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Routine Chest Radiographs after Uncomplicated Thoracentesis
The “Things We Do for No Reason” series reviews practices which have become common parts of hospital care, but which may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent “black and white” conclusions or clinical practice standards, but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion. https://www.choosingwisely.org/
Bedside thoracentesis can cause serious complications, such as pneumothorax, re-expansion pulmonary edema, or hemorrhage. These rare complications have led many hospitalists to routinely order chest radiographs (CXRs) following thoracentesis. However, post-thoracentesis CXRs are usually not indicated and can lead to unnecessary radiation exposure and expense. Rather than obtaining routine CXRs, hospitalists should use postprocedural signs and symptoms to identify the occasional patients who require imaging. A risk-stratified approach is a safe and cost-effective way to avoid unnecessary radiographs.
CASE REPORT
A 52-year-old man with decompensated liver disease and hepatic hydrothorax is hospitalized for increasing dyspnea caused by a recurrent pleural effusion. Diuretics do not improve his dyspnea, and his hospitalist recommends a therapeutic thoracentesis for symptom relief. The patient does not have any significant procedural risk factors: He does not have preexisting pulmonary or pleural disease, his platelet count is 105,000 × 103/µl, and his international normalized ratio is 1.3. Bedside sonography demonstrates a large, free-flowing, right-sided pleural effusion. The hospitalist performs an uncomplicated ultrasound-guided removal of 1.5 L of straw-colored fluid with a catheter-over-needle kit. The patient does not have any pain or increased shortness of breath during or after the procedure. The hospitalist reflexively orders a routine chest radiograph to assess for pneumothorax.
Why You Might Think a Chest Radiograph is Helpful after Thoracentesis
Pleural effusions are newly diagnosed in more than 1.5 million Americans annually,1 and hospitalists frequently care for patients requiring thoracentesis. Internal medicine residents traditionally learn to perform this procedure during residency, and thoracentesis remains a common task for both residents and hospitalists.2 Patients typically tolerate thoracentesis well, but they can develop serious complications such as pneumothorax, re-expansion pulmonary edema, or hemothorax. Before the advent of bedside ultrasound, these complications occurred relatively commonly; a 2010 systematic review, for example, found that the rate of pneumothorax from thoracentesis performed without ultrasound was 9.3%.3 Other studies have identified even higher rates of complications, including two case series in which investigators found a 14% rate of major complications4 and a pneumothorax rate of nearly 30%.5 Postprocedure radiographs became common practice because of the high rate of complications, and this practice has persisted for many practitioners despite the substantial safety improvements introduced by bedside ultrasonography.6
Hospitalists might think routine CXRs are helpful after ultrasound-guided thoracentesis for additional reasons. First, modern guidelines reflecting the low risk of complications after ultrasound-guided procedures have not been released by United States pulmonary medicine societies, and some clinicians may continue to follow practices acquired during the era of unguided thoracentesis. Second, performing postprocedure imaging has become ingrained as a standard part of some institutional procedure checklists6 and some prominent textbooks continue to recommend the practice.7 For some hospitalists, this testing reflex may be reinforced by other common procedures, such as placing a nasogastric tube or a central venous catheter, for which a postprocedure CXR is standard practice. Thus, ordering postprocedure imaging can become internalized as the safe, checklist-based final step of a procedure. Third, hospitalists may order a postprocedure CXR for reasons other than detecting procedural complications. The pleural effusion might be thought to obscure a parenchymal or endobronchial lesion for which a postprocedure CXR may reveal an important finding. Finally, a CXR also may also satisfy the clinician’s curiosity regarding the completeness of drainage.
Why a Routine Postprocedure Chest Radiograph is Not Helpful after Thoracentesis
A routine post-thoracentesis CXR is not necessary for three reasons. First, the use of ultrasound marking or guidance has substantially improved site selection and reduced the rate of complications for experienced operators. For example, a 2010 systematic review found an overall rate of pneumothorax of 4% for ultrasound-guided procedures performed between 1986 and 2006,3 whereas more recently published data suggest the current rate of pneumothorax is closer to 1% when ultrasound marking or guidance is used.8,9 One study of 462 consecutive patients with malignant pleural effusions, for example, showed that the rate of pneumothorax with ultrasound-guided needle-over-catheter thoracentesis was 0.97% (3/310 patients), compared with a rate of 8.89% (12/135 patients) when the procedure was performed without ultrasound.9 Another prospective, randomized study of 160 patients with various causes of pleural effusion showed that the rate of pneumothorax with ultrasound-marked thoracentesis was 1.25% (1/80 patients), compared with 12.5% (10/80 patients) for procedures performed without ultrasound.8 Hospitalists who competently use ultrasound guidance should act on modern estimates of complications and may also choose to incorporate postprocedure ultrasound into their practice. Indeed, the Society of Hospital Medicine recommends against routine chest radiography in asymptomatic patients when sliding lung is visualized on postprocedure ultrasound.10
Second, procedural factors and postprocedural symptoms (new chest pain, dyspnea, or persistent cough) reliably identify patients with high risk of clinically meaningful complications. On one hand, only 1% to 2% of asymptomatic patients have a postprocedure pneumothorax, and clinical monitoring does not lead to chest tube placement in almost all of these cases.11 On the other hand, 67% to 72% of symptomatic patients are found to have complications.12 Doyle et al13 showed that the use of symptoms and procedure-specific factors (such as the aspiration of air, difficult procedure, multiple needle passes, or high operator suspicion of pneumothorax) could obviate the need for routine CXRs in approximately 60% of their procedures without any serious consequences.
Third, postprocedural CXRs very rarely reveal new or unexpected findings. For example, in one series,12 only 3.8% of postdrainage radiographs uncovered new findings, none of which clarified the underlying diagnosis or changed management. To assess the utility of an initial thoracentesis and decide about repeat procedures, begin by asking the patient about symptoms and perform a physical exam.
Why PostProcedural CHEST RADIOGRAPHS Might be Helpful in Certain Circumstances
CXRs might be helpful in certain scenarios, even when a complication is not suspected. For example, a postprocedure CXR to detect nonexpandable lung or evaluate the rate of recurrence may guide definitive management of patients with recurrent or malignant pleural effusion. Determining completeness of drainage may also assist with planning for palliative measures such as pleurodesis or indwelling pleural catheter placement. A postprocedure CXR is also helpful in patients with a technically difficult procedure or in those with symptoms during or immediately after the procedure. This recommendation is consistent with the 2010 British Thoracic Society guidelines, which recommend CXRs for procedures where air was withdrawn, the procedure was difficult, multiple needle passes were required, or the patient became symptomatic.14 The Society of Hospital Medicine’s recent Position Statement concurs with these guidelines and recommends against routine chest radiography in asymptomatic patients when sliding lung is visualized by postprocedure ultrasound.10
What You Should Do Instead
Hospitalists should not rountinely obtain post-thoracentesis CXRs in asymptomatic patients. Clinical monitoring with subsequent symptom-guided evaluation lowers costs, avoids unnecessary radiation exposure, and has been shown to be successful in a large case series of more than 9,300 patients.15 Some coughing should be expected with all large-volume thoracenteses as a normal response to re-expansion of atelectatic lung. The coughing should not persist past the immediate postprocedure period. If symptoms arise or if a complication is expected, the test of choice is either CXR or, if the hospitalist is a competent sonographer, bedside sonography. Bedside sonography is a low-cost, noninvasive method and has been well studied in the diagnosis of post-thoracentesis pneumothorax.16 CXRs may still be needed to confirm findings by sonography, to investigate postprocedural symptoms in those with pleural adhesions or other lung/pleural diseases (because ultrasonography is less reliable in these patients), or if reexpansion pulmonary edema or other complications are suspected. A robust quality improvement strategy to reduce unnecessary post-thoracentesis CXRs could result in cost savings and spare patients from radiation exposure, because a recent study of almost 1,000 thoracenteses performed at an academic medical center demonstrated that internal medicine residents, pulmonologists, and interventional radiologists order a CXR following 95% of thoracenteses.17 For a hypothetical hospital that orders 100 unnecessary post-thoracentesis CXRs annually, hospitalists could avoid approximately $7,000 in wasted expense per year.18
RECOMMENDATIONS:
- Do not routinely order post-thoracentesis CXRs.
- Order a post-thoracentesis CXR if (1) the patient had new chest pain, dyspnea, or persistent cough during or after the procedure; (2) procedural features suggest increased risk of a complication (multiple needle passes, aspiration of air, difficulty obtaining fluid); or (3) a definitive palliative procedure will be arranged based on lung expansion.
- If qualified, use bedside sonography as a first step in the diagnosis of pneumothorax, reserving CXRs for those patients in whom accurate sonography is not possible, an alternative diagnosis is suspected, or when sonography findings are equivocal.
CONCLUSION
Following the uncomplicated thoracentesis, the hospitalist reconsidered the initial decision to order a CXR and rapidly assessed the patient’s risk of complications. Because the procedure required only one needle pass, air was not aspirated, and the patient did not experience prolonged coughing or pain, the CXR order was canceled. The patient recovered uneventfully and was spared the cost and radiation associated with the proposed CXR.
Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason?” Share what you do in your practice and join in the conversation online by retweeting it on Twitter (#TWDFNR) and liking it on Facebook. We invite you to propose ideas for other “Things We Do for No Reason” topics by emailing [email protected].cknowledgments
Acknowledgements
The authors would like to thank Patricia Kritek and Somnath Mookherjee for their comments on an early version of this manuscript.
Disclosures
The au
1. Light RW. Pleural effusions. Med Clin North Am. 2011;95:1055-1070. doi: 10.1016/j.mcna.2011.08.005. PubMed
2. ABIM Policies and Procedures for Certification. http://www.abim.org/~/media/ABIM Public/Files/pdf/publications/certification-guides/policies-and-procedures.pdf. Accessed 10th February 2018.
3. Gordon CE, Feller-Kopman D, Balk EM, Smetana GW. Pneumothorax following thoracentesis: a systematic review and meta-analysis. Arch Intern Med. 2010;170:332-339. doi: 10.1001/archinternmed.2009.548. PubMed
4. Seneff MG, Corwin RW, Gold LH, Irwin RS. Complications associated with thoracocentesis. Chest. 1986;90:97-100. doi: 10.1378/chest.90.1.97 PubMed
5. Grogan DR, Irwin RS, Channick R, Raptopoulos V, Curley FJ, Bartter T. Complications associated with thoracentesis a prospective, randomized study comparing three different methods. Arch Intern Med. 1990;150:873-877. doi: 10.1001/archinte.150.4.873 PubMed
6. Berg D, Berg K, Riesenberg LA, et al. The development of a validated checklist for thoracentesis preliminary results. Am J Med Qual. 2013;28:220-226. doi: 10.1177/1062860612459881. PubMed
7. Morris CA, Wolf A. Video 482e-1 clinical procedure tutorial: thoracentesis. Harrison’s Principles of Internal Medicine, 19th edition. http://accessmedicine.mhmedical.com/MultimediaPlayer.aspx?MultimediaID=12986897. Accessed 28th September 2017.
8. Perazzo A, Gatto P, Barlascini C, Ferrari-Bravo M, Nicolini A. Can ultrasound guidance reduce the risk of pneumothorax following thoracentesis?* , ** A ultrassonografia pode reduzir o risco de pneumotórax após toracocentese? J Bras Pneumol. 2013;40:6-12. doi: 10.1590/S1806-37132014000100002 PubMed
9. Cavanna L, Mordenti P, Bertè R, et al. Ultrasound guidance reduces pneumothorax rate and improves safety of thoracentesis in malignant pleural effusion: report on 445 consecutive patients with advanced cancer. World J Surg Oncol. 2014;12:139. doi: 10.1186/1477-7819-12-139. PubMed
10. Dancel R, Schnobrich D, Puri N, et al. Recommendations on the use of ultrasound guidance for adult thoracentesis: a position statement of the Society of Hospital Medicine. J Hosp Med. 2018;13:126-135. doi: 10.12788/jhm.2940. PubMed
11. Alemán C, Alegre J, Armadans L, et al. The value of chest roentgenography in the diagnosis of pneumothorax after thoracentesis. Am J Med. 1999;107:340-343. doi: 10.1016/S0002-9343(99)00238-7 PubMed
12. Petersen WG, Zimmerman R. Limited utility of chest radiograph after thoracentesis. Chest. 2000;117:1038-1042. doi: 10.1378/chest.117.4.1038 PubMed
13. Doyle JJ, Hnatiuk OW, Torrington KG, Slade AR, Howard RS. Necessity of routine chest roentgenography after thoracentesis. Ann Intern Med. 1996;124: 816-820. doi: 10.7326/0003-4819-124-9-199605010-00005 PubMed
14. BTS- British Thoracic Society. BTS Pleural Disease Guideline 2010. Thorax 2010;65:1-76. doi: 10.1136/thx.2010.137026.
15. Ault MJ, Rosen BT, Scher J, Feinglass J, Barsuk JH. Thoracentesis outcomes: a 12-year experience. Thorax 2015;70:127-132. 10.1136/thoraxjnl-2014-206114. PubMed
16. Shostak E, Brylka D, Krepp J, Pua B, Sanders A. Bedside ultrasonography in detection of post procedure pneumothorax. J Ultrasound Med. 2013;32:1003-1009. doi: 10.7863/ultra.32.6.1003 PubMed
17. Barsuk JH, Cohen ER, Williams MV, et al. Simulation-based mastery learning for thoracentesis skills improves patient outcomes. Acad Med. 2017; doi: 10.1097/ACM.0000000000001965 PubMed
18. Healthcare Bluebook. https://www.healthcarebluebook.com/page_ProcedureDetails.aspx?cftId=137&g=Chest+X-Ray. Accessed 10th February 2018.
The “Things We Do for No Reason” series reviews practices which have become common parts of hospital care, but which may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent “black and white” conclusions or clinical practice standards, but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion. https://www.choosingwisely.org/
Bedside thoracentesis can cause serious complications, such as pneumothorax, re-expansion pulmonary edema, or hemorrhage. These rare complications have led many hospitalists to routinely order chest radiographs (CXRs) following thoracentesis. However, post-thoracentesis CXRs are usually not indicated and can lead to unnecessary radiation exposure and expense. Rather than obtaining routine CXRs, hospitalists should use postprocedural signs and symptoms to identify the occasional patients who require imaging. A risk-stratified approach is a safe and cost-effective way to avoid unnecessary radiographs.
CASE REPORT
A 52-year-old man with decompensated liver disease and hepatic hydrothorax is hospitalized for increasing dyspnea caused by a recurrent pleural effusion. Diuretics do not improve his dyspnea, and his hospitalist recommends a therapeutic thoracentesis for symptom relief. The patient does not have any significant procedural risk factors: He does not have preexisting pulmonary or pleural disease, his platelet count is 105,000 × 103/µl, and his international normalized ratio is 1.3. Bedside sonography demonstrates a large, free-flowing, right-sided pleural effusion. The hospitalist performs an uncomplicated ultrasound-guided removal of 1.5 L of straw-colored fluid with a catheter-over-needle kit. The patient does not have any pain or increased shortness of breath during or after the procedure. The hospitalist reflexively orders a routine chest radiograph to assess for pneumothorax.
Why You Might Think a Chest Radiograph is Helpful after Thoracentesis
Pleural effusions are newly diagnosed in more than 1.5 million Americans annually,1 and hospitalists frequently care for patients requiring thoracentesis. Internal medicine residents traditionally learn to perform this procedure during residency, and thoracentesis remains a common task for both residents and hospitalists.2 Patients typically tolerate thoracentesis well, but they can develop serious complications such as pneumothorax, re-expansion pulmonary edema, or hemothorax. Before the advent of bedside ultrasound, these complications occurred relatively commonly; a 2010 systematic review, for example, found that the rate of pneumothorax from thoracentesis performed without ultrasound was 9.3%.3 Other studies have identified even higher rates of complications, including two case series in which investigators found a 14% rate of major complications4 and a pneumothorax rate of nearly 30%.5 Postprocedure radiographs became common practice because of the high rate of complications, and this practice has persisted for many practitioners despite the substantial safety improvements introduced by bedside ultrasonography.6
Hospitalists might think routine CXRs are helpful after ultrasound-guided thoracentesis for additional reasons. First, modern guidelines reflecting the low risk of complications after ultrasound-guided procedures have not been released by United States pulmonary medicine societies, and some clinicians may continue to follow practices acquired during the era of unguided thoracentesis. Second, performing postprocedure imaging has become ingrained as a standard part of some institutional procedure checklists6 and some prominent textbooks continue to recommend the practice.7 For some hospitalists, this testing reflex may be reinforced by other common procedures, such as placing a nasogastric tube or a central venous catheter, for which a postprocedure CXR is standard practice. Thus, ordering postprocedure imaging can become internalized as the safe, checklist-based final step of a procedure. Third, hospitalists may order a postprocedure CXR for reasons other than detecting procedural complications. The pleural effusion might be thought to obscure a parenchymal or endobronchial lesion for which a postprocedure CXR may reveal an important finding. Finally, a CXR also may also satisfy the clinician’s curiosity regarding the completeness of drainage.
Why a Routine Postprocedure Chest Radiograph is Not Helpful after Thoracentesis
A routine post-thoracentesis CXR is not necessary for three reasons. First, the use of ultrasound marking or guidance has substantially improved site selection and reduced the rate of complications for experienced operators. For example, a 2010 systematic review found an overall rate of pneumothorax of 4% for ultrasound-guided procedures performed between 1986 and 2006,3 whereas more recently published data suggest the current rate of pneumothorax is closer to 1% when ultrasound marking or guidance is used.8,9 One study of 462 consecutive patients with malignant pleural effusions, for example, showed that the rate of pneumothorax with ultrasound-guided needle-over-catheter thoracentesis was 0.97% (3/310 patients), compared with a rate of 8.89% (12/135 patients) when the procedure was performed without ultrasound.9 Another prospective, randomized study of 160 patients with various causes of pleural effusion showed that the rate of pneumothorax with ultrasound-marked thoracentesis was 1.25% (1/80 patients), compared with 12.5% (10/80 patients) for procedures performed without ultrasound.8 Hospitalists who competently use ultrasound guidance should act on modern estimates of complications and may also choose to incorporate postprocedure ultrasound into their practice. Indeed, the Society of Hospital Medicine recommends against routine chest radiography in asymptomatic patients when sliding lung is visualized on postprocedure ultrasound.10
Second, procedural factors and postprocedural symptoms (new chest pain, dyspnea, or persistent cough) reliably identify patients with high risk of clinically meaningful complications. On one hand, only 1% to 2% of asymptomatic patients have a postprocedure pneumothorax, and clinical monitoring does not lead to chest tube placement in almost all of these cases.11 On the other hand, 67% to 72% of symptomatic patients are found to have complications.12 Doyle et al13 showed that the use of symptoms and procedure-specific factors (such as the aspiration of air, difficult procedure, multiple needle passes, or high operator suspicion of pneumothorax) could obviate the need for routine CXRs in approximately 60% of their procedures without any serious consequences.
Third, postprocedural CXRs very rarely reveal new or unexpected findings. For example, in one series,12 only 3.8% of postdrainage radiographs uncovered new findings, none of which clarified the underlying diagnosis or changed management. To assess the utility of an initial thoracentesis and decide about repeat procedures, begin by asking the patient about symptoms and perform a physical exam.
Why PostProcedural CHEST RADIOGRAPHS Might be Helpful in Certain Circumstances
CXRs might be helpful in certain scenarios, even when a complication is not suspected. For example, a postprocedure CXR to detect nonexpandable lung or evaluate the rate of recurrence may guide definitive management of patients with recurrent or malignant pleural effusion. Determining completeness of drainage may also assist with planning for palliative measures such as pleurodesis or indwelling pleural catheter placement. A postprocedure CXR is also helpful in patients with a technically difficult procedure or in those with symptoms during or immediately after the procedure. This recommendation is consistent with the 2010 British Thoracic Society guidelines, which recommend CXRs for procedures where air was withdrawn, the procedure was difficult, multiple needle passes were required, or the patient became symptomatic.14 The Society of Hospital Medicine’s recent Position Statement concurs with these guidelines and recommends against routine chest radiography in asymptomatic patients when sliding lung is visualized by postprocedure ultrasound.10
What You Should Do Instead
Hospitalists should not rountinely obtain post-thoracentesis CXRs in asymptomatic patients. Clinical monitoring with subsequent symptom-guided evaluation lowers costs, avoids unnecessary radiation exposure, and has been shown to be successful in a large case series of more than 9,300 patients.15 Some coughing should be expected with all large-volume thoracenteses as a normal response to re-expansion of atelectatic lung. The coughing should not persist past the immediate postprocedure period. If symptoms arise or if a complication is expected, the test of choice is either CXR or, if the hospitalist is a competent sonographer, bedside sonography. Bedside sonography is a low-cost, noninvasive method and has been well studied in the diagnosis of post-thoracentesis pneumothorax.16 CXRs may still be needed to confirm findings by sonography, to investigate postprocedural symptoms in those with pleural adhesions or other lung/pleural diseases (because ultrasonography is less reliable in these patients), or if reexpansion pulmonary edema or other complications are suspected. A robust quality improvement strategy to reduce unnecessary post-thoracentesis CXRs could result in cost savings and spare patients from radiation exposure, because a recent study of almost 1,000 thoracenteses performed at an academic medical center demonstrated that internal medicine residents, pulmonologists, and interventional radiologists order a CXR following 95% of thoracenteses.17 For a hypothetical hospital that orders 100 unnecessary post-thoracentesis CXRs annually, hospitalists could avoid approximately $7,000 in wasted expense per year.18
RECOMMENDATIONS:
- Do not routinely order post-thoracentesis CXRs.
- Order a post-thoracentesis CXR if (1) the patient had new chest pain, dyspnea, or persistent cough during or after the procedure; (2) procedural features suggest increased risk of a complication (multiple needle passes, aspiration of air, difficulty obtaining fluid); or (3) a definitive palliative procedure will be arranged based on lung expansion.
- If qualified, use bedside sonography as a first step in the diagnosis of pneumothorax, reserving CXRs for those patients in whom accurate sonography is not possible, an alternative diagnosis is suspected, or when sonography findings are equivocal.
CONCLUSION
Following the uncomplicated thoracentesis, the hospitalist reconsidered the initial decision to order a CXR and rapidly assessed the patient’s risk of complications. Because the procedure required only one needle pass, air was not aspirated, and the patient did not experience prolonged coughing or pain, the CXR order was canceled. The patient recovered uneventfully and was spared the cost and radiation associated with the proposed CXR.
Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason?” Share what you do in your practice and join in the conversation online by retweeting it on Twitter (#TWDFNR) and liking it on Facebook. We invite you to propose ideas for other “Things We Do for No Reason” topics by emailing [email protected].cknowledgments
Acknowledgements
The authors would like to thank Patricia Kritek and Somnath Mookherjee for their comments on an early version of this manuscript.
Disclosures
The au
The “Things We Do for No Reason” series reviews practices which have become common parts of hospital care, but which may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent “black and white” conclusions or clinical practice standards, but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion. https://www.choosingwisely.org/
Bedside thoracentesis can cause serious complications, such as pneumothorax, re-expansion pulmonary edema, or hemorrhage. These rare complications have led many hospitalists to routinely order chest radiographs (CXRs) following thoracentesis. However, post-thoracentesis CXRs are usually not indicated and can lead to unnecessary radiation exposure and expense. Rather than obtaining routine CXRs, hospitalists should use postprocedural signs and symptoms to identify the occasional patients who require imaging. A risk-stratified approach is a safe and cost-effective way to avoid unnecessary radiographs.
CASE REPORT
A 52-year-old man with decompensated liver disease and hepatic hydrothorax is hospitalized for increasing dyspnea caused by a recurrent pleural effusion. Diuretics do not improve his dyspnea, and his hospitalist recommends a therapeutic thoracentesis for symptom relief. The patient does not have any significant procedural risk factors: He does not have preexisting pulmonary or pleural disease, his platelet count is 105,000 × 103/µl, and his international normalized ratio is 1.3. Bedside sonography demonstrates a large, free-flowing, right-sided pleural effusion. The hospitalist performs an uncomplicated ultrasound-guided removal of 1.5 L of straw-colored fluid with a catheter-over-needle kit. The patient does not have any pain or increased shortness of breath during or after the procedure. The hospitalist reflexively orders a routine chest radiograph to assess for pneumothorax.
Why You Might Think a Chest Radiograph is Helpful after Thoracentesis
Pleural effusions are newly diagnosed in more than 1.5 million Americans annually,1 and hospitalists frequently care for patients requiring thoracentesis. Internal medicine residents traditionally learn to perform this procedure during residency, and thoracentesis remains a common task for both residents and hospitalists.2 Patients typically tolerate thoracentesis well, but they can develop serious complications such as pneumothorax, re-expansion pulmonary edema, or hemothorax. Before the advent of bedside ultrasound, these complications occurred relatively commonly; a 2010 systematic review, for example, found that the rate of pneumothorax from thoracentesis performed without ultrasound was 9.3%.3 Other studies have identified even higher rates of complications, including two case series in which investigators found a 14% rate of major complications4 and a pneumothorax rate of nearly 30%.5 Postprocedure radiographs became common practice because of the high rate of complications, and this practice has persisted for many practitioners despite the substantial safety improvements introduced by bedside ultrasonography.6
Hospitalists might think routine CXRs are helpful after ultrasound-guided thoracentesis for additional reasons. First, modern guidelines reflecting the low risk of complications after ultrasound-guided procedures have not been released by United States pulmonary medicine societies, and some clinicians may continue to follow practices acquired during the era of unguided thoracentesis. Second, performing postprocedure imaging has become ingrained as a standard part of some institutional procedure checklists6 and some prominent textbooks continue to recommend the practice.7 For some hospitalists, this testing reflex may be reinforced by other common procedures, such as placing a nasogastric tube or a central venous catheter, for which a postprocedure CXR is standard practice. Thus, ordering postprocedure imaging can become internalized as the safe, checklist-based final step of a procedure. Third, hospitalists may order a postprocedure CXR for reasons other than detecting procedural complications. The pleural effusion might be thought to obscure a parenchymal or endobronchial lesion for which a postprocedure CXR may reveal an important finding. Finally, a CXR also may also satisfy the clinician’s curiosity regarding the completeness of drainage.
Why a Routine Postprocedure Chest Radiograph is Not Helpful after Thoracentesis
A routine post-thoracentesis CXR is not necessary for three reasons. First, the use of ultrasound marking or guidance has substantially improved site selection and reduced the rate of complications for experienced operators. For example, a 2010 systematic review found an overall rate of pneumothorax of 4% for ultrasound-guided procedures performed between 1986 and 2006,3 whereas more recently published data suggest the current rate of pneumothorax is closer to 1% when ultrasound marking or guidance is used.8,9 One study of 462 consecutive patients with malignant pleural effusions, for example, showed that the rate of pneumothorax with ultrasound-guided needle-over-catheter thoracentesis was 0.97% (3/310 patients), compared with a rate of 8.89% (12/135 patients) when the procedure was performed without ultrasound.9 Another prospective, randomized study of 160 patients with various causes of pleural effusion showed that the rate of pneumothorax with ultrasound-marked thoracentesis was 1.25% (1/80 patients), compared with 12.5% (10/80 patients) for procedures performed without ultrasound.8 Hospitalists who competently use ultrasound guidance should act on modern estimates of complications and may also choose to incorporate postprocedure ultrasound into their practice. Indeed, the Society of Hospital Medicine recommends against routine chest radiography in asymptomatic patients when sliding lung is visualized on postprocedure ultrasound.10
Second, procedural factors and postprocedural symptoms (new chest pain, dyspnea, or persistent cough) reliably identify patients with high risk of clinically meaningful complications. On one hand, only 1% to 2% of asymptomatic patients have a postprocedure pneumothorax, and clinical monitoring does not lead to chest tube placement in almost all of these cases.11 On the other hand, 67% to 72% of symptomatic patients are found to have complications.12 Doyle et al13 showed that the use of symptoms and procedure-specific factors (such as the aspiration of air, difficult procedure, multiple needle passes, or high operator suspicion of pneumothorax) could obviate the need for routine CXRs in approximately 60% of their procedures without any serious consequences.
Third, postprocedural CXRs very rarely reveal new or unexpected findings. For example, in one series,12 only 3.8% of postdrainage radiographs uncovered new findings, none of which clarified the underlying diagnosis or changed management. To assess the utility of an initial thoracentesis and decide about repeat procedures, begin by asking the patient about symptoms and perform a physical exam.
Why PostProcedural CHEST RADIOGRAPHS Might be Helpful in Certain Circumstances
CXRs might be helpful in certain scenarios, even when a complication is not suspected. For example, a postprocedure CXR to detect nonexpandable lung or evaluate the rate of recurrence may guide definitive management of patients with recurrent or malignant pleural effusion. Determining completeness of drainage may also assist with planning for palliative measures such as pleurodesis or indwelling pleural catheter placement. A postprocedure CXR is also helpful in patients with a technically difficult procedure or in those with symptoms during or immediately after the procedure. This recommendation is consistent with the 2010 British Thoracic Society guidelines, which recommend CXRs for procedures where air was withdrawn, the procedure was difficult, multiple needle passes were required, or the patient became symptomatic.14 The Society of Hospital Medicine’s recent Position Statement concurs with these guidelines and recommends against routine chest radiography in asymptomatic patients when sliding lung is visualized by postprocedure ultrasound.10
What You Should Do Instead
Hospitalists should not rountinely obtain post-thoracentesis CXRs in asymptomatic patients. Clinical monitoring with subsequent symptom-guided evaluation lowers costs, avoids unnecessary radiation exposure, and has been shown to be successful in a large case series of more than 9,300 patients.15 Some coughing should be expected with all large-volume thoracenteses as a normal response to re-expansion of atelectatic lung. The coughing should not persist past the immediate postprocedure period. If symptoms arise or if a complication is expected, the test of choice is either CXR or, if the hospitalist is a competent sonographer, bedside sonography. Bedside sonography is a low-cost, noninvasive method and has been well studied in the diagnosis of post-thoracentesis pneumothorax.16 CXRs may still be needed to confirm findings by sonography, to investigate postprocedural symptoms in those with pleural adhesions or other lung/pleural diseases (because ultrasonography is less reliable in these patients), or if reexpansion pulmonary edema or other complications are suspected. A robust quality improvement strategy to reduce unnecessary post-thoracentesis CXRs could result in cost savings and spare patients from radiation exposure, because a recent study of almost 1,000 thoracenteses performed at an academic medical center demonstrated that internal medicine residents, pulmonologists, and interventional radiologists order a CXR following 95% of thoracenteses.17 For a hypothetical hospital that orders 100 unnecessary post-thoracentesis CXRs annually, hospitalists could avoid approximately $7,000 in wasted expense per year.18
RECOMMENDATIONS:
- Do not routinely order post-thoracentesis CXRs.
- Order a post-thoracentesis CXR if (1) the patient had new chest pain, dyspnea, or persistent cough during or after the procedure; (2) procedural features suggest increased risk of a complication (multiple needle passes, aspiration of air, difficulty obtaining fluid); or (3) a definitive palliative procedure will be arranged based on lung expansion.
- If qualified, use bedside sonography as a first step in the diagnosis of pneumothorax, reserving CXRs for those patients in whom accurate sonography is not possible, an alternative diagnosis is suspected, or when sonography findings are equivocal.
CONCLUSION
Following the uncomplicated thoracentesis, the hospitalist reconsidered the initial decision to order a CXR and rapidly assessed the patient’s risk of complications. Because the procedure required only one needle pass, air was not aspirated, and the patient did not experience prolonged coughing or pain, the CXR order was canceled. The patient recovered uneventfully and was spared the cost and radiation associated with the proposed CXR.
Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason?” Share what you do in your practice and join in the conversation online by retweeting it on Twitter (#TWDFNR) and liking it on Facebook. We invite you to propose ideas for other “Things We Do for No Reason” topics by emailing [email protected].cknowledgments
Acknowledgements
The authors would like to thank Patricia Kritek and Somnath Mookherjee for their comments on an early version of this manuscript.
Disclosures
The au
1. Light RW. Pleural effusions. Med Clin North Am. 2011;95:1055-1070. doi: 10.1016/j.mcna.2011.08.005. PubMed
2. ABIM Policies and Procedures for Certification. http://www.abim.org/~/media/ABIM Public/Files/pdf/publications/certification-guides/policies-and-procedures.pdf. Accessed 10th February 2018.
3. Gordon CE, Feller-Kopman D, Balk EM, Smetana GW. Pneumothorax following thoracentesis: a systematic review and meta-analysis. Arch Intern Med. 2010;170:332-339. doi: 10.1001/archinternmed.2009.548. PubMed
4. Seneff MG, Corwin RW, Gold LH, Irwin RS. Complications associated with thoracocentesis. Chest. 1986;90:97-100. doi: 10.1378/chest.90.1.97 PubMed
5. Grogan DR, Irwin RS, Channick R, Raptopoulos V, Curley FJ, Bartter T. Complications associated with thoracentesis a prospective, randomized study comparing three different methods. Arch Intern Med. 1990;150:873-877. doi: 10.1001/archinte.150.4.873 PubMed
6. Berg D, Berg K, Riesenberg LA, et al. The development of a validated checklist for thoracentesis preliminary results. Am J Med Qual. 2013;28:220-226. doi: 10.1177/1062860612459881. PubMed
7. Morris CA, Wolf A. Video 482e-1 clinical procedure tutorial: thoracentesis. Harrison’s Principles of Internal Medicine, 19th edition. http://accessmedicine.mhmedical.com/MultimediaPlayer.aspx?MultimediaID=12986897. Accessed 28th September 2017.
8. Perazzo A, Gatto P, Barlascini C, Ferrari-Bravo M, Nicolini A. Can ultrasound guidance reduce the risk of pneumothorax following thoracentesis?* , ** A ultrassonografia pode reduzir o risco de pneumotórax após toracocentese? J Bras Pneumol. 2013;40:6-12. doi: 10.1590/S1806-37132014000100002 PubMed
9. Cavanna L, Mordenti P, Bertè R, et al. Ultrasound guidance reduces pneumothorax rate and improves safety of thoracentesis in malignant pleural effusion: report on 445 consecutive patients with advanced cancer. World J Surg Oncol. 2014;12:139. doi: 10.1186/1477-7819-12-139. PubMed
10. Dancel R, Schnobrich D, Puri N, et al. Recommendations on the use of ultrasound guidance for adult thoracentesis: a position statement of the Society of Hospital Medicine. J Hosp Med. 2018;13:126-135. doi: 10.12788/jhm.2940. PubMed
11. Alemán C, Alegre J, Armadans L, et al. The value of chest roentgenography in the diagnosis of pneumothorax after thoracentesis. Am J Med. 1999;107:340-343. doi: 10.1016/S0002-9343(99)00238-7 PubMed
12. Petersen WG, Zimmerman R. Limited utility of chest radiograph after thoracentesis. Chest. 2000;117:1038-1042. doi: 10.1378/chest.117.4.1038 PubMed
13. Doyle JJ, Hnatiuk OW, Torrington KG, Slade AR, Howard RS. Necessity of routine chest roentgenography after thoracentesis. Ann Intern Med. 1996;124: 816-820. doi: 10.7326/0003-4819-124-9-199605010-00005 PubMed
14. BTS- British Thoracic Society. BTS Pleural Disease Guideline 2010. Thorax 2010;65:1-76. doi: 10.1136/thx.2010.137026.
15. Ault MJ, Rosen BT, Scher J, Feinglass J, Barsuk JH. Thoracentesis outcomes: a 12-year experience. Thorax 2015;70:127-132. 10.1136/thoraxjnl-2014-206114. PubMed
16. Shostak E, Brylka D, Krepp J, Pua B, Sanders A. Bedside ultrasonography in detection of post procedure pneumothorax. J Ultrasound Med. 2013;32:1003-1009. doi: 10.7863/ultra.32.6.1003 PubMed
17. Barsuk JH, Cohen ER, Williams MV, et al. Simulation-based mastery learning for thoracentesis skills improves patient outcomes. Acad Med. 2017; doi: 10.1097/ACM.0000000000001965 PubMed
18. Healthcare Bluebook. https://www.healthcarebluebook.com/page_ProcedureDetails.aspx?cftId=137&g=Chest+X-Ray. Accessed 10th February 2018.
1. Light RW. Pleural effusions. Med Clin North Am. 2011;95:1055-1070. doi: 10.1016/j.mcna.2011.08.005. PubMed
2. ABIM Policies and Procedures for Certification. http://www.abim.org/~/media/ABIM Public/Files/pdf/publications/certification-guides/policies-and-procedures.pdf. Accessed 10th February 2018.
3. Gordon CE, Feller-Kopman D, Balk EM, Smetana GW. Pneumothorax following thoracentesis: a systematic review and meta-analysis. Arch Intern Med. 2010;170:332-339. doi: 10.1001/archinternmed.2009.548. PubMed
4. Seneff MG, Corwin RW, Gold LH, Irwin RS. Complications associated with thoracocentesis. Chest. 1986;90:97-100. doi: 10.1378/chest.90.1.97 PubMed
5. Grogan DR, Irwin RS, Channick R, Raptopoulos V, Curley FJ, Bartter T. Complications associated with thoracentesis a prospective, randomized study comparing three different methods. Arch Intern Med. 1990;150:873-877. doi: 10.1001/archinte.150.4.873 PubMed
6. Berg D, Berg K, Riesenberg LA, et al. The development of a validated checklist for thoracentesis preliminary results. Am J Med Qual. 2013;28:220-226. doi: 10.1177/1062860612459881. PubMed
7. Morris CA, Wolf A. Video 482e-1 clinical procedure tutorial: thoracentesis. Harrison’s Principles of Internal Medicine, 19th edition. http://accessmedicine.mhmedical.com/MultimediaPlayer.aspx?MultimediaID=12986897. Accessed 28th September 2017.
8. Perazzo A, Gatto P, Barlascini C, Ferrari-Bravo M, Nicolini A. Can ultrasound guidance reduce the risk of pneumothorax following thoracentesis?* , ** A ultrassonografia pode reduzir o risco de pneumotórax após toracocentese? J Bras Pneumol. 2013;40:6-12. doi: 10.1590/S1806-37132014000100002 PubMed
9. Cavanna L, Mordenti P, Bertè R, et al. Ultrasound guidance reduces pneumothorax rate and improves safety of thoracentesis in malignant pleural effusion: report on 445 consecutive patients with advanced cancer. World J Surg Oncol. 2014;12:139. doi: 10.1186/1477-7819-12-139. PubMed
10. Dancel R, Schnobrich D, Puri N, et al. Recommendations on the use of ultrasound guidance for adult thoracentesis: a position statement of the Society of Hospital Medicine. J Hosp Med. 2018;13:126-135. doi: 10.12788/jhm.2940. PubMed
11. Alemán C, Alegre J, Armadans L, et al. The value of chest roentgenography in the diagnosis of pneumothorax after thoracentesis. Am J Med. 1999;107:340-343. doi: 10.1016/S0002-9343(99)00238-7 PubMed
12. Petersen WG, Zimmerman R. Limited utility of chest radiograph after thoracentesis. Chest. 2000;117:1038-1042. doi: 10.1378/chest.117.4.1038 PubMed
13. Doyle JJ, Hnatiuk OW, Torrington KG, Slade AR, Howard RS. Necessity of routine chest roentgenography after thoracentesis. Ann Intern Med. 1996;124: 816-820. doi: 10.7326/0003-4819-124-9-199605010-00005 PubMed
14. BTS- British Thoracic Society. BTS Pleural Disease Guideline 2010. Thorax 2010;65:1-76. doi: 10.1136/thx.2010.137026.
15. Ault MJ, Rosen BT, Scher J, Feinglass J, Barsuk JH. Thoracentesis outcomes: a 12-year experience. Thorax 2015;70:127-132. 10.1136/thoraxjnl-2014-206114. PubMed
16. Shostak E, Brylka D, Krepp J, Pua B, Sanders A. Bedside ultrasonography in detection of post procedure pneumothorax. J Ultrasound Med. 2013;32:1003-1009. doi: 10.7863/ultra.32.6.1003 PubMed
17. Barsuk JH, Cohen ER, Williams MV, et al. Simulation-based mastery learning for thoracentesis skills improves patient outcomes. Acad Med. 2017; doi: 10.1097/ACM.0000000000001965 PubMed
18. Healthcare Bluebook. https://www.healthcarebluebook.com/page_ProcedureDetails.aspx?cftId=137&g=Chest+X-Ray. Accessed 10th February 2018.
© 2018 Society of Hospital Medicine
Smoking Cessation after Hospital Discharge: Factors Associated with Abstinence
Cigarette smoking is the leading cause of preventable deaths in the United States.1 Smoking contributes to several health problems that require hospitalization. Hospitalization also offers smokers an opportunity to quit because hospital policies prohibit smoking indoors while a health threat increases the motivation to quit.2 Brief bedside smoking cessation counseling with follow-up contact after discharge increases postdischarge tobacco abstinence rates by 37%.2 Identifying the characteristics of patients who are most likely to stop smoking after hospital discharge could identify strategies for interventions to help more smokers to succeed. It could also guide hospital clinicians’ efforts to provide effective brief messages to promote cessation by inpatients under their care during this teachable moment.
Sociodemographic factors, tobacco use, and psychological and medical factors have been associated with successful quit attempts by smokers in the general population.3,4 Far less is known about the predictors of success in quitting smoking and maintaining abstinence after hospitalization. The characteristics associated with abstinence at postdischarge follow-up in prior studies of hospitalized smokers were male gender, greater confidence in quitting, greater readiness to quit, less nicotine dependence, and having a smoking-related illness.5-8 However, most of the prior studies were limited to 1 geographic region,5,6 focused only on a specific subgroup (eg, coronary patients9), or did not biochemically verify tobacco abstinence.8 In fact, to our knowledge, only one prior study has examined the predictors of quitting among a broad sample of hospital patients enrolled across multiple hospitals and biochemically verified abstinence.6 That study was conducted nearly two decades ago in one Midwestern state.
Thus, the present study aimed to identify factors independently associated with sustained postdischarge tobacco abstinence among hospitalized smokers who planned to quit smoking.10 Building on previous work, this study includes a large number of smokers with varied diagnoses admitted to one of three hospitals in two states, uses biochemically verified abstinence as the outcome measure, and examines multiple variables that were identified during the inpatient stay. We hypothesize that consistent with prior literature on this topic, factors independently associated with cessation in the present study will include confidence and intention to quit, degree of nicotine dependence, and a discharge diagnosis of a smoking-related disease.
METHODS
We analyzed data from the Helping HAND2 Trial (HH2; NCT01714323), a randomized clinical trial conducted at the following three hospitals: Massachusetts General Hospital (MGH) in Boston, MA; University of Pittsburgh Medical Center (UPMC) in Pittsburgh, PA; and North Shore Medical Center (NSMC) in Salem, MA. Enrollment occurred from December 2012 to July 2014. The study methodology has been reported elsewhere.11 This study was approved by the Institutional Review Boards of Partners HealthCare and University of Pittsburgh.
PARTICIPANTS
Hospital inpatients were eligible for enrollment if they were
- >18 years old, daily smokers, received smoking cessation counseling in the hospital (ie, standard of care for inpatient smokers), and planned to quit or try to quit smoking after discharge. Exclusion criteria included no access to a telephone, not speaking English, psychiatric or cognitive impairment, medical instability, or admission to obstetric or psychiatric units. All participants were offered nicotine replacement and one counseling session by a tobacco treatment specialist during hospitalization.
STUDY CONDITIONS
Participants were enrolled before discharge and randomly assigned to Sustained Care (Intervention) or Standard Care (Control) conditions.10,11 In the Standard Care condition, participants received advice to call a free telephone quit line and a tailored recommendation for postdischarge pharmacotherapy. Participants randomized to Sustained Care received a free 30-day supply of their choice of FDA-approved tobacco cessation pharmacotherapy at hospital discharge (refillable twice) and five automated interactive voice response calls over three months postdischarge to allow them to access counseling or refill medications.
MEASURES
Baseline Demographic and Smoking Characteristics
A baseline survey assessed demographic variables (age, gender, race/ethnicity, education), tobacco use (cigarettes smoked per day, time to first morning cigarette,12 other tobacco use, and prior quit attempts), intention to quit after discharge (ie,“What is your plan about smoking after you leave the hospital,” with the intent measured across four categorical response options), perceived importance of and confidence in quitting after discharge (five-point Likert scales ranging from “not at all” to “very”), and the presence of another smoker at home. Depression and anxiety symptoms were assessed using the Patient Health Questionnaire (PHQ-413). Alcohol use (AUDIT-C14) and past-year use of cocaine, stimulants, opioids, and marijuana were also measured. Health insurance, length of stay, and primary discharge diagnoses were abstracted from the medical record. Smoking-related disease categories were derived from the 2014 U.S. Surgeon General’s Report.1
Follow-up Assessment
Telephone surveys were administered by the research staff sixmonths after hospital discharge. Participants who reported past seven-day tobacco abstinence (ie, abstinence from tobacco for the past seven days reported at the 6-month call) were asked to provide a mailed saliva sample to assay for cotinine, a nicotine metabolite, to verify self-reported abstinence. Participants who reported nicotine replacement therapy use were asked to provide an in-person measurement of expired air carbon monoxide (CO) instead. Self-reported abstinence was biochemically verified if saliva cotinine was <10 ng/ml or if CO was <9 ppm.11
Outcomes
The dependent variable, consistent with the parent trial, was biochemically confirmed past seven-day tobacco abstinence at six-month follow-up. Nonrespondents and those failing to provide a sample for confirmation were considered as smokers. In addition, a sensitivity analysis used complete cases only, excluding cases with missing smoking status outcomes.
Analysis
Bivariate associations of baseline predictor variables and biochemically confirmed abstinence were examined using chi-square tests for categorical variables and t tests or Wilcoxon rank sum tests for continuous variables. Using multiple logistic regression analyses, we identified variables that were independently associated with confirmed abstinence. The final models included all factors that were associated with cessation in the bivariate analysis (P < .10), factors associated with abstinence in the literature regardless of statistical significance (gender, AUDIT-C score),4 study site, and study condition. A two-sided p value of <.05 was considered to be statistically significant. Analyses were conducted using SAS version 9.4 (SAS Institute, Cary, NC).
RESULTS
Baseline characteristics of the 1,357 smokers enrolled in the trial are reported in Table 1. One-third of participants had a smoking-related discharge diagnosis. The median self-reported confidence in quitting was three on a five-point scale, and nearly half of the participants reported planning to stay abstinent after discharge. At six-month follow-up, 75% of participants completed the assessment, and seven-day tobacco abstinence was reported by 389 participants (29%) and biochemically confirmed in 218 participants (16%).
Results of the multiple logistic regression analysis predicting biochemically confirmed abstinence at six months are presented in Table 2. Factors independently associated with confirmed abstinence were a smoking-related primary discharge diagnosis (AOR = 1.98, 95% CI: 1.41-2.77), greater confidence in the ability to quit smoking (AOR = 1.31, 95% CI: 1.07-1.60), and stronger intention to quit (plan to stay abstinent after discharge vs. try to stay abstinent; AOR = 1.68, 95% CI: 1.19-2.38). Similar variables emerged as independent predictors of abstinence when the analysis was limited to complete cases, with an exception that one additional predictor, time to first cigarette after 30 minutes of waking, had statistical significance at the 0.05 level (Table 2).
DISCUSSION
We examined the associations between factors that were identifiable in the hospital and postdischarge tobacco abstinence among a general sample of hospitalized patients enrolled in a smoking cessation trial. The odds of biochemically confirmed abstinence at six months were higher among participants who reported higher levels of confidence in quitting smoking, those reporting having a definite plan to quit (vs. try to) after discharge, and those with a smoking-related primary discharge diagnosis.
Our findings are largely consistent with the prior literature on this topic, which has demonstrated that increased confidence in quitting, having a plan to quit smoking, and the presence of a smoking-related disease are associated with quit success at follow-up among hospital patients as well as in the general adult population.3-7 Our finding that nicotine dependence predicted quit success in the complete case analysis, but not when imputing smoking status, aligns with prior studies of hospitalized smokers, which have shown an inconclusive relationship between nicotine dependence and quit success.6,8 Despite a clear relationship of dependence to quit success among adult smokers, evidence in the hospital literature has been inconsistent. This inconsistency is likely due to the differing interventions across studies (eg, counseling vs. pharmacotherapy), the differing outcome variables (eg, self-report vs. biochemically verified), as well as the different patient populations selected to participate.
Unfortunately, smoking cessation is infrequently addressed in routine health care settings,15,16 highlighting a gap in care. For example, one survey study16 found that while many health care professionals report asking about smoking status and advising smokers to quit, fewer clinicians assess smokers’ interest or intention to stop smoking, assist with cessation, or arrange follow-up. Our results indicate that assessing an inpatient smoker’s intentions, motivation, and confidence for cessation and attempting to improve low levels of these factors could enhance cessation success. Because motivation is a malleable construct, repeated assessment by hospital clinicians of a patient’s motivation and confidence to quit is needed.
Our results also confirm that inpatient efforts to improve smoking cessation postdischarge should target smokers’ resolve to quit and confidence in the ability to succeed. Motivational interventions and cognitive-behavioral therapy are effective strategies that can resolve ambivalence and increase confidence to quit and should be components of brief interventions delivered in inpatient settings.17,18 Although individuals with a smoking-related illness may already possess some resolve to quit based on their illness, they may be candidates for interventions focused primarily on developing self-efficacy. Indeed, supporting self-efficacy is a major goal of effective bedside counseling and can be bolstered via problem-solving, motivational techniques, and education about pharmacotherapy during a tobacco-specific consult such as the one that these participants experienced. Armed with these resources, smokers with and without a smoking-related disease may be more likely to execute a plan to quit after discharge.
A study limitation is that our results can be generalized only to hospital inpatients who were willing to try to quit smoking after discharge, because the parent trial excluded smokers with lower levels of motivation. Similarly, these results may not be generalizable to obstetric or psychiatric inpatients, who were excluded from this trial.
In conclusion, our results underscore the importance of assessing motivation and self-efficacy in hospitalized smokers and targeting these factors in intervention efforts. Although future research should aim to identify better methods to alter these factors, in the short run, hospital clinicians could target these factors when discussing tobacco use with inpatient smokers.
Acknowledgments
The authors are grateful for the hard work of MGH, NSMC, and UPMC’s tobacco treatment services, the hospital providers, and study research staff.
Disclosures
Drs. Rigotti and Park received royalties from UpToDate and have received a research grant from Pfizer regarding smoking cessation. Dr. Rigotti has consulted (without pay) for Pfizer. Dr. Singer has served as a consultant to Pfizer but on a topic separate from smoking cessation. No other authors have conflicts of interest to disclose.
Role of Funding Source: The study was funded by NIH/NHLBI [grant #R01-HL11821]. The funding organization had no role in the study design, collection, analysis, and interpretation of the data, preparation of the manuscript, or decision to submit the manuscript for publication.
Clinical Trial Registration: NCT01714323
1. U.S. Department of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General, 2014 | SurgeonGeneral.Gov. Office on Smoking and Health: Centers for Disease Control and Prevention; 2014:944. http://www.surgeongeneral.gov/library/reports/50-years-of-progress/index.html. Accessed May 22, 2016.
2. Rigotti NA, Clair C, Munafò MR, Stead LF. Interventions for smoking cessation in hospitalised patients. Cochrane Database Syst Rev. 2012;(5):CD001837. 10.1002/14651858.CD001837.pub3 PubMed
3. Vangeli E, Stapleton J, Smit ES, Borland R, West R. Predictors of attempts to stop smoking and their success in adult general population samples: a systematic review. Addict Abingdon Engl. 2011;106(12):2110-2121. 10.1111/j.1360-0443.2011.03565.x PubMed
4. Ockene JK, Emmons KM, Mermelstein RJ, et al. Relapse and maintenance issues for smoking cessation. Health Psychol. 2000;19(1S):17-31. 10.1037/0278-6133.19.Suppl1.17 PubMed
5. Harrington K, Young-Il K, Meifang C, et al. Web-based intervention for transitioning smokers from inpatient to outpatient care: an RCT. Am J Prev Med. 2016;51(4):620-629. 10.1016/j.amepre.2016.04.008 PubMed
6. Lando H, Hennrikus D, McCarty M, Vessey J. Predictors of quitting in hospitalized smokers. Nicotine Tob Res. 2003;5(2):215-222. 10.1080/0955300031000083436 PubMed
7. Hennrikus DJ, Lando HA, McCarty MC, et al. The TEAM project: the effectiveness of smoking cessation intervention with hospital patients. Prev Med. 2005;40(3):249-258. 10.1016/j.ypmed.2004.05.030 PubMed
8. MacKenzie TD, Pereira RI, Mehler PS. Smoking abstinence after hospitalization: predictors of success. Prev Med. 2004;39(6):1087-1092. 10.1016/j.ypmed.2004.04.054 PubMed
9. Holtrop JS, Stommel M, Corser W, Holmes-Rovner M. Predictors of smoking cessation and relapse after hospitalization for acute coronary syndrome. J Hosp Med. 2009;4(3):E3-E9. 10.1002/jhm.415 PubMed
10. Rigotti NA, Tindle HA, Regan S, et al. A post-discharge smoking-cessation intervention for hospital patients: helping Hand 2 randomized clinical trial. Am J Prev Med. 2016;51(4):597-608. 10.1016/j.amepre.2016.04.005 PubMed
11. Reid ZZ, Regan S, Kelley JHK, et al. Comparative effectiveness of post-discharge strategies for hospitalized smokers: study protocol for the helping HAND 2 randomized controlled trial. BMC Public Health. 2015;15:109. 10.1186/s12889-015-1484-0 PubMed
12. Heatherton TF, Kozlowski LT, Frecker RC, Rickert W, Robinson J. Measuring the heaviness of smoking: using self-reported time to the first cigarette of the day and number of cigarettes smoked per day. Br J Addict. 1989;84(7):791-799. http://dx.doi.org/10.1111/j.1360-0443.1989.tb03059.x PubMed
13. Melchior LA, Huba GJ, Brown VB, Reback CJ. A short depression index for women. Educ Psychol Meas. 1993;53(4):1117-1125. 10.1177/0013164493053004024
14. Bush K, Kivlahan DR, McDonell MB, Fihn SD, Bradley KA. The AUDIT alcohol consumption questions (AUDIT-C): an effective brief screening test for problem drinking. Ambulatory Care Quality Improvement Project (ACQUIP). Alcohol Use Disorders Identification Test. Arch Intern Med. 1998;158(16):1789-1795. 10.1001/archinte.158.16.1789 PubMed
15. Kruger J, Shaw L, Kahende J, Frank E. Health care providers’ advice to quit smoking, National Health Interview Survey, 2000, 2005, and 2010. Prev Chronic Dis. 2012;9:E130. 10.5888/pcd9.110340 PubMed
16. Tong EK, Strouse R, Hall J, Kovac M, Schroeder SA. National survey of U.S. health professionals’ smoking prevalence, cessation practices, and beliefs. Nicotine Tob Res. 2010;12(7):724-733. 10.1093/ntr/ntq071 PubMed
17. Lindson-Hawley N, Thompson TP, Begh R. Motivational interviewing for smoking cessation. Cochrane Database Syst Rev. 2015;(3):CD006936. 10.1002/14651858.CD006936.pub3 PubMed
18. Hendricks PS, Delucchi KL, Hall SM. Mechanisms of change in extended cognitive behavioral treatment for tobacco dependence. Drug Alcohol Depend. 2010;109(1-3):114-119. 10.1016/j.drugalcdep.2009.12.021 PubMed
Cigarette smoking is the leading cause of preventable deaths in the United States.1 Smoking contributes to several health problems that require hospitalization. Hospitalization also offers smokers an opportunity to quit because hospital policies prohibit smoking indoors while a health threat increases the motivation to quit.2 Brief bedside smoking cessation counseling with follow-up contact after discharge increases postdischarge tobacco abstinence rates by 37%.2 Identifying the characteristics of patients who are most likely to stop smoking after hospital discharge could identify strategies for interventions to help more smokers to succeed. It could also guide hospital clinicians’ efforts to provide effective brief messages to promote cessation by inpatients under their care during this teachable moment.
Sociodemographic factors, tobacco use, and psychological and medical factors have been associated with successful quit attempts by smokers in the general population.3,4 Far less is known about the predictors of success in quitting smoking and maintaining abstinence after hospitalization. The characteristics associated with abstinence at postdischarge follow-up in prior studies of hospitalized smokers were male gender, greater confidence in quitting, greater readiness to quit, less nicotine dependence, and having a smoking-related illness.5-8 However, most of the prior studies were limited to 1 geographic region,5,6 focused only on a specific subgroup (eg, coronary patients9), or did not biochemically verify tobacco abstinence.8 In fact, to our knowledge, only one prior study has examined the predictors of quitting among a broad sample of hospital patients enrolled across multiple hospitals and biochemically verified abstinence.6 That study was conducted nearly two decades ago in one Midwestern state.
Thus, the present study aimed to identify factors independently associated with sustained postdischarge tobacco abstinence among hospitalized smokers who planned to quit smoking.10 Building on previous work, this study includes a large number of smokers with varied diagnoses admitted to one of three hospitals in two states, uses biochemically verified abstinence as the outcome measure, and examines multiple variables that were identified during the inpatient stay. We hypothesize that consistent with prior literature on this topic, factors independently associated with cessation in the present study will include confidence and intention to quit, degree of nicotine dependence, and a discharge diagnosis of a smoking-related disease.
METHODS
We analyzed data from the Helping HAND2 Trial (HH2; NCT01714323), a randomized clinical trial conducted at the following three hospitals: Massachusetts General Hospital (MGH) in Boston, MA; University of Pittsburgh Medical Center (UPMC) in Pittsburgh, PA; and North Shore Medical Center (NSMC) in Salem, MA. Enrollment occurred from December 2012 to July 2014. The study methodology has been reported elsewhere.11 This study was approved by the Institutional Review Boards of Partners HealthCare and University of Pittsburgh.
PARTICIPANTS
Hospital inpatients were eligible for enrollment if they were
- >18 years old, daily smokers, received smoking cessation counseling in the hospital (ie, standard of care for inpatient smokers), and planned to quit or try to quit smoking after discharge. Exclusion criteria included no access to a telephone, not speaking English, psychiatric or cognitive impairment, medical instability, or admission to obstetric or psychiatric units. All participants were offered nicotine replacement and one counseling session by a tobacco treatment specialist during hospitalization.
STUDY CONDITIONS
Participants were enrolled before discharge and randomly assigned to Sustained Care (Intervention) or Standard Care (Control) conditions.10,11 In the Standard Care condition, participants received advice to call a free telephone quit line and a tailored recommendation for postdischarge pharmacotherapy. Participants randomized to Sustained Care received a free 30-day supply of their choice of FDA-approved tobacco cessation pharmacotherapy at hospital discharge (refillable twice) and five automated interactive voice response calls over three months postdischarge to allow them to access counseling or refill medications.
MEASURES
Baseline Demographic and Smoking Characteristics
A baseline survey assessed demographic variables (age, gender, race/ethnicity, education), tobacco use (cigarettes smoked per day, time to first morning cigarette,12 other tobacco use, and prior quit attempts), intention to quit after discharge (ie,“What is your plan about smoking after you leave the hospital,” with the intent measured across four categorical response options), perceived importance of and confidence in quitting after discharge (five-point Likert scales ranging from “not at all” to “very”), and the presence of another smoker at home. Depression and anxiety symptoms were assessed using the Patient Health Questionnaire (PHQ-413). Alcohol use (AUDIT-C14) and past-year use of cocaine, stimulants, opioids, and marijuana were also measured. Health insurance, length of stay, and primary discharge diagnoses were abstracted from the medical record. Smoking-related disease categories were derived from the 2014 U.S. Surgeon General’s Report.1
Follow-up Assessment
Telephone surveys were administered by the research staff sixmonths after hospital discharge. Participants who reported past seven-day tobacco abstinence (ie, abstinence from tobacco for the past seven days reported at the 6-month call) were asked to provide a mailed saliva sample to assay for cotinine, a nicotine metabolite, to verify self-reported abstinence. Participants who reported nicotine replacement therapy use were asked to provide an in-person measurement of expired air carbon monoxide (CO) instead. Self-reported abstinence was biochemically verified if saliva cotinine was <10 ng/ml or if CO was <9 ppm.11
Outcomes
The dependent variable, consistent with the parent trial, was biochemically confirmed past seven-day tobacco abstinence at six-month follow-up. Nonrespondents and those failing to provide a sample for confirmation were considered as smokers. In addition, a sensitivity analysis used complete cases only, excluding cases with missing smoking status outcomes.
Analysis
Bivariate associations of baseline predictor variables and biochemically confirmed abstinence were examined using chi-square tests for categorical variables and t tests or Wilcoxon rank sum tests for continuous variables. Using multiple logistic regression analyses, we identified variables that were independently associated with confirmed abstinence. The final models included all factors that were associated with cessation in the bivariate analysis (P < .10), factors associated with abstinence in the literature regardless of statistical significance (gender, AUDIT-C score),4 study site, and study condition. A two-sided p value of <.05 was considered to be statistically significant. Analyses were conducted using SAS version 9.4 (SAS Institute, Cary, NC).
RESULTS
Baseline characteristics of the 1,357 smokers enrolled in the trial are reported in Table 1. One-third of participants had a smoking-related discharge diagnosis. The median self-reported confidence in quitting was three on a five-point scale, and nearly half of the participants reported planning to stay abstinent after discharge. At six-month follow-up, 75% of participants completed the assessment, and seven-day tobacco abstinence was reported by 389 participants (29%) and biochemically confirmed in 218 participants (16%).
Results of the multiple logistic regression analysis predicting biochemically confirmed abstinence at six months are presented in Table 2. Factors independently associated with confirmed abstinence were a smoking-related primary discharge diagnosis (AOR = 1.98, 95% CI: 1.41-2.77), greater confidence in the ability to quit smoking (AOR = 1.31, 95% CI: 1.07-1.60), and stronger intention to quit (plan to stay abstinent after discharge vs. try to stay abstinent; AOR = 1.68, 95% CI: 1.19-2.38). Similar variables emerged as independent predictors of abstinence when the analysis was limited to complete cases, with an exception that one additional predictor, time to first cigarette after 30 minutes of waking, had statistical significance at the 0.05 level (Table 2).
DISCUSSION
We examined the associations between factors that were identifiable in the hospital and postdischarge tobacco abstinence among a general sample of hospitalized patients enrolled in a smoking cessation trial. The odds of biochemically confirmed abstinence at six months were higher among participants who reported higher levels of confidence in quitting smoking, those reporting having a definite plan to quit (vs. try to) after discharge, and those with a smoking-related primary discharge diagnosis.
Our findings are largely consistent with the prior literature on this topic, which has demonstrated that increased confidence in quitting, having a plan to quit smoking, and the presence of a smoking-related disease are associated with quit success at follow-up among hospital patients as well as in the general adult population.3-7 Our finding that nicotine dependence predicted quit success in the complete case analysis, but not when imputing smoking status, aligns with prior studies of hospitalized smokers, which have shown an inconclusive relationship between nicotine dependence and quit success.6,8 Despite a clear relationship of dependence to quit success among adult smokers, evidence in the hospital literature has been inconsistent. This inconsistency is likely due to the differing interventions across studies (eg, counseling vs. pharmacotherapy), the differing outcome variables (eg, self-report vs. biochemically verified), as well as the different patient populations selected to participate.
Unfortunately, smoking cessation is infrequently addressed in routine health care settings,15,16 highlighting a gap in care. For example, one survey study16 found that while many health care professionals report asking about smoking status and advising smokers to quit, fewer clinicians assess smokers’ interest or intention to stop smoking, assist with cessation, or arrange follow-up. Our results indicate that assessing an inpatient smoker’s intentions, motivation, and confidence for cessation and attempting to improve low levels of these factors could enhance cessation success. Because motivation is a malleable construct, repeated assessment by hospital clinicians of a patient’s motivation and confidence to quit is needed.
Our results also confirm that inpatient efforts to improve smoking cessation postdischarge should target smokers’ resolve to quit and confidence in the ability to succeed. Motivational interventions and cognitive-behavioral therapy are effective strategies that can resolve ambivalence and increase confidence to quit and should be components of brief interventions delivered in inpatient settings.17,18 Although individuals with a smoking-related illness may already possess some resolve to quit based on their illness, they may be candidates for interventions focused primarily on developing self-efficacy. Indeed, supporting self-efficacy is a major goal of effective bedside counseling and can be bolstered via problem-solving, motivational techniques, and education about pharmacotherapy during a tobacco-specific consult such as the one that these participants experienced. Armed with these resources, smokers with and without a smoking-related disease may be more likely to execute a plan to quit after discharge.
A study limitation is that our results can be generalized only to hospital inpatients who were willing to try to quit smoking after discharge, because the parent trial excluded smokers with lower levels of motivation. Similarly, these results may not be generalizable to obstetric or psychiatric inpatients, who were excluded from this trial.
In conclusion, our results underscore the importance of assessing motivation and self-efficacy in hospitalized smokers and targeting these factors in intervention efforts. Although future research should aim to identify better methods to alter these factors, in the short run, hospital clinicians could target these factors when discussing tobacco use with inpatient smokers.
Acknowledgments
The authors are grateful for the hard work of MGH, NSMC, and UPMC’s tobacco treatment services, the hospital providers, and study research staff.
Disclosures
Drs. Rigotti and Park received royalties from UpToDate and have received a research grant from Pfizer regarding smoking cessation. Dr. Rigotti has consulted (without pay) for Pfizer. Dr. Singer has served as a consultant to Pfizer but on a topic separate from smoking cessation. No other authors have conflicts of interest to disclose.
Role of Funding Source: The study was funded by NIH/NHLBI [grant #R01-HL11821]. The funding organization had no role in the study design, collection, analysis, and interpretation of the data, preparation of the manuscript, or decision to submit the manuscript for publication.
Clinical Trial Registration: NCT01714323
Cigarette smoking is the leading cause of preventable deaths in the United States.1 Smoking contributes to several health problems that require hospitalization. Hospitalization also offers smokers an opportunity to quit because hospital policies prohibit smoking indoors while a health threat increases the motivation to quit.2 Brief bedside smoking cessation counseling with follow-up contact after discharge increases postdischarge tobacco abstinence rates by 37%.2 Identifying the characteristics of patients who are most likely to stop smoking after hospital discharge could identify strategies for interventions to help more smokers to succeed. It could also guide hospital clinicians’ efforts to provide effective brief messages to promote cessation by inpatients under their care during this teachable moment.
Sociodemographic factors, tobacco use, and psychological and medical factors have been associated with successful quit attempts by smokers in the general population.3,4 Far less is known about the predictors of success in quitting smoking and maintaining abstinence after hospitalization. The characteristics associated with abstinence at postdischarge follow-up in prior studies of hospitalized smokers were male gender, greater confidence in quitting, greater readiness to quit, less nicotine dependence, and having a smoking-related illness.5-8 However, most of the prior studies were limited to 1 geographic region,5,6 focused only on a specific subgroup (eg, coronary patients9), or did not biochemically verify tobacco abstinence.8 In fact, to our knowledge, only one prior study has examined the predictors of quitting among a broad sample of hospital patients enrolled across multiple hospitals and biochemically verified abstinence.6 That study was conducted nearly two decades ago in one Midwestern state.
Thus, the present study aimed to identify factors independently associated with sustained postdischarge tobacco abstinence among hospitalized smokers who planned to quit smoking.10 Building on previous work, this study includes a large number of smokers with varied diagnoses admitted to one of three hospitals in two states, uses biochemically verified abstinence as the outcome measure, and examines multiple variables that were identified during the inpatient stay. We hypothesize that consistent with prior literature on this topic, factors independently associated with cessation in the present study will include confidence and intention to quit, degree of nicotine dependence, and a discharge diagnosis of a smoking-related disease.
METHODS
We analyzed data from the Helping HAND2 Trial (HH2; NCT01714323), a randomized clinical trial conducted at the following three hospitals: Massachusetts General Hospital (MGH) in Boston, MA; University of Pittsburgh Medical Center (UPMC) in Pittsburgh, PA; and North Shore Medical Center (NSMC) in Salem, MA. Enrollment occurred from December 2012 to July 2014. The study methodology has been reported elsewhere.11 This study was approved by the Institutional Review Boards of Partners HealthCare and University of Pittsburgh.
PARTICIPANTS
Hospital inpatients were eligible for enrollment if they were
- >18 years old, daily smokers, received smoking cessation counseling in the hospital (ie, standard of care for inpatient smokers), and planned to quit or try to quit smoking after discharge. Exclusion criteria included no access to a telephone, not speaking English, psychiatric or cognitive impairment, medical instability, or admission to obstetric or psychiatric units. All participants were offered nicotine replacement and one counseling session by a tobacco treatment specialist during hospitalization.
STUDY CONDITIONS
Participants were enrolled before discharge and randomly assigned to Sustained Care (Intervention) or Standard Care (Control) conditions.10,11 In the Standard Care condition, participants received advice to call a free telephone quit line and a tailored recommendation for postdischarge pharmacotherapy. Participants randomized to Sustained Care received a free 30-day supply of their choice of FDA-approved tobacco cessation pharmacotherapy at hospital discharge (refillable twice) and five automated interactive voice response calls over three months postdischarge to allow them to access counseling or refill medications.
MEASURES
Baseline Demographic and Smoking Characteristics
A baseline survey assessed demographic variables (age, gender, race/ethnicity, education), tobacco use (cigarettes smoked per day, time to first morning cigarette,12 other tobacco use, and prior quit attempts), intention to quit after discharge (ie,“What is your plan about smoking after you leave the hospital,” with the intent measured across four categorical response options), perceived importance of and confidence in quitting after discharge (five-point Likert scales ranging from “not at all” to “very”), and the presence of another smoker at home. Depression and anxiety symptoms were assessed using the Patient Health Questionnaire (PHQ-413). Alcohol use (AUDIT-C14) and past-year use of cocaine, stimulants, opioids, and marijuana were also measured. Health insurance, length of stay, and primary discharge diagnoses were abstracted from the medical record. Smoking-related disease categories were derived from the 2014 U.S. Surgeon General’s Report.1
Follow-up Assessment
Telephone surveys were administered by the research staff sixmonths after hospital discharge. Participants who reported past seven-day tobacco abstinence (ie, abstinence from tobacco for the past seven days reported at the 6-month call) were asked to provide a mailed saliva sample to assay for cotinine, a nicotine metabolite, to verify self-reported abstinence. Participants who reported nicotine replacement therapy use were asked to provide an in-person measurement of expired air carbon monoxide (CO) instead. Self-reported abstinence was biochemically verified if saliva cotinine was <10 ng/ml or if CO was <9 ppm.11
Outcomes
The dependent variable, consistent with the parent trial, was biochemically confirmed past seven-day tobacco abstinence at six-month follow-up. Nonrespondents and those failing to provide a sample for confirmation were considered as smokers. In addition, a sensitivity analysis used complete cases only, excluding cases with missing smoking status outcomes.
Analysis
Bivariate associations of baseline predictor variables and biochemically confirmed abstinence were examined using chi-square tests for categorical variables and t tests or Wilcoxon rank sum tests for continuous variables. Using multiple logistic regression analyses, we identified variables that were independently associated with confirmed abstinence. The final models included all factors that were associated with cessation in the bivariate analysis (P < .10), factors associated with abstinence in the literature regardless of statistical significance (gender, AUDIT-C score),4 study site, and study condition. A two-sided p value of <.05 was considered to be statistically significant. Analyses were conducted using SAS version 9.4 (SAS Institute, Cary, NC).
RESULTS
Baseline characteristics of the 1,357 smokers enrolled in the trial are reported in Table 1. One-third of participants had a smoking-related discharge diagnosis. The median self-reported confidence in quitting was three on a five-point scale, and nearly half of the participants reported planning to stay abstinent after discharge. At six-month follow-up, 75% of participants completed the assessment, and seven-day tobacco abstinence was reported by 389 participants (29%) and biochemically confirmed in 218 participants (16%).
Results of the multiple logistic regression analysis predicting biochemically confirmed abstinence at six months are presented in Table 2. Factors independently associated with confirmed abstinence were a smoking-related primary discharge diagnosis (AOR = 1.98, 95% CI: 1.41-2.77), greater confidence in the ability to quit smoking (AOR = 1.31, 95% CI: 1.07-1.60), and stronger intention to quit (plan to stay abstinent after discharge vs. try to stay abstinent; AOR = 1.68, 95% CI: 1.19-2.38). Similar variables emerged as independent predictors of abstinence when the analysis was limited to complete cases, with an exception that one additional predictor, time to first cigarette after 30 minutes of waking, had statistical significance at the 0.05 level (Table 2).
DISCUSSION
We examined the associations between factors that were identifiable in the hospital and postdischarge tobacco abstinence among a general sample of hospitalized patients enrolled in a smoking cessation trial. The odds of biochemically confirmed abstinence at six months were higher among participants who reported higher levels of confidence in quitting smoking, those reporting having a definite plan to quit (vs. try to) after discharge, and those with a smoking-related primary discharge diagnosis.
Our findings are largely consistent with the prior literature on this topic, which has demonstrated that increased confidence in quitting, having a plan to quit smoking, and the presence of a smoking-related disease are associated with quit success at follow-up among hospital patients as well as in the general adult population.3-7 Our finding that nicotine dependence predicted quit success in the complete case analysis, but not when imputing smoking status, aligns with prior studies of hospitalized smokers, which have shown an inconclusive relationship between nicotine dependence and quit success.6,8 Despite a clear relationship of dependence to quit success among adult smokers, evidence in the hospital literature has been inconsistent. This inconsistency is likely due to the differing interventions across studies (eg, counseling vs. pharmacotherapy), the differing outcome variables (eg, self-report vs. biochemically verified), as well as the different patient populations selected to participate.
Unfortunately, smoking cessation is infrequently addressed in routine health care settings,15,16 highlighting a gap in care. For example, one survey study16 found that while many health care professionals report asking about smoking status and advising smokers to quit, fewer clinicians assess smokers’ interest or intention to stop smoking, assist with cessation, or arrange follow-up. Our results indicate that assessing an inpatient smoker’s intentions, motivation, and confidence for cessation and attempting to improve low levels of these factors could enhance cessation success. Because motivation is a malleable construct, repeated assessment by hospital clinicians of a patient’s motivation and confidence to quit is needed.
Our results also confirm that inpatient efforts to improve smoking cessation postdischarge should target smokers’ resolve to quit and confidence in the ability to succeed. Motivational interventions and cognitive-behavioral therapy are effective strategies that can resolve ambivalence and increase confidence to quit and should be components of brief interventions delivered in inpatient settings.17,18 Although individuals with a smoking-related illness may already possess some resolve to quit based on their illness, they may be candidates for interventions focused primarily on developing self-efficacy. Indeed, supporting self-efficacy is a major goal of effective bedside counseling and can be bolstered via problem-solving, motivational techniques, and education about pharmacotherapy during a tobacco-specific consult such as the one that these participants experienced. Armed with these resources, smokers with and without a smoking-related disease may be more likely to execute a plan to quit after discharge.
A study limitation is that our results can be generalized only to hospital inpatients who were willing to try to quit smoking after discharge, because the parent trial excluded smokers with lower levels of motivation. Similarly, these results may not be generalizable to obstetric or psychiatric inpatients, who were excluded from this trial.
In conclusion, our results underscore the importance of assessing motivation and self-efficacy in hospitalized smokers and targeting these factors in intervention efforts. Although future research should aim to identify better methods to alter these factors, in the short run, hospital clinicians could target these factors when discussing tobacco use with inpatient smokers.
Acknowledgments
The authors are grateful for the hard work of MGH, NSMC, and UPMC’s tobacco treatment services, the hospital providers, and study research staff.
Disclosures
Drs. Rigotti and Park received royalties from UpToDate and have received a research grant from Pfizer regarding smoking cessation. Dr. Rigotti has consulted (without pay) for Pfizer. Dr. Singer has served as a consultant to Pfizer but on a topic separate from smoking cessation. No other authors have conflicts of interest to disclose.
Role of Funding Source: The study was funded by NIH/NHLBI [grant #R01-HL11821]. The funding organization had no role in the study design, collection, analysis, and interpretation of the data, preparation of the manuscript, or decision to submit the manuscript for publication.
Clinical Trial Registration: NCT01714323
1. U.S. Department of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General, 2014 | SurgeonGeneral.Gov. Office on Smoking and Health: Centers for Disease Control and Prevention; 2014:944. http://www.surgeongeneral.gov/library/reports/50-years-of-progress/index.html. Accessed May 22, 2016.
2. Rigotti NA, Clair C, Munafò MR, Stead LF. Interventions for smoking cessation in hospitalised patients. Cochrane Database Syst Rev. 2012;(5):CD001837. 10.1002/14651858.CD001837.pub3 PubMed
3. Vangeli E, Stapleton J, Smit ES, Borland R, West R. Predictors of attempts to stop smoking and their success in adult general population samples: a systematic review. Addict Abingdon Engl. 2011;106(12):2110-2121. 10.1111/j.1360-0443.2011.03565.x PubMed
4. Ockene JK, Emmons KM, Mermelstein RJ, et al. Relapse and maintenance issues for smoking cessation. Health Psychol. 2000;19(1S):17-31. 10.1037/0278-6133.19.Suppl1.17 PubMed
5. Harrington K, Young-Il K, Meifang C, et al. Web-based intervention for transitioning smokers from inpatient to outpatient care: an RCT. Am J Prev Med. 2016;51(4):620-629. 10.1016/j.amepre.2016.04.008 PubMed
6. Lando H, Hennrikus D, McCarty M, Vessey J. Predictors of quitting in hospitalized smokers. Nicotine Tob Res. 2003;5(2):215-222. 10.1080/0955300031000083436 PubMed
7. Hennrikus DJ, Lando HA, McCarty MC, et al. The TEAM project: the effectiveness of smoking cessation intervention with hospital patients. Prev Med. 2005;40(3):249-258. 10.1016/j.ypmed.2004.05.030 PubMed
8. MacKenzie TD, Pereira RI, Mehler PS. Smoking abstinence after hospitalization: predictors of success. Prev Med. 2004;39(6):1087-1092. 10.1016/j.ypmed.2004.04.054 PubMed
9. Holtrop JS, Stommel M, Corser W, Holmes-Rovner M. Predictors of smoking cessation and relapse after hospitalization for acute coronary syndrome. J Hosp Med. 2009;4(3):E3-E9. 10.1002/jhm.415 PubMed
10. Rigotti NA, Tindle HA, Regan S, et al. A post-discharge smoking-cessation intervention for hospital patients: helping Hand 2 randomized clinical trial. Am J Prev Med. 2016;51(4):597-608. 10.1016/j.amepre.2016.04.005 PubMed
11. Reid ZZ, Regan S, Kelley JHK, et al. Comparative effectiveness of post-discharge strategies for hospitalized smokers: study protocol for the helping HAND 2 randomized controlled trial. BMC Public Health. 2015;15:109. 10.1186/s12889-015-1484-0 PubMed
12. Heatherton TF, Kozlowski LT, Frecker RC, Rickert W, Robinson J. Measuring the heaviness of smoking: using self-reported time to the first cigarette of the day and number of cigarettes smoked per day. Br J Addict. 1989;84(7):791-799. http://dx.doi.org/10.1111/j.1360-0443.1989.tb03059.x PubMed
13. Melchior LA, Huba GJ, Brown VB, Reback CJ. A short depression index for women. Educ Psychol Meas. 1993;53(4):1117-1125. 10.1177/0013164493053004024
14. Bush K, Kivlahan DR, McDonell MB, Fihn SD, Bradley KA. The AUDIT alcohol consumption questions (AUDIT-C): an effective brief screening test for problem drinking. Ambulatory Care Quality Improvement Project (ACQUIP). Alcohol Use Disorders Identification Test. Arch Intern Med. 1998;158(16):1789-1795. 10.1001/archinte.158.16.1789 PubMed
15. Kruger J, Shaw L, Kahende J, Frank E. Health care providers’ advice to quit smoking, National Health Interview Survey, 2000, 2005, and 2010. Prev Chronic Dis. 2012;9:E130. 10.5888/pcd9.110340 PubMed
16. Tong EK, Strouse R, Hall J, Kovac M, Schroeder SA. National survey of U.S. health professionals’ smoking prevalence, cessation practices, and beliefs. Nicotine Tob Res. 2010;12(7):724-733. 10.1093/ntr/ntq071 PubMed
17. Lindson-Hawley N, Thompson TP, Begh R. Motivational interviewing for smoking cessation. Cochrane Database Syst Rev. 2015;(3):CD006936. 10.1002/14651858.CD006936.pub3 PubMed
18. Hendricks PS, Delucchi KL, Hall SM. Mechanisms of change in extended cognitive behavioral treatment for tobacco dependence. Drug Alcohol Depend. 2010;109(1-3):114-119. 10.1016/j.drugalcdep.2009.12.021 PubMed
1. U.S. Department of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General, 2014 | SurgeonGeneral.Gov. Office on Smoking and Health: Centers for Disease Control and Prevention; 2014:944. http://www.surgeongeneral.gov/library/reports/50-years-of-progress/index.html. Accessed May 22, 2016.
2. Rigotti NA, Clair C, Munafò MR, Stead LF. Interventions for smoking cessation in hospitalised patients. Cochrane Database Syst Rev. 2012;(5):CD001837. 10.1002/14651858.CD001837.pub3 PubMed
3. Vangeli E, Stapleton J, Smit ES, Borland R, West R. Predictors of attempts to stop smoking and their success in adult general population samples: a systematic review. Addict Abingdon Engl. 2011;106(12):2110-2121. 10.1111/j.1360-0443.2011.03565.x PubMed
4. Ockene JK, Emmons KM, Mermelstein RJ, et al. Relapse and maintenance issues for smoking cessation. Health Psychol. 2000;19(1S):17-31. 10.1037/0278-6133.19.Suppl1.17 PubMed
5. Harrington K, Young-Il K, Meifang C, et al. Web-based intervention for transitioning smokers from inpatient to outpatient care: an RCT. Am J Prev Med. 2016;51(4):620-629. 10.1016/j.amepre.2016.04.008 PubMed
6. Lando H, Hennrikus D, McCarty M, Vessey J. Predictors of quitting in hospitalized smokers. Nicotine Tob Res. 2003;5(2):215-222. 10.1080/0955300031000083436 PubMed
7. Hennrikus DJ, Lando HA, McCarty MC, et al. The TEAM project: the effectiveness of smoking cessation intervention with hospital patients. Prev Med. 2005;40(3):249-258. 10.1016/j.ypmed.2004.05.030 PubMed
8. MacKenzie TD, Pereira RI, Mehler PS. Smoking abstinence after hospitalization: predictors of success. Prev Med. 2004;39(6):1087-1092. 10.1016/j.ypmed.2004.04.054 PubMed
9. Holtrop JS, Stommel M, Corser W, Holmes-Rovner M. Predictors of smoking cessation and relapse after hospitalization for acute coronary syndrome. J Hosp Med. 2009;4(3):E3-E9. 10.1002/jhm.415 PubMed
10. Rigotti NA, Tindle HA, Regan S, et al. A post-discharge smoking-cessation intervention for hospital patients: helping Hand 2 randomized clinical trial. Am J Prev Med. 2016;51(4):597-608. 10.1016/j.amepre.2016.04.005 PubMed
11. Reid ZZ, Regan S, Kelley JHK, et al. Comparative effectiveness of post-discharge strategies for hospitalized smokers: study protocol for the helping HAND 2 randomized controlled trial. BMC Public Health. 2015;15:109. 10.1186/s12889-015-1484-0 PubMed
12. Heatherton TF, Kozlowski LT, Frecker RC, Rickert W, Robinson J. Measuring the heaviness of smoking: using self-reported time to the first cigarette of the day and number of cigarettes smoked per day. Br J Addict. 1989;84(7):791-799. http://dx.doi.org/10.1111/j.1360-0443.1989.tb03059.x PubMed
13. Melchior LA, Huba GJ, Brown VB, Reback CJ. A short depression index for women. Educ Psychol Meas. 1993;53(4):1117-1125. 10.1177/0013164493053004024
14. Bush K, Kivlahan DR, McDonell MB, Fihn SD, Bradley KA. The AUDIT alcohol consumption questions (AUDIT-C): an effective brief screening test for problem drinking. Ambulatory Care Quality Improvement Project (ACQUIP). Alcohol Use Disorders Identification Test. Arch Intern Med. 1998;158(16):1789-1795. 10.1001/archinte.158.16.1789 PubMed
15. Kruger J, Shaw L, Kahende J, Frank E. Health care providers’ advice to quit smoking, National Health Interview Survey, 2000, 2005, and 2010. Prev Chronic Dis. 2012;9:E130. 10.5888/pcd9.110340 PubMed
16. Tong EK, Strouse R, Hall J, Kovac M, Schroeder SA. National survey of U.S. health professionals’ smoking prevalence, cessation practices, and beliefs. Nicotine Tob Res. 2010;12(7):724-733. 10.1093/ntr/ntq071 PubMed
17. Lindson-Hawley N, Thompson TP, Begh R. Motivational interviewing for smoking cessation. Cochrane Database Syst Rev. 2015;(3):CD006936. 10.1002/14651858.CD006936.pub3 PubMed
18. Hendricks PS, Delucchi KL, Hall SM. Mechanisms of change in extended cognitive behavioral treatment for tobacco dependence. Drug Alcohol Depend. 2010;109(1-3):114-119. 10.1016/j.drugalcdep.2009.12.021 PubMed
© 2018 Society of Hospital Medicine
Limitations of Using Pediatric Respiratory Illness Readmissions to Compare Hospital Performance
Respiratory illnesses are the leading causes of pediatric hospitalizations in the United States.1 The 30-day hospital readmission rate for respiratory illnesses is being considered for implementation as a national hospital performance measure, as it may be an indicator of lower quality care (eg, poor hospital management of disease, inadequate patient/caretaker education prior to discharge). In adult populations, readmissions can be used to reliably identify variation in hospital performance and successfully drive efforts to improve the value of care.2, 3 In contrast, there are persistent concerns about using pediatric readmissions to identify variation in hospital performance, largely due to lower patient volumes.4-7 To increase the value of pediatric hospital care, it is important to develop ways to meaningfully measure quality of care and further, to better understand the relationship between measures of quality and healthcare costs.
In December 2016, the National Quality Forum (NQF) endorsed a Pediatric Lower Respiratory Infection (LRI) Readmission Measure.8 This measure was developed by the Pediatric Quality Measurement Program, through the Agency for Healthcare Research and Quality. The goal of this program was to “increase the portfolio of evidence-based, consensus pediatric quality measures available to public and private purchasers of children’s healthcare services, providers, and consumers.”9
In anticipation of the national implementation of pediatric readmission measures, we examined whether the Pediatric LRI Readmission Measure could meaningfully identify high and low performers across all types of hospitals admitting children (general hospitals and children’s hospitals) using an all-payer claims database. A recent analysis by Nakamura et al. identified high and low performers using this measure10 but limited the analysis to hospitals with >50 pediatric LRI admissions per year, an approach that excludes many general hospitals. Since general hospitals provide the majority of care for children hospitalized with respiratory infections,11 we aimed to evaluate the measure in a broadly inclusive analysis that included all hospital types. Because low patient volumes might limit use of the measure,4,6 we tested several broadened variations of the measure. We also examined the relationship between hospital performance in pediatric LRI readmissions and healthcare costs.
Our analysis is intended to inform utilizers of pediatric quality metrics and policy makers about the feasibility of using these metrics to publicly report hospital performance and/or identify exceptional hospitals for understanding best practices in pediatric inpatient care.12
METHODS
Study Design and Data Source
We conducted an observational, retrospective cohort analysis using the 2012-2014 California Office of Statewide Health Planning and Development (OSHPD) nonpublic inpatient and emergency department databases.13 The OSHPD databases are compiled annually through mandatory reporting by all licensed nonfederal hospitals in California. The databases contain demographic (eg, age, gender) and utilization data (eg, charges) and can track readmissions to hospitals other than the index hospital. The databases capture administrative claims from approximately 450 hospitals, composed of 16 million inpatients, emergency department patients, and ambulatory surgery patients annually. Data quality is monitored through the California OSHPD.
Study Population
Our study included children aged ≤18 years with LRI, defined using the NQF Pediatric LRI Readmissions Measure: a primary diagnosis of bronchiolitis, influenza, or pneumonia, or a secondary diagnosis of bronchiolitis, influenza, or pneumonia, with a primary diagnosis of asthma, respiratory failure, sepsis, or bacteremia.8 International classification of Diseases, 9th edition (ICD-9) diagnostic codes used are in Appendix 1.
Per the NQF measure specifications,8 records were excluded if they were from hospitals with <80% of records complete with core elements (unique patient identifier, admission date, end-of-service date, and ICD-9 primary diagnosis code). In addition, records were excluded for the following reasons: (1) individual record missing core elements, (2) discharge disposition “death,” (3) 30-day follow-up data not available, (4) primary “newborn” or mental health diagnosis, or (5) primary ICD-9 procedure code for a planned procedure or chemotherapy.
Patient characteristics for hospital admissions with and without 30-day readmissions or 30-day emergency department (ED) revisits were summarized. For the continuous variable age, mean and standard deviation for each group were calculated. For categorical variables (sex, race, payer, and number of chronic conditions), numbers and proportions were determined. Univariate tests of comparison were carried out using the Student’s t test for age and chi-square tests for all categorical variables. Categories of payer with small values were combined for ease of description (categories combined into “other:” workers’ compensation, county indigent programs, other government, other indigent, self-pay, other payer). We identified chronic conditions using the Agency for Healthcare Research and Quality Chronic Condition Indicator (CCI) system, which classifies ICD-9-CM diagnosis codes as chronic or acute and places each code into 1 of 18 mutually exclusive categories (organ systems, disease categories, or other categories). The case-mix adjustment model incorporates a binary variable for each CCI category (0-1, 2, 3, or >4 chronic conditions) per the NQF measure specifications.8 This study was approved by the University of California, San Francisco Institutional Review Board.
Outcomes
Our primary outcome was the hospital-level rate of 30-day readmission after hospital discharge, consistent with the NQF measure.8 We identified outlier hospitals for 30-day readmission rate using the Centers for Medicare and Medicaid Services (CMS) methodology, which defines outlier hospitals as those for whom adjusted readmission rate confidence intervals do not overlap with the overall group mean rate.5, 14
We also determined the hospital-level average cost per index hospitalization (not including costs of readmissions). Since costs of care often differ substantially from charges,15 costs were calculated using cost-to-charge ratios for each hospital (annual total operating expenses/total gross patient revenue, as reported to the OSHPD).16 Costs were subdivided into categories representing $5,000 increments and a top category of >$40,000. Outlier hospitals for costs were defined as those for whom the cost random effect was either greater than the third quartile of the distribution of values by more than 1.5 times the interquartile range or less than the first quartile of the distribution of values by more than 1.5 times the interquartile range.17
ANALYSIS
Primary Analysis
For our primary analysis of 30-day hospital readmission rates, we used hierarchical logistic regression models with hospitals as random effects, adjusting for patient age, sex, and the presence and number of body systems affected by chronic conditions.8 These 4 patient characteristics were selected by the NQF measure developers “because distributions of these characteristics vary across hospitals, and although they are associated with readmission risk, they are independent of hospital quality of care.”10
Because the Centers for Medicare and Medicaid Services (CMS) are in the process of selecting pediatric quality measures for meaningful use reporting,18 we utilized CMS hospital readmissions methodology to calculate risk-adjusted rates and identify outlier hospitals. The CMS modeling strategy stabilizes performance estimates for low-volume hospitals and avoids penalizing these hospitals for high readmission rates that may be due to chance (random effects logistic model to obtain best linear unbiased predictions). This is particularly important in pediatrics, given the low pediatric volumes in many hospitals admitting children.4,19 We then identified outlier hospitals for the 30-day readmission rate using CMS methodology (hospital’s adjusted readmission rate confidence interval does not overlap the overall group mean rate).5, 4 CMS uses this approach for public reporting on HospitalCompare.20
Sensitivity Analyses
We tested several broadening variations of the NQF measure: (1) addition of children admitted with a primary diagnosis of asthma (without requiring LRI as a secondary diagnosis) or a secondary diagnosis of asthma exacerbation (LRIA), (2) inclusion of 30-day ED revisits as an outcome, and (3) merging of 3 years of data. These analyses were all performed using the same modeling strategy as in our primary analysis.
Secondary Outcome Analyses
Our analysis of hospital costs used costs for index admissions over 3 years (2012–2014) and included admissions for asthma. We used hierarchical regression models with hospitals as random effects, adjusting for age, gender, and the presence and number of chronic conditions. The distribution of cost values was highly skewed, so ordinal models were selected after several other modeling approaches failed (log transformation linear model, gamma model, Poisson model, zero-truncated Poisson model).
The relationship between hospital-level costs and hospital-level 30-day readmission or ED revisit rates was analyzed using Spearman’s rank correlation coefficient. Statistical analysis was performed using SAS version 9.4 software (SAS Institute; Cary, North Carolina).
RESULTS
Primary Analysis of 30-day Readmissions (per National Quality Forum Measure)
Our analysis of the 2014 OSHPD database using the specifications of the NQF Pediatric LRI Readmission Measure included a total of 5550 hospitalizations from 174 hospitals, with a mean of 12 eligible hospitalizations per hospital. The mean risk-adjusted readmission rate was 6.5% (362 readmissions). There were no hospitals that were considered outliers based on the risk-adjusted readmission rates (Table 1).
Sensitivity Analyses (Broadening Definitions of National Quality Forum Measure)
We report our testing of the broadened variations of the NQF measure in Table 1. Broadening the population to include children with asthma as a primary diagnosis and children with asthma exacerbations as a secondary diagnosis (LRIA) increased the size of our analysis to 8402 hospitalizations from 190 hospitals. The mean risk-adjusted readmission rate was 5.5%, and no outlier hospitals were identified.
Using the same inclusion criteria of the NQF measure but including 30-day ED revisits as an outcome, we analyzed a total of 5500 hospitalizations from 174 hospitals. The mean risk-adjusted event rate was higher at 7.9%, but there were still no outlier hospitals identified.
Using the broadened population definition (LRIA) and including 30-day ED revisits as an outcome, we analyzed a total of 8402 hospitalizations from 190 hospitals. The mean risk-adjusted event rate was 6.8%, but there were still no outlier hospitals identified.
In our final iteration, we merged 3 years of hospital data (2012-2014) using the broader population definition (LRIA) and including 30-day ED revisits as an outcome. This resulted in 27,873 admissions from 239 hospitals for this analysis, with a mean of 28 eligible hospitalizations per hospital. The mean risk-adjusted event rate was 6.7%, and this approach identified 2 high-performing (risk-adjusted rates: 3.6-5.3) and 7 low-performing hospitals (risk-adjusted rates: 10.1-15.9).
Table 2 presents the demographics of children included in this analysis. Children who had readmissions/revisits were younger, more likely to be white, less likely to have private insurance, and more likely to have a greater number of chronic conditions compared to children without readmissions/revisits.
Secondary Outcome: Hospital Costs
In the analysis of hospital-level costs, we found only 1 outlier high-cost hospital. There was a 20% probability of a hospital respiratory admission costing ≥$40,000 at this hospital. We found no overall relationship between hospital 30-day respiratory readmission rate and hospital costs (Figure 1). However, the hospitals that were outliers for low readmission rates also had low probabilities of excessive hospital costs (3% probability of costs >$40,000; Figure 2).
DISCUSSION
We used a nationally endorsed pediatric quality measure to evaluate hospital performance, defined as 30-day readmission rates for children with respiratory illness. We examined all-payer data from California, which is the most populous state in the country and home to 1 in 8 American children. In this large California dataset, we were unable to identify meaningful variation in hospital performance due to low hospital volumes and event rates. However, when we broadened the measure definition, we were able to identify performance variation. Our findings underscore the importance of testing and potentially modifying existing quality measures in order to more accurately capture the quality of care delivered at hospitals with lower volumes of pediatric patients.21
Our underlying assumption, in light of these prior studies, was that increasing the eligible sample in each hospital by combining respiratory diseases and by using an all-payer claims database rather than a Medicaid-only database would increase the number of detectable outlier hospitals. However, we found that these approaches did not ameliorate the limitations of small volumes. Only through aggregating data over 3 years was it possible to identify any outliers, and this approach identified only 3% of hospitals as outliers. Hence, our analysis reinforces concerns raised by several prior analyses4-7 regarding the limited ability of current pediatric readmission measures to detect meaningful, actionable differences in performance across all types of hospitals (including general/nonchildren’s hospitals). This issue is of particular concern for common pediatric conditions like respiratory illnesses, for which >70% of hospitalizations occur in general hospitals.11
Developers and utilizers of pediatric quality metrics should consider strategies for identifying meaningful, actionable variation in pediatric quality of care at general hospitals. These strategies might include our approach of combining several years of hospital data in order to reach adequate volumes for measuring performance. The potential downside to this approach is performance lag—specifically, hospitals implementing quality improvement readmissions programs may not see changes in their performance for a year or two on a measure aggregating 3 years of data. Alternatively, it is possible that the measure might be used more appropriately across a larger group of hospitals, either to assess performance for multihospital accountable care organization (ACO), or to assess performance for a service area or county. An aggregated group of hospitals would increase the eligible patient volume and, if there is an ACO relationship established, coordinated interventions could be implemented across the hospitals.
We examined the 30-day readmission rate because it is the current standard used by CMS and all NQF-endorsed readmission measures.22,23 Another potential approach is to analyze the 7- or 15-day readmission rate. However, these rates may be similarly limited in identifying hospital performance due to low volumes and event rates. An analysis by Wallace et al. of preventable readmissions to a tertiary children’s hospital found that, while many occurred within 7 days or 15 days, 27% occurred after 7 days and 22%, after 15.24 However, an analysis of several adult 30-day readmission measures used by CMS found that the contribution of hospital-level quality to the readmission rate (measured by intracluster correlation coefficient) reached a nadir at 7 days, which suggests that most readmissions after the seventh day postdischarge were explained by community- and household-level factors beyond hospitals’ control.22 Hence, though 7- or 15-day readmission rates may better represent preventable outcomes under the hospital’s control, the lower event rates and low hospital volumes likely similarly limit the feasibility of their use for performance measurement.
Pediatric quality measures are additionally intended to drive improvements in the value of pediatric care, defined as quality relative to costs.25 In order to better understand the relationship of hospital performance across both the domains of readmissions (quality) and costs, we examined hospital-level costs for care of pediatric respiratory illnesses. We found no overall relationship between hospital readmission rates and costs; however, we found 2 hospitals in California that had significantly lower readmission rates as well as low costs. Close examination of hospitals such as these, which demonstrate exceptional performance in quality and costs, may promote the discovery and dissemination of strategies to improve the value of pediatric care.12
Our study had several limitations. First, the OSHPD database lacked detailed clinical variables to correct for additional case-mix differences between hospitals. However, we used the approach of case-mix adjustment outlined by an NQF-endorsed national quality metric.8 Secondly, since our data were limited to a single state, analyses of other databases may have yielded different results. However, prior analyses using other multistate databases reported similar limitations,5,6 likely due to the limitations of patient volume that are generalizable to settings outside of California. In addition, our cost analysis was performed using cost-to-charge ratios that represent total annual expenses/revenue for the whole hospital.16 These ratios may not be reflective of the specific services provided for children in our analysis; however, service-specific costs were not available, and cost-to-charge ratios are commonly used to report costs.
CONCLUSION
The ability of a nationally-endorsed pediatric respiratory readmissions measure to meaningfully identify variation in hospital performance is limited. General hospitals, which provide the majority of pediatric care for common conditions such as LRI, likely cannot be accurately evaluated using national pediatric quality metrics as they are currently designed. Modifying measures in order to increase hospital-level pediatric patient volumes may facilitate more meaningful evaluation of the quality of pediatric care in general hospitals and identification of exceptional hospitals for understanding best practices in pediatric inpatient care.
Disclosures
Regina Lam consulted for Proximity Health doing market research during the course of developing this manuscript, but this work did not involve any content related to quality metrics, and this entity did not play any role in the development of this manuscript. The remaining authors have no conflicts of interest relevant to this article to disclose.
Funding
Supported by the Agency for Healthcare Research and Quality (K08 HS24592 to SVK and U18HS25297 to MDC and NSB) and the National Institute of Child Health and Human Development (K23HD065836 to NSB). The funding agency played no role in the study design; the collection, analysis, and interpretation of data; the writing of the report; or the decision to submit the manuscript for publication.
1. Agency for Healthcare Research and Quality. Overview of hospital stays for children in the United States. https://www.hcup-us.ahrq.gov/reports/statbriefs/sb187-Hospital-Stays-Children-2012.jsp. Accessed September 1, 2017; 2012. PubMed
2. Mendelson A, Kondo K, Damberg C, et al. The effects of pay-for-performance programs on health, health care use, and processes of care: A systematic review. Ann Intern Med. 2017;166(5):341-353. doi: 10.7326/M16-1881. PubMed
3. Zuckerman RB, Sheingold SH, Orav EJ, Ruhter J, Epstein AM. Readmissions, observation, and the hospital readmissions reduction program. N Engl J Med. 2016;374(16):1543-1551. doi: 10.1056/NEJMsa1513024. PubMed
4. Bardach NS, Chien AT, Dudley RA. Small numbers limit the use of the inpatient pediatric quality indicators for hospital comparison. Acad Pediatr. 2010;10(4):266-273. doi: 10.1016/j.acap.2010.04.025. PubMed
5. Bardach NS, Vittinghoff E, Asteria-Peñaloza R, et al. Measuring hospital quality using pediatric readmission and revisit rates. Pediatrics. 2013;132(3):429-436. doi: 10.1542/peds.2012-3527. PubMed
6. Berry JG, Zaslavsky AM, Toomey SL, et al. Recognizing differences in hospital quality performance for pediatric inpatient care. Pediatrics. 2015;136(2):251-262. doi: 10.1542/peds.2014-3131. PubMed
7. Hain PD, Gay JC, Berutti TW, Whitney GM, Wang W, Saville BR. Preventability of early readmissions at a children’s hospital. Pediatrics. 2013;131(1):e171-e181. doi: 10.1542/peds.2012-0820. PubMed
8. Agency for Healthcare Research and Quality. Pediatric lower respiratory infection readmission measure. https://www.ahrq.gov/sites/default/files/wysiwyg/policymakers/chipra/factsheets/chipra_1415-p008-2-ef.pdf. Accessed September 3, 2017.
9. Agency for Healthcare Research and Quality. CHIPRA Pediatric Quality Measures Program. https://archive.ahrq.gov/policymakers/chipra/pqmpback.html. Accessed October 10, 2017.
10. Nakamura MM, Zaslavsky AM, Toomey SL, et al. Pediatric readmissions After hospitalizations for lower respiratory infections. Pediatrics. 2017;140(2). doi: 10.1542/peds.2016-0938. PubMed
11. Leyenaar JK, Ralston SL, Shieh MS, Pekow PS, Mangione-Smith R, Lindenauer PK. Epidemiology of pediatric hospitalizations at general hospitals and freestanding children’s hospitals in the United States. J Hosp Med. 2016;11(11):743-749. doi: 10.1002/jhm.2624. PubMed
12. Bradley EH, Curry LA, Ramanadhan S, Rowe L, Nembhard IM, Krumholz HM. Research in action: using positive deviance to improve quality of health care. Implement Sci. 2009;4:25. doi: 10.1186/1748-5908-4-25. PubMed
13. California Office of Statewide Health Planning and Development. Data and reports. https://www.oshpd.ca.gov/HID/. Accessed September 3, 2017.
14. QualityNet. Measure methodology reports. https://www.qualitynet.org/dcs/ContentServer?c=Page&pagename=QnetPublic%2FPage%2FQnetTier4&cid=1219069855841. Accessed October 10, 2017.
15. Riley GF. Administrative and claims records as sources of health care cost data. Med Care. 2009;47(7 Suppl 1):S51-S55. doi: 10.1097/MLR.0b013e31819c95aa. PubMed
16. California Office of Statewide Health Planning and Development. Annual financial data. https://www.oshpd.ca.gov/HID/Hospital-Financial.asp. Accessed September 3, 2017.
17. Tukey J. Exploratory Data Analysis: Pearson; London, United Kingdom. 1977.
18. Centers for Medicare and Medicaid Services. Core measures. https://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/QualityMeasures/Core-Measures.html. Accessed September 1, 2017.
19. Berry JG, Toomey SL, Zaslavsky AM, et al. Pediatric readmission prevalence and variability across hospitals. JAMA. 2013;309(4):372-380. doi: 10.1001/jama.2012.188351. PubMed
20. Centers for Medicare and Medicaid Services. HospitalCompare. https://www.medicare.gov/hospitalcompare/search.html. Accessed on October 10, 2017.
21. Mangione-Smith R. The challenges of addressing pediatric quality measurement gaps. Pediatrics. 2017;139(4). doi: 10.1542/peds.2017-0174. PubMed
22. Chin DL, Bang H, Manickam RN, Romano PS. Rethinking thirty-day hospital readmissions: shorter intervals might be better indicators of quality of care. Health Aff (Millwood). 2016;35(10):1867-1875. doi: 10.1377/hlthaff.2016.0205. PubMed
23. National Quality Forum. Measures, reports, and tools. http://www.qualityforum.org/Measures_Reports_Tools.aspx. Accessed March 1, 2018.
24. Wallace SS, Keller SL, Falco CN, et al. An examination of physician-, caregiver-, and disease-related factors associated With readmission From a pediatric hospital medicine service. Hosp Pediatr. 2015;5(11):566-573. doi: 10.1542/hpeds.2015-0015. PubMed
25. Porter ME. What is value in health care? N Engl J Med. 2010;363(26):2477-2481. doi: 10.1056/NEJMp1011024. PubMed
Respiratory illnesses are the leading causes of pediatric hospitalizations in the United States.1 The 30-day hospital readmission rate for respiratory illnesses is being considered for implementation as a national hospital performance measure, as it may be an indicator of lower quality care (eg, poor hospital management of disease, inadequate patient/caretaker education prior to discharge). In adult populations, readmissions can be used to reliably identify variation in hospital performance and successfully drive efforts to improve the value of care.2, 3 In contrast, there are persistent concerns about using pediatric readmissions to identify variation in hospital performance, largely due to lower patient volumes.4-7 To increase the value of pediatric hospital care, it is important to develop ways to meaningfully measure quality of care and further, to better understand the relationship between measures of quality and healthcare costs.
In December 2016, the National Quality Forum (NQF) endorsed a Pediatric Lower Respiratory Infection (LRI) Readmission Measure.8 This measure was developed by the Pediatric Quality Measurement Program, through the Agency for Healthcare Research and Quality. The goal of this program was to “increase the portfolio of evidence-based, consensus pediatric quality measures available to public and private purchasers of children’s healthcare services, providers, and consumers.”9
In anticipation of the national implementation of pediatric readmission measures, we examined whether the Pediatric LRI Readmission Measure could meaningfully identify high and low performers across all types of hospitals admitting children (general hospitals and children’s hospitals) using an all-payer claims database. A recent analysis by Nakamura et al. identified high and low performers using this measure10 but limited the analysis to hospitals with >50 pediatric LRI admissions per year, an approach that excludes many general hospitals. Since general hospitals provide the majority of care for children hospitalized with respiratory infections,11 we aimed to evaluate the measure in a broadly inclusive analysis that included all hospital types. Because low patient volumes might limit use of the measure,4,6 we tested several broadened variations of the measure. We also examined the relationship between hospital performance in pediatric LRI readmissions and healthcare costs.
Our analysis is intended to inform utilizers of pediatric quality metrics and policy makers about the feasibility of using these metrics to publicly report hospital performance and/or identify exceptional hospitals for understanding best practices in pediatric inpatient care.12
METHODS
Study Design and Data Source
We conducted an observational, retrospective cohort analysis using the 2012-2014 California Office of Statewide Health Planning and Development (OSHPD) nonpublic inpatient and emergency department databases.13 The OSHPD databases are compiled annually through mandatory reporting by all licensed nonfederal hospitals in California. The databases contain demographic (eg, age, gender) and utilization data (eg, charges) and can track readmissions to hospitals other than the index hospital. The databases capture administrative claims from approximately 450 hospitals, composed of 16 million inpatients, emergency department patients, and ambulatory surgery patients annually. Data quality is monitored through the California OSHPD.
Study Population
Our study included children aged ≤18 years with LRI, defined using the NQF Pediatric LRI Readmissions Measure: a primary diagnosis of bronchiolitis, influenza, or pneumonia, or a secondary diagnosis of bronchiolitis, influenza, or pneumonia, with a primary diagnosis of asthma, respiratory failure, sepsis, or bacteremia.8 International classification of Diseases, 9th edition (ICD-9) diagnostic codes used are in Appendix 1.
Per the NQF measure specifications,8 records were excluded if they were from hospitals with <80% of records complete with core elements (unique patient identifier, admission date, end-of-service date, and ICD-9 primary diagnosis code). In addition, records were excluded for the following reasons: (1) individual record missing core elements, (2) discharge disposition “death,” (3) 30-day follow-up data not available, (4) primary “newborn” or mental health diagnosis, or (5) primary ICD-9 procedure code for a planned procedure or chemotherapy.
Patient characteristics for hospital admissions with and without 30-day readmissions or 30-day emergency department (ED) revisits were summarized. For the continuous variable age, mean and standard deviation for each group were calculated. For categorical variables (sex, race, payer, and number of chronic conditions), numbers and proportions were determined. Univariate tests of comparison were carried out using the Student’s t test for age and chi-square tests for all categorical variables. Categories of payer with small values were combined for ease of description (categories combined into “other:” workers’ compensation, county indigent programs, other government, other indigent, self-pay, other payer). We identified chronic conditions using the Agency for Healthcare Research and Quality Chronic Condition Indicator (CCI) system, which classifies ICD-9-CM diagnosis codes as chronic or acute and places each code into 1 of 18 mutually exclusive categories (organ systems, disease categories, or other categories). The case-mix adjustment model incorporates a binary variable for each CCI category (0-1, 2, 3, or >4 chronic conditions) per the NQF measure specifications.8 This study was approved by the University of California, San Francisco Institutional Review Board.
Outcomes
Our primary outcome was the hospital-level rate of 30-day readmission after hospital discharge, consistent with the NQF measure.8 We identified outlier hospitals for 30-day readmission rate using the Centers for Medicare and Medicaid Services (CMS) methodology, which defines outlier hospitals as those for whom adjusted readmission rate confidence intervals do not overlap with the overall group mean rate.5, 14
We also determined the hospital-level average cost per index hospitalization (not including costs of readmissions). Since costs of care often differ substantially from charges,15 costs were calculated using cost-to-charge ratios for each hospital (annual total operating expenses/total gross patient revenue, as reported to the OSHPD).16 Costs were subdivided into categories representing $5,000 increments and a top category of >$40,000. Outlier hospitals for costs were defined as those for whom the cost random effect was either greater than the third quartile of the distribution of values by more than 1.5 times the interquartile range or less than the first quartile of the distribution of values by more than 1.5 times the interquartile range.17
ANALYSIS
Primary Analysis
For our primary analysis of 30-day hospital readmission rates, we used hierarchical logistic regression models with hospitals as random effects, adjusting for patient age, sex, and the presence and number of body systems affected by chronic conditions.8 These 4 patient characteristics were selected by the NQF measure developers “because distributions of these characteristics vary across hospitals, and although they are associated with readmission risk, they are independent of hospital quality of care.”10
Because the Centers for Medicare and Medicaid Services (CMS) are in the process of selecting pediatric quality measures for meaningful use reporting,18 we utilized CMS hospital readmissions methodology to calculate risk-adjusted rates and identify outlier hospitals. The CMS modeling strategy stabilizes performance estimates for low-volume hospitals and avoids penalizing these hospitals for high readmission rates that may be due to chance (random effects logistic model to obtain best linear unbiased predictions). This is particularly important in pediatrics, given the low pediatric volumes in many hospitals admitting children.4,19 We then identified outlier hospitals for the 30-day readmission rate using CMS methodology (hospital’s adjusted readmission rate confidence interval does not overlap the overall group mean rate).5, 4 CMS uses this approach for public reporting on HospitalCompare.20
Sensitivity Analyses
We tested several broadening variations of the NQF measure: (1) addition of children admitted with a primary diagnosis of asthma (without requiring LRI as a secondary diagnosis) or a secondary diagnosis of asthma exacerbation (LRIA), (2) inclusion of 30-day ED revisits as an outcome, and (3) merging of 3 years of data. These analyses were all performed using the same modeling strategy as in our primary analysis.
Secondary Outcome Analyses
Our analysis of hospital costs used costs for index admissions over 3 years (2012–2014) and included admissions for asthma. We used hierarchical regression models with hospitals as random effects, adjusting for age, gender, and the presence and number of chronic conditions. The distribution of cost values was highly skewed, so ordinal models were selected after several other modeling approaches failed (log transformation linear model, gamma model, Poisson model, zero-truncated Poisson model).
The relationship between hospital-level costs and hospital-level 30-day readmission or ED revisit rates was analyzed using Spearman’s rank correlation coefficient. Statistical analysis was performed using SAS version 9.4 software (SAS Institute; Cary, North Carolina).
RESULTS
Primary Analysis of 30-day Readmissions (per National Quality Forum Measure)
Our analysis of the 2014 OSHPD database using the specifications of the NQF Pediatric LRI Readmission Measure included a total of 5550 hospitalizations from 174 hospitals, with a mean of 12 eligible hospitalizations per hospital. The mean risk-adjusted readmission rate was 6.5% (362 readmissions). There were no hospitals that were considered outliers based on the risk-adjusted readmission rates (Table 1).
Sensitivity Analyses (Broadening Definitions of National Quality Forum Measure)
We report our testing of the broadened variations of the NQF measure in Table 1. Broadening the population to include children with asthma as a primary diagnosis and children with asthma exacerbations as a secondary diagnosis (LRIA) increased the size of our analysis to 8402 hospitalizations from 190 hospitals. The mean risk-adjusted readmission rate was 5.5%, and no outlier hospitals were identified.
Using the same inclusion criteria of the NQF measure but including 30-day ED revisits as an outcome, we analyzed a total of 5500 hospitalizations from 174 hospitals. The mean risk-adjusted event rate was higher at 7.9%, but there were still no outlier hospitals identified.
Using the broadened population definition (LRIA) and including 30-day ED revisits as an outcome, we analyzed a total of 8402 hospitalizations from 190 hospitals. The mean risk-adjusted event rate was 6.8%, but there were still no outlier hospitals identified.
In our final iteration, we merged 3 years of hospital data (2012-2014) using the broader population definition (LRIA) and including 30-day ED revisits as an outcome. This resulted in 27,873 admissions from 239 hospitals for this analysis, with a mean of 28 eligible hospitalizations per hospital. The mean risk-adjusted event rate was 6.7%, and this approach identified 2 high-performing (risk-adjusted rates: 3.6-5.3) and 7 low-performing hospitals (risk-adjusted rates: 10.1-15.9).
Table 2 presents the demographics of children included in this analysis. Children who had readmissions/revisits were younger, more likely to be white, less likely to have private insurance, and more likely to have a greater number of chronic conditions compared to children without readmissions/revisits.
Secondary Outcome: Hospital Costs
In the analysis of hospital-level costs, we found only 1 outlier high-cost hospital. There was a 20% probability of a hospital respiratory admission costing ≥$40,000 at this hospital. We found no overall relationship between hospital 30-day respiratory readmission rate and hospital costs (Figure 1). However, the hospitals that were outliers for low readmission rates also had low probabilities of excessive hospital costs (3% probability of costs >$40,000; Figure 2).
DISCUSSION
We used a nationally endorsed pediatric quality measure to evaluate hospital performance, defined as 30-day readmission rates for children with respiratory illness. We examined all-payer data from California, which is the most populous state in the country and home to 1 in 8 American children. In this large California dataset, we were unable to identify meaningful variation in hospital performance due to low hospital volumes and event rates. However, when we broadened the measure definition, we were able to identify performance variation. Our findings underscore the importance of testing and potentially modifying existing quality measures in order to more accurately capture the quality of care delivered at hospitals with lower volumes of pediatric patients.21
Our underlying assumption, in light of these prior studies, was that increasing the eligible sample in each hospital by combining respiratory diseases and by using an all-payer claims database rather than a Medicaid-only database would increase the number of detectable outlier hospitals. However, we found that these approaches did not ameliorate the limitations of small volumes. Only through aggregating data over 3 years was it possible to identify any outliers, and this approach identified only 3% of hospitals as outliers. Hence, our analysis reinforces concerns raised by several prior analyses4-7 regarding the limited ability of current pediatric readmission measures to detect meaningful, actionable differences in performance across all types of hospitals (including general/nonchildren’s hospitals). This issue is of particular concern for common pediatric conditions like respiratory illnesses, for which >70% of hospitalizations occur in general hospitals.11
Developers and utilizers of pediatric quality metrics should consider strategies for identifying meaningful, actionable variation in pediatric quality of care at general hospitals. These strategies might include our approach of combining several years of hospital data in order to reach adequate volumes for measuring performance. The potential downside to this approach is performance lag—specifically, hospitals implementing quality improvement readmissions programs may not see changes in their performance for a year or two on a measure aggregating 3 years of data. Alternatively, it is possible that the measure might be used more appropriately across a larger group of hospitals, either to assess performance for multihospital accountable care organization (ACO), or to assess performance for a service area or county. An aggregated group of hospitals would increase the eligible patient volume and, if there is an ACO relationship established, coordinated interventions could be implemented across the hospitals.
We examined the 30-day readmission rate because it is the current standard used by CMS and all NQF-endorsed readmission measures.22,23 Another potential approach is to analyze the 7- or 15-day readmission rate. However, these rates may be similarly limited in identifying hospital performance due to low volumes and event rates. An analysis by Wallace et al. of preventable readmissions to a tertiary children’s hospital found that, while many occurred within 7 days or 15 days, 27% occurred after 7 days and 22%, after 15.24 However, an analysis of several adult 30-day readmission measures used by CMS found that the contribution of hospital-level quality to the readmission rate (measured by intracluster correlation coefficient) reached a nadir at 7 days, which suggests that most readmissions after the seventh day postdischarge were explained by community- and household-level factors beyond hospitals’ control.22 Hence, though 7- or 15-day readmission rates may better represent preventable outcomes under the hospital’s control, the lower event rates and low hospital volumes likely similarly limit the feasibility of their use for performance measurement.
Pediatric quality measures are additionally intended to drive improvements in the value of pediatric care, defined as quality relative to costs.25 In order to better understand the relationship of hospital performance across both the domains of readmissions (quality) and costs, we examined hospital-level costs for care of pediatric respiratory illnesses. We found no overall relationship between hospital readmission rates and costs; however, we found 2 hospitals in California that had significantly lower readmission rates as well as low costs. Close examination of hospitals such as these, which demonstrate exceptional performance in quality and costs, may promote the discovery and dissemination of strategies to improve the value of pediatric care.12
Our study had several limitations. First, the OSHPD database lacked detailed clinical variables to correct for additional case-mix differences between hospitals. However, we used the approach of case-mix adjustment outlined by an NQF-endorsed national quality metric.8 Secondly, since our data were limited to a single state, analyses of other databases may have yielded different results. However, prior analyses using other multistate databases reported similar limitations,5,6 likely due to the limitations of patient volume that are generalizable to settings outside of California. In addition, our cost analysis was performed using cost-to-charge ratios that represent total annual expenses/revenue for the whole hospital.16 These ratios may not be reflective of the specific services provided for children in our analysis; however, service-specific costs were not available, and cost-to-charge ratios are commonly used to report costs.
CONCLUSION
The ability of a nationally-endorsed pediatric respiratory readmissions measure to meaningfully identify variation in hospital performance is limited. General hospitals, which provide the majority of pediatric care for common conditions such as LRI, likely cannot be accurately evaluated using national pediatric quality metrics as they are currently designed. Modifying measures in order to increase hospital-level pediatric patient volumes may facilitate more meaningful evaluation of the quality of pediatric care in general hospitals and identification of exceptional hospitals for understanding best practices in pediatric inpatient care.
Disclosures
Regina Lam consulted for Proximity Health doing market research during the course of developing this manuscript, but this work did not involve any content related to quality metrics, and this entity did not play any role in the development of this manuscript. The remaining authors have no conflicts of interest relevant to this article to disclose.
Funding
Supported by the Agency for Healthcare Research and Quality (K08 HS24592 to SVK and U18HS25297 to MDC and NSB) and the National Institute of Child Health and Human Development (K23HD065836 to NSB). The funding agency played no role in the study design; the collection, analysis, and interpretation of data; the writing of the report; or the decision to submit the manuscript for publication.
Respiratory illnesses are the leading causes of pediatric hospitalizations in the United States.1 The 30-day hospital readmission rate for respiratory illnesses is being considered for implementation as a national hospital performance measure, as it may be an indicator of lower quality care (eg, poor hospital management of disease, inadequate patient/caretaker education prior to discharge). In adult populations, readmissions can be used to reliably identify variation in hospital performance and successfully drive efforts to improve the value of care.2, 3 In contrast, there are persistent concerns about using pediatric readmissions to identify variation in hospital performance, largely due to lower patient volumes.4-7 To increase the value of pediatric hospital care, it is important to develop ways to meaningfully measure quality of care and further, to better understand the relationship between measures of quality and healthcare costs.
In December 2016, the National Quality Forum (NQF) endorsed a Pediatric Lower Respiratory Infection (LRI) Readmission Measure.8 This measure was developed by the Pediatric Quality Measurement Program, through the Agency for Healthcare Research and Quality. The goal of this program was to “increase the portfolio of evidence-based, consensus pediatric quality measures available to public and private purchasers of children’s healthcare services, providers, and consumers.”9
In anticipation of the national implementation of pediatric readmission measures, we examined whether the Pediatric LRI Readmission Measure could meaningfully identify high and low performers across all types of hospitals admitting children (general hospitals and children’s hospitals) using an all-payer claims database. A recent analysis by Nakamura et al. identified high and low performers using this measure10 but limited the analysis to hospitals with >50 pediatric LRI admissions per year, an approach that excludes many general hospitals. Since general hospitals provide the majority of care for children hospitalized with respiratory infections,11 we aimed to evaluate the measure in a broadly inclusive analysis that included all hospital types. Because low patient volumes might limit use of the measure,4,6 we tested several broadened variations of the measure. We also examined the relationship between hospital performance in pediatric LRI readmissions and healthcare costs.
Our analysis is intended to inform utilizers of pediatric quality metrics and policy makers about the feasibility of using these metrics to publicly report hospital performance and/or identify exceptional hospitals for understanding best practices in pediatric inpatient care.12
METHODS
Study Design and Data Source
We conducted an observational, retrospective cohort analysis using the 2012-2014 California Office of Statewide Health Planning and Development (OSHPD) nonpublic inpatient and emergency department databases.13 The OSHPD databases are compiled annually through mandatory reporting by all licensed nonfederal hospitals in California. The databases contain demographic (eg, age, gender) and utilization data (eg, charges) and can track readmissions to hospitals other than the index hospital. The databases capture administrative claims from approximately 450 hospitals, composed of 16 million inpatients, emergency department patients, and ambulatory surgery patients annually. Data quality is monitored through the California OSHPD.
Study Population
Our study included children aged ≤18 years with LRI, defined using the NQF Pediatric LRI Readmissions Measure: a primary diagnosis of bronchiolitis, influenza, or pneumonia, or a secondary diagnosis of bronchiolitis, influenza, or pneumonia, with a primary diagnosis of asthma, respiratory failure, sepsis, or bacteremia.8 International classification of Diseases, 9th edition (ICD-9) diagnostic codes used are in Appendix 1.
Per the NQF measure specifications,8 records were excluded if they were from hospitals with <80% of records complete with core elements (unique patient identifier, admission date, end-of-service date, and ICD-9 primary diagnosis code). In addition, records were excluded for the following reasons: (1) individual record missing core elements, (2) discharge disposition “death,” (3) 30-day follow-up data not available, (4) primary “newborn” or mental health diagnosis, or (5) primary ICD-9 procedure code for a planned procedure or chemotherapy.
Patient characteristics for hospital admissions with and without 30-day readmissions or 30-day emergency department (ED) revisits were summarized. For the continuous variable age, mean and standard deviation for each group were calculated. For categorical variables (sex, race, payer, and number of chronic conditions), numbers and proportions were determined. Univariate tests of comparison were carried out using the Student’s t test for age and chi-square tests for all categorical variables. Categories of payer with small values were combined for ease of description (categories combined into “other:” workers’ compensation, county indigent programs, other government, other indigent, self-pay, other payer). We identified chronic conditions using the Agency for Healthcare Research and Quality Chronic Condition Indicator (CCI) system, which classifies ICD-9-CM diagnosis codes as chronic or acute and places each code into 1 of 18 mutually exclusive categories (organ systems, disease categories, or other categories). The case-mix adjustment model incorporates a binary variable for each CCI category (0-1, 2, 3, or >4 chronic conditions) per the NQF measure specifications.8 This study was approved by the University of California, San Francisco Institutional Review Board.
Outcomes
Our primary outcome was the hospital-level rate of 30-day readmission after hospital discharge, consistent with the NQF measure.8 We identified outlier hospitals for 30-day readmission rate using the Centers for Medicare and Medicaid Services (CMS) methodology, which defines outlier hospitals as those for whom adjusted readmission rate confidence intervals do not overlap with the overall group mean rate.5, 14
We also determined the hospital-level average cost per index hospitalization (not including costs of readmissions). Since costs of care often differ substantially from charges,15 costs were calculated using cost-to-charge ratios for each hospital (annual total operating expenses/total gross patient revenue, as reported to the OSHPD).16 Costs were subdivided into categories representing $5,000 increments and a top category of >$40,000. Outlier hospitals for costs were defined as those for whom the cost random effect was either greater than the third quartile of the distribution of values by more than 1.5 times the interquartile range or less than the first quartile of the distribution of values by more than 1.5 times the interquartile range.17
ANALYSIS
Primary Analysis
For our primary analysis of 30-day hospital readmission rates, we used hierarchical logistic regression models with hospitals as random effects, adjusting for patient age, sex, and the presence and number of body systems affected by chronic conditions.8 These 4 patient characteristics were selected by the NQF measure developers “because distributions of these characteristics vary across hospitals, and although they are associated with readmission risk, they are independent of hospital quality of care.”10
Because the Centers for Medicare and Medicaid Services (CMS) are in the process of selecting pediatric quality measures for meaningful use reporting,18 we utilized CMS hospital readmissions methodology to calculate risk-adjusted rates and identify outlier hospitals. The CMS modeling strategy stabilizes performance estimates for low-volume hospitals and avoids penalizing these hospitals for high readmission rates that may be due to chance (random effects logistic model to obtain best linear unbiased predictions). This is particularly important in pediatrics, given the low pediatric volumes in many hospitals admitting children.4,19 We then identified outlier hospitals for the 30-day readmission rate using CMS methodology (hospital’s adjusted readmission rate confidence interval does not overlap the overall group mean rate).5, 4 CMS uses this approach for public reporting on HospitalCompare.20
Sensitivity Analyses
We tested several broadening variations of the NQF measure: (1) addition of children admitted with a primary diagnosis of asthma (without requiring LRI as a secondary diagnosis) or a secondary diagnosis of asthma exacerbation (LRIA), (2) inclusion of 30-day ED revisits as an outcome, and (3) merging of 3 years of data. These analyses were all performed using the same modeling strategy as in our primary analysis.
Secondary Outcome Analyses
Our analysis of hospital costs used costs for index admissions over 3 years (2012–2014) and included admissions for asthma. We used hierarchical regression models with hospitals as random effects, adjusting for age, gender, and the presence and number of chronic conditions. The distribution of cost values was highly skewed, so ordinal models were selected after several other modeling approaches failed (log transformation linear model, gamma model, Poisson model, zero-truncated Poisson model).
The relationship between hospital-level costs and hospital-level 30-day readmission or ED revisit rates was analyzed using Spearman’s rank correlation coefficient. Statistical analysis was performed using SAS version 9.4 software (SAS Institute; Cary, North Carolina).
RESULTS
Primary Analysis of 30-day Readmissions (per National Quality Forum Measure)
Our analysis of the 2014 OSHPD database using the specifications of the NQF Pediatric LRI Readmission Measure included a total of 5550 hospitalizations from 174 hospitals, with a mean of 12 eligible hospitalizations per hospital. The mean risk-adjusted readmission rate was 6.5% (362 readmissions). There were no hospitals that were considered outliers based on the risk-adjusted readmission rates (Table 1).
Sensitivity Analyses (Broadening Definitions of National Quality Forum Measure)
We report our testing of the broadened variations of the NQF measure in Table 1. Broadening the population to include children with asthma as a primary diagnosis and children with asthma exacerbations as a secondary diagnosis (LRIA) increased the size of our analysis to 8402 hospitalizations from 190 hospitals. The mean risk-adjusted readmission rate was 5.5%, and no outlier hospitals were identified.
Using the same inclusion criteria of the NQF measure but including 30-day ED revisits as an outcome, we analyzed a total of 5500 hospitalizations from 174 hospitals. The mean risk-adjusted event rate was higher at 7.9%, but there were still no outlier hospitals identified.
Using the broadened population definition (LRIA) and including 30-day ED revisits as an outcome, we analyzed a total of 8402 hospitalizations from 190 hospitals. The mean risk-adjusted event rate was 6.8%, but there were still no outlier hospitals identified.
In our final iteration, we merged 3 years of hospital data (2012-2014) using the broader population definition (LRIA) and including 30-day ED revisits as an outcome. This resulted in 27,873 admissions from 239 hospitals for this analysis, with a mean of 28 eligible hospitalizations per hospital. The mean risk-adjusted event rate was 6.7%, and this approach identified 2 high-performing (risk-adjusted rates: 3.6-5.3) and 7 low-performing hospitals (risk-adjusted rates: 10.1-15.9).
Table 2 presents the demographics of children included in this analysis. Children who had readmissions/revisits were younger, more likely to be white, less likely to have private insurance, and more likely to have a greater number of chronic conditions compared to children without readmissions/revisits.
Secondary Outcome: Hospital Costs
In the analysis of hospital-level costs, we found only 1 outlier high-cost hospital. There was a 20% probability of a hospital respiratory admission costing ≥$40,000 at this hospital. We found no overall relationship between hospital 30-day respiratory readmission rate and hospital costs (Figure 1). However, the hospitals that were outliers for low readmission rates also had low probabilities of excessive hospital costs (3% probability of costs >$40,000; Figure 2).
DISCUSSION
We used a nationally endorsed pediatric quality measure to evaluate hospital performance, defined as 30-day readmission rates for children with respiratory illness. We examined all-payer data from California, which is the most populous state in the country and home to 1 in 8 American children. In this large California dataset, we were unable to identify meaningful variation in hospital performance due to low hospital volumes and event rates. However, when we broadened the measure definition, we were able to identify performance variation. Our findings underscore the importance of testing and potentially modifying existing quality measures in order to more accurately capture the quality of care delivered at hospitals with lower volumes of pediatric patients.21
Our underlying assumption, in light of these prior studies, was that increasing the eligible sample in each hospital by combining respiratory diseases and by using an all-payer claims database rather than a Medicaid-only database would increase the number of detectable outlier hospitals. However, we found that these approaches did not ameliorate the limitations of small volumes. Only through aggregating data over 3 years was it possible to identify any outliers, and this approach identified only 3% of hospitals as outliers. Hence, our analysis reinforces concerns raised by several prior analyses4-7 regarding the limited ability of current pediatric readmission measures to detect meaningful, actionable differences in performance across all types of hospitals (including general/nonchildren’s hospitals). This issue is of particular concern for common pediatric conditions like respiratory illnesses, for which >70% of hospitalizations occur in general hospitals.11
Developers and utilizers of pediatric quality metrics should consider strategies for identifying meaningful, actionable variation in pediatric quality of care at general hospitals. These strategies might include our approach of combining several years of hospital data in order to reach adequate volumes for measuring performance. The potential downside to this approach is performance lag—specifically, hospitals implementing quality improvement readmissions programs may not see changes in their performance for a year or two on a measure aggregating 3 years of data. Alternatively, it is possible that the measure might be used more appropriately across a larger group of hospitals, either to assess performance for multihospital accountable care organization (ACO), or to assess performance for a service area or county. An aggregated group of hospitals would increase the eligible patient volume and, if there is an ACO relationship established, coordinated interventions could be implemented across the hospitals.
We examined the 30-day readmission rate because it is the current standard used by CMS and all NQF-endorsed readmission measures.22,23 Another potential approach is to analyze the 7- or 15-day readmission rate. However, these rates may be similarly limited in identifying hospital performance due to low volumes and event rates. An analysis by Wallace et al. of preventable readmissions to a tertiary children’s hospital found that, while many occurred within 7 days or 15 days, 27% occurred after 7 days and 22%, after 15.24 However, an analysis of several adult 30-day readmission measures used by CMS found that the contribution of hospital-level quality to the readmission rate (measured by intracluster correlation coefficient) reached a nadir at 7 days, which suggests that most readmissions after the seventh day postdischarge were explained by community- and household-level factors beyond hospitals’ control.22 Hence, though 7- or 15-day readmission rates may better represent preventable outcomes under the hospital’s control, the lower event rates and low hospital volumes likely similarly limit the feasibility of their use for performance measurement.
Pediatric quality measures are additionally intended to drive improvements in the value of pediatric care, defined as quality relative to costs.25 In order to better understand the relationship of hospital performance across both the domains of readmissions (quality) and costs, we examined hospital-level costs for care of pediatric respiratory illnesses. We found no overall relationship between hospital readmission rates and costs; however, we found 2 hospitals in California that had significantly lower readmission rates as well as low costs. Close examination of hospitals such as these, which demonstrate exceptional performance in quality and costs, may promote the discovery and dissemination of strategies to improve the value of pediatric care.12
Our study had several limitations. First, the OSHPD database lacked detailed clinical variables to correct for additional case-mix differences between hospitals. However, we used the approach of case-mix adjustment outlined by an NQF-endorsed national quality metric.8 Secondly, since our data were limited to a single state, analyses of other databases may have yielded different results. However, prior analyses using other multistate databases reported similar limitations,5,6 likely due to the limitations of patient volume that are generalizable to settings outside of California. In addition, our cost analysis was performed using cost-to-charge ratios that represent total annual expenses/revenue for the whole hospital.16 These ratios may not be reflective of the specific services provided for children in our analysis; however, service-specific costs were not available, and cost-to-charge ratios are commonly used to report costs.
CONCLUSION
The ability of a nationally-endorsed pediatric respiratory readmissions measure to meaningfully identify variation in hospital performance is limited. General hospitals, which provide the majority of pediatric care for common conditions such as LRI, likely cannot be accurately evaluated using national pediatric quality metrics as they are currently designed. Modifying measures in order to increase hospital-level pediatric patient volumes may facilitate more meaningful evaluation of the quality of pediatric care in general hospitals and identification of exceptional hospitals for understanding best practices in pediatric inpatient care.
Disclosures
Regina Lam consulted for Proximity Health doing market research during the course of developing this manuscript, but this work did not involve any content related to quality metrics, and this entity did not play any role in the development of this manuscript. The remaining authors have no conflicts of interest relevant to this article to disclose.
Funding
Supported by the Agency for Healthcare Research and Quality (K08 HS24592 to SVK and U18HS25297 to MDC and NSB) and the National Institute of Child Health and Human Development (K23HD065836 to NSB). The funding agency played no role in the study design; the collection, analysis, and interpretation of data; the writing of the report; or the decision to submit the manuscript for publication.
1. Agency for Healthcare Research and Quality. Overview of hospital stays for children in the United States. https://www.hcup-us.ahrq.gov/reports/statbriefs/sb187-Hospital-Stays-Children-2012.jsp. Accessed September 1, 2017; 2012. PubMed
2. Mendelson A, Kondo K, Damberg C, et al. The effects of pay-for-performance programs on health, health care use, and processes of care: A systematic review. Ann Intern Med. 2017;166(5):341-353. doi: 10.7326/M16-1881. PubMed
3. Zuckerman RB, Sheingold SH, Orav EJ, Ruhter J, Epstein AM. Readmissions, observation, and the hospital readmissions reduction program. N Engl J Med. 2016;374(16):1543-1551. doi: 10.1056/NEJMsa1513024. PubMed
4. Bardach NS, Chien AT, Dudley RA. Small numbers limit the use of the inpatient pediatric quality indicators for hospital comparison. Acad Pediatr. 2010;10(4):266-273. doi: 10.1016/j.acap.2010.04.025. PubMed
5. Bardach NS, Vittinghoff E, Asteria-Peñaloza R, et al. Measuring hospital quality using pediatric readmission and revisit rates. Pediatrics. 2013;132(3):429-436. doi: 10.1542/peds.2012-3527. PubMed
6. Berry JG, Zaslavsky AM, Toomey SL, et al. Recognizing differences in hospital quality performance for pediatric inpatient care. Pediatrics. 2015;136(2):251-262. doi: 10.1542/peds.2014-3131. PubMed
7. Hain PD, Gay JC, Berutti TW, Whitney GM, Wang W, Saville BR. Preventability of early readmissions at a children’s hospital. Pediatrics. 2013;131(1):e171-e181. doi: 10.1542/peds.2012-0820. PubMed
8. Agency for Healthcare Research and Quality. Pediatric lower respiratory infection readmission measure. https://www.ahrq.gov/sites/default/files/wysiwyg/policymakers/chipra/factsheets/chipra_1415-p008-2-ef.pdf. Accessed September 3, 2017.
9. Agency for Healthcare Research and Quality. CHIPRA Pediatric Quality Measures Program. https://archive.ahrq.gov/policymakers/chipra/pqmpback.html. Accessed October 10, 2017.
10. Nakamura MM, Zaslavsky AM, Toomey SL, et al. Pediatric readmissions After hospitalizations for lower respiratory infections. Pediatrics. 2017;140(2). doi: 10.1542/peds.2016-0938. PubMed
11. Leyenaar JK, Ralston SL, Shieh MS, Pekow PS, Mangione-Smith R, Lindenauer PK. Epidemiology of pediatric hospitalizations at general hospitals and freestanding children’s hospitals in the United States. J Hosp Med. 2016;11(11):743-749. doi: 10.1002/jhm.2624. PubMed
12. Bradley EH, Curry LA, Ramanadhan S, Rowe L, Nembhard IM, Krumholz HM. Research in action: using positive deviance to improve quality of health care. Implement Sci. 2009;4:25. doi: 10.1186/1748-5908-4-25. PubMed
13. California Office of Statewide Health Planning and Development. Data and reports. https://www.oshpd.ca.gov/HID/. Accessed September 3, 2017.
14. QualityNet. Measure methodology reports. https://www.qualitynet.org/dcs/ContentServer?c=Page&pagename=QnetPublic%2FPage%2FQnetTier4&cid=1219069855841. Accessed October 10, 2017.
15. Riley GF. Administrative and claims records as sources of health care cost data. Med Care. 2009;47(7 Suppl 1):S51-S55. doi: 10.1097/MLR.0b013e31819c95aa. PubMed
16. California Office of Statewide Health Planning and Development. Annual financial data. https://www.oshpd.ca.gov/HID/Hospital-Financial.asp. Accessed September 3, 2017.
17. Tukey J. Exploratory Data Analysis: Pearson; London, United Kingdom. 1977.
18. Centers for Medicare and Medicaid Services. Core measures. https://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/QualityMeasures/Core-Measures.html. Accessed September 1, 2017.
19. Berry JG, Toomey SL, Zaslavsky AM, et al. Pediatric readmission prevalence and variability across hospitals. JAMA. 2013;309(4):372-380. doi: 10.1001/jama.2012.188351. PubMed
20. Centers for Medicare and Medicaid Services. HospitalCompare. https://www.medicare.gov/hospitalcompare/search.html. Accessed on October 10, 2017.
21. Mangione-Smith R. The challenges of addressing pediatric quality measurement gaps. Pediatrics. 2017;139(4). doi: 10.1542/peds.2017-0174. PubMed
22. Chin DL, Bang H, Manickam RN, Romano PS. Rethinking thirty-day hospital readmissions: shorter intervals might be better indicators of quality of care. Health Aff (Millwood). 2016;35(10):1867-1875. doi: 10.1377/hlthaff.2016.0205. PubMed
23. National Quality Forum. Measures, reports, and tools. http://www.qualityforum.org/Measures_Reports_Tools.aspx. Accessed March 1, 2018.
24. Wallace SS, Keller SL, Falco CN, et al. An examination of physician-, caregiver-, and disease-related factors associated With readmission From a pediatric hospital medicine service. Hosp Pediatr. 2015;5(11):566-573. doi: 10.1542/hpeds.2015-0015. PubMed
25. Porter ME. What is value in health care? N Engl J Med. 2010;363(26):2477-2481. doi: 10.1056/NEJMp1011024. PubMed
1. Agency for Healthcare Research and Quality. Overview of hospital stays for children in the United States. https://www.hcup-us.ahrq.gov/reports/statbriefs/sb187-Hospital-Stays-Children-2012.jsp. Accessed September 1, 2017; 2012. PubMed
2. Mendelson A, Kondo K, Damberg C, et al. The effects of pay-for-performance programs on health, health care use, and processes of care: A systematic review. Ann Intern Med. 2017;166(5):341-353. doi: 10.7326/M16-1881. PubMed
3. Zuckerman RB, Sheingold SH, Orav EJ, Ruhter J, Epstein AM. Readmissions, observation, and the hospital readmissions reduction program. N Engl J Med. 2016;374(16):1543-1551. doi: 10.1056/NEJMsa1513024. PubMed
4. Bardach NS, Chien AT, Dudley RA. Small numbers limit the use of the inpatient pediatric quality indicators for hospital comparison. Acad Pediatr. 2010;10(4):266-273. doi: 10.1016/j.acap.2010.04.025. PubMed
5. Bardach NS, Vittinghoff E, Asteria-Peñaloza R, et al. Measuring hospital quality using pediatric readmission and revisit rates. Pediatrics. 2013;132(3):429-436. doi: 10.1542/peds.2012-3527. PubMed
6. Berry JG, Zaslavsky AM, Toomey SL, et al. Recognizing differences in hospital quality performance for pediatric inpatient care. Pediatrics. 2015;136(2):251-262. doi: 10.1542/peds.2014-3131. PubMed
7. Hain PD, Gay JC, Berutti TW, Whitney GM, Wang W, Saville BR. Preventability of early readmissions at a children’s hospital. Pediatrics. 2013;131(1):e171-e181. doi: 10.1542/peds.2012-0820. PubMed
8. Agency for Healthcare Research and Quality. Pediatric lower respiratory infection readmission measure. https://www.ahrq.gov/sites/default/files/wysiwyg/policymakers/chipra/factsheets/chipra_1415-p008-2-ef.pdf. Accessed September 3, 2017.
9. Agency for Healthcare Research and Quality. CHIPRA Pediatric Quality Measures Program. https://archive.ahrq.gov/policymakers/chipra/pqmpback.html. Accessed October 10, 2017.
10. Nakamura MM, Zaslavsky AM, Toomey SL, et al. Pediatric readmissions After hospitalizations for lower respiratory infections. Pediatrics. 2017;140(2). doi: 10.1542/peds.2016-0938. PubMed
11. Leyenaar JK, Ralston SL, Shieh MS, Pekow PS, Mangione-Smith R, Lindenauer PK. Epidemiology of pediatric hospitalizations at general hospitals and freestanding children’s hospitals in the United States. J Hosp Med. 2016;11(11):743-749. doi: 10.1002/jhm.2624. PubMed
12. Bradley EH, Curry LA, Ramanadhan S, Rowe L, Nembhard IM, Krumholz HM. Research in action: using positive deviance to improve quality of health care. Implement Sci. 2009;4:25. doi: 10.1186/1748-5908-4-25. PubMed
13. California Office of Statewide Health Planning and Development. Data and reports. https://www.oshpd.ca.gov/HID/. Accessed September 3, 2017.
14. QualityNet. Measure methodology reports. https://www.qualitynet.org/dcs/ContentServer?c=Page&pagename=QnetPublic%2FPage%2FQnetTier4&cid=1219069855841. Accessed October 10, 2017.
15. Riley GF. Administrative and claims records as sources of health care cost data. Med Care. 2009;47(7 Suppl 1):S51-S55. doi: 10.1097/MLR.0b013e31819c95aa. PubMed
16. California Office of Statewide Health Planning and Development. Annual financial data. https://www.oshpd.ca.gov/HID/Hospital-Financial.asp. Accessed September 3, 2017.
17. Tukey J. Exploratory Data Analysis: Pearson; London, United Kingdom. 1977.
18. Centers for Medicare and Medicaid Services. Core measures. https://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/QualityMeasures/Core-Measures.html. Accessed September 1, 2017.
19. Berry JG, Toomey SL, Zaslavsky AM, et al. Pediatric readmission prevalence and variability across hospitals. JAMA. 2013;309(4):372-380. doi: 10.1001/jama.2012.188351. PubMed
20. Centers for Medicare and Medicaid Services. HospitalCompare. https://www.medicare.gov/hospitalcompare/search.html. Accessed on October 10, 2017.
21. Mangione-Smith R. The challenges of addressing pediatric quality measurement gaps. Pediatrics. 2017;139(4). doi: 10.1542/peds.2017-0174. PubMed
22. Chin DL, Bang H, Manickam RN, Romano PS. Rethinking thirty-day hospital readmissions: shorter intervals might be better indicators of quality of care. Health Aff (Millwood). 2016;35(10):1867-1875. doi: 10.1377/hlthaff.2016.0205. PubMed
23. National Quality Forum. Measures, reports, and tools. http://www.qualityforum.org/Measures_Reports_Tools.aspx. Accessed March 1, 2018.
24. Wallace SS, Keller SL, Falco CN, et al. An examination of physician-, caregiver-, and disease-related factors associated With readmission From a pediatric hospital medicine service. Hosp Pediatr. 2015;5(11):566-573. doi: 10.1542/hpeds.2015-0015. PubMed
25. Porter ME. What is value in health care? N Engl J Med. 2010;363(26):2477-2481. doi: 10.1056/NEJMp1011024. PubMed
© 2018 Society of Hospital Medicine
The Adoption of an Online Journal Club to Improve Research Dissemination and Social Media Engagement Among Hospitalists
Clinicians, educators, and medical journals are increasingly using the social media outlet, Twitter, as a medium to connect and engage with their colleagues. In particular, online journal clubs have created a space for the timely discussion of research, creation of online communities, and dissemination of research.
Social media-based journal clubs are thought to be one way in which journals can leverage the power of social networks so that researchers can engage with a diverse range of end users4 (including bedside clinicians, administrators, and patients). Several examples of these models exist. For example, #GeriMedJC acts as a complimentary, synchronous chat that takes place at the same time as a live, in-person journal club. #NephJC offers multiple 1-hour chats per month and provides an in-depth summary and analysis of each article, while #UroJC is an asynchronous discussion that takes place over 48 hours. Few data exist to describe whether any of these programs produce measurable improvements in indicators of engagement or dissemination of results.
In 2015, the Journal of Hospital Medicine (JHM) began producing a Twitter-based journal club as a means to connect and engage the Hospital Medicine community and allow for discussion and rapid exchange of information and opinions around a specific clinical topic. This study aims to describe the implementation of the first Journal-sponsored, Twitter-based online journal club and ascertain its impact on both Twitter and journal metrics.
METHODS
#JHMChat was launched in October 2015, and was initially held every 2-3 months until January 2017, when chats began to take place monthly. Each 1-hour chat focused on a recently published article in JHM, was moderated by a JHM social media editor (C.M.W., V.M.A.), and included at least 1 study author or guest expert. Articles were chosen by the social media editors based on the following criteria: (1) attractiveness to possible participants, (2) providing topic variety within the journal club series, and (3) sustainability and topic conduciveness to the online chat model. Chats were held at 9 PM EST in order to engage hospitalists across all US time zones and on different days to accommodate authors’ availability. All sessions were framed by 3-4 questions intended to encourage discussion and presented to chat participants at spaced intervals so as to stimulate a current of responses.
Chats were promoted by way of the JHM (@JHospMedicine, 3400 followers) and Society of Hospital Medicine (SHM; @SHMLive, 5800 followers) Twitter feeds beginning 1 month prior to each session. Visual Abstracts5,6 were used to publicize the sessions, also via Twitter, starting in February 2017.
Continuing Medical Education (CME) credits were offered through the SHM to registered participants, starting in July 2016.7 All sessions were cosponsored by the American Board of Internal Medicine (ABIM) Foundation and the Costs of Care Organization, a non-profit organization aimed at improving healthcare value.
Twitter Metrics
After each session, the following Twitter-based engagement metrics were obtained using the Symplur© Healthcare Hashtag project;8 total number of participants and tweets, tweets/participant, and total impressions (calculated as the number of tweets from each participant multiplied by the number of followers that participant currently had then summed up for all participants). Simply put, impressions can also be thought of as the number of times a single Tweet makes it into someone else’s Twitter feed. So as to avoid artificially inflated metrics, all were obtained 2 hours after the end of the journal club. Participants were defined as anyone who posted an original tweet or retweeted during the session and were encouraged to tag their tweets with the hashtag #JHMChat for post-discussion indexing and measurement. Because authors’ or guests’ popularity on Twitter may influence participation rates, we also assessed the number of followers for each participating author. Spearman’s rank correlation was calculated (Microsoft ExcelTM) where appropriate.
Altmetrics and Page Views
As a means to measure exposure and dissemination external to Twitter, we assessed the change (“Delta”) in the each article’s Altmetric score9, a digital-based metric that quantifies the attention received by a scientific publication on various online platforms including news, blogs, and social media. Delta Altmetric scores were calculated as the difference between the scores on the day of the session and 2 weeks after the respective session, with higher scores indicating greater global online discussion. By measuring the Altmetric score on the day of the discussion, we established a baseline score for comparison purposes. Additionally, this allowed us to better attribute any changes that may have occurred to the discussion itself.
Additionally, using information provided by the journal publisher (John Wiley & Sons Publishing) in 2016, we assessed the effect of #JHMChat on the number of article page views on the JHM website relative to the release of the electronic Table of Contents (eTOC). The eTOC release was chosen as it is historically associated with a high number of page views. In order to isolate the effect of #JHMChat, we only reviewed months in which #JHMChat was not held within 3 days of the eTOC release. Because JHM changed publishers in January 2017, we only assessed page view data on 2016 sessions, as the new publisher lacked enhanced search optimization to obtain these data.
Thematic Analysis
In addition to the above measurements, a thematic analysis of each article was conducted to assess any common themes that would influence our chosen metrics. Themes were assessed and ascribed by one author (C.M.W.) and verified by another (V.M.A.).
Participant and Author Experience
To assess the participant experience, responses to a post-session CME questionnaire that assessed (1) overall quality, (2) comprehensiveness of the discussion, (3) whether the participant would recommend the chat to a colleague, and (4) whether participation would lead to practice-changing measures were reviewed. Registration of each session for CME was also quantified. Finally, each participating author was asked to fill out an electronic post-chat survey (SurveyMonkey®) meant to assess the authors’ experience with the journal club (Appendix).
RESULTS
Between October 2015 and November 2017, a total of 15 sessions were held with a mean of 2.17 (±0.583) million impressions/session, 499 (±129) total tweets/session, and 73 (±24) participants/session (compared to a range of 21-58 participants/session from other online journal clubs, where reported) with 7.2 (±2.0) tweets/participant (Table 1). The total number of participants for all sessions was 1096. Participating authors had on average 1389 (±2714) followers, ranging from a low of 37 to a high of 10,376 (Appendix). No correlation between author following and number of participants (r = 0.19), impressions (r = 0.05), or change in Altmetric score (r = 0.17) was seen.
Thematic analysis revealed 3 predominant themes among the chosen articles: Value-based care (VBC), Quality and Patient Safety (QPS), and Medical Education (ME). Articles focused on VBC had the greatest number of impressions (mean ±SD: 2.61 ± 0.55 million) and participants (mean ±SD: 90 ± 12), while QPS articles had the fewest impressions (mean ±SD: 1.71 ± 0.59 million) and number of participants (mean ±SD: 47 ± 16). The mean increase in the Altmetric score among all discussed articles was 14 (±12), from an average baseline of 30 (±37). Medical Education-themed articles appeared to garner the greatest increase in Altmetric scores, averaging an increase of 32 points, compared with an average baseline score of 31 (±32). In contrast, VBC and QPS articles averaged an increase of 8.6 and 8.4 points, from average baselines of 55 (±53) and 17 (±13), respectively. A 2-month analysis of JHM articles not included in these discussions, in which Altmetric scores were measured in the same way as those from the discussion, revealed a baseline Altmetric score of 27 (±24) with an average increase of 8 (±6) 2 weeks following the chat.
Four articles met the inclusion criteria for page view analysis and suggested that article page views increased to similar levels as the eTOC release (mean: 2668 vs. 2998, respectively; P = .35) (Figure). These increases equate to a 33% and 50% increase in average daily page views (2002) for the chat and eTOC release, respectively.
Ninety-three percent (14/15) of the participating authors responded to the post-discussion survey. All strongly agreed (5/5 on a Likert scale) that the venue allowed for an in-depth discussion about processes and challenges in conducting the study and allowed for greater dissemination and visibility of their work (5/5). Additionally, authors agreed that the journal club was a valuable experience for themselves (4.88/5) and other practitioners (4.88/5). Most agreed that the journal club allowed them to share their work with a different group of participants than usual (4.75/5) and that the experience changed how they would discuss their manuscripts in the future (4.75/5.0); Table 2).
DISCUSSION
The Twitter-based journal club #JHMChat appears to increase social media awareness and dissemination of journal articles and was considered a useful engagement platform by both authors and participants.
Articles with a focus on VBC and ME had the greatest impact on dissemination metrics, particularly, total impressions and Altmetric scores, respectively. Given the strong presence and interest in these topics within Twitter and social media, these findings are not surprising.10,11 For example, over the past several years, the VBC movement has taken shape and grown alongside the expansion of social media, thus giving a space for this community to grow and engage. Of note, the cosponsorship relationship with the ABIM Foundation (which works closely with the Choosing Wisely™ campaign) and the Costs of Care Organization could have influenced the participation and dissemination rates of VBC articles. Medical education articles were also popular and appeared to have increased uptake after chats, based on their Altmetric scores. This may be explained by the fact that medical educators have long utilized social media as a means to connect and engage within their community.12–14 It is also possible that the use of Twitter by trainees (residents, students) may have driven some of the dissemination of ME articles, as this group may not be regular subscribers to JHM.
Online journal clubs offer distinct advantages over traditional in-person journal clubs. First, online journal clubs allow for increased connectivity among online communities, bringing together participants from different geographic areas with diverse training and clinical experiences. Subsequently, this allows for the rapid exchange of both personal and organizational approaches to the topic of discussion.15–17 Second, online journal clubs allow for continual access to the discussion material. For example, while the metrics used in this study only assessed active, synchronous participation, anecdotal evidence and feedback to the authors suggests that many individuals passively engaged by following along or reviewed the chat feed post hoc at their convenience. This asynchronous access is a quality not found in more traditional journal club formats. Finally, because online journal clubs commonly operate with a flattened hierarchy,18 they can break down access barriers to both the researchers who performed the study and thought leaders who commonly participate.17
Several insightful lessons were gleaned in the production and management of this online journal club. On the implementation side, promotion, preparation, and continued organization of an online journal club requires a fair amount of work. In this case, the required time and resources were provided by 2 social media editors in addition to administrative assistance from the SHM. The high attrition rate of online journal clubs over the years attests to these difficulties.24 Additionally, finding incentives to attract and sustain participation can be difficult, as we noted that neither CME nor author popularity (based on their Twitter following) appeared to influence engagement metrics (number of participants, total tweets, and tweets/participant). We also found that partnering with other journal club communities, in particular #NephJC, lead to greater participation rates and impressions. Thus, leveraging connections and topics that span clinical domains may be one way to improve and broaden engagement within these forums. Finally, feedback from participants revealed that the timing of the journal club and the inability to have in-depth discussions, a characteristic commonly associated with traditional journal clubs, were problematic.
This study has several limitations. First, the metrics used to assess social media engagement and dissemination can be easily skewed. For instance, the activity of 1 or 2 individuals with large followings can dramatically influence the number of impressions, giving a falsely elevated sense of broad dissemination. Conversely, there may have been some participants who did not use the #JHMChat hashtag, thus leading to an underestimation in these metrics. Second, while we report total impressions as a measure of dissemination, this metric represents possible interactions and does not guarantee interaction or visualization of that tweet. Additionally, we were unable to characterize our participants and their participation rates over time, as this information is not made available through Symplur© analytics. Third, our page view assessment was limited to 2016 sessions only; therefore, these data may not be an accurate reflection of the impact of #JHMChat on this metric. Fourth, given the marginal response rate to our CME questionnaire, a selection bias could have occurred. Finally, whether social media discussions such as online journal clubs act as leading indicators for future citations remains unclear, as some research has shown an association between increased Altmetric scores and increased citation rates,19-21 while others have not.22,23 Our study was not equipped to assess this correlation.
CONCLUSION
Online journal clubs create new opportunities to connect, engage, and disseminate medical research. These developing forums provide journal editors, researchers, patients, and clinicians with a means to connect and discuss research in ways that were not previously possible. In order to continue to evolve and grow, future research in online journal clubs should explore the downstream effects on citation rates, clinical uptake, and participant knowledge after the sessions.
Acknowledgments
The authors would like to thank Felicia Steele for her assistance in organizing and promoting the chats. Additionally, the authors would like to thank all the authors, guests and participants who took time from their families, work, and daily lives to participate in these activities. Your time and presence were truly appreciated.
Disclosures
The authors of this article operate as the Social Media Editors (C.M.W., V.M.A.) and the Editor-in-Chief (A.A.) for the Journal of Hospital Medicine. Dr. Wray had full access to all the data in the project, takes responsibility for the integrity of the data, and the accuracy of the data analysis.
1. Topf JM, Sparks MA, Phelan PJ, et al. The evolution of the journal club: from osler to twitter. Am J Kidney Dis Off J Natl Kidney Found. 2017;69(6):827-836. doi: 10.1053/j.ajkd.2016.12.012. PubMed
2. Thangasamy IA, Leveridge M, Davies BJ, Finelli A, Stork B, Woo HH. International urology journal club via Twitter: 12-month experience. Eur Urol. 2014;66(1):112-117. doi: 10.1016/j.eururo.2014.01.034. PubMed
3. Gardhouse AI, Budd L, Yang SYC, Wong CL. #GeriMedJC: the Twitter complement to the traditional-format geriatric medicine journal club. J Am Geriatr Soc. 2017;65(6):1347-1351. doi: 10.1111/jgs.14920. PubMed
4. Duque L. How academics and researchers can get more out of social media. Harvard Business Review. https://hbr.org/2016/06/how-academics-and-researchers-can-get-more-out-of-social-media. Accessed November 9, 2017.
5. Wray CM, Arora VM. #VisualAbstract: a revolution in communicating science? Ann Surg. 2017;266(6):e49-e50. doi: 10.1097/SLA.0000000000002339. PubMed
6. Ibrahim AM. Seeing is believing: using visual abstracts to disseminate scientific research. Am J Gastroenterol. 2017:ajg2017268. doi: 10.1038/ajg.2017.268. PubMed
7. #JHMChat. http://shm.hospitalmedicine.org/acton/media/25526/jhmchat. Accessed November 9, 2017.
8. #JHMChat-healthcare social media. Symplur. https://www.symplur.com/search/%23JHMChat. Accessed November 9, 2017.
9. Altmetric. Altmetric. https://www.altmetric.com/. Accessed November 9, 2017.
10. value-based healthcare | Symplur. https://www.symplur.com/topic/value-based-healthcare/. Accessed November 17, 2017.
11. medical education | Symplur. https://www.symplur.com/topic/medical-education/. Accessed November 17, 2017.
12. Sterling M, Leung P, Wright D, Bishop TF. The use of social media in graduate medical education: a systematic review. Acad Med. 2017;92(7):1043. doi: 10.1097/ACM.0000000000001617. PubMed
13. Davis WM, Ho K, Last J. Advancing social media in medical education. CMAJ Can Med Assoc J. 2015;187(8):549-550. doi: 10.1503/cmaj.141417. PubMed
14. Hillman T, Sherbino J. Social media in medical education: a new pedagogical paradigm? Postgrad Med J. 2015;91(1080):544-545. doi: 10.1136/postgradmedj-2015-133686. PubMed
15. Gerds AT, Chan T. Social media in hematology in 2017: dystopia, utopia, or somewhere in-between? Curr Hematol Malig Rep. 2017;12(6):582-591. doi: 10.1007/s11899-017-0424-8. PubMed
16. Mehta N, Flickinger T. The times they are a-changin’: academia, social media and the JGIM Twitter Journal Club. J Gen Intern Med. 2014;29(10):1317-1318. doi: 10.1007/s11606-014-2976-9. PubMed
17. Chan T, Trueger NS, Roland D, Thoma B. Evidence-based medicine in the era of social media: scholarly engagement through participation and online interaction. CJEM. 2017:1-6. doi: 10.1017/cem.2016.407. PubMed
18. Utengen A. The flattening of healthcare: breaking down of barriers in healthcare social media-twitter visualized. https://www.symplur.com/shorts/the-flattening-of-healthcare-twitter-visualized/. Accessed November 8, 2017.
19. Thelwall M, Haustein S, Larivière V, Sugimoto CR. Do altmetrics work? Twitter and ten other social web services. PloS One. 2013;8(5):e64841. doi: 10.1371/journal.pone.0064841. PubMed
20. Peoples BK, Midway SR, Sackett D, Lynch A, Cooney PB. Twitter predicts citation rates of ecological research. PloS One. 2016;11(11):e0166570. doi: 10.1371/journal.pone.0166570. PubMed
21. Eysenbach G. Can tweets predict citations? Metrics of social impact based on Twitter and correlation with traditional metrics of scientific impact. J Med Internet Res. 2011;13(4):e123. doi: 10.2196/jmir.2012. PubMed
22. Winter JCF de. The relationship between tweets, citations, and article views for PLOS ONE articles. Scientometrics. 2015;102(2):1773-1779. doi: 10.1007/s11192-014-1445-x.
23. Haustein S, Peters I, Sugimoto CR, Thelwall M, Larivière V. Tweeting biomedicine: an analysis of tweets and citations in the biomedical literature. J Assoc Inf Sci Technol. 2014;65(4):656-669. doi: 10.1002/asi.23101.
24. Journal club. In: Wikipedia. 2017. https://en.wikipedia.org/w/index.php?title=Journal_club&oldid=807037773. Accessed November 9, 2017.
Clinicians, educators, and medical journals are increasingly using the social media outlet, Twitter, as a medium to connect and engage with their colleagues. In particular, online journal clubs have created a space for the timely discussion of research, creation of online communities, and dissemination of research.
Social media-based journal clubs are thought to be one way in which journals can leverage the power of social networks so that researchers can engage with a diverse range of end users4 (including bedside clinicians, administrators, and patients). Several examples of these models exist. For example, #GeriMedJC acts as a complimentary, synchronous chat that takes place at the same time as a live, in-person journal club. #NephJC offers multiple 1-hour chats per month and provides an in-depth summary and analysis of each article, while #UroJC is an asynchronous discussion that takes place over 48 hours. Few data exist to describe whether any of these programs produce measurable improvements in indicators of engagement or dissemination of results.
In 2015, the Journal of Hospital Medicine (JHM) began producing a Twitter-based journal club as a means to connect and engage the Hospital Medicine community and allow for discussion and rapid exchange of information and opinions around a specific clinical topic. This study aims to describe the implementation of the first Journal-sponsored, Twitter-based online journal club and ascertain its impact on both Twitter and journal metrics.
METHODS
#JHMChat was launched in October 2015, and was initially held every 2-3 months until January 2017, when chats began to take place monthly. Each 1-hour chat focused on a recently published article in JHM, was moderated by a JHM social media editor (C.M.W., V.M.A.), and included at least 1 study author or guest expert. Articles were chosen by the social media editors based on the following criteria: (1) attractiveness to possible participants, (2) providing topic variety within the journal club series, and (3) sustainability and topic conduciveness to the online chat model. Chats were held at 9 PM EST in order to engage hospitalists across all US time zones and on different days to accommodate authors’ availability. All sessions were framed by 3-4 questions intended to encourage discussion and presented to chat participants at spaced intervals so as to stimulate a current of responses.
Chats were promoted by way of the JHM (@JHospMedicine, 3400 followers) and Society of Hospital Medicine (SHM; @SHMLive, 5800 followers) Twitter feeds beginning 1 month prior to each session. Visual Abstracts5,6 were used to publicize the sessions, also via Twitter, starting in February 2017.
Continuing Medical Education (CME) credits were offered through the SHM to registered participants, starting in July 2016.7 All sessions were cosponsored by the American Board of Internal Medicine (ABIM) Foundation and the Costs of Care Organization, a non-profit organization aimed at improving healthcare value.
Twitter Metrics
After each session, the following Twitter-based engagement metrics were obtained using the Symplur© Healthcare Hashtag project;8 total number of participants and tweets, tweets/participant, and total impressions (calculated as the number of tweets from each participant multiplied by the number of followers that participant currently had then summed up for all participants). Simply put, impressions can also be thought of as the number of times a single Tweet makes it into someone else’s Twitter feed. So as to avoid artificially inflated metrics, all were obtained 2 hours after the end of the journal club. Participants were defined as anyone who posted an original tweet or retweeted during the session and were encouraged to tag their tweets with the hashtag #JHMChat for post-discussion indexing and measurement. Because authors’ or guests’ popularity on Twitter may influence participation rates, we also assessed the number of followers for each participating author. Spearman’s rank correlation was calculated (Microsoft ExcelTM) where appropriate.
Altmetrics and Page Views
As a means to measure exposure and dissemination external to Twitter, we assessed the change (“Delta”) in the each article’s Altmetric score9, a digital-based metric that quantifies the attention received by a scientific publication on various online platforms including news, blogs, and social media. Delta Altmetric scores were calculated as the difference between the scores on the day of the session and 2 weeks after the respective session, with higher scores indicating greater global online discussion. By measuring the Altmetric score on the day of the discussion, we established a baseline score for comparison purposes. Additionally, this allowed us to better attribute any changes that may have occurred to the discussion itself.
Additionally, using information provided by the journal publisher (John Wiley & Sons Publishing) in 2016, we assessed the effect of #JHMChat on the number of article page views on the JHM website relative to the release of the electronic Table of Contents (eTOC). The eTOC release was chosen as it is historically associated with a high number of page views. In order to isolate the effect of #JHMChat, we only reviewed months in which #JHMChat was not held within 3 days of the eTOC release. Because JHM changed publishers in January 2017, we only assessed page view data on 2016 sessions, as the new publisher lacked enhanced search optimization to obtain these data.
Thematic Analysis
In addition to the above measurements, a thematic analysis of each article was conducted to assess any common themes that would influence our chosen metrics. Themes were assessed and ascribed by one author (C.M.W.) and verified by another (V.M.A.).
Participant and Author Experience
To assess the participant experience, responses to a post-session CME questionnaire that assessed (1) overall quality, (2) comprehensiveness of the discussion, (3) whether the participant would recommend the chat to a colleague, and (4) whether participation would lead to practice-changing measures were reviewed. Registration of each session for CME was also quantified. Finally, each participating author was asked to fill out an electronic post-chat survey (SurveyMonkey®) meant to assess the authors’ experience with the journal club (Appendix).
RESULTS
Between October 2015 and November 2017, a total of 15 sessions were held with a mean of 2.17 (±0.583) million impressions/session, 499 (±129) total tweets/session, and 73 (±24) participants/session (compared to a range of 21-58 participants/session from other online journal clubs, where reported) with 7.2 (±2.0) tweets/participant (Table 1). The total number of participants for all sessions was 1096. Participating authors had on average 1389 (±2714) followers, ranging from a low of 37 to a high of 10,376 (Appendix). No correlation between author following and number of participants (r = 0.19), impressions (r = 0.05), or change in Altmetric score (r = 0.17) was seen.
Thematic analysis revealed 3 predominant themes among the chosen articles: Value-based care (VBC), Quality and Patient Safety (QPS), and Medical Education (ME). Articles focused on VBC had the greatest number of impressions (mean ±SD: 2.61 ± 0.55 million) and participants (mean ±SD: 90 ± 12), while QPS articles had the fewest impressions (mean ±SD: 1.71 ± 0.59 million) and number of participants (mean ±SD: 47 ± 16). The mean increase in the Altmetric score among all discussed articles was 14 (±12), from an average baseline of 30 (±37). Medical Education-themed articles appeared to garner the greatest increase in Altmetric scores, averaging an increase of 32 points, compared with an average baseline score of 31 (±32). In contrast, VBC and QPS articles averaged an increase of 8.6 and 8.4 points, from average baselines of 55 (±53) and 17 (±13), respectively. A 2-month analysis of JHM articles not included in these discussions, in which Altmetric scores were measured in the same way as those from the discussion, revealed a baseline Altmetric score of 27 (±24) with an average increase of 8 (±6) 2 weeks following the chat.
Four articles met the inclusion criteria for page view analysis and suggested that article page views increased to similar levels as the eTOC release (mean: 2668 vs. 2998, respectively; P = .35) (Figure). These increases equate to a 33% and 50% increase in average daily page views (2002) for the chat and eTOC release, respectively.
Ninety-three percent (14/15) of the participating authors responded to the post-discussion survey. All strongly agreed (5/5 on a Likert scale) that the venue allowed for an in-depth discussion about processes and challenges in conducting the study and allowed for greater dissemination and visibility of their work (5/5). Additionally, authors agreed that the journal club was a valuable experience for themselves (4.88/5) and other practitioners (4.88/5). Most agreed that the journal club allowed them to share their work with a different group of participants than usual (4.75/5) and that the experience changed how they would discuss their manuscripts in the future (4.75/5.0); Table 2).
DISCUSSION
The Twitter-based journal club #JHMChat appears to increase social media awareness and dissemination of journal articles and was considered a useful engagement platform by both authors and participants.
Articles with a focus on VBC and ME had the greatest impact on dissemination metrics, particularly, total impressions and Altmetric scores, respectively. Given the strong presence and interest in these topics within Twitter and social media, these findings are not surprising.10,11 For example, over the past several years, the VBC movement has taken shape and grown alongside the expansion of social media, thus giving a space for this community to grow and engage. Of note, the cosponsorship relationship with the ABIM Foundation (which works closely with the Choosing Wisely™ campaign) and the Costs of Care Organization could have influenced the participation and dissemination rates of VBC articles. Medical education articles were also popular and appeared to have increased uptake after chats, based on their Altmetric scores. This may be explained by the fact that medical educators have long utilized social media as a means to connect and engage within their community.12–14 It is also possible that the use of Twitter by trainees (residents, students) may have driven some of the dissemination of ME articles, as this group may not be regular subscribers to JHM.
Online journal clubs offer distinct advantages over traditional in-person journal clubs. First, online journal clubs allow for increased connectivity among online communities, bringing together participants from different geographic areas with diverse training and clinical experiences. Subsequently, this allows for the rapid exchange of both personal and organizational approaches to the topic of discussion.15–17 Second, online journal clubs allow for continual access to the discussion material. For example, while the metrics used in this study only assessed active, synchronous participation, anecdotal evidence and feedback to the authors suggests that many individuals passively engaged by following along or reviewed the chat feed post hoc at their convenience. This asynchronous access is a quality not found in more traditional journal club formats. Finally, because online journal clubs commonly operate with a flattened hierarchy,18 they can break down access barriers to both the researchers who performed the study and thought leaders who commonly participate.17
Several insightful lessons were gleaned in the production and management of this online journal club. On the implementation side, promotion, preparation, and continued organization of an online journal club requires a fair amount of work. In this case, the required time and resources were provided by 2 social media editors in addition to administrative assistance from the SHM. The high attrition rate of online journal clubs over the years attests to these difficulties.24 Additionally, finding incentives to attract and sustain participation can be difficult, as we noted that neither CME nor author popularity (based on their Twitter following) appeared to influence engagement metrics (number of participants, total tweets, and tweets/participant). We also found that partnering with other journal club communities, in particular #NephJC, lead to greater participation rates and impressions. Thus, leveraging connections and topics that span clinical domains may be one way to improve and broaden engagement within these forums. Finally, feedback from participants revealed that the timing of the journal club and the inability to have in-depth discussions, a characteristic commonly associated with traditional journal clubs, were problematic.
This study has several limitations. First, the metrics used to assess social media engagement and dissemination can be easily skewed. For instance, the activity of 1 or 2 individuals with large followings can dramatically influence the number of impressions, giving a falsely elevated sense of broad dissemination. Conversely, there may have been some participants who did not use the #JHMChat hashtag, thus leading to an underestimation in these metrics. Second, while we report total impressions as a measure of dissemination, this metric represents possible interactions and does not guarantee interaction or visualization of that tweet. Additionally, we were unable to characterize our participants and their participation rates over time, as this information is not made available through Symplur© analytics. Third, our page view assessment was limited to 2016 sessions only; therefore, these data may not be an accurate reflection of the impact of #JHMChat on this metric. Fourth, given the marginal response rate to our CME questionnaire, a selection bias could have occurred. Finally, whether social media discussions such as online journal clubs act as leading indicators for future citations remains unclear, as some research has shown an association between increased Altmetric scores and increased citation rates,19-21 while others have not.22,23 Our study was not equipped to assess this correlation.
CONCLUSION
Online journal clubs create new opportunities to connect, engage, and disseminate medical research. These developing forums provide journal editors, researchers, patients, and clinicians with a means to connect and discuss research in ways that were not previously possible. In order to continue to evolve and grow, future research in online journal clubs should explore the downstream effects on citation rates, clinical uptake, and participant knowledge after the sessions.
Acknowledgments
The authors would like to thank Felicia Steele for her assistance in organizing and promoting the chats. Additionally, the authors would like to thank all the authors, guests and participants who took time from their families, work, and daily lives to participate in these activities. Your time and presence were truly appreciated.
Disclosures
The authors of this article operate as the Social Media Editors (C.M.W., V.M.A.) and the Editor-in-Chief (A.A.) for the Journal of Hospital Medicine. Dr. Wray had full access to all the data in the project, takes responsibility for the integrity of the data, and the accuracy of the data analysis.
Clinicians, educators, and medical journals are increasingly using the social media outlet, Twitter, as a medium to connect and engage with their colleagues. In particular, online journal clubs have created a space for the timely discussion of research, creation of online communities, and dissemination of research.
Social media-based journal clubs are thought to be one way in which journals can leverage the power of social networks so that researchers can engage with a diverse range of end users4 (including bedside clinicians, administrators, and patients). Several examples of these models exist. For example, #GeriMedJC acts as a complimentary, synchronous chat that takes place at the same time as a live, in-person journal club. #NephJC offers multiple 1-hour chats per month and provides an in-depth summary and analysis of each article, while #UroJC is an asynchronous discussion that takes place over 48 hours. Few data exist to describe whether any of these programs produce measurable improvements in indicators of engagement or dissemination of results.
In 2015, the Journal of Hospital Medicine (JHM) began producing a Twitter-based journal club as a means to connect and engage the Hospital Medicine community and allow for discussion and rapid exchange of information and opinions around a specific clinical topic. This study aims to describe the implementation of the first Journal-sponsored, Twitter-based online journal club and ascertain its impact on both Twitter and journal metrics.
METHODS
#JHMChat was launched in October 2015, and was initially held every 2-3 months until January 2017, when chats began to take place monthly. Each 1-hour chat focused on a recently published article in JHM, was moderated by a JHM social media editor (C.M.W., V.M.A.), and included at least 1 study author or guest expert. Articles were chosen by the social media editors based on the following criteria: (1) attractiveness to possible participants, (2) providing topic variety within the journal club series, and (3) sustainability and topic conduciveness to the online chat model. Chats were held at 9 PM EST in order to engage hospitalists across all US time zones and on different days to accommodate authors’ availability. All sessions were framed by 3-4 questions intended to encourage discussion and presented to chat participants at spaced intervals so as to stimulate a current of responses.
Chats were promoted by way of the JHM (@JHospMedicine, 3400 followers) and Society of Hospital Medicine (SHM; @SHMLive, 5800 followers) Twitter feeds beginning 1 month prior to each session. Visual Abstracts5,6 were used to publicize the sessions, also via Twitter, starting in February 2017.
Continuing Medical Education (CME) credits were offered through the SHM to registered participants, starting in July 2016.7 All sessions were cosponsored by the American Board of Internal Medicine (ABIM) Foundation and the Costs of Care Organization, a non-profit organization aimed at improving healthcare value.
Twitter Metrics
After each session, the following Twitter-based engagement metrics were obtained using the Symplur© Healthcare Hashtag project;8 total number of participants and tweets, tweets/participant, and total impressions (calculated as the number of tweets from each participant multiplied by the number of followers that participant currently had then summed up for all participants). Simply put, impressions can also be thought of as the number of times a single Tweet makes it into someone else’s Twitter feed. So as to avoid artificially inflated metrics, all were obtained 2 hours after the end of the journal club. Participants were defined as anyone who posted an original tweet or retweeted during the session and were encouraged to tag their tweets with the hashtag #JHMChat for post-discussion indexing and measurement. Because authors’ or guests’ popularity on Twitter may influence participation rates, we also assessed the number of followers for each participating author. Spearman’s rank correlation was calculated (Microsoft ExcelTM) where appropriate.
Altmetrics and Page Views
As a means to measure exposure and dissemination external to Twitter, we assessed the change (“Delta”) in the each article’s Altmetric score9, a digital-based metric that quantifies the attention received by a scientific publication on various online platforms including news, blogs, and social media. Delta Altmetric scores were calculated as the difference between the scores on the day of the session and 2 weeks after the respective session, with higher scores indicating greater global online discussion. By measuring the Altmetric score on the day of the discussion, we established a baseline score for comparison purposes. Additionally, this allowed us to better attribute any changes that may have occurred to the discussion itself.
Additionally, using information provided by the journal publisher (John Wiley & Sons Publishing) in 2016, we assessed the effect of #JHMChat on the number of article page views on the JHM website relative to the release of the electronic Table of Contents (eTOC). The eTOC release was chosen as it is historically associated with a high number of page views. In order to isolate the effect of #JHMChat, we only reviewed months in which #JHMChat was not held within 3 days of the eTOC release. Because JHM changed publishers in January 2017, we only assessed page view data on 2016 sessions, as the new publisher lacked enhanced search optimization to obtain these data.
Thematic Analysis
In addition to the above measurements, a thematic analysis of each article was conducted to assess any common themes that would influence our chosen metrics. Themes were assessed and ascribed by one author (C.M.W.) and verified by another (V.M.A.).
Participant and Author Experience
To assess the participant experience, responses to a post-session CME questionnaire that assessed (1) overall quality, (2) comprehensiveness of the discussion, (3) whether the participant would recommend the chat to a colleague, and (4) whether participation would lead to practice-changing measures were reviewed. Registration of each session for CME was also quantified. Finally, each participating author was asked to fill out an electronic post-chat survey (SurveyMonkey®) meant to assess the authors’ experience with the journal club (Appendix).
RESULTS
Between October 2015 and November 2017, a total of 15 sessions were held with a mean of 2.17 (±0.583) million impressions/session, 499 (±129) total tweets/session, and 73 (±24) participants/session (compared to a range of 21-58 participants/session from other online journal clubs, where reported) with 7.2 (±2.0) tweets/participant (Table 1). The total number of participants for all sessions was 1096. Participating authors had on average 1389 (±2714) followers, ranging from a low of 37 to a high of 10,376 (Appendix). No correlation between author following and number of participants (r = 0.19), impressions (r = 0.05), or change in Altmetric score (r = 0.17) was seen.
Thematic analysis revealed 3 predominant themes among the chosen articles: Value-based care (VBC), Quality and Patient Safety (QPS), and Medical Education (ME). Articles focused on VBC had the greatest number of impressions (mean ±SD: 2.61 ± 0.55 million) and participants (mean ±SD: 90 ± 12), while QPS articles had the fewest impressions (mean ±SD: 1.71 ± 0.59 million) and number of participants (mean ±SD: 47 ± 16). The mean increase in the Altmetric score among all discussed articles was 14 (±12), from an average baseline of 30 (±37). Medical Education-themed articles appeared to garner the greatest increase in Altmetric scores, averaging an increase of 32 points, compared with an average baseline score of 31 (±32). In contrast, VBC and QPS articles averaged an increase of 8.6 and 8.4 points, from average baselines of 55 (±53) and 17 (±13), respectively. A 2-month analysis of JHM articles not included in these discussions, in which Altmetric scores were measured in the same way as those from the discussion, revealed a baseline Altmetric score of 27 (±24) with an average increase of 8 (±6) 2 weeks following the chat.
Four articles met the inclusion criteria for page view analysis and suggested that article page views increased to similar levels as the eTOC release (mean: 2668 vs. 2998, respectively; P = .35) (Figure). These increases equate to a 33% and 50% increase in average daily page views (2002) for the chat and eTOC release, respectively.
Ninety-three percent (14/15) of the participating authors responded to the post-discussion survey. All strongly agreed (5/5 on a Likert scale) that the venue allowed for an in-depth discussion about processes and challenges in conducting the study and allowed for greater dissemination and visibility of their work (5/5). Additionally, authors agreed that the journal club was a valuable experience for themselves (4.88/5) and other practitioners (4.88/5). Most agreed that the journal club allowed them to share their work with a different group of participants than usual (4.75/5) and that the experience changed how they would discuss their manuscripts in the future (4.75/5.0); Table 2).
DISCUSSION
The Twitter-based journal club #JHMChat appears to increase social media awareness and dissemination of journal articles and was considered a useful engagement platform by both authors and participants.
Articles with a focus on VBC and ME had the greatest impact on dissemination metrics, particularly, total impressions and Altmetric scores, respectively. Given the strong presence and interest in these topics within Twitter and social media, these findings are not surprising.10,11 For example, over the past several years, the VBC movement has taken shape and grown alongside the expansion of social media, thus giving a space for this community to grow and engage. Of note, the cosponsorship relationship with the ABIM Foundation (which works closely with the Choosing Wisely™ campaign) and the Costs of Care Organization could have influenced the participation and dissemination rates of VBC articles. Medical education articles were also popular and appeared to have increased uptake after chats, based on their Altmetric scores. This may be explained by the fact that medical educators have long utilized social media as a means to connect and engage within their community.12–14 It is also possible that the use of Twitter by trainees (residents, students) may have driven some of the dissemination of ME articles, as this group may not be regular subscribers to JHM.
Online journal clubs offer distinct advantages over traditional in-person journal clubs. First, online journal clubs allow for increased connectivity among online communities, bringing together participants from different geographic areas with diverse training and clinical experiences. Subsequently, this allows for the rapid exchange of both personal and organizational approaches to the topic of discussion.15–17 Second, online journal clubs allow for continual access to the discussion material. For example, while the metrics used in this study only assessed active, synchronous participation, anecdotal evidence and feedback to the authors suggests that many individuals passively engaged by following along or reviewed the chat feed post hoc at their convenience. This asynchronous access is a quality not found in more traditional journal club formats. Finally, because online journal clubs commonly operate with a flattened hierarchy,18 they can break down access barriers to both the researchers who performed the study and thought leaders who commonly participate.17
Several insightful lessons were gleaned in the production and management of this online journal club. On the implementation side, promotion, preparation, and continued organization of an online journal club requires a fair amount of work. In this case, the required time and resources were provided by 2 social media editors in addition to administrative assistance from the SHM. The high attrition rate of online journal clubs over the years attests to these difficulties.24 Additionally, finding incentives to attract and sustain participation can be difficult, as we noted that neither CME nor author popularity (based on their Twitter following) appeared to influence engagement metrics (number of participants, total tweets, and tweets/participant). We also found that partnering with other journal club communities, in particular #NephJC, lead to greater participation rates and impressions. Thus, leveraging connections and topics that span clinical domains may be one way to improve and broaden engagement within these forums. Finally, feedback from participants revealed that the timing of the journal club and the inability to have in-depth discussions, a characteristic commonly associated with traditional journal clubs, were problematic.
This study has several limitations. First, the metrics used to assess social media engagement and dissemination can be easily skewed. For instance, the activity of 1 or 2 individuals with large followings can dramatically influence the number of impressions, giving a falsely elevated sense of broad dissemination. Conversely, there may have been some participants who did not use the #JHMChat hashtag, thus leading to an underestimation in these metrics. Second, while we report total impressions as a measure of dissemination, this metric represents possible interactions and does not guarantee interaction or visualization of that tweet. Additionally, we were unable to characterize our participants and their participation rates over time, as this information is not made available through Symplur© analytics. Third, our page view assessment was limited to 2016 sessions only; therefore, these data may not be an accurate reflection of the impact of #JHMChat on this metric. Fourth, given the marginal response rate to our CME questionnaire, a selection bias could have occurred. Finally, whether social media discussions such as online journal clubs act as leading indicators for future citations remains unclear, as some research has shown an association between increased Altmetric scores and increased citation rates,19-21 while others have not.22,23 Our study was not equipped to assess this correlation.
CONCLUSION
Online journal clubs create new opportunities to connect, engage, and disseminate medical research. These developing forums provide journal editors, researchers, patients, and clinicians with a means to connect and discuss research in ways that were not previously possible. In order to continue to evolve and grow, future research in online journal clubs should explore the downstream effects on citation rates, clinical uptake, and participant knowledge after the sessions.
Acknowledgments
The authors would like to thank Felicia Steele for her assistance in organizing and promoting the chats. Additionally, the authors would like to thank all the authors, guests and participants who took time from their families, work, and daily lives to participate in these activities. Your time and presence were truly appreciated.
Disclosures
The authors of this article operate as the Social Media Editors (C.M.W., V.M.A.) and the Editor-in-Chief (A.A.) for the Journal of Hospital Medicine. Dr. Wray had full access to all the data in the project, takes responsibility for the integrity of the data, and the accuracy of the data analysis.
1. Topf JM, Sparks MA, Phelan PJ, et al. The evolution of the journal club: from osler to twitter. Am J Kidney Dis Off J Natl Kidney Found. 2017;69(6):827-836. doi: 10.1053/j.ajkd.2016.12.012. PubMed
2. Thangasamy IA, Leveridge M, Davies BJ, Finelli A, Stork B, Woo HH. International urology journal club via Twitter: 12-month experience. Eur Urol. 2014;66(1):112-117. doi: 10.1016/j.eururo.2014.01.034. PubMed
3. Gardhouse AI, Budd L, Yang SYC, Wong CL. #GeriMedJC: the Twitter complement to the traditional-format geriatric medicine journal club. J Am Geriatr Soc. 2017;65(6):1347-1351. doi: 10.1111/jgs.14920. PubMed
4. Duque L. How academics and researchers can get more out of social media. Harvard Business Review. https://hbr.org/2016/06/how-academics-and-researchers-can-get-more-out-of-social-media. Accessed November 9, 2017.
5. Wray CM, Arora VM. #VisualAbstract: a revolution in communicating science? Ann Surg. 2017;266(6):e49-e50. doi: 10.1097/SLA.0000000000002339. PubMed
6. Ibrahim AM. Seeing is believing: using visual abstracts to disseminate scientific research. Am J Gastroenterol. 2017:ajg2017268. doi: 10.1038/ajg.2017.268. PubMed
7. #JHMChat. http://shm.hospitalmedicine.org/acton/media/25526/jhmchat. Accessed November 9, 2017.
8. #JHMChat-healthcare social media. Symplur. https://www.symplur.com/search/%23JHMChat. Accessed November 9, 2017.
9. Altmetric. Altmetric. https://www.altmetric.com/. Accessed November 9, 2017.
10. value-based healthcare | Symplur. https://www.symplur.com/topic/value-based-healthcare/. Accessed November 17, 2017.
11. medical education | Symplur. https://www.symplur.com/topic/medical-education/. Accessed November 17, 2017.
12. Sterling M, Leung P, Wright D, Bishop TF. The use of social media in graduate medical education: a systematic review. Acad Med. 2017;92(7):1043. doi: 10.1097/ACM.0000000000001617. PubMed
13. Davis WM, Ho K, Last J. Advancing social media in medical education. CMAJ Can Med Assoc J. 2015;187(8):549-550. doi: 10.1503/cmaj.141417. PubMed
14. Hillman T, Sherbino J. Social media in medical education: a new pedagogical paradigm? Postgrad Med J. 2015;91(1080):544-545. doi: 10.1136/postgradmedj-2015-133686. PubMed
15. Gerds AT, Chan T. Social media in hematology in 2017: dystopia, utopia, or somewhere in-between? Curr Hematol Malig Rep. 2017;12(6):582-591. doi: 10.1007/s11899-017-0424-8. PubMed
16. Mehta N, Flickinger T. The times they are a-changin’: academia, social media and the JGIM Twitter Journal Club. J Gen Intern Med. 2014;29(10):1317-1318. doi: 10.1007/s11606-014-2976-9. PubMed
17. Chan T, Trueger NS, Roland D, Thoma B. Evidence-based medicine in the era of social media: scholarly engagement through participation and online interaction. CJEM. 2017:1-6. doi: 10.1017/cem.2016.407. PubMed
18. Utengen A. The flattening of healthcare: breaking down of barriers in healthcare social media-twitter visualized. https://www.symplur.com/shorts/the-flattening-of-healthcare-twitter-visualized/. Accessed November 8, 2017.
19. Thelwall M, Haustein S, Larivière V, Sugimoto CR. Do altmetrics work? Twitter and ten other social web services. PloS One. 2013;8(5):e64841. doi: 10.1371/journal.pone.0064841. PubMed
20. Peoples BK, Midway SR, Sackett D, Lynch A, Cooney PB. Twitter predicts citation rates of ecological research. PloS One. 2016;11(11):e0166570. doi: 10.1371/journal.pone.0166570. PubMed
21. Eysenbach G. Can tweets predict citations? Metrics of social impact based on Twitter and correlation with traditional metrics of scientific impact. J Med Internet Res. 2011;13(4):e123. doi: 10.2196/jmir.2012. PubMed
22. Winter JCF de. The relationship between tweets, citations, and article views for PLOS ONE articles. Scientometrics. 2015;102(2):1773-1779. doi: 10.1007/s11192-014-1445-x.
23. Haustein S, Peters I, Sugimoto CR, Thelwall M, Larivière V. Tweeting biomedicine: an analysis of tweets and citations in the biomedical literature. J Assoc Inf Sci Technol. 2014;65(4):656-669. doi: 10.1002/asi.23101.
24. Journal club. In: Wikipedia. 2017. https://en.wikipedia.org/w/index.php?title=Journal_club&oldid=807037773. Accessed November 9, 2017.
1. Topf JM, Sparks MA, Phelan PJ, et al. The evolution of the journal club: from osler to twitter. Am J Kidney Dis Off J Natl Kidney Found. 2017;69(6):827-836. doi: 10.1053/j.ajkd.2016.12.012. PubMed
2. Thangasamy IA, Leveridge M, Davies BJ, Finelli A, Stork B, Woo HH. International urology journal club via Twitter: 12-month experience. Eur Urol. 2014;66(1):112-117. doi: 10.1016/j.eururo.2014.01.034. PubMed
3. Gardhouse AI, Budd L, Yang SYC, Wong CL. #GeriMedJC: the Twitter complement to the traditional-format geriatric medicine journal club. J Am Geriatr Soc. 2017;65(6):1347-1351. doi: 10.1111/jgs.14920. PubMed
4. Duque L. How academics and researchers can get more out of social media. Harvard Business Review. https://hbr.org/2016/06/how-academics-and-researchers-can-get-more-out-of-social-media. Accessed November 9, 2017.
5. Wray CM, Arora VM. #VisualAbstract: a revolution in communicating science? Ann Surg. 2017;266(6):e49-e50. doi: 10.1097/SLA.0000000000002339. PubMed
6. Ibrahim AM. Seeing is believing: using visual abstracts to disseminate scientific research. Am J Gastroenterol. 2017:ajg2017268. doi: 10.1038/ajg.2017.268. PubMed
7. #JHMChat. http://shm.hospitalmedicine.org/acton/media/25526/jhmchat. Accessed November 9, 2017.
8. #JHMChat-healthcare social media. Symplur. https://www.symplur.com/search/%23JHMChat. Accessed November 9, 2017.
9. Altmetric. Altmetric. https://www.altmetric.com/. Accessed November 9, 2017.
10. value-based healthcare | Symplur. https://www.symplur.com/topic/value-based-healthcare/. Accessed November 17, 2017.
11. medical education | Symplur. https://www.symplur.com/topic/medical-education/. Accessed November 17, 2017.
12. Sterling M, Leung P, Wright D, Bishop TF. The use of social media in graduate medical education: a systematic review. Acad Med. 2017;92(7):1043. doi: 10.1097/ACM.0000000000001617. PubMed
13. Davis WM, Ho K, Last J. Advancing social media in medical education. CMAJ Can Med Assoc J. 2015;187(8):549-550. doi: 10.1503/cmaj.141417. PubMed
14. Hillman T, Sherbino J. Social media in medical education: a new pedagogical paradigm? Postgrad Med J. 2015;91(1080):544-545. doi: 10.1136/postgradmedj-2015-133686. PubMed
15. Gerds AT, Chan T. Social media in hematology in 2017: dystopia, utopia, or somewhere in-between? Curr Hematol Malig Rep. 2017;12(6):582-591. doi: 10.1007/s11899-017-0424-8. PubMed
16. Mehta N, Flickinger T. The times they are a-changin’: academia, social media and the JGIM Twitter Journal Club. J Gen Intern Med. 2014;29(10):1317-1318. doi: 10.1007/s11606-014-2976-9. PubMed
17. Chan T, Trueger NS, Roland D, Thoma B. Evidence-based medicine in the era of social media: scholarly engagement through participation and online interaction. CJEM. 2017:1-6. doi: 10.1017/cem.2016.407. PubMed
18. Utengen A. The flattening of healthcare: breaking down of barriers in healthcare social media-twitter visualized. https://www.symplur.com/shorts/the-flattening-of-healthcare-twitter-visualized/. Accessed November 8, 2017.
19. Thelwall M, Haustein S, Larivière V, Sugimoto CR. Do altmetrics work? Twitter and ten other social web services. PloS One. 2013;8(5):e64841. doi: 10.1371/journal.pone.0064841. PubMed
20. Peoples BK, Midway SR, Sackett D, Lynch A, Cooney PB. Twitter predicts citation rates of ecological research. PloS One. 2016;11(11):e0166570. doi: 10.1371/journal.pone.0166570. PubMed
21. Eysenbach G. Can tweets predict citations? Metrics of social impact based on Twitter and correlation with traditional metrics of scientific impact. J Med Internet Res. 2011;13(4):e123. doi: 10.2196/jmir.2012. PubMed
22. Winter JCF de. The relationship between tweets, citations, and article views for PLOS ONE articles. Scientometrics. 2015;102(2):1773-1779. doi: 10.1007/s11192-014-1445-x.
23. Haustein S, Peters I, Sugimoto CR, Thelwall M, Larivière V. Tweeting biomedicine: an analysis of tweets and citations in the biomedical literature. J Assoc Inf Sci Technol. 2014;65(4):656-669. doi: 10.1002/asi.23101.
24. Journal club. In: Wikipedia. 2017. https://en.wikipedia.org/w/index.php?title=Journal_club&oldid=807037773. Accessed November 9, 2017.
© 2018 Society of Hospital Medicine
Current Perspectives on Transport Medicine in Pediatric Hospital Medicine Fellowships
Transport medicine (TM) involves the provision of care to patients who require transfer to a healthcare facility that can deliver definitive treatment.1 Pediatric interfacility transport occurs in approximately 10% of nonneonatal, nonpregnancy pediatric hospitalizations in the United States.2 Studies document a decline in resident participation in pediatric transports and variability in curricular content.3,4
The Pediatric Hospital Medicine (PHM) Core Competencies include “Transport of the Critically Ill Child.”7 Additionally, the Curriculum Committee of the PHM Fellowship Directors Council proposed a curricular framework that includes a required clinical experience in “Care and Stabilization of the Critically Ill Child,”8 which can occur in a variety of practice settings, including TM. TM is also listed as a potential elective rotation.
In 2014, 60% of PHM fellowships included a required or optional TM rotation.9 A recent study of pediatric emergency, critical care, and neonatal medicine fellowships revealed a paucity of formal or published TM curricula in these programs.10 Furthermore, no standard or published TM curricula have been established for PHM fellowships. The primary objective of our study is to determine attitudes regarding TM training among PHM fellows, recent PHM fellowship graduates, and PHM fellowship program directors (PDs). The secondary objective is to identify how the perspectives of these fellowship stakeholders could influence the design of a TM curriculum.
METHODS
This cross-sectional study focused on 3 stakeholder groups related to PHM fellowships. The subjects included in the study were physicians enrolled in a PHM fellowship (fellow) during the 2015-2016 academic year, graduates of fellowship (graduate) between 2010 and 2015, and fellowship program directors (PD). Unique web-based, anonymous surveys for each group were developed, reviewed by content and methodology experts, and piloted with local pediatric hospitalists. Surveys consisted of unfolding multiple-choice questions and ranking items along Likert scales and the Dreyfus model.
Questions were designed to elicit demographic data, perspectives, and experience related to TM education in PHM fellowships across all respondent groups. Depending on the context, identical or similar questions were asked among the groups. For example, all groups were asked to prioritize learning objectives for a TM rotation. Graduates and PDs reported the most effective teaching methods for use during a TM rotation. Fellows rated their own interest in a TM elective, and PDs were asked to rate the level of interest among their fellows.
Participant contact information was obtained from a website (phmfellows.org) and databases of fellows and graduates, which are maintained by the PHM Fellowship Directors Council (personal communication, Jayne Truckenbrod, DO; February 2, 2017). Between February and April 2016, the participants were individually emailed a link to their respective surveys, and 3 reminder e-mails were sent to nonresponders. The survey was administered through SurveyMonkey (www.surveymonkey.com).
SPSS (IBM SPSS Statistics, IBM Corporation, Armonk, New York) was used for statistical analysis. Descriptive data were presented using mean and standard deviation. Comparisons among fellows, graduates, and PDs were conducted using one-way analyses of variance or Mann-Whitney U test. Frequency of application and self-evaluation of core competency skills before and after the rotation were evaluated using paired sample t-tests. The study protocol was deemed exempt from review by our local Institutional Review Board.
RESULTS
Forty of 70 (57%) fellows, 32 of 87 graduates (37%), and 14 of 32 PDs (44%) responded to the survey. The majority of the participants described their respective programs as 2 years in duration (59% for fellows, 56% for graduates, and 85% for PDs). Most programs (85%) were based at children’s hospitals. Most graduates (84%) practiced in a children’s hospital, and 12% of them practiced in a community site or a combination of sites.
Both fellows and graduates reported limited involvement in several aspects of TM prior to fellowship. Fellows’ interest in completing a TM rotation during fellowship is greater than the interest as perceived by PDs (3.03+1.00 vs. 2.38+1.19, P = .061). Prior TM exposure in residency or perceived proficiency in TM was not associated with lack of interest. Twenty-five percent of graduates completed a TM rotation during PHM fellowship. Many graduates agreed (41%) or strongly agreed (16%) with the statement “I recommend participating in a TM rotation during PHM fellowship.” Graduates who had completed a TM rotation were more likely to agree with this statement (P = .001).
There were similarities between reservations about participating in a TM rotation among fellows and barriers identified by graduates and PDs (Table). However, no graduates cited lack of relevance to a career in PHM as a barrier to participation in a TM rotation. Fellows, graduates, and PDs reported concordant responses regarding the prioritization of learning objectives for a TM rotation (Table). Both graduates and PDs ranked active learning strategies, such as direct patient care and simulation, as the most effective methods for teaching TM.
Discordance was noted between how frequently fellows participated in aspects of TM during fellowship and graduates’ current practice of PHM (Figure). With regard to select TM-related PHM core competencies, such as respiratory failure, shock, and leading a healthcare team, most (63%–90%, depending on the competency) fellows perceived themselves as “competent” prior to the start of the fellowship. Nevertheless, more than 70% of fellows remained very or extremely interested in gaining additional experience in each competency during fellowship.
DISCUSSION
Survey respondents demonstrate variable levels of interest and engagement in TM training; in particular, fellows and graduates often reported greater interest and value in a TM rotation than PDs. Similar to fellows in related fields,10 PHM fellows and graduates selected clinical topics as the most essential elements of TM training. In accordance with the literature, our findings suggest that direct patient care, one-on-one instruction, and simulation would be appropriate and popular methods for delivering this type of educational content.10,11
Curriculum design for a TM rotation should reinforce clinical PHM competencies related to TM while focusing on topics that are specific to the transport environment, such as methods of interfacility transport, handoffs, transitions of care, and team leadership.2,7,12 Trainee comfort level with different forms of transport (eg, fear of flying, motion sickness) and local and state policies regarding interfacility transfer should also be considered. In addition, fellows could engage in clinical research and quality improvement projects related to TM given the overall paucity of literature in the field.13
Several reasons can explain why fellows and graduates place a greater value on a TM rotation than PDs. Fellows and graduates may perceive inherent value in gaining particular knowledge and skills, such as greater understanding of the logistics and personnel involved in transferring patients and experience working with a healthcare team in a unique and dynamic setting.3,10,14
PDs may not be aware of the extent of participation in elements of transport among graduates. A recent workforce survey of pediatric interfacility transport systems indicated that although medical directors are from the fields of emergency, critical care, and neonatal medicine, 20% of medical control physicians are pediatric hospitalists.4 Given that the majority of PHM fellowships are based at children’s hospitals and transport teams are often associated with intensive care or emergency medicine units, PDs may have limited exposure to transport systems that incorporate hospitalists.
Pediatric hospitalists at all practice sites must have clinical and systems skills related to TM. However, the scope of practice for those working at community sites may be more likely to include distinct elements of TM.6 Currently, most fellowship graduates work at free-standing children’s or university-affiliated hospitals and have pursued careers in academic medicine.15 As the field evolves, the number of fellowship-trained pediatric hospitalists working at community sites may increase, making the acquisition of skills relevant to TM during fellowship training more crucial.
This study has several limitations. We attempted to identify all recent PHM fellowship graduates, but sampling bias may exist. Response bias may have been introduced by the self-reporting of skill and proficiency as well as by the small sample size and response rate for some stakeholder groups. The latter may be exacerbated by the fact that we do not have data on the degree or distribution of program representation among the fellow and graduate groups, given the lack of identifying information collected. Finally, we did not collect specific information about existing TM curricula in PHM fellowships.
We report a variable level of interest and engagement in TM among fellowship stakeholders, even though “Transport of the Critically Ill Child” is a PHM Core Competency. Fellows are interested in TM but unsure of its relevance to a PHM career. Graduates support the acquisition of transport skills during fellowship training.
ACKNOWLEDGMENTS
The authors would like to thank Tony Woodward, MD for reviewing the survey tools; Sheree Schrager, PhD and Margaret Trost, MD for their valuable insights into the results; and Grant Christman, MD for reviewing the manuscript.
Disclosures
The authors declare no potential conflicts of interest.
Funding
No funding was secured for this study.
1. Insoft RM, Schwartz HP, Romito J. Guidelines for Air and Ground Transport of Neonatal and Pediatric Patients., 4th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2016.
2. Rosenthal JL, Romano PS, Kokroko J, Gu W, Okumura MJ. Profiling interfacility transfers for hospitalized pediatric patients. Hosp Pediatr. 2017;7(6):335-343. PubMed
3. Kline-Krammes S, Wheeler DS, Schwartz HP, Forbes M, Bigham MT. Missed opportunities during pediatric residency training. Report of a 10-year follow-up survey in critical care transport medicine. Pediatr Emerg Care. 2012;28(1):1-5. PubMed
4. Tanem J, Triscari D, Chan M, Meyer MT. Workforce survey of pediatric interfacility transport systems in the United States. Pediatr Emer Care. 2016;32(6):364-370. PubMed
5. Freed GL, Dunham KM. Pediatric hospitalists: training, current practice, and career goals. J Hosp Med. 2009;4(3):179-186. PubMed
6. Roberts KB. Pediatric hospitalists in community hospitals: hospital-based generalists with expanded roles. Hosp Pediatr. 2015;5(5):290-292. PubMed
7. Stucky ER, Maniscalco J, Ottolini MC, et al. The Pediatric Hospital Medicine Core Competencies Supplement: a Framework for Curriculum Development by the Society of Hospital Medicine with acknowledgement to pediatric hospitalists from the American Academy of Pediatrics and the Academic Pediatric Association. J Hosp Med. 2010;5(suppl 2):i-xv, 1-114. PubMed
8. Jerardi KE, Fisher E, Rassbach C, et al. Development of a Curricular Framework for Pediatric Hospital Medicine Fellowships. Pediatrics. 2017;140(1):1-8. PubMed
9. Shah NH, Rhim HJH, Maniscalco J, Wilson K, Rassbach C. The current state of pediatric hospital medicine fellowships: A survey of program directors. J Hosp Med. 2016;11(5):324-328. PubMed
10. Mickells GE, Goodman DM, Rozenfeld RA. Education of pediatric subspecialty fellows in transport medicine: a national survey. BMC Pediatrics. 2017;17(1):13. PubMed
11. Cross B, Wilson D. High-fidelity simulation for transport team training and competency evaluation. Newborn Inf Nurs Rev. 2009;9(4):200-206.
12. Weingart C, Herstich T, Baker P, et al. Making good better: implementing a standardized handoff in pediatric transport. Air Med J. 2013;32(1):40-46. PubMed
13. Kandil SB, Sanford HA, Northrup V, Bigham MT, Giuliano Jr. JS. Transport disposition using transport risk assessment in pediatrics (TRAP) score. Prehosp Emerg Care. 2012;16(3):366-373. PubMed
14. Giardino AP, Tran XG, King J, Giardino ER, Woodward GA, Durbin DR. A longitudinal view of resident education in pediatric emergency interhospital transport. Pediatr Emerg Care. 2010;26(9):653-658. PubMed
15. Oshimurua JM, Bauer BD, Shah N, Nguyen N, Maniscalco J. Current roles and perceived needs of pediatric hospital medicine fellowship graduates. Hosp Pediatr. 2016;6(10):633-637 PubMed
Transport medicine (TM) involves the provision of care to patients who require transfer to a healthcare facility that can deliver definitive treatment.1 Pediatric interfacility transport occurs in approximately 10% of nonneonatal, nonpregnancy pediatric hospitalizations in the United States.2 Studies document a decline in resident participation in pediatric transports and variability in curricular content.3,4
The Pediatric Hospital Medicine (PHM) Core Competencies include “Transport of the Critically Ill Child.”7 Additionally, the Curriculum Committee of the PHM Fellowship Directors Council proposed a curricular framework that includes a required clinical experience in “Care and Stabilization of the Critically Ill Child,”8 which can occur in a variety of practice settings, including TM. TM is also listed as a potential elective rotation.
In 2014, 60% of PHM fellowships included a required or optional TM rotation.9 A recent study of pediatric emergency, critical care, and neonatal medicine fellowships revealed a paucity of formal or published TM curricula in these programs.10 Furthermore, no standard or published TM curricula have been established for PHM fellowships. The primary objective of our study is to determine attitudes regarding TM training among PHM fellows, recent PHM fellowship graduates, and PHM fellowship program directors (PDs). The secondary objective is to identify how the perspectives of these fellowship stakeholders could influence the design of a TM curriculum.
METHODS
This cross-sectional study focused on 3 stakeholder groups related to PHM fellowships. The subjects included in the study were physicians enrolled in a PHM fellowship (fellow) during the 2015-2016 academic year, graduates of fellowship (graduate) between 2010 and 2015, and fellowship program directors (PD). Unique web-based, anonymous surveys for each group were developed, reviewed by content and methodology experts, and piloted with local pediatric hospitalists. Surveys consisted of unfolding multiple-choice questions and ranking items along Likert scales and the Dreyfus model.
Questions were designed to elicit demographic data, perspectives, and experience related to TM education in PHM fellowships across all respondent groups. Depending on the context, identical or similar questions were asked among the groups. For example, all groups were asked to prioritize learning objectives for a TM rotation. Graduates and PDs reported the most effective teaching methods for use during a TM rotation. Fellows rated their own interest in a TM elective, and PDs were asked to rate the level of interest among their fellows.
Participant contact information was obtained from a website (phmfellows.org) and databases of fellows and graduates, which are maintained by the PHM Fellowship Directors Council (personal communication, Jayne Truckenbrod, DO; February 2, 2017). Between February and April 2016, the participants were individually emailed a link to their respective surveys, and 3 reminder e-mails were sent to nonresponders. The survey was administered through SurveyMonkey (www.surveymonkey.com).
SPSS (IBM SPSS Statistics, IBM Corporation, Armonk, New York) was used for statistical analysis. Descriptive data were presented using mean and standard deviation. Comparisons among fellows, graduates, and PDs were conducted using one-way analyses of variance or Mann-Whitney U test. Frequency of application and self-evaluation of core competency skills before and after the rotation were evaluated using paired sample t-tests. The study protocol was deemed exempt from review by our local Institutional Review Board.
RESULTS
Forty of 70 (57%) fellows, 32 of 87 graduates (37%), and 14 of 32 PDs (44%) responded to the survey. The majority of the participants described their respective programs as 2 years in duration (59% for fellows, 56% for graduates, and 85% for PDs). Most programs (85%) were based at children’s hospitals. Most graduates (84%) practiced in a children’s hospital, and 12% of them practiced in a community site or a combination of sites.
Both fellows and graduates reported limited involvement in several aspects of TM prior to fellowship. Fellows’ interest in completing a TM rotation during fellowship is greater than the interest as perceived by PDs (3.03+1.00 vs. 2.38+1.19, P = .061). Prior TM exposure in residency or perceived proficiency in TM was not associated with lack of interest. Twenty-five percent of graduates completed a TM rotation during PHM fellowship. Many graduates agreed (41%) or strongly agreed (16%) with the statement “I recommend participating in a TM rotation during PHM fellowship.” Graduates who had completed a TM rotation were more likely to agree with this statement (P = .001).
There were similarities between reservations about participating in a TM rotation among fellows and barriers identified by graduates and PDs (Table). However, no graduates cited lack of relevance to a career in PHM as a barrier to participation in a TM rotation. Fellows, graduates, and PDs reported concordant responses regarding the prioritization of learning objectives for a TM rotation (Table). Both graduates and PDs ranked active learning strategies, such as direct patient care and simulation, as the most effective methods for teaching TM.
Discordance was noted between how frequently fellows participated in aspects of TM during fellowship and graduates’ current practice of PHM (Figure). With regard to select TM-related PHM core competencies, such as respiratory failure, shock, and leading a healthcare team, most (63%–90%, depending on the competency) fellows perceived themselves as “competent” prior to the start of the fellowship. Nevertheless, more than 70% of fellows remained very or extremely interested in gaining additional experience in each competency during fellowship.
DISCUSSION
Survey respondents demonstrate variable levels of interest and engagement in TM training; in particular, fellows and graduates often reported greater interest and value in a TM rotation than PDs. Similar to fellows in related fields,10 PHM fellows and graduates selected clinical topics as the most essential elements of TM training. In accordance with the literature, our findings suggest that direct patient care, one-on-one instruction, and simulation would be appropriate and popular methods for delivering this type of educational content.10,11
Curriculum design for a TM rotation should reinforce clinical PHM competencies related to TM while focusing on topics that are specific to the transport environment, such as methods of interfacility transport, handoffs, transitions of care, and team leadership.2,7,12 Trainee comfort level with different forms of transport (eg, fear of flying, motion sickness) and local and state policies regarding interfacility transfer should also be considered. In addition, fellows could engage in clinical research and quality improvement projects related to TM given the overall paucity of literature in the field.13
Several reasons can explain why fellows and graduates place a greater value on a TM rotation than PDs. Fellows and graduates may perceive inherent value in gaining particular knowledge and skills, such as greater understanding of the logistics and personnel involved in transferring patients and experience working with a healthcare team in a unique and dynamic setting.3,10,14
PDs may not be aware of the extent of participation in elements of transport among graduates. A recent workforce survey of pediatric interfacility transport systems indicated that although medical directors are from the fields of emergency, critical care, and neonatal medicine, 20% of medical control physicians are pediatric hospitalists.4 Given that the majority of PHM fellowships are based at children’s hospitals and transport teams are often associated with intensive care or emergency medicine units, PDs may have limited exposure to transport systems that incorporate hospitalists.
Pediatric hospitalists at all practice sites must have clinical and systems skills related to TM. However, the scope of practice for those working at community sites may be more likely to include distinct elements of TM.6 Currently, most fellowship graduates work at free-standing children’s or university-affiliated hospitals and have pursued careers in academic medicine.15 As the field evolves, the number of fellowship-trained pediatric hospitalists working at community sites may increase, making the acquisition of skills relevant to TM during fellowship training more crucial.
This study has several limitations. We attempted to identify all recent PHM fellowship graduates, but sampling bias may exist. Response bias may have been introduced by the self-reporting of skill and proficiency as well as by the small sample size and response rate for some stakeholder groups. The latter may be exacerbated by the fact that we do not have data on the degree or distribution of program representation among the fellow and graduate groups, given the lack of identifying information collected. Finally, we did not collect specific information about existing TM curricula in PHM fellowships.
We report a variable level of interest and engagement in TM among fellowship stakeholders, even though “Transport of the Critically Ill Child” is a PHM Core Competency. Fellows are interested in TM but unsure of its relevance to a PHM career. Graduates support the acquisition of transport skills during fellowship training.
ACKNOWLEDGMENTS
The authors would like to thank Tony Woodward, MD for reviewing the survey tools; Sheree Schrager, PhD and Margaret Trost, MD for their valuable insights into the results; and Grant Christman, MD for reviewing the manuscript.
Disclosures
The authors declare no potential conflicts of interest.
Funding
No funding was secured for this study.
Transport medicine (TM) involves the provision of care to patients who require transfer to a healthcare facility that can deliver definitive treatment.1 Pediatric interfacility transport occurs in approximately 10% of nonneonatal, nonpregnancy pediatric hospitalizations in the United States.2 Studies document a decline in resident participation in pediatric transports and variability in curricular content.3,4
The Pediatric Hospital Medicine (PHM) Core Competencies include “Transport of the Critically Ill Child.”7 Additionally, the Curriculum Committee of the PHM Fellowship Directors Council proposed a curricular framework that includes a required clinical experience in “Care and Stabilization of the Critically Ill Child,”8 which can occur in a variety of practice settings, including TM. TM is also listed as a potential elective rotation.
In 2014, 60% of PHM fellowships included a required or optional TM rotation.9 A recent study of pediatric emergency, critical care, and neonatal medicine fellowships revealed a paucity of formal or published TM curricula in these programs.10 Furthermore, no standard or published TM curricula have been established for PHM fellowships. The primary objective of our study is to determine attitudes regarding TM training among PHM fellows, recent PHM fellowship graduates, and PHM fellowship program directors (PDs). The secondary objective is to identify how the perspectives of these fellowship stakeholders could influence the design of a TM curriculum.
METHODS
This cross-sectional study focused on 3 stakeholder groups related to PHM fellowships. The subjects included in the study were physicians enrolled in a PHM fellowship (fellow) during the 2015-2016 academic year, graduates of fellowship (graduate) between 2010 and 2015, and fellowship program directors (PD). Unique web-based, anonymous surveys for each group were developed, reviewed by content and methodology experts, and piloted with local pediatric hospitalists. Surveys consisted of unfolding multiple-choice questions and ranking items along Likert scales and the Dreyfus model.
Questions were designed to elicit demographic data, perspectives, and experience related to TM education in PHM fellowships across all respondent groups. Depending on the context, identical or similar questions were asked among the groups. For example, all groups were asked to prioritize learning objectives for a TM rotation. Graduates and PDs reported the most effective teaching methods for use during a TM rotation. Fellows rated their own interest in a TM elective, and PDs were asked to rate the level of interest among their fellows.
Participant contact information was obtained from a website (phmfellows.org) and databases of fellows and graduates, which are maintained by the PHM Fellowship Directors Council (personal communication, Jayne Truckenbrod, DO; February 2, 2017). Between February and April 2016, the participants were individually emailed a link to their respective surveys, and 3 reminder e-mails were sent to nonresponders. The survey was administered through SurveyMonkey (www.surveymonkey.com).
SPSS (IBM SPSS Statistics, IBM Corporation, Armonk, New York) was used for statistical analysis. Descriptive data were presented using mean and standard deviation. Comparisons among fellows, graduates, and PDs were conducted using one-way analyses of variance or Mann-Whitney U test. Frequency of application and self-evaluation of core competency skills before and after the rotation were evaluated using paired sample t-tests. The study protocol was deemed exempt from review by our local Institutional Review Board.
RESULTS
Forty of 70 (57%) fellows, 32 of 87 graduates (37%), and 14 of 32 PDs (44%) responded to the survey. The majority of the participants described their respective programs as 2 years in duration (59% for fellows, 56% for graduates, and 85% for PDs). Most programs (85%) were based at children’s hospitals. Most graduates (84%) practiced in a children’s hospital, and 12% of them practiced in a community site or a combination of sites.
Both fellows and graduates reported limited involvement in several aspects of TM prior to fellowship. Fellows’ interest in completing a TM rotation during fellowship is greater than the interest as perceived by PDs (3.03+1.00 vs. 2.38+1.19, P = .061). Prior TM exposure in residency or perceived proficiency in TM was not associated with lack of interest. Twenty-five percent of graduates completed a TM rotation during PHM fellowship. Many graduates agreed (41%) or strongly agreed (16%) with the statement “I recommend participating in a TM rotation during PHM fellowship.” Graduates who had completed a TM rotation were more likely to agree with this statement (P = .001).
There were similarities between reservations about participating in a TM rotation among fellows and barriers identified by graduates and PDs (Table). However, no graduates cited lack of relevance to a career in PHM as a barrier to participation in a TM rotation. Fellows, graduates, and PDs reported concordant responses regarding the prioritization of learning objectives for a TM rotation (Table). Both graduates and PDs ranked active learning strategies, such as direct patient care and simulation, as the most effective methods for teaching TM.
Discordance was noted between how frequently fellows participated in aspects of TM during fellowship and graduates’ current practice of PHM (Figure). With regard to select TM-related PHM core competencies, such as respiratory failure, shock, and leading a healthcare team, most (63%–90%, depending on the competency) fellows perceived themselves as “competent” prior to the start of the fellowship. Nevertheless, more than 70% of fellows remained very or extremely interested in gaining additional experience in each competency during fellowship.
DISCUSSION
Survey respondents demonstrate variable levels of interest and engagement in TM training; in particular, fellows and graduates often reported greater interest and value in a TM rotation than PDs. Similar to fellows in related fields,10 PHM fellows and graduates selected clinical topics as the most essential elements of TM training. In accordance with the literature, our findings suggest that direct patient care, one-on-one instruction, and simulation would be appropriate and popular methods for delivering this type of educational content.10,11
Curriculum design for a TM rotation should reinforce clinical PHM competencies related to TM while focusing on topics that are specific to the transport environment, such as methods of interfacility transport, handoffs, transitions of care, and team leadership.2,7,12 Trainee comfort level with different forms of transport (eg, fear of flying, motion sickness) and local and state policies regarding interfacility transfer should also be considered. In addition, fellows could engage in clinical research and quality improvement projects related to TM given the overall paucity of literature in the field.13
Several reasons can explain why fellows and graduates place a greater value on a TM rotation than PDs. Fellows and graduates may perceive inherent value in gaining particular knowledge and skills, such as greater understanding of the logistics and personnel involved in transferring patients and experience working with a healthcare team in a unique and dynamic setting.3,10,14
PDs may not be aware of the extent of participation in elements of transport among graduates. A recent workforce survey of pediatric interfacility transport systems indicated that although medical directors are from the fields of emergency, critical care, and neonatal medicine, 20% of medical control physicians are pediatric hospitalists.4 Given that the majority of PHM fellowships are based at children’s hospitals and transport teams are often associated with intensive care or emergency medicine units, PDs may have limited exposure to transport systems that incorporate hospitalists.
Pediatric hospitalists at all practice sites must have clinical and systems skills related to TM. However, the scope of practice for those working at community sites may be more likely to include distinct elements of TM.6 Currently, most fellowship graduates work at free-standing children’s or university-affiliated hospitals and have pursued careers in academic medicine.15 As the field evolves, the number of fellowship-trained pediatric hospitalists working at community sites may increase, making the acquisition of skills relevant to TM during fellowship training more crucial.
This study has several limitations. We attempted to identify all recent PHM fellowship graduates, but sampling bias may exist. Response bias may have been introduced by the self-reporting of skill and proficiency as well as by the small sample size and response rate for some stakeholder groups. The latter may be exacerbated by the fact that we do not have data on the degree or distribution of program representation among the fellow and graduate groups, given the lack of identifying information collected. Finally, we did not collect specific information about existing TM curricula in PHM fellowships.
We report a variable level of interest and engagement in TM among fellowship stakeholders, even though “Transport of the Critically Ill Child” is a PHM Core Competency. Fellows are interested in TM but unsure of its relevance to a PHM career. Graduates support the acquisition of transport skills during fellowship training.
ACKNOWLEDGMENTS
The authors would like to thank Tony Woodward, MD for reviewing the survey tools; Sheree Schrager, PhD and Margaret Trost, MD for their valuable insights into the results; and Grant Christman, MD for reviewing the manuscript.
Disclosures
The authors declare no potential conflicts of interest.
Funding
No funding was secured for this study.
1. Insoft RM, Schwartz HP, Romito J. Guidelines for Air and Ground Transport of Neonatal and Pediatric Patients., 4th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2016.
2. Rosenthal JL, Romano PS, Kokroko J, Gu W, Okumura MJ. Profiling interfacility transfers for hospitalized pediatric patients. Hosp Pediatr. 2017;7(6):335-343. PubMed
3. Kline-Krammes S, Wheeler DS, Schwartz HP, Forbes M, Bigham MT. Missed opportunities during pediatric residency training. Report of a 10-year follow-up survey in critical care transport medicine. Pediatr Emerg Care. 2012;28(1):1-5. PubMed
4. Tanem J, Triscari D, Chan M, Meyer MT. Workforce survey of pediatric interfacility transport systems in the United States. Pediatr Emer Care. 2016;32(6):364-370. PubMed
5. Freed GL, Dunham KM. Pediatric hospitalists: training, current practice, and career goals. J Hosp Med. 2009;4(3):179-186. PubMed
6. Roberts KB. Pediatric hospitalists in community hospitals: hospital-based generalists with expanded roles. Hosp Pediatr. 2015;5(5):290-292. PubMed
7. Stucky ER, Maniscalco J, Ottolini MC, et al. The Pediatric Hospital Medicine Core Competencies Supplement: a Framework for Curriculum Development by the Society of Hospital Medicine with acknowledgement to pediatric hospitalists from the American Academy of Pediatrics and the Academic Pediatric Association. J Hosp Med. 2010;5(suppl 2):i-xv, 1-114. PubMed
8. Jerardi KE, Fisher E, Rassbach C, et al. Development of a Curricular Framework for Pediatric Hospital Medicine Fellowships. Pediatrics. 2017;140(1):1-8. PubMed
9. Shah NH, Rhim HJH, Maniscalco J, Wilson K, Rassbach C. The current state of pediatric hospital medicine fellowships: A survey of program directors. J Hosp Med. 2016;11(5):324-328. PubMed
10. Mickells GE, Goodman DM, Rozenfeld RA. Education of pediatric subspecialty fellows in transport medicine: a national survey. BMC Pediatrics. 2017;17(1):13. PubMed
11. Cross B, Wilson D. High-fidelity simulation for transport team training and competency evaluation. Newborn Inf Nurs Rev. 2009;9(4):200-206.
12. Weingart C, Herstich T, Baker P, et al. Making good better: implementing a standardized handoff in pediatric transport. Air Med J. 2013;32(1):40-46. PubMed
13. Kandil SB, Sanford HA, Northrup V, Bigham MT, Giuliano Jr. JS. Transport disposition using transport risk assessment in pediatrics (TRAP) score. Prehosp Emerg Care. 2012;16(3):366-373. PubMed
14. Giardino AP, Tran XG, King J, Giardino ER, Woodward GA, Durbin DR. A longitudinal view of resident education in pediatric emergency interhospital transport. Pediatr Emerg Care. 2010;26(9):653-658. PubMed
15. Oshimurua JM, Bauer BD, Shah N, Nguyen N, Maniscalco J. Current roles and perceived needs of pediatric hospital medicine fellowship graduates. Hosp Pediatr. 2016;6(10):633-637 PubMed
1. Insoft RM, Schwartz HP, Romito J. Guidelines for Air and Ground Transport of Neonatal and Pediatric Patients., 4th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2016.
2. Rosenthal JL, Romano PS, Kokroko J, Gu W, Okumura MJ. Profiling interfacility transfers for hospitalized pediatric patients. Hosp Pediatr. 2017;7(6):335-343. PubMed
3. Kline-Krammes S, Wheeler DS, Schwartz HP, Forbes M, Bigham MT. Missed opportunities during pediatric residency training. Report of a 10-year follow-up survey in critical care transport medicine. Pediatr Emerg Care. 2012;28(1):1-5. PubMed
4. Tanem J, Triscari D, Chan M, Meyer MT. Workforce survey of pediatric interfacility transport systems in the United States. Pediatr Emer Care. 2016;32(6):364-370. PubMed
5. Freed GL, Dunham KM. Pediatric hospitalists: training, current practice, and career goals. J Hosp Med. 2009;4(3):179-186. PubMed
6. Roberts KB. Pediatric hospitalists in community hospitals: hospital-based generalists with expanded roles. Hosp Pediatr. 2015;5(5):290-292. PubMed
7. Stucky ER, Maniscalco J, Ottolini MC, et al. The Pediatric Hospital Medicine Core Competencies Supplement: a Framework for Curriculum Development by the Society of Hospital Medicine with acknowledgement to pediatric hospitalists from the American Academy of Pediatrics and the Academic Pediatric Association. J Hosp Med. 2010;5(suppl 2):i-xv, 1-114. PubMed
8. Jerardi KE, Fisher E, Rassbach C, et al. Development of a Curricular Framework for Pediatric Hospital Medicine Fellowships. Pediatrics. 2017;140(1):1-8. PubMed
9. Shah NH, Rhim HJH, Maniscalco J, Wilson K, Rassbach C. The current state of pediatric hospital medicine fellowships: A survey of program directors. J Hosp Med. 2016;11(5):324-328. PubMed
10. Mickells GE, Goodman DM, Rozenfeld RA. Education of pediatric subspecialty fellows in transport medicine: a national survey. BMC Pediatrics. 2017;17(1):13. PubMed
11. Cross B, Wilson D. High-fidelity simulation for transport team training and competency evaluation. Newborn Inf Nurs Rev. 2009;9(4):200-206.
12. Weingart C, Herstich T, Baker P, et al. Making good better: implementing a standardized handoff in pediatric transport. Air Med J. 2013;32(1):40-46. PubMed
13. Kandil SB, Sanford HA, Northrup V, Bigham MT, Giuliano Jr. JS. Transport disposition using transport risk assessment in pediatrics (TRAP) score. Prehosp Emerg Care. 2012;16(3):366-373. PubMed
14. Giardino AP, Tran XG, King J, Giardino ER, Woodward GA, Durbin DR. A longitudinal view of resident education in pediatric emergency interhospital transport. Pediatr Emerg Care. 2010;26(9):653-658. PubMed
15. Oshimurua JM, Bauer BD, Shah N, Nguyen N, Maniscalco J. Current roles and perceived needs of pediatric hospital medicine fellowship graduates. Hosp Pediatr. 2016;6(10):633-637 PubMed
© 2018 Society of Hospital Medicine
“We’ve Learned It’s a Medical Illness, Not a Moral Choice”: Qualitative Study of the Effects of a Multicomponent Addiction Intervention on Hospital Providers’ Attitudes and Experiences
Substance use disorders (SUD) represent a national epidemic with death rates exceeding those of HIV at its peak.1 Hospitals are increasingly filled with people suffering from medical complications of addiction.2,3 While the US health system spends billions of dollars annually on hospital care for medical problems resulting from SUD,4 most hospitals lack expertise or care systems to directly address SUD or connect people to treatment after discharge. 5,6
Patients with SUD often feel stigmatized in healthcare settings and want providers who understand SUD and how to treat it.7 Providers feel underprepared8 and commonly have negative attitudes toward patients with SUD.9,10 Caring for patients can be a source of resentment, dissatisfaction, and burnout.9 Such negative attitudes can adversely affect patient care. Studies show that patients who perceive discrimination by providers are less likely to complete treatment11 and providers’ negative attitudes may disempower patients.9
Evaluations of hospital interventions for adults with SUD focus primarily on patient-level outcomes of SUD severity,12 healthcare utilization,13 and treatment engagement.14,15 Little is known about how such interventions can affect interprofessional providers’ attitudes and experiences, or how systems-level interventions influence hospital culture.16
We performed a qualitative study of multidisciplinary hospital providers to 1) understand the challenges that hospital providers face in managing care for patients with SUD, and 2) explore how integrating SUD treatment in a hospital setting affects providers’ attitudes, experiences, and perceptions of the care environment. This study was part of a formative evaluation of the Improving Addiction Care Team (IMPACT). IMPACT includes a hospital-based, interprofessional addiction medicine consultation service and rapid-access pathways to community addiction care after hospitalization.17. IMPACT is an intensive intervention that includes SUD assessments, withdrawal management, medications for addiction (eg, methadone, buprenorphine induction), counseling and behavioral SUD treatment, peer engagement and support, and linkages to community-based addiction care. We described the rationale and design of IMPACT in earlier publications.7,17
METHODS
Setting
We conducted in-person interviews and focus groups (FGs) with interprofessional hospital providers at a single urban academic medical center between February and July 2016, six months after starting IMPACT implementation. Oregon Health and Science University’s (OHSU) institutional review board approved the protocol.
Participants
We conducted 12 individual informant interviews (IIs) and 6 (FGs) (each comprising 3-6 participants) with a wide range of providers, including physicians, nurses, social workers, residents, patient advocates, case managers, and pharmacists. In total, 34 providers participated. We used purposive sampling to choose participants with experience both caring for patients with SUD and with exposure to IMPACT. Participant characteristics are summarized in Table 1.
Data Collection
We employed 2 different types of interviews. In situations where multiple providers occupied a similar role (eg, social workers), we chose to use a focus group format to elicit a range of perspectives and experiences through participant interaction.18 We conducted individual interviews to gain input from key informants who had unique roles in the program (eg, a cardiac surgeon) and to include providers who would otherwise be unable to participate due to scheduling barriers (eg, residents). We interviewed all participants using a semi-structured interview guide that was developed by an interdisciplinary team, including expert qualitative researchers, IMPACT clinical team members, and other OHSU clinicians (Appendix A). An interviewer who was not a part of the IMPACT clinical team asked all participants about their experience caring for patients with SUD, their experience with IMPACT, and how they might improve care. FGs lasted between 41-57 minutes, and individual key informant interviews lasted between 11-38 minutes. We ended recruitment after reaching theme saturation. Our goal was to achieve saturation across the sample as a whole and not within distinct participant groups. We noted if certain themes were more salient for 1 particular group. We audio-recorded all interviews and FGs. Recordings were transcribed, de-identified, and transferred to ATLAS.ti for data analysis.
Analysis
We conducted a thematic analysis using an inductive approach at the semantic level.19 Using an iterative process, we generated a preliminary coding schema after reviewing an initial selection of transcripts. Coders then independently coded transcripts and met in dyads to both discuss and reconcile codes, and resolve any discrepancies through discussion until reaching a consensus. One coder (DC) coded all transcripts; 3 coders (EP, SPP, MR) divided the transcripts evenly. All authors met periodically to discuss codebook revisions and emergent themes. We identified themes that represented patterns, had meaning to study participants, and captured important findings related to our research questions.19
As expected, the style of IIs differed from that of FGs and informants were able to provide information specific to their roles. Overall, the information provided by IIs was complementary to that of FGs and helped triangulate findings. Thus, we combined them in the results.18
RESULTS
We organized our findings into 3 main groupings, including (1) care before IMPACT, (2) care with IMPACT, and (3) perceived limitations of IMPACT. We included a table (Table 2) with additional quotations, beyond those in the body of the results, to support emergent themes described below.
Care before IMPACT
Providers felt hospitalization did not address addiction for many reasons, including ethical and legal concerns, medical knowledge gaps, and lack of treatment options.
Before IMPACT, many participants noted that hospitalization ignored or avoided addressing addiction, leading to a chaotic care environment that adversely affected patient care and provider experience. As one social worker stated, “prior to IMPACT we provided assessments, and we provided resources. But we didn’t address addiction.”
Providers cited multiple explanations for this, including the common misperception that using methadone to treat withdrawal violated federal regulations, and concerns about the ethicality of using opioids in patients with SUD. Across disciplines, providers described a “huge knowledge gap” and little confidence in addressing withdrawal, complex chronic pain, medications for addiction, and challenging patient behaviors. Providers also described limited expertise and scarce treatment options as a deterrent. As one attending reflected, “I would ask those questions [about SUD] before, but then … I had the information, but I couldn’t do anything with it.”
Providers felt the failure to address SUD adversely affected patient care, leading to untreated withdrawal, disruptive behaviors, and patients leaving against medical advice (AMA).
Participants across disciplines described wide variability in the medical management of SUD, particularly around the management of opioid withdrawal and pain, with some providers who “simply wouldn’t prescribe methadone or any opiates” and others who prescribed high doses without anticipating risks. As one attending recalled:
“You would see this pattern, especially in the intravenous drug-using population: left AMA, left AMA, left AMA … nine times out of ten, nobody was dealing with the fact that they were gonna go into withdrawal.”
Respondents recalled that disruptive behaviors from patients’ active use or withdrawal frequently threatened safety; imposed a tremendous burden on staff time and morale; and were a consistent source of providers’ distress. As one patient advocate explained:
“[Providers] get called to the unit because the person is yelling and throwing things or comes back after being gone for a long period and appears impaired … it often blows up, and they get discharged or they leave against medical advice or they go out and don’t come back. We don’t really know what happened to them, and they’re vulnerable. And the staff are vulnerable. And other patients are distressed by the disruption and commotion.”
Absent standards and systems to address SUD, providers felt they were “left to their own,” resulting in a reactive and chaotic care environment.
Providers noted inconsistent rules and policies regarding smoke breaks, room searches, and visitors. As a result, care felt “reckless and risky” and led to a “nonalliance” across disciplines. Providers frequently described inconsistent and loose expectations until an event -- often active use – triggered an ad hoc ratcheting up of the rules, damaging patient-provider relationships and limiting providers’ ability to provide medical care. Facing these conflicts, “staff gets escalated, and everybody gets kind of spun up.” As one attending reflected:
“I could not get any sort of engagement even in just her medical issues … I was trying to talk to her and educate her about heart failure and salt intake and food intake, but every time I walked in the room … I’d have to come in and be like, ‘your UDS [urine drug screen] was positive again, so here’s the changes to your behavioral plan, and OK, let’s talk about your heart failure …’ At that point, the relationship had completely disintegrated until it was very nonproductive.”
Providers described widespread “moral distress,” burnout, and feelings of futility before IMPACT.
Consequently, providers felt that caring for people with SUD was “very emotionally draining and very time consuming.” As one patient advocate described:
“We’ve been watching staff try to manage these patients for years without the experts and the resources and the skills that they need … As a result, there was a crescendo effect of moral distress, and [staff] bring in all of their past experiences which influence the interaction … Some staff are very skilled, but you also saw some really punitive responses.”
Many felt that providing intensive medical care without addressing people’s underlying SUD was a waste of time and resources. As one cardiac surgeon reflected:
“[Patients] ended up either dead or reinfected. Nobody wanted to do stuff because we felt it was futile. Well, of course, it’s futile …. you’re basically trying to fix the symptoms. It’s like having a leaky roof and just running around with a bunch of buckets, which is like surgery. You gotta fix the roof…otherwise they will continue to inject bacteria into their bodies.”
Care with IMPACT:
Providers felt integrating hospital-based systems to address SUD legitimized addiction as a treatable disease.
Participants described IMPACT as a “sea change” that “completely reframes” addiction as “a medical condition that actually has a treatment.” As one social worker observed, “when it’s somebody in a white coat with expertise who’s talking to another doctor it really can shift mindsets in an amazing way.” Others echoed this, stating that an addiction team “legitimized the fact that this is an actual disease that we need to treat - and a failure to treat it is a failure to be a good doctor.”
Providers felt that by addressing addiction directly, “IMPACT elevated the consciousness of providers and nurses … that substance use disorders are brain disorders and not bad behavior.” They described that this legitimization, combined with seeing firsthand the stabilizing effects of medications for addiction, allowed providers to understand SUD as a chronic disease, and not a moral failing.
Providers felt IMPACT improved patient engagement and humanized care by treating withdrawal, directly communicating about SUD, and modeling compassionate care.
Providers noted that treating withdrawal had a dramatic effect on patient engagement and care. One surgeon explained, “by managing their opioid dependence and other substance abuse issues … it’s easier for the staff to take care of them, it’s safer, and the patients feel better taken care of because the staff will engage with them.” Many noted that conflict-ridden “conversations were able to go to the side, and we were able to talk about other things to build rapport.” Others noted that this shift felt like “more productive time.”
In addition, providers repeatedly emphasized that having clear hospital standards and a process to engage patients “really helps … establish rapport with patients: ‘This is how we work this. These are your boundaries. And this is what will happen if you push those boundaries.’ There it is.” Providers attributed improved patient-provider communication to “frank conversation,” “the right amount of empathy,” and a less judgmental environment. As one attending described, “I don’t know if it gives them a voice or allows us to hear them better … but something’s happening with communication.”
Many participants highlighted that IMPACT modeled compassionate bedside interactions, exposed the role of trauma in many patients’ lives, and helped providers see SUD as a disease spectrum. One attending noted that to “actually appreciate the subtleties – just the severity of the disorder – has been powerful.” One resident said:
“There’s definitely a lot of stigma around patients with use disorders that probably shows itself in subtle ways throughout their hospitalization. I think IMPACT does a good job … keeping the patient in the center and keeping their use disorder contextualized in the greater person … [IMPACT] role models bedside interactions and how to treat people like humans.”
Providers valued post-hospital SUD treatment pathways.
Providers valued previously nonexistent post-hospital SUD treatment pathways, stating “this relationship with [community treatment] … it’s like an answer to prayers,” and “this isn’t just like we’re being nicer.” One attending described:
“Starting them on [methadone or buprenorphine-naloxone] and then making the next step in the outpatient world happen has been huge. That transition is so critical … that’s been probably the biggest impact.”
Providers felt relief after IMPACT implementation.
Providers felt that by addressing SUD treatment gaps and providing addiction expertise, IMPACT helped alleviate the previously widespread feelings of “moral distress.” One resident explained “having [IMPACT] as a lifeline, it just feels so good.” As an infectious disease consultant noted, “it makes people more open to treating people if they don’t feel isolated and out of their depth.” Others noted that IMPACT supported better multidisciplinary collaboration, which “reduced a lot of tension between the teams.” One nurse summarized:
“I think you feel more empowered when you’ve got the right medication, … the knowledge, and you feel like you have the resources. You actually feel like you’re making a difference.”
Respondents acknowledged that even with IMPACT, some patients leave AMA or relapse. However, by understanding addiction as a relapsing and remitting disease, providers reconceptualized “success,” further reducing feelings of emotional burnout and stress: “there will be ups and downs, it’s not gonna be a straight linear success.” One case manager reflected,
“Maybe that’s part of the nature of the illness, you progress, and then you kind of hold your breath and then it slips again … at least with IMPACT at the table I can say we’ve done the best we can for this person.”
Perceived limitations of IMPACT:
Providers noted several key limitations of IMPACT, including that hospital-based interventions do not address poverty and have limited ability to address socioeconomic determinants such as “social support, … housing, or nutrition.” Providers also felt that IMPACT had limited ability to alleviate patients’ feelings of boredom and isolation associated with prolonged hospitalization, and that IMPACT had limited effectiveness for highly ambivalent patients (Table 2).
Finally, while many described increased confidence managing SUD after working with IMPACT, others cautioned against deferring too much to specialists. As one resident doctor said:
“We shouldn’t forget that all providers should know how to handle some form of people with addiction … I just don’t want it to be like, ‘oh, well, no, I don’t need to think about this … because we have an addiction specialist.’”
Participants across disciplines repeatedly suggested formal, ongoing initiatives to educate and train providers to manage SUD independently.
DISCUSSION
This study explores provider perspectives on care for hospitalized adults with SUD. Before IMPACT, providers felt care was chaotic, unsafe, and frustrating. Providers perceived variable care quality, resulting in untreated withdrawal, inconsistent care plans, and poor patient outcomes, leading to widespread “moral distress” and feelings of futility among providers. Yet this experience was not inevitable. Providers described that a hospital-based intervention to treat SUD reframed addiction as a treatable chronic disease, transformed culture, and improved patient care and provider experience.
Our findings are consistent with and build on previous research in several ways. First, widespread anxiety and difficulty managing patients with SUD was not unique to our hospital. In a systematic review, van Boekel and colleagues describe that healthcare providers perceived violence, manipulation, and poor motivation as factors impeding care for patients with SUD.9 Our study demonstrates the resulting feelings of powerlessness and frustration may be alleviated through an intervention that provides SUD care.
Second, our study is consistent with a recent survey-based study by Wakeman and colleagues that found that a hospital-based SUD intervention improved providers’ feelings of preparedness and satisfaction.20 Our study provides a rich qualitative description and elucidates mechanisms by which such interventions may work.
The finding that a hospital-based SUD intervention can shift providers’ views of addiction is important. Earlier studies have shown that providers who perceive addiction as a choice are more likely to have negative attitudes toward people with SUD.11 While our intervention did not provide formal education aimed at changing attitudes, participants reported that seeing firsthand effects of treatment on patient behaviors was a powerful tool that radically shifted providers’ understanding and reduced stigma.
Stigma can occur at both individual and organizational levels. Structural stigma refers to practices, policies, and norms of institutions that exclude needs of a particular group.21 The absence of systems to address SUD sends a message to both patients and providers that addiction is a not a treatable or worthy disease. IMPACT was in and of itself a systems-level intervention; by creating a consultation service, hospital-wide policies, and pathways to care after hospitalization, IMPACT ‘legitimized’ SUD and reduced institutional stigma.
Several studies have shown the feasibility and effectiveness of starting medications for addiction (MAT) in the hospital.13-15 Our study builds on this work by highlighting systems-level elements valued by providers. These elements may be important to support and scale widespread adoption of MAT in hospitals. Specifically, providers felt that IMPACT’s attention to hospital policies, use of addiction medicine specialists, and direct linkages to outpatient SUD treatment proved instrumental in shifting care systems.
Our study has several limitations. As a single-site study, our goal was not generalizability, but transferability. As such, we aimed to obtain rich, in-depth information that can inform implementation of similar efforts. Because our study was conducted after the implementation of IMPACT, providers’ perspectives on care before IMPACT may have been influenced by the intervention. However, this also strengthens our findings by allowing participants the opportunity for insights under a different system. It likely leads to distinct findings compared to what we might have uncovered in a pre-post study. While respondents noted perceived limitations of IMPACT, there were few instances of negative remarks in the data we collected. It is possible that providers with more negative interpretations chose not to participate in interviews; however, we elicited wide viewpoints and encouraged participants to share both strengths and weaknesses. Finally, IMPACT implementation depends on regional as well as local factors such as Medicaid expansion, community treatment resources, and the existence of addiction medicine expertise that will differ across settings.
Despite these limitations, our study has several important implications. For clinical practice, our findings highlight the importance of treating withdrawal to address challenging patient behaviors and the value of integrating MAT into the hospital setting. Our findings also underscore the role of expert consultation for addiction. Importantly, our results emphasize that reframing SUD as a brain disease can have significant implications for clinical care and providers’ well-being. Provider distress is not inevitable and can change with the right support and systems.
At the hospital and health systems level, our findings suggest that hospitals can and should address SUD. This may include forming interprofessional teams with SUD expertise, providing standardized guidelines for addiction care such as patient safety plans and methadone policies, and creating rapid-access pathways to outpatient SUD care. By addressing SUD, hospitals may simultaneously improve care and reduce provider burnout. Providers’ important concerns about shifting SUD treatment to a specialty team and their discomfort managing SUD pre-IMPACT suggest the need to integrate SUD education across all levels of interprofessional education. Furthermore, provider concerns that IMPACT has limited ability to engage ambivalent patients underscores the need for hospital-based approaches that emphasize harm reduction strategies.
As the SUD epidemic worsens, SUD-related hospitalizations are skyrocketing, and people are dying at unprecedented rates.2,3 Many efforts to address SUD have been in primary care or community settings. While important, many people with SUD are unable or unlikely to seek primary care. 22 Hospitals need a workforce and systems that can address both the physical and behavioral health needs of this population. By implementing SUD improvements, hospitals can support staff and reduce burnout, better engage patients, improve care, and reduce stigma from this devastating disease
Disclosures
The authors have no conflicts of interest to disclose.
1. Rossen L, Bastian B, Warner M, Khan D, Chong Y. Drug poisoning mortality: United States, 1999-2015. 2017; https://www.cdc.gov/nchs/data-visualization/drug-poisoning-mortality/. Accessed 7-11, 2017.
2. Tedesco D, Asch SM, Curtin C, et al. Opioid abuse and poisoning: trends in inpatient and emergency department discharges. Health Aff (Millwood). 2017;36(10):1748-1753. http:// doi.org/10.1377/hlthaff.2017.0260. PubMed
3. Weiss AJ, Elixhauser A, Barrett ML, Steiner CA, Bailey MK, O’Malley L. Statistical Brief #219: Opioid-Related Inpatient Stays and Emergency Department Visits by State, 2009-2014. 2017; https://hcup-us.ahrq.gov/reports/statbriefs/sb219-Opioid-Hospital-Stays-ED-Visits-by-State.jsp?utm_source=AHRQ&utm_medium=EN-2&utm_term=&utm_content=2&utm_campaign=AHRQ_EN12_20_2016. Accessed July 11, 2017. PubMed
4. Ronan MV, Herzig SJ. Hospitalizations related to opioid abuse/dependence and associated serious infections increased sharply, 2002-12. Health Aff (Millwood). 2016;35(5):832-837. http:// doi.org/10.1377/hlthaff.2015.1424. PubMed
5. Infectious Diseases Society of America Emerging Infections Network. Report for Query: ‘Injection Drug Use (IDU) and Infectious Disease Practice’. 2017; https://www.int-med.uiowa.edu/Research/EIN/FinalReport_IDUandID.pdf. Accessed July 11, 2017.
6. Rosenthal ES, Karchmer AW, Theisen-Toupal J, Castillo RA, Rowley CF. Suboptimal addiction interventions for patients hospitalized with injection drug use-associated infective endocarditis. Am J Med. 2016;129(5):481-485. http:// doi.org/10.1016/j.amjmed.2015.09.024. PubMed
7. Velez CM, Nicolaidis C, Korthuis PT, Englander H. “It’s been an Experience, a Life Learning Experience”: A qualitative study of hospitalized patients with substance use disorders. J Gen Intern Med. 2017;32(3):296-303. http:// doi.org/10.1007/s11606-016-3919-4. PubMed
8. Wakeman SE, Pham-Kanter G, Donelan K. Attitudes, practices, and preparedness to care for patients with substance use disorder: Results from a survey of general internists. Subst Abus. 2016;37(4):635-641. http:// doi.org/10.1080/08897077.2016.1187240. PubMed
9. van Boekel LC, Brouwers EP, van Weeghel J, Garretsen HF. Stigma among health professionals towards patients with substance use disorders and its consequences for healthcare delivery: systematic review. Drug Alcohol Depend. 2013;131(1-2):23-35. http:// doi.org/10.1016/j.drugalcdep.2013.02.018 PubMed
10. Merrill JO, Rhodes LA, Deyo RA, Marlatt GA, Bradley KA. Mutual mistrust in the medical care of drug users: the keys to the “narc” cabinet. J Gen Intern Med. 2002;17(5):327-333. http:// doi.org/10.1046/j.1525-1497.2002.10625.x. PubMed
11. Brener L, Von Hippel W, Kippax S, Preacher KJ. The role of physician and nurse attitudes in the health care of injecting drug users. Subst Use Misuse. 2010;45(7-8):1007-1018. http:// doi.org/10.3109/10826081003659543. PubMed
12. Wakeman SE, Metlay JP, Chang Y, Herman GE, Rigotti NA. Inpatient addiction consultation for hospitalized patients increases post-discharge abstinence and reduces addiction severity. J Gen Intern Med. 2017;32(8):909-916. http:// doi.org/10.1007/s11606-017-4077-z. PubMed
13. Wei J, Defries T, Lozada M, Young N, Huen W, Tulsky J. An inpatient treatment and discharge planning protocol for alcohol dependence: efficacy in reducing 30-day readmissions and emergency department visits. J Gen Intern Med. 2015;30(3):365-370. http:// doi.org/10.1007/s11606-014-2968-9. PubMed
14. Liebschutz JM, Crooks D, Herman D, et al. Buprenorphine treatment for hospitalized, opioid-dependent patients: a randomized clinical trial. JAMA Intern Med. 2014;174(8):1369-1376. http:// doi.org/10.1001/jamainternmed.2014.2556. PubMed
15. Shanahan CW, Beers D, Alford DP, Brigandi E, Samet JH. A transitional opioid program to engage hospitalized drug users. J Gen Intern Med. 2010;25(8):803-808. http:// doi.org/10.1007/s11606-010-1311-3. PubMed
16. Parmelli E, Flodgren G, Beyer F, Baillie N, Schaafsma ME, Eccles MP. The effectiveness of strategies to change organisational culture to improve healthcare performance: a systematic review. Implement Sci. 2011;6(1):33. http:// doi.org/10.1186/1748-5908-6-33. PubMed
17. Englander H, Weimer M, Solotaroff R, et al. Planning and designing the improving addiction care team (IMPACT) for hospitalized adults with substance use disorder. J Hosp Med. 2017;12(5):339-342. http:// doi.org/10.12788/jhm.2736. PubMed
18. Lambert SD, Loiselle CG. Combining individual interviews and focus groups to enhance data richness. J Adv Nurs. 2008;62(2):228-237. http:// doi.org/10.1111/j.1365-2648.2007.04559.x. PubMed
19. Braun VC, Victoria. Using thematic analysis in psychology. Qual Res Psychol. 2006;3:25. http://dx.doi.org/10.1191/1478088706qp063oa.
20. Wakeman SE, Kanter GP, Donelan K. Institutional substance use disorder intervention improves general internist preparedness, attitudes, and clinical practice. J Addict Med. 2017;11(4):308-314. http:// doi.org/10.1097/ADM.0000000000000314. PubMed
21. Paterson B, Hirsch G, Andres K. Structural factors that promote stigmatization of drug users with hepatitis C in hospital emergency departments. Int J Drug Policy. 2013;24(5):471-478. http:// doi.org/10.1016/j.drugpo.2013.01.008 PubMed
22. Ross LE, Vigod S, Wishart J, et al. Barriers and facilitators to primary care for people with mental health and/or substance use issues: a qualitative study. BMC Fam Pract. 2015;16:135. http:// doi.org/10.1186/s12875-015-0353-3. PubMed
Substance use disorders (SUD) represent a national epidemic with death rates exceeding those of HIV at its peak.1 Hospitals are increasingly filled with people suffering from medical complications of addiction.2,3 While the US health system spends billions of dollars annually on hospital care for medical problems resulting from SUD,4 most hospitals lack expertise or care systems to directly address SUD or connect people to treatment after discharge. 5,6
Patients with SUD often feel stigmatized in healthcare settings and want providers who understand SUD and how to treat it.7 Providers feel underprepared8 and commonly have negative attitudes toward patients with SUD.9,10 Caring for patients can be a source of resentment, dissatisfaction, and burnout.9 Such negative attitudes can adversely affect patient care. Studies show that patients who perceive discrimination by providers are less likely to complete treatment11 and providers’ negative attitudes may disempower patients.9
Evaluations of hospital interventions for adults with SUD focus primarily on patient-level outcomes of SUD severity,12 healthcare utilization,13 and treatment engagement.14,15 Little is known about how such interventions can affect interprofessional providers’ attitudes and experiences, or how systems-level interventions influence hospital culture.16
We performed a qualitative study of multidisciplinary hospital providers to 1) understand the challenges that hospital providers face in managing care for patients with SUD, and 2) explore how integrating SUD treatment in a hospital setting affects providers’ attitudes, experiences, and perceptions of the care environment. This study was part of a formative evaluation of the Improving Addiction Care Team (IMPACT). IMPACT includes a hospital-based, interprofessional addiction medicine consultation service and rapid-access pathways to community addiction care after hospitalization.17. IMPACT is an intensive intervention that includes SUD assessments, withdrawal management, medications for addiction (eg, methadone, buprenorphine induction), counseling and behavioral SUD treatment, peer engagement and support, and linkages to community-based addiction care. We described the rationale and design of IMPACT in earlier publications.7,17
METHODS
Setting
We conducted in-person interviews and focus groups (FGs) with interprofessional hospital providers at a single urban academic medical center between February and July 2016, six months after starting IMPACT implementation. Oregon Health and Science University’s (OHSU) institutional review board approved the protocol.
Participants
We conducted 12 individual informant interviews (IIs) and 6 (FGs) (each comprising 3-6 participants) with a wide range of providers, including physicians, nurses, social workers, residents, patient advocates, case managers, and pharmacists. In total, 34 providers participated. We used purposive sampling to choose participants with experience both caring for patients with SUD and with exposure to IMPACT. Participant characteristics are summarized in Table 1.
Data Collection
We employed 2 different types of interviews. In situations where multiple providers occupied a similar role (eg, social workers), we chose to use a focus group format to elicit a range of perspectives and experiences through participant interaction.18 We conducted individual interviews to gain input from key informants who had unique roles in the program (eg, a cardiac surgeon) and to include providers who would otherwise be unable to participate due to scheduling barriers (eg, residents). We interviewed all participants using a semi-structured interview guide that was developed by an interdisciplinary team, including expert qualitative researchers, IMPACT clinical team members, and other OHSU clinicians (Appendix A). An interviewer who was not a part of the IMPACT clinical team asked all participants about their experience caring for patients with SUD, their experience with IMPACT, and how they might improve care. FGs lasted between 41-57 minutes, and individual key informant interviews lasted between 11-38 minutes. We ended recruitment after reaching theme saturation. Our goal was to achieve saturation across the sample as a whole and not within distinct participant groups. We noted if certain themes were more salient for 1 particular group. We audio-recorded all interviews and FGs. Recordings were transcribed, de-identified, and transferred to ATLAS.ti for data analysis.
Analysis
We conducted a thematic analysis using an inductive approach at the semantic level.19 Using an iterative process, we generated a preliminary coding schema after reviewing an initial selection of transcripts. Coders then independently coded transcripts and met in dyads to both discuss and reconcile codes, and resolve any discrepancies through discussion until reaching a consensus. One coder (DC) coded all transcripts; 3 coders (EP, SPP, MR) divided the transcripts evenly. All authors met periodically to discuss codebook revisions and emergent themes. We identified themes that represented patterns, had meaning to study participants, and captured important findings related to our research questions.19
As expected, the style of IIs differed from that of FGs and informants were able to provide information specific to their roles. Overall, the information provided by IIs was complementary to that of FGs and helped triangulate findings. Thus, we combined them in the results.18
RESULTS
We organized our findings into 3 main groupings, including (1) care before IMPACT, (2) care with IMPACT, and (3) perceived limitations of IMPACT. We included a table (Table 2) with additional quotations, beyond those in the body of the results, to support emergent themes described below.
Care before IMPACT
Providers felt hospitalization did not address addiction for many reasons, including ethical and legal concerns, medical knowledge gaps, and lack of treatment options.
Before IMPACT, many participants noted that hospitalization ignored or avoided addressing addiction, leading to a chaotic care environment that adversely affected patient care and provider experience. As one social worker stated, “prior to IMPACT we provided assessments, and we provided resources. But we didn’t address addiction.”
Providers cited multiple explanations for this, including the common misperception that using methadone to treat withdrawal violated federal regulations, and concerns about the ethicality of using opioids in patients with SUD. Across disciplines, providers described a “huge knowledge gap” and little confidence in addressing withdrawal, complex chronic pain, medications for addiction, and challenging patient behaviors. Providers also described limited expertise and scarce treatment options as a deterrent. As one attending reflected, “I would ask those questions [about SUD] before, but then … I had the information, but I couldn’t do anything with it.”
Providers felt the failure to address SUD adversely affected patient care, leading to untreated withdrawal, disruptive behaviors, and patients leaving against medical advice (AMA).
Participants across disciplines described wide variability in the medical management of SUD, particularly around the management of opioid withdrawal and pain, with some providers who “simply wouldn’t prescribe methadone or any opiates” and others who prescribed high doses without anticipating risks. As one attending recalled:
“You would see this pattern, especially in the intravenous drug-using population: left AMA, left AMA, left AMA … nine times out of ten, nobody was dealing with the fact that they were gonna go into withdrawal.”
Respondents recalled that disruptive behaviors from patients’ active use or withdrawal frequently threatened safety; imposed a tremendous burden on staff time and morale; and were a consistent source of providers’ distress. As one patient advocate explained:
“[Providers] get called to the unit because the person is yelling and throwing things or comes back after being gone for a long period and appears impaired … it often blows up, and they get discharged or they leave against medical advice or they go out and don’t come back. We don’t really know what happened to them, and they’re vulnerable. And the staff are vulnerable. And other patients are distressed by the disruption and commotion.”
Absent standards and systems to address SUD, providers felt they were “left to their own,” resulting in a reactive and chaotic care environment.
Providers noted inconsistent rules and policies regarding smoke breaks, room searches, and visitors. As a result, care felt “reckless and risky” and led to a “nonalliance” across disciplines. Providers frequently described inconsistent and loose expectations until an event -- often active use – triggered an ad hoc ratcheting up of the rules, damaging patient-provider relationships and limiting providers’ ability to provide medical care. Facing these conflicts, “staff gets escalated, and everybody gets kind of spun up.” As one attending reflected:
“I could not get any sort of engagement even in just her medical issues … I was trying to talk to her and educate her about heart failure and salt intake and food intake, but every time I walked in the room … I’d have to come in and be like, ‘your UDS [urine drug screen] was positive again, so here’s the changes to your behavioral plan, and OK, let’s talk about your heart failure …’ At that point, the relationship had completely disintegrated until it was very nonproductive.”
Providers described widespread “moral distress,” burnout, and feelings of futility before IMPACT.
Consequently, providers felt that caring for people with SUD was “very emotionally draining and very time consuming.” As one patient advocate described:
“We’ve been watching staff try to manage these patients for years without the experts and the resources and the skills that they need … As a result, there was a crescendo effect of moral distress, and [staff] bring in all of their past experiences which influence the interaction … Some staff are very skilled, but you also saw some really punitive responses.”
Many felt that providing intensive medical care without addressing people’s underlying SUD was a waste of time and resources. As one cardiac surgeon reflected:
“[Patients] ended up either dead or reinfected. Nobody wanted to do stuff because we felt it was futile. Well, of course, it’s futile …. you’re basically trying to fix the symptoms. It’s like having a leaky roof and just running around with a bunch of buckets, which is like surgery. You gotta fix the roof…otherwise they will continue to inject bacteria into their bodies.”
Care with IMPACT:
Providers felt integrating hospital-based systems to address SUD legitimized addiction as a treatable disease.
Participants described IMPACT as a “sea change” that “completely reframes” addiction as “a medical condition that actually has a treatment.” As one social worker observed, “when it’s somebody in a white coat with expertise who’s talking to another doctor it really can shift mindsets in an amazing way.” Others echoed this, stating that an addiction team “legitimized the fact that this is an actual disease that we need to treat - and a failure to treat it is a failure to be a good doctor.”
Providers felt that by addressing addiction directly, “IMPACT elevated the consciousness of providers and nurses … that substance use disorders are brain disorders and not bad behavior.” They described that this legitimization, combined with seeing firsthand the stabilizing effects of medications for addiction, allowed providers to understand SUD as a chronic disease, and not a moral failing.
Providers felt IMPACT improved patient engagement and humanized care by treating withdrawal, directly communicating about SUD, and modeling compassionate care.
Providers noted that treating withdrawal had a dramatic effect on patient engagement and care. One surgeon explained, “by managing their opioid dependence and other substance abuse issues … it’s easier for the staff to take care of them, it’s safer, and the patients feel better taken care of because the staff will engage with them.” Many noted that conflict-ridden “conversations were able to go to the side, and we were able to talk about other things to build rapport.” Others noted that this shift felt like “more productive time.”
In addition, providers repeatedly emphasized that having clear hospital standards and a process to engage patients “really helps … establish rapport with patients: ‘This is how we work this. These are your boundaries. And this is what will happen if you push those boundaries.’ There it is.” Providers attributed improved patient-provider communication to “frank conversation,” “the right amount of empathy,” and a less judgmental environment. As one attending described, “I don’t know if it gives them a voice or allows us to hear them better … but something’s happening with communication.”
Many participants highlighted that IMPACT modeled compassionate bedside interactions, exposed the role of trauma in many patients’ lives, and helped providers see SUD as a disease spectrum. One attending noted that to “actually appreciate the subtleties – just the severity of the disorder – has been powerful.” One resident said:
“There’s definitely a lot of stigma around patients with use disorders that probably shows itself in subtle ways throughout their hospitalization. I think IMPACT does a good job … keeping the patient in the center and keeping their use disorder contextualized in the greater person … [IMPACT] role models bedside interactions and how to treat people like humans.”
Providers valued post-hospital SUD treatment pathways.
Providers valued previously nonexistent post-hospital SUD treatment pathways, stating “this relationship with [community treatment] … it’s like an answer to prayers,” and “this isn’t just like we’re being nicer.” One attending described:
“Starting them on [methadone or buprenorphine-naloxone] and then making the next step in the outpatient world happen has been huge. That transition is so critical … that’s been probably the biggest impact.”
Providers felt relief after IMPACT implementation.
Providers felt that by addressing SUD treatment gaps and providing addiction expertise, IMPACT helped alleviate the previously widespread feelings of “moral distress.” One resident explained “having [IMPACT] as a lifeline, it just feels so good.” As an infectious disease consultant noted, “it makes people more open to treating people if they don’t feel isolated and out of their depth.” Others noted that IMPACT supported better multidisciplinary collaboration, which “reduced a lot of tension between the teams.” One nurse summarized:
“I think you feel more empowered when you’ve got the right medication, … the knowledge, and you feel like you have the resources. You actually feel like you’re making a difference.”
Respondents acknowledged that even with IMPACT, some patients leave AMA or relapse. However, by understanding addiction as a relapsing and remitting disease, providers reconceptualized “success,” further reducing feelings of emotional burnout and stress: “there will be ups and downs, it’s not gonna be a straight linear success.” One case manager reflected,
“Maybe that’s part of the nature of the illness, you progress, and then you kind of hold your breath and then it slips again … at least with IMPACT at the table I can say we’ve done the best we can for this person.”
Perceived limitations of IMPACT:
Providers noted several key limitations of IMPACT, including that hospital-based interventions do not address poverty and have limited ability to address socioeconomic determinants such as “social support, … housing, or nutrition.” Providers also felt that IMPACT had limited ability to alleviate patients’ feelings of boredom and isolation associated with prolonged hospitalization, and that IMPACT had limited effectiveness for highly ambivalent patients (Table 2).
Finally, while many described increased confidence managing SUD after working with IMPACT, others cautioned against deferring too much to specialists. As one resident doctor said:
“We shouldn’t forget that all providers should know how to handle some form of people with addiction … I just don’t want it to be like, ‘oh, well, no, I don’t need to think about this … because we have an addiction specialist.’”
Participants across disciplines repeatedly suggested formal, ongoing initiatives to educate and train providers to manage SUD independently.
DISCUSSION
This study explores provider perspectives on care for hospitalized adults with SUD. Before IMPACT, providers felt care was chaotic, unsafe, and frustrating. Providers perceived variable care quality, resulting in untreated withdrawal, inconsistent care plans, and poor patient outcomes, leading to widespread “moral distress” and feelings of futility among providers. Yet this experience was not inevitable. Providers described that a hospital-based intervention to treat SUD reframed addiction as a treatable chronic disease, transformed culture, and improved patient care and provider experience.
Our findings are consistent with and build on previous research in several ways. First, widespread anxiety and difficulty managing patients with SUD was not unique to our hospital. In a systematic review, van Boekel and colleagues describe that healthcare providers perceived violence, manipulation, and poor motivation as factors impeding care for patients with SUD.9 Our study demonstrates the resulting feelings of powerlessness and frustration may be alleviated through an intervention that provides SUD care.
Second, our study is consistent with a recent survey-based study by Wakeman and colleagues that found that a hospital-based SUD intervention improved providers’ feelings of preparedness and satisfaction.20 Our study provides a rich qualitative description and elucidates mechanisms by which such interventions may work.
The finding that a hospital-based SUD intervention can shift providers’ views of addiction is important. Earlier studies have shown that providers who perceive addiction as a choice are more likely to have negative attitudes toward people with SUD.11 While our intervention did not provide formal education aimed at changing attitudes, participants reported that seeing firsthand effects of treatment on patient behaviors was a powerful tool that radically shifted providers’ understanding and reduced stigma.
Stigma can occur at both individual and organizational levels. Structural stigma refers to practices, policies, and norms of institutions that exclude needs of a particular group.21 The absence of systems to address SUD sends a message to both patients and providers that addiction is a not a treatable or worthy disease. IMPACT was in and of itself a systems-level intervention; by creating a consultation service, hospital-wide policies, and pathways to care after hospitalization, IMPACT ‘legitimized’ SUD and reduced institutional stigma.
Several studies have shown the feasibility and effectiveness of starting medications for addiction (MAT) in the hospital.13-15 Our study builds on this work by highlighting systems-level elements valued by providers. These elements may be important to support and scale widespread adoption of MAT in hospitals. Specifically, providers felt that IMPACT’s attention to hospital policies, use of addiction medicine specialists, and direct linkages to outpatient SUD treatment proved instrumental in shifting care systems.
Our study has several limitations. As a single-site study, our goal was not generalizability, but transferability. As such, we aimed to obtain rich, in-depth information that can inform implementation of similar efforts. Because our study was conducted after the implementation of IMPACT, providers’ perspectives on care before IMPACT may have been influenced by the intervention. However, this also strengthens our findings by allowing participants the opportunity for insights under a different system. It likely leads to distinct findings compared to what we might have uncovered in a pre-post study. While respondents noted perceived limitations of IMPACT, there were few instances of negative remarks in the data we collected. It is possible that providers with more negative interpretations chose not to participate in interviews; however, we elicited wide viewpoints and encouraged participants to share both strengths and weaknesses. Finally, IMPACT implementation depends on regional as well as local factors such as Medicaid expansion, community treatment resources, and the existence of addiction medicine expertise that will differ across settings.
Despite these limitations, our study has several important implications. For clinical practice, our findings highlight the importance of treating withdrawal to address challenging patient behaviors and the value of integrating MAT into the hospital setting. Our findings also underscore the role of expert consultation for addiction. Importantly, our results emphasize that reframing SUD as a brain disease can have significant implications for clinical care and providers’ well-being. Provider distress is not inevitable and can change with the right support and systems.
At the hospital and health systems level, our findings suggest that hospitals can and should address SUD. This may include forming interprofessional teams with SUD expertise, providing standardized guidelines for addiction care such as patient safety plans and methadone policies, and creating rapid-access pathways to outpatient SUD care. By addressing SUD, hospitals may simultaneously improve care and reduce provider burnout. Providers’ important concerns about shifting SUD treatment to a specialty team and their discomfort managing SUD pre-IMPACT suggest the need to integrate SUD education across all levels of interprofessional education. Furthermore, provider concerns that IMPACT has limited ability to engage ambivalent patients underscores the need for hospital-based approaches that emphasize harm reduction strategies.
As the SUD epidemic worsens, SUD-related hospitalizations are skyrocketing, and people are dying at unprecedented rates.2,3 Many efforts to address SUD have been in primary care or community settings. While important, many people with SUD are unable or unlikely to seek primary care. 22 Hospitals need a workforce and systems that can address both the physical and behavioral health needs of this population. By implementing SUD improvements, hospitals can support staff and reduce burnout, better engage patients, improve care, and reduce stigma from this devastating disease
Disclosures
The authors have no conflicts of interest to disclose.
Substance use disorders (SUD) represent a national epidemic with death rates exceeding those of HIV at its peak.1 Hospitals are increasingly filled with people suffering from medical complications of addiction.2,3 While the US health system spends billions of dollars annually on hospital care for medical problems resulting from SUD,4 most hospitals lack expertise or care systems to directly address SUD or connect people to treatment after discharge. 5,6
Patients with SUD often feel stigmatized in healthcare settings and want providers who understand SUD and how to treat it.7 Providers feel underprepared8 and commonly have negative attitudes toward patients with SUD.9,10 Caring for patients can be a source of resentment, dissatisfaction, and burnout.9 Such negative attitudes can adversely affect patient care. Studies show that patients who perceive discrimination by providers are less likely to complete treatment11 and providers’ negative attitudes may disempower patients.9
Evaluations of hospital interventions for adults with SUD focus primarily on patient-level outcomes of SUD severity,12 healthcare utilization,13 and treatment engagement.14,15 Little is known about how such interventions can affect interprofessional providers’ attitudes and experiences, or how systems-level interventions influence hospital culture.16
We performed a qualitative study of multidisciplinary hospital providers to 1) understand the challenges that hospital providers face in managing care for patients with SUD, and 2) explore how integrating SUD treatment in a hospital setting affects providers’ attitudes, experiences, and perceptions of the care environment. This study was part of a formative evaluation of the Improving Addiction Care Team (IMPACT). IMPACT includes a hospital-based, interprofessional addiction medicine consultation service and rapid-access pathways to community addiction care after hospitalization.17. IMPACT is an intensive intervention that includes SUD assessments, withdrawal management, medications for addiction (eg, methadone, buprenorphine induction), counseling and behavioral SUD treatment, peer engagement and support, and linkages to community-based addiction care. We described the rationale and design of IMPACT in earlier publications.7,17
METHODS
Setting
We conducted in-person interviews and focus groups (FGs) with interprofessional hospital providers at a single urban academic medical center between February and July 2016, six months after starting IMPACT implementation. Oregon Health and Science University’s (OHSU) institutional review board approved the protocol.
Participants
We conducted 12 individual informant interviews (IIs) and 6 (FGs) (each comprising 3-6 participants) with a wide range of providers, including physicians, nurses, social workers, residents, patient advocates, case managers, and pharmacists. In total, 34 providers participated. We used purposive sampling to choose participants with experience both caring for patients with SUD and with exposure to IMPACT. Participant characteristics are summarized in Table 1.
Data Collection
We employed 2 different types of interviews. In situations where multiple providers occupied a similar role (eg, social workers), we chose to use a focus group format to elicit a range of perspectives and experiences through participant interaction.18 We conducted individual interviews to gain input from key informants who had unique roles in the program (eg, a cardiac surgeon) and to include providers who would otherwise be unable to participate due to scheduling barriers (eg, residents). We interviewed all participants using a semi-structured interview guide that was developed by an interdisciplinary team, including expert qualitative researchers, IMPACT clinical team members, and other OHSU clinicians (Appendix A). An interviewer who was not a part of the IMPACT clinical team asked all participants about their experience caring for patients with SUD, their experience with IMPACT, and how they might improve care. FGs lasted between 41-57 minutes, and individual key informant interviews lasted between 11-38 minutes. We ended recruitment after reaching theme saturation. Our goal was to achieve saturation across the sample as a whole and not within distinct participant groups. We noted if certain themes were more salient for 1 particular group. We audio-recorded all interviews and FGs. Recordings were transcribed, de-identified, and transferred to ATLAS.ti for data analysis.
Analysis
We conducted a thematic analysis using an inductive approach at the semantic level.19 Using an iterative process, we generated a preliminary coding schema after reviewing an initial selection of transcripts. Coders then independently coded transcripts and met in dyads to both discuss and reconcile codes, and resolve any discrepancies through discussion until reaching a consensus. One coder (DC) coded all transcripts; 3 coders (EP, SPP, MR) divided the transcripts evenly. All authors met periodically to discuss codebook revisions and emergent themes. We identified themes that represented patterns, had meaning to study participants, and captured important findings related to our research questions.19
As expected, the style of IIs differed from that of FGs and informants were able to provide information specific to their roles. Overall, the information provided by IIs was complementary to that of FGs and helped triangulate findings. Thus, we combined them in the results.18
RESULTS
We organized our findings into 3 main groupings, including (1) care before IMPACT, (2) care with IMPACT, and (3) perceived limitations of IMPACT. We included a table (Table 2) with additional quotations, beyond those in the body of the results, to support emergent themes described below.
Care before IMPACT
Providers felt hospitalization did not address addiction for many reasons, including ethical and legal concerns, medical knowledge gaps, and lack of treatment options.
Before IMPACT, many participants noted that hospitalization ignored or avoided addressing addiction, leading to a chaotic care environment that adversely affected patient care and provider experience. As one social worker stated, “prior to IMPACT we provided assessments, and we provided resources. But we didn’t address addiction.”
Providers cited multiple explanations for this, including the common misperception that using methadone to treat withdrawal violated federal regulations, and concerns about the ethicality of using opioids in patients with SUD. Across disciplines, providers described a “huge knowledge gap” and little confidence in addressing withdrawal, complex chronic pain, medications for addiction, and challenging patient behaviors. Providers also described limited expertise and scarce treatment options as a deterrent. As one attending reflected, “I would ask those questions [about SUD] before, but then … I had the information, but I couldn’t do anything with it.”
Providers felt the failure to address SUD adversely affected patient care, leading to untreated withdrawal, disruptive behaviors, and patients leaving against medical advice (AMA).
Participants across disciplines described wide variability in the medical management of SUD, particularly around the management of opioid withdrawal and pain, with some providers who “simply wouldn’t prescribe methadone or any opiates” and others who prescribed high doses without anticipating risks. As one attending recalled:
“You would see this pattern, especially in the intravenous drug-using population: left AMA, left AMA, left AMA … nine times out of ten, nobody was dealing with the fact that they were gonna go into withdrawal.”
Respondents recalled that disruptive behaviors from patients’ active use or withdrawal frequently threatened safety; imposed a tremendous burden on staff time and morale; and were a consistent source of providers’ distress. As one patient advocate explained:
“[Providers] get called to the unit because the person is yelling and throwing things or comes back after being gone for a long period and appears impaired … it often blows up, and they get discharged or they leave against medical advice or they go out and don’t come back. We don’t really know what happened to them, and they’re vulnerable. And the staff are vulnerable. And other patients are distressed by the disruption and commotion.”
Absent standards and systems to address SUD, providers felt they were “left to their own,” resulting in a reactive and chaotic care environment.
Providers noted inconsistent rules and policies regarding smoke breaks, room searches, and visitors. As a result, care felt “reckless and risky” and led to a “nonalliance” across disciplines. Providers frequently described inconsistent and loose expectations until an event -- often active use – triggered an ad hoc ratcheting up of the rules, damaging patient-provider relationships and limiting providers’ ability to provide medical care. Facing these conflicts, “staff gets escalated, and everybody gets kind of spun up.” As one attending reflected:
“I could not get any sort of engagement even in just her medical issues … I was trying to talk to her and educate her about heart failure and salt intake and food intake, but every time I walked in the room … I’d have to come in and be like, ‘your UDS [urine drug screen] was positive again, so here’s the changes to your behavioral plan, and OK, let’s talk about your heart failure …’ At that point, the relationship had completely disintegrated until it was very nonproductive.”
Providers described widespread “moral distress,” burnout, and feelings of futility before IMPACT.
Consequently, providers felt that caring for people with SUD was “very emotionally draining and very time consuming.” As one patient advocate described:
“We’ve been watching staff try to manage these patients for years without the experts and the resources and the skills that they need … As a result, there was a crescendo effect of moral distress, and [staff] bring in all of their past experiences which influence the interaction … Some staff are very skilled, but you also saw some really punitive responses.”
Many felt that providing intensive medical care without addressing people’s underlying SUD was a waste of time and resources. As one cardiac surgeon reflected:
“[Patients] ended up either dead or reinfected. Nobody wanted to do stuff because we felt it was futile. Well, of course, it’s futile …. you’re basically trying to fix the symptoms. It’s like having a leaky roof and just running around with a bunch of buckets, which is like surgery. You gotta fix the roof…otherwise they will continue to inject bacteria into their bodies.”
Care with IMPACT:
Providers felt integrating hospital-based systems to address SUD legitimized addiction as a treatable disease.
Participants described IMPACT as a “sea change” that “completely reframes” addiction as “a medical condition that actually has a treatment.” As one social worker observed, “when it’s somebody in a white coat with expertise who’s talking to another doctor it really can shift mindsets in an amazing way.” Others echoed this, stating that an addiction team “legitimized the fact that this is an actual disease that we need to treat - and a failure to treat it is a failure to be a good doctor.”
Providers felt that by addressing addiction directly, “IMPACT elevated the consciousness of providers and nurses … that substance use disorders are brain disorders and not bad behavior.” They described that this legitimization, combined with seeing firsthand the stabilizing effects of medications for addiction, allowed providers to understand SUD as a chronic disease, and not a moral failing.
Providers felt IMPACT improved patient engagement and humanized care by treating withdrawal, directly communicating about SUD, and modeling compassionate care.
Providers noted that treating withdrawal had a dramatic effect on patient engagement and care. One surgeon explained, “by managing their opioid dependence and other substance abuse issues … it’s easier for the staff to take care of them, it’s safer, and the patients feel better taken care of because the staff will engage with them.” Many noted that conflict-ridden “conversations were able to go to the side, and we were able to talk about other things to build rapport.” Others noted that this shift felt like “more productive time.”
In addition, providers repeatedly emphasized that having clear hospital standards and a process to engage patients “really helps … establish rapport with patients: ‘This is how we work this. These are your boundaries. And this is what will happen if you push those boundaries.’ There it is.” Providers attributed improved patient-provider communication to “frank conversation,” “the right amount of empathy,” and a less judgmental environment. As one attending described, “I don’t know if it gives them a voice or allows us to hear them better … but something’s happening with communication.”
Many participants highlighted that IMPACT modeled compassionate bedside interactions, exposed the role of trauma in many patients’ lives, and helped providers see SUD as a disease spectrum. One attending noted that to “actually appreciate the subtleties – just the severity of the disorder – has been powerful.” One resident said:
“There’s definitely a lot of stigma around patients with use disorders that probably shows itself in subtle ways throughout their hospitalization. I think IMPACT does a good job … keeping the patient in the center and keeping their use disorder contextualized in the greater person … [IMPACT] role models bedside interactions and how to treat people like humans.”
Providers valued post-hospital SUD treatment pathways.
Providers valued previously nonexistent post-hospital SUD treatment pathways, stating “this relationship with [community treatment] … it’s like an answer to prayers,” and “this isn’t just like we’re being nicer.” One attending described:
“Starting them on [methadone or buprenorphine-naloxone] and then making the next step in the outpatient world happen has been huge. That transition is so critical … that’s been probably the biggest impact.”
Providers felt relief after IMPACT implementation.
Providers felt that by addressing SUD treatment gaps and providing addiction expertise, IMPACT helped alleviate the previously widespread feelings of “moral distress.” One resident explained “having [IMPACT] as a lifeline, it just feels so good.” As an infectious disease consultant noted, “it makes people more open to treating people if they don’t feel isolated and out of their depth.” Others noted that IMPACT supported better multidisciplinary collaboration, which “reduced a lot of tension between the teams.” One nurse summarized:
“I think you feel more empowered when you’ve got the right medication, … the knowledge, and you feel like you have the resources. You actually feel like you’re making a difference.”
Respondents acknowledged that even with IMPACT, some patients leave AMA or relapse. However, by understanding addiction as a relapsing and remitting disease, providers reconceptualized “success,” further reducing feelings of emotional burnout and stress: “there will be ups and downs, it’s not gonna be a straight linear success.” One case manager reflected,
“Maybe that’s part of the nature of the illness, you progress, and then you kind of hold your breath and then it slips again … at least with IMPACT at the table I can say we’ve done the best we can for this person.”
Perceived limitations of IMPACT:
Providers noted several key limitations of IMPACT, including that hospital-based interventions do not address poverty and have limited ability to address socioeconomic determinants such as “social support, … housing, or nutrition.” Providers also felt that IMPACT had limited ability to alleviate patients’ feelings of boredom and isolation associated with prolonged hospitalization, and that IMPACT had limited effectiveness for highly ambivalent patients (Table 2).
Finally, while many described increased confidence managing SUD after working with IMPACT, others cautioned against deferring too much to specialists. As one resident doctor said:
“We shouldn’t forget that all providers should know how to handle some form of people with addiction … I just don’t want it to be like, ‘oh, well, no, I don’t need to think about this … because we have an addiction specialist.’”
Participants across disciplines repeatedly suggested formal, ongoing initiatives to educate and train providers to manage SUD independently.
DISCUSSION
This study explores provider perspectives on care for hospitalized adults with SUD. Before IMPACT, providers felt care was chaotic, unsafe, and frustrating. Providers perceived variable care quality, resulting in untreated withdrawal, inconsistent care plans, and poor patient outcomes, leading to widespread “moral distress” and feelings of futility among providers. Yet this experience was not inevitable. Providers described that a hospital-based intervention to treat SUD reframed addiction as a treatable chronic disease, transformed culture, and improved patient care and provider experience.
Our findings are consistent with and build on previous research in several ways. First, widespread anxiety and difficulty managing patients with SUD was not unique to our hospital. In a systematic review, van Boekel and colleagues describe that healthcare providers perceived violence, manipulation, and poor motivation as factors impeding care for patients with SUD.9 Our study demonstrates the resulting feelings of powerlessness and frustration may be alleviated through an intervention that provides SUD care.
Second, our study is consistent with a recent survey-based study by Wakeman and colleagues that found that a hospital-based SUD intervention improved providers’ feelings of preparedness and satisfaction.20 Our study provides a rich qualitative description and elucidates mechanisms by which such interventions may work.
The finding that a hospital-based SUD intervention can shift providers’ views of addiction is important. Earlier studies have shown that providers who perceive addiction as a choice are more likely to have negative attitudes toward people with SUD.11 While our intervention did not provide formal education aimed at changing attitudes, participants reported that seeing firsthand effects of treatment on patient behaviors was a powerful tool that radically shifted providers’ understanding and reduced stigma.
Stigma can occur at both individual and organizational levels. Structural stigma refers to practices, policies, and norms of institutions that exclude needs of a particular group.21 The absence of systems to address SUD sends a message to both patients and providers that addiction is a not a treatable or worthy disease. IMPACT was in and of itself a systems-level intervention; by creating a consultation service, hospital-wide policies, and pathways to care after hospitalization, IMPACT ‘legitimized’ SUD and reduced institutional stigma.
Several studies have shown the feasibility and effectiveness of starting medications for addiction (MAT) in the hospital.13-15 Our study builds on this work by highlighting systems-level elements valued by providers. These elements may be important to support and scale widespread adoption of MAT in hospitals. Specifically, providers felt that IMPACT’s attention to hospital policies, use of addiction medicine specialists, and direct linkages to outpatient SUD treatment proved instrumental in shifting care systems.
Our study has several limitations. As a single-site study, our goal was not generalizability, but transferability. As such, we aimed to obtain rich, in-depth information that can inform implementation of similar efforts. Because our study was conducted after the implementation of IMPACT, providers’ perspectives on care before IMPACT may have been influenced by the intervention. However, this also strengthens our findings by allowing participants the opportunity for insights under a different system. It likely leads to distinct findings compared to what we might have uncovered in a pre-post study. While respondents noted perceived limitations of IMPACT, there were few instances of negative remarks in the data we collected. It is possible that providers with more negative interpretations chose not to participate in interviews; however, we elicited wide viewpoints and encouraged participants to share both strengths and weaknesses. Finally, IMPACT implementation depends on regional as well as local factors such as Medicaid expansion, community treatment resources, and the existence of addiction medicine expertise that will differ across settings.
Despite these limitations, our study has several important implications. For clinical practice, our findings highlight the importance of treating withdrawal to address challenging patient behaviors and the value of integrating MAT into the hospital setting. Our findings also underscore the role of expert consultation for addiction. Importantly, our results emphasize that reframing SUD as a brain disease can have significant implications for clinical care and providers’ well-being. Provider distress is not inevitable and can change with the right support and systems.
At the hospital and health systems level, our findings suggest that hospitals can and should address SUD. This may include forming interprofessional teams with SUD expertise, providing standardized guidelines for addiction care such as patient safety plans and methadone policies, and creating rapid-access pathways to outpatient SUD care. By addressing SUD, hospitals may simultaneously improve care and reduce provider burnout. Providers’ important concerns about shifting SUD treatment to a specialty team and their discomfort managing SUD pre-IMPACT suggest the need to integrate SUD education across all levels of interprofessional education. Furthermore, provider concerns that IMPACT has limited ability to engage ambivalent patients underscores the need for hospital-based approaches that emphasize harm reduction strategies.
As the SUD epidemic worsens, SUD-related hospitalizations are skyrocketing, and people are dying at unprecedented rates.2,3 Many efforts to address SUD have been in primary care or community settings. While important, many people with SUD are unable or unlikely to seek primary care. 22 Hospitals need a workforce and systems that can address both the physical and behavioral health needs of this population. By implementing SUD improvements, hospitals can support staff and reduce burnout, better engage patients, improve care, and reduce stigma from this devastating disease
Disclosures
The authors have no conflicts of interest to disclose.
1. Rossen L, Bastian B, Warner M, Khan D, Chong Y. Drug poisoning mortality: United States, 1999-2015. 2017; https://www.cdc.gov/nchs/data-visualization/drug-poisoning-mortality/. Accessed 7-11, 2017.
2. Tedesco D, Asch SM, Curtin C, et al. Opioid abuse and poisoning: trends in inpatient and emergency department discharges. Health Aff (Millwood). 2017;36(10):1748-1753. http:// doi.org/10.1377/hlthaff.2017.0260. PubMed
3. Weiss AJ, Elixhauser A, Barrett ML, Steiner CA, Bailey MK, O’Malley L. Statistical Brief #219: Opioid-Related Inpatient Stays and Emergency Department Visits by State, 2009-2014. 2017; https://hcup-us.ahrq.gov/reports/statbriefs/sb219-Opioid-Hospital-Stays-ED-Visits-by-State.jsp?utm_source=AHRQ&utm_medium=EN-2&utm_term=&utm_content=2&utm_campaign=AHRQ_EN12_20_2016. Accessed July 11, 2017. PubMed
4. Ronan MV, Herzig SJ. Hospitalizations related to opioid abuse/dependence and associated serious infections increased sharply, 2002-12. Health Aff (Millwood). 2016;35(5):832-837. http:// doi.org/10.1377/hlthaff.2015.1424. PubMed
5. Infectious Diseases Society of America Emerging Infections Network. Report for Query: ‘Injection Drug Use (IDU) and Infectious Disease Practice’. 2017; https://www.int-med.uiowa.edu/Research/EIN/FinalReport_IDUandID.pdf. Accessed July 11, 2017.
6. Rosenthal ES, Karchmer AW, Theisen-Toupal J, Castillo RA, Rowley CF. Suboptimal addiction interventions for patients hospitalized with injection drug use-associated infective endocarditis. Am J Med. 2016;129(5):481-485. http:// doi.org/10.1016/j.amjmed.2015.09.024. PubMed
7. Velez CM, Nicolaidis C, Korthuis PT, Englander H. “It’s been an Experience, a Life Learning Experience”: A qualitative study of hospitalized patients with substance use disorders. J Gen Intern Med. 2017;32(3):296-303. http:// doi.org/10.1007/s11606-016-3919-4. PubMed
8. Wakeman SE, Pham-Kanter G, Donelan K. Attitudes, practices, and preparedness to care for patients with substance use disorder: Results from a survey of general internists. Subst Abus. 2016;37(4):635-641. http:// doi.org/10.1080/08897077.2016.1187240. PubMed
9. van Boekel LC, Brouwers EP, van Weeghel J, Garretsen HF. Stigma among health professionals towards patients with substance use disorders and its consequences for healthcare delivery: systematic review. Drug Alcohol Depend. 2013;131(1-2):23-35. http:// doi.org/10.1016/j.drugalcdep.2013.02.018 PubMed
10. Merrill JO, Rhodes LA, Deyo RA, Marlatt GA, Bradley KA. Mutual mistrust in the medical care of drug users: the keys to the “narc” cabinet. J Gen Intern Med. 2002;17(5):327-333. http:// doi.org/10.1046/j.1525-1497.2002.10625.x. PubMed
11. Brener L, Von Hippel W, Kippax S, Preacher KJ. The role of physician and nurse attitudes in the health care of injecting drug users. Subst Use Misuse. 2010;45(7-8):1007-1018. http:// doi.org/10.3109/10826081003659543. PubMed
12. Wakeman SE, Metlay JP, Chang Y, Herman GE, Rigotti NA. Inpatient addiction consultation for hospitalized patients increases post-discharge abstinence and reduces addiction severity. J Gen Intern Med. 2017;32(8):909-916. http:// doi.org/10.1007/s11606-017-4077-z. PubMed
13. Wei J, Defries T, Lozada M, Young N, Huen W, Tulsky J. An inpatient treatment and discharge planning protocol for alcohol dependence: efficacy in reducing 30-day readmissions and emergency department visits. J Gen Intern Med. 2015;30(3):365-370. http:// doi.org/10.1007/s11606-014-2968-9. PubMed
14. Liebschutz JM, Crooks D, Herman D, et al. Buprenorphine treatment for hospitalized, opioid-dependent patients: a randomized clinical trial. JAMA Intern Med. 2014;174(8):1369-1376. http:// doi.org/10.1001/jamainternmed.2014.2556. PubMed
15. Shanahan CW, Beers D, Alford DP, Brigandi E, Samet JH. A transitional opioid program to engage hospitalized drug users. J Gen Intern Med. 2010;25(8):803-808. http:// doi.org/10.1007/s11606-010-1311-3. PubMed
16. Parmelli E, Flodgren G, Beyer F, Baillie N, Schaafsma ME, Eccles MP. The effectiveness of strategies to change organisational culture to improve healthcare performance: a systematic review. Implement Sci. 2011;6(1):33. http:// doi.org/10.1186/1748-5908-6-33. PubMed
17. Englander H, Weimer M, Solotaroff R, et al. Planning and designing the improving addiction care team (IMPACT) for hospitalized adults with substance use disorder. J Hosp Med. 2017;12(5):339-342. http:// doi.org/10.12788/jhm.2736. PubMed
18. Lambert SD, Loiselle CG. Combining individual interviews and focus groups to enhance data richness. J Adv Nurs. 2008;62(2):228-237. http:// doi.org/10.1111/j.1365-2648.2007.04559.x. PubMed
19. Braun VC, Victoria. Using thematic analysis in psychology. Qual Res Psychol. 2006;3:25. http://dx.doi.org/10.1191/1478088706qp063oa.
20. Wakeman SE, Kanter GP, Donelan K. Institutional substance use disorder intervention improves general internist preparedness, attitudes, and clinical practice. J Addict Med. 2017;11(4):308-314. http:// doi.org/10.1097/ADM.0000000000000314. PubMed
21. Paterson B, Hirsch G, Andres K. Structural factors that promote stigmatization of drug users with hepatitis C in hospital emergency departments. Int J Drug Policy. 2013;24(5):471-478. http:// doi.org/10.1016/j.drugpo.2013.01.008 PubMed
22. Ross LE, Vigod S, Wishart J, et al. Barriers and facilitators to primary care for people with mental health and/or substance use issues: a qualitative study. BMC Fam Pract. 2015;16:135. http:// doi.org/10.1186/s12875-015-0353-3. PubMed
1. Rossen L, Bastian B, Warner M, Khan D, Chong Y. Drug poisoning mortality: United States, 1999-2015. 2017; https://www.cdc.gov/nchs/data-visualization/drug-poisoning-mortality/. Accessed 7-11, 2017.
2. Tedesco D, Asch SM, Curtin C, et al. Opioid abuse and poisoning: trends in inpatient and emergency department discharges. Health Aff (Millwood). 2017;36(10):1748-1753. http:// doi.org/10.1377/hlthaff.2017.0260. PubMed
3. Weiss AJ, Elixhauser A, Barrett ML, Steiner CA, Bailey MK, O’Malley L. Statistical Brief #219: Opioid-Related Inpatient Stays and Emergency Department Visits by State, 2009-2014. 2017; https://hcup-us.ahrq.gov/reports/statbriefs/sb219-Opioid-Hospital-Stays-ED-Visits-by-State.jsp?utm_source=AHRQ&utm_medium=EN-2&utm_term=&utm_content=2&utm_campaign=AHRQ_EN12_20_2016. Accessed July 11, 2017. PubMed
4. Ronan MV, Herzig SJ. Hospitalizations related to opioid abuse/dependence and associated serious infections increased sharply, 2002-12. Health Aff (Millwood). 2016;35(5):832-837. http:// doi.org/10.1377/hlthaff.2015.1424. PubMed
5. Infectious Diseases Society of America Emerging Infections Network. Report for Query: ‘Injection Drug Use (IDU) and Infectious Disease Practice’. 2017; https://www.int-med.uiowa.edu/Research/EIN/FinalReport_IDUandID.pdf. Accessed July 11, 2017.
6. Rosenthal ES, Karchmer AW, Theisen-Toupal J, Castillo RA, Rowley CF. Suboptimal addiction interventions for patients hospitalized with injection drug use-associated infective endocarditis. Am J Med. 2016;129(5):481-485. http:// doi.org/10.1016/j.amjmed.2015.09.024. PubMed
7. Velez CM, Nicolaidis C, Korthuis PT, Englander H. “It’s been an Experience, a Life Learning Experience”: A qualitative study of hospitalized patients with substance use disorders. J Gen Intern Med. 2017;32(3):296-303. http:// doi.org/10.1007/s11606-016-3919-4. PubMed
8. Wakeman SE, Pham-Kanter G, Donelan K. Attitudes, practices, and preparedness to care for patients with substance use disorder: Results from a survey of general internists. Subst Abus. 2016;37(4):635-641. http:// doi.org/10.1080/08897077.2016.1187240. PubMed
9. van Boekel LC, Brouwers EP, van Weeghel J, Garretsen HF. Stigma among health professionals towards patients with substance use disorders and its consequences for healthcare delivery: systematic review. Drug Alcohol Depend. 2013;131(1-2):23-35. http:// doi.org/10.1016/j.drugalcdep.2013.02.018 PubMed
10. Merrill JO, Rhodes LA, Deyo RA, Marlatt GA, Bradley KA. Mutual mistrust in the medical care of drug users: the keys to the “narc” cabinet. J Gen Intern Med. 2002;17(5):327-333. http:// doi.org/10.1046/j.1525-1497.2002.10625.x. PubMed
11. Brener L, Von Hippel W, Kippax S, Preacher KJ. The role of physician and nurse attitudes in the health care of injecting drug users. Subst Use Misuse. 2010;45(7-8):1007-1018. http:// doi.org/10.3109/10826081003659543. PubMed
12. Wakeman SE, Metlay JP, Chang Y, Herman GE, Rigotti NA. Inpatient addiction consultation for hospitalized patients increases post-discharge abstinence and reduces addiction severity. J Gen Intern Med. 2017;32(8):909-916. http:// doi.org/10.1007/s11606-017-4077-z. PubMed
13. Wei J, Defries T, Lozada M, Young N, Huen W, Tulsky J. An inpatient treatment and discharge planning protocol for alcohol dependence: efficacy in reducing 30-day readmissions and emergency department visits. J Gen Intern Med. 2015;30(3):365-370. http:// doi.org/10.1007/s11606-014-2968-9. PubMed
14. Liebschutz JM, Crooks D, Herman D, et al. Buprenorphine treatment for hospitalized, opioid-dependent patients: a randomized clinical trial. JAMA Intern Med. 2014;174(8):1369-1376. http:// doi.org/10.1001/jamainternmed.2014.2556. PubMed
15. Shanahan CW, Beers D, Alford DP, Brigandi E, Samet JH. A transitional opioid program to engage hospitalized drug users. J Gen Intern Med. 2010;25(8):803-808. http:// doi.org/10.1007/s11606-010-1311-3. PubMed
16. Parmelli E, Flodgren G, Beyer F, Baillie N, Schaafsma ME, Eccles MP. The effectiveness of strategies to change organisational culture to improve healthcare performance: a systematic review. Implement Sci. 2011;6(1):33. http:// doi.org/10.1186/1748-5908-6-33. PubMed
17. Englander H, Weimer M, Solotaroff R, et al. Planning and designing the improving addiction care team (IMPACT) for hospitalized adults with substance use disorder. J Hosp Med. 2017;12(5):339-342. http:// doi.org/10.12788/jhm.2736. PubMed
18. Lambert SD, Loiselle CG. Combining individual interviews and focus groups to enhance data richness. J Adv Nurs. 2008;62(2):228-237. http:// doi.org/10.1111/j.1365-2648.2007.04559.x. PubMed
19. Braun VC, Victoria. Using thematic analysis in psychology. Qual Res Psychol. 2006;3:25. http://dx.doi.org/10.1191/1478088706qp063oa.
20. Wakeman SE, Kanter GP, Donelan K. Institutional substance use disorder intervention improves general internist preparedness, attitudes, and clinical practice. J Addict Med. 2017;11(4):308-314. http:// doi.org/10.1097/ADM.0000000000000314. PubMed
21. Paterson B, Hirsch G, Andres K. Structural factors that promote stigmatization of drug users with hepatitis C in hospital emergency departments. Int J Drug Policy. 2013;24(5):471-478. http:// doi.org/10.1016/j.drugpo.2013.01.008 PubMed
22. Ross LE, Vigod S, Wishart J, et al. Barriers and facilitators to primary care for people with mental health and/or substance use issues: a qualitative study. BMC Fam Pract. 2015;16:135. http:// doi.org/10.1186/s12875-015-0353-3. PubMed
© 2018 Society of Hospital Medicine
TENS improves fibromyalgia pain
Also today, brisk walking may decrease total knee replacement, smoking is neglected in the treatment of some patients with peripheral arterial disease, and the ACP beefs up its firearms policy in the wake of the shooting in Pittsburgh.
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Also today, brisk walking may decrease total knee replacement, smoking is neglected in the treatment of some patients with peripheral arterial disease, and the ACP beefs up its firearms policy in the wake of the shooting in Pittsburgh.
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Apple Podcasts
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Also today, brisk walking may decrease total knee replacement, smoking is neglected in the treatment of some patients with peripheral arterial disease, and the ACP beefs up its firearms policy in the wake of the shooting in Pittsburgh.
Amazon Alexa
Apple Podcasts
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Treatment-resistant OCD: There’s more we can do
Treatment-resistant OCD can be a debilitating condition. Diagnostic clarity is crucial to fully elicit symptoms and identify comorbid conditions in order to develop practical, evidence-based treatment strategies and improve the patient’s and family’s quality of life. In this article, we delineate first-line strategies for treatment-resistant OCD and then review augmentation strategies, with an emphasis on glutamate-modulating agents.
Making the diagnosis
The diagnosis of OCD is made when a patient meets DSM-5 criteria for the presence of obsessions and/or compulsions, which are defined as unwanted, distressing, intrusive, recurrent thoughts or images (obsessions) and repetitive behaviors or mental acts (compulsions).1 OCD is considered a chronic waxing and waning disorder; stress and lack of sleep lead to worsening symptoms. The hidden nature of symptoms and the reinforcement provided by the reduction in anxiety after performing a compulsion contribute to sustained illness. Eliciting symptoms from patients may be challenging due to the shame they may feel. When reviewing symptoms on the Y-BOCS, it is helpful to preface questions with statements such as “Many people report excessive concern or disgust with…” to help the patient feel understood and less anxious, rather than using direct queries, such as “Are you bothered by…?”
Consider comorbid conditions
After making the initial diagnosis of OCD, it is important to assess whether the symptoms are better accounted for by another condition, and whether comorbid conditions are present (Table 1).
CASE CONTINUED
Ruling out other diagnoses
_
Initial treatment: CBT
Cognitive-behavioral therapy with exposures and response prevention (from here on referred to as CBT) has been established as a first-line, evidence-based treatment for OCD in both children and adults.2,3 For patients with treatment-resistant OCD, intensive daily CBT in a partial hospitalization or inpatient setting that is a tailor-made, patient-specific program is one of the most effective treatments, with response rates of up to 70%4-8 CBT’s advantages over medication include lower relapse rates and no known adverse effects. Unfortunately, CBT is underused9-11 due in part to a shortage of trained clinicians, and because patients may favor the ease of taking medication over the time, effort, and cost involved in CBT.
First-line pharmacologic options for treating OCD are SSRIs and clomipramine, as supported by multiple randomized controlled trials (RCTs), meta-analyses, expert guidelines, and consensus statements (Table 22,12-14). No significant difference has been found among SSRIs for the treatment of OCD in a review of 17 studies that included more than 3,000 patients.15 Treatment with SSRIs or clomipramine is effective for 50% to 60% of patients.16 Many clinicians view the combination of an SSRI and CBT as the treatment of choice for OCD.2
Continue to: Reluctance to engage in CBT
CASE CONTINUED
Reluctance to engage in CBT
To determine the next course of action, you review Mr. S’s treatment history. He has received adequate doses of 2 SSRIs and currently is taking clomipramine, 100 mg twice daily. He recently began CBT, which includes homework to help face his fears; however, Mr. S is reluctant to complete the exposure assignments, and after pausing for a few seconds as he tries to resist sending an apology email to his coworkers, he then returns to his compulsive behavior.
Facing treatment resistance
Although currently there isn’t a cure to resolve all traces of OCD, the goal of treatment is to decrease distress, interference, and the frequency of symptoms to a minimal level such that only the patients themselves are aware of symptoms. In broad terms, “response” has been defined as a decrease in symptoms, and “remission” has been defined as minimal symptoms after treatment.
Close to half of adults treated for OCD respond well to standard-of-care treatment (CBT and/or an SSRI), while the other 50% are considered partial responders or nonresponders.2 For patients with OCD, researchers often define “treatment response” as a ≥25% reduction in symptom severity score on the Y-BOCS. Approximately 30% of adults with OCD do not respond substantially to the first-line treatments, and even those who are defined as “responders” in research studies typically continue to have significant symptoms that impact their quality of life.2 In children, a clinical definition for treatment-refractory OCD has been presented as failing to achieve adequate symptom relief despite receiving an adequate course of CBT and at least 2 adequate trials of an SSRI or clomipramine.17 In the Pediatric OCD Treatment Study (POTS) trial, >46% of youth did not achieve remission from their OCD symptoms, even after receiving evidence-based care provided by experienced clinicians (combined treatment with CBT and an SSRI).18
_
Challenges in psychotherapy
Compassion is a key element in developing rapport with patients to help them face increasingly more challenging exposures. Making OCD the problem, not the person, is an essential element in helping patients move forward. Some clinicians may become frustrated with patients when treatment is not moving along well, referring to resistance, denial, or sabotage. According to March and Mulle,19 these terms lack the recognition and compassion that exposures are inherently difficult.19
Another challenge for therapists is if the patient’s presenting symptoms are personally offensive or a sensitive topic. For example, a therapist who is disgusted by public restrooms will find it difficult to tolerate the risks associated with exposure to germs and support a patient in touching objects in the restroom. Therapists also may be challenged when the patient’s fears align with the therapist’s religious beliefs. In these situations, consider transferring care to another therapist.
Family members need to learn about the nature of the illness and their roles in helping patients improve. Family members may unknowingly enable symptoms or criticize patients for their lack of motivation, which can lead to conflict in the home. Family dysfunction can in turn worsen OCD symptoms.
The most likely cause of lack of response to therapy is inexpert CBT.19 Deep breathing and relaxation training have been used as an active placebo in studies20; in a meta-analysis examining the effective components of CBT, studies that added relaxation training were not more effective than those that employed exposures alone.21 Patients receiving CBT should be able to articulate the hierarchical approach used to gradually face their fears.
Continue to: Pharmacologic augmentation strategies
Pharmacologic augmentation strategies
Selective serotonin reuptake inhibitors. While most OCD research trials have assessed SSRIs in 12-week studies, clinicians may consider extending SSRI treatment for an additional 12 weeks for nonresponders because some patients will continue to make gains. In the past, it was generally believed that higher doses of SSRIs are needed for treating OCD than for treating major depressive disorder. For instance, greater improvement was seen with 250 to 400 mg/d of sertraline compared with 200 mg/d22 and with escitalopram after an increase of dose up to 50 mg/d.23 However, more recently, this notion of higher doses being necessary for treatment response has been called into question. For example, a study of escitalopram found similar responses to 10 mg/d vs 20 mg/d after 24 weeks.24 A meta-analysis of adult studies of SSRIs for OCD supported higher doses as being more effective, but noted that the drop-out rate from treatment was greater in patients treated with higher doses.25 As a note of caution, long-term, high-dose maintenance therapy increases the risk of adverse reactions.26
Following a failed treatment with a first SSRI, it remains debatable as to what ought to be the second pharmacologic treatment. Although clomipramine is often reserved for treatment after 2 failed trials of an SSRI due to its greater risk of adverse effects, in an open-label study, switching from an SSRI to clomipramine led to greater response than switching from one SSRI to another.27 On the other hand, while meta-analyses have reported greater treatment effect for oral clomipramine than for SSRIs, direct head-to-head comparisons have not supported this notion.28 To get the best of both worlds, some clinicians employ a strategy of combining clomipramine with an SSRI, while monitoring for adverse effects and interactions such as serotonin syndrome.29-31
Benzodiazepines. Although benzodiazepines are useful for brief treatment of an anxiety disorder (eg, for a person with a fear of heights who needs to take an airplane),32 they have not been shown to be effective for OCD33 or as augmentation to an SSRI.34
N-acetylcysteine (NAC). Two RCTs of adults with OCD who received adjunctive NAC, 3 g/d in divided doses, found no significant difference in the treatment arms by the conclusion of 16 weeks—either both groups improved, or both groups failed to improve.35,36 In a 10-week study of patients with moderate to severe OCD symptoms, NAC, 2 g/d, as augmentation to fluvoxamine, 200 mg/d, showed a significant time x interaction in the treatment group.37 No follow-up information is available, however.
In a multicenter RCT of NAC given to children and adolescents with OCD as augmentation to citalopram, symptoms decreased and the quality-of-life score improved, with a large treatment effect size in the NAC group.38 However, in a study aimed at examining NAC in youth with Tourette syndrome, OCD symptoms were measured as a secondary outcome and there was no benefit of NAC over placebo.39
Memantine. Four 8- to 12-week RCTs in adults with OCD favored adjunctive memantine, 20 mg/d, taken with an SSRI, over placebo.40-43 A small study suggests that patients with OCD may be more likely to respond to memantine than patients with generalized anxiety disorder.44 Case reports have noted that memantine has been beneficial for pediatric patients with refractory OCD.45
Continue to: Topiramate
Topiramate. Three 12-week RCTs examined topiramate augmentation at 100 to 400 mg/d in patients with OCD who had failed at least 1 previous trial of an SSRI. The earliest study was most encouraging: Y-BOCS scores decreased by 32% in the topiramate group but by only 2.4% in the placebo group.46 However, the other 2 studies found no difference in the final OCD symptom severity score between active treatment and placebo groups,47,48 and the use of topiramate, particularly at higher doses, was limited by its adverse effects.
Lamotrigine. Initially, lamotrigine augmentation of SSRIs in OCD did not appear to be helpful.49 More recently, several case studies reported that lamotrigine, 100 to 200 mg/d, added to paroxetine or clomipramine, resulted in dramatic improvement in Y-BOCS scores for patients with long-standing refractory symptoms.50,51 In a retrospective review of 22 patients who received augmentation with lamotrigine, 150 mg/d, 20 had a significant response; the mean decrease in Y-BOCS score was 67%.52 Finally, in a 16-week RCT, lamotrigine, 100 mg/d, added to an SSRI led to a significant decrease in both Y-BOCS score and depressive symptoms while also improving semantic fluency.53
Ketamine. Ketamine is drawing increased attention for its nearly instantaneous antidepressant effect that lasts for up to 2 weeks after a single infusion.54 In a study of 15 medication-free adults with continuous intrusive obsessions, 4 of 8 patients who received a single IV infusion of ketamine, 0.5 mg/kg, met the criteria for treatment response (>35% reduction in Y-BOCS score measured 1 week later); none of the patients who received a placebo infusion of saline met this criteria.55 A small open-label trial of 10 treatment-refractory patients found that an infusion of ketamine, 0.5 mg/kg, was beneficial for comorbid depression but had only a minimal effect on OCD symptoms measured 3 days post-infusion.56 A short-term follow-up on these patients revealed dysphoria in some responders.57
D-cycloserine. The idea of using a pharmacologic agent to increase the speed or efficacy of behavioral therapy is intriguing. Proof of concept was demonstrated in a study that found that giving D-cycloserine prior to computerized exposure therapy significantly improved clinical response in patients with acrophobia.58 However, using this approach to treating OCD netted mixed results; D-cycloserine was found to be most helpful during early stages of treatment.59,60
Table 3 outlines the mechanisms of action and common uses for NAC, memantine, ketamine, topiramate, lamotrigine, and D-cycloserine. Table 4 summarizes the literature on the efficacy of some of the augmentation strategies for treating OCD described in this article.
Continue to: Alternative strategies
Alternative strategies
Augmentation strategies with neuroleptics,61 transcranial magnetic stimulation,62 and deep brain stimulation63 have recently been reviewed. Space limitations preclude a comprehensive review of these strategies, but in a cross-sectional study of augmentation strategies in OCD, no difference was found in terms of symptom severity between those prescribed SSRI monotherapy or augmentation with neuroleptics, benzodiazepines, or antidepressants.64
CASE CONTINUED
Progress in CBT
Mr. S agrees to a trial of NAC as an augmentation strategy, but after 8 weeks of treatment with NAC, 600 mg twice daily, his Y-BOCS had declined by only 2 points. He also complains of nausea and does not want to increase the dose. You discontinue NAC and opt to further explore his reaction to CBT. Mr. S shares that he has been seeing his psychologist only once every 3 weeks because he does not want to miss work. You encourage him to increase to weekly CBT sessions, and you obtain his permission to contact his therapist and his family members. Fortunately, his therapist is highly qualified, but unfortunately, Mr. S’s father has been sending him multiple critical emails about not advancing at his job and for being “lazy” at work. You schedule a session with Mr. S and his father. Great progress is made after Mr. S and his father both share their frustrations and come to understand and appreciate each other’s struggles. Four weeks later, after weekly CBT appointments, Mr. S has a Y-BOCS of 18 and spends <2 hours/d checking emails for errors and apologizing.
Bottom Line
It is unrealistic to expect OCD symptoms to be cured. Many ‘treatment-resistant’ patients have not received properly delivered cognitive-behavioral therapy, and this first-line treatment modality should be considered in every eligible patient, and augmented with a selective serotonin reuptake inhibitor (SSRI) when needed. Glutamatergic agents, in turn, can augment SSRIs.
Related Resources
- Yale-Brown Obsessive-Compulsive Scale. https://iocdf.org/ wp-content/uploads/2014/08/Assessment-Tools.pdf.
- The International OCD Foundation. https://iocdf.org.
Drug Brand Names
Citalopram • Celexa
Clomipramine • Anafranil
Escitalopram • Lexapro
Fluoxetine • Prozac
Fluvoxamine • Luvox
Ketamine • Ketalar
Lamotrigine • Lamictal
Memantine • Namenda
Paroxetine • Paxil
Sertraline • Zoloft
Topiramate • Topomax
1. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Koran LM, Hanna GL, Hollander E, et al. Practice guideline for the treatment of patients with obsessive-compulsive disorder. Am J Psychiatry; 2007;164(suppl 7):5-53.
3. Practice parameter for the assessment and treatment of children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry. 2012;51(1):98-113.
4. Bystritsky A, Munford PR, Rosen RM, et al. A preliminary study of partial hospital management of severe obsessive-compulsive disorder. Psychiatr Serv. 1996;47(2):170-174.
5. Calvocoressi L, McDougle CI, Wasylink S, et al. Inpatient treatment of patients with severe obsessive-compulsive disorder. Hosp Community Psychiatry. 1993;44(12):1150-1154.
6. Eddy KT, Dutra L, Bradley R, et al. A multidimensional meta-analysis of psychotherapy and pharmacotherapy for obsessive-compulsive disorder. Clin Psychol Rev. 2004;24(8):1011-1030.
7. Abramowitz JS. The psychological treatment of obsessive-compulsive disorder. Can J Psychiatry. 2006;51(7):407-416.
8. Simpson HB, Huppert JD, Petkova E, et al. Response versus remission in obsessive-compulsive disorder. J Clin Psychiatry. 2006;67(2):269-276.
9. Marques L, LeBlanc NJ, Weingarden HM, et al. Barriers to treatment and service utilization in an internet sample of individuals with obsessive-compulsive symptoms. Depress Anxiety. 2010;27(5):470-475.
10. Goodwin R, Koenen KC, Hellman F, et al. Helpseeking and access to mental health treatment for obsessive-compulsive disorder. Acta Psychiatr Scand. 2002;106(2):143-149.
11. Kohn R, Saxena S, Levav I, et al. The treatment gap in mental health care. Bull World Health Organ. 2004;82(11):858-866.
12. Baldwin DS, Anderson IM, Nutt DJ, et al. Evidence-based pharmacological treatment of anxiety disorders, post-traumatic stress disorder and obsessive-compulsive disorder: a revision of the 2005 guidelines from the British Association for Psychopharmacology. J Psychopharmacol. 2014;28(5):403-439.
13. Lovell K, Bee P. Implementing the NICE OCD/BDD guidelines. Psychol Psychother. 2008;81(Pt 4):365-376.
14. Bandelow B, Sher L, Bunevicius R, et al. Guidelines for the pharmacological treatment of anxiety disorders, obsessive-compulsive disorder and posttraumatic stress disorder in primary care. Int J Psychiatry Clin Pract. 2012;16(2):77-84.
15. Soomro GM, Altman D, Rajagopal S, et al. Selective serotonin re-uptake inhibitors (SSRIs) versus placebo for obsessive compulsive disorder (OCD). Cochrane Database Syst Rev. 2008;(1):CD001765.
16. Pittenger C, Bloch MH. Pharmacological treatment of obsessive-compulsive disorder. Psychiatr Clin North Am. 2014;37(3):375-391.
17. Bloch MH, Storch EA. Assessment and management of treatment-refractory obsessive-compulsive disorder in children. J Am Acad Child Adolesc Psychiatry. 2015;54(4):251-262.
18. Pediatric OCD Treatment Study (POTS) Team. Cognitive-behavior therapy, sertraline, and their combination for children and adolescents with obsessive-compulsive disorder: the Pediatric OCD Treatment Study (POTS) randomized controlled trial. JAMA. 2004;292(16):1969-1976.
19. March JS, Mulle K. OCD in children and adolescents: a cognitive-behavioral treatment manual. New York, NY: Guilford Press; 1998.
20. Marks IM. Fears, phobias, and rituals: Panic, anxiety, and their disorders. 1987, New York, NY: Oxford University Press; 1987.
21. Ale CM, McCarthy DM, Rothschild LM, et al. Components of cognitive behavioral therapy related to outcome in childhood anxiety disorders. Clin Child Fam Psychol Rev. 2015;18(3):240-251.
22. Ninan PT, Koran LM, Kiev A, et al. High-dose sertraline strategy for nonresponders to acute treatment for obsessive-compulsive disorder: a multicenter double-blind trial. J Clin Psychiatry. 2006;67(1):15-22.
23. Rabinowitz I, Baruch Y, Barak Y. High-dose escitalopram for the treatment of obsessive-compulsive disorder. Int Clin Psychopharmacol. 2008;23(1):49-53.
24. Stein DJ, Andersen EW, Tonnoir B, et al. Escitalopram in obsessive-compulsive disorder: a randomized, placebo-controlled, paroxetine-referenced, fixed-dose, 24-week study. Curr Med Res Opin. 2007;23(4):701-711.
25. Bloch MH, McGuire J, Landeros-Weisenberger A, et al. Meta-analysis of the dose-response relationship of SSRI in obsessive-compulsive disorder. Mol Psychiatry. 2010;15(8):850-855.
26. Sayyah M, Majzoob S, Sayyah M. Metabolic and toxicological considerations for obsessive-compulsive disorder drug therapy. Expert Opin Drug Metab Toxicol. 2013;9(6):657-673.
27. Hollander E, Bienstock CA, Koran LM, et al. Refractory obsessive-compulsive disorder: state-of-the-art treatment. J Clin Psychiatry. 2002;63(suppl 6):20-29.
28. Fineberg NA, Gale TM. Evidence-based pharmacotherapy of obsessive-compulsive disorder. Int J Neuropsychopharmacol. 2005;8(1):107-129.
29. Marazziti D, Golia F, Consoli G, et al. Effectiveness of long-term augmentation with citalopram to clomipramine in treatment-resistant OCD patients. CNS Spectr. 2008;13(11):971-976.
30. Browne M, Horn E, Jones TT. The benefits of clomipramine-fluoxetine combination in obsessive compulsive disorder. Can J Psychiatry. 1993;38(4):242-243.
31. Ravizza L, Barzega G, Bellino S, et al. Drug treatment of obsessive-compulsive disorder (OCD): long-term trial with clomipramine and selective serotonin reuptake inhibitors (SSRIs). Psychopharmacol Bull. 1996;32(1):167-173.
32. Koen N, Stein DJ. Pharmacotherapy of anxiety disorders: a critical review. Dialogues Clin Neurosci. 2011;13(4):423-437.
33. Hollander E, Kaplan A, Stahl SM. A double-blind, placebo-controlled trial of clonazepam in obsessive-compulsive disorder. World J Biol Psychiatry. 2003;4(1):30-34.
34. Crockett BA, Churchill E, Davidson JR. A double-blind combination study of clonazepam with sertraline in obsessive-compulsive disorder. Ann Clin Psychiatry. 2004;16(3):127-132.
35. Costa DLC, Diniz JB, Requena G, et al. Randomized, double-blind, placebo-controlled trial of n-acetylcysteine augmentation for treatment-resistant obsessive-compulsive disorder. J Clin Psychiatry. 2017;78(7):e766-e773.
36. Sarris J, Oliver G, Camfield DA, et al. N-Acetyl Cysteine (NAC) in the treatment of obsessive-compulsive disorder: a 16-week, double-blind, randomised, placebo-controlled study. CNS Drugs. 2015;29(9):801-809.
37. Paydary K, Akamaloo A, Ahmadipour A, et al. N-acetylcysteine augmentation therapy for moderate-to-severe obsessive-compulsive disorder: randomized, double-blind, placebo-controlled trial. J Clin Pharm Ther. 2016;41(2):214-219.
38. Ghanizadeh A, Mohammadi MR, Bahraini S, et al. Efficacy of N-acetylcysteine augmentation on obsessive compulsive disorder: a multicenter randomized double blind placebo controlled clinical trial. Iran J Psychiatry. 2017;12(2):134-141.
39. Bloch MH, Panza KE, Yaffa A, et al. N-acetylcysteine in the treatment of pediatric tourette syndrome: randomized, double-blind, placebo-controlled add-on trial. J Child Adolesc Psychopharmacol. 2016;26(4):327-334.
40. Ghaleiha A, Entezari N, Modabbernia A, et al. Memantine add-on in moderate to severe obsessive-compulsive disorder: randomized double-blind placebo-controlled study. J Psychiatr Res. 2013;47(2):175-180.
41. Stewart SE, Jenike EA, Hezel DM, et al. A single-blinded case-control study of memantine in severe obsessive-compulsive disorder. J Clin Psychopharmacol. 2010;30(1):34-39.
42. Modarresi A, Sayyah M, Razooghi S, et al. Memantine augmentation improves symptoms in serotonin reuptake inhibitor-refractory obsessive-compulsive disorder: a randomized controlled trial. Pharmacopsychiatry. 2017. doi: 10.1055/s-0043-120268. [Epub ahead of print].
43. Haghighi M, Jahangard L, Mohammad-Beigi H, et al. In a double-blind, randomized and placebo-controlled trial, adjuvant memantine improved symptoms in inpatients suffering from refractory obsessive-compulsive disorders (OCD). Psychopharmacology (Berl). 2013;228(4):633-640.
44. Feusner JD, Kerwin L, Saxena S, et al. Differential efficacy of memantine for obsessive-compulsive disorder vs. generalized anxiety disorder: an open-label trial. Psychopharmacol Bull. 2009;42(1):81-93.
45. Hezel DM, Beattie K, Stewart SE. Memantine as an augmenting agent for severe pediatric OCD. Am J Psychiatry. 2009;166(2):237.
46. Mowla A, Khajeian AM, Sahraian A, et al. topiramate augmentation in resistant ocd: a double-blind placebo-controlled clinical trial. CNS Spectr. 2010;15(11):613-617.
47. Berlin H, Koran LM, Jenike MA, et al. Double-blind, placebo-controlled trial of topiramate augmentation in treatment-resistant obsessive-compulsive disorder. J Clin Psychiatry. 2011;72(5):716-721.
48. Afshar H, Akuchekian S, Mahaky B, et al. Topiramate augmentation in refractory obsessive-compulsive disorder: A randomized, double-blind, placebo-controlled trial. J Res Med Sci. 2014;19(10):976-981.
49. Kumar TC, Khanna S. Lamotrigine augmentation of serotonin re-uptake inhibitors in obsessive-compulsive disorder. Aust N Z J Psychiatry. 2000;34(3):527-528.
50. Arrojo-Romero M, Tajes Alonso M, de Leon J. Lamotrigine augmentation of serotonin reuptake inhibitors in severe and long-term treatment-resistant obsessive-compulsive disorder. Case Rep Psychiatry. 2013;2013:612459.
51. Uzun O. Lamotrigine as an augmentation agent in treatment-resistant obsessive-compulsive disorder: a case report. J Psychopharmacol. 2010;24(3):425-427.
52. Hussain A, Dar MA, Wani RA, et al. Role of lamotrigine augmentation in treatment-resistant obsessive compulsive disorder: a retrospective case review from South Asia. Indian J Psychol Med. 2015;37(2):154-158.
53. Bruno A, Micò U, Pandolfo G, et al. Lamotrigine augmentation of serotonin reuptake inhibitors in treatment-resistant obsessive-compulsive disorder: a double-blind, placebo-controlled study. J Psychopharmacol. 2012;26(11):1456-1462.
54. Krystal JH, Sanacora G, Duman RS. Rapid-acting glutamatergic antidepressants: the path to ketamine and beyond. Biol Psychiatry. 2013;73(12):113311-41.
55. Rodriguez CI, Kegeles LS, Levinson A, et al. Randomized controlled crossover trial of ketamine in obsessive-compulsive disorder: proof-of-concept. Neuropsychopharmacology. 2013;38(12):2475-2483.
56. Bloch MH, Wasylink S, Landeros-Weisenberger A,, et al. Effects of ketamine in treatment-refractory obsessive-compulsive disorder. Biol Psychiatry. 2012;72(11):964-970.
57. Niciu MJ, Grunschel BD, Corlett PR, et al. Two cases of delayed-onset suicidal ideation, dysphoria and anxiety after ketamine infusion in patients with obsessive-compulsive disorder and a history of major depressive disorder. J Psychopharmacol. 2013;27(7):651-654.
58. Ressler KJ, Rothbaum BO, Tannenbaum L, et al. Cognitive enhancers as adjuncts to psychotherapy: use of D-cycloserine in phobic individuals to facilitate extinction of fear. Arch Gen Psychiatry. 2004;61(11):1136-1144.
59. Norberg MM, Krystal JH, Tolin DF. A meta-analysis of D-cycloserine and the facilitation of fear extinction and exposure therapy. Biol Psychiatry. 2008;63(12):1118-1126.
60. Xia J, Du Y, Han J, et al. D-cycloserine augmentation in behavioral therapy for obsessive-compulsive disorder: a meta-analysis. Drug Des Devel Ther. 2015;9:2101-2117.
61. Veale D, Miles S, Smallcombe N, et al. Atypical antipsychotic augmentation in SSRI treatment refractory obsessive-compulsive disorder: a systematic review and meta-analysis. BMC Psychiatry. 2014;14:317.
62. Guo Q, Li C, Wang J. Updated review on the clinical use of repetitive transcranial magnetic stimulation in psychiatric disorders. Neurosci Bull. 2017;33(6):747-756.
63. Naesström, M, Blomstedt P, Bodlund O. A systematic review of psychiatric indications for deep brain stimulation, with focus on major depressive and obsessive-compulsive disorder. Nord J Psychiatry. 2016;70(7):483-491.
64. Van Ameringen M, Simpson W, Patterson B, et al. Pharmacological treatment strategies in obsessive compulsive disorder: A cross-sectional view in nine international OCD centers. J Psychopharmacol, 2014;28(6):596-602.
Treatment-resistant OCD can be a debilitating condition. Diagnostic clarity is crucial to fully elicit symptoms and identify comorbid conditions in order to develop practical, evidence-based treatment strategies and improve the patient’s and family’s quality of life. In this article, we delineate first-line strategies for treatment-resistant OCD and then review augmentation strategies, with an emphasis on glutamate-modulating agents.
Making the diagnosis
The diagnosis of OCD is made when a patient meets DSM-5 criteria for the presence of obsessions and/or compulsions, which are defined as unwanted, distressing, intrusive, recurrent thoughts or images (obsessions) and repetitive behaviors or mental acts (compulsions).1 OCD is considered a chronic waxing and waning disorder; stress and lack of sleep lead to worsening symptoms. The hidden nature of symptoms and the reinforcement provided by the reduction in anxiety after performing a compulsion contribute to sustained illness. Eliciting symptoms from patients may be challenging due to the shame they may feel. When reviewing symptoms on the Y-BOCS, it is helpful to preface questions with statements such as “Many people report excessive concern or disgust with…” to help the patient feel understood and less anxious, rather than using direct queries, such as “Are you bothered by…?”
Consider comorbid conditions
After making the initial diagnosis of OCD, it is important to assess whether the symptoms are better accounted for by another condition, and whether comorbid conditions are present (Table 1).
CASE CONTINUED
Ruling out other diagnoses
_
Initial treatment: CBT
Cognitive-behavioral therapy with exposures and response prevention (from here on referred to as CBT) has been established as a first-line, evidence-based treatment for OCD in both children and adults.2,3 For patients with treatment-resistant OCD, intensive daily CBT in a partial hospitalization or inpatient setting that is a tailor-made, patient-specific program is one of the most effective treatments, with response rates of up to 70%4-8 CBT’s advantages over medication include lower relapse rates and no known adverse effects. Unfortunately, CBT is underused9-11 due in part to a shortage of trained clinicians, and because patients may favor the ease of taking medication over the time, effort, and cost involved in CBT.
First-line pharmacologic options for treating OCD are SSRIs and clomipramine, as supported by multiple randomized controlled trials (RCTs), meta-analyses, expert guidelines, and consensus statements (Table 22,12-14). No significant difference has been found among SSRIs for the treatment of OCD in a review of 17 studies that included more than 3,000 patients.15 Treatment with SSRIs or clomipramine is effective for 50% to 60% of patients.16 Many clinicians view the combination of an SSRI and CBT as the treatment of choice for OCD.2
Continue to: Reluctance to engage in CBT
CASE CONTINUED
Reluctance to engage in CBT
To determine the next course of action, you review Mr. S’s treatment history. He has received adequate doses of 2 SSRIs and currently is taking clomipramine, 100 mg twice daily. He recently began CBT, which includes homework to help face his fears; however, Mr. S is reluctant to complete the exposure assignments, and after pausing for a few seconds as he tries to resist sending an apology email to his coworkers, he then returns to his compulsive behavior.
Facing treatment resistance
Although currently there isn’t a cure to resolve all traces of OCD, the goal of treatment is to decrease distress, interference, and the frequency of symptoms to a minimal level such that only the patients themselves are aware of symptoms. In broad terms, “response” has been defined as a decrease in symptoms, and “remission” has been defined as minimal symptoms after treatment.
Close to half of adults treated for OCD respond well to standard-of-care treatment (CBT and/or an SSRI), while the other 50% are considered partial responders or nonresponders.2 For patients with OCD, researchers often define “treatment response” as a ≥25% reduction in symptom severity score on the Y-BOCS. Approximately 30% of adults with OCD do not respond substantially to the first-line treatments, and even those who are defined as “responders” in research studies typically continue to have significant symptoms that impact their quality of life.2 In children, a clinical definition for treatment-refractory OCD has been presented as failing to achieve adequate symptom relief despite receiving an adequate course of CBT and at least 2 adequate trials of an SSRI or clomipramine.17 In the Pediatric OCD Treatment Study (POTS) trial, >46% of youth did not achieve remission from their OCD symptoms, even after receiving evidence-based care provided by experienced clinicians (combined treatment with CBT and an SSRI).18
_
Challenges in psychotherapy
Compassion is a key element in developing rapport with patients to help them face increasingly more challenging exposures. Making OCD the problem, not the person, is an essential element in helping patients move forward. Some clinicians may become frustrated with patients when treatment is not moving along well, referring to resistance, denial, or sabotage. According to March and Mulle,19 these terms lack the recognition and compassion that exposures are inherently difficult.19
Another challenge for therapists is if the patient’s presenting symptoms are personally offensive or a sensitive topic. For example, a therapist who is disgusted by public restrooms will find it difficult to tolerate the risks associated with exposure to germs and support a patient in touching objects in the restroom. Therapists also may be challenged when the patient’s fears align with the therapist’s religious beliefs. In these situations, consider transferring care to another therapist.
Family members need to learn about the nature of the illness and their roles in helping patients improve. Family members may unknowingly enable symptoms or criticize patients for their lack of motivation, which can lead to conflict in the home. Family dysfunction can in turn worsen OCD symptoms.
The most likely cause of lack of response to therapy is inexpert CBT.19 Deep breathing and relaxation training have been used as an active placebo in studies20; in a meta-analysis examining the effective components of CBT, studies that added relaxation training were not more effective than those that employed exposures alone.21 Patients receiving CBT should be able to articulate the hierarchical approach used to gradually face their fears.
Continue to: Pharmacologic augmentation strategies
Pharmacologic augmentation strategies
Selective serotonin reuptake inhibitors. While most OCD research trials have assessed SSRIs in 12-week studies, clinicians may consider extending SSRI treatment for an additional 12 weeks for nonresponders because some patients will continue to make gains. In the past, it was generally believed that higher doses of SSRIs are needed for treating OCD than for treating major depressive disorder. For instance, greater improvement was seen with 250 to 400 mg/d of sertraline compared with 200 mg/d22 and with escitalopram after an increase of dose up to 50 mg/d.23 However, more recently, this notion of higher doses being necessary for treatment response has been called into question. For example, a study of escitalopram found similar responses to 10 mg/d vs 20 mg/d after 24 weeks.24 A meta-analysis of adult studies of SSRIs for OCD supported higher doses as being more effective, but noted that the drop-out rate from treatment was greater in patients treated with higher doses.25 As a note of caution, long-term, high-dose maintenance therapy increases the risk of adverse reactions.26
Following a failed treatment with a first SSRI, it remains debatable as to what ought to be the second pharmacologic treatment. Although clomipramine is often reserved for treatment after 2 failed trials of an SSRI due to its greater risk of adverse effects, in an open-label study, switching from an SSRI to clomipramine led to greater response than switching from one SSRI to another.27 On the other hand, while meta-analyses have reported greater treatment effect for oral clomipramine than for SSRIs, direct head-to-head comparisons have not supported this notion.28 To get the best of both worlds, some clinicians employ a strategy of combining clomipramine with an SSRI, while monitoring for adverse effects and interactions such as serotonin syndrome.29-31
Benzodiazepines. Although benzodiazepines are useful for brief treatment of an anxiety disorder (eg, for a person with a fear of heights who needs to take an airplane),32 they have not been shown to be effective for OCD33 or as augmentation to an SSRI.34
N-acetylcysteine (NAC). Two RCTs of adults with OCD who received adjunctive NAC, 3 g/d in divided doses, found no significant difference in the treatment arms by the conclusion of 16 weeks—either both groups improved, or both groups failed to improve.35,36 In a 10-week study of patients with moderate to severe OCD symptoms, NAC, 2 g/d, as augmentation to fluvoxamine, 200 mg/d, showed a significant time x interaction in the treatment group.37 No follow-up information is available, however.
In a multicenter RCT of NAC given to children and adolescents with OCD as augmentation to citalopram, symptoms decreased and the quality-of-life score improved, with a large treatment effect size in the NAC group.38 However, in a study aimed at examining NAC in youth with Tourette syndrome, OCD symptoms were measured as a secondary outcome and there was no benefit of NAC over placebo.39
Memantine. Four 8- to 12-week RCTs in adults with OCD favored adjunctive memantine, 20 mg/d, taken with an SSRI, over placebo.40-43 A small study suggests that patients with OCD may be more likely to respond to memantine than patients with generalized anxiety disorder.44 Case reports have noted that memantine has been beneficial for pediatric patients with refractory OCD.45
Continue to: Topiramate
Topiramate. Three 12-week RCTs examined topiramate augmentation at 100 to 400 mg/d in patients with OCD who had failed at least 1 previous trial of an SSRI. The earliest study was most encouraging: Y-BOCS scores decreased by 32% in the topiramate group but by only 2.4% in the placebo group.46 However, the other 2 studies found no difference in the final OCD symptom severity score between active treatment and placebo groups,47,48 and the use of topiramate, particularly at higher doses, was limited by its adverse effects.
Lamotrigine. Initially, lamotrigine augmentation of SSRIs in OCD did not appear to be helpful.49 More recently, several case studies reported that lamotrigine, 100 to 200 mg/d, added to paroxetine or clomipramine, resulted in dramatic improvement in Y-BOCS scores for patients with long-standing refractory symptoms.50,51 In a retrospective review of 22 patients who received augmentation with lamotrigine, 150 mg/d, 20 had a significant response; the mean decrease in Y-BOCS score was 67%.52 Finally, in a 16-week RCT, lamotrigine, 100 mg/d, added to an SSRI led to a significant decrease in both Y-BOCS score and depressive symptoms while also improving semantic fluency.53
Ketamine. Ketamine is drawing increased attention for its nearly instantaneous antidepressant effect that lasts for up to 2 weeks after a single infusion.54 In a study of 15 medication-free adults with continuous intrusive obsessions, 4 of 8 patients who received a single IV infusion of ketamine, 0.5 mg/kg, met the criteria for treatment response (>35% reduction in Y-BOCS score measured 1 week later); none of the patients who received a placebo infusion of saline met this criteria.55 A small open-label trial of 10 treatment-refractory patients found that an infusion of ketamine, 0.5 mg/kg, was beneficial for comorbid depression but had only a minimal effect on OCD symptoms measured 3 days post-infusion.56 A short-term follow-up on these patients revealed dysphoria in some responders.57
D-cycloserine. The idea of using a pharmacologic agent to increase the speed or efficacy of behavioral therapy is intriguing. Proof of concept was demonstrated in a study that found that giving D-cycloserine prior to computerized exposure therapy significantly improved clinical response in patients with acrophobia.58 However, using this approach to treating OCD netted mixed results; D-cycloserine was found to be most helpful during early stages of treatment.59,60
Table 3 outlines the mechanisms of action and common uses for NAC, memantine, ketamine, topiramate, lamotrigine, and D-cycloserine. Table 4 summarizes the literature on the efficacy of some of the augmentation strategies for treating OCD described in this article.
Continue to: Alternative strategies
Alternative strategies
Augmentation strategies with neuroleptics,61 transcranial magnetic stimulation,62 and deep brain stimulation63 have recently been reviewed. Space limitations preclude a comprehensive review of these strategies, but in a cross-sectional study of augmentation strategies in OCD, no difference was found in terms of symptom severity between those prescribed SSRI monotherapy or augmentation with neuroleptics, benzodiazepines, or antidepressants.64
CASE CONTINUED
Progress in CBT
Mr. S agrees to a trial of NAC as an augmentation strategy, but after 8 weeks of treatment with NAC, 600 mg twice daily, his Y-BOCS had declined by only 2 points. He also complains of nausea and does not want to increase the dose. You discontinue NAC and opt to further explore his reaction to CBT. Mr. S shares that he has been seeing his psychologist only once every 3 weeks because he does not want to miss work. You encourage him to increase to weekly CBT sessions, and you obtain his permission to contact his therapist and his family members. Fortunately, his therapist is highly qualified, but unfortunately, Mr. S’s father has been sending him multiple critical emails about not advancing at his job and for being “lazy” at work. You schedule a session with Mr. S and his father. Great progress is made after Mr. S and his father both share their frustrations and come to understand and appreciate each other’s struggles. Four weeks later, after weekly CBT appointments, Mr. S has a Y-BOCS of 18 and spends <2 hours/d checking emails for errors and apologizing.
Bottom Line
It is unrealistic to expect OCD symptoms to be cured. Many ‘treatment-resistant’ patients have not received properly delivered cognitive-behavioral therapy, and this first-line treatment modality should be considered in every eligible patient, and augmented with a selective serotonin reuptake inhibitor (SSRI) when needed. Glutamatergic agents, in turn, can augment SSRIs.
Related Resources
- Yale-Brown Obsessive-Compulsive Scale. https://iocdf.org/ wp-content/uploads/2014/08/Assessment-Tools.pdf.
- The International OCD Foundation. https://iocdf.org.
Drug Brand Names
Citalopram • Celexa
Clomipramine • Anafranil
Escitalopram • Lexapro
Fluoxetine • Prozac
Fluvoxamine • Luvox
Ketamine • Ketalar
Lamotrigine • Lamictal
Memantine • Namenda
Paroxetine • Paxil
Sertraline • Zoloft
Topiramate • Topomax
Treatment-resistant OCD can be a debilitating condition. Diagnostic clarity is crucial to fully elicit symptoms and identify comorbid conditions in order to develop practical, evidence-based treatment strategies and improve the patient’s and family’s quality of life. In this article, we delineate first-line strategies for treatment-resistant OCD and then review augmentation strategies, with an emphasis on glutamate-modulating agents.
Making the diagnosis
The diagnosis of OCD is made when a patient meets DSM-5 criteria for the presence of obsessions and/or compulsions, which are defined as unwanted, distressing, intrusive, recurrent thoughts or images (obsessions) and repetitive behaviors or mental acts (compulsions).1 OCD is considered a chronic waxing and waning disorder; stress and lack of sleep lead to worsening symptoms. The hidden nature of symptoms and the reinforcement provided by the reduction in anxiety after performing a compulsion contribute to sustained illness. Eliciting symptoms from patients may be challenging due to the shame they may feel. When reviewing symptoms on the Y-BOCS, it is helpful to preface questions with statements such as “Many people report excessive concern or disgust with…” to help the patient feel understood and less anxious, rather than using direct queries, such as “Are you bothered by…?”
Consider comorbid conditions
After making the initial diagnosis of OCD, it is important to assess whether the symptoms are better accounted for by another condition, and whether comorbid conditions are present (Table 1).
CASE CONTINUED
Ruling out other diagnoses
_
Initial treatment: CBT
Cognitive-behavioral therapy with exposures and response prevention (from here on referred to as CBT) has been established as a first-line, evidence-based treatment for OCD in both children and adults.2,3 For patients with treatment-resistant OCD, intensive daily CBT in a partial hospitalization or inpatient setting that is a tailor-made, patient-specific program is one of the most effective treatments, with response rates of up to 70%4-8 CBT’s advantages over medication include lower relapse rates and no known adverse effects. Unfortunately, CBT is underused9-11 due in part to a shortage of trained clinicians, and because patients may favor the ease of taking medication over the time, effort, and cost involved in CBT.
First-line pharmacologic options for treating OCD are SSRIs and clomipramine, as supported by multiple randomized controlled trials (RCTs), meta-analyses, expert guidelines, and consensus statements (Table 22,12-14). No significant difference has been found among SSRIs for the treatment of OCD in a review of 17 studies that included more than 3,000 patients.15 Treatment with SSRIs or clomipramine is effective for 50% to 60% of patients.16 Many clinicians view the combination of an SSRI and CBT as the treatment of choice for OCD.2
Continue to: Reluctance to engage in CBT
CASE CONTINUED
Reluctance to engage in CBT
To determine the next course of action, you review Mr. S’s treatment history. He has received adequate doses of 2 SSRIs and currently is taking clomipramine, 100 mg twice daily. He recently began CBT, which includes homework to help face his fears; however, Mr. S is reluctant to complete the exposure assignments, and after pausing for a few seconds as he tries to resist sending an apology email to his coworkers, he then returns to his compulsive behavior.
Facing treatment resistance
Although currently there isn’t a cure to resolve all traces of OCD, the goal of treatment is to decrease distress, interference, and the frequency of symptoms to a minimal level such that only the patients themselves are aware of symptoms. In broad terms, “response” has been defined as a decrease in symptoms, and “remission” has been defined as minimal symptoms after treatment.
Close to half of adults treated for OCD respond well to standard-of-care treatment (CBT and/or an SSRI), while the other 50% are considered partial responders or nonresponders.2 For patients with OCD, researchers often define “treatment response” as a ≥25% reduction in symptom severity score on the Y-BOCS. Approximately 30% of adults with OCD do not respond substantially to the first-line treatments, and even those who are defined as “responders” in research studies typically continue to have significant symptoms that impact their quality of life.2 In children, a clinical definition for treatment-refractory OCD has been presented as failing to achieve adequate symptom relief despite receiving an adequate course of CBT and at least 2 adequate trials of an SSRI or clomipramine.17 In the Pediatric OCD Treatment Study (POTS) trial, >46% of youth did not achieve remission from their OCD symptoms, even after receiving evidence-based care provided by experienced clinicians (combined treatment with CBT and an SSRI).18
_
Challenges in psychotherapy
Compassion is a key element in developing rapport with patients to help them face increasingly more challenging exposures. Making OCD the problem, not the person, is an essential element in helping patients move forward. Some clinicians may become frustrated with patients when treatment is not moving along well, referring to resistance, denial, or sabotage. According to March and Mulle,19 these terms lack the recognition and compassion that exposures are inherently difficult.19
Another challenge for therapists is if the patient’s presenting symptoms are personally offensive or a sensitive topic. For example, a therapist who is disgusted by public restrooms will find it difficult to tolerate the risks associated with exposure to germs and support a patient in touching objects in the restroom. Therapists also may be challenged when the patient’s fears align with the therapist’s religious beliefs. In these situations, consider transferring care to another therapist.
Family members need to learn about the nature of the illness and their roles in helping patients improve. Family members may unknowingly enable symptoms or criticize patients for their lack of motivation, which can lead to conflict in the home. Family dysfunction can in turn worsen OCD symptoms.
The most likely cause of lack of response to therapy is inexpert CBT.19 Deep breathing and relaxation training have been used as an active placebo in studies20; in a meta-analysis examining the effective components of CBT, studies that added relaxation training were not more effective than those that employed exposures alone.21 Patients receiving CBT should be able to articulate the hierarchical approach used to gradually face their fears.
Continue to: Pharmacologic augmentation strategies
Pharmacologic augmentation strategies
Selective serotonin reuptake inhibitors. While most OCD research trials have assessed SSRIs in 12-week studies, clinicians may consider extending SSRI treatment for an additional 12 weeks for nonresponders because some patients will continue to make gains. In the past, it was generally believed that higher doses of SSRIs are needed for treating OCD than for treating major depressive disorder. For instance, greater improvement was seen with 250 to 400 mg/d of sertraline compared with 200 mg/d22 and with escitalopram after an increase of dose up to 50 mg/d.23 However, more recently, this notion of higher doses being necessary for treatment response has been called into question. For example, a study of escitalopram found similar responses to 10 mg/d vs 20 mg/d after 24 weeks.24 A meta-analysis of adult studies of SSRIs for OCD supported higher doses as being more effective, but noted that the drop-out rate from treatment was greater in patients treated with higher doses.25 As a note of caution, long-term, high-dose maintenance therapy increases the risk of adverse reactions.26
Following a failed treatment with a first SSRI, it remains debatable as to what ought to be the second pharmacologic treatment. Although clomipramine is often reserved for treatment after 2 failed trials of an SSRI due to its greater risk of adverse effects, in an open-label study, switching from an SSRI to clomipramine led to greater response than switching from one SSRI to another.27 On the other hand, while meta-analyses have reported greater treatment effect for oral clomipramine than for SSRIs, direct head-to-head comparisons have not supported this notion.28 To get the best of both worlds, some clinicians employ a strategy of combining clomipramine with an SSRI, while monitoring for adverse effects and interactions such as serotonin syndrome.29-31
Benzodiazepines. Although benzodiazepines are useful for brief treatment of an anxiety disorder (eg, for a person with a fear of heights who needs to take an airplane),32 they have not been shown to be effective for OCD33 or as augmentation to an SSRI.34
N-acetylcysteine (NAC). Two RCTs of adults with OCD who received adjunctive NAC, 3 g/d in divided doses, found no significant difference in the treatment arms by the conclusion of 16 weeks—either both groups improved, or both groups failed to improve.35,36 In a 10-week study of patients with moderate to severe OCD symptoms, NAC, 2 g/d, as augmentation to fluvoxamine, 200 mg/d, showed a significant time x interaction in the treatment group.37 No follow-up information is available, however.
In a multicenter RCT of NAC given to children and adolescents with OCD as augmentation to citalopram, symptoms decreased and the quality-of-life score improved, with a large treatment effect size in the NAC group.38 However, in a study aimed at examining NAC in youth with Tourette syndrome, OCD symptoms were measured as a secondary outcome and there was no benefit of NAC over placebo.39
Memantine. Four 8- to 12-week RCTs in adults with OCD favored adjunctive memantine, 20 mg/d, taken with an SSRI, over placebo.40-43 A small study suggests that patients with OCD may be more likely to respond to memantine than patients with generalized anxiety disorder.44 Case reports have noted that memantine has been beneficial for pediatric patients with refractory OCD.45
Continue to: Topiramate
Topiramate. Three 12-week RCTs examined topiramate augmentation at 100 to 400 mg/d in patients with OCD who had failed at least 1 previous trial of an SSRI. The earliest study was most encouraging: Y-BOCS scores decreased by 32% in the topiramate group but by only 2.4% in the placebo group.46 However, the other 2 studies found no difference in the final OCD symptom severity score between active treatment and placebo groups,47,48 and the use of topiramate, particularly at higher doses, was limited by its adverse effects.
Lamotrigine. Initially, lamotrigine augmentation of SSRIs in OCD did not appear to be helpful.49 More recently, several case studies reported that lamotrigine, 100 to 200 mg/d, added to paroxetine or clomipramine, resulted in dramatic improvement in Y-BOCS scores for patients with long-standing refractory symptoms.50,51 In a retrospective review of 22 patients who received augmentation with lamotrigine, 150 mg/d, 20 had a significant response; the mean decrease in Y-BOCS score was 67%.52 Finally, in a 16-week RCT, lamotrigine, 100 mg/d, added to an SSRI led to a significant decrease in both Y-BOCS score and depressive symptoms while also improving semantic fluency.53
Ketamine. Ketamine is drawing increased attention for its nearly instantaneous antidepressant effect that lasts for up to 2 weeks after a single infusion.54 In a study of 15 medication-free adults with continuous intrusive obsessions, 4 of 8 patients who received a single IV infusion of ketamine, 0.5 mg/kg, met the criteria for treatment response (>35% reduction in Y-BOCS score measured 1 week later); none of the patients who received a placebo infusion of saline met this criteria.55 A small open-label trial of 10 treatment-refractory patients found that an infusion of ketamine, 0.5 mg/kg, was beneficial for comorbid depression but had only a minimal effect on OCD symptoms measured 3 days post-infusion.56 A short-term follow-up on these patients revealed dysphoria in some responders.57
D-cycloserine. The idea of using a pharmacologic agent to increase the speed or efficacy of behavioral therapy is intriguing. Proof of concept was demonstrated in a study that found that giving D-cycloserine prior to computerized exposure therapy significantly improved clinical response in patients with acrophobia.58 However, using this approach to treating OCD netted mixed results; D-cycloserine was found to be most helpful during early stages of treatment.59,60
Table 3 outlines the mechanisms of action and common uses for NAC, memantine, ketamine, topiramate, lamotrigine, and D-cycloserine. Table 4 summarizes the literature on the efficacy of some of the augmentation strategies for treating OCD described in this article.
Continue to: Alternative strategies
Alternative strategies
Augmentation strategies with neuroleptics,61 transcranial magnetic stimulation,62 and deep brain stimulation63 have recently been reviewed. Space limitations preclude a comprehensive review of these strategies, but in a cross-sectional study of augmentation strategies in OCD, no difference was found in terms of symptom severity between those prescribed SSRI monotherapy or augmentation with neuroleptics, benzodiazepines, or antidepressants.64
CASE CONTINUED
Progress in CBT
Mr. S agrees to a trial of NAC as an augmentation strategy, but after 8 weeks of treatment with NAC, 600 mg twice daily, his Y-BOCS had declined by only 2 points. He also complains of nausea and does not want to increase the dose. You discontinue NAC and opt to further explore his reaction to CBT. Mr. S shares that he has been seeing his psychologist only once every 3 weeks because he does not want to miss work. You encourage him to increase to weekly CBT sessions, and you obtain his permission to contact his therapist and his family members. Fortunately, his therapist is highly qualified, but unfortunately, Mr. S’s father has been sending him multiple critical emails about not advancing at his job and for being “lazy” at work. You schedule a session with Mr. S and his father. Great progress is made after Mr. S and his father both share their frustrations and come to understand and appreciate each other’s struggles. Four weeks later, after weekly CBT appointments, Mr. S has a Y-BOCS of 18 and spends <2 hours/d checking emails for errors and apologizing.
Bottom Line
It is unrealistic to expect OCD symptoms to be cured. Many ‘treatment-resistant’ patients have not received properly delivered cognitive-behavioral therapy, and this first-line treatment modality should be considered in every eligible patient, and augmented with a selective serotonin reuptake inhibitor (SSRI) when needed. Glutamatergic agents, in turn, can augment SSRIs.
Related Resources
- Yale-Brown Obsessive-Compulsive Scale. https://iocdf.org/ wp-content/uploads/2014/08/Assessment-Tools.pdf.
- The International OCD Foundation. https://iocdf.org.
Drug Brand Names
Citalopram • Celexa
Clomipramine • Anafranil
Escitalopram • Lexapro
Fluoxetine • Prozac
Fluvoxamine • Luvox
Ketamine • Ketalar
Lamotrigine • Lamictal
Memantine • Namenda
Paroxetine • Paxil
Sertraline • Zoloft
Topiramate • Topomax
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3. Practice parameter for the assessment and treatment of children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry. 2012;51(1):98-113.
4. Bystritsky A, Munford PR, Rosen RM, et al. A preliminary study of partial hospital management of severe obsessive-compulsive disorder. Psychiatr Serv. 1996;47(2):170-174.
5. Calvocoressi L, McDougle CI, Wasylink S, et al. Inpatient treatment of patients with severe obsessive-compulsive disorder. Hosp Community Psychiatry. 1993;44(12):1150-1154.
6. Eddy KT, Dutra L, Bradley R, et al. A multidimensional meta-analysis of psychotherapy and pharmacotherapy for obsessive-compulsive disorder. Clin Psychol Rev. 2004;24(8):1011-1030.
7. Abramowitz JS. The psychological treatment of obsessive-compulsive disorder. Can J Psychiatry. 2006;51(7):407-416.
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20. Marks IM. Fears, phobias, and rituals: Panic, anxiety, and their disorders. 1987, New York, NY: Oxford University Press; 1987.
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22. Ninan PT, Koran LM, Kiev A, et al. High-dose sertraline strategy for nonresponders to acute treatment for obsessive-compulsive disorder: a multicenter double-blind trial. J Clin Psychiatry. 2006;67(1):15-22.
23. Rabinowitz I, Baruch Y, Barak Y. High-dose escitalopram for the treatment of obsessive-compulsive disorder. Int Clin Psychopharmacol. 2008;23(1):49-53.
24. Stein DJ, Andersen EW, Tonnoir B, et al. Escitalopram in obsessive-compulsive disorder: a randomized, placebo-controlled, paroxetine-referenced, fixed-dose, 24-week study. Curr Med Res Opin. 2007;23(4):701-711.
25. Bloch MH, McGuire J, Landeros-Weisenberger A, et al. Meta-analysis of the dose-response relationship of SSRI in obsessive-compulsive disorder. Mol Psychiatry. 2010;15(8):850-855.
26. Sayyah M, Majzoob S, Sayyah M. Metabolic and toxicological considerations for obsessive-compulsive disorder drug therapy. Expert Opin Drug Metab Toxicol. 2013;9(6):657-673.
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29. Marazziti D, Golia F, Consoli G, et al. Effectiveness of long-term augmentation with citalopram to clomipramine in treatment-resistant OCD patients. CNS Spectr. 2008;13(11):971-976.
30. Browne M, Horn E, Jones TT. The benefits of clomipramine-fluoxetine combination in obsessive compulsive disorder. Can J Psychiatry. 1993;38(4):242-243.
31. Ravizza L, Barzega G, Bellino S, et al. Drug treatment of obsessive-compulsive disorder (OCD): long-term trial with clomipramine and selective serotonin reuptake inhibitors (SSRIs). Psychopharmacol Bull. 1996;32(1):167-173.
32. Koen N, Stein DJ. Pharmacotherapy of anxiety disorders: a critical review. Dialogues Clin Neurosci. 2011;13(4):423-437.
33. Hollander E, Kaplan A, Stahl SM. A double-blind, placebo-controlled trial of clonazepam in obsessive-compulsive disorder. World J Biol Psychiatry. 2003;4(1):30-34.
34. Crockett BA, Churchill E, Davidson JR. A double-blind combination study of clonazepam with sertraline in obsessive-compulsive disorder. Ann Clin Psychiatry. 2004;16(3):127-132.
35. Costa DLC, Diniz JB, Requena G, et al. Randomized, double-blind, placebo-controlled trial of n-acetylcysteine augmentation for treatment-resistant obsessive-compulsive disorder. J Clin Psychiatry. 2017;78(7):e766-e773.
36. Sarris J, Oliver G, Camfield DA, et al. N-Acetyl Cysteine (NAC) in the treatment of obsessive-compulsive disorder: a 16-week, double-blind, randomised, placebo-controlled study. CNS Drugs. 2015;29(9):801-809.
37. Paydary K, Akamaloo A, Ahmadipour A, et al. N-acetylcysteine augmentation therapy for moderate-to-severe obsessive-compulsive disorder: randomized, double-blind, placebo-controlled trial. J Clin Pharm Ther. 2016;41(2):214-219.
38. Ghanizadeh A, Mohammadi MR, Bahraini S, et al. Efficacy of N-acetylcysteine augmentation on obsessive compulsive disorder: a multicenter randomized double blind placebo controlled clinical trial. Iran J Psychiatry. 2017;12(2):134-141.
39. Bloch MH, Panza KE, Yaffa A, et al. N-acetylcysteine in the treatment of pediatric tourette syndrome: randomized, double-blind, placebo-controlled add-on trial. J Child Adolesc Psychopharmacol. 2016;26(4):327-334.
40. Ghaleiha A, Entezari N, Modabbernia A, et al. Memantine add-on in moderate to severe obsessive-compulsive disorder: randomized double-blind placebo-controlled study. J Psychiatr Res. 2013;47(2):175-180.
41. Stewart SE, Jenike EA, Hezel DM, et al. A single-blinded case-control study of memantine in severe obsessive-compulsive disorder. J Clin Psychopharmacol. 2010;30(1):34-39.
42. Modarresi A, Sayyah M, Razooghi S, et al. Memantine augmentation improves symptoms in serotonin reuptake inhibitor-refractory obsessive-compulsive disorder: a randomized controlled trial. Pharmacopsychiatry. 2017. doi: 10.1055/s-0043-120268. [Epub ahead of print].
43. Haghighi M, Jahangard L, Mohammad-Beigi H, et al. In a double-blind, randomized and placebo-controlled trial, adjuvant memantine improved symptoms in inpatients suffering from refractory obsessive-compulsive disorders (OCD). Psychopharmacology (Berl). 2013;228(4):633-640.
44. Feusner JD, Kerwin L, Saxena S, et al. Differential efficacy of memantine for obsessive-compulsive disorder vs. generalized anxiety disorder: an open-label trial. Psychopharmacol Bull. 2009;42(1):81-93.
45. Hezel DM, Beattie K, Stewart SE. Memantine as an augmenting agent for severe pediatric OCD. Am J Psychiatry. 2009;166(2):237.
46. Mowla A, Khajeian AM, Sahraian A, et al. topiramate augmentation in resistant ocd: a double-blind placebo-controlled clinical trial. CNS Spectr. 2010;15(11):613-617.
47. Berlin H, Koran LM, Jenike MA, et al. Double-blind, placebo-controlled trial of topiramate augmentation in treatment-resistant obsessive-compulsive disorder. J Clin Psychiatry. 2011;72(5):716-721.
48. Afshar H, Akuchekian S, Mahaky B, et al. Topiramate augmentation in refractory obsessive-compulsive disorder: A randomized, double-blind, placebo-controlled trial. J Res Med Sci. 2014;19(10):976-981.
49. Kumar TC, Khanna S. Lamotrigine augmentation of serotonin re-uptake inhibitors in obsessive-compulsive disorder. Aust N Z J Psychiatry. 2000;34(3):527-528.
50. Arrojo-Romero M, Tajes Alonso M, de Leon J. Lamotrigine augmentation of serotonin reuptake inhibitors in severe and long-term treatment-resistant obsessive-compulsive disorder. Case Rep Psychiatry. 2013;2013:612459.
51. Uzun O. Lamotrigine as an augmentation agent in treatment-resistant obsessive-compulsive disorder: a case report. J Psychopharmacol. 2010;24(3):425-427.
52. Hussain A, Dar MA, Wani RA, et al. Role of lamotrigine augmentation in treatment-resistant obsessive compulsive disorder: a retrospective case review from South Asia. Indian J Psychol Med. 2015;37(2):154-158.
53. Bruno A, Micò U, Pandolfo G, et al. Lamotrigine augmentation of serotonin reuptake inhibitors in treatment-resistant obsessive-compulsive disorder: a double-blind, placebo-controlled study. J Psychopharmacol. 2012;26(11):1456-1462.
54. Krystal JH, Sanacora G, Duman RS. Rapid-acting glutamatergic antidepressants: the path to ketamine and beyond. Biol Psychiatry. 2013;73(12):113311-41.
55. Rodriguez CI, Kegeles LS, Levinson A, et al. Randomized controlled crossover trial of ketamine in obsessive-compulsive disorder: proof-of-concept. Neuropsychopharmacology. 2013;38(12):2475-2483.
56. Bloch MH, Wasylink S, Landeros-Weisenberger A,, et al. Effects of ketamine in treatment-refractory obsessive-compulsive disorder. Biol Psychiatry. 2012;72(11):964-970.
57. Niciu MJ, Grunschel BD, Corlett PR, et al. Two cases of delayed-onset suicidal ideation, dysphoria and anxiety after ketamine infusion in patients with obsessive-compulsive disorder and a history of major depressive disorder. J Psychopharmacol. 2013;27(7):651-654.
58. Ressler KJ, Rothbaum BO, Tannenbaum L, et al. Cognitive enhancers as adjuncts to psychotherapy: use of D-cycloserine in phobic individuals to facilitate extinction of fear. Arch Gen Psychiatry. 2004;61(11):1136-1144.
59. Norberg MM, Krystal JH, Tolin DF. A meta-analysis of D-cycloserine and the facilitation of fear extinction and exposure therapy. Biol Psychiatry. 2008;63(12):1118-1126.
60. Xia J, Du Y, Han J, et al. D-cycloserine augmentation in behavioral therapy for obsessive-compulsive disorder: a meta-analysis. Drug Des Devel Ther. 2015;9:2101-2117.
61. Veale D, Miles S, Smallcombe N, et al. Atypical antipsychotic augmentation in SSRI treatment refractory obsessive-compulsive disorder: a systematic review and meta-analysis. BMC Psychiatry. 2014;14:317.
62. Guo Q, Li C, Wang J. Updated review on the clinical use of repetitive transcranial magnetic stimulation in psychiatric disorders. Neurosci Bull. 2017;33(6):747-756.
63. Naesström, M, Blomstedt P, Bodlund O. A systematic review of psychiatric indications for deep brain stimulation, with focus on major depressive and obsessive-compulsive disorder. Nord J Psychiatry. 2016;70(7):483-491.
64. Van Ameringen M, Simpson W, Patterson B, et al. Pharmacological treatment strategies in obsessive compulsive disorder: A cross-sectional view in nine international OCD centers. J Psychopharmacol, 2014;28(6):596-602.
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12. Baldwin DS, Anderson IM, Nutt DJ, et al. Evidence-based pharmacological treatment of anxiety disorders, post-traumatic stress disorder and obsessive-compulsive disorder: a revision of the 2005 guidelines from the British Association for Psychopharmacology. J Psychopharmacol. 2014;28(5):403-439.
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15. Soomro GM, Altman D, Rajagopal S, et al. Selective serotonin re-uptake inhibitors (SSRIs) versus placebo for obsessive compulsive disorder (OCD). Cochrane Database Syst Rev. 2008;(1):CD001765.
16. Pittenger C, Bloch MH. Pharmacological treatment of obsessive-compulsive disorder. Psychiatr Clin North Am. 2014;37(3):375-391.
17. Bloch MH, Storch EA. Assessment and management of treatment-refractory obsessive-compulsive disorder in children. J Am Acad Child Adolesc Psychiatry. 2015;54(4):251-262.
18. Pediatric OCD Treatment Study (POTS) Team. Cognitive-behavior therapy, sertraline, and their combination for children and adolescents with obsessive-compulsive disorder: the Pediatric OCD Treatment Study (POTS) randomized controlled trial. JAMA. 2004;292(16):1969-1976.
19. March JS, Mulle K. OCD in children and adolescents: a cognitive-behavioral treatment manual. New York, NY: Guilford Press; 1998.
20. Marks IM. Fears, phobias, and rituals: Panic, anxiety, and their disorders. 1987, New York, NY: Oxford University Press; 1987.
21. Ale CM, McCarthy DM, Rothschild LM, et al. Components of cognitive behavioral therapy related to outcome in childhood anxiety disorders. Clin Child Fam Psychol Rev. 2015;18(3):240-251.
22. Ninan PT, Koran LM, Kiev A, et al. High-dose sertraline strategy for nonresponders to acute treatment for obsessive-compulsive disorder: a multicenter double-blind trial. J Clin Psychiatry. 2006;67(1):15-22.
23. Rabinowitz I, Baruch Y, Barak Y. High-dose escitalopram for the treatment of obsessive-compulsive disorder. Int Clin Psychopharmacol. 2008;23(1):49-53.
24. Stein DJ, Andersen EW, Tonnoir B, et al. Escitalopram in obsessive-compulsive disorder: a randomized, placebo-controlled, paroxetine-referenced, fixed-dose, 24-week study. Curr Med Res Opin. 2007;23(4):701-711.
25. Bloch MH, McGuire J, Landeros-Weisenberger A, et al. Meta-analysis of the dose-response relationship of SSRI in obsessive-compulsive disorder. Mol Psychiatry. 2010;15(8):850-855.
26. Sayyah M, Majzoob S, Sayyah M. Metabolic and toxicological considerations for obsessive-compulsive disorder drug therapy. Expert Opin Drug Metab Toxicol. 2013;9(6):657-673.
27. Hollander E, Bienstock CA, Koran LM, et al. Refractory obsessive-compulsive disorder: state-of-the-art treatment. J Clin Psychiatry. 2002;63(suppl 6):20-29.
28. Fineberg NA, Gale TM. Evidence-based pharmacotherapy of obsessive-compulsive disorder. Int J Neuropsychopharmacol. 2005;8(1):107-129.
29. Marazziti D, Golia F, Consoli G, et al. Effectiveness of long-term augmentation with citalopram to clomipramine in treatment-resistant OCD patients. CNS Spectr. 2008;13(11):971-976.
30. Browne M, Horn E, Jones TT. The benefits of clomipramine-fluoxetine combination in obsessive compulsive disorder. Can J Psychiatry. 1993;38(4):242-243.
31. Ravizza L, Barzega G, Bellino S, et al. Drug treatment of obsessive-compulsive disorder (OCD): long-term trial with clomipramine and selective serotonin reuptake inhibitors (SSRIs). Psychopharmacol Bull. 1996;32(1):167-173.
32. Koen N, Stein DJ. Pharmacotherapy of anxiety disorders: a critical review. Dialogues Clin Neurosci. 2011;13(4):423-437.
33. Hollander E, Kaplan A, Stahl SM. A double-blind, placebo-controlled trial of clonazepam in obsessive-compulsive disorder. World J Biol Psychiatry. 2003;4(1):30-34.
34. Crockett BA, Churchill E, Davidson JR. A double-blind combination study of clonazepam with sertraline in obsessive-compulsive disorder. Ann Clin Psychiatry. 2004;16(3):127-132.
35. Costa DLC, Diniz JB, Requena G, et al. Randomized, double-blind, placebo-controlled trial of n-acetylcysteine augmentation for treatment-resistant obsessive-compulsive disorder. J Clin Psychiatry. 2017;78(7):e766-e773.
36. Sarris J, Oliver G, Camfield DA, et al. N-Acetyl Cysteine (NAC) in the treatment of obsessive-compulsive disorder: a 16-week, double-blind, randomised, placebo-controlled study. CNS Drugs. 2015;29(9):801-809.
37. Paydary K, Akamaloo A, Ahmadipour A, et al. N-acetylcysteine augmentation therapy for moderate-to-severe obsessive-compulsive disorder: randomized, double-blind, placebo-controlled trial. J Clin Pharm Ther. 2016;41(2):214-219.
38. Ghanizadeh A, Mohammadi MR, Bahraini S, et al. Efficacy of N-acetylcysteine augmentation on obsessive compulsive disorder: a multicenter randomized double blind placebo controlled clinical trial. Iran J Psychiatry. 2017;12(2):134-141.
39. Bloch MH, Panza KE, Yaffa A, et al. N-acetylcysteine in the treatment of pediatric tourette syndrome: randomized, double-blind, placebo-controlled add-on trial. J Child Adolesc Psychopharmacol. 2016;26(4):327-334.
40. Ghaleiha A, Entezari N, Modabbernia A, et al. Memantine add-on in moderate to severe obsessive-compulsive disorder: randomized double-blind placebo-controlled study. J Psychiatr Res. 2013;47(2):175-180.
41. Stewart SE, Jenike EA, Hezel DM, et al. A single-blinded case-control study of memantine in severe obsessive-compulsive disorder. J Clin Psychopharmacol. 2010;30(1):34-39.
42. Modarresi A, Sayyah M, Razooghi S, et al. Memantine augmentation improves symptoms in serotonin reuptake inhibitor-refractory obsessive-compulsive disorder: a randomized controlled trial. Pharmacopsychiatry. 2017. doi: 10.1055/s-0043-120268. [Epub ahead of print].
43. Haghighi M, Jahangard L, Mohammad-Beigi H, et al. In a double-blind, randomized and placebo-controlled trial, adjuvant memantine improved symptoms in inpatients suffering from refractory obsessive-compulsive disorders (OCD). Psychopharmacology (Berl). 2013;228(4):633-640.
44. Feusner JD, Kerwin L, Saxena S, et al. Differential efficacy of memantine for obsessive-compulsive disorder vs. generalized anxiety disorder: an open-label trial. Psychopharmacol Bull. 2009;42(1):81-93.
45. Hezel DM, Beattie K, Stewart SE. Memantine as an augmenting agent for severe pediatric OCD. Am J Psychiatry. 2009;166(2):237.
46. Mowla A, Khajeian AM, Sahraian A, et al. topiramate augmentation in resistant ocd: a double-blind placebo-controlled clinical trial. CNS Spectr. 2010;15(11):613-617.
47. Berlin H, Koran LM, Jenike MA, et al. Double-blind, placebo-controlled trial of topiramate augmentation in treatment-resistant obsessive-compulsive disorder. J Clin Psychiatry. 2011;72(5):716-721.
48. Afshar H, Akuchekian S, Mahaky B, et al. Topiramate augmentation in refractory obsessive-compulsive disorder: A randomized, double-blind, placebo-controlled trial. J Res Med Sci. 2014;19(10):976-981.
49. Kumar TC, Khanna S. Lamotrigine augmentation of serotonin re-uptake inhibitors in obsessive-compulsive disorder. Aust N Z J Psychiatry. 2000;34(3):527-528.
50. Arrojo-Romero M, Tajes Alonso M, de Leon J. Lamotrigine augmentation of serotonin reuptake inhibitors in severe and long-term treatment-resistant obsessive-compulsive disorder. Case Rep Psychiatry. 2013;2013:612459.
51. Uzun O. Lamotrigine as an augmentation agent in treatment-resistant obsessive-compulsive disorder: a case report. J Psychopharmacol. 2010;24(3):425-427.
52. Hussain A, Dar MA, Wani RA, et al. Role of lamotrigine augmentation in treatment-resistant obsessive compulsive disorder: a retrospective case review from South Asia. Indian J Psychol Med. 2015;37(2):154-158.
53. Bruno A, Micò U, Pandolfo G, et al. Lamotrigine augmentation of serotonin reuptake inhibitors in treatment-resistant obsessive-compulsive disorder: a double-blind, placebo-controlled study. J Psychopharmacol. 2012;26(11):1456-1462.
54. Krystal JH, Sanacora G, Duman RS. Rapid-acting glutamatergic antidepressants: the path to ketamine and beyond. Biol Psychiatry. 2013;73(12):113311-41.
55. Rodriguez CI, Kegeles LS, Levinson A, et al. Randomized controlled crossover trial of ketamine in obsessive-compulsive disorder: proof-of-concept. Neuropsychopharmacology. 2013;38(12):2475-2483.
56. Bloch MH, Wasylink S, Landeros-Weisenberger A,, et al. Effects of ketamine in treatment-refractory obsessive-compulsive disorder. Biol Psychiatry. 2012;72(11):964-970.
57. Niciu MJ, Grunschel BD, Corlett PR, et al. Two cases of delayed-onset suicidal ideation, dysphoria and anxiety after ketamine infusion in patients with obsessive-compulsive disorder and a history of major depressive disorder. J Psychopharmacol. 2013;27(7):651-654.
58. Ressler KJ, Rothbaum BO, Tannenbaum L, et al. Cognitive enhancers as adjuncts to psychotherapy: use of D-cycloserine in phobic individuals to facilitate extinction of fear. Arch Gen Psychiatry. 2004;61(11):1136-1144.
59. Norberg MM, Krystal JH, Tolin DF. A meta-analysis of D-cycloserine and the facilitation of fear extinction and exposure therapy. Biol Psychiatry. 2008;63(12):1118-1126.
60. Xia J, Du Y, Han J, et al. D-cycloserine augmentation in behavioral therapy for obsessive-compulsive disorder: a meta-analysis. Drug Des Devel Ther. 2015;9:2101-2117.
61. Veale D, Miles S, Smallcombe N, et al. Atypical antipsychotic augmentation in SSRI treatment refractory obsessive-compulsive disorder: a systematic review and meta-analysis. BMC Psychiatry. 2014;14:317.
62. Guo Q, Li C, Wang J. Updated review on the clinical use of repetitive transcranial magnetic stimulation in psychiatric disorders. Neurosci Bull. 2017;33(6):747-756.
63. Naesström, M, Blomstedt P, Bodlund O. A systematic review of psychiatric indications for deep brain stimulation, with focus on major depressive and obsessive-compulsive disorder. Nord J Psychiatry. 2016;70(7):483-491.
64. Van Ameringen M, Simpson W, Patterson B, et al. Pharmacological treatment strategies in obsessive compulsive disorder: A cross-sectional view in nine international OCD centers. J Psychopharmacol, 2014;28(6):596-602.
Disruptive mood dysregulation disorder: A better understanding
Disruptive mood dysregulation disorder (DMDD)—a childhood condition of extreme irritability, anger, and frequent, intense temper outbursts—has been a source of controversy among clinicians in the field of pediatric mental health. Before DSM-5 was published, the validity of DMDD had been questioned because DMDD had failed a field trial; agreement between clinicians on the diagnosis of DMDD was poor.1 Axelson2 and Birmaher et al3 examined its validity in their COBY (Course and Outcome of Bipolar Youth) sample. They concluded that only 19% met the criteria for DMDD in 3 times of follow-up. Furthermore, most DMDD criteria overlap with those of other common pediatric psychiatric disorders, including oppositional defiant disorder (ODD), attention-deficit/hyperactivity disorder (ADHD), and pediatric bipolar disorder (BD). Because diagnosis of pediatric BD increased drastically from 2.9% to 15.1% between 1990 and 2000,4 it was believed that introducing DMDD as a diagnosis might lessen the overdiagnosis of pediatric BD by identifying children with chronic irritability and temper tantrums who previously would have been diagnosed with BD.
It is important to recognize that in pediatric patients, mood disorders present differently than they do in adults.5 In children/adolescents, mood disorders are less likely to present as distinct episodes (narrow band), but more likely to present as chronic, broad symptoms. Also, irritability is a common presentation in many pediatric psychiatric disorders, such as ODD, BD (irritability without elation),6 and depression. Thus, for many clinicians, determining the correct mood disorder diagnosis in pediatric patients can be challenging.
This article describes the diagnosis of DMDD, and how its presentation is similar to—and different from—those of other common pediatric psychiatric disorders.
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The origin of DMDD
Many researchers have investigated the broadband phenotypical presentation of pediatric mood disorders, which have been mostly diagnosed in the psychiatric community as pediatric BD. Leibenluft7 identified a subtype of mood disorder that they termed “severe mood dysregulation” (SMD). Compared with the narrow-band, clearly episodic BD, SMD has a different trajectory, outcome, and findings on brain imaging. SMD is characterized by chronic irritability with abnormal mood (anger or sadness) at least half of the day on most days, with 3 hyperarousal symptoms, including pressured speech, racing thoughts or flight of ideas, intrusiveness, distractibility, insomnia, and agitation.8 Eventually, SMD became the foundation of the development of DMDD.
DSM-5 diagnostic criteria for DMDD include severe recurrent temper outbursts that are out of proportion to the situation, inconsistent with developmental level, and occurring on average ≥3 times per week, plus persistently irritable or angry mood for most of the day nearly every day.9 Additional criteria include the presence of symptoms for at least 12 months (without a symptom-free period of at least 3 consecutive months) in ≥2 settings (at home, at school, or with peers) with onset before age 10. The course of DMDD typically is chronic with accompanying severe temperament. The estimated 6-month to 1-year prevalence is 2% to 5%; the diagnosis is more common among males and school-age children than it is in females and adolescents.9,10
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DMDD or bipolar disorder?
A patient cannot be dually diagnosed with both disorders. If a patient exhibits a manic episode for more than 1 day, that would null and void the DMDD diagnosis. However, in a study to evaluate BD in pediatric patients, researchers divided BD symptoms into BD-specific categories (elevated mood, grandiosity, and increased goal-directed activity) and nonspecific symptoms such as irritability and talkativeness, distractibility, and flight of ideas or racing thoughts. They found that in the absence of specific symptoms, a diagnosis of BD is unlikely to be the correct diagnosis.11 Hence, as a nonspecific symptom, chronic irritability should be attributed to the symptom count for DMDD, rather than BD. Most epidemiologic studies have concluded that depression and anxiety, and not irritability, are typically the preceeding presentations prior to the development of BD in young adults.12 Chronic irritability, however, predicts major depressive disorder and anxiety disorders in later adolescence and one’s early twenties.13 Furthermore, BD commonly presents with infrequent and discrete episodes and a later age of onset, while DMDD presents with chronic and frequent, severe temper outbursts. Some differences between DMDD and BD are illustrated in Table 1.11-13
Continue to: CASE 1
CASE 1
Irritable and taking risks
Ms. N, age 16, is brought to the outpatient psychiatry clinic by her parents for evaluation of mood symptoms, including irritability. Her mother claims her daughter was an introverted, anxious, shy child, but by the beginning of middle school, she began to feel irritable and frequently stayed up at night with little sleep. In high school, Ms. N had displayed several episodes of risk-taking behaviors, including taking her father’s vehicle for a drive despite not having a driver’s permit, running away for 2 days, and having unprotected sex.
During her assessment, Ms. N is pleasant and claims she usually has a great mood. She fought with her mother several times this year, which led her to run away. Her parents had divorced when Ms. N was 5 years old and have shared custody. Ms. N is doing well in school despite her parents’ concerns.
Diagnosis. The most likely diagnosis is emerging BD. Notice that Ms. N may have had anxiety symptoms before she developed irritability. She had a relatively late onset of symptoms that were episodic in nature, which further supports a diagnosis of BD.
_
>
DMDD or oppositional defiant disorder?
DMDD and ODD cannot be dually diagnosed. However, if a patient meets the criteria for both DMDD and ODD, only the DMDD diagnosis should be considered. One of many issues of DMDD is its similarity to ODD. In fact, more than 70% of patients with DMDD also meet the diagnostic criteria for ODD.10,14 Some researchers have conceptualized DMDD as a severe form of ODD. However, there are a few differences that clinicians can use to distinguish the 2 disorders.
Compared with patients with ODD, those with DMDD more frequently experience severe irritability.15 Patients with ODD may present with delinquent behaviors and trouble with authority figures. Moreover, comorbidity with ADHD is twice as common in ODD; more than 65% of patients with ADHD have ODD vs 30% who have DMDD.10,16 Finally, in general, children with DMDD have more social impairments compared with those with ODD. Differences between DMDD and BD are illustrated in Table 2.10,14-16
Continue to: CASE 2
CASE 2
Angry and defiant
Mr. R, age 14, is brought to the emergency department (ED) by his parents after becoming very aggressive with them. He punched a wall and vandalized his room after his parents grounded him because of his previous defiant behavior. He had been suspended from school that day for disrespecting his teacher after he was caught fighting another student.
His parents describe Mr. R as a strong-willed, stubborn child. He has difficulty with rules and refuses to follow them. He is grouchy and irritable around adults, including the ED staff. Mr. R enjoys being with his friends and playing video games. He had been diagnosed with ADHD when he was in kindergarten, when his teacher noticed he had a poor attention span and could not sit still. According to his parents, Mr. R has “blown up” a few times before, smashing items in his room and shouting obscenities. Mr. R’s parents noticed that he is more defiant in concurrence with discontinuing his ADHD stimulant medication.
Diagnosis. The most likely diagnosis for Mr. R is ODD. Notice the comorbidity of ADHD, which is more commonly associated with ODD. The frequency and severity of his outbursts and irritability symptoms were lower than that typically associated with DMDD.
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Treatment strategies for DMDD
Management of DMDD should focus on helping children and adolescents improve their emotional dysregulation.
Clinicians should always consider behavioral therapy as a first-line intervention. The behavioral planning team may include (but is not limited to) a behavior specialist, child psychiatrist, psychologist, therapist, skills trainer, teachers, and the caregiver(s). The plan should be implemented across all settings, including home and school. Furthermore, social skills training is necessary for many children with DMDD, who may require intensive behavioral modification planning. Comorbidity with ADHD should be addressed with a combination of behavioral planning and stimulant medications.17 If available, parent training and parent-child interactive therapy can help to improve defiant behavior.
Pharmacotherapy
Currently, no medications are FDA-approved for treating DMDD. Most pharmacologic trials that included patients with DMDD focused on managing chronic irritability and/or stabilizing comorbid disorders (ie, ADHD, depression, and anxiety).
Continue to: Stimulants
Stimulants. Previous trials examined the benefit of CNS stimulant medications, alone or in conjunction with behavioral therapy, in treating DMDD and comorbid ADHD. Methylphenidate results in a significant reduction in aggression18 with a dosing recommendation range from 1 to 1.2 mg/kg/d. CNS stimulants should be considered as first-line pharmacotherapy for DMDD, especially for patients with comorbid ADHD.
Anticonvulsants. Divalproex sodium is superior to placebo in treating aggression in children and adolescents.19 Trials found that divalproex sodium reduces irritability and aggression whether it is prescribed as monotherapy or combined with stimulant medications.19
Lithium is one of the main treatment options for mania in BD. The benefits of lithium for controlling aggression in DMDD are still under investigation. Earlier studies found that lithium significantly improves aggressive behavior in hospitalized pediatric with conduct disorder.20,21 However, a later study that evaluated lithium vs placebo for children with SMD (which arguably is phenotypically related to the DMDD) found there were no significant differences in improvement of irritability symptoms between groups.22 More research is needed to determine if lithium may play a role in treating patients with DMDD.
Antipsychotics. Aripiprazole and risperidone are FDA-approved for treating irritability in autism. A 2017 meta-analysis found both medications were effective in controlling irritability and aggression in other diagnoses as well.23 Other antipsychotic medications did not show sufficient benefits in treating irritability.23 When considering antipsychotics, clinicians should weigh the risks of metabolic adverse effects and follow practice guidelines.
Antidepressants. A systematic review did not find that selective serotonin reuptake inhibitors or serotonin-norepinephrine reuptake inhibitors effectively reduce irritability.24 However, in most of the studies evaluated, irritability was not the primary outcome measure.24
Other medications. Alpha-2 agonists (guanfacine, clonidine), and atomoxetine may help irritability indirectly by improving ADHD symptoms.25
Bottom Line
Disruptive mood dysregulation disorder (DMDD), bipolar disorder, and oppositional defiant disorder have similar presentations and diagnostic criteria. The frequency and severity of irritability can be a distinguishing factor. Behavioral therapy is a first-line treatment. No medications are FDA-approved for treating DMDD, but pharmacotherapy may help reduce irritability and aggression.
Related Resources
- Rao U. DSM-5: disruptive mood dysregulation disorder. Asian J Psychiatr. 2014;11:119-123.
- Roy AK, Lopes V, Klein RG. Disruptive mood dysregulation disorder: a new diagnostic approach to chronic irritability in youth. Am J Psychiatry. 2014;171(9):918-924.
Drug Brand Names
Aripiprazole • Abilify
Atomoxetine • Strattera
Clonidine • Catapres
Divalproex sodium • Depakote, Depakote ER
Guanfacine • Intuniv, Tenex
Lithium • Eskalith, Lithobid
Methylphenidate • Concerta, Ritalin
Risperidone • Risperdal
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20. Campbell M, Adams PB, Small AM, et al. Lithium in hospitalized aggressive children with conduct disorder: a double-blind and placebo-controlled study. J Am Acad Child Adolesc Psychiatry. 1995;34(4):445-453.
21. Malone RP, Delaney MA, Luebbert JF, et al. A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Arch Gen Psychiatry. 2000;57(7):649-654.
22. Dickstein DP, Towbin KE, Van Der Veen JW, et al. Randomized double-blind placebo-controlled trial of lithium in youths with severe mood dysregulation. J Child Adolesc Psychopharmacol. 2009;19(1):61-73.
23. van Schalkwyk GI, Lewis AS, Beyer C, et al. Efficacy of antipsychotics for irritability and aggression in children: a meta-analysis. Expert Rev Neurother. 2017;17(10):1045-1053.
24. Kim S, Boylan K. Effectiveness of antidepressant medications for symptoms of irritability and disruptive behaviors in children and adolescents. J Child Adolesc Psychopharmacol. 2016;26(8):694-704.
25. Scahill L, Chappell PB, Kim YS, et al. A placebo-controlled study of guanfacine in the treatment of children with tic disorders and attention deficit hyperactivity disorder. Am J Psychiatry. 2001;158(7):1067-1074.
Disruptive mood dysregulation disorder (DMDD)—a childhood condition of extreme irritability, anger, and frequent, intense temper outbursts—has been a source of controversy among clinicians in the field of pediatric mental health. Before DSM-5 was published, the validity of DMDD had been questioned because DMDD had failed a field trial; agreement between clinicians on the diagnosis of DMDD was poor.1 Axelson2 and Birmaher et al3 examined its validity in their COBY (Course and Outcome of Bipolar Youth) sample. They concluded that only 19% met the criteria for DMDD in 3 times of follow-up. Furthermore, most DMDD criteria overlap with those of other common pediatric psychiatric disorders, including oppositional defiant disorder (ODD), attention-deficit/hyperactivity disorder (ADHD), and pediatric bipolar disorder (BD). Because diagnosis of pediatric BD increased drastically from 2.9% to 15.1% between 1990 and 2000,4 it was believed that introducing DMDD as a diagnosis might lessen the overdiagnosis of pediatric BD by identifying children with chronic irritability and temper tantrums who previously would have been diagnosed with BD.
It is important to recognize that in pediatric patients, mood disorders present differently than they do in adults.5 In children/adolescents, mood disorders are less likely to present as distinct episodes (narrow band), but more likely to present as chronic, broad symptoms. Also, irritability is a common presentation in many pediatric psychiatric disorders, such as ODD, BD (irritability without elation),6 and depression. Thus, for many clinicians, determining the correct mood disorder diagnosis in pediatric patients can be challenging.
This article describes the diagnosis of DMDD, and how its presentation is similar to—and different from—those of other common pediatric psychiatric disorders.
_
The origin of DMDD
Many researchers have investigated the broadband phenotypical presentation of pediatric mood disorders, which have been mostly diagnosed in the psychiatric community as pediatric BD. Leibenluft7 identified a subtype of mood disorder that they termed “severe mood dysregulation” (SMD). Compared with the narrow-band, clearly episodic BD, SMD has a different trajectory, outcome, and findings on brain imaging. SMD is characterized by chronic irritability with abnormal mood (anger or sadness) at least half of the day on most days, with 3 hyperarousal symptoms, including pressured speech, racing thoughts or flight of ideas, intrusiveness, distractibility, insomnia, and agitation.8 Eventually, SMD became the foundation of the development of DMDD.
DSM-5 diagnostic criteria for DMDD include severe recurrent temper outbursts that are out of proportion to the situation, inconsistent with developmental level, and occurring on average ≥3 times per week, plus persistently irritable or angry mood for most of the day nearly every day.9 Additional criteria include the presence of symptoms for at least 12 months (without a symptom-free period of at least 3 consecutive months) in ≥2 settings (at home, at school, or with peers) with onset before age 10. The course of DMDD typically is chronic with accompanying severe temperament. The estimated 6-month to 1-year prevalence is 2% to 5%; the diagnosis is more common among males and school-age children than it is in females and adolescents.9,10
_
DMDD or bipolar disorder?
A patient cannot be dually diagnosed with both disorders. If a patient exhibits a manic episode for more than 1 day, that would null and void the DMDD diagnosis. However, in a study to evaluate BD in pediatric patients, researchers divided BD symptoms into BD-specific categories (elevated mood, grandiosity, and increased goal-directed activity) and nonspecific symptoms such as irritability and talkativeness, distractibility, and flight of ideas or racing thoughts. They found that in the absence of specific symptoms, a diagnosis of BD is unlikely to be the correct diagnosis.11 Hence, as a nonspecific symptom, chronic irritability should be attributed to the symptom count for DMDD, rather than BD. Most epidemiologic studies have concluded that depression and anxiety, and not irritability, are typically the preceeding presentations prior to the development of BD in young adults.12 Chronic irritability, however, predicts major depressive disorder and anxiety disorders in later adolescence and one’s early twenties.13 Furthermore, BD commonly presents with infrequent and discrete episodes and a later age of onset, while DMDD presents with chronic and frequent, severe temper outbursts. Some differences between DMDD and BD are illustrated in Table 1.11-13
Continue to: CASE 1
CASE 1
Irritable and taking risks
Ms. N, age 16, is brought to the outpatient psychiatry clinic by her parents for evaluation of mood symptoms, including irritability. Her mother claims her daughter was an introverted, anxious, shy child, but by the beginning of middle school, she began to feel irritable and frequently stayed up at night with little sleep. In high school, Ms. N had displayed several episodes of risk-taking behaviors, including taking her father’s vehicle for a drive despite not having a driver’s permit, running away for 2 days, and having unprotected sex.
During her assessment, Ms. N is pleasant and claims she usually has a great mood. She fought with her mother several times this year, which led her to run away. Her parents had divorced when Ms. N was 5 years old and have shared custody. Ms. N is doing well in school despite her parents’ concerns.
Diagnosis. The most likely diagnosis is emerging BD. Notice that Ms. N may have had anxiety symptoms before she developed irritability. She had a relatively late onset of symptoms that were episodic in nature, which further supports a diagnosis of BD.
_
>
DMDD or oppositional defiant disorder?
DMDD and ODD cannot be dually diagnosed. However, if a patient meets the criteria for both DMDD and ODD, only the DMDD diagnosis should be considered. One of many issues of DMDD is its similarity to ODD. In fact, more than 70% of patients with DMDD also meet the diagnostic criteria for ODD.10,14 Some researchers have conceptualized DMDD as a severe form of ODD. However, there are a few differences that clinicians can use to distinguish the 2 disorders.
Compared with patients with ODD, those with DMDD more frequently experience severe irritability.15 Patients with ODD may present with delinquent behaviors and trouble with authority figures. Moreover, comorbidity with ADHD is twice as common in ODD; more than 65% of patients with ADHD have ODD vs 30% who have DMDD.10,16 Finally, in general, children with DMDD have more social impairments compared with those with ODD. Differences between DMDD and BD are illustrated in Table 2.10,14-16
Continue to: CASE 2
CASE 2
Angry and defiant
Mr. R, age 14, is brought to the emergency department (ED) by his parents after becoming very aggressive with them. He punched a wall and vandalized his room after his parents grounded him because of his previous defiant behavior. He had been suspended from school that day for disrespecting his teacher after he was caught fighting another student.
His parents describe Mr. R as a strong-willed, stubborn child. He has difficulty with rules and refuses to follow them. He is grouchy and irritable around adults, including the ED staff. Mr. R enjoys being with his friends and playing video games. He had been diagnosed with ADHD when he was in kindergarten, when his teacher noticed he had a poor attention span and could not sit still. According to his parents, Mr. R has “blown up” a few times before, smashing items in his room and shouting obscenities. Mr. R’s parents noticed that he is more defiant in concurrence with discontinuing his ADHD stimulant medication.
Diagnosis. The most likely diagnosis for Mr. R is ODD. Notice the comorbidity of ADHD, which is more commonly associated with ODD. The frequency and severity of his outbursts and irritability symptoms were lower than that typically associated with DMDD.
_
Treatment strategies for DMDD
Management of DMDD should focus on helping children and adolescents improve their emotional dysregulation.
Clinicians should always consider behavioral therapy as a first-line intervention. The behavioral planning team may include (but is not limited to) a behavior specialist, child psychiatrist, psychologist, therapist, skills trainer, teachers, and the caregiver(s). The plan should be implemented across all settings, including home and school. Furthermore, social skills training is necessary for many children with DMDD, who may require intensive behavioral modification planning. Comorbidity with ADHD should be addressed with a combination of behavioral planning and stimulant medications.17 If available, parent training and parent-child interactive therapy can help to improve defiant behavior.
Pharmacotherapy
Currently, no medications are FDA-approved for treating DMDD. Most pharmacologic trials that included patients with DMDD focused on managing chronic irritability and/or stabilizing comorbid disorders (ie, ADHD, depression, and anxiety).
Continue to: Stimulants
Stimulants. Previous trials examined the benefit of CNS stimulant medications, alone or in conjunction with behavioral therapy, in treating DMDD and comorbid ADHD. Methylphenidate results in a significant reduction in aggression18 with a dosing recommendation range from 1 to 1.2 mg/kg/d. CNS stimulants should be considered as first-line pharmacotherapy for DMDD, especially for patients with comorbid ADHD.
Anticonvulsants. Divalproex sodium is superior to placebo in treating aggression in children and adolescents.19 Trials found that divalproex sodium reduces irritability and aggression whether it is prescribed as monotherapy or combined with stimulant medications.19
Lithium is one of the main treatment options for mania in BD. The benefits of lithium for controlling aggression in DMDD are still under investigation. Earlier studies found that lithium significantly improves aggressive behavior in hospitalized pediatric with conduct disorder.20,21 However, a later study that evaluated lithium vs placebo for children with SMD (which arguably is phenotypically related to the DMDD) found there were no significant differences in improvement of irritability symptoms between groups.22 More research is needed to determine if lithium may play a role in treating patients with DMDD.
Antipsychotics. Aripiprazole and risperidone are FDA-approved for treating irritability in autism. A 2017 meta-analysis found both medications were effective in controlling irritability and aggression in other diagnoses as well.23 Other antipsychotic medications did not show sufficient benefits in treating irritability.23 When considering antipsychotics, clinicians should weigh the risks of metabolic adverse effects and follow practice guidelines.
Antidepressants. A systematic review did not find that selective serotonin reuptake inhibitors or serotonin-norepinephrine reuptake inhibitors effectively reduce irritability.24 However, in most of the studies evaluated, irritability was not the primary outcome measure.24
Other medications. Alpha-2 agonists (guanfacine, clonidine), and atomoxetine may help irritability indirectly by improving ADHD symptoms.25
Bottom Line
Disruptive mood dysregulation disorder (DMDD), bipolar disorder, and oppositional defiant disorder have similar presentations and diagnostic criteria. The frequency and severity of irritability can be a distinguishing factor. Behavioral therapy is a first-line treatment. No medications are FDA-approved for treating DMDD, but pharmacotherapy may help reduce irritability and aggression.
Related Resources
- Rao U. DSM-5: disruptive mood dysregulation disorder. Asian J Psychiatr. 2014;11:119-123.
- Roy AK, Lopes V, Klein RG. Disruptive mood dysregulation disorder: a new diagnostic approach to chronic irritability in youth. Am J Psychiatry. 2014;171(9):918-924.
Drug Brand Names
Aripiprazole • Abilify
Atomoxetine • Strattera
Clonidine • Catapres
Divalproex sodium • Depakote, Depakote ER
Guanfacine • Intuniv, Tenex
Lithium • Eskalith, Lithobid
Methylphenidate • Concerta, Ritalin
Risperidone • Risperdal
Disruptive mood dysregulation disorder (DMDD)—a childhood condition of extreme irritability, anger, and frequent, intense temper outbursts—has been a source of controversy among clinicians in the field of pediatric mental health. Before DSM-5 was published, the validity of DMDD had been questioned because DMDD had failed a field trial; agreement between clinicians on the diagnosis of DMDD was poor.1 Axelson2 and Birmaher et al3 examined its validity in their COBY (Course and Outcome of Bipolar Youth) sample. They concluded that only 19% met the criteria for DMDD in 3 times of follow-up. Furthermore, most DMDD criteria overlap with those of other common pediatric psychiatric disorders, including oppositional defiant disorder (ODD), attention-deficit/hyperactivity disorder (ADHD), and pediatric bipolar disorder (BD). Because diagnosis of pediatric BD increased drastically from 2.9% to 15.1% between 1990 and 2000,4 it was believed that introducing DMDD as a diagnosis might lessen the overdiagnosis of pediatric BD by identifying children with chronic irritability and temper tantrums who previously would have been diagnosed with BD.
It is important to recognize that in pediatric patients, mood disorders present differently than they do in adults.5 In children/adolescents, mood disorders are less likely to present as distinct episodes (narrow band), but more likely to present as chronic, broad symptoms. Also, irritability is a common presentation in many pediatric psychiatric disorders, such as ODD, BD (irritability without elation),6 and depression. Thus, for many clinicians, determining the correct mood disorder diagnosis in pediatric patients can be challenging.
This article describes the diagnosis of DMDD, and how its presentation is similar to—and different from—those of other common pediatric psychiatric disorders.
_
The origin of DMDD
Many researchers have investigated the broadband phenotypical presentation of pediatric mood disorders, which have been mostly diagnosed in the psychiatric community as pediatric BD. Leibenluft7 identified a subtype of mood disorder that they termed “severe mood dysregulation” (SMD). Compared with the narrow-band, clearly episodic BD, SMD has a different trajectory, outcome, and findings on brain imaging. SMD is characterized by chronic irritability with abnormal mood (anger or sadness) at least half of the day on most days, with 3 hyperarousal symptoms, including pressured speech, racing thoughts or flight of ideas, intrusiveness, distractibility, insomnia, and agitation.8 Eventually, SMD became the foundation of the development of DMDD.
DSM-5 diagnostic criteria for DMDD include severe recurrent temper outbursts that are out of proportion to the situation, inconsistent with developmental level, and occurring on average ≥3 times per week, plus persistently irritable or angry mood for most of the day nearly every day.9 Additional criteria include the presence of symptoms for at least 12 months (without a symptom-free period of at least 3 consecutive months) in ≥2 settings (at home, at school, or with peers) with onset before age 10. The course of DMDD typically is chronic with accompanying severe temperament. The estimated 6-month to 1-year prevalence is 2% to 5%; the diagnosis is more common among males and school-age children than it is in females and adolescents.9,10
_
DMDD or bipolar disorder?
A patient cannot be dually diagnosed with both disorders. If a patient exhibits a manic episode for more than 1 day, that would null and void the DMDD diagnosis. However, in a study to evaluate BD in pediatric patients, researchers divided BD symptoms into BD-specific categories (elevated mood, grandiosity, and increased goal-directed activity) and nonspecific symptoms such as irritability and talkativeness, distractibility, and flight of ideas or racing thoughts. They found that in the absence of specific symptoms, a diagnosis of BD is unlikely to be the correct diagnosis.11 Hence, as a nonspecific symptom, chronic irritability should be attributed to the symptom count for DMDD, rather than BD. Most epidemiologic studies have concluded that depression and anxiety, and not irritability, are typically the preceeding presentations prior to the development of BD in young adults.12 Chronic irritability, however, predicts major depressive disorder and anxiety disorders in later adolescence and one’s early twenties.13 Furthermore, BD commonly presents with infrequent and discrete episodes and a later age of onset, while DMDD presents with chronic and frequent, severe temper outbursts. Some differences between DMDD and BD are illustrated in Table 1.11-13
Continue to: CASE 1
CASE 1
Irritable and taking risks
Ms. N, age 16, is brought to the outpatient psychiatry clinic by her parents for evaluation of mood symptoms, including irritability. Her mother claims her daughter was an introverted, anxious, shy child, but by the beginning of middle school, she began to feel irritable and frequently stayed up at night with little sleep. In high school, Ms. N had displayed several episodes of risk-taking behaviors, including taking her father’s vehicle for a drive despite not having a driver’s permit, running away for 2 days, and having unprotected sex.
During her assessment, Ms. N is pleasant and claims she usually has a great mood. She fought with her mother several times this year, which led her to run away. Her parents had divorced when Ms. N was 5 years old and have shared custody. Ms. N is doing well in school despite her parents’ concerns.
Diagnosis. The most likely diagnosis is emerging BD. Notice that Ms. N may have had anxiety symptoms before she developed irritability. She had a relatively late onset of symptoms that were episodic in nature, which further supports a diagnosis of BD.
_
>
DMDD or oppositional defiant disorder?
DMDD and ODD cannot be dually diagnosed. However, if a patient meets the criteria for both DMDD and ODD, only the DMDD diagnosis should be considered. One of many issues of DMDD is its similarity to ODD. In fact, more than 70% of patients with DMDD also meet the diagnostic criteria for ODD.10,14 Some researchers have conceptualized DMDD as a severe form of ODD. However, there are a few differences that clinicians can use to distinguish the 2 disorders.
Compared with patients with ODD, those with DMDD more frequently experience severe irritability.15 Patients with ODD may present with delinquent behaviors and trouble with authority figures. Moreover, comorbidity with ADHD is twice as common in ODD; more than 65% of patients with ADHD have ODD vs 30% who have DMDD.10,16 Finally, in general, children with DMDD have more social impairments compared with those with ODD. Differences between DMDD and BD are illustrated in Table 2.10,14-16
Continue to: CASE 2
CASE 2
Angry and defiant
Mr. R, age 14, is brought to the emergency department (ED) by his parents after becoming very aggressive with them. He punched a wall and vandalized his room after his parents grounded him because of his previous defiant behavior. He had been suspended from school that day for disrespecting his teacher after he was caught fighting another student.
His parents describe Mr. R as a strong-willed, stubborn child. He has difficulty with rules and refuses to follow them. He is grouchy and irritable around adults, including the ED staff. Mr. R enjoys being with his friends and playing video games. He had been diagnosed with ADHD when he was in kindergarten, when his teacher noticed he had a poor attention span and could not sit still. According to his parents, Mr. R has “blown up” a few times before, smashing items in his room and shouting obscenities. Mr. R’s parents noticed that he is more defiant in concurrence with discontinuing his ADHD stimulant medication.
Diagnosis. The most likely diagnosis for Mr. R is ODD. Notice the comorbidity of ADHD, which is more commonly associated with ODD. The frequency and severity of his outbursts and irritability symptoms were lower than that typically associated with DMDD.
_
Treatment strategies for DMDD
Management of DMDD should focus on helping children and adolescents improve their emotional dysregulation.
Clinicians should always consider behavioral therapy as a first-line intervention. The behavioral planning team may include (but is not limited to) a behavior specialist, child psychiatrist, psychologist, therapist, skills trainer, teachers, and the caregiver(s). The plan should be implemented across all settings, including home and school. Furthermore, social skills training is necessary for many children with DMDD, who may require intensive behavioral modification planning. Comorbidity with ADHD should be addressed with a combination of behavioral planning and stimulant medications.17 If available, parent training and parent-child interactive therapy can help to improve defiant behavior.
Pharmacotherapy
Currently, no medications are FDA-approved for treating DMDD. Most pharmacologic trials that included patients with DMDD focused on managing chronic irritability and/or stabilizing comorbid disorders (ie, ADHD, depression, and anxiety).
Continue to: Stimulants
Stimulants. Previous trials examined the benefit of CNS stimulant medications, alone or in conjunction with behavioral therapy, in treating DMDD and comorbid ADHD. Methylphenidate results in a significant reduction in aggression18 with a dosing recommendation range from 1 to 1.2 mg/kg/d. CNS stimulants should be considered as first-line pharmacotherapy for DMDD, especially for patients with comorbid ADHD.
Anticonvulsants. Divalproex sodium is superior to placebo in treating aggression in children and adolescents.19 Trials found that divalproex sodium reduces irritability and aggression whether it is prescribed as monotherapy or combined with stimulant medications.19
Lithium is one of the main treatment options for mania in BD. The benefits of lithium for controlling aggression in DMDD are still under investigation. Earlier studies found that lithium significantly improves aggressive behavior in hospitalized pediatric with conduct disorder.20,21 However, a later study that evaluated lithium vs placebo for children with SMD (which arguably is phenotypically related to the DMDD) found there were no significant differences in improvement of irritability symptoms between groups.22 More research is needed to determine if lithium may play a role in treating patients with DMDD.
Antipsychotics. Aripiprazole and risperidone are FDA-approved for treating irritability in autism. A 2017 meta-analysis found both medications were effective in controlling irritability and aggression in other diagnoses as well.23 Other antipsychotic medications did not show sufficient benefits in treating irritability.23 When considering antipsychotics, clinicians should weigh the risks of metabolic adverse effects and follow practice guidelines.
Antidepressants. A systematic review did not find that selective serotonin reuptake inhibitors or serotonin-norepinephrine reuptake inhibitors effectively reduce irritability.24 However, in most of the studies evaluated, irritability was not the primary outcome measure.24
Other medications. Alpha-2 agonists (guanfacine, clonidine), and atomoxetine may help irritability indirectly by improving ADHD symptoms.25
Bottom Line
Disruptive mood dysregulation disorder (DMDD), bipolar disorder, and oppositional defiant disorder have similar presentations and diagnostic criteria. The frequency and severity of irritability can be a distinguishing factor. Behavioral therapy is a first-line treatment. No medications are FDA-approved for treating DMDD, but pharmacotherapy may help reduce irritability and aggression.
Related Resources
- Rao U. DSM-5: disruptive mood dysregulation disorder. Asian J Psychiatr. 2014;11:119-123.
- Roy AK, Lopes V, Klein RG. Disruptive mood dysregulation disorder: a new diagnostic approach to chronic irritability in youth. Am J Psychiatry. 2014;171(9):918-924.
Drug Brand Names
Aripiprazole • Abilify
Atomoxetine • Strattera
Clonidine • Catapres
Divalproex sodium • Depakote, Depakote ER
Guanfacine • Intuniv, Tenex
Lithium • Eskalith, Lithobid
Methylphenidate • Concerta, Ritalin
Risperidone • Risperdal
1. Regier DA, Narrow WE, Clarke DE, et al. DSM-5 field trials in the United States and Canada, Part II: test-retest reliability of selected categorical diagnoses. Am J Psychiatry. 2013;170(1):59-70.
2. Axelson D. Taking disruptive mood dysregulation disorder out for a test drive. Am J Psychiatry. 2013;170(2):136-139.
3. Birmaher B, Axelson D, Goldstein B, et al. Four-year longitudinal course of children and adolescents with bipolar spectrum disorders: the Course and Outcome of Bipolar Youth (COBY) study. Am J Psychiatry. 2009;166(7):795-804.
4. Case BG, Olfson M, Marcus SC, et al. Trends in the inpatient mental health treatment of children and adolescents in US community hospitals between 1990 and 2000. Arch Gen Psychiatry. 2007;64(1):89-96.
5. Pliszka S; AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2007;46(7):894-921.
6. Hunt J, Birmaher B, Leonard H, et al. Irritability without elation in a large bipolar youth sample: frequency and clinical description. J Am Acad Child Adolesc Psychiatry. 2009;48(7):730-739.
7. Leibenluft E. Severe mood dysregulation, irritability, and the diagnostic boundaries of bipolar disorder in youths. Am J Psychiatry. 2011;168(2):129-142.
8. Rich BA, Carver FW, Holroyd T, et al. Different neural pathways to negative affect in youth with pediatric bipolar disorder and severe mood dysregulation. J Psychiatr Res. 2011;45(10):1283-1294.
9. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
10. Copeland WE, Angold A, Costello EJ, et al. Prevalence, comorbidity, and correlates of DSM-5 proposed disruptive mood dysregulation disorder. Am J Psychiatry. 2013;170(2):173-179.
11. Elmaadawi AZ, Jensen PS, Arnold LE, et al. Risk for emerging bipolar disorder, variants, and symptoms in children with attention deficit hyperactivity disorder, now grown up. World J Psychiatry. 2015;5(4):412-424.
12. Duffy A. The early natural history of bipolar disorder: what we have learned from longitudinal high-risk research. Can J Psychiatry. 2010;55(8):477-485.
13. Stringaris A, Cohen P, Pine DS, et al. Adult outcomes of youth irritability: a 20-year prospective community-based study. Am J Psychiatry. 2009;166(9):1048-1054.
14. Mayes SD, Waxmonsky JD, Calhoun SL, et al. Disruptive mood dysregulation disorder symptoms and association with oppositional defiant and other disorders in a general population child sample. J Child Adolesc Psychopharmacol. 2016;26(2):101-106.
15. Stringaris A, Vidal-Ribas P, Brotman MA, et al. Practitioner review: definition, recognition, and treatment challenges of irritability in young people. J Child Psychol Psychiatry. 2018;59(7):721-739.
16. Angold A, Costello EJ, Erkanli A. Comorbidity. J Child Psychol Psychiatry. 1999;40(1):57-87.
17. Fernandez de la Cruz L, Simonoff E, McGough JJ, et al. Treatment of children with attention-deficit/hyperactivity disorder (ADHD) and irritability: results from the multimodal treatment study of children with ADHD (MTA). J Am Acad Child Adolesc Psychiatry. 2015;54(1):62-70.
18. Pappadopulos E, Woolston S, Chait A, et al. Pharmacotherapy of aggression in children and adolescents: efficacy and effect size. J Can Acad Child Adolesc Psychiatry. 2006;15(1):27-39.
19. Donovan SJ, Stewart JW, Nunes EV, et al. Divalproex treatment for youth with explosive temper and mood lability: a double-blind, placebo-controlled crossover design. Am J Psychiatry. 2000;157(5):818-820.
20. Campbell M, Adams PB, Small AM, et al. Lithium in hospitalized aggressive children with conduct disorder: a double-blind and placebo-controlled study. J Am Acad Child Adolesc Psychiatry. 1995;34(4):445-453.
21. Malone RP, Delaney MA, Luebbert JF, et al. A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Arch Gen Psychiatry. 2000;57(7):649-654.
22. Dickstein DP, Towbin KE, Van Der Veen JW, et al. Randomized double-blind placebo-controlled trial of lithium in youths with severe mood dysregulation. J Child Adolesc Psychopharmacol. 2009;19(1):61-73.
23. van Schalkwyk GI, Lewis AS, Beyer C, et al. Efficacy of antipsychotics for irritability and aggression in children: a meta-analysis. Expert Rev Neurother. 2017;17(10):1045-1053.
24. Kim S, Boylan K. Effectiveness of antidepressant medications for symptoms of irritability and disruptive behaviors in children and adolescents. J Child Adolesc Psychopharmacol. 2016;26(8):694-704.
25. Scahill L, Chappell PB, Kim YS, et al. A placebo-controlled study of guanfacine in the treatment of children with tic disorders and attention deficit hyperactivity disorder. Am J Psychiatry. 2001;158(7):1067-1074.
1. Regier DA, Narrow WE, Clarke DE, et al. DSM-5 field trials in the United States and Canada, Part II: test-retest reliability of selected categorical diagnoses. Am J Psychiatry. 2013;170(1):59-70.
2. Axelson D. Taking disruptive mood dysregulation disorder out for a test drive. Am J Psychiatry. 2013;170(2):136-139.
3. Birmaher B, Axelson D, Goldstein B, et al. Four-year longitudinal course of children and adolescents with bipolar spectrum disorders: the Course and Outcome of Bipolar Youth (COBY) study. Am J Psychiatry. 2009;166(7):795-804.
4. Case BG, Olfson M, Marcus SC, et al. Trends in the inpatient mental health treatment of children and adolescents in US community hospitals between 1990 and 2000. Arch Gen Psychiatry. 2007;64(1):89-96.
5. Pliszka S; AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2007;46(7):894-921.
6. Hunt J, Birmaher B, Leonard H, et al. Irritability without elation in a large bipolar youth sample: frequency and clinical description. J Am Acad Child Adolesc Psychiatry. 2009;48(7):730-739.
7. Leibenluft E. Severe mood dysregulation, irritability, and the diagnostic boundaries of bipolar disorder in youths. Am J Psychiatry. 2011;168(2):129-142.
8. Rich BA, Carver FW, Holroyd T, et al. Different neural pathways to negative affect in youth with pediatric bipolar disorder and severe mood dysregulation. J Psychiatr Res. 2011;45(10):1283-1294.
9. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
10. Copeland WE, Angold A, Costello EJ, et al. Prevalence, comorbidity, and correlates of DSM-5 proposed disruptive mood dysregulation disorder. Am J Psychiatry. 2013;170(2):173-179.
11. Elmaadawi AZ, Jensen PS, Arnold LE, et al. Risk for emerging bipolar disorder, variants, and symptoms in children with attention deficit hyperactivity disorder, now grown up. World J Psychiatry. 2015;5(4):412-424.
12. Duffy A. The early natural history of bipolar disorder: what we have learned from longitudinal high-risk research. Can J Psychiatry. 2010;55(8):477-485.
13. Stringaris A, Cohen P, Pine DS, et al. Adult outcomes of youth irritability: a 20-year prospective community-based study. Am J Psychiatry. 2009;166(9):1048-1054.
14. Mayes SD, Waxmonsky JD, Calhoun SL, et al. Disruptive mood dysregulation disorder symptoms and association with oppositional defiant and other disorders in a general population child sample. J Child Adolesc Psychopharmacol. 2016;26(2):101-106.
15. Stringaris A, Vidal-Ribas P, Brotman MA, et al. Practitioner review: definition, recognition, and treatment challenges of irritability in young people. J Child Psychol Psychiatry. 2018;59(7):721-739.
16. Angold A, Costello EJ, Erkanli A. Comorbidity. J Child Psychol Psychiatry. 1999;40(1):57-87.
17. Fernandez de la Cruz L, Simonoff E, McGough JJ, et al. Treatment of children with attention-deficit/hyperactivity disorder (ADHD) and irritability: results from the multimodal treatment study of children with ADHD (MTA). J Am Acad Child Adolesc Psychiatry. 2015;54(1):62-70.
18. Pappadopulos E, Woolston S, Chait A, et al. Pharmacotherapy of aggression in children and adolescents: efficacy and effect size. J Can Acad Child Adolesc Psychiatry. 2006;15(1):27-39.
19. Donovan SJ, Stewart JW, Nunes EV, et al. Divalproex treatment for youth with explosive temper and mood lability: a double-blind, placebo-controlled crossover design. Am J Psychiatry. 2000;157(5):818-820.
20. Campbell M, Adams PB, Small AM, et al. Lithium in hospitalized aggressive children with conduct disorder: a double-blind and placebo-controlled study. J Am Acad Child Adolesc Psychiatry. 1995;34(4):445-453.
21. Malone RP, Delaney MA, Luebbert JF, et al. A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Arch Gen Psychiatry. 2000;57(7):649-654.
22. Dickstein DP, Towbin KE, Van Der Veen JW, et al. Randomized double-blind placebo-controlled trial of lithium in youths with severe mood dysregulation. J Child Adolesc Psychopharmacol. 2009;19(1):61-73.
23. van Schalkwyk GI, Lewis AS, Beyer C, et al. Efficacy of antipsychotics for irritability and aggression in children: a meta-analysis. Expert Rev Neurother. 2017;17(10):1045-1053.
24. Kim S, Boylan K. Effectiveness of antidepressant medications for symptoms of irritability and disruptive behaviors in children and adolescents. J Child Adolesc Psychopharmacol. 2016;26(8):694-704.
25. Scahill L, Chappell PB, Kim YS, et al. A placebo-controlled study of guanfacine in the treatment of children with tic disorders and attention deficit hyperactivity disorder. Am J Psychiatry. 2001;158(7):1067-1074.
Bright light therapy for bipolar depression
Bright light therapy (BLT) refers to the use of bright light to treat symptoms of depression. BLT was initially prescribed as a treatment for patients with seasonal affective disorder.1 It was later found helpful for nonseasonal depression,2 premenstrual dysphoric disorder, postpartum depression, and phase shift circadian disorders, including for patients with dementia whose cognitive function improved after treatment with BLT.3 More recent studies suggest year-round benefit for nonseasonal depression.2 The American Psychiatric Association practice guidelines for the treatment of depression list BLT as an alternative and/or addition to pharmacologic and psychological treatment.4 BLT also may be beneficial for patients who are in the depressive phase of bipolar illness.
This article describes the evidence, rationale for use, mechanism of action, benefits, and safety profile of BLT for treating patients with bipolar depression.
Circadian rhythm disruption in bipolar disorder
Clinical manifestation. Patients with bipolar disorder (BD) spend more time in depression than in mania.5 Sleep disturbance is a core symptom of BD; patients typically have little need for sleep during a manic episode, and excess sleepiness during a depressive episode. Sleep complaints can be both precipitating factors and consequences of mood disorders. Patients with seasonal depression have excess sleepiness and weight gain in the winter followed by hypomanic-like symptoms in the spring, including decreased need for sleep and weight loss with psychomotor activation. In a recent review of sleep problems in patients with BD, Steinan et al6 reported that 20% of patients with euthymic mood in bipolar disorder experience a sleep disorder. Circadian disruption and “eveningness” (being more active during the evening) have been associated with mood episodes, functional impairment, poor quality of life, and treatment resistance.7-10
Pathophysiology. Existing hypotheses for the biological mechanism underlying dysregulation of circadian rhythm in BD include changes in melatonin levels, expression of melatonin receptors in the CNS, and daily cortisol profiles.11 Genetic evidence also links circadian rhythm dysregulation with BD. Two polymorphisms on the circadian locomotor output cycles kaput (CLOCK) gene that control circadian rhythm—aryl hydrocarbon receptor nuclear translocator-like (ARNTL) and timeless circadian clock (TIMELESS)—have been linked to lithium responsiveness in BD.12 In addition, Per2, Cry1, and Rev-Erbα expression—all components of the circadian clock—have been found to increase individual susceptibility to the therapeutic effects of lithium in mice.13 In addition, circadian rhythm dysregulation is associated with metabolic problems encountered by patients with BD, including weight gain, diabetes mellitus, and cardiovascular disease.14
Rationale for use
Regulation of a patient’s circadian rhythm disruption is a potential treatment for BD. Hashimoto et al15 demonstrated that midday bright light exposure can phase advance and increase the amplitude of nocturnal melatonin production in healthy individuals. Morning light therapy has been shown to increase blood serotonin throughout the day in both healthy individuals and in patients with nonseasonal depression; the effect was apparent with light intensities as low as 50 lux.16 Lithium may exert its therapeutic effect through its influence on the retino-hypothalamic-pineal tract and thus its effect on melatonin secretion.17
BLT is a logical choice to treat the depression phase of BD when exposure to sunlight is not feasible due to geographical location, season, or other factor. For patients who live in areas that receive frequent sunshine, an outside stroll for half an hour will likely achieve similar benefit to BLT.
The precise mechanism of action of BLT for bipolar depression has not yet been determined. It may be attributed to a phase-resetting effect via melanopsin and the suprachiasmatic nucleus (Box18-24).
Box
Bright light therapy: How it works
The mechanism of action of bright light therapy is yet to be elucidated. The suprachiasmatic nucleus (SCN) in the hypothalamus is the center of circadian rhythm regulation and receives direct input from the retina through the retinohypothalamic tract.18 Melanopsin, a short-wavelength, light-sensitive G-protein–coupled receptor located in human retinal ganglion cells, is known to transduce short-wavelength light signals into neural signals.19 Since melanopsin is primarily responsible for resetting the timing of the SCN, suppressing pineal gland melatonin secretion and improving alertness and electroencephalogram-derived correlates of arousal,20 short-wavelength light with a low light intensity might be a better stimulator for melanopsin-containing retinal ganglion cells and the behaviors mediated via this photoreceptor system.21,22 Whether the antidepressant effect of light is also related to its alerting property is unclear.23 However, the acute alerting and performance-enhancing effects of light are increasingly taken into account for the design of indoor light standards in office environments.24 Response to light therapy is thus attributed to its phase-resetting effect.
Continue to: BLT for BD...
BLT for BD: What’s the evidence?
Several studies and case reports have evaluated the use of BLT for bipolar depression. The number of participants in these studies is small, and there is no uniformity of methodology or patient selection.
Dauphinais et al (2012)25 randomly assigned 44 patients with bipolar depression to BLT or a high-density or low-density negative ion generator for 8 weeks. They reported no difference in outcome between the various groups (50% vs 55.6%, remission and response rate). Only one patient in each group showed a switch to hypomania.
Carmadese et al (2015)26 reported an open-label study of adjunctive BLT in 31 difficult-to-treat patients with depression (16 unipolar and 15 bipolar). Significant improvement was noted within 3 weeks and was sustained in 1 patient with bipolar depression 5 weeks after cessation of BLT.
Papatheodorou and Kutcher (1995)27 treated 7 adolescents with bipolar depression with adjunctive BLT (10,000 lux twice per day). Three patients showed a marked response (>70% decrease from baseline Beck Depression Inventory and Symptom Check List scores). Two patients had a moderate response (40% to 47% decrease) and 2 patients obtained mild to no response. There were no reported adverse effects.
Benedetti et al (2014)28 studied 141 patients with treatment-resistant bipolar depression. Approximately one-quarter (23%) had a history of attempted suicide, and 83% had a history of drug resistance. The authors found a combination of total sleep deprivation, BLT, and lithium rapidly decreased suicidality and improved patients’ depressive symptoms.
Liebenluft et al (1995)29 administered 13 trials of BLT to 9 patients with rapid-cycling BD during a 3-month period. Five patients received the treatment in the morning, 5 around midday, and 3 in the evening. Patients who received BLT at midday had the best outcome, while 3 of the 5 patients who received morning BLT developed unstable mood. The authors recommended titrating the duration of light exposure so that patients could skip a treatment if their mood was trending toward hypomania.
Sit et al (2007)30 evaluated BLT in a case series of 9 women with bipolar I or II disorder in the depression phase. Patients were exposed to 50 lux of red light for 2 weeks, and then they received 7,000 lux BLT for 15, 30, and 45 minutes daily for 2 weeks (4 patients received morning light and 5 received midday light). Mood was assessed using the Structured Interview Guide for the Hamilton Depression Rating Scale with Atypical Depression Supplement and the Mania Rating Scale. Of the 4 patients receiving morning BLT, one patient had a full response and the other 3 developed hypomania. Of the 5 patients who received midday BLT, 2 achieved full response, 2 showed early improvement but required a dose increase, and one remained depressed but had a full response when she was switched to morning BLT.
Tseng et al (2016)31 reported a meta-analysis of BLT for bipolar depression that included a total of 567 patients from 11 studies. They reported significant improvement with BLT alone or in combination with antidepressants or total sleep deprivation. They also reported significant improvement with BLT in 130 patients who were not receiving other treatments. There was no difference in the frequency of mood shifts between patients on BLT alone or in combination with other modalities. The authors reported no mood shift in any of the patients receiving concurrent mood stabilizers. They also reported no difference with the color of light, gender, or duration of illness.
Yorguner et al (2017)32 conducted a 2-week randomized, single-blind study of BLT as an add-on treatment for 32 patients with bipolar depression. Patients were randomly assigned to BLT or dim light, which they were administered each morning for 30 mins for 2 weeks. Sixteen patients who received BLT showed a significantly greater reduction in Hamilton Depression Rating Scale scores (mean score of 24 at baseline down to 12) compared with 16 patients who received dim light (mean score of 24 at baseline down to 18). The authors also reported remission in 4 out of 4 patients who had seasonal depression, compared with 3 out of 12 who did not have seasonal depression (the other 9 showed response but not remission).
Zhou et al (2018)33 conducted a multi-center, randomized, single-blind clinical trial of 63 patients with bipolar depression. Thirty-three patients received morning BLT, and 30 received dim red light therapy (control group). The authors reported a significantly higher response rate in the BLT group (78%) compared with the control group (43%).
Sit et al (2018)34 conducted a 6-week randomized, double-blind, placebo-controlled trial of BLT vs dim red light in patients with bipolar I or II depression. Twenty-three patients were administered 7,000 lux bright white light, and 23 patients received 50 lux dim red light, at midday 5 days a week. The light dose was increased by 15 minutes every week up to 60 minutes by Week 4, unless the patient achieved remission. Patients were maintained on their usual medications, which included mood stabilizers and/or antidepressants. At Week 6, the group randomized to BLT had a significantly higher remission rate (68%) compared with patients who received dim red light (22%). Improvement was noted by Week 4. Patients receiving BLT also had significantly fewer depressive symptoms, and no mood polarity switch was noted.
Prescribing bright light therapy
Light box selection criteria. When selecting a light box or related BLT treatment apparatus, the Center for Environmental Therapeutics recommends consideration of the following factors35:
- clinical efficacy
- ocular and dermatologic safety
- visual comfort.
Selecting a dose. The dose received is determined by the intensity emitted from the light source, distance from the light box, and duration of exposure.36 Begin with midday light therapy between 12 noon and 2
Monitor for adverse effects. Generally, BLT is well tolerated.37 Adverse effects are rare; the most common ones include headache, eyestrain, nausea, and agitation.38 One study found no adverse ocular effects from light therapy after 5 years of treatment.39 Adverse effects tend to remit spontaneously or after dose reduction.35 Evening administration of BLT may increase the incidence of sleep disturbances.40 Like other biologic treatments for bipolar depression, BLT can precipitate manic/hypomanic and mixed states in susceptible patients, although the light dose can be titrated against emergent symptoms of hypomania.41
Bottom Line
Evidence suggests that bright light therapy is an effective, well tolerated, and affordable adjunct treatment for bipolar depression. Exposure to 5,000 to 7,000 lux around noon for 15 to 60 minutes will enhance the remission rate.
Related Resource
Mostert M, Dubovsky S. When bipolar treatment fails: what’s your next step? Current Psychiatry. 2008;7(1):39-46.
Drug Brand Name
Lithium • Eskalith, Lithobid
1. Pjrek E, Winkler D, Stastny J, et al. Bright light therapy in seasonal affective disorder--does it suffice? Eur Neuropsychopharmacol. 2004.14(4):347-351.
2. Al-Karawi D, Jubair L. Bright light therapy for nonseasonal depression: meta-analysis of clinical trials. J Affect Disord. 2016;198:64-71.
3. Sekiguchi H, Iritani S, Fujita K. Bright light therapy for sleep disturbance in dementia is most effective for mild to moderate Alzheimer’s type dementia: a case series. Psychogeriatrics, 2017;17(5):275-281.
4. Gelenberg AJ, Freeman MP, Markowitz JC, et al. Practice guideline for the treatment of patients with major depressive disorder, third edition. https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/mdd.pdf American Psychiatric Association. 2010. Accessed August, 10, 2017.
5. Kupka RW, Altshuler LL, Nolen WA, et al. Three times more days depressed than manic or hypomanic in both bipolar I and bipolar II disorder. Bipolar Disord. 2007;9(5):531-535.
6. Steinan MK, Krane-Gartiser K, Morken G, et al. Sleep problems in euthymic bipolar disorders: a review of clinical studies. Current Psychiatry Reviews. 2015;11:235-243.
7. Cudney LE, Frey BN, Streiner D, et al. Biological rhythms are independently associated with quality of life in bipolar disorder. Int J Bipolar Disord. 2016;4(1):9.
8. Duarte FA, Cardoso TA, Campos MT, et al. Biological rhythms in bipolar and depressive disorders: a community study with drug-naive young adults. J Affect Disord, 2015;186:145-148.
9. Pinho M, Sehmbi M, Cudney LE, et al. The association between biological rhythms, depression, and functioning in bipolar disorder: a large multi-center study. Acta Psychiatr Scand. 2015:133(2);102-108.
10. Ng TH, Chung KF, Lee CT, et al. Eveningness and its associated impairments in remitted bipolar disorder. Behav Sleep Med. 2016:14(6):650-664.
11. Wu YH, Ursinus J, Zahn JN, et al. Alterations of melatonin receptors MT1 and MT2 in the hypothalamic suprachiasmatic nucleus during depression. J Affect Disord, 2013:148(2-3):357-367.
12. Rybakowski JK, Dmitrzak-Weglar M, Kliwicki S, et al. Polymorphism of circadian clock genes and prophylactic lithium response. Bipolar Disord. 2014;16(2):151-158.
13. Schnell A, Sandrelli F, Ranc V, et al. Mice lacking circadian clock components display different mood-related behaviors and do not respond uniformly to chronic lithium treatment. Chronobiol Int. 2015;32(8):1075-1089.
14. Kim Y, Santos R, Gage FH, et al. Molecular mechanisms of bipolar disorder: progress made and future challenges. Front Cell Neurosci. 2017;11:30.
15. Hashimoto S, Kohsaka M, Nakamura K. Midday exposure to bright light changes the circadian organization of plasma melatonin rhythm in humans. Neurosci Lett. 1997;221(2-3):
89-92.
16. Rao ML, Müller-Oerlinghausen B, Mackert A, et al. The influence of phototherapy on serotonin and melatonin in non-seasonal depression. Pharmacopsychiatry.1990;23(3):155-158.
17. Moreira J, Geoffroy PA. Lithium and bipolar disorder: impacts from molecular to behavioural circadian rhythms. Chronobiol Int. 2016;33(4):351-373.
18. Oldham MA, Ciraulo DA. Bright light therapy for depression: a review of its effects on chronobiology and the autonomic nervous system. Chronobiol Int. 2014;31(3):305-319.
19. Berson DM, Dunn FA, Takao M. Phototransduction by retinal ganglion cells that set the circadian clock. Science. 2002;295(5557):1070-1073.
20. Peirson S, Foster RG. Melanopsin: another way of signaling light. Neuron. 2006;49(3):331-339.
21. Anderson JL, Glod CA, Dai J, et al. Lux vs. wavelength in light treatment of seasonal affective disorder. Acta Psychiatr Scand. 2009;120(3):203-212.
22. Wirz-Justice A, Graw P, Kräuchi K, et al. Effect of light on unmasked circadian rhythms in winter depression. In: Wetterberg L, ed. Light and biological rhythms in man. Oxford, United Kingdom:Pergamon Press;1993:385-393.
23. Cajochen C. Alerting effects of light. Sleep Med Rev. 2007;11(6):453-464.
24. Aries MBC. Human lighting demands: healthy lighting in an office environment. Eindhoven, Eindhoven University Press. 2005;158. doi:10.6100/IR594257.
25. Dauphinais DR, Rosenthal JZ, Terman M, et al. Controlled trial of safety and efficacy of bright light therapy vs. negative air ions in patients with bipolar depression. Psychiatry Res. 2012;196(1):57-61.
26. Camardese G, Leone B, Serrani R, et al. Augmentation of light therapy in difficult-to-treat depressed patients: an open-label trial in both unipolar and bipolar patients. Neuropsychiatr Dis Treat. 2015;11:2331-2338.
27. Papatheodorou G, Kutcher S. The effect of adjunctive light therapy on ameliorating breakthrough depressive symptoms in adolescent-onset bipolar disorder.
J Psychiatry Neurosci. 1995;20(3):226-232.
28. Benedetti F, Riccaboni R, Locatelli C, et al. Rapid treatment response of suicidal symptoms to lithium, sleep deprivation, and light therapy (chronotherapeutics) in drug-resistant bipolar depression. J Clin Psychiatry. 2014;75(2):133-140.
29. Liebenluft E, Turner EH, Felman-Naim S, et al. Light therapy in patients with rapid cycling bipolar disorder: preliminary results. Psychopharmacol Bull. 1995;31(4):
705-710.
30. Sit DK, Wisner KL, Hanusa BH, et al. Light therapy for bipolar disorder: a case series in women. Bipolar Disord. 2007;9(8):918-927.
31. Tseng PT, Chen YW, Tu KY, et al. Light therapy in the treatment of patients with bipolar depression: a meta-analytic study. Eur Neuropsychopharmacol. 2016;26(6):
1037-1047.
32. Yorguner KN, Bulut NS, Carkaxhiu BG, et al. Efficacy of bright light therapy in bipolar depression. Psychiatry Res. 2017;260:432-438.
33. Zhou TH, Dang WM, Ma YT, et al. Clinical efficacy, onset time and safety of bright light therapy in acute bipolar depression as an adjunctive therapy: a randomized controlled trial. J Affect Disord. 2018;227:90-96.
34. Sit DK, McGowan J, Wiltrout C, et al. Adjunctive bright light therapy for bipolar depression: a randomized double-blind placebo-controlled trial. Am J Psychiatry. 2018;175(2):
131-139.
35. Center for Environmental Therapeutics. https://www.cet.org/. Center for Environmental Therapeutics. Accessed November 15, 2017.
36. Lam RW, Levitt AJ. Canadian consensus guidelines for the treatment of seasonal affective disorder. https://mdsc.ca/documents/Consumer%20and%20Family%20Support/CCG_on_Seasonal_Affective_Disorder.pdf. 1999. Accessed August 2, 2017.
37. Terman M, Terman JS. Bright light therapy: side effects and benefits across the symptom spectrum. J Clin Psychiatry. 1999; 60(11):799-808;quiz 809.
38. Labbate LA, et al. Side effects induced by bright light treatment for seasonal affective disorder. J Clin Psychiatry. 1994; 55(5):189-191.
39. Gallin PF, et al. Ophthalmologic examination of patients with seasonal affective disorder, before and after bright light therapy. Am J Ophthalmol. 1995;119(2):202-210.
40. Chan PK, Lam RW, Perry KF. Mania precipitated by light therapy for patients with SAD. J Clin Psychiatry. 1994;55(10):454.
41. Kripke DF. Timing of phototherapy and occurrence of mania. Biol Psychiatry. 1991; 29(11):1156-1157.
Bright light therapy (BLT) refers to the use of bright light to treat symptoms of depression. BLT was initially prescribed as a treatment for patients with seasonal affective disorder.1 It was later found helpful for nonseasonal depression,2 premenstrual dysphoric disorder, postpartum depression, and phase shift circadian disorders, including for patients with dementia whose cognitive function improved after treatment with BLT.3 More recent studies suggest year-round benefit for nonseasonal depression.2 The American Psychiatric Association practice guidelines for the treatment of depression list BLT as an alternative and/or addition to pharmacologic and psychological treatment.4 BLT also may be beneficial for patients who are in the depressive phase of bipolar illness.
This article describes the evidence, rationale for use, mechanism of action, benefits, and safety profile of BLT for treating patients with bipolar depression.
Circadian rhythm disruption in bipolar disorder
Clinical manifestation. Patients with bipolar disorder (BD) spend more time in depression than in mania.5 Sleep disturbance is a core symptom of BD; patients typically have little need for sleep during a manic episode, and excess sleepiness during a depressive episode. Sleep complaints can be both precipitating factors and consequences of mood disorders. Patients with seasonal depression have excess sleepiness and weight gain in the winter followed by hypomanic-like symptoms in the spring, including decreased need for sleep and weight loss with psychomotor activation. In a recent review of sleep problems in patients with BD, Steinan et al6 reported that 20% of patients with euthymic mood in bipolar disorder experience a sleep disorder. Circadian disruption and “eveningness” (being more active during the evening) have been associated with mood episodes, functional impairment, poor quality of life, and treatment resistance.7-10
Pathophysiology. Existing hypotheses for the biological mechanism underlying dysregulation of circadian rhythm in BD include changes in melatonin levels, expression of melatonin receptors in the CNS, and daily cortisol profiles.11 Genetic evidence also links circadian rhythm dysregulation with BD. Two polymorphisms on the circadian locomotor output cycles kaput (CLOCK) gene that control circadian rhythm—aryl hydrocarbon receptor nuclear translocator-like (ARNTL) and timeless circadian clock (TIMELESS)—have been linked to lithium responsiveness in BD.12 In addition, Per2, Cry1, and Rev-Erbα expression—all components of the circadian clock—have been found to increase individual susceptibility to the therapeutic effects of lithium in mice.13 In addition, circadian rhythm dysregulation is associated with metabolic problems encountered by patients with BD, including weight gain, diabetes mellitus, and cardiovascular disease.14
Rationale for use
Regulation of a patient’s circadian rhythm disruption is a potential treatment for BD. Hashimoto et al15 demonstrated that midday bright light exposure can phase advance and increase the amplitude of nocturnal melatonin production in healthy individuals. Morning light therapy has been shown to increase blood serotonin throughout the day in both healthy individuals and in patients with nonseasonal depression; the effect was apparent with light intensities as low as 50 lux.16 Lithium may exert its therapeutic effect through its influence on the retino-hypothalamic-pineal tract and thus its effect on melatonin secretion.17
BLT is a logical choice to treat the depression phase of BD when exposure to sunlight is not feasible due to geographical location, season, or other factor. For patients who live in areas that receive frequent sunshine, an outside stroll for half an hour will likely achieve similar benefit to BLT.
The precise mechanism of action of BLT for bipolar depression has not yet been determined. It may be attributed to a phase-resetting effect via melanopsin and the suprachiasmatic nucleus (Box18-24).
Box
Bright light therapy: How it works
The mechanism of action of bright light therapy is yet to be elucidated. The suprachiasmatic nucleus (SCN) in the hypothalamus is the center of circadian rhythm regulation and receives direct input from the retina through the retinohypothalamic tract.18 Melanopsin, a short-wavelength, light-sensitive G-protein–coupled receptor located in human retinal ganglion cells, is known to transduce short-wavelength light signals into neural signals.19 Since melanopsin is primarily responsible for resetting the timing of the SCN, suppressing pineal gland melatonin secretion and improving alertness and electroencephalogram-derived correlates of arousal,20 short-wavelength light with a low light intensity might be a better stimulator for melanopsin-containing retinal ganglion cells and the behaviors mediated via this photoreceptor system.21,22 Whether the antidepressant effect of light is also related to its alerting property is unclear.23 However, the acute alerting and performance-enhancing effects of light are increasingly taken into account for the design of indoor light standards in office environments.24 Response to light therapy is thus attributed to its phase-resetting effect.
Continue to: BLT for BD...
BLT for BD: What’s the evidence?
Several studies and case reports have evaluated the use of BLT for bipolar depression. The number of participants in these studies is small, and there is no uniformity of methodology or patient selection.
Dauphinais et al (2012)25 randomly assigned 44 patients with bipolar depression to BLT or a high-density or low-density negative ion generator for 8 weeks. They reported no difference in outcome between the various groups (50% vs 55.6%, remission and response rate). Only one patient in each group showed a switch to hypomania.
Carmadese et al (2015)26 reported an open-label study of adjunctive BLT in 31 difficult-to-treat patients with depression (16 unipolar and 15 bipolar). Significant improvement was noted within 3 weeks and was sustained in 1 patient with bipolar depression 5 weeks after cessation of BLT.
Papatheodorou and Kutcher (1995)27 treated 7 adolescents with bipolar depression with adjunctive BLT (10,000 lux twice per day). Three patients showed a marked response (>70% decrease from baseline Beck Depression Inventory and Symptom Check List scores). Two patients had a moderate response (40% to 47% decrease) and 2 patients obtained mild to no response. There were no reported adverse effects.
Benedetti et al (2014)28 studied 141 patients with treatment-resistant bipolar depression. Approximately one-quarter (23%) had a history of attempted suicide, and 83% had a history of drug resistance. The authors found a combination of total sleep deprivation, BLT, and lithium rapidly decreased suicidality and improved patients’ depressive symptoms.
Liebenluft et al (1995)29 administered 13 trials of BLT to 9 patients with rapid-cycling BD during a 3-month period. Five patients received the treatment in the morning, 5 around midday, and 3 in the evening. Patients who received BLT at midday had the best outcome, while 3 of the 5 patients who received morning BLT developed unstable mood. The authors recommended titrating the duration of light exposure so that patients could skip a treatment if their mood was trending toward hypomania.
Sit et al (2007)30 evaluated BLT in a case series of 9 women with bipolar I or II disorder in the depression phase. Patients were exposed to 50 lux of red light for 2 weeks, and then they received 7,000 lux BLT for 15, 30, and 45 minutes daily for 2 weeks (4 patients received morning light and 5 received midday light). Mood was assessed using the Structured Interview Guide for the Hamilton Depression Rating Scale with Atypical Depression Supplement and the Mania Rating Scale. Of the 4 patients receiving morning BLT, one patient had a full response and the other 3 developed hypomania. Of the 5 patients who received midday BLT, 2 achieved full response, 2 showed early improvement but required a dose increase, and one remained depressed but had a full response when she was switched to morning BLT.
Tseng et al (2016)31 reported a meta-analysis of BLT for bipolar depression that included a total of 567 patients from 11 studies. They reported significant improvement with BLT alone or in combination with antidepressants or total sleep deprivation. They also reported significant improvement with BLT in 130 patients who were not receiving other treatments. There was no difference in the frequency of mood shifts between patients on BLT alone or in combination with other modalities. The authors reported no mood shift in any of the patients receiving concurrent mood stabilizers. They also reported no difference with the color of light, gender, or duration of illness.
Yorguner et al (2017)32 conducted a 2-week randomized, single-blind study of BLT as an add-on treatment for 32 patients with bipolar depression. Patients were randomly assigned to BLT or dim light, which they were administered each morning for 30 mins for 2 weeks. Sixteen patients who received BLT showed a significantly greater reduction in Hamilton Depression Rating Scale scores (mean score of 24 at baseline down to 12) compared with 16 patients who received dim light (mean score of 24 at baseline down to 18). The authors also reported remission in 4 out of 4 patients who had seasonal depression, compared with 3 out of 12 who did not have seasonal depression (the other 9 showed response but not remission).
Zhou et al (2018)33 conducted a multi-center, randomized, single-blind clinical trial of 63 patients with bipolar depression. Thirty-three patients received morning BLT, and 30 received dim red light therapy (control group). The authors reported a significantly higher response rate in the BLT group (78%) compared with the control group (43%).
Sit et al (2018)34 conducted a 6-week randomized, double-blind, placebo-controlled trial of BLT vs dim red light in patients with bipolar I or II depression. Twenty-three patients were administered 7,000 lux bright white light, and 23 patients received 50 lux dim red light, at midday 5 days a week. The light dose was increased by 15 minutes every week up to 60 minutes by Week 4, unless the patient achieved remission. Patients were maintained on their usual medications, which included mood stabilizers and/or antidepressants. At Week 6, the group randomized to BLT had a significantly higher remission rate (68%) compared with patients who received dim red light (22%). Improvement was noted by Week 4. Patients receiving BLT also had significantly fewer depressive symptoms, and no mood polarity switch was noted.
Prescribing bright light therapy
Light box selection criteria. When selecting a light box or related BLT treatment apparatus, the Center for Environmental Therapeutics recommends consideration of the following factors35:
- clinical efficacy
- ocular and dermatologic safety
- visual comfort.
Selecting a dose. The dose received is determined by the intensity emitted from the light source, distance from the light box, and duration of exposure.36 Begin with midday light therapy between 12 noon and 2
Monitor for adverse effects. Generally, BLT is well tolerated.37 Adverse effects are rare; the most common ones include headache, eyestrain, nausea, and agitation.38 One study found no adverse ocular effects from light therapy after 5 years of treatment.39 Adverse effects tend to remit spontaneously or after dose reduction.35 Evening administration of BLT may increase the incidence of sleep disturbances.40 Like other biologic treatments for bipolar depression, BLT can precipitate manic/hypomanic and mixed states in susceptible patients, although the light dose can be titrated against emergent symptoms of hypomania.41
Bottom Line
Evidence suggests that bright light therapy is an effective, well tolerated, and affordable adjunct treatment for bipolar depression. Exposure to 5,000 to 7,000 lux around noon for 15 to 60 minutes will enhance the remission rate.
Related Resource
Mostert M, Dubovsky S. When bipolar treatment fails: what’s your next step? Current Psychiatry. 2008;7(1):39-46.
Drug Brand Name
Lithium • Eskalith, Lithobid
Bright light therapy (BLT) refers to the use of bright light to treat symptoms of depression. BLT was initially prescribed as a treatment for patients with seasonal affective disorder.1 It was later found helpful for nonseasonal depression,2 premenstrual dysphoric disorder, postpartum depression, and phase shift circadian disorders, including for patients with dementia whose cognitive function improved after treatment with BLT.3 More recent studies suggest year-round benefit for nonseasonal depression.2 The American Psychiatric Association practice guidelines for the treatment of depression list BLT as an alternative and/or addition to pharmacologic and psychological treatment.4 BLT also may be beneficial for patients who are in the depressive phase of bipolar illness.
This article describes the evidence, rationale for use, mechanism of action, benefits, and safety profile of BLT for treating patients with bipolar depression.
Circadian rhythm disruption in bipolar disorder
Clinical manifestation. Patients with bipolar disorder (BD) spend more time in depression than in mania.5 Sleep disturbance is a core symptom of BD; patients typically have little need for sleep during a manic episode, and excess sleepiness during a depressive episode. Sleep complaints can be both precipitating factors and consequences of mood disorders. Patients with seasonal depression have excess sleepiness and weight gain in the winter followed by hypomanic-like symptoms in the spring, including decreased need for sleep and weight loss with psychomotor activation. In a recent review of sleep problems in patients with BD, Steinan et al6 reported that 20% of patients with euthymic mood in bipolar disorder experience a sleep disorder. Circadian disruption and “eveningness” (being more active during the evening) have been associated with mood episodes, functional impairment, poor quality of life, and treatment resistance.7-10
Pathophysiology. Existing hypotheses for the biological mechanism underlying dysregulation of circadian rhythm in BD include changes in melatonin levels, expression of melatonin receptors in the CNS, and daily cortisol profiles.11 Genetic evidence also links circadian rhythm dysregulation with BD. Two polymorphisms on the circadian locomotor output cycles kaput (CLOCK) gene that control circadian rhythm—aryl hydrocarbon receptor nuclear translocator-like (ARNTL) and timeless circadian clock (TIMELESS)—have been linked to lithium responsiveness in BD.12 In addition, Per2, Cry1, and Rev-Erbα expression—all components of the circadian clock—have been found to increase individual susceptibility to the therapeutic effects of lithium in mice.13 In addition, circadian rhythm dysregulation is associated with metabolic problems encountered by patients with BD, including weight gain, diabetes mellitus, and cardiovascular disease.14
Rationale for use
Regulation of a patient’s circadian rhythm disruption is a potential treatment for BD. Hashimoto et al15 demonstrated that midday bright light exposure can phase advance and increase the amplitude of nocturnal melatonin production in healthy individuals. Morning light therapy has been shown to increase blood serotonin throughout the day in both healthy individuals and in patients with nonseasonal depression; the effect was apparent with light intensities as low as 50 lux.16 Lithium may exert its therapeutic effect through its influence on the retino-hypothalamic-pineal tract and thus its effect on melatonin secretion.17
BLT is a logical choice to treat the depression phase of BD when exposure to sunlight is not feasible due to geographical location, season, or other factor. For patients who live in areas that receive frequent sunshine, an outside stroll for half an hour will likely achieve similar benefit to BLT.
The precise mechanism of action of BLT for bipolar depression has not yet been determined. It may be attributed to a phase-resetting effect via melanopsin and the suprachiasmatic nucleus (Box18-24).
Box
Bright light therapy: How it works
The mechanism of action of bright light therapy is yet to be elucidated. The suprachiasmatic nucleus (SCN) in the hypothalamus is the center of circadian rhythm regulation and receives direct input from the retina through the retinohypothalamic tract.18 Melanopsin, a short-wavelength, light-sensitive G-protein–coupled receptor located in human retinal ganglion cells, is known to transduce short-wavelength light signals into neural signals.19 Since melanopsin is primarily responsible for resetting the timing of the SCN, suppressing pineal gland melatonin secretion and improving alertness and electroencephalogram-derived correlates of arousal,20 short-wavelength light with a low light intensity might be a better stimulator for melanopsin-containing retinal ganglion cells and the behaviors mediated via this photoreceptor system.21,22 Whether the antidepressant effect of light is also related to its alerting property is unclear.23 However, the acute alerting and performance-enhancing effects of light are increasingly taken into account for the design of indoor light standards in office environments.24 Response to light therapy is thus attributed to its phase-resetting effect.
Continue to: BLT for BD...
BLT for BD: What’s the evidence?
Several studies and case reports have evaluated the use of BLT for bipolar depression. The number of participants in these studies is small, and there is no uniformity of methodology or patient selection.
Dauphinais et al (2012)25 randomly assigned 44 patients with bipolar depression to BLT or a high-density or low-density negative ion generator for 8 weeks. They reported no difference in outcome between the various groups (50% vs 55.6%, remission and response rate). Only one patient in each group showed a switch to hypomania.
Carmadese et al (2015)26 reported an open-label study of adjunctive BLT in 31 difficult-to-treat patients with depression (16 unipolar and 15 bipolar). Significant improvement was noted within 3 weeks and was sustained in 1 patient with bipolar depression 5 weeks after cessation of BLT.
Papatheodorou and Kutcher (1995)27 treated 7 adolescents with bipolar depression with adjunctive BLT (10,000 lux twice per day). Three patients showed a marked response (>70% decrease from baseline Beck Depression Inventory and Symptom Check List scores). Two patients had a moderate response (40% to 47% decrease) and 2 patients obtained mild to no response. There were no reported adverse effects.
Benedetti et al (2014)28 studied 141 patients with treatment-resistant bipolar depression. Approximately one-quarter (23%) had a history of attempted suicide, and 83% had a history of drug resistance. The authors found a combination of total sleep deprivation, BLT, and lithium rapidly decreased suicidality and improved patients’ depressive symptoms.
Liebenluft et al (1995)29 administered 13 trials of BLT to 9 patients with rapid-cycling BD during a 3-month period. Five patients received the treatment in the morning, 5 around midday, and 3 in the evening. Patients who received BLT at midday had the best outcome, while 3 of the 5 patients who received morning BLT developed unstable mood. The authors recommended titrating the duration of light exposure so that patients could skip a treatment if their mood was trending toward hypomania.
Sit et al (2007)30 evaluated BLT in a case series of 9 women with bipolar I or II disorder in the depression phase. Patients were exposed to 50 lux of red light for 2 weeks, and then they received 7,000 lux BLT for 15, 30, and 45 minutes daily for 2 weeks (4 patients received morning light and 5 received midday light). Mood was assessed using the Structured Interview Guide for the Hamilton Depression Rating Scale with Atypical Depression Supplement and the Mania Rating Scale. Of the 4 patients receiving morning BLT, one patient had a full response and the other 3 developed hypomania. Of the 5 patients who received midday BLT, 2 achieved full response, 2 showed early improvement but required a dose increase, and one remained depressed but had a full response when she was switched to morning BLT.
Tseng et al (2016)31 reported a meta-analysis of BLT for bipolar depression that included a total of 567 patients from 11 studies. They reported significant improvement with BLT alone or in combination with antidepressants or total sleep deprivation. They also reported significant improvement with BLT in 130 patients who were not receiving other treatments. There was no difference in the frequency of mood shifts between patients on BLT alone or in combination with other modalities. The authors reported no mood shift in any of the patients receiving concurrent mood stabilizers. They also reported no difference with the color of light, gender, or duration of illness.
Yorguner et al (2017)32 conducted a 2-week randomized, single-blind study of BLT as an add-on treatment for 32 patients with bipolar depression. Patients were randomly assigned to BLT or dim light, which they were administered each morning for 30 mins for 2 weeks. Sixteen patients who received BLT showed a significantly greater reduction in Hamilton Depression Rating Scale scores (mean score of 24 at baseline down to 12) compared with 16 patients who received dim light (mean score of 24 at baseline down to 18). The authors also reported remission in 4 out of 4 patients who had seasonal depression, compared with 3 out of 12 who did not have seasonal depression (the other 9 showed response but not remission).
Zhou et al (2018)33 conducted a multi-center, randomized, single-blind clinical trial of 63 patients with bipolar depression. Thirty-three patients received morning BLT, and 30 received dim red light therapy (control group). The authors reported a significantly higher response rate in the BLT group (78%) compared with the control group (43%).
Sit et al (2018)34 conducted a 6-week randomized, double-blind, placebo-controlled trial of BLT vs dim red light in patients with bipolar I or II depression. Twenty-three patients were administered 7,000 lux bright white light, and 23 patients received 50 lux dim red light, at midday 5 days a week. The light dose was increased by 15 minutes every week up to 60 minutes by Week 4, unless the patient achieved remission. Patients were maintained on their usual medications, which included mood stabilizers and/or antidepressants. At Week 6, the group randomized to BLT had a significantly higher remission rate (68%) compared with patients who received dim red light (22%). Improvement was noted by Week 4. Patients receiving BLT also had significantly fewer depressive symptoms, and no mood polarity switch was noted.
Prescribing bright light therapy
Light box selection criteria. When selecting a light box or related BLT treatment apparatus, the Center for Environmental Therapeutics recommends consideration of the following factors35:
- clinical efficacy
- ocular and dermatologic safety
- visual comfort.
Selecting a dose. The dose received is determined by the intensity emitted from the light source, distance from the light box, and duration of exposure.36 Begin with midday light therapy between 12 noon and 2
Monitor for adverse effects. Generally, BLT is well tolerated.37 Adverse effects are rare; the most common ones include headache, eyestrain, nausea, and agitation.38 One study found no adverse ocular effects from light therapy after 5 years of treatment.39 Adverse effects tend to remit spontaneously or after dose reduction.35 Evening administration of BLT may increase the incidence of sleep disturbances.40 Like other biologic treatments for bipolar depression, BLT can precipitate manic/hypomanic and mixed states in susceptible patients, although the light dose can be titrated against emergent symptoms of hypomania.41
Bottom Line
Evidence suggests that bright light therapy is an effective, well tolerated, and affordable adjunct treatment for bipolar depression. Exposure to 5,000 to 7,000 lux around noon for 15 to 60 minutes will enhance the remission rate.
Related Resource
Mostert M, Dubovsky S. When bipolar treatment fails: what’s your next step? Current Psychiatry. 2008;7(1):39-46.
Drug Brand Name
Lithium • Eskalith, Lithobid
1. Pjrek E, Winkler D, Stastny J, et al. Bright light therapy in seasonal affective disorder--does it suffice? Eur Neuropsychopharmacol. 2004.14(4):347-351.
2. Al-Karawi D, Jubair L. Bright light therapy for nonseasonal depression: meta-analysis of clinical trials. J Affect Disord. 2016;198:64-71.
3. Sekiguchi H, Iritani S, Fujita K. Bright light therapy for sleep disturbance in dementia is most effective for mild to moderate Alzheimer’s type dementia: a case series. Psychogeriatrics, 2017;17(5):275-281.
4. Gelenberg AJ, Freeman MP, Markowitz JC, et al. Practice guideline for the treatment of patients with major depressive disorder, third edition. https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/mdd.pdf American Psychiatric Association. 2010. Accessed August, 10, 2017.
5. Kupka RW, Altshuler LL, Nolen WA, et al. Three times more days depressed than manic or hypomanic in both bipolar I and bipolar II disorder. Bipolar Disord. 2007;9(5):531-535.
6. Steinan MK, Krane-Gartiser K, Morken G, et al. Sleep problems in euthymic bipolar disorders: a review of clinical studies. Current Psychiatry Reviews. 2015;11:235-243.
7. Cudney LE, Frey BN, Streiner D, et al. Biological rhythms are independently associated with quality of life in bipolar disorder. Int J Bipolar Disord. 2016;4(1):9.
8. Duarte FA, Cardoso TA, Campos MT, et al. Biological rhythms in bipolar and depressive disorders: a community study with drug-naive young adults. J Affect Disord, 2015;186:145-148.
9. Pinho M, Sehmbi M, Cudney LE, et al. The association between biological rhythms, depression, and functioning in bipolar disorder: a large multi-center study. Acta Psychiatr Scand. 2015:133(2);102-108.
10. Ng TH, Chung KF, Lee CT, et al. Eveningness and its associated impairments in remitted bipolar disorder. Behav Sleep Med. 2016:14(6):650-664.
11. Wu YH, Ursinus J, Zahn JN, et al. Alterations of melatonin receptors MT1 and MT2 in the hypothalamic suprachiasmatic nucleus during depression. J Affect Disord, 2013:148(2-3):357-367.
12. Rybakowski JK, Dmitrzak-Weglar M, Kliwicki S, et al. Polymorphism of circadian clock genes and prophylactic lithium response. Bipolar Disord. 2014;16(2):151-158.
13. Schnell A, Sandrelli F, Ranc V, et al. Mice lacking circadian clock components display different mood-related behaviors and do not respond uniformly to chronic lithium treatment. Chronobiol Int. 2015;32(8):1075-1089.
14. Kim Y, Santos R, Gage FH, et al. Molecular mechanisms of bipolar disorder: progress made and future challenges. Front Cell Neurosci. 2017;11:30.
15. Hashimoto S, Kohsaka M, Nakamura K. Midday exposure to bright light changes the circadian organization of plasma melatonin rhythm in humans. Neurosci Lett. 1997;221(2-3):
89-92.
16. Rao ML, Müller-Oerlinghausen B, Mackert A, et al. The influence of phototherapy on serotonin and melatonin in non-seasonal depression. Pharmacopsychiatry.1990;23(3):155-158.
17. Moreira J, Geoffroy PA. Lithium and bipolar disorder: impacts from molecular to behavioural circadian rhythms. Chronobiol Int. 2016;33(4):351-373.
18. Oldham MA, Ciraulo DA. Bright light therapy for depression: a review of its effects on chronobiology and the autonomic nervous system. Chronobiol Int. 2014;31(3):305-319.
19. Berson DM, Dunn FA, Takao M. Phototransduction by retinal ganglion cells that set the circadian clock. Science. 2002;295(5557):1070-1073.
20. Peirson S, Foster RG. Melanopsin: another way of signaling light. Neuron. 2006;49(3):331-339.
21. Anderson JL, Glod CA, Dai J, et al. Lux vs. wavelength in light treatment of seasonal affective disorder. Acta Psychiatr Scand. 2009;120(3):203-212.
22. Wirz-Justice A, Graw P, Kräuchi K, et al. Effect of light on unmasked circadian rhythms in winter depression. In: Wetterberg L, ed. Light and biological rhythms in man. Oxford, United Kingdom:Pergamon Press;1993:385-393.
23. Cajochen C. Alerting effects of light. Sleep Med Rev. 2007;11(6):453-464.
24. Aries MBC. Human lighting demands: healthy lighting in an office environment. Eindhoven, Eindhoven University Press. 2005;158. doi:10.6100/IR594257.
25. Dauphinais DR, Rosenthal JZ, Terman M, et al. Controlled trial of safety and efficacy of bright light therapy vs. negative air ions in patients with bipolar depression. Psychiatry Res. 2012;196(1):57-61.
26. Camardese G, Leone B, Serrani R, et al. Augmentation of light therapy in difficult-to-treat depressed patients: an open-label trial in both unipolar and bipolar patients. Neuropsychiatr Dis Treat. 2015;11:2331-2338.
27. Papatheodorou G, Kutcher S. The effect of adjunctive light therapy on ameliorating breakthrough depressive symptoms in adolescent-onset bipolar disorder.
J Psychiatry Neurosci. 1995;20(3):226-232.
28. Benedetti F, Riccaboni R, Locatelli C, et al. Rapid treatment response of suicidal symptoms to lithium, sleep deprivation, and light therapy (chronotherapeutics) in drug-resistant bipolar depression. J Clin Psychiatry. 2014;75(2):133-140.
29. Liebenluft E, Turner EH, Felman-Naim S, et al. Light therapy in patients with rapid cycling bipolar disorder: preliminary results. Psychopharmacol Bull. 1995;31(4):
705-710.
30. Sit DK, Wisner KL, Hanusa BH, et al. Light therapy for bipolar disorder: a case series in women. Bipolar Disord. 2007;9(8):918-927.
31. Tseng PT, Chen YW, Tu KY, et al. Light therapy in the treatment of patients with bipolar depression: a meta-analytic study. Eur Neuropsychopharmacol. 2016;26(6):
1037-1047.
32. Yorguner KN, Bulut NS, Carkaxhiu BG, et al. Efficacy of bright light therapy in bipolar depression. Psychiatry Res. 2017;260:432-438.
33. Zhou TH, Dang WM, Ma YT, et al. Clinical efficacy, onset time and safety of bright light therapy in acute bipolar depression as an adjunctive therapy: a randomized controlled trial. J Affect Disord. 2018;227:90-96.
34. Sit DK, McGowan J, Wiltrout C, et al. Adjunctive bright light therapy for bipolar depression: a randomized double-blind placebo-controlled trial. Am J Psychiatry. 2018;175(2):
131-139.
35. Center for Environmental Therapeutics. https://www.cet.org/. Center for Environmental Therapeutics. Accessed November 15, 2017.
36. Lam RW, Levitt AJ. Canadian consensus guidelines for the treatment of seasonal affective disorder. https://mdsc.ca/documents/Consumer%20and%20Family%20Support/CCG_on_Seasonal_Affective_Disorder.pdf. 1999. Accessed August 2, 2017.
37. Terman M, Terman JS. Bright light therapy: side effects and benefits across the symptom spectrum. J Clin Psychiatry. 1999; 60(11):799-808;quiz 809.
38. Labbate LA, et al. Side effects induced by bright light treatment for seasonal affective disorder. J Clin Psychiatry. 1994; 55(5):189-191.
39. Gallin PF, et al. Ophthalmologic examination of patients with seasonal affective disorder, before and after bright light therapy. Am J Ophthalmol. 1995;119(2):202-210.
40. Chan PK, Lam RW, Perry KF. Mania precipitated by light therapy for patients with SAD. J Clin Psychiatry. 1994;55(10):454.
41. Kripke DF. Timing of phototherapy and occurrence of mania. Biol Psychiatry. 1991; 29(11):1156-1157.
1. Pjrek E, Winkler D, Stastny J, et al. Bright light therapy in seasonal affective disorder--does it suffice? Eur Neuropsychopharmacol. 2004.14(4):347-351.
2. Al-Karawi D, Jubair L. Bright light therapy for nonseasonal depression: meta-analysis of clinical trials. J Affect Disord. 2016;198:64-71.
3. Sekiguchi H, Iritani S, Fujita K. Bright light therapy for sleep disturbance in dementia is most effective for mild to moderate Alzheimer’s type dementia: a case series. Psychogeriatrics, 2017;17(5):275-281.
4. Gelenberg AJ, Freeman MP, Markowitz JC, et al. Practice guideline for the treatment of patients with major depressive disorder, third edition. https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/mdd.pdf American Psychiatric Association. 2010. Accessed August, 10, 2017.
5. Kupka RW, Altshuler LL, Nolen WA, et al. Three times more days depressed than manic or hypomanic in both bipolar I and bipolar II disorder. Bipolar Disord. 2007;9(5):531-535.
6. Steinan MK, Krane-Gartiser K, Morken G, et al. Sleep problems in euthymic bipolar disorders: a review of clinical studies. Current Psychiatry Reviews. 2015;11:235-243.
7. Cudney LE, Frey BN, Streiner D, et al. Biological rhythms are independently associated with quality of life in bipolar disorder. Int J Bipolar Disord. 2016;4(1):9.
8. Duarte FA, Cardoso TA, Campos MT, et al. Biological rhythms in bipolar and depressive disorders: a community study with drug-naive young adults. J Affect Disord, 2015;186:145-148.
9. Pinho M, Sehmbi M, Cudney LE, et al. The association between biological rhythms, depression, and functioning in bipolar disorder: a large multi-center study. Acta Psychiatr Scand. 2015:133(2);102-108.
10. Ng TH, Chung KF, Lee CT, et al. Eveningness and its associated impairments in remitted bipolar disorder. Behav Sleep Med. 2016:14(6):650-664.
11. Wu YH, Ursinus J, Zahn JN, et al. Alterations of melatonin receptors MT1 and MT2 in the hypothalamic suprachiasmatic nucleus during depression. J Affect Disord, 2013:148(2-3):357-367.
12. Rybakowski JK, Dmitrzak-Weglar M, Kliwicki S, et al. Polymorphism of circadian clock genes and prophylactic lithium response. Bipolar Disord. 2014;16(2):151-158.
13. Schnell A, Sandrelli F, Ranc V, et al. Mice lacking circadian clock components display different mood-related behaviors and do not respond uniformly to chronic lithium treatment. Chronobiol Int. 2015;32(8):1075-1089.
14. Kim Y, Santos R, Gage FH, et al. Molecular mechanisms of bipolar disorder: progress made and future challenges. Front Cell Neurosci. 2017;11:30.
15. Hashimoto S, Kohsaka M, Nakamura K. Midday exposure to bright light changes the circadian organization of plasma melatonin rhythm in humans. Neurosci Lett. 1997;221(2-3):
89-92.
16. Rao ML, Müller-Oerlinghausen B, Mackert A, et al. The influence of phototherapy on serotonin and melatonin in non-seasonal depression. Pharmacopsychiatry.1990;23(3):155-158.
17. Moreira J, Geoffroy PA. Lithium and bipolar disorder: impacts from molecular to behavioural circadian rhythms. Chronobiol Int. 2016;33(4):351-373.
18. Oldham MA, Ciraulo DA. Bright light therapy for depression: a review of its effects on chronobiology and the autonomic nervous system. Chronobiol Int. 2014;31(3):305-319.
19. Berson DM, Dunn FA, Takao M. Phototransduction by retinal ganglion cells that set the circadian clock. Science. 2002;295(5557):1070-1073.
20. Peirson S, Foster RG. Melanopsin: another way of signaling light. Neuron. 2006;49(3):331-339.
21. Anderson JL, Glod CA, Dai J, et al. Lux vs. wavelength in light treatment of seasonal affective disorder. Acta Psychiatr Scand. 2009;120(3):203-212.
22. Wirz-Justice A, Graw P, Kräuchi K, et al. Effect of light on unmasked circadian rhythms in winter depression. In: Wetterberg L, ed. Light and biological rhythms in man. Oxford, United Kingdom:Pergamon Press;1993:385-393.
23. Cajochen C. Alerting effects of light. Sleep Med Rev. 2007;11(6):453-464.
24. Aries MBC. Human lighting demands: healthy lighting in an office environment. Eindhoven, Eindhoven University Press. 2005;158. doi:10.6100/IR594257.
25. Dauphinais DR, Rosenthal JZ, Terman M, et al. Controlled trial of safety and efficacy of bright light therapy vs. negative air ions in patients with bipolar depression. Psychiatry Res. 2012;196(1):57-61.
26. Camardese G, Leone B, Serrani R, et al. Augmentation of light therapy in difficult-to-treat depressed patients: an open-label trial in both unipolar and bipolar patients. Neuropsychiatr Dis Treat. 2015;11:2331-2338.
27. Papatheodorou G, Kutcher S. The effect of adjunctive light therapy on ameliorating breakthrough depressive symptoms in adolescent-onset bipolar disorder.
J Psychiatry Neurosci. 1995;20(3):226-232.
28. Benedetti F, Riccaboni R, Locatelli C, et al. Rapid treatment response of suicidal symptoms to lithium, sleep deprivation, and light therapy (chronotherapeutics) in drug-resistant bipolar depression. J Clin Psychiatry. 2014;75(2):133-140.
29. Liebenluft E, Turner EH, Felman-Naim S, et al. Light therapy in patients with rapid cycling bipolar disorder: preliminary results. Psychopharmacol Bull. 1995;31(4):
705-710.
30. Sit DK, Wisner KL, Hanusa BH, et al. Light therapy for bipolar disorder: a case series in women. Bipolar Disord. 2007;9(8):918-927.
31. Tseng PT, Chen YW, Tu KY, et al. Light therapy in the treatment of patients with bipolar depression: a meta-analytic study. Eur Neuropsychopharmacol. 2016;26(6):
1037-1047.
32. Yorguner KN, Bulut NS, Carkaxhiu BG, et al. Efficacy of bright light therapy in bipolar depression. Psychiatry Res. 2017;260:432-438.
33. Zhou TH, Dang WM, Ma YT, et al. Clinical efficacy, onset time and safety of bright light therapy in acute bipolar depression as an adjunctive therapy: a randomized controlled trial. J Affect Disord. 2018;227:90-96.
34. Sit DK, McGowan J, Wiltrout C, et al. Adjunctive bright light therapy for bipolar depression: a randomized double-blind placebo-controlled trial. Am J Psychiatry. 2018;175(2):
131-139.
35. Center for Environmental Therapeutics. https://www.cet.org/. Center for Environmental Therapeutics. Accessed November 15, 2017.
36. Lam RW, Levitt AJ. Canadian consensus guidelines for the treatment of seasonal affective disorder. https://mdsc.ca/documents/Consumer%20and%20Family%20Support/CCG_on_Seasonal_Affective_Disorder.pdf. 1999. Accessed August 2, 2017.
37. Terman M, Terman JS. Bright light therapy: side effects and benefits across the symptom spectrum. J Clin Psychiatry. 1999; 60(11):799-808;quiz 809.
38. Labbate LA, et al. Side effects induced by bright light treatment for seasonal affective disorder. J Clin Psychiatry. 1994; 55(5):189-191.
39. Gallin PF, et al. Ophthalmologic examination of patients with seasonal affective disorder, before and after bright light therapy. Am J Ophthalmol. 1995;119(2):202-210.
40. Chan PK, Lam RW, Perry KF. Mania precipitated by light therapy for patients with SAD. J Clin Psychiatry. 1994;55(10):454.
41. Kripke DF. Timing of phototherapy and occurrence of mania. Biol Psychiatry. 1991; 29(11):1156-1157.