Cleveland Clinic Journal of Medicine

A 39-year-old woman presented to the emergency department with a 2-day history of exertional dyspnea, left-sided chest pain with pleuritic characteristics, and cough without fever or chills. She had a history of severe postprandial nausea and vomiting, weight loss, and malnutrition, which had necessitated placement of a peripherally inserted central catheter in her right arm for total parenteral nutrition.

On physical examination, the patient was afebrile but tachycardic and tachypneic. Her oxygen saturation on room air by pulse oximetry was 91%, though she was not in significant distress. Breath sounds were equal bilaterally and clear, with symmetrical chest wall expansion.

Her white blood cell count was 18.5 × 10⁹/L (reference range 3.5–10.5), with 19.3% eosinophils (reference range 1%–7%); her D-dimer level was also elevated.

Conditions to consider in a patient with these imaging findings in the setting of leukocytosis and eosinophilia include mycobacterial infection, hypersensitivity reaction, diffuse fungal infiltrates, and possibly metastatic disease such as thyroid carcinoma or melanoma. The patient reported having had a purified protein derivative test that was positive for tuberculosis, but she denied having had active disease.

She underwent bronchosocopy. Bronchoalveolar lavage specimen study showed an elevated eosinophil count of 17%. Acid-fast staining detected no organisms. Transbronchial biopsy study revealed foreign-body granulomas from microcrystalline cellulose microemboli deposited in the microvasculature of the patient’s lungs. Upon further questioning the patient admitted she had crushed oral tablets of prescribed opioids and injected them intravenously.

A COMPLICATION OF INJECTING ORAL TABLETS

Oral tablets typically contain talc, cellulose, cornstarch, or combinations of these substances as binding agents. When pulverized, the powder can be combined with water to form an injectable solution with higher and more rapid bioavailability.^1,2 The binders, however, are insoluble and accumulate in various tissues.

Intravenous injection of microcellulose has been shown to produce pulmonary and peripheral eosinophilia in birds. In humans, the immune response in foreign body granulomatosis can vary, and case reports have not mentioned eosinophils in the lungs or serum.^3,4

Deposition of these particles in pulmonary vessels is common and can trigger a potentially fatal reaction, presenting as acute onset of cough, chest pain, dyspnea, fever, and pulmonary hypertension. The severity of these clinical findings is relative to the degree of pulmonary hypertension created by the arteriolar involvement of these emboli.^2,5

Our patient’s exertional dyspnea and hypoxemia resolved during 1 week of hospitalization with conservative management and supplemental oxygen. She was referred to our pain rehabilitation clinic, where she was successfully weaned from narcotics. Her pulmonary findings on computed tomography were still present 3 years after her initial images, though less prominent.

A 39-year-old woman presented to the emergency department with a 2-day history of exertional dyspnea, left-sided chest pain with pleuritic characteristics, and cough without fever or chills. She had a history of severe postprandial nausea and vomiting, weight loss, and malnutrition, which had necessitated placement of a peripherally inserted central catheter in her right arm for total parenteral nutrition.

On physical examination, the patient was afebrile but tachycardic and tachypneic. Her oxygen saturation on room air by pulse oximetry was 91%, though she was not in significant distress. Breath sounds were equal bilaterally and clear, with symmetrical chest wall expansion.

Her white blood cell count was 18.5 × 10⁹/L (reference range 3.5–10.5), with 19.3% eosinophils (reference range 1%–7%); her D-dimer level was also elevated.

Conditions to consider in a patient with these imaging findings in the setting of leukocytosis and eosinophilia include mycobacterial infection, hypersensitivity reaction, diffuse fungal infiltrates, and possibly metastatic disease such as thyroid carcinoma or melanoma. The patient reported having had a purified protein derivative test that was positive for tuberculosis, but she denied having had active disease.

She underwent bronchosocopy. Bronchoalveolar lavage specimen study showed an elevated eosinophil count of 17%. Acid-fast staining detected no organisms. Transbronchial biopsy study revealed foreign-body granulomas from microcrystalline cellulose microemboli deposited in the microvasculature of the patient’s lungs. Upon further questioning the patient admitted she had crushed oral tablets of prescribed opioids and injected them intravenously.

A COMPLICATION OF INJECTING ORAL TABLETS

Oral tablets typically contain talc, cellulose, cornstarch, or combinations of these substances as binding agents. When pulverized, the powder can be combined with water to form an injectable solution with higher and more rapid bioavailability.^1,2 The binders, however, are insoluble and accumulate in various tissues.

Intravenous injection of microcellulose has been shown to produce pulmonary and peripheral eosinophilia in birds. In humans, the immune response in foreign body granulomatosis can vary, and case reports have not mentioned eosinophils in the lungs or serum.^3,4

Deposition of these particles in pulmonary vessels is common and can trigger a potentially fatal reaction, presenting as acute onset of cough, chest pain, dyspnea, fever, and pulmonary hypertension. The severity of these clinical findings is relative to the degree of pulmonary hypertension created by the arteriolar involvement of these emboli.^2,5

Our patient’s exertional dyspnea and hypoxemia resolved during 1 week of hospitalization with conservative management and supplemental oxygen. She was referred to our pain rehabilitation clinic, where she was successfully weaned from narcotics. Her pulmonary findings on computed tomography were still present 3 years after her initial images, though less prominent.

A 39-year-old woman presented to the emergency department with a 2-day history of exertional dyspnea, left-sided chest pain with pleuritic characteristics, and cough without fever or chills. She had a history of severe postprandial nausea and vomiting, weight loss, and malnutrition, which had necessitated placement of a peripherally inserted central catheter in her right arm for total parenteral nutrition.

On physical examination, the patient was afebrile but tachycardic and tachypneic. Her oxygen saturation on room air by pulse oximetry was 91%, though she was not in significant distress. Breath sounds were equal bilaterally and clear, with symmetrical chest wall expansion.

Her white blood cell count was 18.5 × 10⁹/L (reference range 3.5–10.5), with 19.3% eosinophils (reference range 1%–7%); her D-dimer level was also elevated.

Conditions to consider in a patient with these imaging findings in the setting of leukocytosis and eosinophilia include mycobacterial infection, hypersensitivity reaction, diffuse fungal infiltrates, and possibly metastatic disease such as thyroid carcinoma or melanoma. The patient reported having had a purified protein derivative test that was positive for tuberculosis, but she denied having had active disease.

She underwent bronchosocopy. Bronchoalveolar lavage specimen study showed an elevated eosinophil count of 17%. Acid-fast staining detected no organisms. Transbronchial biopsy study revealed foreign-body granulomas from microcrystalline cellulose microemboli deposited in the microvasculature of the patient’s lungs. Upon further questioning the patient admitted she had crushed oral tablets of prescribed opioids and injected them intravenously.

A COMPLICATION OF INJECTING ORAL TABLETS

Oral tablets typically contain talc, cellulose, cornstarch, or combinations of these substances as binding agents. When pulverized, the powder can be combined with water to form an injectable solution with higher and more rapid bioavailability.^1,2 The binders, however, are insoluble and accumulate in various tissues.

Intravenous injection of microcellulose has been shown to produce pulmonary and peripheral eosinophilia in birds. In humans, the immune response in foreign body granulomatosis can vary, and case reports have not mentioned eosinophils in the lungs or serum.^3,4

Deposition of these particles in pulmonary vessels is common and can trigger a potentially fatal reaction, presenting as acute onset of cough, chest pain, dyspnea, fever, and pulmonary hypertension. The severity of these clinical findings is relative to the degree of pulmonary hypertension created by the arteriolar involvement of these emboli.^2,5

Our patient’s exertional dyspnea and hypoxemia resolved during 1 week of hospitalization with conservative management and supplemental oxygen. She was referred to our pain rehabilitation clinic, where she was successfully weaned from narcotics. Her pulmonary findings on computed tomography were still present 3 years after her initial images, though less prominent.

An 82-year-old man with poorly controlled diabetes mellitus presented to our emergency department with a 1-day history of confusion and coffee-ground emesis.

Biopsy study revealed necrosis of the esophageal mucosa. A diagnosis of acute necrotizing esophagitis was made.

ACUTE NECROTIZING ESOPHAGITIS

Acute necrotizing esophagitis is thought to arise from a combination of an ischemic insult to the esophagus, an impaired mucosal barrier system, and a backflow injury from chemical contents of gastric secretions.¹ The tissue hypoperfusion derives from vasculopathy, hypotension, or malnutrition. It is associated with diabetes mellitus, diabetic ketoacidosis, lactic acidosis, alcohol abuse, cirrhosis, renal insufficiency, malignancy, antibiotic use, esophageal infections, and aortic dissection.

The esophagus has a diverse blood supply. The upper esophagus is supplied by the inferior thyroid arteries, the mid-esophagus by the bronchial, proper esophageal, and intercostal arteries, and the distal esophagus by the left gastric and left inferior phrenic arteries.¹

KEY FEATURES AND DIAGNOSTIC CLUES

The necrotic changes are prominent in the distal esophagus, which is more susceptible to ischemia and mucosal injury. The characteristic endoscopic finding is a diffuse black esophagus with a sharp transition to normal mucosa at the gastroesophageal junction.

The differential diagnosis includes melanosis, pseudomelanosis, malignant melanoma, acanthosis nigricans, coal dust deposition, caustic ingestion, radiation esophagitis, and infectious esophagitis caused by cytomegalovirus, herpes simplex virus, Candida albicans, or Klebsiella pneumoniae.^2–4

TREATMENT AND OUTCOME

Avoidance of oral intake and gastric acid suppression with intravenous proton pump inhibitors are recommended to prevent additional injury of the esophageal mucosa.

The condition generally resolves with restored blood flow and treatment of any coexisting illness. However, it may be complicated by perforation (6.8%), mediastinitis (5.7%), or subsequent development of esophageal stricture (10.2%).⁵ Patients with esophageal stricture require endoscopic dilation after mucosal recovery.

The overall risk of death in acute necrotizing esophagitis is high (31.8%) and most often due to the underlying disease, such as sepsis, malignancy, cardiogenic shock, or hypovolemic shock.⁵ The mortality rate directly attributed to complications of acute necrotizing esophagitis is much lower (5.7%).⁵     

An 82-year-old man with poorly controlled diabetes mellitus presented to our emergency department with a 1-day history of confusion and coffee-ground emesis.

Biopsy study revealed necrosis of the esophageal mucosa. A diagnosis of acute necrotizing esophagitis was made.

ACUTE NECROTIZING ESOPHAGITIS

Acute necrotizing esophagitis is thought to arise from a combination of an ischemic insult to the esophagus, an impaired mucosal barrier system, and a backflow injury from chemical contents of gastric secretions.¹ The tissue hypoperfusion derives from vasculopathy, hypotension, or malnutrition. It is associated with diabetes mellitus, diabetic ketoacidosis, lactic acidosis, alcohol abuse, cirrhosis, renal insufficiency, malignancy, antibiotic use, esophageal infections, and aortic dissection.

The esophagus has a diverse blood supply. The upper esophagus is supplied by the inferior thyroid arteries, the mid-esophagus by the bronchial, proper esophageal, and intercostal arteries, and the distal esophagus by the left gastric and left inferior phrenic arteries.¹

KEY FEATURES AND DIAGNOSTIC CLUES

The necrotic changes are prominent in the distal esophagus, which is more susceptible to ischemia and mucosal injury. The characteristic endoscopic finding is a diffuse black esophagus with a sharp transition to normal mucosa at the gastroesophageal junction.

The differential diagnosis includes melanosis, pseudomelanosis, malignant melanoma, acanthosis nigricans, coal dust deposition, caustic ingestion, radiation esophagitis, and infectious esophagitis caused by cytomegalovirus, herpes simplex virus, Candida albicans, or Klebsiella pneumoniae.^2–4

TREATMENT AND OUTCOME

Avoidance of oral intake and gastric acid suppression with intravenous proton pump inhibitors are recommended to prevent additional injury of the esophageal mucosa.

The condition generally resolves with restored blood flow and treatment of any coexisting illness. However, it may be complicated by perforation (6.8%), mediastinitis (5.7%), or subsequent development of esophageal stricture (10.2%).⁵ Patients with esophageal stricture require endoscopic dilation after mucosal recovery.

The overall risk of death in acute necrotizing esophagitis is high (31.8%) and most often due to the underlying disease, such as sepsis, malignancy, cardiogenic shock, or hypovolemic shock.⁵ The mortality rate directly attributed to complications of acute necrotizing esophagitis is much lower (5.7%).⁵     

An 82-year-old man with poorly controlled diabetes mellitus presented to our emergency department with a 1-day history of confusion and coffee-ground emesis.

Biopsy study revealed necrosis of the esophageal mucosa. A diagnosis of acute necrotizing esophagitis was made.

ACUTE NECROTIZING ESOPHAGITIS

Acute necrotizing esophagitis is thought to arise from a combination of an ischemic insult to the esophagus, an impaired mucosal barrier system, and a backflow injury from chemical contents of gastric secretions.¹ The tissue hypoperfusion derives from vasculopathy, hypotension, or malnutrition. It is associated with diabetes mellitus, diabetic ketoacidosis, lactic acidosis, alcohol abuse, cirrhosis, renal insufficiency, malignancy, antibiotic use, esophageal infections, and aortic dissection.

The esophagus has a diverse blood supply. The upper esophagus is supplied by the inferior thyroid arteries, the mid-esophagus by the bronchial, proper esophageal, and intercostal arteries, and the distal esophagus by the left gastric and left inferior phrenic arteries.¹

KEY FEATURES AND DIAGNOSTIC CLUES

The necrotic changes are prominent in the distal esophagus, which is more susceptible to ischemia and mucosal injury. The characteristic endoscopic finding is a diffuse black esophagus with a sharp transition to normal mucosa at the gastroesophageal junction.

The differential diagnosis includes melanosis, pseudomelanosis, malignant melanoma, acanthosis nigricans, coal dust deposition, caustic ingestion, radiation esophagitis, and infectious esophagitis caused by cytomegalovirus, herpes simplex virus, Candida albicans, or Klebsiella pneumoniae.^2–4

TREATMENT AND OUTCOME

Avoidance of oral intake and gastric acid suppression with intravenous proton pump inhibitors are recommended to prevent additional injury of the esophageal mucosa.

The condition generally resolves with restored blood flow and treatment of any coexisting illness. However, it may be complicated by perforation (6.8%), mediastinitis (5.7%), or subsequent development of esophageal stricture (10.2%).⁵ Patients with esophageal stricture require endoscopic dilation after mucosal recovery.

The overall risk of death in acute necrotizing esophagitis is high (31.8%) and most often due to the underlying disease, such as sepsis, malignancy, cardiogenic shock, or hypovolemic shock.⁵ The mortality rate directly attributed to complications of acute necrotizing esophagitis is much lower (5.7%).⁵     

Vasovagal syncope is usually benign, and although it often recurs, increasing fluid and salt intake and performing counter-pressure maneuvers are usually sufficient.¹ However, if patients continue to have syncopal episodes despite these first-line measures, other options include drug therapy with midodrine, fludrocortisone, beta-blockers, or selective serotonin reuptake inhibitors; orthostatic training; and, in some cases, pacemaker implantation. The 2017 guidelines from the American College of Cardiology, American Heart Association, and Heart Rhythm Society (ACC/AHA/HRS) are helpful in the management of these patients.¹

RATIONALE

Although vasovagal syncope is considered benign, it can result in injury and can significantly affect quality of life.

The diagnosis can often be established in the initial evaluation with a structured history, physical examination, and electrocardiography. If the diagnosis is still unclear, tilt-table testing can be useful and has an ACC/AHA/HRS class IIa (moderate) recommendation.¹ Once the diagnosis of vasovagal syncope is made, first-line measures can be instituted.

FIRST-LINE MEASURES

An explanation of the diagnosis, education on avoiding triggers such as prolonged standing and warm environments, coping with potentially stressful visits to the doctor or dentist, and reassurance that the condition is benign are all strongly recommended (class I).¹

Initial measures include performing physical counter-pressure maneuvers (class IIa), increasing salt and fluid intake (class IIb) in the absence of contraindications, and, in selected patients, reducing or withdrawing hypotensive medications when appropriate (class IIb).

Physical counter-pressure maneuvers are recommended for patients whose syncopal episodes have a sufficiently long prodromal period. Maneuvers include the following:

• Leg crossing: crossing the legs while tensing leg, abdominal, and buttock muscles
• Handgrip: maximally contracting a rubber ball or other object in the dominant hand
• Squatting
• Limb or abdominal contractions
• Arm tensing: contracting both arms by gripping one hand with the other and abducting both arms.²

The effectiveness of counter-pressure maneuvers was studied by van Dijk et al² in a multicenter prospective randomized clinical trial that included 223 patients with recurrent vasovagal syncope associated with prodromal symptoms. They concluded that these maneuvers decreased the recurrence of syncopal episodes, with a relative risk reduction of 0.36 (95% confidence interval 0.11–0.53, P < .005) and were low-cost and risk-free.

Confirming the diagnosis of vasovagal syncope with tilt-table testing may reassure the patient. It can also help the patient learn to identify the symptoms associated with a vasovagal episode, which in turn may encourage timely use of physical counter-pressure maneuvers at the onset.

The evidence for increasing salt and fluid intake for patients with vasovagal syncope is limited. But in the absence of a contraindication such as hypertension, renal disease, or heart failure, it may be reasonable to encourage the ingestion of 2 L to 3 L of fluid per day and a total of 6 g to 9 g of salt per day (around 1 to 2 heaping teaspoons of salt).¹

In patients who continue to have syncopal episodes despite adequate use of first-line measures, medical therapy can be considered. Unfortunately, evidence supporting drug therapy for recurrent syncope is limited.³ Options include midodrine (class IIa), fludrocortisone (class IIb), beta-blockers (class IIb), and selective serotonin reuptake inhibitors (class IIb).¹

Midodrine has the strongest recommendation and is a reasonable option if there is no history of hypertension, heart failure, or urinary retention. It is a peripheral alpha-agonist that ameliorates the reduction in peripheral sympathetic neural outflow responsible for venous pooling and vasodepression in vasovagal syncope.^4–6

Fludrocortisone results in increased blood volume due to mineralocorticoid activity. In the Prevention of Syncope Trial 2 of fludrocortisone vs placebo, patients on fludrocortisone had a “marginally nonsignificant” reduction in recurrence of syncope over 1 year (hazard ratio 0.69, P = .069).⁷

Overall, beta-blockers have failed to prevent syncope in randomized controlled trials. But in a meta-analysis that included patients from the Prevention of Syncope Trial,⁸ an age-dependent benefit of beta-blockers was noted in patients age 42 and older.⁹ Therefore, a beta-blocker may be a reasonable option in patients in this age group with recurrent vasovagal syncope.¹

Serotonin has central effects on blood pressure and heart rate that can induce syncope. However, evidence for the effectiveness of selective serotonin reuptake inhibitors in the prevention of recurrent vasovagal syncope has been contradictory in small trials.^10,11

When choosing a drug, contraindications should be considered, including possible effects during pregnancy in women of childbearing age.

OTHER MEASURES

Orthostatic training, with repetitive tilt-table testing until a test is negative, or with daily standing quietly against a wall for prolonged periods of time, has not been shown to have sustained benefit in reducing the recurrence of syncopal episodes (class IIb recommendation).¹

Dual-chamber pacing can be considered in carefully selected patients age 40 or older with syncope and documented asystole of at least 3 seconds or spontaneous pauses of at least 6 seconds without syncope on implantable loop recorder monitoring (class IIb recommendation).^1,12,13 Strict patient selection increases the likelihood that pacing will be effective.¹ For example, patients with documented asystole during syncope and a tilt-table test that induces minimal or no vasodepressor response are more likely to respond than patients with a positive tilt-table test with a vasodepressor (hypotensive) response.¹³

Tilt-table testing may also be considered to identify patients with a hypotensive response who would be less likely to respond to permanent cardiac pacing.¹⁴ 


Compression garments carry a class IIa recommendation for orthostatic hypotension,1 but they have not been adequately studied in vasovagal syncope.

Vasovagal syncope is usually benign, and although it often recurs, increasing fluid and salt intake and performing counter-pressure maneuvers are usually sufficient.¹ However, if patients continue to have syncopal episodes despite these first-line measures, other options include drug therapy with midodrine, fludrocortisone, beta-blockers, or selective serotonin reuptake inhibitors; orthostatic training; and, in some cases, pacemaker implantation. The 2017 guidelines from the American College of Cardiology, American Heart Association, and Heart Rhythm Society (ACC/AHA/HRS) are helpful in the management of these patients.¹

RATIONALE

Although vasovagal syncope is considered benign, it can result in injury and can significantly affect quality of life.

The diagnosis can often be established in the initial evaluation with a structured history, physical examination, and electrocardiography. If the diagnosis is still unclear, tilt-table testing can be useful and has an ACC/AHA/HRS class IIa (moderate) recommendation.¹ Once the diagnosis of vasovagal syncope is made, first-line measures can be instituted.

FIRST-LINE MEASURES

An explanation of the diagnosis, education on avoiding triggers such as prolonged standing and warm environments, coping with potentially stressful visits to the doctor or dentist, and reassurance that the condition is benign are all strongly recommended (class I).¹

Initial measures include performing physical counter-pressure maneuvers (class IIa), increasing salt and fluid intake (class IIb) in the absence of contraindications, and, in selected patients, reducing or withdrawing hypotensive medications when appropriate (class IIb).

Physical counter-pressure maneuvers are recommended for patients whose syncopal episodes have a sufficiently long prodromal period. Maneuvers include the following:

• Leg crossing: crossing the legs while tensing leg, abdominal, and buttock muscles
• Handgrip: maximally contracting a rubber ball or other object in the dominant hand
• Squatting
• Limb or abdominal contractions
• Arm tensing: contracting both arms by gripping one hand with the other and abducting both arms.²

The effectiveness of counter-pressure maneuvers was studied by van Dijk et al² in a multicenter prospective randomized clinical trial that included 223 patients with recurrent vasovagal syncope associated with prodromal symptoms. They concluded that these maneuvers decreased the recurrence of syncopal episodes, with a relative risk reduction of 0.36 (95% confidence interval 0.11–0.53, P < .005) and were low-cost and risk-free.

Confirming the diagnosis of vasovagal syncope with tilt-table testing may reassure the patient. It can also help the patient learn to identify the symptoms associated with a vasovagal episode, which in turn may encourage timely use of physical counter-pressure maneuvers at the onset.

The evidence for increasing salt and fluid intake for patients with vasovagal syncope is limited. But in the absence of a contraindication such as hypertension, renal disease, or heart failure, it may be reasonable to encourage the ingestion of 2 L to 3 L of fluid per day and a total of 6 g to 9 g of salt per day (around 1 to 2 heaping teaspoons of salt).¹

In patients who continue to have syncopal episodes despite adequate use of first-line measures, medical therapy can be considered. Unfortunately, evidence supporting drug therapy for recurrent syncope is limited.³ Options include midodrine (class IIa), fludrocortisone (class IIb), beta-blockers (class IIb), and selective serotonin reuptake inhibitors (class IIb).¹

Midodrine has the strongest recommendation and is a reasonable option if there is no history of hypertension, heart failure, or urinary retention. It is a peripheral alpha-agonist that ameliorates the reduction in peripheral sympathetic neural outflow responsible for venous pooling and vasodepression in vasovagal syncope.^4–6

Fludrocortisone results in increased blood volume due to mineralocorticoid activity. In the Prevention of Syncope Trial 2 of fludrocortisone vs placebo, patients on fludrocortisone had a “marginally nonsignificant” reduction in recurrence of syncope over 1 year (hazard ratio 0.69, P = .069).⁷

Overall, beta-blockers have failed to prevent syncope in randomized controlled trials. But in a meta-analysis that included patients from the Prevention of Syncope Trial,⁸ an age-dependent benefit of beta-blockers was noted in patients age 42 and older.⁹ Therefore, a beta-blocker may be a reasonable option in patients in this age group with recurrent vasovagal syncope.¹

Serotonin has central effects on blood pressure and heart rate that can induce syncope. However, evidence for the effectiveness of selective serotonin reuptake inhibitors in the prevention of recurrent vasovagal syncope has been contradictory in small trials.^10,11

When choosing a drug, contraindications should be considered, including possible effects during pregnancy in women of childbearing age.

OTHER MEASURES

Orthostatic training, with repetitive tilt-table testing until a test is negative, or with daily standing quietly against a wall for prolonged periods of time, has not been shown to have sustained benefit in reducing the recurrence of syncopal episodes (class IIb recommendation).¹

Dual-chamber pacing can be considered in carefully selected patients age 40 or older with syncope and documented asystole of at least 3 seconds or spontaneous pauses of at least 6 seconds without syncope on implantable loop recorder monitoring (class IIb recommendation).^1,12,13 Strict patient selection increases the likelihood that pacing will be effective.¹ For example, patients with documented asystole during syncope and a tilt-table test that induces minimal or no vasodepressor response are more likely to respond than patients with a positive tilt-table test with a vasodepressor (hypotensive) response.¹³

Tilt-table testing may also be considered to identify patients with a hypotensive response who would be less likely to respond to permanent cardiac pacing.¹⁴ 


Compression garments carry a class IIa recommendation for orthostatic hypotension,1 but they have not been adequately studied in vasovagal syncope.

Vasovagal syncope is usually benign, and although it often recurs, increasing fluid and salt intake and performing counter-pressure maneuvers are usually sufficient.¹ However, if patients continue to have syncopal episodes despite these first-line measures, other options include drug therapy with midodrine, fludrocortisone, beta-blockers, or selective serotonin reuptake inhibitors; orthostatic training; and, in some cases, pacemaker implantation. The 2017 guidelines from the American College of Cardiology, American Heart Association, and Heart Rhythm Society (ACC/AHA/HRS) are helpful in the management of these patients.¹

RATIONALE

Although vasovagal syncope is considered benign, it can result in injury and can significantly affect quality of life.

The diagnosis can often be established in the initial evaluation with a structured history, physical examination, and electrocardiography. If the diagnosis is still unclear, tilt-table testing can be useful and has an ACC/AHA/HRS class IIa (moderate) recommendation.¹ Once the diagnosis of vasovagal syncope is made, first-line measures can be instituted.

FIRST-LINE MEASURES

An explanation of the diagnosis, education on avoiding triggers such as prolonged standing and warm environments, coping with potentially stressful visits to the doctor or dentist, and reassurance that the condition is benign are all strongly recommended (class I).¹

Initial measures include performing physical counter-pressure maneuvers (class IIa), increasing salt and fluid intake (class IIb) in the absence of contraindications, and, in selected patients, reducing or withdrawing hypotensive medications when appropriate (class IIb).

Physical counter-pressure maneuvers are recommended for patients whose syncopal episodes have a sufficiently long prodromal period. Maneuvers include the following:

• Leg crossing: crossing the legs while tensing leg, abdominal, and buttock muscles
• Handgrip: maximally contracting a rubber ball or other object in the dominant hand
• Squatting
• Limb or abdominal contractions
• Arm tensing: contracting both arms by gripping one hand with the other and abducting both arms.²

The effectiveness of counter-pressure maneuvers was studied by van Dijk et al² in a multicenter prospective randomized clinical trial that included 223 patients with recurrent vasovagal syncope associated with prodromal symptoms. They concluded that these maneuvers decreased the recurrence of syncopal episodes, with a relative risk reduction of 0.36 (95% confidence interval 0.11–0.53, P < .005) and were low-cost and risk-free.

Confirming the diagnosis of vasovagal syncope with tilt-table testing may reassure the patient. It can also help the patient learn to identify the symptoms associated with a vasovagal episode, which in turn may encourage timely use of physical counter-pressure maneuvers at the onset.

The evidence for increasing salt and fluid intake for patients with vasovagal syncope is limited. But in the absence of a contraindication such as hypertension, renal disease, or heart failure, it may be reasonable to encourage the ingestion of 2 L to 3 L of fluid per day and a total of 6 g to 9 g of salt per day (around 1 to 2 heaping teaspoons of salt).¹

In patients who continue to have syncopal episodes despite adequate use of first-line measures, medical therapy can be considered. Unfortunately, evidence supporting drug therapy for recurrent syncope is limited.³ Options include midodrine (class IIa), fludrocortisone (class IIb), beta-blockers (class IIb), and selective serotonin reuptake inhibitors (class IIb).¹

Midodrine has the strongest recommendation and is a reasonable option if there is no history of hypertension, heart failure, or urinary retention. It is a peripheral alpha-agonist that ameliorates the reduction in peripheral sympathetic neural outflow responsible for venous pooling and vasodepression in vasovagal syncope.^4–6

Fludrocortisone results in increased blood volume due to mineralocorticoid activity. In the Prevention of Syncope Trial 2 of fludrocortisone vs placebo, patients on fludrocortisone had a “marginally nonsignificant” reduction in recurrence of syncope over 1 year (hazard ratio 0.69, P = .069).⁷

Overall, beta-blockers have failed to prevent syncope in randomized controlled trials. But in a meta-analysis that included patients from the Prevention of Syncope Trial,⁸ an age-dependent benefit of beta-blockers was noted in patients age 42 and older.⁹ Therefore, a beta-blocker may be a reasonable option in patients in this age group with recurrent vasovagal syncope.¹

Serotonin has central effects on blood pressure and heart rate that can induce syncope. However, evidence for the effectiveness of selective serotonin reuptake inhibitors in the prevention of recurrent vasovagal syncope has been contradictory in small trials.^10,11

When choosing a drug, contraindications should be considered, including possible effects during pregnancy in women of childbearing age.

OTHER MEASURES

Orthostatic training, with repetitive tilt-table testing until a test is negative, or with daily standing quietly against a wall for prolonged periods of time, has not been shown to have sustained benefit in reducing the recurrence of syncopal episodes (class IIb recommendation).¹

Dual-chamber pacing can be considered in carefully selected patients age 40 or older with syncope and documented asystole of at least 3 seconds or spontaneous pauses of at least 6 seconds without syncope on implantable loop recorder monitoring (class IIb recommendation).^1,12,13 Strict patient selection increases the likelihood that pacing will be effective.¹ For example, patients with documented asystole during syncope and a tilt-table test that induces minimal or no vasodepressor response are more likely to respond than patients with a positive tilt-table test with a vasodepressor (hypotensive) response.¹³

Tilt-table testing may also be considered to identify patients with a hypotensive response who would be less likely to respond to permanent cardiac pacing.¹⁴ 


Compression garments carry a class IIa recommendation for orthostatic hypotension,1 but they have not been adequately studied in vasovagal syncope.

Yes, anti-tumor necrosis factor (anti-TNF) therapy for inflammatory bowel disease (IBD) can be continued during pregnancy.

IBD is often diagnosed and treated in women during their reproductive years. Consequently, these patients face important decisions about the management of their disease and the safety of their baby. Clinicians should be prepared to offer guidance by discussing the risks and benefits of anti-TNF agents with their pregnant patients who have IBD, as well as with those considering pregnancy.

STUDIES OF THE POTENTIAL RISKS

Anti-TNF agents are monoclonal antibodies. Infliximab, adalimumab, and golimumab are actively transported into the fetal circulation via the placenta, mainly during the second and third trimesters. Certolizumab crosses the placenta only by passive means, because it lacks the fragment crystallizable (Fc) region required for placental transfer.¹

Effects on pregnancy outcomes

In a 2016 meta-analysis,² of 1,242 pregnancies in women with IBD, 482 were in women on anti-TNF therapy. It found no statistically significant difference in rates of adverse pregnancy outcomes including congenital abnormality, preterm birth, and low birth weight.

A meta-analysis of 1,216 pregnant women with IBD found no statistically significant differences in rates of spontaneous or elective abortion, preterm birth, low birth weight, or congenital malformation in those on anti-TNF therapy vs controls.³

A systematic review of 58 studies including more than 1,500 pregnant women with IBD who were exposed to anti-TNF agents concluded that there was no association with adverse pregnancy outcomes such as spontaneous abortion, preterm delivery, stillbirth, low birth weight, congenital malformation, or infection.⁴

A retrospective cohort study of 66 pregnant patients with IBD from several centers in Spain found that anti-TNF or thiopurine therapy during pregnancy did not increase the risk of pregnancy complications or neonatal complications.⁵

Effects on newborns

Cord blood studies have shown that maternal use of infliximab and adalimumab results in a detectable serum level in newborns, while cord blood levels of certolizumab are much lower.^1,6 In some studies, anti-TNF drugs were detectable in infants for up to 6 months after birth, whereas other studies found that detectable serum levels dropped soon after birth.^1,7

Addressing concern about an increased risk of infection or dysfunctional immune development in newborns exposed to anti-TNF drugs in utero, a systematic review found no increased risk.⁴ A retrospective multicenter cohort study of 841 children also reported no association between in utero exposure to anti-TNF agents and risk of severe infection in the short term or long term (mean of 4 years).⁸ Additional studies are under way to determine long-term risk to the newborn.⁷

The Toronto consensus guidelines strongly recommend continuing anti-TNF therapy during pregnancy in women with IBD who began maintenance therapy before conception.⁶

If a patient strongly prefers to stop therapy during pregnancy to limit fetal exposure, the Toronto consensus recommends giving the last dose at 22 to 24 weeks of gestation. However, this should only be considered in patients whose IBD is in remission and at low risk of relapse.^6,9

Although anti-TNF drugs may differ in terms of placental transfer, agents should not be switched in stable patients, as switching increases the risk of relapse.¹⁰

BENEFITS OF CONTINUING THERAPY

Active IBD poses a significantly greater risk to the mother and the baby than continuing anti-TNF therapy during pregnancy.^1,7 The primary benefit of continuing therapy is to maintain disease remission.

Among women with active IBD at the time of conception, one-third will have improvement in disease activity during the course of their pregnancy, one-third will have no change, and one-third will have worsening of disease activity. But if IBD is in remission at the time of conception, it will remain in remission in nearly 80% of women during pregnancy.¹

Women with active IBD are at increased risk of preterm delivery, low birth weight, and intrauterine growth restriction.^1,2,5 Also, women with IBD have an increased risk of venous thromboembolism, particularly if they have active disease during pregnancy.¹ Therefore, achieving and maintaining remission are vital in the management of the pregnant patient with IBD.

CONSIDERATIONS AFTER BIRTH: BREAST-FEEDING AND VACCINATION

Breast-feeding is considered safe. Minuscule amounts of infliximab or adalimumab are transferred in breast milk but are unlikely to result in systemic immune suppression in the infant.⁷

Live-attenuated vaccines should be avoided for the first 6 months in infants exposed to anti-TNF agents in utero.^1,7,11 All other vaccines, including hepatitis B virus vaccine, should be given according to standard schedules.⁶

OUR RECOMMENDATIONS

The goal of managing IBD in women of reproductive age is to minimize the risk of adverse outcomes for both mother and baby. We recommend a team approach, working closely with a gastroenterologist and a high-risk-pregnancy obstetrician, if available.

Patients should continue anti-TNF therapy during pregnancy because evidence supports its safety. If a woman wants to stop therapy and is at low risk of relapse, we recommend giving the last dose at 22 to 24 weeks of gestation, then promptly resuming therapy postpartum.

Live-attenuated vaccines (eg, influenza, rotavirus) should be avoided for the first 6 months in babies born to mothers on anti-TNF therapy.

Yes, anti-tumor necrosis factor (anti-TNF) therapy for inflammatory bowel disease (IBD) can be continued during pregnancy.

IBD is often diagnosed and treated in women during their reproductive years. Consequently, these patients face important decisions about the management of their disease and the safety of their baby. Clinicians should be prepared to offer guidance by discussing the risks and benefits of anti-TNF agents with their pregnant patients who have IBD, as well as with those considering pregnancy.

STUDIES OF THE POTENTIAL RISKS

Anti-TNF agents are monoclonal antibodies. Infliximab, adalimumab, and golimumab are actively transported into the fetal circulation via the placenta, mainly during the second and third trimesters. Certolizumab crosses the placenta only by passive means, because it lacks the fragment crystallizable (Fc) region required for placental transfer.¹

Effects on pregnancy outcomes

In a 2016 meta-analysis,² of 1,242 pregnancies in women with IBD, 482 were in women on anti-TNF therapy. It found no statistically significant difference in rates of adverse pregnancy outcomes including congenital abnormality, preterm birth, and low birth weight.

A meta-analysis of 1,216 pregnant women with IBD found no statistically significant differences in rates of spontaneous or elective abortion, preterm birth, low birth weight, or congenital malformation in those on anti-TNF therapy vs controls.³

A systematic review of 58 studies including more than 1,500 pregnant women with IBD who were exposed to anti-TNF agents concluded that there was no association with adverse pregnancy outcomes such as spontaneous abortion, preterm delivery, stillbirth, low birth weight, congenital malformation, or infection.⁴

A retrospective cohort study of 66 pregnant patients with IBD from several centers in Spain found that anti-TNF or thiopurine therapy during pregnancy did not increase the risk of pregnancy complications or neonatal complications.⁵

Effects on newborns

Cord blood studies have shown that maternal use of infliximab and adalimumab results in a detectable serum level in newborns, while cord blood levels of certolizumab are much lower.^1,6 In some studies, anti-TNF drugs were detectable in infants for up to 6 months after birth, whereas other studies found that detectable serum levels dropped soon after birth.^1,7

Addressing concern about an increased risk of infection or dysfunctional immune development in newborns exposed to anti-TNF drugs in utero, a systematic review found no increased risk.⁴ A retrospective multicenter cohort study of 841 children also reported no association between in utero exposure to anti-TNF agents and risk of severe infection in the short term or long term (mean of 4 years).⁸ Additional studies are under way to determine long-term risk to the newborn.⁷

The Toronto consensus guidelines strongly recommend continuing anti-TNF therapy during pregnancy in women with IBD who began maintenance therapy before conception.⁶

If a patient strongly prefers to stop therapy during pregnancy to limit fetal exposure, the Toronto consensus recommends giving the last dose at 22 to 24 weeks of gestation. However, this should only be considered in patients whose IBD is in remission and at low risk of relapse.^6,9

Although anti-TNF drugs may differ in terms of placental transfer, agents should not be switched in stable patients, as switching increases the risk of relapse.¹⁰

BENEFITS OF CONTINUING THERAPY

Active IBD poses a significantly greater risk to the mother and the baby than continuing anti-TNF therapy during pregnancy.^1,7 The primary benefit of continuing therapy is to maintain disease remission.

Among women with active IBD at the time of conception, one-third will have improvement in disease activity during the course of their pregnancy, one-third will have no change, and one-third will have worsening of disease activity. But if IBD is in remission at the time of conception, it will remain in remission in nearly 80% of women during pregnancy.¹

Women with active IBD are at increased risk of preterm delivery, low birth weight, and intrauterine growth restriction.^1,2,5 Also, women with IBD have an increased risk of venous thromboembolism, particularly if they have active disease during pregnancy.¹ Therefore, achieving and maintaining remission are vital in the management of the pregnant patient with IBD.

CONSIDERATIONS AFTER BIRTH: BREAST-FEEDING AND VACCINATION

Breast-feeding is considered safe. Minuscule amounts of infliximab or adalimumab are transferred in breast milk but are unlikely to result in systemic immune suppression in the infant.⁷

Live-attenuated vaccines should be avoided for the first 6 months in infants exposed to anti-TNF agents in utero.^1,7,11 All other vaccines, including hepatitis B virus vaccine, should be given according to standard schedules.⁶

OUR RECOMMENDATIONS

The goal of managing IBD in women of reproductive age is to minimize the risk of adverse outcomes for both mother and baby. We recommend a team approach, working closely with a gastroenterologist and a high-risk-pregnancy obstetrician, if available.

Patients should continue anti-TNF therapy during pregnancy because evidence supports its safety. If a woman wants to stop therapy and is at low risk of relapse, we recommend giving the last dose at 22 to 24 weeks of gestation, then promptly resuming therapy postpartum.

Live-attenuated vaccines (eg, influenza, rotavirus) should be avoided for the first 6 months in babies born to mothers on anti-TNF therapy.

Yes, anti-tumor necrosis factor (anti-TNF) therapy for inflammatory bowel disease (IBD) can be continued during pregnancy.

IBD is often diagnosed and treated in women during their reproductive years. Consequently, these patients face important decisions about the management of their disease and the safety of their baby. Clinicians should be prepared to offer guidance by discussing the risks and benefits of anti-TNF agents with their pregnant patients who have IBD, as well as with those considering pregnancy.

STUDIES OF THE POTENTIAL RISKS

Anti-TNF agents are monoclonal antibodies. Infliximab, adalimumab, and golimumab are actively transported into the fetal circulation via the placenta, mainly during the second and third trimesters. Certolizumab crosses the placenta only by passive means, because it lacks the fragment crystallizable (Fc) region required for placental transfer.¹

Effects on pregnancy outcomes

In a 2016 meta-analysis,² of 1,242 pregnancies in women with IBD, 482 were in women on anti-TNF therapy. It found no statistically significant difference in rates of adverse pregnancy outcomes including congenital abnormality, preterm birth, and low birth weight.

A meta-analysis of 1,216 pregnant women with IBD found no statistically significant differences in rates of spontaneous or elective abortion, preterm birth, low birth weight, or congenital malformation in those on anti-TNF therapy vs controls.³

A systematic review of 58 studies including more than 1,500 pregnant women with IBD who were exposed to anti-TNF agents concluded that there was no association with adverse pregnancy outcomes such as spontaneous abortion, preterm delivery, stillbirth, low birth weight, congenital malformation, or infection.⁴

A retrospective cohort study of 66 pregnant patients with IBD from several centers in Spain found that anti-TNF or thiopurine therapy during pregnancy did not increase the risk of pregnancy complications or neonatal complications.⁵

Effects on newborns

Cord blood studies have shown that maternal use of infliximab and adalimumab results in a detectable serum level in newborns, while cord blood levels of certolizumab are much lower.^1,6 In some studies, anti-TNF drugs were detectable in infants for up to 6 months after birth, whereas other studies found that detectable serum levels dropped soon after birth.^1,7

Addressing concern about an increased risk of infection or dysfunctional immune development in newborns exposed to anti-TNF drugs in utero, a systematic review found no increased risk.⁴ A retrospective multicenter cohort study of 841 children also reported no association between in utero exposure to anti-TNF agents and risk of severe infection in the short term or long term (mean of 4 years).⁸ Additional studies are under way to determine long-term risk to the newborn.⁷

The Toronto consensus guidelines strongly recommend continuing anti-TNF therapy during pregnancy in women with IBD who began maintenance therapy before conception.⁶

If a patient strongly prefers to stop therapy during pregnancy to limit fetal exposure, the Toronto consensus recommends giving the last dose at 22 to 24 weeks of gestation. However, this should only be considered in patients whose IBD is in remission and at low risk of relapse.^6,9

Although anti-TNF drugs may differ in terms of placental transfer, agents should not be switched in stable patients, as switching increases the risk of relapse.¹⁰

BENEFITS OF CONTINUING THERAPY

Active IBD poses a significantly greater risk to the mother and the baby than continuing anti-TNF therapy during pregnancy.^1,7 The primary benefit of continuing therapy is to maintain disease remission.

Among women with active IBD at the time of conception, one-third will have improvement in disease activity during the course of their pregnancy, one-third will have no change, and one-third will have worsening of disease activity. But if IBD is in remission at the time of conception, it will remain in remission in nearly 80% of women during pregnancy.¹

Women with active IBD are at increased risk of preterm delivery, low birth weight, and intrauterine growth restriction.^1,2,5 Also, women with IBD have an increased risk of venous thromboembolism, particularly if they have active disease during pregnancy.¹ Therefore, achieving and maintaining remission are vital in the management of the pregnant patient with IBD.

CONSIDERATIONS AFTER BIRTH: BREAST-FEEDING AND VACCINATION

Breast-feeding is considered safe. Minuscule amounts of infliximab or adalimumab are transferred in breast milk but are unlikely to result in systemic immune suppression in the infant.⁷

Live-attenuated vaccines should be avoided for the first 6 months in infants exposed to anti-TNF agents in utero.^1,7,11 All other vaccines, including hepatitis B virus vaccine, should be given according to standard schedules.⁶

OUR RECOMMENDATIONS

The goal of managing IBD in women of reproductive age is to minimize the risk of adverse outcomes for both mother and baby. We recommend a team approach, working closely with a gastroenterologist and a high-risk-pregnancy obstetrician, if available.

Patients should continue anti-TNF therapy during pregnancy because evidence supports its safety. If a woman wants to stop therapy and is at low risk of relapse, we recommend giving the last dose at 22 to 24 weeks of gestation, then promptly resuming therapy postpartum.

Live-attenuated vaccines (eg, influenza, rotavirus) should be avoided for the first 6 months in babies born to mothers on anti-TNF therapy.

No. Continuous monitoring for changes in heart rhythm with cardiac telemetry is recommended for all patients admitted to an intensive care unit (ICU). But routine telemetry monitoring for patients in non-ICU beds is not recommended, as it leads to unnecessary testing and treatment, increasing the cost of care and hospital length of stay.

RISK STRATIFICATION AND INDICATIONS

Telemetry is generally recommended for patients admitted with any type of heart disease, including:

• Acute myocardial infarction with ST-segment elevation or Q waves on 12-lead electrocardiography (ECG)
• Acute ischemia suggested by ST-segment depression or T-wave inversion on ECG
• Systolic blood pressure less than 100 mm Hg
• Acute decompensated heart failure with bilateral rales above the lung bases
• Chest pain that is worse than or the same as that in prior angina or myocardial infarction.^1,2

Indications for telemetry are less clear in patients with no history of heart disease. The American Heart Association (AHA)³ has classified admitted patients based on the presence or absence of heart disease³:

• Class I (high risk of arrhythmia): acute coronary syndrome, new arrhythmia (eg, atrial fibrillation or flutter), severe electrolyte imbalance; telemetry is warranted
• Class II (moderate risk): acute decompensated heart failure with stable hemodynamic status, a surgical or medical diagnosis with underlying paced rhythms (ie, with a pacemaker), and chronic arrhythmia (atrial fibrillation or flutter); in these cases, telemetry monitoring may be considered
• Class III (low risk): no history of cardiac disease or arrhythmias, admitted for medical or surgical reasons; in these cases, telemetry is generally not indicated³

Telemetry should also be considered in patients admitted with syncope or stroke, critical illness, or palpitations.

Syncope and stroke

Despite the wide use of telemetry for patients admitted with syncope, current evidence does not support this practice. However, the AHA recommends routine telemetry for patients admitted with idiopathic syncope when there is a high level of suspicion for underlying cardiac arrhythmias as a cause of syncope (risk class II-b).³ In 30% of patients admitted with stroke or transient ischemic attack, the cause is cardioembolic. Therefore, telemetry is indicated to rule out an underlying cardiac cause.⁴

Critical illness

Patients hospitalized with major trauma, acute respiratory failure, sepsis, shock, or acute pulmonary embolism or for major noncardiac surgery (especially elderly patients with coronary artery disease or at high risk of coronary events) require cardiac telemetry (risk class I-b). Patients admitted with kidney failure, significant electrolyte abnormalities, drug or substance toxicity (especially with known arrhythmogenic drugs) also require cardiac telemetry at the time of admission (risk class I-b).

Recurrent palpitations, arrhythmia

Most patients with palpitations can be evaluated in an outpatient setting.⁵ However, patients hospitalized for recurrent palpitations or for suspected underlying cardiac disease require telemetric monitoring (risk class II-b).³ Patients with high-degree atrioventricular block admitted after percutaneous temporary pacemaker implantation should be monitored, as should patients with a permanent pacemaker for 12 to 24 hours after implantation (risk class I-c). Also, patients hospitalized after implantable cardioverter-defibrillator (ICD) shock need to be monitored.^3,6

Patients with a paced rhythm who do not meet the above criteria do not require routine telemetric monitoring (risk class III-c).⁷

Off-site telemetry monitoring can identify significant arrhythmias during hospitalization. It also saves time on nursing staff to focus on bedside patient care. However, its convenience can lower the threshold for ordering it. This can lead to overuse with a major impact on healthcare costs.

Routine use of cardiac telemetry is associated with increased hospitalization costs with little benefit.⁸ The use of off-site services for continuous monitoring can activate many alarms throughout the day, triggering unnecessary workups and leading to densensitization to alarms (“alarm fatigue”).⁹

Despite the precise indications outlined in the AHA updated practice standards for inpatient electrocardiographic monitoring,¹⁰ telemetry use is expanding to non-ICU units without evidence of benefit,⁸ and this overuse can result in harmful clinical outcomes and a financial burden. Telemetry monitoring of low-risk patients can cause delays in emergency department and ICU admissions and transfers^8,11 of patients who may be sicker and need intensive care.

In a prospective observational study,¹² only 11 (6%) of 182 patients admitted to a general medical floor met AHA class I criteria for telemetry; very few patients developed a significant telemetry event such as atrial fibrillation or flutter that necessitated a change in management. Most overprescribers of telemetry monitoring reason that it will catch arrhythmias early.¹² In fact, in a study of patients in a cardiac unit, telemetry detected just 50% of in-house cardiac arrest cases, with a potential survival benefit of only 0.02%.¹³

Another study showed that only 0.01% of all telemetry alarms represented a real emergency. Only 37.2% of emergency alarms were classified as clinically important, and only 48.3% of these led to a change in management within 1 hour.¹⁴

Moreover, in a report of trauma patients with abnormal results on ECG at the time of admission, telemetry had negligible clinical benefit.¹⁵ And in a study of 414 patients, only 4% of those admitted with chest pain and normal initial ECG had cardiac interventions.¹⁶

Another study⁸ showed that hospital intervention to restrict the use of telemetry guided by AHA recommendations resulted in a 43% reduction in telemetry orders, a 47% reduction in telemetry duration, and a 70% reduction in the mean daily number of patients monitored, with no changes in hospital census or rates of code blue, death, or rapid response team activation.⁸

The financial cost can be seen in the backup of patients in the emergency department. A study showed that 91% of patients being admitted for chest pain were delayed by more than 3 hours while waiting for monitored beds. This translated into an annual cost of $168,300 to the hospital.¹⁷ Adherence to guidelines for appropriate use of telemetry can significantly decrease costs. Applying a simple algorithm for telemetry use was shown⁸ to decrease daily non-ICU cardiac telemetry costs from $18,971 to $5,772.

CURRENT GUIDELINES ARE LIMITED

The current American College of Cardiology and AHA guidelines are based mostly on expert opinion rather than randomized clinical trials, while most telemetry trials have been performed on patients with a cardiac or possible cardiac diagnosis.³ Current guidelines need to be updated, and more studies are needed to specify the optimal duration of cardiac monitoring in indicated cases. Many noncardiac conditions raise a legitimate concern of dysrhythmia, an indication for cardiac monitoring, but precise recommendations for telemetry for such conditions are lacking.

RECOMMENDATIONS


Raising awareness of the clinical and financial burdens associated with unwise telemetry utilization is critical. We suggest use of a pop-up notification in the electronic medical record to remind the provider of the existing telemetry order and to specify the duration of telemetry monitoring when placing the initial order. The goal is to identify patients in true need of a telemetry bed, to decrease unnecessary testing, and to reduce hospitalization costs.

No. Continuous monitoring for changes in heart rhythm with cardiac telemetry is recommended for all patients admitted to an intensive care unit (ICU). But routine telemetry monitoring for patients in non-ICU beds is not recommended, as it leads to unnecessary testing and treatment, increasing the cost of care and hospital length of stay.

RISK STRATIFICATION AND INDICATIONS

Telemetry is generally recommended for patients admitted with any type of heart disease, including:

• Acute myocardial infarction with ST-segment elevation or Q waves on 12-lead electrocardiography (ECG)
• Acute ischemia suggested by ST-segment depression or T-wave inversion on ECG
• Systolic blood pressure less than 100 mm Hg
• Acute decompensated heart failure with bilateral rales above the lung bases
• Chest pain that is worse than or the same as that in prior angina or myocardial infarction.^1,2

Indications for telemetry are less clear in patients with no history of heart disease. The American Heart Association (AHA)³ has classified admitted patients based on the presence or absence of heart disease³:

• Class I (high risk of arrhythmia): acute coronary syndrome, new arrhythmia (eg, atrial fibrillation or flutter), severe electrolyte imbalance; telemetry is warranted
• Class II (moderate risk): acute decompensated heart failure with stable hemodynamic status, a surgical or medical diagnosis with underlying paced rhythms (ie, with a pacemaker), and chronic arrhythmia (atrial fibrillation or flutter); in these cases, telemetry monitoring may be considered
• Class III (low risk): no history of cardiac disease or arrhythmias, admitted for medical or surgical reasons; in these cases, telemetry is generally not indicated³

Telemetry should also be considered in patients admitted with syncope or stroke, critical illness, or palpitations.

Syncope and stroke

Despite the wide use of telemetry for patients admitted with syncope, current evidence does not support this practice. However, the AHA recommends routine telemetry for patients admitted with idiopathic syncope when there is a high level of suspicion for underlying cardiac arrhythmias as a cause of syncope (risk class II-b).³ In 30% of patients admitted with stroke or transient ischemic attack, the cause is cardioembolic. Therefore, telemetry is indicated to rule out an underlying cardiac cause.⁴

Critical illness

Patients hospitalized with major trauma, acute respiratory failure, sepsis, shock, or acute pulmonary embolism or for major noncardiac surgery (especially elderly patients with coronary artery disease or at high risk of coronary events) require cardiac telemetry (risk class I-b). Patients admitted with kidney failure, significant electrolyte abnormalities, drug or substance toxicity (especially with known arrhythmogenic drugs) also require cardiac telemetry at the time of admission (risk class I-b).

Recurrent palpitations, arrhythmia

Most patients with palpitations can be evaluated in an outpatient setting.⁵ However, patients hospitalized for recurrent palpitations or for suspected underlying cardiac disease require telemetric monitoring (risk class II-b).³ Patients with high-degree atrioventricular block admitted after percutaneous temporary pacemaker implantation should be monitored, as should patients with a permanent pacemaker for 12 to 24 hours after implantation (risk class I-c). Also, patients hospitalized after implantable cardioverter-defibrillator (ICD) shock need to be monitored.^3,6

Patients with a paced rhythm who do not meet the above criteria do not require routine telemetric monitoring (risk class III-c).⁷

Off-site telemetry monitoring can identify significant arrhythmias during hospitalization. It also saves time on nursing staff to focus on bedside patient care. However, its convenience can lower the threshold for ordering it. This can lead to overuse with a major impact on healthcare costs.

Routine use of cardiac telemetry is associated with increased hospitalization costs with little benefit.⁸ The use of off-site services for continuous monitoring can activate many alarms throughout the day, triggering unnecessary workups and leading to densensitization to alarms (“alarm fatigue”).⁹

Despite the precise indications outlined in the AHA updated practice standards for inpatient electrocardiographic monitoring,¹⁰ telemetry use is expanding to non-ICU units without evidence of benefit,⁸ and this overuse can result in harmful clinical outcomes and a financial burden. Telemetry monitoring of low-risk patients can cause delays in emergency department and ICU admissions and transfers^8,11 of patients who may be sicker and need intensive care.

In a prospective observational study,¹² only 11 (6%) of 182 patients admitted to a general medical floor met AHA class I criteria for telemetry; very few patients developed a significant telemetry event such as atrial fibrillation or flutter that necessitated a change in management. Most overprescribers of telemetry monitoring reason that it will catch arrhythmias early.¹² In fact, in a study of patients in a cardiac unit, telemetry detected just 50% of in-house cardiac arrest cases, with a potential survival benefit of only 0.02%.¹³

Another study showed that only 0.01% of all telemetry alarms represented a real emergency. Only 37.2% of emergency alarms were classified as clinically important, and only 48.3% of these led to a change in management within 1 hour.¹⁴

Moreover, in a report of trauma patients with abnormal results on ECG at the time of admission, telemetry had negligible clinical benefit.¹⁵ And in a study of 414 patients, only 4% of those admitted with chest pain and normal initial ECG had cardiac interventions.¹⁶

Another study⁸ showed that hospital intervention to restrict the use of telemetry guided by AHA recommendations resulted in a 43% reduction in telemetry orders, a 47% reduction in telemetry duration, and a 70% reduction in the mean daily number of patients monitored, with no changes in hospital census or rates of code blue, death, or rapid response team activation.⁸

The financial cost can be seen in the backup of patients in the emergency department. A study showed that 91% of patients being admitted for chest pain were delayed by more than 3 hours while waiting for monitored beds. This translated into an annual cost of $168,300 to the hospital.¹⁷ Adherence to guidelines for appropriate use of telemetry can significantly decrease costs. Applying a simple algorithm for telemetry use was shown⁸ to decrease daily non-ICU cardiac telemetry costs from $18,971 to $5,772.

CURRENT GUIDELINES ARE LIMITED

The current American College of Cardiology and AHA guidelines are based mostly on expert opinion rather than randomized clinical trials, while most telemetry trials have been performed on patients with a cardiac or possible cardiac diagnosis.³ Current guidelines need to be updated, and more studies are needed to specify the optimal duration of cardiac monitoring in indicated cases. Many noncardiac conditions raise a legitimate concern of dysrhythmia, an indication for cardiac monitoring, but precise recommendations for telemetry for such conditions are lacking.

RECOMMENDATIONS


Raising awareness of the clinical and financial burdens associated with unwise telemetry utilization is critical. We suggest use of a pop-up notification in the electronic medical record to remind the provider of the existing telemetry order and to specify the duration of telemetry monitoring when placing the initial order. The goal is to identify patients in true need of a telemetry bed, to decrease unnecessary testing, and to reduce hospitalization costs.

No. Continuous monitoring for changes in heart rhythm with cardiac telemetry is recommended for all patients admitted to an intensive care unit (ICU). But routine telemetry monitoring for patients in non-ICU beds is not recommended, as it leads to unnecessary testing and treatment, increasing the cost of care and hospital length of stay.

RISK STRATIFICATION AND INDICATIONS

Telemetry is generally recommended for patients admitted with any type of heart disease, including:

• Acute myocardial infarction with ST-segment elevation or Q waves on 12-lead electrocardiography (ECG)
• Acute ischemia suggested by ST-segment depression or T-wave inversion on ECG
• Systolic blood pressure less than 100 mm Hg
• Acute decompensated heart failure with bilateral rales above the lung bases
• Chest pain that is worse than or the same as that in prior angina or myocardial infarction.^1,2

Indications for telemetry are less clear in patients with no history of heart disease. The American Heart Association (AHA)³ has classified admitted patients based on the presence or absence of heart disease³:

• Class I (high risk of arrhythmia): acute coronary syndrome, new arrhythmia (eg, atrial fibrillation or flutter), severe electrolyte imbalance; telemetry is warranted
• Class II (moderate risk): acute decompensated heart failure with stable hemodynamic status, a surgical or medical diagnosis with underlying paced rhythms (ie, with a pacemaker), and chronic arrhythmia (atrial fibrillation or flutter); in these cases, telemetry monitoring may be considered
• Class III (low risk): no history of cardiac disease or arrhythmias, admitted for medical or surgical reasons; in these cases, telemetry is generally not indicated³

Telemetry should also be considered in patients admitted with syncope or stroke, critical illness, or palpitations.

Syncope and stroke

Despite the wide use of telemetry for patients admitted with syncope, current evidence does not support this practice. However, the AHA recommends routine telemetry for patients admitted with idiopathic syncope when there is a high level of suspicion for underlying cardiac arrhythmias as a cause of syncope (risk class II-b).³ In 30% of patients admitted with stroke or transient ischemic attack, the cause is cardioembolic. Therefore, telemetry is indicated to rule out an underlying cardiac cause.⁴

Critical illness

Patients hospitalized with major trauma, acute respiratory failure, sepsis, shock, or acute pulmonary embolism or for major noncardiac surgery (especially elderly patients with coronary artery disease or at high risk of coronary events) require cardiac telemetry (risk class I-b). Patients admitted with kidney failure, significant electrolyte abnormalities, drug or substance toxicity (especially with known arrhythmogenic drugs) also require cardiac telemetry at the time of admission (risk class I-b).

Recurrent palpitations, arrhythmia

Most patients with palpitations can be evaluated in an outpatient setting.⁵ However, patients hospitalized for recurrent palpitations or for suspected underlying cardiac disease require telemetric monitoring (risk class II-b).³ Patients with high-degree atrioventricular block admitted after percutaneous temporary pacemaker implantation should be monitored, as should patients with a permanent pacemaker for 12 to 24 hours after implantation (risk class I-c). Also, patients hospitalized after implantable cardioverter-defibrillator (ICD) shock need to be monitored.^3,6

Patients with a paced rhythm who do not meet the above criteria do not require routine telemetric monitoring (risk class III-c).⁷

Off-site telemetry monitoring can identify significant arrhythmias during hospitalization. It also saves time on nursing staff to focus on bedside patient care. However, its convenience can lower the threshold for ordering it. This can lead to overuse with a major impact on healthcare costs.

Routine use of cardiac telemetry is associated with increased hospitalization costs with little benefit.⁸ The use of off-site services for continuous monitoring can activate many alarms throughout the day, triggering unnecessary workups and leading to densensitization to alarms (“alarm fatigue”).⁹

Despite the precise indications outlined in the AHA updated practice standards for inpatient electrocardiographic monitoring,¹⁰ telemetry use is expanding to non-ICU units without evidence of benefit,⁸ and this overuse can result in harmful clinical outcomes and a financial burden. Telemetry monitoring of low-risk patients can cause delays in emergency department and ICU admissions and transfers^8,11 of patients who may be sicker and need intensive care.

In a prospective observational study,¹² only 11 (6%) of 182 patients admitted to a general medical floor met AHA class I criteria for telemetry; very few patients developed a significant telemetry event such as atrial fibrillation or flutter that necessitated a change in management. Most overprescribers of telemetry monitoring reason that it will catch arrhythmias early.¹² In fact, in a study of patients in a cardiac unit, telemetry detected just 50% of in-house cardiac arrest cases, with a potential survival benefit of only 0.02%.¹³

Another study showed that only 0.01% of all telemetry alarms represented a real emergency. Only 37.2% of emergency alarms were classified as clinically important, and only 48.3% of these led to a change in management within 1 hour.¹⁴

Moreover, in a report of trauma patients with abnormal results on ECG at the time of admission, telemetry had negligible clinical benefit.¹⁵ And in a study of 414 patients, only 4% of those admitted with chest pain and normal initial ECG had cardiac interventions.¹⁶

Another study⁸ showed that hospital intervention to restrict the use of telemetry guided by AHA recommendations resulted in a 43% reduction in telemetry orders, a 47% reduction in telemetry duration, and a 70% reduction in the mean daily number of patients monitored, with no changes in hospital census or rates of code blue, death, or rapid response team activation.⁸

The financial cost can be seen in the backup of patients in the emergency department. A study showed that 91% of patients being admitted for chest pain were delayed by more than 3 hours while waiting for monitored beds. This translated into an annual cost of $168,300 to the hospital.¹⁷ Adherence to guidelines for appropriate use of telemetry can significantly decrease costs. Applying a simple algorithm for telemetry use was shown⁸ to decrease daily non-ICU cardiac telemetry costs from $18,971 to $5,772.

CURRENT GUIDELINES ARE LIMITED

The current American College of Cardiology and AHA guidelines are based mostly on expert opinion rather than randomized clinical trials, while most telemetry trials have been performed on patients with a cardiac or possible cardiac diagnosis.³ Current guidelines need to be updated, and more studies are needed to specify the optimal duration of cardiac monitoring in indicated cases. Many noncardiac conditions raise a legitimate concern of dysrhythmia, an indication for cardiac monitoring, but precise recommendations for telemetry for such conditions are lacking.

RECOMMENDATIONS


Raising awareness of the clinical and financial burdens associated with unwise telemetry utilization is critical. We suggest use of a pop-up notification in the electronic medical record to remind the provider of the existing telemetry order and to specify the duration of telemetry monitoring when placing the initial order. The goal is to identify patients in true need of a telemetry bed, to decrease unnecessary testing, and to reduce hospitalization costs.

Telemedicine has been used successfully to improve patient access to medical care while reducing healthcare costs. In 2016, an estimated 61% of US healthcare institutions and 40% to 50% of US hospitals used telemedicine.¹ From 2012 to 2013, the telemedicine market grew by 60%. However, its widespread use has been limited by low reimbursement rates and interstate licensing and practice issues.

In this commentary, we discuss the history of telemedicine, current uses and challenges, and areas of future growth.

DEFINITION AND HISTORY

The World Health Organization defines telemedicine as “the delivery of health care services, where distance is a critical factor, by all health care professionals using information and communication technologies for the exchange of valid information for diagnosis, treatment and prevention of disease and injuries, research and evaluation, and for the continuing education of healthcare providers, all in the interests of advancing the health of individuals and their communities.”²

Modern telemedicine began in the early 1900s in the Netherlands with the transmission of heart rhythms over the telephone,³ which was followed by transmissions to radio consultation centers in Europe in the 1920s. In the 1940s, radiographic images were transmitted by telephone between cities in Pennsylvania.⁴

Today, telemedicine is used in a variety of specialties including radiology, neurology, and pathology⁵ and by organizations in the United States ranging from the National Aeronautics and Space Administration and Kaiser Permanente to the US Department of Veterans Affairs (VA). The VA, in particular, is a leader in telemedicine. In 2012, it reduced mental health hospitalizations by over 40%, heart failure hospitalizations by 25%, and diabetes and chronic obstructive pulmonary disease hospitalizations by about 20% using telemedicine programs.⁶ In 2015, it provided about 2.1 million telemedicine consultations to 677,000 veterans.⁷

TYPES OF TELEMEDICINE PROGRAMS

There are 2 types of telemedicine programs.

Synchronous programs take place in real time and are a live 2-way interaction between the patient and healthcare provider. This includes virtual appointments that are conducted using the patient’s smartphone, tablet, or computer with a camera. When using a smartphone or tablet, patients must first download an app that connects them with a provider.

Asynchronous programs, also known as “store and forward” applications, are not live and involve the transfer of images, videos, and other clinical information that a healthcare provider views and responds to at a later time. In this case, patients may wear medical devices to monitor and track health information (eg, blood pressure) in a personal health application that they forward to their healthcare provider.

IMPROVING PATIENT ACCESS TO CARE WHILE REDUCING COSTS

Telemedicine allows patients living in both rural and urban areas to access healthcare when they need it. Currently, about 59 million Americans reside in health professional-shortage areas, which are rural and urban areas with shortages of primary care providers.¹ These patients often experience long delays when attempting to schedule a healthcare visit⁷ and may experience issues with continuity of care if they are unable to see the same care provider at every visit.

It also provides access to care to patients without reliable transportation or those who may be too sick to travel long distances. For some patients, such as those with cystic fibrosis who do not want to come to the hospital for fear of contracting multiple antibiotic-resistant bacteria, a virtual office visit may be safer.

At the same time, telemedicine helps reduce healthcare costs. For example, it:

• Optimizes staff distribution and healthcare resources within a healthcare facility and across an entire system
• Enables primary care providers to conduct appointments without additional office staff at any time, thereby extending office hours and availability
• Reduces the financial impact of patient no-shows
• Improves patient engagement and outcomes
• Reduces unnecessary office and emergency room visits and hospital admissions.

The last point is especially important for senior living and skilled nursing centers whose residents are known to have high rates of hospital admissions.^8,9 In these facilities, 24-hour medical assistance may not be available, and telemedicine can help troubleshoot common problems.

LOW REIMBURSEMENT RATES CURTAIL USE

Limited reimbursement has curtailed the widespread use of telemedicine. Although rules for reimbursement are evolving, telemedicine still represents a small amount of total healthcare expenditures. In 2015, Medicare spent approximately $14.4 million on services delivered via telemedicine—less than 0.01% of total spending on healthcare services.¹

Currently, 31 states and the District of Columbia have telemedicine parity laws that mandate private commercial insurers to pay for telemedicine services.¹⁰ Unfortunately, there is a lack of uniformity in the specifics of these laws, resulting in variations in reimbursement rates. Furthermore, a large number of larger insurers such as Medicare and Medicaid and many self-insured plans do not fall under these mandates.

Another factor that affects reimbursement for telemedicine services is the setting of the medical encounter. Medicare reimburses providers for telemedicine services only when they are conducted at specific sites such as physician’s offices, hospitals, rural health centers, and skilled nursing facilities. Additionally, Medicare only reimburses for services in areas with a shortage of healthcare professionals and in non-metropolitan areas, which excludes many urban patients.¹¹

In contrast, more commercial reimbursement is occurring for online urgent care, and options for commercial reimbursement of online behavioral services are being explored.

Current licensure laws also limit the ability of many healthcare providers to offer telemedicine services. Federal law requires providers to be fully licensed to practice medicine in the state where the patient is physically located. In cases of health systems that have locations in more than one state, providers may need to apply for and pay to maintain multiple licenses (current interstate licensing laws vary across states).

Interstate licensure is one way to solve this problem. Thus far, a number of states have joined the Interstate Medical Licensure Compact that intends to allow physicians to obtain expedited licenses to practice in multiple states.¹²

The federal TELE-MED Act was introduced in 2015 but not passed. It proposed to “allow a Medicare provider to provide telemedicine services to a Medicare beneficiary who is in a different state from the one in which the provider is licensed or authorized to provide healthcare services.”

CAN TELEMEDICINE FOSTER A GOOD PROVIDER-PATIENT RELATIONSHIP?

In-person encounters provide healthcare providers with the opportunity to build a therapeutic relationship with their patients. Face-to-face encounters also increase patient satisfaction scores and outcomes. As such, critics fear that patient relationships may suffer with the use of telemedicine. However, using video technology for new patient encounters may help overcome this challenge. During a video encounter, the provider can see the patient’s facial expressions and take cues from nonverbal behaviors.

At times, the element of distance may enhance the encounter. For example, in behavioral health, patients often feel more comfortable in their home environment than in a sterile office environment.

Telemedicine patients often have positive experiences, given the speed of access, precision, time savings, and the ability to stay in contact with healthcare providers from the comfort of their homes. Ultimately, these virtual visits may help improve compliance with follow-up consultations since the barriers of distance and transportation are circumvented.

WHO CAN CONDUCT TELEMEDICINE VISITS?

Although a patient’s healthcare team is likely to consist of members who are not physicians, including nurse practitioners, physician assistants, social workers, and psychologists, not everyone can, by law, conduct telemedicine visits. Currently, the rules and regulations addressing ancillary team members’ participation in telemedicine vary from state to state.

TELEMEDICINE VISITS AT CLEVELAND CLINIC

Our health system has several telemedicine programs, including our eHospital program. Launched in 2014, this program provides patients at 4 hospitals with input from staff intensivists and experienced critical care nurses during the night (7 pm to 7 am) via remote monitoring. These remote caregivers have full access to patient charts and, when signalled, can activate an in-room camera to initiate 2-way audio communication with patients, their families, and bedside caregivers.

In addition, new patient consults are being offered via telemedicine for several services including dermatology, where pictures of skin lesions are reviewed and triaged, and management recommendations are provided accordingly.

In 2016, Cleveland Clinic launched its Remote Hypertension Improvement Program—an enterprise-wide initiative to minimize hypertension-associated mortality and morbidity with the assistance of telehealth services. The program was first piloted in a group of 80 high-risk hypertensive patients who were monitored and followed through a Bluetooth-enabled remote monitoring tool, which exported blood pressure readings to a central dashboard. A multidisciplinary team of doctors, nurses, and pharmacists used this dashboard to adjust medication when needed and provide virtual lifestyle coaching. Over a 24-week period, the patients’ systolic blood pressure decreased by an average of 7.5 mm Hg and diastolic blood pressure by 3.1 mm Hg (unpublished data).

Beginning this year, blood pressure readings will be directly exported from the remote monitoring tool into the patient’s electronic medical record, providing the healthcare team with the information needed to make informed decisions to remotely manage patients with hypertension.

Remote monitoring of patients with hypertension is also being used at other institutions such as the VA. In 2016, almost 19,000 veterans were using the remote monitoring system, and this number is expected to increase with the enhanced adaptation of telemedicine services.¹³

FUTURE DIRECTIONS

About 50% of all adults in the United States have at least 1 chronic disease. In all, chronic disease accounts for roughly 75% of the total healthcare expenditure and 70% of all deaths.^7,14 Recent data suggest that virtual chronic disease management represents an untapped market for telemedicine, given its relative underutilization compared to other services such as telebehavorial health and specialty telemedicine. These patients require frequent visits to the doctor, and targeting this patient population with telemedicine may decrease the number of emergency room visits and hospital admissions.

Another growing area in the field of telemedicine is the “hospital at home” model in which patients who meet the criteria for hospitalization but are otherwise stable are treated at home for diseases such as chronic obstructive pulmonary disease, pneumonia, and heart failure. Studies have shown that the hospital-at-home model, when used appropriately, is not only more cost-effective than hospitalization but results in a shorter treatment duration and lower rates of delirium.^15–17

Finally, in the acute setting, we have seen wide success with telemedicine programs in stroke care, radiology, intensive care, and psychiatry, and several studies have shown mortality rates comparable to those with the traditional model.^18,19 These encounters often require specialized skills and are the focus of multiple ongoing studies.           

Acknowledgment: The authors would like to acknowledge and thank Matthew Faiman, MD, for providing information regarding the Remote Hypertension Program.

Telemedicine has been used successfully to improve patient access to medical care while reducing healthcare costs. In 2016, an estimated 61% of US healthcare institutions and 40% to 50% of US hospitals used telemedicine.¹ From 2012 to 2013, the telemedicine market grew by 60%. However, its widespread use has been limited by low reimbursement rates and interstate licensing and practice issues.

In this commentary, we discuss the history of telemedicine, current uses and challenges, and areas of future growth.

DEFINITION AND HISTORY

The World Health Organization defines telemedicine as “the delivery of health care services, where distance is a critical factor, by all health care professionals using information and communication technologies for the exchange of valid information for diagnosis, treatment and prevention of disease and injuries, research and evaluation, and for the continuing education of healthcare providers, all in the interests of advancing the health of individuals and their communities.”²

Modern telemedicine began in the early 1900s in the Netherlands with the transmission of heart rhythms over the telephone,³ which was followed by transmissions to radio consultation centers in Europe in the 1920s. In the 1940s, radiographic images were transmitted by telephone between cities in Pennsylvania.⁴

Today, telemedicine is used in a variety of specialties including radiology, neurology, and pathology⁵ and by organizations in the United States ranging from the National Aeronautics and Space Administration and Kaiser Permanente to the US Department of Veterans Affairs (VA). The VA, in particular, is a leader in telemedicine. In 2012, it reduced mental health hospitalizations by over 40%, heart failure hospitalizations by 25%, and diabetes and chronic obstructive pulmonary disease hospitalizations by about 20% using telemedicine programs.⁶ In 2015, it provided about 2.1 million telemedicine consultations to 677,000 veterans.⁷

TYPES OF TELEMEDICINE PROGRAMS

There are 2 types of telemedicine programs.

Synchronous programs take place in real time and are a live 2-way interaction between the patient and healthcare provider. This includes virtual appointments that are conducted using the patient’s smartphone, tablet, or computer with a camera. When using a smartphone or tablet, patients must first download an app that connects them with a provider.

Asynchronous programs, also known as “store and forward” applications, are not live and involve the transfer of images, videos, and other clinical information that a healthcare provider views and responds to at a later time. In this case, patients may wear medical devices to monitor and track health information (eg, blood pressure) in a personal health application that they forward to their healthcare provider.

IMPROVING PATIENT ACCESS TO CARE WHILE REDUCING COSTS

Telemedicine allows patients living in both rural and urban areas to access healthcare when they need it. Currently, about 59 million Americans reside in health professional-shortage areas, which are rural and urban areas with shortages of primary care providers.¹ These patients often experience long delays when attempting to schedule a healthcare visit⁷ and may experience issues with continuity of care if they are unable to see the same care provider at every visit.

It also provides access to care to patients without reliable transportation or those who may be too sick to travel long distances. For some patients, such as those with cystic fibrosis who do not want to come to the hospital for fear of contracting multiple antibiotic-resistant bacteria, a virtual office visit may be safer.

At the same time, telemedicine helps reduce healthcare costs. For example, it:

• Optimizes staff distribution and healthcare resources within a healthcare facility and across an entire system
• Enables primary care providers to conduct appointments without additional office staff at any time, thereby extending office hours and availability
• Reduces the financial impact of patient no-shows
• Improves patient engagement and outcomes
• Reduces unnecessary office and emergency room visits and hospital admissions.

The last point is especially important for senior living and skilled nursing centers whose residents are known to have high rates of hospital admissions.^8,9 In these facilities, 24-hour medical assistance may not be available, and telemedicine can help troubleshoot common problems.

LOW REIMBURSEMENT RATES CURTAIL USE

Limited reimbursement has curtailed the widespread use of telemedicine. Although rules for reimbursement are evolving, telemedicine still represents a small amount of total healthcare expenditures. In 2015, Medicare spent approximately $14.4 million on services delivered via telemedicine—less than 0.01% of total spending on healthcare services.¹

Currently, 31 states and the District of Columbia have telemedicine parity laws that mandate private commercial insurers to pay for telemedicine services.¹⁰ Unfortunately, there is a lack of uniformity in the specifics of these laws, resulting in variations in reimbursement rates. Furthermore, a large number of larger insurers such as Medicare and Medicaid and many self-insured plans do not fall under these mandates.

Another factor that affects reimbursement for telemedicine services is the setting of the medical encounter. Medicare reimburses providers for telemedicine services only when they are conducted at specific sites such as physician’s offices, hospitals, rural health centers, and skilled nursing facilities. Additionally, Medicare only reimburses for services in areas with a shortage of healthcare professionals and in non-metropolitan areas, which excludes many urban patients.¹¹

In contrast, more commercial reimbursement is occurring for online urgent care, and options for commercial reimbursement of online behavioral services are being explored.

Current licensure laws also limit the ability of many healthcare providers to offer telemedicine services. Federal law requires providers to be fully licensed to practice medicine in the state where the patient is physically located. In cases of health systems that have locations in more than one state, providers may need to apply for and pay to maintain multiple licenses (current interstate licensing laws vary across states).

Interstate licensure is one way to solve this problem. Thus far, a number of states have joined the Interstate Medical Licensure Compact that intends to allow physicians to obtain expedited licenses to practice in multiple states.¹²

The federal TELE-MED Act was introduced in 2015 but not passed. It proposed to “allow a Medicare provider to provide telemedicine services to a Medicare beneficiary who is in a different state from the one in which the provider is licensed or authorized to provide healthcare services.”

CAN TELEMEDICINE FOSTER A GOOD PROVIDER-PATIENT RELATIONSHIP?

In-person encounters provide healthcare providers with the opportunity to build a therapeutic relationship with their patients. Face-to-face encounters also increase patient satisfaction scores and outcomes. As such, critics fear that patient relationships may suffer with the use of telemedicine. However, using video technology for new patient encounters may help overcome this challenge. During a video encounter, the provider can see the patient’s facial expressions and take cues from nonverbal behaviors.

At times, the element of distance may enhance the encounter. For example, in behavioral health, patients often feel more comfortable in their home environment than in a sterile office environment.

Telemedicine patients often have positive experiences, given the speed of access, precision, time savings, and the ability to stay in contact with healthcare providers from the comfort of their homes. Ultimately, these virtual visits may help improve compliance with follow-up consultations since the barriers of distance and transportation are circumvented.

WHO CAN CONDUCT TELEMEDICINE VISITS?

Although a patient’s healthcare team is likely to consist of members who are not physicians, including nurse practitioners, physician assistants, social workers, and psychologists, not everyone can, by law, conduct telemedicine visits. Currently, the rules and regulations addressing ancillary team members’ participation in telemedicine vary from state to state.

TELEMEDICINE VISITS AT CLEVELAND CLINIC

Our health system has several telemedicine programs, including our eHospital program. Launched in 2014, this program provides patients at 4 hospitals with input from staff intensivists and experienced critical care nurses during the night (7 pm to 7 am) via remote monitoring. These remote caregivers have full access to patient charts and, when signalled, can activate an in-room camera to initiate 2-way audio communication with patients, their families, and bedside caregivers.

In addition, new patient consults are being offered via telemedicine for several services including dermatology, where pictures of skin lesions are reviewed and triaged, and management recommendations are provided accordingly.

In 2016, Cleveland Clinic launched its Remote Hypertension Improvement Program—an enterprise-wide initiative to minimize hypertension-associated mortality and morbidity with the assistance of telehealth services. The program was first piloted in a group of 80 high-risk hypertensive patients who were monitored and followed through a Bluetooth-enabled remote monitoring tool, which exported blood pressure readings to a central dashboard. A multidisciplinary team of doctors, nurses, and pharmacists used this dashboard to adjust medication when needed and provide virtual lifestyle coaching. Over a 24-week period, the patients’ systolic blood pressure decreased by an average of 7.5 mm Hg and diastolic blood pressure by 3.1 mm Hg (unpublished data).

Beginning this year, blood pressure readings will be directly exported from the remote monitoring tool into the patient’s electronic medical record, providing the healthcare team with the information needed to make informed decisions to remotely manage patients with hypertension.

Remote monitoring of patients with hypertension is also being used at other institutions such as the VA. In 2016, almost 19,000 veterans were using the remote monitoring system, and this number is expected to increase with the enhanced adaptation of telemedicine services.¹³

FUTURE DIRECTIONS

About 50% of all adults in the United States have at least 1 chronic disease. In all, chronic disease accounts for roughly 75% of the total healthcare expenditure and 70% of all deaths.^7,14 Recent data suggest that virtual chronic disease management represents an untapped market for telemedicine, given its relative underutilization compared to other services such as telebehavorial health and specialty telemedicine. These patients require frequent visits to the doctor, and targeting this patient population with telemedicine may decrease the number of emergency room visits and hospital admissions.

Another growing area in the field of telemedicine is the “hospital at home” model in which patients who meet the criteria for hospitalization but are otherwise stable are treated at home for diseases such as chronic obstructive pulmonary disease, pneumonia, and heart failure. Studies have shown that the hospital-at-home model, when used appropriately, is not only more cost-effective than hospitalization but results in a shorter treatment duration and lower rates of delirium.^15–17

Finally, in the acute setting, we have seen wide success with telemedicine programs in stroke care, radiology, intensive care, and psychiatry, and several studies have shown mortality rates comparable to those with the traditional model.^18,19 These encounters often require specialized skills and are the focus of multiple ongoing studies.           

Acknowledgment: The authors would like to acknowledge and thank Matthew Faiman, MD, for providing information regarding the Remote Hypertension Program.

Telemedicine has been used successfully to improve patient access to medical care while reducing healthcare costs. In 2016, an estimated 61% of US healthcare institutions and 40% to 50% of US hospitals used telemedicine.¹ From 2012 to 2013, the telemedicine market grew by 60%. However, its widespread use has been limited by low reimbursement rates and interstate licensing and practice issues.

In this commentary, we discuss the history of telemedicine, current uses and challenges, and areas of future growth.

DEFINITION AND HISTORY

The World Health Organization defines telemedicine as “the delivery of health care services, where distance is a critical factor, by all health care professionals using information and communication technologies for the exchange of valid information for diagnosis, treatment and prevention of disease and injuries, research and evaluation, and for the continuing education of healthcare providers, all in the interests of advancing the health of individuals and their communities.”²

Modern telemedicine began in the early 1900s in the Netherlands with the transmission of heart rhythms over the telephone,³ which was followed by transmissions to radio consultation centers in Europe in the 1920s. In the 1940s, radiographic images were transmitted by telephone between cities in Pennsylvania.⁴

Today, telemedicine is used in a variety of specialties including radiology, neurology, and pathology⁵ and by organizations in the United States ranging from the National Aeronautics and Space Administration and Kaiser Permanente to the US Department of Veterans Affairs (VA). The VA, in particular, is a leader in telemedicine. In 2012, it reduced mental health hospitalizations by over 40%, heart failure hospitalizations by 25%, and diabetes and chronic obstructive pulmonary disease hospitalizations by about 20% using telemedicine programs.⁶ In 2015, it provided about 2.1 million telemedicine consultations to 677,000 veterans.⁷

TYPES OF TELEMEDICINE PROGRAMS

There are 2 types of telemedicine programs.

Synchronous programs take place in real time and are a live 2-way interaction between the patient and healthcare provider. This includes virtual appointments that are conducted using the patient’s smartphone, tablet, or computer with a camera. When using a smartphone or tablet, patients must first download an app that connects them with a provider.

Asynchronous programs, also known as “store and forward” applications, are not live and involve the transfer of images, videos, and other clinical information that a healthcare provider views and responds to at a later time. In this case, patients may wear medical devices to monitor and track health information (eg, blood pressure) in a personal health application that they forward to their healthcare provider.

IMPROVING PATIENT ACCESS TO CARE WHILE REDUCING COSTS

Telemedicine allows patients living in both rural and urban areas to access healthcare when they need it. Currently, about 59 million Americans reside in health professional-shortage areas, which are rural and urban areas with shortages of primary care providers.¹ These patients often experience long delays when attempting to schedule a healthcare visit⁷ and may experience issues with continuity of care if they are unable to see the same care provider at every visit.

It also provides access to care to patients without reliable transportation or those who may be too sick to travel long distances. For some patients, such as those with cystic fibrosis who do not want to come to the hospital for fear of contracting multiple antibiotic-resistant bacteria, a virtual office visit may be safer.

At the same time, telemedicine helps reduce healthcare costs. For example, it:

• Optimizes staff distribution and healthcare resources within a healthcare facility and across an entire system
• Enables primary care providers to conduct appointments without additional office staff at any time, thereby extending office hours and availability
• Reduces the financial impact of patient no-shows
• Improves patient engagement and outcomes
• Reduces unnecessary office and emergency room visits and hospital admissions.

The last point is especially important for senior living and skilled nursing centers whose residents are known to have high rates of hospital admissions.^8,9 In these facilities, 24-hour medical assistance may not be available, and telemedicine can help troubleshoot common problems.

LOW REIMBURSEMENT RATES CURTAIL USE

Limited reimbursement has curtailed the widespread use of telemedicine. Although rules for reimbursement are evolving, telemedicine still represents a small amount of total healthcare expenditures. In 2015, Medicare spent approximately $14.4 million on services delivered via telemedicine—less than 0.01% of total spending on healthcare services.¹

Currently, 31 states and the District of Columbia have telemedicine parity laws that mandate private commercial insurers to pay for telemedicine services.¹⁰ Unfortunately, there is a lack of uniformity in the specifics of these laws, resulting in variations in reimbursement rates. Furthermore, a large number of larger insurers such as Medicare and Medicaid and many self-insured plans do not fall under these mandates.

Another factor that affects reimbursement for telemedicine services is the setting of the medical encounter. Medicare reimburses providers for telemedicine services only when they are conducted at specific sites such as physician’s offices, hospitals, rural health centers, and skilled nursing facilities. Additionally, Medicare only reimburses for services in areas with a shortage of healthcare professionals and in non-metropolitan areas, which excludes many urban patients.¹¹

In contrast, more commercial reimbursement is occurring for online urgent care, and options for commercial reimbursement of online behavioral services are being explored.

Current licensure laws also limit the ability of many healthcare providers to offer telemedicine services. Federal law requires providers to be fully licensed to practice medicine in the state where the patient is physically located. In cases of health systems that have locations in more than one state, providers may need to apply for and pay to maintain multiple licenses (current interstate licensing laws vary across states).

Interstate licensure is one way to solve this problem. Thus far, a number of states have joined the Interstate Medical Licensure Compact that intends to allow physicians to obtain expedited licenses to practice in multiple states.¹²

The federal TELE-MED Act was introduced in 2015 but not passed. It proposed to “allow a Medicare provider to provide telemedicine services to a Medicare beneficiary who is in a different state from the one in which the provider is licensed or authorized to provide healthcare services.”

CAN TELEMEDICINE FOSTER A GOOD PROVIDER-PATIENT RELATIONSHIP?

In-person encounters provide healthcare providers with the opportunity to build a therapeutic relationship with their patients. Face-to-face encounters also increase patient satisfaction scores and outcomes. As such, critics fear that patient relationships may suffer with the use of telemedicine. However, using video technology for new patient encounters may help overcome this challenge. During a video encounter, the provider can see the patient’s facial expressions and take cues from nonverbal behaviors.

At times, the element of distance may enhance the encounter. For example, in behavioral health, patients often feel more comfortable in their home environment than in a sterile office environment.

Telemedicine patients often have positive experiences, given the speed of access, precision, time savings, and the ability to stay in contact with healthcare providers from the comfort of their homes. Ultimately, these virtual visits may help improve compliance with follow-up consultations since the barriers of distance and transportation are circumvented.

WHO CAN CONDUCT TELEMEDICINE VISITS?

Although a patient’s healthcare team is likely to consist of members who are not physicians, including nurse practitioners, physician assistants, social workers, and psychologists, not everyone can, by law, conduct telemedicine visits. Currently, the rules and regulations addressing ancillary team members’ participation in telemedicine vary from state to state.

TELEMEDICINE VISITS AT CLEVELAND CLINIC

Our health system has several telemedicine programs, including our eHospital program. Launched in 2014, this program provides patients at 4 hospitals with input from staff intensivists and experienced critical care nurses during the night (7 pm to 7 am) via remote monitoring. These remote caregivers have full access to patient charts and, when signalled, can activate an in-room camera to initiate 2-way audio communication with patients, their families, and bedside caregivers.

In addition, new patient consults are being offered via telemedicine for several services including dermatology, where pictures of skin lesions are reviewed and triaged, and management recommendations are provided accordingly.

In 2016, Cleveland Clinic launched its Remote Hypertension Improvement Program—an enterprise-wide initiative to minimize hypertension-associated mortality and morbidity with the assistance of telehealth services. The program was first piloted in a group of 80 high-risk hypertensive patients who were monitored and followed through a Bluetooth-enabled remote monitoring tool, which exported blood pressure readings to a central dashboard. A multidisciplinary team of doctors, nurses, and pharmacists used this dashboard to adjust medication when needed and provide virtual lifestyle coaching. Over a 24-week period, the patients’ systolic blood pressure decreased by an average of 7.5 mm Hg and diastolic blood pressure by 3.1 mm Hg (unpublished data).

Beginning this year, blood pressure readings will be directly exported from the remote monitoring tool into the patient’s electronic medical record, providing the healthcare team with the information needed to make informed decisions to remotely manage patients with hypertension.

Remote monitoring of patients with hypertension is also being used at other institutions such as the VA. In 2016, almost 19,000 veterans were using the remote monitoring system, and this number is expected to increase with the enhanced adaptation of telemedicine services.¹³

FUTURE DIRECTIONS

About 50% of all adults in the United States have at least 1 chronic disease. In all, chronic disease accounts for roughly 75% of the total healthcare expenditure and 70% of all deaths.^7,14 Recent data suggest that virtual chronic disease management represents an untapped market for telemedicine, given its relative underutilization compared to other services such as telebehavorial health and specialty telemedicine. These patients require frequent visits to the doctor, and targeting this patient population with telemedicine may decrease the number of emergency room visits and hospital admissions.

Another growing area in the field of telemedicine is the “hospital at home” model in which patients who meet the criteria for hospitalization but are otherwise stable are treated at home for diseases such as chronic obstructive pulmonary disease, pneumonia, and heart failure. Studies have shown that the hospital-at-home model, when used appropriately, is not only more cost-effective than hospitalization but results in a shorter treatment duration and lower rates of delirium.^15–17

Finally, in the acute setting, we have seen wide success with telemedicine programs in stroke care, radiology, intensive care, and psychiatry, and several studies have shown mortality rates comparable to those with the traditional model.^18,19 These encounters often require specialized skills and are the focus of multiple ongoing studies.           

Acknowledgment: The authors would like to acknowledge and thank Matthew Faiman, MD, for providing information regarding the Remote Hypertension Program.

The narrative review by Modesto-Lowe et al¹ in this issue on the potential therapeutic use of cannabis for peripheral neuropathy is only the latest in a vogue string of examinations on how medical marijuana may be used to manage complex conditions. While the authors should be lauded for acknowledging that the role of cannabis in treating peripheral neuropathy is far from settled (“the unknown” in their title), the high stakes involved warrant even more stringent scrutiny than they suggest.

See related article

We are in the midst of an epidemic of chronic opioid use with massive repercussions, and it did not start overnight. Mounting calls for liberalizing narcotic use across a broad range of pain conditions accumulated gradually during the patient-advocacy era of the 1990s, with supporting “evidence” coming mostly from small uncontrolled studies, anecdotal reports, and industry pressure.² Although cannabis and opioids are not interchangeable, we should be cautious about concluding that cannabis is effective and that it should be used to treat chronic pain.

CHRONIC PAIN IS COMPLICATED

Peripheral neuropathy, by definition, is a chronic pain condition. Unlike acute pain, chronic pain is characterized by biologic, psychologic, and social complexities that require nuance to manage and study.

Such nuance is lacking in most recent reviews of the medical use of cannabis. The conditions in question are often studied as if they were transient and acute, eg, employing short-term studies and rudimentary measures such as numeric pain-rating scales or other snapshots of pain intensity. Results of these shortsighted assessments are impossible to extrapolate to long-term outcomes.

Whether cannabis therapy for chronic pain conditions is sustainable remains to be seen. Outcomes in chronic pain should not be defined simply by pain reduction, but by other dimensions such as changes in pain-related disability and quality of life, development of pharmacologic tolerance or dependence, adverse effects, and other “collateral damage.” We are far from understanding these issues, which require highly controlled and regulated longitudinal studies.

A recent Cochrane review³ of the efficacy of cannabis-based medicines for chronic neuropathic pain found that harms might outweigh the benefits. The quality of evidence was rated as very low to moderate; the reviewers cited small sample sizes and exclusion of important subgroups of patients (eg, those with substance abuse or other psychiatric comorbidities). Such exclusions are the crux of a major problem with cannabis research: studies are not naturalistic. The gritty reality of chronic pain management is paramount, and failing to consider the high-risk biopsychosocial factors typical of patients with chronic pain is naïve and, frankly, dangerous.

The true danger of cannabis lies in what we already know with certainty. As the authors discuss, cannabis undisputedly results in dose-dependent cognitive and motivational problems. If we are preaching physical therapy and home exercise to counter deconditioning, socialization to reverse depression, cognitive-behavioral therapy to increase coping, returning to work to prevent prolonged disability, and other active measures to prevent pain from becoming chronic, then why would we suggest treatments known to blunt motivation, energy, concentration, and overall mood? As a general central nervous system suppressant,⁴ cannabis works broadly against our best efforts to rehabilitate patients and restore their overall function.

ALL CANNABIS IS NOT THE SAME

The authors use the general term cannabis in their title, yet rightly unpack the differences between medical marijuana, tetrahydrocannabinol (THC), and cannabidiol (CBD). However, in the minds of untrained and pain-stricken patients seeking rapid relief and practical solutions, such distinctions are likely irrelevant.

The danger in the barrage of publications examining cannabis vs medical marijuana vs THC vs CBD is that they all communicate an unintentional yet problematic message: that marijuana of some sort for pain is acceptable to try. And in the face of financial pressures, changing legal landscapes, insurance coverage volatility, and access issues, are patients really going to always secure prescriptions for well-regulated CBD (lacking psychoactive THC) from thoughtful and well-informed physicians, or will they turn to convenient street suppliers?

Simplified perceptions of safety and efficacy across all cannabis products do not help. More troublesome would be to extrapolate safety to other forms of marijuana known to be dangerous, such as synthetic cannabinoids, which in some instances have been associated with catastrophic outcomes.⁵ The slippery slope is real: if the message becomes that some (or most) marijuana is benign or even therapeutic, what is to curb a widespread and unregulated epidemic?

YOUTH AT RISK

Some groups are more vulnerable than others to the potential negative effects of cannabis. In a study at a medical cannabis dispensary in San Francisco,⁶ adolescents and young adults used more marijuana than older users did and had higher rates of “use when bored” and eventual pharmacologic dependence. Sustained use of marijuana by young people places them at risk of serious psychiatric disorders, with numerous studies demonstrating the unfolding of schizophrenia, depression, bipolar disorder, and more.⁷

As the authors point out, cannabis may be contraindicated in those already burdened with mental health problems. If we recall that comorbid psychiatric disorders are the norm rather than the exception in chronic pain conditions,⁸ can we recommend cannabis therapy for most patients with chronic pain with confidence that it will not cause unintended problems? Evidence already shows that even well-established medical marijuana services attract (and perhaps unintentionally debilitate) a certain high-risk demographic: young, socioeconomically disadvantaged men with other comorbid psychiatric and substance use disorders, who ultimately rank poorly in functional health measures compared with the general population.⁹

NOT REEFER MADNESS, BUT REEFER CAUTION

I am not advocating the fear-mongering misinformation campaigns of the past. We should not exaggerate and warn about “reefer madness” or equate marijuana with untruths about random violence or complete bedlam. Nonetheless, concerns for widespread amotivation, worsening psychiatric states, chronic disability, and chemical dependence are very real.

Needed are tightly regulated, well-controlled, and long-term prospective studies involving isolated CBD formulations lacking THC. Over time, perhaps only formulations approved by the US Food and Drug Administration will be embraced. In the meantime, more comprehensive approaches should be recommended, such as team-based interdisciplinary rehabilitation programs that have shown efficacy in handling chronic pain complexities.^10,11

If such steps are unlikely, physicians should nonetheless stand united in sending a message of cautious optimism regarding medical marijuana, educating their patients not only about recently advertised potential yet inconclusive benefits, but also about the well-known and actual certitudes of its harms for use in chronic pain management. There is plenty of bad and worse information to share with patients, and there is a slippery slope of epidemic proportions to be wary about.

The narrative review by Modesto-Lowe et al¹ in this issue on the potential therapeutic use of cannabis for peripheral neuropathy is only the latest in a vogue string of examinations on how medical marijuana may be used to manage complex conditions. While the authors should be lauded for acknowledging that the role of cannabis in treating peripheral neuropathy is far from settled (“the unknown” in their title), the high stakes involved warrant even more stringent scrutiny than they suggest.

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We are in the midst of an epidemic of chronic opioid use with massive repercussions, and it did not start overnight. Mounting calls for liberalizing narcotic use across a broad range of pain conditions accumulated gradually during the patient-advocacy era of the 1990s, with supporting “evidence” coming mostly from small uncontrolled studies, anecdotal reports, and industry pressure.² Although cannabis and opioids are not interchangeable, we should be cautious about concluding that cannabis is effective and that it should be used to treat chronic pain.

CHRONIC PAIN IS COMPLICATED

Peripheral neuropathy, by definition, is a chronic pain condition. Unlike acute pain, chronic pain is characterized by biologic, psychologic, and social complexities that require nuance to manage and study.

Such nuance is lacking in most recent reviews of the medical use of cannabis. The conditions in question are often studied as if they were transient and acute, eg, employing short-term studies and rudimentary measures such as numeric pain-rating scales or other snapshots of pain intensity. Results of these shortsighted assessments are impossible to extrapolate to long-term outcomes.

Whether cannabis therapy for chronic pain conditions is sustainable remains to be seen. Outcomes in chronic pain should not be defined simply by pain reduction, but by other dimensions such as changes in pain-related disability and quality of life, development of pharmacologic tolerance or dependence, adverse effects, and other “collateral damage.” We are far from understanding these issues, which require highly controlled and regulated longitudinal studies.

A recent Cochrane review³ of the efficacy of cannabis-based medicines for chronic neuropathic pain found that harms might outweigh the benefits. The quality of evidence was rated as very low to moderate; the reviewers cited small sample sizes and exclusion of important subgroups of patients (eg, those with substance abuse or other psychiatric comorbidities). Such exclusions are the crux of a major problem with cannabis research: studies are not naturalistic. The gritty reality of chronic pain management is paramount, and failing to consider the high-risk biopsychosocial factors typical of patients with chronic pain is naïve and, frankly, dangerous.

The true danger of cannabis lies in what we already know with certainty. As the authors discuss, cannabis undisputedly results in dose-dependent cognitive and motivational problems. If we are preaching physical therapy and home exercise to counter deconditioning, socialization to reverse depression, cognitive-behavioral therapy to increase coping, returning to work to prevent prolonged disability, and other active measures to prevent pain from becoming chronic, then why would we suggest treatments known to blunt motivation, energy, concentration, and overall mood? As a general central nervous system suppressant,⁴ cannabis works broadly against our best efforts to rehabilitate patients and restore their overall function.

ALL CANNABIS IS NOT THE SAME

The authors use the general term cannabis in their title, yet rightly unpack the differences between medical marijuana, tetrahydrocannabinol (THC), and cannabidiol (CBD). However, in the minds of untrained and pain-stricken patients seeking rapid relief and practical solutions, such distinctions are likely irrelevant.

The danger in the barrage of publications examining cannabis vs medical marijuana vs THC vs CBD is that they all communicate an unintentional yet problematic message: that marijuana of some sort for pain is acceptable to try. And in the face of financial pressures, changing legal landscapes, insurance coverage volatility, and access issues, are patients really going to always secure prescriptions for well-regulated CBD (lacking psychoactive THC) from thoughtful and well-informed physicians, or will they turn to convenient street suppliers?

Simplified perceptions of safety and efficacy across all cannabis products do not help. More troublesome would be to extrapolate safety to other forms of marijuana known to be dangerous, such as synthetic cannabinoids, which in some instances have been associated with catastrophic outcomes.⁵ The slippery slope is real: if the message becomes that some (or most) marijuana is benign or even therapeutic, what is to curb a widespread and unregulated epidemic?

YOUTH AT RISK

Some groups are more vulnerable than others to the potential negative effects of cannabis. In a study at a medical cannabis dispensary in San Francisco,⁶ adolescents and young adults used more marijuana than older users did and had higher rates of “use when bored” and eventual pharmacologic dependence. Sustained use of marijuana by young people places them at risk of serious psychiatric disorders, with numerous studies demonstrating the unfolding of schizophrenia, depression, bipolar disorder, and more.⁷

As the authors point out, cannabis may be contraindicated in those already burdened with mental health problems. If we recall that comorbid psychiatric disorders are the norm rather than the exception in chronic pain conditions,⁸ can we recommend cannabis therapy for most patients with chronic pain with confidence that it will not cause unintended problems? Evidence already shows that even well-established medical marijuana services attract (and perhaps unintentionally debilitate) a certain high-risk demographic: young, socioeconomically disadvantaged men with other comorbid psychiatric and substance use disorders, who ultimately rank poorly in functional health measures compared with the general population.⁹

NOT REEFER MADNESS, BUT REEFER CAUTION

I am not advocating the fear-mongering misinformation campaigns of the past. We should not exaggerate and warn about “reefer madness” or equate marijuana with untruths about random violence or complete bedlam. Nonetheless, concerns for widespread amotivation, worsening psychiatric states, chronic disability, and chemical dependence are very real.

Needed are tightly regulated, well-controlled, and long-term prospective studies involving isolated CBD formulations lacking THC. Over time, perhaps only formulations approved by the US Food and Drug Administration will be embraced. In the meantime, more comprehensive approaches should be recommended, such as team-based interdisciplinary rehabilitation programs that have shown efficacy in handling chronic pain complexities.^10,11

If such steps are unlikely, physicians should nonetheless stand united in sending a message of cautious optimism regarding medical marijuana, educating their patients not only about recently advertised potential yet inconclusive benefits, but also about the well-known and actual certitudes of its harms for use in chronic pain management. There is plenty of bad and worse information to share with patients, and there is a slippery slope of epidemic proportions to be wary about.