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Radiation exposure exceeds 50 mSv in 2% of ICU patients
MONTREAL – Some of the sickest patients treated at U.S. hospitals receive high levels of radiation exposure, based on a review of more than 4,000 medical ICU patients treated recently at one U.S. quaternary-care center.
During 2013, 98 patients admitted to the medical ICU at the Cleveland Clinic – 2% of the 4,155 patients who passed through the medical ICU that year – had cumulative radiation exposure of at least 50 mSv while in the ICU, thereby exceeding the U.S. standard for maximum annual workplace exposure, Dr. Sudhir Krishnan said at the annual meeting of the American College of Chest Physicians. The finding raises questions of whether all these exposures are appropriate and whether they reflect overuse of certain imaging modalities.
Dr. Krishnan and his associates ran a retrospective review of case records for the medical ICU–admitted patients at the Cleveland Clinic during 2013 (Chest. 2015 Oct 25. doi: 10.1378/chest.2278486). During their ICU stay, 3,490 patients (84%) received some amount of radiation exposure. Exposure averaged 7 mSv, with a median of 1.5 mSv. The radiation exposure came primarily from imaging and more specifically from CT examinations, which produced more than half of all radiation-exposure episodes. Other sources included x-rays, nuclear scans, and interventional procedures.
Based on typical radiation dosages received during each type of procedure, the researchers calculated an estimated total radiation dosage received by each patient during their ICU stay. Nearly two-thirds of patients had an exposure of less than 3 mSv, the average annual exposure a person receives from ambient radiation. A quarter of the patients had an exposure of 3-14 mSv, 11% had an exposure of 15-49 mSv, and 2% – 98 patients – had exposure during their ICU stay that ran to 50 mSv or greater, exceeding the U.S. workplace annual maximum . Thirteen patients had an exposure level during their ICU stay that reached 100 mSv or higher; the maximum exposure level was in a patient with cumulative exposure of 176 mSv, said Dr. Krishnan, a critical-care medicine specialist at the Cleveland Clinic.
He and his coworkers did a multivariate analysis to identify factors that linked with a higher likelihood of having high radiation exposure. Patients at greatest risk for high exposure levels were sicker patients with higher APACHE 3 scores, longer stays in the ICU, and the presence of cirrhosis, but those most at risk also tended to be younger. Rates of both ICU deaths and deaths during the entire hospitalization were significantly higher among those with radiation exposure that was 50 mSv or greater.
Dr. Krishnan cautioned that he has not run any analysis that assessed the appropriateness of the imaging that the ICU patients received, nor did he have any data documenting the clinical consequences to the patients who had higher radiation exposure. Despite that uncertainty, he suggested that efforts focus on avoiding unnecessary radiation exposure to patients.
On Twitter @mitchelzoler
MONTREAL – Some of the sickest patients treated at U.S. hospitals receive high levels of radiation exposure, based on a review of more than 4,000 medical ICU patients treated recently at one U.S. quaternary-care center.
During 2013, 98 patients admitted to the medical ICU at the Cleveland Clinic – 2% of the 4,155 patients who passed through the medical ICU that year – had cumulative radiation exposure of at least 50 mSv while in the ICU, thereby exceeding the U.S. standard for maximum annual workplace exposure, Dr. Sudhir Krishnan said at the annual meeting of the American College of Chest Physicians. The finding raises questions of whether all these exposures are appropriate and whether they reflect overuse of certain imaging modalities.
Dr. Krishnan and his associates ran a retrospective review of case records for the medical ICU–admitted patients at the Cleveland Clinic during 2013 (Chest. 2015 Oct 25. doi: 10.1378/chest.2278486). During their ICU stay, 3,490 patients (84%) received some amount of radiation exposure. Exposure averaged 7 mSv, with a median of 1.5 mSv. The radiation exposure came primarily from imaging and more specifically from CT examinations, which produced more than half of all radiation-exposure episodes. Other sources included x-rays, nuclear scans, and interventional procedures.
Based on typical radiation dosages received during each type of procedure, the researchers calculated an estimated total radiation dosage received by each patient during their ICU stay. Nearly two-thirds of patients had an exposure of less than 3 mSv, the average annual exposure a person receives from ambient radiation. A quarter of the patients had an exposure of 3-14 mSv, 11% had an exposure of 15-49 mSv, and 2% – 98 patients – had exposure during their ICU stay that ran to 50 mSv or greater, exceeding the U.S. workplace annual maximum . Thirteen patients had an exposure level during their ICU stay that reached 100 mSv or higher; the maximum exposure level was in a patient with cumulative exposure of 176 mSv, said Dr. Krishnan, a critical-care medicine specialist at the Cleveland Clinic.
He and his coworkers did a multivariate analysis to identify factors that linked with a higher likelihood of having high radiation exposure. Patients at greatest risk for high exposure levels were sicker patients with higher APACHE 3 scores, longer stays in the ICU, and the presence of cirrhosis, but those most at risk also tended to be younger. Rates of both ICU deaths and deaths during the entire hospitalization were significantly higher among those with radiation exposure that was 50 mSv or greater.
Dr. Krishnan cautioned that he has not run any analysis that assessed the appropriateness of the imaging that the ICU patients received, nor did he have any data documenting the clinical consequences to the patients who had higher radiation exposure. Despite that uncertainty, he suggested that efforts focus on avoiding unnecessary radiation exposure to patients.
On Twitter @mitchelzoler
MONTREAL – Some of the sickest patients treated at U.S. hospitals receive high levels of radiation exposure, based on a review of more than 4,000 medical ICU patients treated recently at one U.S. quaternary-care center.
During 2013, 98 patients admitted to the medical ICU at the Cleveland Clinic – 2% of the 4,155 patients who passed through the medical ICU that year – had cumulative radiation exposure of at least 50 mSv while in the ICU, thereby exceeding the U.S. standard for maximum annual workplace exposure, Dr. Sudhir Krishnan said at the annual meeting of the American College of Chest Physicians. The finding raises questions of whether all these exposures are appropriate and whether they reflect overuse of certain imaging modalities.
Dr. Krishnan and his associates ran a retrospective review of case records for the medical ICU–admitted patients at the Cleveland Clinic during 2013 (Chest. 2015 Oct 25. doi: 10.1378/chest.2278486). During their ICU stay, 3,490 patients (84%) received some amount of radiation exposure. Exposure averaged 7 mSv, with a median of 1.5 mSv. The radiation exposure came primarily from imaging and more specifically from CT examinations, which produced more than half of all radiation-exposure episodes. Other sources included x-rays, nuclear scans, and interventional procedures.
Based on typical radiation dosages received during each type of procedure, the researchers calculated an estimated total radiation dosage received by each patient during their ICU stay. Nearly two-thirds of patients had an exposure of less than 3 mSv, the average annual exposure a person receives from ambient radiation. A quarter of the patients had an exposure of 3-14 mSv, 11% had an exposure of 15-49 mSv, and 2% – 98 patients – had exposure during their ICU stay that ran to 50 mSv or greater, exceeding the U.S. workplace annual maximum . Thirteen patients had an exposure level during their ICU stay that reached 100 mSv or higher; the maximum exposure level was in a patient with cumulative exposure of 176 mSv, said Dr. Krishnan, a critical-care medicine specialist at the Cleveland Clinic.
He and his coworkers did a multivariate analysis to identify factors that linked with a higher likelihood of having high radiation exposure. Patients at greatest risk for high exposure levels were sicker patients with higher APACHE 3 scores, longer stays in the ICU, and the presence of cirrhosis, but those most at risk also tended to be younger. Rates of both ICU deaths and deaths during the entire hospitalization were significantly higher among those with radiation exposure that was 50 mSv or greater.
Dr. Krishnan cautioned that he has not run any analysis that assessed the appropriateness of the imaging that the ICU patients received, nor did he have any data documenting the clinical consequences to the patients who had higher radiation exposure. Despite that uncertainty, he suggested that efforts focus on avoiding unnecessary radiation exposure to patients.
On Twitter @mitchelzoler
AT CHEST 2015
Key clinical point: A small but significant percentage of medical ICU patients receive cumulative radiation doses that exceed federal standards for annual workplace exposure.
Major finding: Two percent of medical ICU patients received at least 50 mSv of radiation exposure during their ICU stay.
Data source: Single-center, retrospective study with 4,155 consecutive medical ICU patients during 2013.
Disclosures: Dr. Krishnan had no disclosures.
Malpractice Counsel: Aneurysm, Falls
Sued If You Do, Sued If You Don’t
A 52-year-old woman presented to the ED with complaints of abdominal pain, vaginal bleeding, and left leg pain. The patient stated that the symptoms, which she had been experiencing over the past few days, were becoming progressively worse. She denied fevers, chills, nausea, vomiting, diarrhea, or constipation. Her surgical history was
remarkable for an appendectomy 30 years prior. The patient was not currently on any medications. Regarding social history, she denied alcohol or tobacco use. She also denied any allergies to medications.
On physical examination, all of the patient’s vital signs were normal. The head, eyes, ears, nose, and throat, and lung and heart examinations were also normal; however, on abdominal examination, she exhibited tenderness throughout the lower abdomen, but without guarding or rebound. There was no costovertebral angle tenderness of the back. The pelvic examination was remarkable for a small amount of blood from the cervical os and a slightly enlarged uterus. The adnexa were normal and without tenderness.
The patient sued both the EP and the hospital, claiming that the CT scan was unnecessary and had it not been performed, she would not have experienced the stroke. The defense asserted that the CT scan with contrast was appropriate given the patient’s symptoms and physical findings, and that the contrast dye used was not the cause of the stroke. The jury awarded the plaintiff $3.6 million.
Discussion
This case is unique in that the EP was sued for ordering a CT scan. In the overwhelming majority of malpractice cases, EPs are sued for not obtaining a certain test—frequently a CT scan. It does not appear the jury in this case was correct in their judgment as there was no conceivable way the EP could have anticipated this type of unusual reaction, especially in a patient with no history of medication allergies.
This jury ruling places EPs in an untenable situation: If they order a test and anything bad happens, they will be sued. If they do not order a test and something bad happens, they will be sued. In legal theory, there must be proximal cause between what the physician did (ie, order the CT scan) and the bad outcome, or negligence (ie, SAH). For this case, the two events seem true-true and unrelated. The contrast dye clearly did not cause the cerebral aneurysm, which was a preexisting condition.
Nonidiosyncratic reactions are due to direct toxic or osmolar effects. Symptoms include bradycardia, hypotension, vasovagal reactions, sensation of warmth, metallic taste in the mouth, and nausea and vomiting.1
Ironically, the majority of adverse reactions to ICM involve hypotension, not hypertension. This includes cardiovascular reactions to ICM, which typically involve bradycardia, peripheral vasodilation, and hypotension.1 The incidence and severity of an adverse reaction to ICM also depends on whether ionic or nonionic ICM was used. (Unfortunately, the type of ICM administered to the patient in this case was not disclosed.)
The incidence and severity of adverse reactions to ICM are less with nonionic compared to ionic ICM. More than 90% of adverse reactions to nonionic ICM are anaphlyactoid.2 In general, adverse reactions occur in 4% to 12% of patients receiving ionic ICM compared to 1% to 3% of those receiving nonionic ICM.2 In a study of more than 300,000 contrast administrations, Katayama et al,3 found the overall risk for severe adverse reaction to be 0.2% for ionic ICM compared to 0.04% for nonionic ICM.
The bottom line in this case is that the patient’s event was a very rare and completely unforeseen result temporally related to the contrast CT scan ordered to evaluate the etiology of this patient’s abdominal pain.
Falls
A 67-year-old woman with a chief complaint of lightheadedness and dizziness was transferred from a dialysis center to the ED by emergency medical services (EMS). She stated that her symptoms came on suddenly right after she had completed her scheduled dialysis.
As the patient was being rolled on a stretcher from the ambulance to the ED entrance, the stretcher collapsed and tipped over, causing the patient to fall and strike her head on the pavement. The patient suffered a severe intraparenchymal brain hemorrhage, requiring intubation, ventilation, and admission to the intensive care unit. On the second day of admission, the patient’s family signed “do not resuscitate” orders and, in accordance with their wishes, life support was withdrawn and the patient died.
The family sued the ambulance company, stating the patient’s death was a direct result of negligent training and supervision of EMS personnel. The plaintiff further claimed the incident was caused by the failure to properly secure a locking mechanism on the stretcher, which caused it to tip. The ambulance company disputed the liability, asserting that what occurred was a tragic accident, not negligence. The jury found in favor of the plaintiff and awarded $1.5 million.
Discussion
While this is not a true ED case since the patient’s fall occurred just outside the ED, it does emphasize the importance of falls and the challenges of fall prevention within the hospital—including the ED. The incidence of falls within hospitals ranges from 1.3 to 9 falls per 1,000 occupied bed days (OBD).1 This incidence, however, is not evenly distributed across hospital departments. Not surprisingly, the highest rates are reported in areas such as geriatric, neurology, and rehabilitation units.1 The highest rates, 17 to 67 per 1,000 OBDs, appear to occur in geropsychiatric units,2,3 and a significant number of such patient falls are serious, with some type of injury resulting from the fall in 30% to 51% of cases.1 The percentage of falls resulting in a fracture ranges from 1% to 3%.1
As previously noted, the ED is not immune to patient falls. A review of one academic medical center ED with 75,000 annual visits found an incidence of 1.3 falls per month, 31% of which resulted in patient injury.4
Some relatively simple steps can be taken to reduce the incidence of falls. For example, identifying patients at high risk of falling (eg, patients who are elderly, confused, dizzy) and ensuring other care-team workers are aware of the risk, can be very helpful.4,5 In addition, brightly colored signs on the stretcher or colored wrist bands indicating the patient is at high-risk for falls helps to engage the entire healthcare team in fall-prevention measures.4 Sitters with high-risk patients can also help minimize fall risk.
Although side rails on hospital beds are intended to increase patient safety, their use is not without controversy. Most hospitals require staff to have side rails up for obvious reasons. Some hospitals, however, are concerned that the use of side rails can cause a fall from a higher position and increase the risk of injury when a patient attempts to get out of bed. Additional important steps include ensuring that all wet surfaces are quickly identified and cleaned, and making sure everyone is aware of the importance of fall-prevention measures.
The employment of the abovementioned fall-prevention measures is especially important in relation to the aging US population. As the number of elderly patients in the United States continues to grow, the risk of patient falls is expected to increase. Therefore, hospitals should be proactive in implementing preventive measures to reduce the risk of patient falls and injury.
- Sued If You Do, Sued If You Don't
- Siddiqi NH, Lin EC. Contrast medium reactions. http://emedicine.medscape.com/article. Updated September 29, 2015. Accessed October 8, 2015.
- Cochran ST. Anaphylactoid reactions to radiocontrast media. Curr Allergy Asthma Rep. 2005;5(1):28-31.
- Katayama H, Yamaguchi K, Kozuka T, Takashima T, Seez P, Matsuura K. Adverse reactions to ionic and nonionic contrast media. A report from the Japanese Committee on the Safety of Contrast Media. Radiology. 1990;175(3):621-128.
- Falls
- Oliver D, Healey F, Haines TP. Preventing falls and fall-related injuries in hospitals. Clin Geriatr Med. 2010;26(4):645-692.
- Nyberg L, Gustafson Y, Janson A, Sandman PO, Eriksson S. Incidence of falls in three different types of geriatric care. A Swedish prospective study. Scand J Soc Med. 1997;25(1):8-13.
- Weintraub D, Spurlock M. Change in the rate of restraint use and falls on a psychogeriatric inpatient unit: impact of the health care financing administration’s new restraint and seclusion standards for hospitals. J Geriatr Psychiatry Neurol. 2002;15(2):91-94.
- Rosenthal A. Preventing falls in the emergency department: a program that works (Abstract). Virginia Henderson Global Nursing e-Repository Web site. http://www.nursinglibrary.org/vhl/handle/10755/162669. Accessed October 7, 2015.
- Alexander D, Kinsley TL, Waszinski C. Journey to a safe environment: fall precaution in an emergency department at a level I trauma center. J Emerg Nurs. 2013;39(4):346-352.
Sued If You Do, Sued If You Don’t
A 52-year-old woman presented to the ED with complaints of abdominal pain, vaginal bleeding, and left leg pain. The patient stated that the symptoms, which she had been experiencing over the past few days, were becoming progressively worse. She denied fevers, chills, nausea, vomiting, diarrhea, or constipation. Her surgical history was
remarkable for an appendectomy 30 years prior. The patient was not currently on any medications. Regarding social history, she denied alcohol or tobacco use. She also denied any allergies to medications.
On physical examination, all of the patient’s vital signs were normal. The head, eyes, ears, nose, and throat, and lung and heart examinations were also normal; however, on abdominal examination, she exhibited tenderness throughout the lower abdomen, but without guarding or rebound. There was no costovertebral angle tenderness of the back. The pelvic examination was remarkable for a small amount of blood from the cervical os and a slightly enlarged uterus. The adnexa were normal and without tenderness.
The patient sued both the EP and the hospital, claiming that the CT scan was unnecessary and had it not been performed, she would not have experienced the stroke. The defense asserted that the CT scan with contrast was appropriate given the patient’s symptoms and physical findings, and that the contrast dye used was not the cause of the stroke. The jury awarded the plaintiff $3.6 million.
Discussion
This case is unique in that the EP was sued for ordering a CT scan. In the overwhelming majority of malpractice cases, EPs are sued for not obtaining a certain test—frequently a CT scan. It does not appear the jury in this case was correct in their judgment as there was no conceivable way the EP could have anticipated this type of unusual reaction, especially in a patient with no history of medication allergies.
This jury ruling places EPs in an untenable situation: If they order a test and anything bad happens, they will be sued. If they do not order a test and something bad happens, they will be sued. In legal theory, there must be proximal cause between what the physician did (ie, order the CT scan) and the bad outcome, or negligence (ie, SAH). For this case, the two events seem true-true and unrelated. The contrast dye clearly did not cause the cerebral aneurysm, which was a preexisting condition.
Nonidiosyncratic reactions are due to direct toxic or osmolar effects. Symptoms include bradycardia, hypotension, vasovagal reactions, sensation of warmth, metallic taste in the mouth, and nausea and vomiting.1
Ironically, the majority of adverse reactions to ICM involve hypotension, not hypertension. This includes cardiovascular reactions to ICM, which typically involve bradycardia, peripheral vasodilation, and hypotension.1 The incidence and severity of an adverse reaction to ICM also depends on whether ionic or nonionic ICM was used. (Unfortunately, the type of ICM administered to the patient in this case was not disclosed.)
The incidence and severity of adverse reactions to ICM are less with nonionic compared to ionic ICM. More than 90% of adverse reactions to nonionic ICM are anaphlyactoid.2 In general, adverse reactions occur in 4% to 12% of patients receiving ionic ICM compared to 1% to 3% of those receiving nonionic ICM.2 In a study of more than 300,000 contrast administrations, Katayama et al,3 found the overall risk for severe adverse reaction to be 0.2% for ionic ICM compared to 0.04% for nonionic ICM.
The bottom line in this case is that the patient’s event was a very rare and completely unforeseen result temporally related to the contrast CT scan ordered to evaluate the etiology of this patient’s abdominal pain.
Falls
A 67-year-old woman with a chief complaint of lightheadedness and dizziness was transferred from a dialysis center to the ED by emergency medical services (EMS). She stated that her symptoms came on suddenly right after she had completed her scheduled dialysis.
As the patient was being rolled on a stretcher from the ambulance to the ED entrance, the stretcher collapsed and tipped over, causing the patient to fall and strike her head on the pavement. The patient suffered a severe intraparenchymal brain hemorrhage, requiring intubation, ventilation, and admission to the intensive care unit. On the second day of admission, the patient’s family signed “do not resuscitate” orders and, in accordance with their wishes, life support was withdrawn and the patient died.
The family sued the ambulance company, stating the patient’s death was a direct result of negligent training and supervision of EMS personnel. The plaintiff further claimed the incident was caused by the failure to properly secure a locking mechanism on the stretcher, which caused it to tip. The ambulance company disputed the liability, asserting that what occurred was a tragic accident, not negligence. The jury found in favor of the plaintiff and awarded $1.5 million.
Discussion
While this is not a true ED case since the patient’s fall occurred just outside the ED, it does emphasize the importance of falls and the challenges of fall prevention within the hospital—including the ED. The incidence of falls within hospitals ranges from 1.3 to 9 falls per 1,000 occupied bed days (OBD).1 This incidence, however, is not evenly distributed across hospital departments. Not surprisingly, the highest rates are reported in areas such as geriatric, neurology, and rehabilitation units.1 The highest rates, 17 to 67 per 1,000 OBDs, appear to occur in geropsychiatric units,2,3 and a significant number of such patient falls are serious, with some type of injury resulting from the fall in 30% to 51% of cases.1 The percentage of falls resulting in a fracture ranges from 1% to 3%.1
As previously noted, the ED is not immune to patient falls. A review of one academic medical center ED with 75,000 annual visits found an incidence of 1.3 falls per month, 31% of which resulted in patient injury.4
Some relatively simple steps can be taken to reduce the incidence of falls. For example, identifying patients at high risk of falling (eg, patients who are elderly, confused, dizzy) and ensuring other care-team workers are aware of the risk, can be very helpful.4,5 In addition, brightly colored signs on the stretcher or colored wrist bands indicating the patient is at high-risk for falls helps to engage the entire healthcare team in fall-prevention measures.4 Sitters with high-risk patients can also help minimize fall risk.
Although side rails on hospital beds are intended to increase patient safety, their use is not without controversy. Most hospitals require staff to have side rails up for obvious reasons. Some hospitals, however, are concerned that the use of side rails can cause a fall from a higher position and increase the risk of injury when a patient attempts to get out of bed. Additional important steps include ensuring that all wet surfaces are quickly identified and cleaned, and making sure everyone is aware of the importance of fall-prevention measures.
The employment of the abovementioned fall-prevention measures is especially important in relation to the aging US population. As the number of elderly patients in the United States continues to grow, the risk of patient falls is expected to increase. Therefore, hospitals should be proactive in implementing preventive measures to reduce the risk of patient falls and injury.
Sued If You Do, Sued If You Don’t
A 52-year-old woman presented to the ED with complaints of abdominal pain, vaginal bleeding, and left leg pain. The patient stated that the symptoms, which she had been experiencing over the past few days, were becoming progressively worse. She denied fevers, chills, nausea, vomiting, diarrhea, or constipation. Her surgical history was
remarkable for an appendectomy 30 years prior. The patient was not currently on any medications. Regarding social history, she denied alcohol or tobacco use. She also denied any allergies to medications.
On physical examination, all of the patient’s vital signs were normal. The head, eyes, ears, nose, and throat, and lung and heart examinations were also normal; however, on abdominal examination, she exhibited tenderness throughout the lower abdomen, but without guarding or rebound. There was no costovertebral angle tenderness of the back. The pelvic examination was remarkable for a small amount of blood from the cervical os and a slightly enlarged uterus. The adnexa were normal and without tenderness.
The patient sued both the EP and the hospital, claiming that the CT scan was unnecessary and had it not been performed, she would not have experienced the stroke. The defense asserted that the CT scan with contrast was appropriate given the patient’s symptoms and physical findings, and that the contrast dye used was not the cause of the stroke. The jury awarded the plaintiff $3.6 million.
Discussion
This case is unique in that the EP was sued for ordering a CT scan. In the overwhelming majority of malpractice cases, EPs are sued for not obtaining a certain test—frequently a CT scan. It does not appear the jury in this case was correct in their judgment as there was no conceivable way the EP could have anticipated this type of unusual reaction, especially in a patient with no history of medication allergies.
This jury ruling places EPs in an untenable situation: If they order a test and anything bad happens, they will be sued. If they do not order a test and something bad happens, they will be sued. In legal theory, there must be proximal cause between what the physician did (ie, order the CT scan) and the bad outcome, or negligence (ie, SAH). For this case, the two events seem true-true and unrelated. The contrast dye clearly did not cause the cerebral aneurysm, which was a preexisting condition.
Nonidiosyncratic reactions are due to direct toxic or osmolar effects. Symptoms include bradycardia, hypotension, vasovagal reactions, sensation of warmth, metallic taste in the mouth, and nausea and vomiting.1
Ironically, the majority of adverse reactions to ICM involve hypotension, not hypertension. This includes cardiovascular reactions to ICM, which typically involve bradycardia, peripheral vasodilation, and hypotension.1 The incidence and severity of an adverse reaction to ICM also depends on whether ionic or nonionic ICM was used. (Unfortunately, the type of ICM administered to the patient in this case was not disclosed.)
The incidence and severity of adverse reactions to ICM are less with nonionic compared to ionic ICM. More than 90% of adverse reactions to nonionic ICM are anaphlyactoid.2 In general, adverse reactions occur in 4% to 12% of patients receiving ionic ICM compared to 1% to 3% of those receiving nonionic ICM.2 In a study of more than 300,000 contrast administrations, Katayama et al,3 found the overall risk for severe adverse reaction to be 0.2% for ionic ICM compared to 0.04% for nonionic ICM.
The bottom line in this case is that the patient’s event was a very rare and completely unforeseen result temporally related to the contrast CT scan ordered to evaluate the etiology of this patient’s abdominal pain.
Falls
A 67-year-old woman with a chief complaint of lightheadedness and dizziness was transferred from a dialysis center to the ED by emergency medical services (EMS). She stated that her symptoms came on suddenly right after she had completed her scheduled dialysis.
As the patient was being rolled on a stretcher from the ambulance to the ED entrance, the stretcher collapsed and tipped over, causing the patient to fall and strike her head on the pavement. The patient suffered a severe intraparenchymal brain hemorrhage, requiring intubation, ventilation, and admission to the intensive care unit. On the second day of admission, the patient’s family signed “do not resuscitate” orders and, in accordance with their wishes, life support was withdrawn and the patient died.
The family sued the ambulance company, stating the patient’s death was a direct result of negligent training and supervision of EMS personnel. The plaintiff further claimed the incident was caused by the failure to properly secure a locking mechanism on the stretcher, which caused it to tip. The ambulance company disputed the liability, asserting that what occurred was a tragic accident, not negligence. The jury found in favor of the plaintiff and awarded $1.5 million.
Discussion
While this is not a true ED case since the patient’s fall occurred just outside the ED, it does emphasize the importance of falls and the challenges of fall prevention within the hospital—including the ED. The incidence of falls within hospitals ranges from 1.3 to 9 falls per 1,000 occupied bed days (OBD).1 This incidence, however, is not evenly distributed across hospital departments. Not surprisingly, the highest rates are reported in areas such as geriatric, neurology, and rehabilitation units.1 The highest rates, 17 to 67 per 1,000 OBDs, appear to occur in geropsychiatric units,2,3 and a significant number of such patient falls are serious, with some type of injury resulting from the fall in 30% to 51% of cases.1 The percentage of falls resulting in a fracture ranges from 1% to 3%.1
As previously noted, the ED is not immune to patient falls. A review of one academic medical center ED with 75,000 annual visits found an incidence of 1.3 falls per month, 31% of which resulted in patient injury.4
Some relatively simple steps can be taken to reduce the incidence of falls. For example, identifying patients at high risk of falling (eg, patients who are elderly, confused, dizzy) and ensuring other care-team workers are aware of the risk, can be very helpful.4,5 In addition, brightly colored signs on the stretcher or colored wrist bands indicating the patient is at high-risk for falls helps to engage the entire healthcare team in fall-prevention measures.4 Sitters with high-risk patients can also help minimize fall risk.
Although side rails on hospital beds are intended to increase patient safety, their use is not without controversy. Most hospitals require staff to have side rails up for obvious reasons. Some hospitals, however, are concerned that the use of side rails can cause a fall from a higher position and increase the risk of injury when a patient attempts to get out of bed. Additional important steps include ensuring that all wet surfaces are quickly identified and cleaned, and making sure everyone is aware of the importance of fall-prevention measures.
The employment of the abovementioned fall-prevention measures is especially important in relation to the aging US population. As the number of elderly patients in the United States continues to grow, the risk of patient falls is expected to increase. Therefore, hospitals should be proactive in implementing preventive measures to reduce the risk of patient falls and injury.
- Sued If You Do, Sued If You Don't
- Siddiqi NH, Lin EC. Contrast medium reactions. http://emedicine.medscape.com/article. Updated September 29, 2015. Accessed October 8, 2015.
- Cochran ST. Anaphylactoid reactions to radiocontrast media. Curr Allergy Asthma Rep. 2005;5(1):28-31.
- Katayama H, Yamaguchi K, Kozuka T, Takashima T, Seez P, Matsuura K. Adverse reactions to ionic and nonionic contrast media. A report from the Japanese Committee on the Safety of Contrast Media. Radiology. 1990;175(3):621-128.
- Falls
- Oliver D, Healey F, Haines TP. Preventing falls and fall-related injuries in hospitals. Clin Geriatr Med. 2010;26(4):645-692.
- Nyberg L, Gustafson Y, Janson A, Sandman PO, Eriksson S. Incidence of falls in three different types of geriatric care. A Swedish prospective study. Scand J Soc Med. 1997;25(1):8-13.
- Weintraub D, Spurlock M. Change in the rate of restraint use and falls on a psychogeriatric inpatient unit: impact of the health care financing administration’s new restraint and seclusion standards for hospitals. J Geriatr Psychiatry Neurol. 2002;15(2):91-94.
- Rosenthal A. Preventing falls in the emergency department: a program that works (Abstract). Virginia Henderson Global Nursing e-Repository Web site. http://www.nursinglibrary.org/vhl/handle/10755/162669. Accessed October 7, 2015.
- Alexander D, Kinsley TL, Waszinski C. Journey to a safe environment: fall precaution in an emergency department at a level I trauma center. J Emerg Nurs. 2013;39(4):346-352.
- Sued If You Do, Sued If You Don't
- Siddiqi NH, Lin EC. Contrast medium reactions. http://emedicine.medscape.com/article. Updated September 29, 2015. Accessed October 8, 2015.
- Cochran ST. Anaphylactoid reactions to radiocontrast media. Curr Allergy Asthma Rep. 2005;5(1):28-31.
- Katayama H, Yamaguchi K, Kozuka T, Takashima T, Seez P, Matsuura K. Adverse reactions to ionic and nonionic contrast media. A report from the Japanese Committee on the Safety of Contrast Media. Radiology. 1990;175(3):621-128.
- Falls
- Oliver D, Healey F, Haines TP. Preventing falls and fall-related injuries in hospitals. Clin Geriatr Med. 2010;26(4):645-692.
- Nyberg L, Gustafson Y, Janson A, Sandman PO, Eriksson S. Incidence of falls in three different types of geriatric care. A Swedish prospective study. Scand J Soc Med. 1997;25(1):8-13.
- Weintraub D, Spurlock M. Change in the rate of restraint use and falls on a psychogeriatric inpatient unit: impact of the health care financing administration’s new restraint and seclusion standards for hospitals. J Geriatr Psychiatry Neurol. 2002;15(2):91-94.
- Rosenthal A. Preventing falls in the emergency department: a program that works (Abstract). Virginia Henderson Global Nursing e-Repository Web site. http://www.nursinglibrary.org/vhl/handle/10755/162669. Accessed October 7, 2015.
- Alexander D, Kinsley TL, Waszinski C. Journey to a safe environment: fall precaution in an emergency department at a level I trauma center. J Emerg Nurs. 2013;39(4):346-352.
Case Report: Not Just Another Kidney Stone
Case
A 36-year-old woman with a 2-week history of left flank pain presented to the ED via emergency medical services. The patient, who had a history of nephrolithiasis, assumed her pain was due to another kidney stone. She stated that while waiting for the presumed stone to pass, the pain in her left flank worsened and she felt lightheaded and weak.
The patient’s vital signs at presentation were: heart rate, 96 beats/minute; blood pressure, 133/76 mm Hg; respiratory rate, 20 breaths/minute; and temperature, 98.9˚F. Oxygen saturation was 98% on room air. On physical examination, the patient had left lower quadrant pain and left costovertebral angle tenderness. Laboratory studies were remarkable for a negative urine pregnancy test, a hemoglobin level of 6.8 g/dL, and a hematocrit of 21.1%. Based on the patient’s history and symptoms, axial and coronal computed tomography (CT) scans were ordered, revealing a ruptured left renal calyx with hemorrhage from ureterolithiasis (Figures 1a and 1b).
Rupture of renal calyx and extravasation of blood or urine is a potential complication of nephrolithiasis. Stone size, degree of obstruction, and length of symptomatic presentation presumably contribute to complications from nephrolithiasis. Stones that are symptomatic for more than 4 weeks are estimated to have an increased complication rate of up to 20%.1
Calyx or fornix rupture results from increased intraluminal pressure. Rupture of these structures is thought to be a type of “safety-valve” function to relieve obstructive uropathy.2
Obstructions from small leaks to large urinomas can cause extravasation of urine. In most cases, urinary extravasation is confined to the subcapsular space or perirenal space within the Gerota’s fascia;3 however, as seen in this patient, mixed hematoma/urinomas can form.
Causes
In cases of nontraumatic calyx rupture, the cause of the obstruction is most often a distal obstructing ureteral stone.4 Other causes of rupture include extrinsic compression from malignant and benign masses, ureteric junction obstructions, or iatrogenic causes.4 Interestingly, in one small study, the median size of the obstructing stone was only 4 mm. The same study also noted that proximal ureteral obstruction occurred when larger stones where present.4
Conservative Versus Nonconservative Management
Potential complications of urinomas include abscess formation, sepsis, hydronephrosis, and paralytic ileus.3 Despite possible adverse sequelae, uncomplicated urinomas may be managed conservatively with supportive care. According to a study by Chapman et al,5 about 40% of patients managed conservatively recover without complications. In addition, in a retrospective study by Doehn et al6 involving 160 cases of fornix rupture treated with endoscopic therapy or nephrostomy tube supplemented with antibiotics, no instances of perinephric abscess or other complications requiring a second procedure were noted.
Management of suspected ureterolithiasis in the ED is focused on analgesia and supportive care. Acute analgesia is often provided parenterally with opioids alone or with an opioid/nonsteroidal anti-inflammatory drug (NSAID) combination.7 Frequent reassessment of the patient is required to ensure adequate pain control and to prevent sedation. Other symptoms, such as nausea, vomiting, and dehydration, may be treated with intravenous (IV) fluids and antiemetic medications. Further radiographic evaluation is needed once analgesia is achieved.7,8
Imaging Studies
Radiological evaluation of patients with suspected ureterolithiasis may involve several imaging modalities. Noncontrast helical CT scan is the standard for rapid and efficient identification of ureteral stones while allowing visualization of other potential pathology (eg, urinoma).7-9 Other modalities, such as ultrasonography; radiography of the kidneys, ureters, and bladder; and an IV pyelogram with contrasted CT, may be ordered if noncontrast helical CT scan is not available on-site or if there are comorbidities. In addition to imaging studies, basic laboratory studies (eg, serum creatinine and blood urea nitrogen testing) are indicated to assess overall renal function and direct the choice of radiological study.7
Disposition
Clinical decision-making is key when recommending inpatient versus outpatient treatment in patients with ureterolithiasis. Patients with uncontrolled pain or vomiting may require inpatient admission for supportive care, while those demonstrating acute renal failure, pyuria with bacteriuria, complete bilateral ureteral obstruction, urinoma, or signs of sepsis demand emergent urology consultation. Specifically, patients with urinoma require ureteroscopy versus nephrostomy6,10 to allow drainage while carefully monitoring for development of subsequent bleeding and infection.
When discharging patients from the ED, expulsive therapy using tamsulosin9 and analgesia with combination of oral opioids and NSAIDs are most commonly effective.11 Outpatient urology referrals are recommended for ureteral stones greater than 5 mm in size or if the stones have been present in the ureter for greater than 4 weeks.1 Proper evaluation and management of ureterolithiasis in the ED is crucial for positive outcomes and to reduce long-term complications.
Case Conclusion
Computed tomography revealed a ruptured renal calyx on the left side with free fluid in the abdomen. Urology services were consulted and the patient was taken to the operating room for cystoscopy, ureteral stent placement, and laser lithotripsy. Following surgery, she subsequently developed urosepsis for which she was successfully treated with IV antibiotics and discharged on hospital day 15.
Mr Eisenstat is a fourth-year medical student at the University of South Carolina School of Medicine, Greenville. Dr Fabiano is an emergency physician, department of emergency medicine, Greenville Health Systems, Greenville, South Carolina. Dr Collins is family medicine physician, department of emergency medicine, Greenville Health Systems, Greenville, South Carolina.
- Hübner WA, Irby P, Stoller M. Natural history and current concepts for the treatment of small ureteral calculi. Eur Urol. 1993;24(2):172-176.
- Lin DY, Fang YC, Huang DY, Lin SP. Spontaneous rupture of the ureter secondary to urolithiasis and extravasation of calyceal fornix due to acute urinary bladder distension: four case reports. Chin J Radiology. 2004;29:269-275.
- Behzad-Noori M, Blandon JA, Negrin Exposito JE, Sarmiento JL, Dias AL, Hernandez GT. Urinoma: a rare complication from being between a rock and soft organ. El Paso Physician. 2010;33(6):5-6.
- Gershman B, Kulkarni N, Sahani DV, Eisner BH. Causes of renal forniceal rupture. BJU Int. 2011;108(11):1909-1911.
- Chapman JP, Gonzalez J, Diokno AC. Significance of urinary extravasation during renal colic. Urology. 1987;30(6):541-545.
- Doehn C, Fiola L, Peter M, Jocham D. Outcome analysis of fornix ruptures in 162 consecutive patients. J Endourol. 2010;24(11):1869-1873
- Portis AJ, Sundaram CP. Diagnosis and initial management of kidney stones. Am Fam Physician. 2001;63(7):1329-1338
- Smith RC, Verga M, Dalrymple N, McCarthy S, Rosenfield AT. Acute ureteral obstruction: value of secondary signs of helical unenhanced CT. AJR Am J Roentgenol. 1996;167(5):1109-1113.Burke TA, Wisniewski T, Ernst FR. Resource utilization and costs associated with chemotherapy-induced nausea and vomiting (CINV) following highly or moderately emetogenic chemotherapy administered in the US outpatient hospital setting. Support Care Cancer. 2011;19(1):131-140.
- Ha M, MacDonald RD. Impact of CT scan in patients with first episode of suspected nephrolithiasis. J Emerg Med. 2004;27(3):225-231.
- Tawfiek ER, Bagley DH. Management of upper urinary tract calculi with ureteroscopic techniques. Urology. 1999;53(1):25-31.
- Larkin GL, Peacock WF 4th, Pearl SM, Blair GA, D'Amico F. Efficacy of ketorolac tromethamine versus meperidine in the ED treatment of acute renal colic. Am J Emerg Med. 1999;17(1):6-10.
Case
A 36-year-old woman with a 2-week history of left flank pain presented to the ED via emergency medical services. The patient, who had a history of nephrolithiasis, assumed her pain was due to another kidney stone. She stated that while waiting for the presumed stone to pass, the pain in her left flank worsened and she felt lightheaded and weak.
The patient’s vital signs at presentation were: heart rate, 96 beats/minute; blood pressure, 133/76 mm Hg; respiratory rate, 20 breaths/minute; and temperature, 98.9˚F. Oxygen saturation was 98% on room air. On physical examination, the patient had left lower quadrant pain and left costovertebral angle tenderness. Laboratory studies were remarkable for a negative urine pregnancy test, a hemoglobin level of 6.8 g/dL, and a hematocrit of 21.1%. Based on the patient’s history and symptoms, axial and coronal computed tomography (CT) scans were ordered, revealing a ruptured left renal calyx with hemorrhage from ureterolithiasis (Figures 1a and 1b).
Rupture of renal calyx and extravasation of blood or urine is a potential complication of nephrolithiasis. Stone size, degree of obstruction, and length of symptomatic presentation presumably contribute to complications from nephrolithiasis. Stones that are symptomatic for more than 4 weeks are estimated to have an increased complication rate of up to 20%.1
Calyx or fornix rupture results from increased intraluminal pressure. Rupture of these structures is thought to be a type of “safety-valve” function to relieve obstructive uropathy.2
Obstructions from small leaks to large urinomas can cause extravasation of urine. In most cases, urinary extravasation is confined to the subcapsular space or perirenal space within the Gerota’s fascia;3 however, as seen in this patient, mixed hematoma/urinomas can form.
Causes
In cases of nontraumatic calyx rupture, the cause of the obstruction is most often a distal obstructing ureteral stone.4 Other causes of rupture include extrinsic compression from malignant and benign masses, ureteric junction obstructions, or iatrogenic causes.4 Interestingly, in one small study, the median size of the obstructing stone was only 4 mm. The same study also noted that proximal ureteral obstruction occurred when larger stones where present.4
Conservative Versus Nonconservative Management
Potential complications of urinomas include abscess formation, sepsis, hydronephrosis, and paralytic ileus.3 Despite possible adverse sequelae, uncomplicated urinomas may be managed conservatively with supportive care. According to a study by Chapman et al,5 about 40% of patients managed conservatively recover without complications. In addition, in a retrospective study by Doehn et al6 involving 160 cases of fornix rupture treated with endoscopic therapy or nephrostomy tube supplemented with antibiotics, no instances of perinephric abscess or other complications requiring a second procedure were noted.
Management of suspected ureterolithiasis in the ED is focused on analgesia and supportive care. Acute analgesia is often provided parenterally with opioids alone or with an opioid/nonsteroidal anti-inflammatory drug (NSAID) combination.7 Frequent reassessment of the patient is required to ensure adequate pain control and to prevent sedation. Other symptoms, such as nausea, vomiting, and dehydration, may be treated with intravenous (IV) fluids and antiemetic medications. Further radiographic evaluation is needed once analgesia is achieved.7,8
Imaging Studies
Radiological evaluation of patients with suspected ureterolithiasis may involve several imaging modalities. Noncontrast helical CT scan is the standard for rapid and efficient identification of ureteral stones while allowing visualization of other potential pathology (eg, urinoma).7-9 Other modalities, such as ultrasonography; radiography of the kidneys, ureters, and bladder; and an IV pyelogram with contrasted CT, may be ordered if noncontrast helical CT scan is not available on-site or if there are comorbidities. In addition to imaging studies, basic laboratory studies (eg, serum creatinine and blood urea nitrogen testing) are indicated to assess overall renal function and direct the choice of radiological study.7
Disposition
Clinical decision-making is key when recommending inpatient versus outpatient treatment in patients with ureterolithiasis. Patients with uncontrolled pain or vomiting may require inpatient admission for supportive care, while those demonstrating acute renal failure, pyuria with bacteriuria, complete bilateral ureteral obstruction, urinoma, or signs of sepsis demand emergent urology consultation. Specifically, patients with urinoma require ureteroscopy versus nephrostomy6,10 to allow drainage while carefully monitoring for development of subsequent bleeding and infection.
When discharging patients from the ED, expulsive therapy using tamsulosin9 and analgesia with combination of oral opioids and NSAIDs are most commonly effective.11 Outpatient urology referrals are recommended for ureteral stones greater than 5 mm in size or if the stones have been present in the ureter for greater than 4 weeks.1 Proper evaluation and management of ureterolithiasis in the ED is crucial for positive outcomes and to reduce long-term complications.
Case Conclusion
Computed tomography revealed a ruptured renal calyx on the left side with free fluid in the abdomen. Urology services were consulted and the patient was taken to the operating room for cystoscopy, ureteral stent placement, and laser lithotripsy. Following surgery, she subsequently developed urosepsis for which she was successfully treated with IV antibiotics and discharged on hospital day 15.
Mr Eisenstat is a fourth-year medical student at the University of South Carolina School of Medicine, Greenville. Dr Fabiano is an emergency physician, department of emergency medicine, Greenville Health Systems, Greenville, South Carolina. Dr Collins is family medicine physician, department of emergency medicine, Greenville Health Systems, Greenville, South Carolina.
Case
A 36-year-old woman with a 2-week history of left flank pain presented to the ED via emergency medical services. The patient, who had a history of nephrolithiasis, assumed her pain was due to another kidney stone. She stated that while waiting for the presumed stone to pass, the pain in her left flank worsened and she felt lightheaded and weak.
The patient’s vital signs at presentation were: heart rate, 96 beats/minute; blood pressure, 133/76 mm Hg; respiratory rate, 20 breaths/minute; and temperature, 98.9˚F. Oxygen saturation was 98% on room air. On physical examination, the patient had left lower quadrant pain and left costovertebral angle tenderness. Laboratory studies were remarkable for a negative urine pregnancy test, a hemoglobin level of 6.8 g/dL, and a hematocrit of 21.1%. Based on the patient’s history and symptoms, axial and coronal computed tomography (CT) scans were ordered, revealing a ruptured left renal calyx with hemorrhage from ureterolithiasis (Figures 1a and 1b).
Rupture of renal calyx and extravasation of blood or urine is a potential complication of nephrolithiasis. Stone size, degree of obstruction, and length of symptomatic presentation presumably contribute to complications from nephrolithiasis. Stones that are symptomatic for more than 4 weeks are estimated to have an increased complication rate of up to 20%.1
Calyx or fornix rupture results from increased intraluminal pressure. Rupture of these structures is thought to be a type of “safety-valve” function to relieve obstructive uropathy.2
Obstructions from small leaks to large urinomas can cause extravasation of urine. In most cases, urinary extravasation is confined to the subcapsular space or perirenal space within the Gerota’s fascia;3 however, as seen in this patient, mixed hematoma/urinomas can form.
Causes
In cases of nontraumatic calyx rupture, the cause of the obstruction is most often a distal obstructing ureteral stone.4 Other causes of rupture include extrinsic compression from malignant and benign masses, ureteric junction obstructions, or iatrogenic causes.4 Interestingly, in one small study, the median size of the obstructing stone was only 4 mm. The same study also noted that proximal ureteral obstruction occurred when larger stones where present.4
Conservative Versus Nonconservative Management
Potential complications of urinomas include abscess formation, sepsis, hydronephrosis, and paralytic ileus.3 Despite possible adverse sequelae, uncomplicated urinomas may be managed conservatively with supportive care. According to a study by Chapman et al,5 about 40% of patients managed conservatively recover without complications. In addition, in a retrospective study by Doehn et al6 involving 160 cases of fornix rupture treated with endoscopic therapy or nephrostomy tube supplemented with antibiotics, no instances of perinephric abscess or other complications requiring a second procedure were noted.
Management of suspected ureterolithiasis in the ED is focused on analgesia and supportive care. Acute analgesia is often provided parenterally with opioids alone or with an opioid/nonsteroidal anti-inflammatory drug (NSAID) combination.7 Frequent reassessment of the patient is required to ensure adequate pain control and to prevent sedation. Other symptoms, such as nausea, vomiting, and dehydration, may be treated with intravenous (IV) fluids and antiemetic medications. Further radiographic evaluation is needed once analgesia is achieved.7,8
Imaging Studies
Radiological evaluation of patients with suspected ureterolithiasis may involve several imaging modalities. Noncontrast helical CT scan is the standard for rapid and efficient identification of ureteral stones while allowing visualization of other potential pathology (eg, urinoma).7-9 Other modalities, such as ultrasonography; radiography of the kidneys, ureters, and bladder; and an IV pyelogram with contrasted CT, may be ordered if noncontrast helical CT scan is not available on-site or if there are comorbidities. In addition to imaging studies, basic laboratory studies (eg, serum creatinine and blood urea nitrogen testing) are indicated to assess overall renal function and direct the choice of radiological study.7
Disposition
Clinical decision-making is key when recommending inpatient versus outpatient treatment in patients with ureterolithiasis. Patients with uncontrolled pain or vomiting may require inpatient admission for supportive care, while those demonstrating acute renal failure, pyuria with bacteriuria, complete bilateral ureteral obstruction, urinoma, or signs of sepsis demand emergent urology consultation. Specifically, patients with urinoma require ureteroscopy versus nephrostomy6,10 to allow drainage while carefully monitoring for development of subsequent bleeding and infection.
When discharging patients from the ED, expulsive therapy using tamsulosin9 and analgesia with combination of oral opioids and NSAIDs are most commonly effective.11 Outpatient urology referrals are recommended for ureteral stones greater than 5 mm in size or if the stones have been present in the ureter for greater than 4 weeks.1 Proper evaluation and management of ureterolithiasis in the ED is crucial for positive outcomes and to reduce long-term complications.
Case Conclusion
Computed tomography revealed a ruptured renal calyx on the left side with free fluid in the abdomen. Urology services were consulted and the patient was taken to the operating room for cystoscopy, ureteral stent placement, and laser lithotripsy. Following surgery, she subsequently developed urosepsis for which she was successfully treated with IV antibiotics and discharged on hospital day 15.
Mr Eisenstat is a fourth-year medical student at the University of South Carolina School of Medicine, Greenville. Dr Fabiano is an emergency physician, department of emergency medicine, Greenville Health Systems, Greenville, South Carolina. Dr Collins is family medicine physician, department of emergency medicine, Greenville Health Systems, Greenville, South Carolina.
- Hübner WA, Irby P, Stoller M. Natural history and current concepts for the treatment of small ureteral calculi. Eur Urol. 1993;24(2):172-176.
- Lin DY, Fang YC, Huang DY, Lin SP. Spontaneous rupture of the ureter secondary to urolithiasis and extravasation of calyceal fornix due to acute urinary bladder distension: four case reports. Chin J Radiology. 2004;29:269-275.
- Behzad-Noori M, Blandon JA, Negrin Exposito JE, Sarmiento JL, Dias AL, Hernandez GT. Urinoma: a rare complication from being between a rock and soft organ. El Paso Physician. 2010;33(6):5-6.
- Gershman B, Kulkarni N, Sahani DV, Eisner BH. Causes of renal forniceal rupture. BJU Int. 2011;108(11):1909-1911.
- Chapman JP, Gonzalez J, Diokno AC. Significance of urinary extravasation during renal colic. Urology. 1987;30(6):541-545.
- Doehn C, Fiola L, Peter M, Jocham D. Outcome analysis of fornix ruptures in 162 consecutive patients. J Endourol. 2010;24(11):1869-1873
- Portis AJ, Sundaram CP. Diagnosis and initial management of kidney stones. Am Fam Physician. 2001;63(7):1329-1338
- Smith RC, Verga M, Dalrymple N, McCarthy S, Rosenfield AT. Acute ureteral obstruction: value of secondary signs of helical unenhanced CT. AJR Am J Roentgenol. 1996;167(5):1109-1113.Burke TA, Wisniewski T, Ernst FR. Resource utilization and costs associated with chemotherapy-induced nausea and vomiting (CINV) following highly or moderately emetogenic chemotherapy administered in the US outpatient hospital setting. Support Care Cancer. 2011;19(1):131-140.
- Ha M, MacDonald RD. Impact of CT scan in patients with first episode of suspected nephrolithiasis. J Emerg Med. 2004;27(3):225-231.
- Tawfiek ER, Bagley DH. Management of upper urinary tract calculi with ureteroscopic techniques. Urology. 1999;53(1):25-31.
- Larkin GL, Peacock WF 4th, Pearl SM, Blair GA, D'Amico F. Efficacy of ketorolac tromethamine versus meperidine in the ED treatment of acute renal colic. Am J Emerg Med. 1999;17(1):6-10.
- Hübner WA, Irby P, Stoller M. Natural history and current concepts for the treatment of small ureteral calculi. Eur Urol. 1993;24(2):172-176.
- Lin DY, Fang YC, Huang DY, Lin SP. Spontaneous rupture of the ureter secondary to urolithiasis and extravasation of calyceal fornix due to acute urinary bladder distension: four case reports. Chin J Radiology. 2004;29:269-275.
- Behzad-Noori M, Blandon JA, Negrin Exposito JE, Sarmiento JL, Dias AL, Hernandez GT. Urinoma: a rare complication from being between a rock and soft organ. El Paso Physician. 2010;33(6):5-6.
- Gershman B, Kulkarni N, Sahani DV, Eisner BH. Causes of renal forniceal rupture. BJU Int. 2011;108(11):1909-1911.
- Chapman JP, Gonzalez J, Diokno AC. Significance of urinary extravasation during renal colic. Urology. 1987;30(6):541-545.
- Doehn C, Fiola L, Peter M, Jocham D. Outcome analysis of fornix ruptures in 162 consecutive patients. J Endourol. 2010;24(11):1869-1873
- Portis AJ, Sundaram CP. Diagnosis and initial management of kidney stones. Am Fam Physician. 2001;63(7):1329-1338
- Smith RC, Verga M, Dalrymple N, McCarthy S, Rosenfield AT. Acute ureteral obstruction: value of secondary signs of helical unenhanced CT. AJR Am J Roentgenol. 1996;167(5):1109-1113.Burke TA, Wisniewski T, Ernst FR. Resource utilization and costs associated with chemotherapy-induced nausea and vomiting (CINV) following highly or moderately emetogenic chemotherapy administered in the US outpatient hospital setting. Support Care Cancer. 2011;19(1):131-140.
- Ha M, MacDonald RD. Impact of CT scan in patients with first episode of suspected nephrolithiasis. J Emerg Med. 2004;27(3):225-231.
- Tawfiek ER, Bagley DH. Management of upper urinary tract calculi with ureteroscopic techniques. Urology. 1999;53(1):25-31.
- Larkin GL, Peacock WF 4th, Pearl SM, Blair GA, D'Amico F. Efficacy of ketorolac tromethamine versus meperidine in the ED treatment of acute renal colic. Am J Emerg Med. 1999;17(1):6-10.
Emergency Imaging
30-year-old woman with a history of alcoholism and anxiety presented to the ED for evaluation of abdominal distension and pain. She reported new social stressors at home and increased alcohol consumption. She also noted gradually increasing abdominal distension over the past several weeks. As patient’s liver function tests were elevated, supine radiographs of the abdomen were acquired for further evaluation; a representative image is presented below (Figure 1a).
What is the suspected diagnosis?
Is any additional imaging required?
Answer
Centralization of bowel is suggestive of abdominopelvic ascites.1 Additional radiographic findings that may be seen with ascites include diffusely increased density of the abdomen and bulging of the peritoneal fat stripes/flanks. In the average adult, a minimum of approximately 800 mL of ascitic fluid is required to medially displace bowel loops or abdominal viscera.2 While there are many causes of ascites, the radiograph in this case suggests the underlying etiology of cirrhosis. Although the top of the liver is not visualized on the radiograph, the liver contour appears enlarged (red arrow, Figure 1b).
In the ED, ultrasound is the imaging modality of choice to confirm the presence of ascites as it is widely available, quick, relatively inexpensive, and does not require ionizing radiation. Ultrasound is also useful when examining the abdominal viscera since it may detect the underlying cause of ascites.3 The ultrasound image of the abdominal viscera in this case demonstrated a hypoechoic (dark) signal (red arrow, Figure 1c) between the abdominal wall (red asterisk, Figure 1c) and bowel loops (letter ‘B,” Figure 1c). This finding confirmed the presence of ascites because simple fluid does not reflect the ultrasound beam, but instead results in the hypoechoic signal seen in Figure 1c. An additional sonographic image confirmed the presence of an enlarged liver (white asterisk, Figure 1d) and ascites in the right upper quadrant (red arrow, Figure 1d).
The patient was admitted for further workup and treatment of alcoholic cirrhosis. A
Dr Lyons is a resident in the department of radiology at New York Presbyterian Hospital/Weill Cornell Medical College in New York City. Dr Wladyka is an assistant professor of radiology at Weill Cornell Medical College in New York City and an assistant attending radiologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. Dr Hentel is an associate professor of clinical radiology at Weill Cornell Medical College in New York City. He is also chief of emergency/musculoskeletal imaging and executive vice-chairman for the department of radiology at New York-
- Meschan I. Analysis of Roentgen Signs in General Radiology. Philadelphia, PA: Saunders; 1973:1231.
- Keeffee EJ, Gagliardi RA, Pfister RC. The roentgenographic evaluation of ascites. Am J Roentgenol. 1967;101(2):388-396.
- Goldberg BB, Goodman GA, Clearfield HR. Evaluation of ascites by ultrasound. Radiology. 1970;96(1):15-22.
30-year-old woman with a history of alcoholism and anxiety presented to the ED for evaluation of abdominal distension and pain. She reported new social stressors at home and increased alcohol consumption. She also noted gradually increasing abdominal distension over the past several weeks. As patient’s liver function tests were elevated, supine radiographs of the abdomen were acquired for further evaluation; a representative image is presented below (Figure 1a).
What is the suspected diagnosis?
Is any additional imaging required?
Answer
Centralization of bowel is suggestive of abdominopelvic ascites.1 Additional radiographic findings that may be seen with ascites include diffusely increased density of the abdomen and bulging of the peritoneal fat stripes/flanks. In the average adult, a minimum of approximately 800 mL of ascitic fluid is required to medially displace bowel loops or abdominal viscera.2 While there are many causes of ascites, the radiograph in this case suggests the underlying etiology of cirrhosis. Although the top of the liver is not visualized on the radiograph, the liver contour appears enlarged (red arrow, Figure 1b).
In the ED, ultrasound is the imaging modality of choice to confirm the presence of ascites as it is widely available, quick, relatively inexpensive, and does not require ionizing radiation. Ultrasound is also useful when examining the abdominal viscera since it may detect the underlying cause of ascites.3 The ultrasound image of the abdominal viscera in this case demonstrated a hypoechoic (dark) signal (red arrow, Figure 1c) between the abdominal wall (red asterisk, Figure 1c) and bowel loops (letter ‘B,” Figure 1c). This finding confirmed the presence of ascites because simple fluid does not reflect the ultrasound beam, but instead results in the hypoechoic signal seen in Figure 1c. An additional sonographic image confirmed the presence of an enlarged liver (white asterisk, Figure 1d) and ascites in the right upper quadrant (red arrow, Figure 1d).
The patient was admitted for further workup and treatment of alcoholic cirrhosis. A
Dr Lyons is a resident in the department of radiology at New York Presbyterian Hospital/Weill Cornell Medical College in New York City. Dr Wladyka is an assistant professor of radiology at Weill Cornell Medical College in New York City and an assistant attending radiologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. Dr Hentel is an associate professor of clinical radiology at Weill Cornell Medical College in New York City. He is also chief of emergency/musculoskeletal imaging and executive vice-chairman for the department of radiology at New York-
30-year-old woman with a history of alcoholism and anxiety presented to the ED for evaluation of abdominal distension and pain. She reported new social stressors at home and increased alcohol consumption. She also noted gradually increasing abdominal distension over the past several weeks. As patient’s liver function tests were elevated, supine radiographs of the abdomen were acquired for further evaluation; a representative image is presented below (Figure 1a).
What is the suspected diagnosis?
Is any additional imaging required?
Answer
Centralization of bowel is suggestive of abdominopelvic ascites.1 Additional radiographic findings that may be seen with ascites include diffusely increased density of the abdomen and bulging of the peritoneal fat stripes/flanks. In the average adult, a minimum of approximately 800 mL of ascitic fluid is required to medially displace bowel loops or abdominal viscera.2 While there are many causes of ascites, the radiograph in this case suggests the underlying etiology of cirrhosis. Although the top of the liver is not visualized on the radiograph, the liver contour appears enlarged (red arrow, Figure 1b).
In the ED, ultrasound is the imaging modality of choice to confirm the presence of ascites as it is widely available, quick, relatively inexpensive, and does not require ionizing radiation. Ultrasound is also useful when examining the abdominal viscera since it may detect the underlying cause of ascites.3 The ultrasound image of the abdominal viscera in this case demonstrated a hypoechoic (dark) signal (red arrow, Figure 1c) between the abdominal wall (red asterisk, Figure 1c) and bowel loops (letter ‘B,” Figure 1c). This finding confirmed the presence of ascites because simple fluid does not reflect the ultrasound beam, but instead results in the hypoechoic signal seen in Figure 1c. An additional sonographic image confirmed the presence of an enlarged liver (white asterisk, Figure 1d) and ascites in the right upper quadrant (red arrow, Figure 1d).
The patient was admitted for further workup and treatment of alcoholic cirrhosis. A
Dr Lyons is a resident in the department of radiology at New York Presbyterian Hospital/Weill Cornell Medical College in New York City. Dr Wladyka is an assistant professor of radiology at Weill Cornell Medical College in New York City and an assistant attending radiologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. Dr Hentel is an associate professor of clinical radiology at Weill Cornell Medical College in New York City. He is also chief of emergency/musculoskeletal imaging and executive vice-chairman for the department of radiology at New York-
- Meschan I. Analysis of Roentgen Signs in General Radiology. Philadelphia, PA: Saunders; 1973:1231.
- Keeffee EJ, Gagliardi RA, Pfister RC. The roentgenographic evaluation of ascites. Am J Roentgenol. 1967;101(2):388-396.
- Goldberg BB, Goodman GA, Clearfield HR. Evaluation of ascites by ultrasound. Radiology. 1970;96(1):15-22.
- Meschan I. Analysis of Roentgen Signs in General Radiology. Philadelphia, PA: Saunders; 1973:1231.
- Keeffee EJ, Gagliardi RA, Pfister RC. The roentgenographic evaluation of ascites. Am J Roentgenol. 1967;101(2):388-396.
- Goldberg BB, Goodman GA, Clearfield HR. Evaluation of ascites by ultrasound. Radiology. 1970;96(1):15-22.
Surgical Management of Gorham-Stout Disease of the Pelvis Refractory to Medical and Radiation Therapy
Gorham-Stout disease (GSD) is a rare condition characterized by spontaneous idiopathic resorption of bone with lymphovascular proliferation and an absence of malignant features. It was originally described by Jackson1 in an 1838 report of a 36-year-old man whose “arm bone, between the shoulder and elbow” had completely vanished after 2 fractures. The disease was defined and its pathology characterized by Gorham and Stout2 in 1955 in a series of 24 patients. Despite about 200 reported cases in the literature,3 its etiology remains unclear. Any bone in the skeleton may be affected by GSD, although there is a predilection for the skull, humerus, clavicle, ribs, pelvis, and femur.4-6 It commonly manifests within the first 3 decades of life, but case reports range from as early as 2 months of age to the eighth decade.5,7
Gorham-Stout disease is a diagnosis of exclusion that requires careful consideration of the clinical context, radiographic findings, and histopathology. Typical histopathologic findings include benign lymphatic or vascular proliferation, involution of adipose tissue within the bone marrow, and thinning of bony trabeculae.6 Fibrous tissue may replace vascular tissue after the initial vasoproliferative, osteolytic phase.6 Some authors describe the disease as having 2 phases, the first with massive osteolysis followed by relative dormancy and the second without progression or re-ossification.8,9 Treatment remains controversial and is guided by management of the disease’s complications. Options range from careful observation and supportive management to aggressive surgical resection and reconstruction, with positive outcomes reported using many different modalities.10 Most treatment successes, however, hinge on halting bony resorption using medical and radiation therapy. Surgery is usually reserved as a salvage option for patients who have failed medical modalities and have residual symptoms or functional limitations.6
This case report describes the successful surgical management of a patient with pelvic GSD who had progressive pain and functional limitation despite exhaustive medical and radiation therapy. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A healthy 27-year-old man sought medical attention after a fall while mowing his lawn that resulted in difficulty ambulating. Radiographic studies showed discontinuous lytic lesions in the right periacetabular region and the right sacroiliac (SI) joint. Biopsy at an outside institution revealed an infiltration of thin-walled branching vascular channels involving intertrabecular marrow spaces and periosteal connective tissue. The vessels were devoid of a muscular coat and lined by flattened epithelium; these features were seen as consistent with GSD.
The patient was managed medically at the outside institution for approximately 2 years, with regimens consisting of zoledronate, denosumab, sorafenib, vincristine, sirolimus, and bevacizumab. Because there is no standard chemotherapy protocol for GSD, this broad regimen was likely an attempt by treating physicians to control disease progression before considering radiation or surgery. Zoledronate, a bisphosphonate, and denosumab, a monoclonal antibody against the receptor activator of nuclear factor κβ ligand (RANKL), both inhibit bone resorption, making them logical choices in treating an osteolytic disease. Sorafenib, vincristine, sirolimus, and bevacizumab may be of clinical benefit in GSD via inhibition of vascular proliferation, which is a key histologic feature in GSD. Sorafenib inhibits the vascular endothelial growth factor (VEGF) receptor, vincristine and sirolimus inhibit VEGF production, and bevacizumab is a monoclonal antibody targeting VEGF.
The patient’s disease continued to involve more of his right hemipelvis despite this extensive regimen of chemotherapy, and he experienced significant functional decline about 2 years after initial presentation, when he was no longer able to ambulate unassisted. Radiation therapy to the pelvis was attempted at the outside institution (6/15 MV photons, 5040 cGy, 28 fractions) without improvement. Three years after his initial injury, he presented to our clinic.
Now age 30 years, the patient ambulated only with crutches and endorsed minimal improvement in his pain over 3 years of treatment. Physical examination of the patient revealed that he was a tall, thin man in visible discomfort. Sensation was intact to light touch in the bilateral L1 to S1 nerve distributions. There was marked weakness of the right lower extremity, and his examination was limited by pain. He could not perform a straight leg raise on the right side. Right quadriceps strength was 4/5, and right hamstrings strength was 3/5. There was no weakness in the left leg. Reflexes were normal and symmetric bilaterally at the patellar and gastrocnemius soleus tendons. Distal circulatory status in both extremities was normal, and there were no deformities of the skin.
Figure 1 shows the patient’s computed tomography (CT) scan. Figures 1A and 1B reveal fragmentation of the posterior ilia and sacrum along both SI joints. Dislocation of the pubic symphysis is shown in Figures 1C and 1D, and discontinuous involvement of the ischium and posterior wall of the acetabulum is visible in Figure 1E.
Serum studies, including C-reactive protein, erythrocyte sedimentation rate, and a complete blood count, were within normal limits. A CT-guided core needle biopsy and aspiration of the right SI joint revealed no infection; pathology was nondiagnostic. Anesthetic injection of the hip joint resulted in no relief. As this man was severely functionally limited and had exhausted all medical and radiation treatment options, a collaborative decision was made to proceed with surgical management. Surgical options included spinopelvic fusion unilaterally or bilaterally, hip arthroplasty, or sacropelvic resection with or without reconstruction. The patient opted for intralesional surgery and spinopelvic fusion in place of more radical options.
Thirty-seven months after his initial presentation, he underwent posterior spinal fusion L5 to S1, SI fusion, and anterior locking plate fixation of the pubic symphysis, as seen in Figure 2. Pathology from surgical specimens, seen at original magnification ×20 and ×100 in Figures 3A and 3B, respectively, showed prominent vascular proliferation in the right ilium, with reactive bone changes in the left ilium and right sacrum. A lytic lesion showed fibrous tissue with an embedded fragment of necrotic bone.
Six weeks after surgery, the patient had substantial improvement in his pain and was partially weight-bearing. He was able to ambulate with crutches and returned to work. The patient’s overall clinical status continued to improve throughout the postoperative course. He developed low back pain 7 months after surgery and was found to have a sacrococcygeal abscess and coccygeal fracture anterior to the sacrum. He underwent irrigation and débridement of the abscess and distal coccygectomy and was treated with 6 weeks of intravenous cefazolin and long-term suppression with levofloxacin and rifampin for methicillin-sensitive Staphylococcus aureus hardware infection and osteomyelitis. The patient’s clinical course subsequently improved. At latest follow-up 16 months after the index operation, pain was reported as manageable and mostly an annoyance. He was prescribed up to 40 mg of oxycodone daily for pain. The patient returned to work, ambulates with a cane (no other assistive devices), and reports being able to get around without any difficulty.
Discussion
Gorham-Stout disease is an exceedingly rare condition resulting in spontaneous osteolysis. Approximately 200 cases have been reported with no apparent gender, race, or familial predilection or systemic symptoms differentiating it from other etiologies of idiopathic osteolysis.6 These patients often seek medical attention after sustaining a pathologic fracture,6 when a broad differential diagnosis narrows to GSD only after biopsy excludes other possibilities and demonstrates characteristic angiomatosis without malignant features.2,4,6,8,10 Gorham-Stout disease appears more frequently at particular sites within the skeleton, and pelvic involvement is common—more than 20% of cases in 1 review.5,10 Limitations in the patient’s ability to ambulate invariably result from osteolysis of the pelvis, which is concerning considering the young age at which GSD typically presents. A variety of treatment modalities have been described for pelvic GSD, but surgery has been undertaken in relatively few cases.5
The diagnosis is one of exclusion after considering the clinical context and radiologic and pathologic findings. In this case, a pathologic fracture was discovered with osteolytic lesions throughout the hemipelvis. Biopsy excluded malignancy and demonstrated the key hemangiomatous vascular proliferation with thin-walled vessels that is classic for GSD. While our patient initially appeared to have 2 sites of disease, the surgical specimen revealed a primary site of vascular proliferation in the right ilium from which 2 apparent foci had spread, consistent with the typical monocentric presentation of GSD.11 A broad differential diagnosis must be considered at initial presentation, including osteomyelitis, metastatic disease, multiple myeloma, and primary bone sarcoma. Upon identifying a primary osteolytic process, several considerations besides GSD remain, such as Hajdu-Cheney syndrome, Winchester syndrome, multicentric osteolysis with nephropathy, familial osteolysis, Farber disease, and neurogenic osteolysis; most of these etiologies involve familial predispositions and/or systemic symptoms.
Treatment options for GSD include supportive care, medical therapy, radiation, and surgery. For pelvic GSD, numerous reports have demonstrated good outcomes with supportive management, since osteolysis often spontaneously arrests.8,9,12 Others have had success with medical treatments in attempts to halt bone resorption.6,13-15 Bisphosphonates are the cornerstone of medical therapy in GSD, as they appear to halt further osteoclastic bone breakdown. The levels of VEGF have been shown to be elevated in GSD,13 likely consistent with the vascular proliferation evident on pathology, and therapies such as bevacizumab and interferon α-2b have been used to target osteolysis via this pathway with good outcome.13,14,16 External beam-radiation therapy has been shown to prevent local progression of osteolysis in up to 80% of cases.4 However, even with arrest of bone resorption, damage to affected bone may have progressed to the point of significant functional limitation. This may be especially true in the pelvis.
We present a case of a patient who continued to deteriorate after maximal medical and radiation therapy. Many reported cases of pelvic GSD have had good outcomes with some combination of conservative management, medical therapy, and radiation. However, in our patient, the pelvis and lumbosacral spine were unstable as a result of significant bone loss and fracture, and his clinical deterioration was dramatic. We considered reasonable surgical approaches, including local intralesional débridement and massive en bloc resection with structural allograft. We chose the less radical procedure given the patient’s age, minimal surgical history, and personal preference. Although structural pelvic allograft has been successful in a few cases, there remains a high risk of complications, such as fracture, resorption, or infection.17 We considered the addition of hip arthroplasty with either scenario, but we elected not to perform this component given his young age and lack of symptomatic improvement with diagnostic anesthetic hip injection. The key to this patient’s surgical reconstruction, aside from eliminating gross disease, was the stabilization of the spinopelvic junction and pelvic ring. His functional improvement as early as 6 weeks after surgery demonstrates that surgery can have an important role for patients with pelvic GSD who fail medical and radiation therapy.
1. Jackson JBS. A boneless arm. Boston Med Surg J. 1838;18:368-369.
2. Gorham LW, Stout AP. Massive osteolysis (acute spontaneous absorption of bone, phantom bone, disappearing bone): its relation to hemangiomatosis. J Bone Joint Surg Am. 1955;37(5):985-1004.
3. Lehmann G, Pfeil A, Böttcher J, et al. Benefit of a 17-year long-term bisphosphonate therapy in a patient with Gorham-Stout syndrome. Arch Orthop Trauma Surg. 2009;129(7):967-972.
4. Heyd R, Micke O, Surholt C, et al; German Cooperative Group on Radiotherapy for Benign Diseases (GCG-BD). Radiation therapy for Gorham-Stout syndrome: results of a national patterns-of-care study and literature review. Int J Radiat Oncol Biol Phys. 2011;81(3):e179-e185.
5. Kulenkampff HA, Richter GM, Hasse WE, Adler CP. Massive pelvic osteolysis in the Gorham-Stout syndrome. Int Orthop. 1990;14(4):361-366.
6. Ruggieri P, Montalti M, Angelini A, Alberghini M, Mercuri M. Gorham-Stout disease: the experience of the Rizzoli Institute and review of the literature. Skeletal Radiol. 2011;40(11):1391-1397.
7. Vinée P, Tanyü MO, Hauenstein KH, Sigmund G, Stöver B, Adler CP. CT and MRI of Gorham syndrome. J Comput Assist Tomogr. 1994;18(6):985-989.
8. Boyer P, Bourgeois P, Boyer O, Catonné Y, Saillant G. Massive Gorham-Stout syndrome of the pelvis. Clin Rheumatol. 2005;24(5):551-555.
9. Malde R, Agrawal HM, Ghosh SL, Dinshaw KA. Vanishing bone disease involving the pelvis. J Cancer Res Ther. 2005;1(4):227-228.
10. Kuriyama DK, McElligott SC, Glaser DW, Thompson KS. Treatment of Gorham-Stout disease with zoledronic acid and interferon-α: a case report and literature review. J Pediatr Hematol Oncol. 2010;32(8):579-584.
11. Tie ML, Poland GA, Rosenow EC III. Chylothorax in Gorham’s syndrome. A common complication of a rare disease. Chest. 1994;105(1):208-213.
12. Möller G, Priemel M, Amling M, Werner M, Kuhlmey AS, Delling G. The Gorham-Stout syndrome (Gorham’s massive osteolysis). A report of six cases with histopathological findings. J Bone Joint Surg Br. 1999;81(3):501-506.
13. Dupond JL, Bermont L, Runge M, de Billy M. Plasma VEGF determination in disseminated lymphangiomatosis—Gorham-Stout syndrome: a marker of activity? A case report with a 5-year follow-up. Bone. 2010;46(3):873-876.
14. Wang JD, Chang TK, Cheng YY, et al. A child with dyspnea and unstable gait. Pediatr Hemat Oncol. 2007;24(4):321-324.
15. Zheng MW, Yang M, Qiu JX, et al. Gorham-Stout syndrome presenting in a 5-year-old girl with a successful bisphosphonate therapeutic effect. Exp Ther Med. 2012;4(3):449-451.
16. Timke C, Krause MF, Oppermann HC, Leuschner I, Claviez A. Interferon alpha 2b treatment in an eleven-year-old boy with disseminated lymphangiomatosis. Pediatr Blood Cancer. 2007;48(1):108-111.
17. Stöve J, Reichelt A. Massive osteolysis of the pelvis, femur and sacral bone with a Gorham-Stout syndrome. Arch Orthop Trauma Surg. 1995;114(4):207-210.
Gorham-Stout disease (GSD) is a rare condition characterized by spontaneous idiopathic resorption of bone with lymphovascular proliferation and an absence of malignant features. It was originally described by Jackson1 in an 1838 report of a 36-year-old man whose “arm bone, between the shoulder and elbow” had completely vanished after 2 fractures. The disease was defined and its pathology characterized by Gorham and Stout2 in 1955 in a series of 24 patients. Despite about 200 reported cases in the literature,3 its etiology remains unclear. Any bone in the skeleton may be affected by GSD, although there is a predilection for the skull, humerus, clavicle, ribs, pelvis, and femur.4-6 It commonly manifests within the first 3 decades of life, but case reports range from as early as 2 months of age to the eighth decade.5,7
Gorham-Stout disease is a diagnosis of exclusion that requires careful consideration of the clinical context, radiographic findings, and histopathology. Typical histopathologic findings include benign lymphatic or vascular proliferation, involution of adipose tissue within the bone marrow, and thinning of bony trabeculae.6 Fibrous tissue may replace vascular tissue after the initial vasoproliferative, osteolytic phase.6 Some authors describe the disease as having 2 phases, the first with massive osteolysis followed by relative dormancy and the second without progression or re-ossification.8,9 Treatment remains controversial and is guided by management of the disease’s complications. Options range from careful observation and supportive management to aggressive surgical resection and reconstruction, with positive outcomes reported using many different modalities.10 Most treatment successes, however, hinge on halting bony resorption using medical and radiation therapy. Surgery is usually reserved as a salvage option for patients who have failed medical modalities and have residual symptoms or functional limitations.6
This case report describes the successful surgical management of a patient with pelvic GSD who had progressive pain and functional limitation despite exhaustive medical and radiation therapy. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A healthy 27-year-old man sought medical attention after a fall while mowing his lawn that resulted in difficulty ambulating. Radiographic studies showed discontinuous lytic lesions in the right periacetabular region and the right sacroiliac (SI) joint. Biopsy at an outside institution revealed an infiltration of thin-walled branching vascular channels involving intertrabecular marrow spaces and periosteal connective tissue. The vessels were devoid of a muscular coat and lined by flattened epithelium; these features were seen as consistent with GSD.
The patient was managed medically at the outside institution for approximately 2 years, with regimens consisting of zoledronate, denosumab, sorafenib, vincristine, sirolimus, and bevacizumab. Because there is no standard chemotherapy protocol for GSD, this broad regimen was likely an attempt by treating physicians to control disease progression before considering radiation or surgery. Zoledronate, a bisphosphonate, and denosumab, a monoclonal antibody against the receptor activator of nuclear factor κβ ligand (RANKL), both inhibit bone resorption, making them logical choices in treating an osteolytic disease. Sorafenib, vincristine, sirolimus, and bevacizumab may be of clinical benefit in GSD via inhibition of vascular proliferation, which is a key histologic feature in GSD. Sorafenib inhibits the vascular endothelial growth factor (VEGF) receptor, vincristine and sirolimus inhibit VEGF production, and bevacizumab is a monoclonal antibody targeting VEGF.
The patient’s disease continued to involve more of his right hemipelvis despite this extensive regimen of chemotherapy, and he experienced significant functional decline about 2 years after initial presentation, when he was no longer able to ambulate unassisted. Radiation therapy to the pelvis was attempted at the outside institution (6/15 MV photons, 5040 cGy, 28 fractions) without improvement. Three years after his initial injury, he presented to our clinic.
Now age 30 years, the patient ambulated only with crutches and endorsed minimal improvement in his pain over 3 years of treatment. Physical examination of the patient revealed that he was a tall, thin man in visible discomfort. Sensation was intact to light touch in the bilateral L1 to S1 nerve distributions. There was marked weakness of the right lower extremity, and his examination was limited by pain. He could not perform a straight leg raise on the right side. Right quadriceps strength was 4/5, and right hamstrings strength was 3/5. There was no weakness in the left leg. Reflexes were normal and symmetric bilaterally at the patellar and gastrocnemius soleus tendons. Distal circulatory status in both extremities was normal, and there were no deformities of the skin.
Figure 1 shows the patient’s computed tomography (CT) scan. Figures 1A and 1B reveal fragmentation of the posterior ilia and sacrum along both SI joints. Dislocation of the pubic symphysis is shown in Figures 1C and 1D, and discontinuous involvement of the ischium and posterior wall of the acetabulum is visible in Figure 1E.
Serum studies, including C-reactive protein, erythrocyte sedimentation rate, and a complete blood count, were within normal limits. A CT-guided core needle biopsy and aspiration of the right SI joint revealed no infection; pathology was nondiagnostic. Anesthetic injection of the hip joint resulted in no relief. As this man was severely functionally limited and had exhausted all medical and radiation treatment options, a collaborative decision was made to proceed with surgical management. Surgical options included spinopelvic fusion unilaterally or bilaterally, hip arthroplasty, or sacropelvic resection with or without reconstruction. The patient opted for intralesional surgery and spinopelvic fusion in place of more radical options.
Thirty-seven months after his initial presentation, he underwent posterior spinal fusion L5 to S1, SI fusion, and anterior locking plate fixation of the pubic symphysis, as seen in Figure 2. Pathology from surgical specimens, seen at original magnification ×20 and ×100 in Figures 3A and 3B, respectively, showed prominent vascular proliferation in the right ilium, with reactive bone changes in the left ilium and right sacrum. A lytic lesion showed fibrous tissue with an embedded fragment of necrotic bone.
Six weeks after surgery, the patient had substantial improvement in his pain and was partially weight-bearing. He was able to ambulate with crutches and returned to work. The patient’s overall clinical status continued to improve throughout the postoperative course. He developed low back pain 7 months after surgery and was found to have a sacrococcygeal abscess and coccygeal fracture anterior to the sacrum. He underwent irrigation and débridement of the abscess and distal coccygectomy and was treated with 6 weeks of intravenous cefazolin and long-term suppression with levofloxacin and rifampin for methicillin-sensitive Staphylococcus aureus hardware infection and osteomyelitis. The patient’s clinical course subsequently improved. At latest follow-up 16 months after the index operation, pain was reported as manageable and mostly an annoyance. He was prescribed up to 40 mg of oxycodone daily for pain. The patient returned to work, ambulates with a cane (no other assistive devices), and reports being able to get around without any difficulty.
Discussion
Gorham-Stout disease is an exceedingly rare condition resulting in spontaneous osteolysis. Approximately 200 cases have been reported with no apparent gender, race, or familial predilection or systemic symptoms differentiating it from other etiologies of idiopathic osteolysis.6 These patients often seek medical attention after sustaining a pathologic fracture,6 when a broad differential diagnosis narrows to GSD only after biopsy excludes other possibilities and demonstrates characteristic angiomatosis without malignant features.2,4,6,8,10 Gorham-Stout disease appears more frequently at particular sites within the skeleton, and pelvic involvement is common—more than 20% of cases in 1 review.5,10 Limitations in the patient’s ability to ambulate invariably result from osteolysis of the pelvis, which is concerning considering the young age at which GSD typically presents. A variety of treatment modalities have been described for pelvic GSD, but surgery has been undertaken in relatively few cases.5
The diagnosis is one of exclusion after considering the clinical context and radiologic and pathologic findings. In this case, a pathologic fracture was discovered with osteolytic lesions throughout the hemipelvis. Biopsy excluded malignancy and demonstrated the key hemangiomatous vascular proliferation with thin-walled vessels that is classic for GSD. While our patient initially appeared to have 2 sites of disease, the surgical specimen revealed a primary site of vascular proliferation in the right ilium from which 2 apparent foci had spread, consistent with the typical monocentric presentation of GSD.11 A broad differential diagnosis must be considered at initial presentation, including osteomyelitis, metastatic disease, multiple myeloma, and primary bone sarcoma. Upon identifying a primary osteolytic process, several considerations besides GSD remain, such as Hajdu-Cheney syndrome, Winchester syndrome, multicentric osteolysis with nephropathy, familial osteolysis, Farber disease, and neurogenic osteolysis; most of these etiologies involve familial predispositions and/or systemic symptoms.
Treatment options for GSD include supportive care, medical therapy, radiation, and surgery. For pelvic GSD, numerous reports have demonstrated good outcomes with supportive management, since osteolysis often spontaneously arrests.8,9,12 Others have had success with medical treatments in attempts to halt bone resorption.6,13-15 Bisphosphonates are the cornerstone of medical therapy in GSD, as they appear to halt further osteoclastic bone breakdown. The levels of VEGF have been shown to be elevated in GSD,13 likely consistent with the vascular proliferation evident on pathology, and therapies such as bevacizumab and interferon α-2b have been used to target osteolysis via this pathway with good outcome.13,14,16 External beam-radiation therapy has been shown to prevent local progression of osteolysis in up to 80% of cases.4 However, even with arrest of bone resorption, damage to affected bone may have progressed to the point of significant functional limitation. This may be especially true in the pelvis.
We present a case of a patient who continued to deteriorate after maximal medical and radiation therapy. Many reported cases of pelvic GSD have had good outcomes with some combination of conservative management, medical therapy, and radiation. However, in our patient, the pelvis and lumbosacral spine were unstable as a result of significant bone loss and fracture, and his clinical deterioration was dramatic. We considered reasonable surgical approaches, including local intralesional débridement and massive en bloc resection with structural allograft. We chose the less radical procedure given the patient’s age, minimal surgical history, and personal preference. Although structural pelvic allograft has been successful in a few cases, there remains a high risk of complications, such as fracture, resorption, or infection.17 We considered the addition of hip arthroplasty with either scenario, but we elected not to perform this component given his young age and lack of symptomatic improvement with diagnostic anesthetic hip injection. The key to this patient’s surgical reconstruction, aside from eliminating gross disease, was the stabilization of the spinopelvic junction and pelvic ring. His functional improvement as early as 6 weeks after surgery demonstrates that surgery can have an important role for patients with pelvic GSD who fail medical and radiation therapy.
Gorham-Stout disease (GSD) is a rare condition characterized by spontaneous idiopathic resorption of bone with lymphovascular proliferation and an absence of malignant features. It was originally described by Jackson1 in an 1838 report of a 36-year-old man whose “arm bone, between the shoulder and elbow” had completely vanished after 2 fractures. The disease was defined and its pathology characterized by Gorham and Stout2 in 1955 in a series of 24 patients. Despite about 200 reported cases in the literature,3 its etiology remains unclear. Any bone in the skeleton may be affected by GSD, although there is a predilection for the skull, humerus, clavicle, ribs, pelvis, and femur.4-6 It commonly manifests within the first 3 decades of life, but case reports range from as early as 2 months of age to the eighth decade.5,7
Gorham-Stout disease is a diagnosis of exclusion that requires careful consideration of the clinical context, radiographic findings, and histopathology. Typical histopathologic findings include benign lymphatic or vascular proliferation, involution of adipose tissue within the bone marrow, and thinning of bony trabeculae.6 Fibrous tissue may replace vascular tissue after the initial vasoproliferative, osteolytic phase.6 Some authors describe the disease as having 2 phases, the first with massive osteolysis followed by relative dormancy and the second without progression or re-ossification.8,9 Treatment remains controversial and is guided by management of the disease’s complications. Options range from careful observation and supportive management to aggressive surgical resection and reconstruction, with positive outcomes reported using many different modalities.10 Most treatment successes, however, hinge on halting bony resorption using medical and radiation therapy. Surgery is usually reserved as a salvage option for patients who have failed medical modalities and have residual symptoms or functional limitations.6
This case report describes the successful surgical management of a patient with pelvic GSD who had progressive pain and functional limitation despite exhaustive medical and radiation therapy. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A healthy 27-year-old man sought medical attention after a fall while mowing his lawn that resulted in difficulty ambulating. Radiographic studies showed discontinuous lytic lesions in the right periacetabular region and the right sacroiliac (SI) joint. Biopsy at an outside institution revealed an infiltration of thin-walled branching vascular channels involving intertrabecular marrow spaces and periosteal connective tissue. The vessels were devoid of a muscular coat and lined by flattened epithelium; these features were seen as consistent with GSD.
The patient was managed medically at the outside institution for approximately 2 years, with regimens consisting of zoledronate, denosumab, sorafenib, vincristine, sirolimus, and bevacizumab. Because there is no standard chemotherapy protocol for GSD, this broad regimen was likely an attempt by treating physicians to control disease progression before considering radiation or surgery. Zoledronate, a bisphosphonate, and denosumab, a monoclonal antibody against the receptor activator of nuclear factor κβ ligand (RANKL), both inhibit bone resorption, making them logical choices in treating an osteolytic disease. Sorafenib, vincristine, sirolimus, and bevacizumab may be of clinical benefit in GSD via inhibition of vascular proliferation, which is a key histologic feature in GSD. Sorafenib inhibits the vascular endothelial growth factor (VEGF) receptor, vincristine and sirolimus inhibit VEGF production, and bevacizumab is a monoclonal antibody targeting VEGF.
The patient’s disease continued to involve more of his right hemipelvis despite this extensive regimen of chemotherapy, and he experienced significant functional decline about 2 years after initial presentation, when he was no longer able to ambulate unassisted. Radiation therapy to the pelvis was attempted at the outside institution (6/15 MV photons, 5040 cGy, 28 fractions) without improvement. Three years after his initial injury, he presented to our clinic.
Now age 30 years, the patient ambulated only with crutches and endorsed minimal improvement in his pain over 3 years of treatment. Physical examination of the patient revealed that he was a tall, thin man in visible discomfort. Sensation was intact to light touch in the bilateral L1 to S1 nerve distributions. There was marked weakness of the right lower extremity, and his examination was limited by pain. He could not perform a straight leg raise on the right side. Right quadriceps strength was 4/5, and right hamstrings strength was 3/5. There was no weakness in the left leg. Reflexes were normal and symmetric bilaterally at the patellar and gastrocnemius soleus tendons. Distal circulatory status in both extremities was normal, and there were no deformities of the skin.
Figure 1 shows the patient’s computed tomography (CT) scan. Figures 1A and 1B reveal fragmentation of the posterior ilia and sacrum along both SI joints. Dislocation of the pubic symphysis is shown in Figures 1C and 1D, and discontinuous involvement of the ischium and posterior wall of the acetabulum is visible in Figure 1E.
Serum studies, including C-reactive protein, erythrocyte sedimentation rate, and a complete blood count, were within normal limits. A CT-guided core needle biopsy and aspiration of the right SI joint revealed no infection; pathology was nondiagnostic. Anesthetic injection of the hip joint resulted in no relief. As this man was severely functionally limited and had exhausted all medical and radiation treatment options, a collaborative decision was made to proceed with surgical management. Surgical options included spinopelvic fusion unilaterally or bilaterally, hip arthroplasty, or sacropelvic resection with or without reconstruction. The patient opted for intralesional surgery and spinopelvic fusion in place of more radical options.
Thirty-seven months after his initial presentation, he underwent posterior spinal fusion L5 to S1, SI fusion, and anterior locking plate fixation of the pubic symphysis, as seen in Figure 2. Pathology from surgical specimens, seen at original magnification ×20 and ×100 in Figures 3A and 3B, respectively, showed prominent vascular proliferation in the right ilium, with reactive bone changes in the left ilium and right sacrum. A lytic lesion showed fibrous tissue with an embedded fragment of necrotic bone.
Six weeks after surgery, the patient had substantial improvement in his pain and was partially weight-bearing. He was able to ambulate with crutches and returned to work. The patient’s overall clinical status continued to improve throughout the postoperative course. He developed low back pain 7 months after surgery and was found to have a sacrococcygeal abscess and coccygeal fracture anterior to the sacrum. He underwent irrigation and débridement of the abscess and distal coccygectomy and was treated with 6 weeks of intravenous cefazolin and long-term suppression with levofloxacin and rifampin for methicillin-sensitive Staphylococcus aureus hardware infection and osteomyelitis. The patient’s clinical course subsequently improved. At latest follow-up 16 months after the index operation, pain was reported as manageable and mostly an annoyance. He was prescribed up to 40 mg of oxycodone daily for pain. The patient returned to work, ambulates with a cane (no other assistive devices), and reports being able to get around without any difficulty.
Discussion
Gorham-Stout disease is an exceedingly rare condition resulting in spontaneous osteolysis. Approximately 200 cases have been reported with no apparent gender, race, or familial predilection or systemic symptoms differentiating it from other etiologies of idiopathic osteolysis.6 These patients often seek medical attention after sustaining a pathologic fracture,6 when a broad differential diagnosis narrows to GSD only after biopsy excludes other possibilities and demonstrates characteristic angiomatosis without malignant features.2,4,6,8,10 Gorham-Stout disease appears more frequently at particular sites within the skeleton, and pelvic involvement is common—more than 20% of cases in 1 review.5,10 Limitations in the patient’s ability to ambulate invariably result from osteolysis of the pelvis, which is concerning considering the young age at which GSD typically presents. A variety of treatment modalities have been described for pelvic GSD, but surgery has been undertaken in relatively few cases.5
The diagnosis is one of exclusion after considering the clinical context and radiologic and pathologic findings. In this case, a pathologic fracture was discovered with osteolytic lesions throughout the hemipelvis. Biopsy excluded malignancy and demonstrated the key hemangiomatous vascular proliferation with thin-walled vessels that is classic for GSD. While our patient initially appeared to have 2 sites of disease, the surgical specimen revealed a primary site of vascular proliferation in the right ilium from which 2 apparent foci had spread, consistent with the typical monocentric presentation of GSD.11 A broad differential diagnosis must be considered at initial presentation, including osteomyelitis, metastatic disease, multiple myeloma, and primary bone sarcoma. Upon identifying a primary osteolytic process, several considerations besides GSD remain, such as Hajdu-Cheney syndrome, Winchester syndrome, multicentric osteolysis with nephropathy, familial osteolysis, Farber disease, and neurogenic osteolysis; most of these etiologies involve familial predispositions and/or systemic symptoms.
Treatment options for GSD include supportive care, medical therapy, radiation, and surgery. For pelvic GSD, numerous reports have demonstrated good outcomes with supportive management, since osteolysis often spontaneously arrests.8,9,12 Others have had success with medical treatments in attempts to halt bone resorption.6,13-15 Bisphosphonates are the cornerstone of medical therapy in GSD, as they appear to halt further osteoclastic bone breakdown. The levels of VEGF have been shown to be elevated in GSD,13 likely consistent with the vascular proliferation evident on pathology, and therapies such as bevacizumab and interferon α-2b have been used to target osteolysis via this pathway with good outcome.13,14,16 External beam-radiation therapy has been shown to prevent local progression of osteolysis in up to 80% of cases.4 However, even with arrest of bone resorption, damage to affected bone may have progressed to the point of significant functional limitation. This may be especially true in the pelvis.
We present a case of a patient who continued to deteriorate after maximal medical and radiation therapy. Many reported cases of pelvic GSD have had good outcomes with some combination of conservative management, medical therapy, and radiation. However, in our patient, the pelvis and lumbosacral spine were unstable as a result of significant bone loss and fracture, and his clinical deterioration was dramatic. We considered reasonable surgical approaches, including local intralesional débridement and massive en bloc resection with structural allograft. We chose the less radical procedure given the patient’s age, minimal surgical history, and personal preference. Although structural pelvic allograft has been successful in a few cases, there remains a high risk of complications, such as fracture, resorption, or infection.17 We considered the addition of hip arthroplasty with either scenario, but we elected not to perform this component given his young age and lack of symptomatic improvement with diagnostic anesthetic hip injection. The key to this patient’s surgical reconstruction, aside from eliminating gross disease, was the stabilization of the spinopelvic junction and pelvic ring. His functional improvement as early as 6 weeks after surgery demonstrates that surgery can have an important role for patients with pelvic GSD who fail medical and radiation therapy.
1. Jackson JBS. A boneless arm. Boston Med Surg J. 1838;18:368-369.
2. Gorham LW, Stout AP. Massive osteolysis (acute spontaneous absorption of bone, phantom bone, disappearing bone): its relation to hemangiomatosis. J Bone Joint Surg Am. 1955;37(5):985-1004.
3. Lehmann G, Pfeil A, Böttcher J, et al. Benefit of a 17-year long-term bisphosphonate therapy in a patient with Gorham-Stout syndrome. Arch Orthop Trauma Surg. 2009;129(7):967-972.
4. Heyd R, Micke O, Surholt C, et al; German Cooperative Group on Radiotherapy for Benign Diseases (GCG-BD). Radiation therapy for Gorham-Stout syndrome: results of a national patterns-of-care study and literature review. Int J Radiat Oncol Biol Phys. 2011;81(3):e179-e185.
5. Kulenkampff HA, Richter GM, Hasse WE, Adler CP. Massive pelvic osteolysis in the Gorham-Stout syndrome. Int Orthop. 1990;14(4):361-366.
6. Ruggieri P, Montalti M, Angelini A, Alberghini M, Mercuri M. Gorham-Stout disease: the experience of the Rizzoli Institute and review of the literature. Skeletal Radiol. 2011;40(11):1391-1397.
7. Vinée P, Tanyü MO, Hauenstein KH, Sigmund G, Stöver B, Adler CP. CT and MRI of Gorham syndrome. J Comput Assist Tomogr. 1994;18(6):985-989.
8. Boyer P, Bourgeois P, Boyer O, Catonné Y, Saillant G. Massive Gorham-Stout syndrome of the pelvis. Clin Rheumatol. 2005;24(5):551-555.
9. Malde R, Agrawal HM, Ghosh SL, Dinshaw KA. Vanishing bone disease involving the pelvis. J Cancer Res Ther. 2005;1(4):227-228.
10. Kuriyama DK, McElligott SC, Glaser DW, Thompson KS. Treatment of Gorham-Stout disease with zoledronic acid and interferon-α: a case report and literature review. J Pediatr Hematol Oncol. 2010;32(8):579-584.
11. Tie ML, Poland GA, Rosenow EC III. Chylothorax in Gorham’s syndrome. A common complication of a rare disease. Chest. 1994;105(1):208-213.
12. Möller G, Priemel M, Amling M, Werner M, Kuhlmey AS, Delling G. The Gorham-Stout syndrome (Gorham’s massive osteolysis). A report of six cases with histopathological findings. J Bone Joint Surg Br. 1999;81(3):501-506.
13. Dupond JL, Bermont L, Runge M, de Billy M. Plasma VEGF determination in disseminated lymphangiomatosis—Gorham-Stout syndrome: a marker of activity? A case report with a 5-year follow-up. Bone. 2010;46(3):873-876.
14. Wang JD, Chang TK, Cheng YY, et al. A child with dyspnea and unstable gait. Pediatr Hemat Oncol. 2007;24(4):321-324.
15. Zheng MW, Yang M, Qiu JX, et al. Gorham-Stout syndrome presenting in a 5-year-old girl with a successful bisphosphonate therapeutic effect. Exp Ther Med. 2012;4(3):449-451.
16. Timke C, Krause MF, Oppermann HC, Leuschner I, Claviez A. Interferon alpha 2b treatment in an eleven-year-old boy with disseminated lymphangiomatosis. Pediatr Blood Cancer. 2007;48(1):108-111.
17. Stöve J, Reichelt A. Massive osteolysis of the pelvis, femur and sacral bone with a Gorham-Stout syndrome. Arch Orthop Trauma Surg. 1995;114(4):207-210.
1. Jackson JBS. A boneless arm. Boston Med Surg J. 1838;18:368-369.
2. Gorham LW, Stout AP. Massive osteolysis (acute spontaneous absorption of bone, phantom bone, disappearing bone): its relation to hemangiomatosis. J Bone Joint Surg Am. 1955;37(5):985-1004.
3. Lehmann G, Pfeil A, Böttcher J, et al. Benefit of a 17-year long-term bisphosphonate therapy in a patient with Gorham-Stout syndrome. Arch Orthop Trauma Surg. 2009;129(7):967-972.
4. Heyd R, Micke O, Surholt C, et al; German Cooperative Group on Radiotherapy for Benign Diseases (GCG-BD). Radiation therapy for Gorham-Stout syndrome: results of a national patterns-of-care study and literature review. Int J Radiat Oncol Biol Phys. 2011;81(3):e179-e185.
5. Kulenkampff HA, Richter GM, Hasse WE, Adler CP. Massive pelvic osteolysis in the Gorham-Stout syndrome. Int Orthop. 1990;14(4):361-366.
6. Ruggieri P, Montalti M, Angelini A, Alberghini M, Mercuri M. Gorham-Stout disease: the experience of the Rizzoli Institute and review of the literature. Skeletal Radiol. 2011;40(11):1391-1397.
7. Vinée P, Tanyü MO, Hauenstein KH, Sigmund G, Stöver B, Adler CP. CT and MRI of Gorham syndrome. J Comput Assist Tomogr. 1994;18(6):985-989.
8. Boyer P, Bourgeois P, Boyer O, Catonné Y, Saillant G. Massive Gorham-Stout syndrome of the pelvis. Clin Rheumatol. 2005;24(5):551-555.
9. Malde R, Agrawal HM, Ghosh SL, Dinshaw KA. Vanishing bone disease involving the pelvis. J Cancer Res Ther. 2005;1(4):227-228.
10. Kuriyama DK, McElligott SC, Glaser DW, Thompson KS. Treatment of Gorham-Stout disease with zoledronic acid and interferon-α: a case report and literature review. J Pediatr Hematol Oncol. 2010;32(8):579-584.
11. Tie ML, Poland GA, Rosenow EC III. Chylothorax in Gorham’s syndrome. A common complication of a rare disease. Chest. 1994;105(1):208-213.
12. Möller G, Priemel M, Amling M, Werner M, Kuhlmey AS, Delling G. The Gorham-Stout syndrome (Gorham’s massive osteolysis). A report of six cases with histopathological findings. J Bone Joint Surg Br. 1999;81(3):501-506.
13. Dupond JL, Bermont L, Runge M, de Billy M. Plasma VEGF determination in disseminated lymphangiomatosis—Gorham-Stout syndrome: a marker of activity? A case report with a 5-year follow-up. Bone. 2010;46(3):873-876.
14. Wang JD, Chang TK, Cheng YY, et al. A child with dyspnea and unstable gait. Pediatr Hemat Oncol. 2007;24(4):321-324.
15. Zheng MW, Yang M, Qiu JX, et al. Gorham-Stout syndrome presenting in a 5-year-old girl with a successful bisphosphonate therapeutic effect. Exp Ther Med. 2012;4(3):449-451.
16. Timke C, Krause MF, Oppermann HC, Leuschner I, Claviez A. Interferon alpha 2b treatment in an eleven-year-old boy with disseminated lymphangiomatosis. Pediatr Blood Cancer. 2007;48(1):108-111.
17. Stöve J, Reichelt A. Massive osteolysis of the pelvis, femur and sacral bone with a Gorham-Stout syndrome. Arch Orthop Trauma Surg. 1995;114(4):207-210.
Coracoid Fracture After Reverse Total Shoulder Arthroplasty: A Report of 2 Cases
Reverse total shoulder arthroplasty (RTSA) performed in carefully selected patients often leads to satisfactory outcomes.1,2 In recent years, its indications and the number performed per year have expanded. Subsequently, there has been a concomitant rise in reported complications,2,3 with a rate ranging from 19% to 68%.2,3 Some common complications include scapular notching,2-4 fracture,2,3,5-7 dislocation,2,3,7 and infection.2,3,7
In this series, we describe 2 cases of coracoid fracture after RTSA. The patients provided written informed consent for print and electronic publication of these case reports.
Case Series
Case 1
An independently functioning 81-year-old right hand–dominant woman (BMI, 22.1 [height, 160 cm; weight, 56.7 kg]) presented with increasing left shoulder pain and dysfunction after a motor vehicle accident 2 months earlier. She had reported vague chronic left shoulder pain in the past, but after the accident her pain was significantly worse. A subacromial corticosteroid injection by her primary care physician provided temporary symptomatic relief, but her symptoms recurred.
On presentation, there was obvious anterior superior escape of the humeral head, which was accentuated by shoulder shrug. Her deltoid motor function was found to be intact, and her active shoulder range of motion was severely limited (pseudoparesis). There was notable crepitation as well as significant weakness and pain with abduction and external rotation strength testing.
Radiographic imaging showed anterior superior escape of the humeral head with some early degenerative changes (Seebauer type IIB8 [Figure 1A]). Magnetic resonance imaging confirmed a full-thickness retracted massive rotator cuff tear with complete involvement of the supraspinatus, infraspinatus, and most of the subscapularis muscles. Significant glenohumeral degenerative changes consistent with cuff tear arthropathy were also seen without any evidence of fracture.
After thorough discussion of options, risks, and benefits, the decision was made to proceed with RTSA. The patient underwent the procedure without complications. A DePuy Delta Xtend prosthesis was used with a cemented humeral stem, polyethylene, and glenosphere, sizes of 12, +3, and 38, respectively. The glenosphere component, positioned inferiorly to avoid scapular notching, was secured with 3 screws, and the stem was placed in neutral version. The patient’s shoulder was reduced, ranged, and noted to be stable, allowing for supple passive range of motion without evidence of excessive tightness. She was placed in a sling with the shoulder positioned in neutral alignment. Her postoperative radiograph (Figure 1B) showed satisfactory implantation of the reverse total shoulder prosthesis. Her postoperative course was uneventful, and rehabilitation consisted of 6 weeks of sling protection, with advancing passive and active range of motion. Strengthening exercises were initiated 6 weeks after surgery.
At the patient’s 6-week postoperative visit, she demonstrated pain-free passive elevation to 80° and active forward elevation to 70°. At her 3-month postoperative visit, she reported a 1-week onset of anterior shoulder pain accompanied by a strange noise at the anterior aspect of the operative shoulder. She denied any recent trauma. She continued to have minimal shoulder pain with passive forward flexion of 80°; however, her active forward elevation was very limited because of pain in the anterior aspect of her shoulder. Active external rotation was noted to be 20° and internal rotation was to her buttock. She had pain to palpation of the coracoid process. Radiographs were unchanged from immediate postoperative radiographs. Computed tomography (CT), which was ordered to ensure that the implant was stable with no loosening, showed satisfactory alignment of the prosthesis and no loosening. However, CT was notable for a nondisplaced fracture through the base of the coracoid (Figures 2A-2D). The patient stopped formal physical therapy, and sling immobilization was initiated. After 3 weeks, the sling was discontinued and physical therapy was begun again. She responded satisfactorily to this treatment approach, and, at her 6-month postoperative follow-up, she was without pain, instability, or crepitation. Her range of motion had improved with pain-free active forward flexion, external rotation, and abduction of 100°, 15°, and 90°, respectively. At 28-month postoperative follow-up, her visual analog scale, American Shoulder and Elbow Surgeons score, and Simple Shoulder Test score were 3, 73, and 67, respectively.
Case 2
A 68-year-old, right-handed woman (BMI, 22.5 [height, 160 cm; weight, 57.6 kg]) presented with right shoulder pain and dysfunction of 3 years’ duration. She had undergone an open rotator cuff repair at an outside facility 4 years ago that was unsuccessful. At the time of her presentation to our institution, she had already undergone a failed course of physical therapy. A trial of corticosteroid subacromial injections did not adequately manage her symptoms.
On presentation, her active forward flexion, abduction, and external rotation were 40°, 30°, and 10°, respectively. She had full passive range of motion and pain with active and passive shoulder motion. Radiographic imaging showed superior migration of the humeral head with evidence of glenohumeral arthropathy suggestive of rotator cuff arthropathy (Seebauer type IIA8). After thorough discussion of options, risks, and benefits, the decision was made to proceed with RTSA. She underwent the procedure without complications. A DePuy Delta Xtend prosthesis was used with a cemented humeral stem, polyethylene, and glenosphere, sizes of 8, +3, and 38, respectively. The glenosphere component, positioned inferiorly to avoid scapular notching, was secured with 4 screws, and the stem was placed in neutral version. Her shoulder was reduced, ranged, and noted to be stable, allowing for supple passive range of motion without evidence of excessive tightness. She was placed in a sling with the shoulder positioned in neutral alignment. Her postoperative radiographs revealed satisfactory implantation of the reverse total shoulder prosthesis. Her postoperative course was uneventful. She was taken out of her shoulder immobilizer 4 weeks after surgery and began home-based physical therapy.
At 1 year after surgery, the patient had minimal shoulder pain with active forward flexion, external rotation, and abduction of 135°, 20°, and 85°, respectively. She presented to our clinic 15 months after RTSA with acute onset of pain about her anterior shoulder. She denied any recent trauma or infectious exposures. On examination, her motion was unchanged from prior examinations. However, she was tender on palpation of the coracoid. Radiographs at that time were unchanged (Figures 3A, 3B). Laboratory tests (erythrocyte sedimentation rate, C-reactive protein, and complete blood count with differential) that were subsequently ordered to rule out an occult infection were within normal limits. Computed tomography, which was ordered for further assessment and to ensure that the implant was stable with no loosening, showed satisfactory alignment of the prosthesis without loosening. However, a lucency was noted in the midportion of the coracoid that was suggestive of a fracture (Figures 4A, 4B). A conservative plan of treatment was advised with sling immobilization for 3 weeks and follow-up visits. The patient responded satisfactorily to this treatment approach, and, at her latest follow-up, 8 months after presenting with a coracoid fracture, she was pain-free. At the 5-year postoperative follow-up, her visual analog scale, American Shoulder and Elbow Surgeons score, and Simple Shoulder Test score were 1-2, 78, and 75, respectively.
Discussion
The reverse prosthesis, a semi-constrained ball-and-socket device, provides satisfactory functional outcomes when used in carefully selected patients with rotator cuff arthropathy and pseudoparalysis, failed shoulder arthroplasty, and fracture sequelae.1,9-11 By the traditional Grammont principles of medializing the center of rotation and lowering the humerus, shear forces about the glenoid are reduced and the deltoid muscle is tensioned, allowing for adequate torque generation, required to facilitate shoulder motion.12,13 While long-term outcomes concerning durability and survivorship are pending, some studies have attempted to improve our understanding of implant and functional longevity. Guery and colleagues14 noted an implant survival of 91% at 120 months. However, increased pain and decreased function were seen at the 6-year mark.14 A more recent study by Cuff and colleagues15 revealed 94% implant survivorship and sustained improvement in range of motion and pain at 5 years.
Despite considerable success, RTSA can be associated with a myriad of complications. The most common complications of RTSA include scapular notching (44%-96%), glenoid side failure (5%-40%), instability (2.4%-31%), and infection (1%-15.3%).2,3 In the setting of inflammatory arthropathy, there is an increased risk for intraoperative and postoperative fractures.16,17 To date, there are only 2 reported cases of coracoid process fractures after RTSA.18,19 In the case by Nolan and colleagues,18 conservative management with a sling for 6 weeks led to successful resolution of symptoms. Although little information is provided on the management of these rare fractures, literature on the slightly more common scapular (0.9%-7.2%) and acromial (0.9%-4.9%) fractures suggest that periscapular fractures are on the rise, may increase the risk for revision surgery, and can lead to inferior outcomes when compared with patients without fractures.5,20,21
Acromial fractures after RTSA have been reported to occur at a rate of 0.9% to 4.9%.5,21 This is a concern because of RTSA reliance on a functional deltoid.5,6 The cause of these fractures remains to be fully elucidated. Wahlquist and colleagues6 in 2011 reported the cases of 5 patients that sustained acromial base fractures after RTSA. All 5 patients were noted to have unsatisfactory functional results despite achieving union (3 were treated with open reduction and internal fixation, and 2 were treated nonoperatively). Acromial fractures tend to present with pain within 6 months of surgery, which may indicate excessive constraint about the scapula, eventually leading to fracture. Furthermore, disruption of this bony structure can lead to devastating results because the acromial base serves as a fulcrum for the deltoid.
Despite a well-placed reverse prosthesis, there is increased reliance on surrounding glenohumeral musculature, resulting from poor rotator cuff function and biomechanical differences compared with a native shoulder. Both our patients were found to have relatively small body habitus. It is possible that, by nature of their smaller statures, they were more susceptible to consequences of excessive joint and soft-tissue tension after RTSA. One explanation for acromial fractures after RTSA is that, by excessively lengthening and/or lateralizing the deltoid, the tension on the acromion in these elderly patients may be sufficient to cause a fracture. A similar mechanism may explain their coracoid fractures. As the arm is lengthened and the prosthesis is tightened, the conjoint tendon is significantly tensioned. We routinely check the tension of these muscles as an extra confirmation of joint stability. However, excessive tension for a significant duration may provide too much stress for bone turnover to match with the inherent repair process, potentially causing a fracture. Recent evidence has also found that bone mineral density of the coracoid diminishes with age, suggesting some predisposition to fracture with lower-energy mechanisms.22
Another possible cause for coracoid fractures may be the orientation of the implants. While we did not have mechanistic evidence, it is possible that, with adduction and internal rotation, prosthetic impingement against the coracoid is feasible, particularly in patients of small stature. Although a glenoid implant placed high can increase the chance for coracoid–implant impingement, the fact that the patients improved without revision makes chronic mechanical impingement less likely. Drill holes, especially multiple ones, placed throughout the base of the coracoid may also predispose to coracoid fractures.
Patients with periscapular fractures (acromion, scapular spine, or coracoid) after RTSA often present with pain and occasional deficits in function. Both patients in this series noted pain out of proportion to examination. The onset of this pain differed, with 1 patient noting pain within the first 3 months and 1 noting discomfort later. Neither patient had any trauma. In the presence of significant symptoms, negative radiographs, and a poor response to conservative treatment, we recommend advanced imaging to rule out fracture. However, prior to obtaining advanced imaging, proper radiographic techniques should be utilized. Eyres and colleagues,23 in a series of 12 fractures of the coracoid process, relied primarily on coracoid views directed 45° in a cephalic direction and thin-slice CT. An isotope bone scan identified 1 case not initially found on radiographs.23
Conservative management with use of a sling until resolution of symptoms was successful in our series. If symptoms persist, a bone stimulator can be used prior to implementing a surgical solution; however, current evidence does not expound on timing and utility of such modalities. Perhaps as important as treatment is education of the patient and the rehabilitation team about the importance of identifying increasing pain as a potential sign of impending fracture in this population. Subsequent activity modification until the pain resolves can help avoid the setback in postoperative recovery that this complication may cause.
Conclusion
We present 2 patients with coracoid fractures encountered at 3 months and 15 months after RTSA. Nonoperative management proved adequate in treating both cases. We suggest a high level of suspicion for possible fracture in the patient who comes in with new-onset pain in a localized region with or without functional deficits.
1. Lawrence TM, Ahmadi S, Sanchez-Sotelo J, Sperling JW, Cofield RH. Patient reported activities after reverse shoulder arthroplasty: part II. J Shoulder Elbow Surg. 2012;21(11):1464-1469.
2. Cheung E, Willis M, Walker M, Clark R, Frankle MA. Complications in reverse total shoulder arthroplasty. J Am Acad Orthop Surg. 2011;19(7):439-449.
3. Affonso J, Nicholson GP, Frankle MA, et al. Complications of the reverse prosthesis: prevention and treatment. Instr Course Lect. 2012;61:157-168.
4. Lévigne C, Garret J, Boileau P, Alami G, Favard L, Walch G. Scapular notching in reverse shoulder arthroplasty: is it important to avoid it and how? Clin Orthop Relat Res. 2011;469(9):2512-2520.
5. Hamid N, Connor PM, Fleischli JF, D’Alessandro DF. Acromial fracture after reverse shoulder arthroplasty. Am J Orthop. 2011;40(7):E125-E129.
6. Wahlquist TC, Hunt AF, Braman JP. Acromial base fractures after reverse total shoulder arthroplasty: report of five cases. J Shoulder Elbow Surg. 2011;20(7):1178-1183.
7. Zumstein MA, Pinedo M, Old J, Boileau P. Problems, complications, reoperations, and revisions in reverse total shoulder arthroplasty: a systematic review. J Shoulder Elbow Surg. 2011;20(1):146-157.
8. Visotsky JL, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am. 2004;86(suppl 2):35-40.
9. Gamradt SC, Gelber J, Zhang AL. Shoulder function and pain level after revision of failed reverse shoulder replacement to hemiarthroplasty. Int J Shoulder Surg. 2012;6(2):29-35.
10. Garrigues GE, Johnston PS, Pepe MD, Tucker BS, Ramsey ML, Austin LS. Hemiarthroplasty versus reverse total shoulder arthroplasty for acute proximal humerus fractures in elderly patients. Orthopedics. 2012;35(5):e703-e708.
11. Patel DN, Young B, Onyekwelu I, Zuckerman JD, Kwon YW. Reverse total shoulder arthroplasty for failed shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(11):1473-1483.
12. Grammont PM, Baulot E. The classic: Delta shoulder prosthesis for rotator cuff rupture. 1993. Clin Orthop Relat Res. 2011;469(9):2424.
13. Schwartz DG, Kang SH, Lynch TS, et al. The anterior deltoid’s importance in reverse shoulder arthroplasty: a cadaveric biomechanical study. J Shoulder Elbow Surg. 2013;22(3):357-364.
14. Guery J, Favard L, Sirveaux F, Oudet D, Mole D, Walch G. Reverse total shoulder arthroplasty. Survivorship analysis of eighty replacements followed for five to ten years. J Bone Joint Surg Am. 2006;88(8):1742-1747.
15. Cuff D, Clark R, Pupello D, Frankle M. Reverse shoulder arthroplasty for the treatment of rotator cuff deficiency: a concise follow-up, at a minimum of five years, of a previous report. J Bone Joint Surg Am. 2012;94(21):1996-2000.
16. Young AA, Smith MM, Bacle G, Moraga C, Walch G. Early results of reverse shoulder arthroplasty in patients with rheumatoid arthritis. J Bone Joint Surg. 2011;93(20):1915-1923.
17. Hattrup SJ, Sanchez-Sotelo J, Sperling JW, Cofield RH. Reverse shoulder replacement for patients with inflammatory arthritis. J Hand Surg Am. 2012;37(9):1888-1894.
18. Nolan BM, Ankerson E, Wiater JM. Reverse total shoulder arthroplasty improves function in cuff tear arthropathy. Clin Orthop Relat Res. 2011;469(9):2476-2482.
19. Stechel A, Fuhrmann U, Irlenbusch L, Rott O, Irlenbusch U. Reversed shoulder arthroplasty in cuff tear arthritis, fracture sequelae, and revision arthroplasty. Acta Orthop. 2010;81(3):367-372.
20. Teusink MJ, Otto RJ, Cottrell BJ, Frankle MA. What is the effect of postoperative scapular fracture on outcomes of reverse shoulder arthroplasty? J Shoulder Elbow Surg. 2014;23(6):782-790.
21. Walch G, Bacle G, Lädermann A, Nové-Josserand L, Smithers CJ. Do the indications, results, and complications of reverse shoulder arthroplasty change with surgeon’s experience? J Shoulder Elbow Surg. 2012;21(11):1470-1477.
22. Beranger JS, Maqdes A, Pujol N, Desmoineaux P, Beaufils P. Bone mineral density of the coracoid process decreases with age [published online ahead of print December 17, 2014]. Knee Surg Sports Traumatol Arthrosc.
23. Eyres KS, Brooks A, Stanley D. Fractures of the coracoid process. J Bone Joint Surg Br. 1995;77(3):425-428.
Reverse total shoulder arthroplasty (RTSA) performed in carefully selected patients often leads to satisfactory outcomes.1,2 In recent years, its indications and the number performed per year have expanded. Subsequently, there has been a concomitant rise in reported complications,2,3 with a rate ranging from 19% to 68%.2,3 Some common complications include scapular notching,2-4 fracture,2,3,5-7 dislocation,2,3,7 and infection.2,3,7
In this series, we describe 2 cases of coracoid fracture after RTSA. The patients provided written informed consent for print and electronic publication of these case reports.
Case Series
Case 1
An independently functioning 81-year-old right hand–dominant woman (BMI, 22.1 [height, 160 cm; weight, 56.7 kg]) presented with increasing left shoulder pain and dysfunction after a motor vehicle accident 2 months earlier. She had reported vague chronic left shoulder pain in the past, but after the accident her pain was significantly worse. A subacromial corticosteroid injection by her primary care physician provided temporary symptomatic relief, but her symptoms recurred.
On presentation, there was obvious anterior superior escape of the humeral head, which was accentuated by shoulder shrug. Her deltoid motor function was found to be intact, and her active shoulder range of motion was severely limited (pseudoparesis). There was notable crepitation as well as significant weakness and pain with abduction and external rotation strength testing.
Radiographic imaging showed anterior superior escape of the humeral head with some early degenerative changes (Seebauer type IIB8 [Figure 1A]). Magnetic resonance imaging confirmed a full-thickness retracted massive rotator cuff tear with complete involvement of the supraspinatus, infraspinatus, and most of the subscapularis muscles. Significant glenohumeral degenerative changes consistent with cuff tear arthropathy were also seen without any evidence of fracture.
After thorough discussion of options, risks, and benefits, the decision was made to proceed with RTSA. The patient underwent the procedure without complications. A DePuy Delta Xtend prosthesis was used with a cemented humeral stem, polyethylene, and glenosphere, sizes of 12, +3, and 38, respectively. The glenosphere component, positioned inferiorly to avoid scapular notching, was secured with 3 screws, and the stem was placed in neutral version. The patient’s shoulder was reduced, ranged, and noted to be stable, allowing for supple passive range of motion without evidence of excessive tightness. She was placed in a sling with the shoulder positioned in neutral alignment. Her postoperative radiograph (Figure 1B) showed satisfactory implantation of the reverse total shoulder prosthesis. Her postoperative course was uneventful, and rehabilitation consisted of 6 weeks of sling protection, with advancing passive and active range of motion. Strengthening exercises were initiated 6 weeks after surgery.
At the patient’s 6-week postoperative visit, she demonstrated pain-free passive elevation to 80° and active forward elevation to 70°. At her 3-month postoperative visit, she reported a 1-week onset of anterior shoulder pain accompanied by a strange noise at the anterior aspect of the operative shoulder. She denied any recent trauma. She continued to have minimal shoulder pain with passive forward flexion of 80°; however, her active forward elevation was very limited because of pain in the anterior aspect of her shoulder. Active external rotation was noted to be 20° and internal rotation was to her buttock. She had pain to palpation of the coracoid process. Radiographs were unchanged from immediate postoperative radiographs. Computed tomography (CT), which was ordered to ensure that the implant was stable with no loosening, showed satisfactory alignment of the prosthesis and no loosening. However, CT was notable for a nondisplaced fracture through the base of the coracoid (Figures 2A-2D). The patient stopped formal physical therapy, and sling immobilization was initiated. After 3 weeks, the sling was discontinued and physical therapy was begun again. She responded satisfactorily to this treatment approach, and, at her 6-month postoperative follow-up, she was without pain, instability, or crepitation. Her range of motion had improved with pain-free active forward flexion, external rotation, and abduction of 100°, 15°, and 90°, respectively. At 28-month postoperative follow-up, her visual analog scale, American Shoulder and Elbow Surgeons score, and Simple Shoulder Test score were 3, 73, and 67, respectively.
Case 2
A 68-year-old, right-handed woman (BMI, 22.5 [height, 160 cm; weight, 57.6 kg]) presented with right shoulder pain and dysfunction of 3 years’ duration. She had undergone an open rotator cuff repair at an outside facility 4 years ago that was unsuccessful. At the time of her presentation to our institution, she had already undergone a failed course of physical therapy. A trial of corticosteroid subacromial injections did not adequately manage her symptoms.
On presentation, her active forward flexion, abduction, and external rotation were 40°, 30°, and 10°, respectively. She had full passive range of motion and pain with active and passive shoulder motion. Radiographic imaging showed superior migration of the humeral head with evidence of glenohumeral arthropathy suggestive of rotator cuff arthropathy (Seebauer type IIA8). After thorough discussion of options, risks, and benefits, the decision was made to proceed with RTSA. She underwent the procedure without complications. A DePuy Delta Xtend prosthesis was used with a cemented humeral stem, polyethylene, and glenosphere, sizes of 8, +3, and 38, respectively. The glenosphere component, positioned inferiorly to avoid scapular notching, was secured with 4 screws, and the stem was placed in neutral version. Her shoulder was reduced, ranged, and noted to be stable, allowing for supple passive range of motion without evidence of excessive tightness. She was placed in a sling with the shoulder positioned in neutral alignment. Her postoperative radiographs revealed satisfactory implantation of the reverse total shoulder prosthesis. Her postoperative course was uneventful. She was taken out of her shoulder immobilizer 4 weeks after surgery and began home-based physical therapy.
At 1 year after surgery, the patient had minimal shoulder pain with active forward flexion, external rotation, and abduction of 135°, 20°, and 85°, respectively. She presented to our clinic 15 months after RTSA with acute onset of pain about her anterior shoulder. She denied any recent trauma or infectious exposures. On examination, her motion was unchanged from prior examinations. However, she was tender on palpation of the coracoid. Radiographs at that time were unchanged (Figures 3A, 3B). Laboratory tests (erythrocyte sedimentation rate, C-reactive protein, and complete blood count with differential) that were subsequently ordered to rule out an occult infection were within normal limits. Computed tomography, which was ordered for further assessment and to ensure that the implant was stable with no loosening, showed satisfactory alignment of the prosthesis without loosening. However, a lucency was noted in the midportion of the coracoid that was suggestive of a fracture (Figures 4A, 4B). A conservative plan of treatment was advised with sling immobilization for 3 weeks and follow-up visits. The patient responded satisfactorily to this treatment approach, and, at her latest follow-up, 8 months after presenting with a coracoid fracture, she was pain-free. At the 5-year postoperative follow-up, her visual analog scale, American Shoulder and Elbow Surgeons score, and Simple Shoulder Test score were 1-2, 78, and 75, respectively.
Discussion
The reverse prosthesis, a semi-constrained ball-and-socket device, provides satisfactory functional outcomes when used in carefully selected patients with rotator cuff arthropathy and pseudoparalysis, failed shoulder arthroplasty, and fracture sequelae.1,9-11 By the traditional Grammont principles of medializing the center of rotation and lowering the humerus, shear forces about the glenoid are reduced and the deltoid muscle is tensioned, allowing for adequate torque generation, required to facilitate shoulder motion.12,13 While long-term outcomes concerning durability and survivorship are pending, some studies have attempted to improve our understanding of implant and functional longevity. Guery and colleagues14 noted an implant survival of 91% at 120 months. However, increased pain and decreased function were seen at the 6-year mark.14 A more recent study by Cuff and colleagues15 revealed 94% implant survivorship and sustained improvement in range of motion and pain at 5 years.
Despite considerable success, RTSA can be associated with a myriad of complications. The most common complications of RTSA include scapular notching (44%-96%), glenoid side failure (5%-40%), instability (2.4%-31%), and infection (1%-15.3%).2,3 In the setting of inflammatory arthropathy, there is an increased risk for intraoperative and postoperative fractures.16,17 To date, there are only 2 reported cases of coracoid process fractures after RTSA.18,19 In the case by Nolan and colleagues,18 conservative management with a sling for 6 weeks led to successful resolution of symptoms. Although little information is provided on the management of these rare fractures, literature on the slightly more common scapular (0.9%-7.2%) and acromial (0.9%-4.9%) fractures suggest that periscapular fractures are on the rise, may increase the risk for revision surgery, and can lead to inferior outcomes when compared with patients without fractures.5,20,21
Acromial fractures after RTSA have been reported to occur at a rate of 0.9% to 4.9%.5,21 This is a concern because of RTSA reliance on a functional deltoid.5,6 The cause of these fractures remains to be fully elucidated. Wahlquist and colleagues6 in 2011 reported the cases of 5 patients that sustained acromial base fractures after RTSA. All 5 patients were noted to have unsatisfactory functional results despite achieving union (3 were treated with open reduction and internal fixation, and 2 were treated nonoperatively). Acromial fractures tend to present with pain within 6 months of surgery, which may indicate excessive constraint about the scapula, eventually leading to fracture. Furthermore, disruption of this bony structure can lead to devastating results because the acromial base serves as a fulcrum for the deltoid.
Despite a well-placed reverse prosthesis, there is increased reliance on surrounding glenohumeral musculature, resulting from poor rotator cuff function and biomechanical differences compared with a native shoulder. Both our patients were found to have relatively small body habitus. It is possible that, by nature of their smaller statures, they were more susceptible to consequences of excessive joint and soft-tissue tension after RTSA. One explanation for acromial fractures after RTSA is that, by excessively lengthening and/or lateralizing the deltoid, the tension on the acromion in these elderly patients may be sufficient to cause a fracture. A similar mechanism may explain their coracoid fractures. As the arm is lengthened and the prosthesis is tightened, the conjoint tendon is significantly tensioned. We routinely check the tension of these muscles as an extra confirmation of joint stability. However, excessive tension for a significant duration may provide too much stress for bone turnover to match with the inherent repair process, potentially causing a fracture. Recent evidence has also found that bone mineral density of the coracoid diminishes with age, suggesting some predisposition to fracture with lower-energy mechanisms.22
Another possible cause for coracoid fractures may be the orientation of the implants. While we did not have mechanistic evidence, it is possible that, with adduction and internal rotation, prosthetic impingement against the coracoid is feasible, particularly in patients of small stature. Although a glenoid implant placed high can increase the chance for coracoid–implant impingement, the fact that the patients improved without revision makes chronic mechanical impingement less likely. Drill holes, especially multiple ones, placed throughout the base of the coracoid may also predispose to coracoid fractures.
Patients with periscapular fractures (acromion, scapular spine, or coracoid) after RTSA often present with pain and occasional deficits in function. Both patients in this series noted pain out of proportion to examination. The onset of this pain differed, with 1 patient noting pain within the first 3 months and 1 noting discomfort later. Neither patient had any trauma. In the presence of significant symptoms, negative radiographs, and a poor response to conservative treatment, we recommend advanced imaging to rule out fracture. However, prior to obtaining advanced imaging, proper radiographic techniques should be utilized. Eyres and colleagues,23 in a series of 12 fractures of the coracoid process, relied primarily on coracoid views directed 45° in a cephalic direction and thin-slice CT. An isotope bone scan identified 1 case not initially found on radiographs.23
Conservative management with use of a sling until resolution of symptoms was successful in our series. If symptoms persist, a bone stimulator can be used prior to implementing a surgical solution; however, current evidence does not expound on timing and utility of such modalities. Perhaps as important as treatment is education of the patient and the rehabilitation team about the importance of identifying increasing pain as a potential sign of impending fracture in this population. Subsequent activity modification until the pain resolves can help avoid the setback in postoperative recovery that this complication may cause.
Conclusion
We present 2 patients with coracoid fractures encountered at 3 months and 15 months after RTSA. Nonoperative management proved adequate in treating both cases. We suggest a high level of suspicion for possible fracture in the patient who comes in with new-onset pain in a localized region with or without functional deficits.
Reverse total shoulder arthroplasty (RTSA) performed in carefully selected patients often leads to satisfactory outcomes.1,2 In recent years, its indications and the number performed per year have expanded. Subsequently, there has been a concomitant rise in reported complications,2,3 with a rate ranging from 19% to 68%.2,3 Some common complications include scapular notching,2-4 fracture,2,3,5-7 dislocation,2,3,7 and infection.2,3,7
In this series, we describe 2 cases of coracoid fracture after RTSA. The patients provided written informed consent for print and electronic publication of these case reports.
Case Series
Case 1
An independently functioning 81-year-old right hand–dominant woman (BMI, 22.1 [height, 160 cm; weight, 56.7 kg]) presented with increasing left shoulder pain and dysfunction after a motor vehicle accident 2 months earlier. She had reported vague chronic left shoulder pain in the past, but after the accident her pain was significantly worse. A subacromial corticosteroid injection by her primary care physician provided temporary symptomatic relief, but her symptoms recurred.
On presentation, there was obvious anterior superior escape of the humeral head, which was accentuated by shoulder shrug. Her deltoid motor function was found to be intact, and her active shoulder range of motion was severely limited (pseudoparesis). There was notable crepitation as well as significant weakness and pain with abduction and external rotation strength testing.
Radiographic imaging showed anterior superior escape of the humeral head with some early degenerative changes (Seebauer type IIB8 [Figure 1A]). Magnetic resonance imaging confirmed a full-thickness retracted massive rotator cuff tear with complete involvement of the supraspinatus, infraspinatus, and most of the subscapularis muscles. Significant glenohumeral degenerative changes consistent with cuff tear arthropathy were also seen without any evidence of fracture.
After thorough discussion of options, risks, and benefits, the decision was made to proceed with RTSA. The patient underwent the procedure without complications. A DePuy Delta Xtend prosthesis was used with a cemented humeral stem, polyethylene, and glenosphere, sizes of 12, +3, and 38, respectively. The glenosphere component, positioned inferiorly to avoid scapular notching, was secured with 3 screws, and the stem was placed in neutral version. The patient’s shoulder was reduced, ranged, and noted to be stable, allowing for supple passive range of motion without evidence of excessive tightness. She was placed in a sling with the shoulder positioned in neutral alignment. Her postoperative radiograph (Figure 1B) showed satisfactory implantation of the reverse total shoulder prosthesis. Her postoperative course was uneventful, and rehabilitation consisted of 6 weeks of sling protection, with advancing passive and active range of motion. Strengthening exercises were initiated 6 weeks after surgery.
At the patient’s 6-week postoperative visit, she demonstrated pain-free passive elevation to 80° and active forward elevation to 70°. At her 3-month postoperative visit, she reported a 1-week onset of anterior shoulder pain accompanied by a strange noise at the anterior aspect of the operative shoulder. She denied any recent trauma. She continued to have minimal shoulder pain with passive forward flexion of 80°; however, her active forward elevation was very limited because of pain in the anterior aspect of her shoulder. Active external rotation was noted to be 20° and internal rotation was to her buttock. She had pain to palpation of the coracoid process. Radiographs were unchanged from immediate postoperative radiographs. Computed tomography (CT), which was ordered to ensure that the implant was stable with no loosening, showed satisfactory alignment of the prosthesis and no loosening. However, CT was notable for a nondisplaced fracture through the base of the coracoid (Figures 2A-2D). The patient stopped formal physical therapy, and sling immobilization was initiated. After 3 weeks, the sling was discontinued and physical therapy was begun again. She responded satisfactorily to this treatment approach, and, at her 6-month postoperative follow-up, she was without pain, instability, or crepitation. Her range of motion had improved with pain-free active forward flexion, external rotation, and abduction of 100°, 15°, and 90°, respectively. At 28-month postoperative follow-up, her visual analog scale, American Shoulder and Elbow Surgeons score, and Simple Shoulder Test score were 3, 73, and 67, respectively.
Case 2
A 68-year-old, right-handed woman (BMI, 22.5 [height, 160 cm; weight, 57.6 kg]) presented with right shoulder pain and dysfunction of 3 years’ duration. She had undergone an open rotator cuff repair at an outside facility 4 years ago that was unsuccessful. At the time of her presentation to our institution, she had already undergone a failed course of physical therapy. A trial of corticosteroid subacromial injections did not adequately manage her symptoms.
On presentation, her active forward flexion, abduction, and external rotation were 40°, 30°, and 10°, respectively. She had full passive range of motion and pain with active and passive shoulder motion. Radiographic imaging showed superior migration of the humeral head with evidence of glenohumeral arthropathy suggestive of rotator cuff arthropathy (Seebauer type IIA8). After thorough discussion of options, risks, and benefits, the decision was made to proceed with RTSA. She underwent the procedure without complications. A DePuy Delta Xtend prosthesis was used with a cemented humeral stem, polyethylene, and glenosphere, sizes of 8, +3, and 38, respectively. The glenosphere component, positioned inferiorly to avoid scapular notching, was secured with 4 screws, and the stem was placed in neutral version. Her shoulder was reduced, ranged, and noted to be stable, allowing for supple passive range of motion without evidence of excessive tightness. She was placed in a sling with the shoulder positioned in neutral alignment. Her postoperative radiographs revealed satisfactory implantation of the reverse total shoulder prosthesis. Her postoperative course was uneventful. She was taken out of her shoulder immobilizer 4 weeks after surgery and began home-based physical therapy.
At 1 year after surgery, the patient had minimal shoulder pain with active forward flexion, external rotation, and abduction of 135°, 20°, and 85°, respectively. She presented to our clinic 15 months after RTSA with acute onset of pain about her anterior shoulder. She denied any recent trauma or infectious exposures. On examination, her motion was unchanged from prior examinations. However, she was tender on palpation of the coracoid. Radiographs at that time were unchanged (Figures 3A, 3B). Laboratory tests (erythrocyte sedimentation rate, C-reactive protein, and complete blood count with differential) that were subsequently ordered to rule out an occult infection were within normal limits. Computed tomography, which was ordered for further assessment and to ensure that the implant was stable with no loosening, showed satisfactory alignment of the prosthesis without loosening. However, a lucency was noted in the midportion of the coracoid that was suggestive of a fracture (Figures 4A, 4B). A conservative plan of treatment was advised with sling immobilization for 3 weeks and follow-up visits. The patient responded satisfactorily to this treatment approach, and, at her latest follow-up, 8 months after presenting with a coracoid fracture, she was pain-free. At the 5-year postoperative follow-up, her visual analog scale, American Shoulder and Elbow Surgeons score, and Simple Shoulder Test score were 1-2, 78, and 75, respectively.
Discussion
The reverse prosthesis, a semi-constrained ball-and-socket device, provides satisfactory functional outcomes when used in carefully selected patients with rotator cuff arthropathy and pseudoparalysis, failed shoulder arthroplasty, and fracture sequelae.1,9-11 By the traditional Grammont principles of medializing the center of rotation and lowering the humerus, shear forces about the glenoid are reduced and the deltoid muscle is tensioned, allowing for adequate torque generation, required to facilitate shoulder motion.12,13 While long-term outcomes concerning durability and survivorship are pending, some studies have attempted to improve our understanding of implant and functional longevity. Guery and colleagues14 noted an implant survival of 91% at 120 months. However, increased pain and decreased function were seen at the 6-year mark.14 A more recent study by Cuff and colleagues15 revealed 94% implant survivorship and sustained improvement in range of motion and pain at 5 years.
Despite considerable success, RTSA can be associated with a myriad of complications. The most common complications of RTSA include scapular notching (44%-96%), glenoid side failure (5%-40%), instability (2.4%-31%), and infection (1%-15.3%).2,3 In the setting of inflammatory arthropathy, there is an increased risk for intraoperative and postoperative fractures.16,17 To date, there are only 2 reported cases of coracoid process fractures after RTSA.18,19 In the case by Nolan and colleagues,18 conservative management with a sling for 6 weeks led to successful resolution of symptoms. Although little information is provided on the management of these rare fractures, literature on the slightly more common scapular (0.9%-7.2%) and acromial (0.9%-4.9%) fractures suggest that periscapular fractures are on the rise, may increase the risk for revision surgery, and can lead to inferior outcomes when compared with patients without fractures.5,20,21
Acromial fractures after RTSA have been reported to occur at a rate of 0.9% to 4.9%.5,21 This is a concern because of RTSA reliance on a functional deltoid.5,6 The cause of these fractures remains to be fully elucidated. Wahlquist and colleagues6 in 2011 reported the cases of 5 patients that sustained acromial base fractures after RTSA. All 5 patients were noted to have unsatisfactory functional results despite achieving union (3 were treated with open reduction and internal fixation, and 2 were treated nonoperatively). Acromial fractures tend to present with pain within 6 months of surgery, which may indicate excessive constraint about the scapula, eventually leading to fracture. Furthermore, disruption of this bony structure can lead to devastating results because the acromial base serves as a fulcrum for the deltoid.
Despite a well-placed reverse prosthesis, there is increased reliance on surrounding glenohumeral musculature, resulting from poor rotator cuff function and biomechanical differences compared with a native shoulder. Both our patients were found to have relatively small body habitus. It is possible that, by nature of their smaller statures, they were more susceptible to consequences of excessive joint and soft-tissue tension after RTSA. One explanation for acromial fractures after RTSA is that, by excessively lengthening and/or lateralizing the deltoid, the tension on the acromion in these elderly patients may be sufficient to cause a fracture. A similar mechanism may explain their coracoid fractures. As the arm is lengthened and the prosthesis is tightened, the conjoint tendon is significantly tensioned. We routinely check the tension of these muscles as an extra confirmation of joint stability. However, excessive tension for a significant duration may provide too much stress for bone turnover to match with the inherent repair process, potentially causing a fracture. Recent evidence has also found that bone mineral density of the coracoid diminishes with age, suggesting some predisposition to fracture with lower-energy mechanisms.22
Another possible cause for coracoid fractures may be the orientation of the implants. While we did not have mechanistic evidence, it is possible that, with adduction and internal rotation, prosthetic impingement against the coracoid is feasible, particularly in patients of small stature. Although a glenoid implant placed high can increase the chance for coracoid–implant impingement, the fact that the patients improved without revision makes chronic mechanical impingement less likely. Drill holes, especially multiple ones, placed throughout the base of the coracoid may also predispose to coracoid fractures.
Patients with periscapular fractures (acromion, scapular spine, or coracoid) after RTSA often present with pain and occasional deficits in function. Both patients in this series noted pain out of proportion to examination. The onset of this pain differed, with 1 patient noting pain within the first 3 months and 1 noting discomfort later. Neither patient had any trauma. In the presence of significant symptoms, negative radiographs, and a poor response to conservative treatment, we recommend advanced imaging to rule out fracture. However, prior to obtaining advanced imaging, proper radiographic techniques should be utilized. Eyres and colleagues,23 in a series of 12 fractures of the coracoid process, relied primarily on coracoid views directed 45° in a cephalic direction and thin-slice CT. An isotope bone scan identified 1 case not initially found on radiographs.23
Conservative management with use of a sling until resolution of symptoms was successful in our series. If symptoms persist, a bone stimulator can be used prior to implementing a surgical solution; however, current evidence does not expound on timing and utility of such modalities. Perhaps as important as treatment is education of the patient and the rehabilitation team about the importance of identifying increasing pain as a potential sign of impending fracture in this population. Subsequent activity modification until the pain resolves can help avoid the setback in postoperative recovery that this complication may cause.
Conclusion
We present 2 patients with coracoid fractures encountered at 3 months and 15 months after RTSA. Nonoperative management proved adequate in treating both cases. We suggest a high level of suspicion for possible fracture in the patient who comes in with new-onset pain in a localized region with or without functional deficits.
1. Lawrence TM, Ahmadi S, Sanchez-Sotelo J, Sperling JW, Cofield RH. Patient reported activities after reverse shoulder arthroplasty: part II. J Shoulder Elbow Surg. 2012;21(11):1464-1469.
2. Cheung E, Willis M, Walker M, Clark R, Frankle MA. Complications in reverse total shoulder arthroplasty. J Am Acad Orthop Surg. 2011;19(7):439-449.
3. Affonso J, Nicholson GP, Frankle MA, et al. Complications of the reverse prosthesis: prevention and treatment. Instr Course Lect. 2012;61:157-168.
4. Lévigne C, Garret J, Boileau P, Alami G, Favard L, Walch G. Scapular notching in reverse shoulder arthroplasty: is it important to avoid it and how? Clin Orthop Relat Res. 2011;469(9):2512-2520.
5. Hamid N, Connor PM, Fleischli JF, D’Alessandro DF. Acromial fracture after reverse shoulder arthroplasty. Am J Orthop. 2011;40(7):E125-E129.
6. Wahlquist TC, Hunt AF, Braman JP. Acromial base fractures after reverse total shoulder arthroplasty: report of five cases. J Shoulder Elbow Surg. 2011;20(7):1178-1183.
7. Zumstein MA, Pinedo M, Old J, Boileau P. Problems, complications, reoperations, and revisions in reverse total shoulder arthroplasty: a systematic review. J Shoulder Elbow Surg. 2011;20(1):146-157.
8. Visotsky JL, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am. 2004;86(suppl 2):35-40.
9. Gamradt SC, Gelber J, Zhang AL. Shoulder function and pain level after revision of failed reverse shoulder replacement to hemiarthroplasty. Int J Shoulder Surg. 2012;6(2):29-35.
10. Garrigues GE, Johnston PS, Pepe MD, Tucker BS, Ramsey ML, Austin LS. Hemiarthroplasty versus reverse total shoulder arthroplasty for acute proximal humerus fractures in elderly patients. Orthopedics. 2012;35(5):e703-e708.
11. Patel DN, Young B, Onyekwelu I, Zuckerman JD, Kwon YW. Reverse total shoulder arthroplasty for failed shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(11):1473-1483.
12. Grammont PM, Baulot E. The classic: Delta shoulder prosthesis for rotator cuff rupture. 1993. Clin Orthop Relat Res. 2011;469(9):2424.
13. Schwartz DG, Kang SH, Lynch TS, et al. The anterior deltoid’s importance in reverse shoulder arthroplasty: a cadaveric biomechanical study. J Shoulder Elbow Surg. 2013;22(3):357-364.
14. Guery J, Favard L, Sirveaux F, Oudet D, Mole D, Walch G. Reverse total shoulder arthroplasty. Survivorship analysis of eighty replacements followed for five to ten years. J Bone Joint Surg Am. 2006;88(8):1742-1747.
15. Cuff D, Clark R, Pupello D, Frankle M. Reverse shoulder arthroplasty for the treatment of rotator cuff deficiency: a concise follow-up, at a minimum of five years, of a previous report. J Bone Joint Surg Am. 2012;94(21):1996-2000.
16. Young AA, Smith MM, Bacle G, Moraga C, Walch G. Early results of reverse shoulder arthroplasty in patients with rheumatoid arthritis. J Bone Joint Surg. 2011;93(20):1915-1923.
17. Hattrup SJ, Sanchez-Sotelo J, Sperling JW, Cofield RH. Reverse shoulder replacement for patients with inflammatory arthritis. J Hand Surg Am. 2012;37(9):1888-1894.
18. Nolan BM, Ankerson E, Wiater JM. Reverse total shoulder arthroplasty improves function in cuff tear arthropathy. Clin Orthop Relat Res. 2011;469(9):2476-2482.
19. Stechel A, Fuhrmann U, Irlenbusch L, Rott O, Irlenbusch U. Reversed shoulder arthroplasty in cuff tear arthritis, fracture sequelae, and revision arthroplasty. Acta Orthop. 2010;81(3):367-372.
20. Teusink MJ, Otto RJ, Cottrell BJ, Frankle MA. What is the effect of postoperative scapular fracture on outcomes of reverse shoulder arthroplasty? J Shoulder Elbow Surg. 2014;23(6):782-790.
21. Walch G, Bacle G, Lädermann A, Nové-Josserand L, Smithers CJ. Do the indications, results, and complications of reverse shoulder arthroplasty change with surgeon’s experience? J Shoulder Elbow Surg. 2012;21(11):1470-1477.
22. Beranger JS, Maqdes A, Pujol N, Desmoineaux P, Beaufils P. Bone mineral density of the coracoid process decreases with age [published online ahead of print December 17, 2014]. Knee Surg Sports Traumatol Arthrosc.
23. Eyres KS, Brooks A, Stanley D. Fractures of the coracoid process. J Bone Joint Surg Br. 1995;77(3):425-428.
1. Lawrence TM, Ahmadi S, Sanchez-Sotelo J, Sperling JW, Cofield RH. Patient reported activities after reverse shoulder arthroplasty: part II. J Shoulder Elbow Surg. 2012;21(11):1464-1469.
2. Cheung E, Willis M, Walker M, Clark R, Frankle MA. Complications in reverse total shoulder arthroplasty. J Am Acad Orthop Surg. 2011;19(7):439-449.
3. Affonso J, Nicholson GP, Frankle MA, et al. Complications of the reverse prosthesis: prevention and treatment. Instr Course Lect. 2012;61:157-168.
4. Lévigne C, Garret J, Boileau P, Alami G, Favard L, Walch G. Scapular notching in reverse shoulder arthroplasty: is it important to avoid it and how? Clin Orthop Relat Res. 2011;469(9):2512-2520.
5. Hamid N, Connor PM, Fleischli JF, D’Alessandro DF. Acromial fracture after reverse shoulder arthroplasty. Am J Orthop. 2011;40(7):E125-E129.
6. Wahlquist TC, Hunt AF, Braman JP. Acromial base fractures after reverse total shoulder arthroplasty: report of five cases. J Shoulder Elbow Surg. 2011;20(7):1178-1183.
7. Zumstein MA, Pinedo M, Old J, Boileau P. Problems, complications, reoperations, and revisions in reverse total shoulder arthroplasty: a systematic review. J Shoulder Elbow Surg. 2011;20(1):146-157.
8. Visotsky JL, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am. 2004;86(suppl 2):35-40.
9. Gamradt SC, Gelber J, Zhang AL. Shoulder function and pain level after revision of failed reverse shoulder replacement to hemiarthroplasty. Int J Shoulder Surg. 2012;6(2):29-35.
10. Garrigues GE, Johnston PS, Pepe MD, Tucker BS, Ramsey ML, Austin LS. Hemiarthroplasty versus reverse total shoulder arthroplasty for acute proximal humerus fractures in elderly patients. Orthopedics. 2012;35(5):e703-e708.
11. Patel DN, Young B, Onyekwelu I, Zuckerman JD, Kwon YW. Reverse total shoulder arthroplasty for failed shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(11):1473-1483.
12. Grammont PM, Baulot E. The classic: Delta shoulder prosthesis for rotator cuff rupture. 1993. Clin Orthop Relat Res. 2011;469(9):2424.
13. Schwartz DG, Kang SH, Lynch TS, et al. The anterior deltoid’s importance in reverse shoulder arthroplasty: a cadaveric biomechanical study. J Shoulder Elbow Surg. 2013;22(3):357-364.
14. Guery J, Favard L, Sirveaux F, Oudet D, Mole D, Walch G. Reverse total shoulder arthroplasty. Survivorship analysis of eighty replacements followed for five to ten years. J Bone Joint Surg Am. 2006;88(8):1742-1747.
15. Cuff D, Clark R, Pupello D, Frankle M. Reverse shoulder arthroplasty for the treatment of rotator cuff deficiency: a concise follow-up, at a minimum of five years, of a previous report. J Bone Joint Surg Am. 2012;94(21):1996-2000.
16. Young AA, Smith MM, Bacle G, Moraga C, Walch G. Early results of reverse shoulder arthroplasty in patients with rheumatoid arthritis. J Bone Joint Surg. 2011;93(20):1915-1923.
17. Hattrup SJ, Sanchez-Sotelo J, Sperling JW, Cofield RH. Reverse shoulder replacement for patients with inflammatory arthritis. J Hand Surg Am. 2012;37(9):1888-1894.
18. Nolan BM, Ankerson E, Wiater JM. Reverse total shoulder arthroplasty improves function in cuff tear arthropathy. Clin Orthop Relat Res. 2011;469(9):2476-2482.
19. Stechel A, Fuhrmann U, Irlenbusch L, Rott O, Irlenbusch U. Reversed shoulder arthroplasty in cuff tear arthritis, fracture sequelae, and revision arthroplasty. Acta Orthop. 2010;81(3):367-372.
20. Teusink MJ, Otto RJ, Cottrell BJ, Frankle MA. What is the effect of postoperative scapular fracture on outcomes of reverse shoulder arthroplasty? J Shoulder Elbow Surg. 2014;23(6):782-790.
21. Walch G, Bacle G, Lädermann A, Nové-Josserand L, Smithers CJ. Do the indications, results, and complications of reverse shoulder arthroplasty change with surgeon’s experience? J Shoulder Elbow Surg. 2012;21(11):1470-1477.
22. Beranger JS, Maqdes A, Pujol N, Desmoineaux P, Beaufils P. Bone mineral density of the coracoid process decreases with age [published online ahead of print December 17, 2014]. Knee Surg Sports Traumatol Arthrosc.
23. Eyres KS, Brooks A, Stanley D. Fractures of the coracoid process. J Bone Joint Surg Br. 1995;77(3):425-428.
Medicaid Insurance Is Associated With Larger Curves in Patients Who Require Scoliosis Surgery
Rising health care costs have led many health insurers to limit benefits, which may be a problem for children in need of specialty care. Uninsured children have poorer access to specialty care than insured children. Children with public health coverage have better access to specialty care than uninsured children but inferior access compared with privately insured children.1,2 It is well documented that children with government insurance have limited access to orthopedic care for fractures, ligamentous knee injuries, and other injuries.1,3-5 Adolescent idiopathic scoliosis (AIS) differs from many other conditions managed by pediatric orthopedists, as it may be progressive, with management becoming increasingly more complex as the curve magnitude increases.6 The ability to access care earlier in the disease process may allow for earlier nonoperative interventions, such as bracing. For patients who require spinal fusion, earlier diagnosis and referral to a specialist could potentially result in shorter fusions and preserve distal motion segments. The ability to access the health care system in a timely fashion would therefore be of utmost importance for patients with scoliosis.
The literature on AIS is lacking in studies focused on care access based on insurance coverage and the potential impact that this may have on curve progression.7-9 We conducted a study to determine whether there is a difference between patients with and without private insurance who present to a busy urban pediatric orthopedic practice for management of scoliosis that eventually resulted in surgical treatment.
Materials and Methods
After obtaining institutional review board approval for this study, we retrospectively reviewed the medical records of patients (age, 10-18 years) who underwent posterior spinal fusion (PSF) for newly diagnosed AIS between 2008 and 2012. We excluded patients treated with growing spine instrumentation (growing rods), patients younger than 10 years or older than 18 years at presentation, and patients without adequate radiographs or clinical data, including insurance status. To focus on newly diagnosed scoliosis, we also excluded patients who had been seen for second opinions or whose scoliosis had been managed elsewhere in the past. Patients with syndromic, neuromuscular, or congenital scoliosis were also excluded.
Medical records were checked to ascertain time from initial evaluation to decision for surgery, time from recommendation for surgery until actual procedure, and insurance status. Distance traveled was figured from patients’ home addresses. Cobb angles were calculated from initial preoperative and final preoperative posteroanterior (PA) radiographs. Curves as seen on PA, lateral, and maximal effort, supine bending thoracic and lumbar radiographs from the initial preoperative visit were classified using the system of Lenke and colleagues.10 Hospital records were queried to determine number of levels fused at surgery, number of implants placed, and length of stay. Patients were evaluated without prior screening of insurance status and without prior consultation with referring physicians. Surgical procedures were scheduled on a first-come, first-served basis without preference for insurance status.
Results
We identified 135 consecutive patients with newly diagnosed AIS treated with PSF by our group between January 2008 and December 2012 (Table 1). Sixty-one percent had private insurance; 39% had Medicaid. There was no difference in age or ASA (American Society of Anesthesiologists) score between groups. Mean (SD) Cobb angle at initial presentation was 47.5° (14.3°) (range, 18.0°-86.0°) for the private insurance group and 57.2° (15.7°) (range, 23.0°-95.0°) for the Medicaid group (P < .0001). At time of surgery, mean (SD) Cobb angles were 54.6° (11.7°) and 60.6° (13.9°) for the private insurance and Medicaid groups, respectively (P = .008). There was no difference in curve types (Lenke and colleagues10 classification) between groups (Table 2, P = .83). Medicaid patients traveled a shorter mean (SD) distance for care, 56.3 (57.0) miles, versus 73.7 (66.7) miles (P = .05). There was no statistical difference (P = .14) in mean (SD) surgical wait time from surgery recommendation to actual surgery, 103.1 (62.4) days and 128.8 (137.5) days for the private insurance and Medicaid groups, respectively. The difference between patient groups in mean (SD) number of levels fused did not reach statistical significance (P = .16), 10.3 (2.2) levels for the Medicaid group and 9.7 (2.3) levels for the private insurance group. Mean (SD) estimated blood loss was higher for Medicaid patients, 445.7 (415.9) mL versus 335.1 (271.5) mL (P = .06), though there was no difference in use of posterior column osteotomies between groups. There was no difference (P = .11) in mean (SD) length of hospital stay between Medicaid patients, 2.6 (0.8) days, and private insurance patients, 2.4 (0.5) days.
Discussion
According to an extensive body of literature, patients with government insurance have limited access to specialty care.1,11,12 Medicaid-insured children in need of orthopedic care are no exception. Sabharwal and colleagues13 examined a database of pediatric fracture cases and found that 52% of the privately insured patients and 22% of the publicly insured patients received orthopedic care (P = .013).13 When Pierce and colleagues14 called 42 orthopedic practices regarding a fictitious 14-year-old patient with an anterior cruciate ligament tear, 38 offered an appointment within 2 weeks to a privately insured patient, and 6 offered such an appointment to a publicly insured patient. Skaggs and colleagues4 surveyed 230 orthopedic practices nationally and found that Medicaid-insured children had limited access to orthopedic care; 41 practices (18%) would not see a child with Medicaid under any circumstances. Using a fictitious case of a 10-year-old boy with a forearm fracture, Iobst and colleagues3 tried making an appointment at 100 orthopedic offices. Eight gave an appointment within 1 week to a Medicaid-insured patient, and 36 gave an appointment to a privately insured patient.3
There are few data regarding insurance status and scoliosis care in children. Spinal deformity differs from simple fractures and ligamentous injuries, as timely care may result in a less invasive treatment (bracing) if the curvature is caught early. Goldstein and colleagues9 recently evaluated 642 patients who presented for scoliosis evaluation over a 10-year period. There was no difference in curve magnitudes between patients with and without Medicaid insurance. Thirty-two percent of these patients were evaluated for a second opinion, and the authors chose not to subdivide patients on the basis of curve severity and treatment needed, noting only no difference between groups. There was no discussion of the potential difference between patients with and without private insurance with respect to surgically versus nonsurgically treated curves. We wanted to focus specifically on patients who required surgical intervention, as our experience has been that many patients with government insurance present with either very mild scoliosis (10°) or very large curves that were not identified because of lack of primary care access or inadequate school screening. Although summing these 2 groups would result in a similar average, they would represent a different cohort than patients with curves along a bell curve. Furthermore, it is the group of patients who would require surgical intervention that is so critical to identify early in order to intervene.
Our data suggest a difference in presenting curves between patients with and without private insurance. The approximately 10° difference between patient groups in this study could potentially represent the difference between bracing and surgery. Furthermore, Miyanji and colleagues6 evaluated the relationship between Cobb angle and health care consumption and correlated larger curve magnitudes with more levels fused, longer surgeries, and higher rates of transfusion. Specifically, every 10° increase in curve magnitude resulted in 7.8 more minutes of operative time, 0.3 extra levels fused, and 1.5 times increased risk for requiring a blood transfusion.
Cho and Egorova15 recently evaluated insurance status with respect to surgical outcomes using a national inpatient database and found that 42.4% of surgeries for AIS in children with Medicaid had fusions involving 9 or more levels, whereas only 33.6% of privately insured patients had fusions of 9 or more levels. There was no difference in osteotomy or reoperation for pseudarthrosis between groups, but there was a slightly higher rate of infectious (1.1% vs 0.6%) and hemorrhagic (2.5% vs 1.7%) complications in the Medicaid group. Hospital stay was longer in patients with Medicaid, though complications were not different between groups.
The mean difference in the magnitude of the curves treated in our study was not more than 10° between patients with and without Medicaid, perhaps explaining the lack of a statistically significant difference in number of levels fused between groups. Although the groups were similar with respect to the percentage requiring posterior column spinal osteotomies, we noted a difference in estimated blood loss between groups, likely explained by the fact that a junior surgeon was added just before initiation of the study period, potentially skewing the estimated blood loss as this surgeon gained experience. Payer status has been correlated to length of hospital stay in children with scoliosis. Vitale and colleagues8 reviewed the effect of payer status on surgical outcomes in 3606 scoliosis patients from a statewide database in California and concluded that, compared with patients having all other payment sources, Medicaid patients had higher odds for complications and longer hospital stay. Our hospital has adopted a highly coordinated care pathway that allows for discharge on postoperative day 2, likely explaining the lack of any difference in postoperative stay.16
The disparity in curve magnitudes among patients with and without private insurance is striking and probably multifactorial. Very likely, the combination of schools with limited screening programs within urban or rural school systems,17 restricted access to pediatricians,18,19 and longer waits to see orthopedic specialists20 all contribute to this disparity. It should be noted that school screening is mandatory in our state. This discrepancy may be related to a previously established tendency in minority populations toward waiting longer to seek care and refusing surgical recommendations, though we were unable to query socioeconomic factors such as race and household income.21,22 It is clearly important to increase access to care for underinsured patients with scoliosis. A comprehensive approach, including providing better education in the schools, establishing communication with referring primary care providers, and increasing access through more physicians or physician extenders, is likely needed. Orthopedists should perhaps treat scoliosis evaluation with the same sense of urgency given to minor fractures, and primary care providers should try to ensure that appropriate referrals for scoliosis are made. Also curious was the shorter travel distance for Medicaid patients versus private insurance patients in this study. We hypothesize this is related to our urban location and its large Medicaid population.
Our study had several limitations. Our electronic medical records (EMR) system does not store data related to the time a patient calls for an initial appointment, limiting our ability to determine how long patients waited for their initial consultation. Furthermore, the decision to undergo surgery is multifactorial and cannot be simplified into time from initial recommendation to surgery, as some patients delay surgery because of school or other obligations. These data should be reasonably consistent over time, as patients seen in the early spring in both groups may delay surgery until the summer, and those diagnosed in June may prefer earlier surgery.
Summary
Children with AIS are at risk for curve progression. Therefore, delays in providing timely care may result in worsening scoliosis. Compared with private insurance patients, Medicaid patients presented with larger curve magnitudes. Further study is needed to better delineate ways to improve care access for patients with scoliosis in communities with larger Medicaid populations.
1. Skaggs DL. Less access to care for children with Medicaid. Orthopedics. 2003;26(12):1184, 1186.
2. Skinner AC, Mayer ML. Effects of insurance status on children’s access to specialty care: a systematic review of the literature. BMC Health Serv Res. 2007;7:194.
3. Iobst C, King W, Baitner A, Tidwell M, Swirsky S, Skaggs DL. Access to care for children with fractures. J Pediatr Orthop. 2010;30(3):244-247.
4. Skaggs DL, Lehmann CL, Rice C, et al. Access to orthopaedic care for children with Medicaid versus private insurance: results of a national survey. J Pediatr Orthop. 2006;26(3):400-404.
5. Skaggs DL, Oda JE, Lerman L, et al. Insurance status and delay in orthotic treatment in children. J Pediatr Orthop. 2007;27(1):94-97.
6. Miyanji F, Slobogean GP, Samdani AF, et al. Is larger scoliosis curve magnitude associated with increased perioperative health-care resource utilization? A multicenter analysis of 325 adolescent idiopathic scoliosis curves. J Bone Joint Surg Am. 2012;94(9):809-813.
7. Nuno M, Drazin DG, Acosta FL Jr. Differences in treatments and outcomes for idiopathic scoliosis patients treated in the United States from 1998 to 2007: impact of socioeconomic variables and ethnicity. Spine J. 2013;13(2):116-123.
8. Vitale MA, Arons RR, Hyman JE, Skaggs DL, Roye DP, Vitale MG. The contribution of hospital volume, payer status, and other factors on the surgical outcomes of scoliosis patients: a review of 3,606 cases in the state of California. J Pediatr Orthop. 2005;25(3):393-399.
9. Goldstein RY, Joiner ER, Skaggs DL. Insurance status does not predict curve magnitude in adolescent idiopathic scoliosis at first presentation to an orthopaedic surgeon. J Pediatr Orthop. 2015;35(1):39-42.
10. Lenke LG, Betz RR, Harms J, et al. Adolescent idiopathic scoliosis: a new classification to determine extent of spinal arthrodesis. J Bone Joint Surg Am. 2001;83(8):1169-1181.
11. Alosh H, Riley LH 3rd, Skolasky RL. Insurance status, geography, race, and ethnicity as predictors of anterior cervical spine surgery rates and in-hospital mortality: an examination of United States trends from 1992 to 2005. Spine. 2009;34(18):1956-1962.
12. Newacheck PW, Hughes DC, Hung YY, Wong S, Stoddard JJ. The unmet health needs of America’s children. Pediatrics. 2000;105(4 pt 2):989-997.
13. Sabharwal S, Zhao C, McClemens E, Kaufmann A. Pediatric orthopaedic patients presenting to a university emergency department after visiting another emergency department: demographics and health insurance status. J Pediatr Orthop. 2007;27(6):690-694.
14. Pierce TR, Mehlman CT, Tamai J, Skaggs DL. Access to care for the adolescent anterior cruciate ligament patient with Medicaid versus private insurance. J Pediatr Orthop. 2012;32(3):245-248.
15. Cho SK, Egorova NN. The association between insurance status and complications, length of stay, and costs for pediatric idiopathic scoliosis. Spine. 2015;40(4):247-256.
16. Fletcher ND, Shourbaji N, Mitchell PM, Oswald TS, Devito DP, Bruce RW Jr. Clinical and economic implications of early discharge following posterior spinal fusion for adolescent idiopathic scoliosis. J Child Orthop. 2014;8(3):257-263.
17. Kasper MJ, Robbins L, Root L, Peterson MG, Allegrante JP. A musculoskeletal outreach screening, treatment, and education program for urban minority children. Arthritis Care Res. 1993;6(3):126-133.
18. Berman S, Dolins J, Tang SF, Yudkowsky B. Factors that influence the willingness of private primary care pediatricians to accept more Medicaid patients. Pediatrics. 2002;110(2 pt 1):239-248.
19. Sommers BD. Protecting low-income children’s access to care: are physician visits associated with reduced patient dropout from Medicaid and the Children’s Health Insurance Program? Pediatrics. 2006;118(1):e36-e42.
20. Bisgaier J, Polsky D, Rhodes KV. Academic medical centers and equity in specialty care access for children. Arch Pediatr Adolesc Med. 2012;166(4):304-310.
21. Sedlis SP, Fisher VJ, Tice D, Esposito R, Madmon L, Steinberg EH. Racial differences in performance of invasive cardiac procedures in a Department of Veterans Affairs medical center. J Clin Epidemiol. 1997;50(8):899-901.
22. Mitchell JB, McCormack LA. Time trends in late-stage diagnosis of cervical cancer. Differences by race/ethnicity and income. Med Care. 1997;35(12):1220-1224.
Rising health care costs have led many health insurers to limit benefits, which may be a problem for children in need of specialty care. Uninsured children have poorer access to specialty care than insured children. Children with public health coverage have better access to specialty care than uninsured children but inferior access compared with privately insured children.1,2 It is well documented that children with government insurance have limited access to orthopedic care for fractures, ligamentous knee injuries, and other injuries.1,3-5 Adolescent idiopathic scoliosis (AIS) differs from many other conditions managed by pediatric orthopedists, as it may be progressive, with management becoming increasingly more complex as the curve magnitude increases.6 The ability to access care earlier in the disease process may allow for earlier nonoperative interventions, such as bracing. For patients who require spinal fusion, earlier diagnosis and referral to a specialist could potentially result in shorter fusions and preserve distal motion segments. The ability to access the health care system in a timely fashion would therefore be of utmost importance for patients with scoliosis.
The literature on AIS is lacking in studies focused on care access based on insurance coverage and the potential impact that this may have on curve progression.7-9 We conducted a study to determine whether there is a difference between patients with and without private insurance who present to a busy urban pediatric orthopedic practice for management of scoliosis that eventually resulted in surgical treatment.
Materials and Methods
After obtaining institutional review board approval for this study, we retrospectively reviewed the medical records of patients (age, 10-18 years) who underwent posterior spinal fusion (PSF) for newly diagnosed AIS between 2008 and 2012. We excluded patients treated with growing spine instrumentation (growing rods), patients younger than 10 years or older than 18 years at presentation, and patients without adequate radiographs or clinical data, including insurance status. To focus on newly diagnosed scoliosis, we also excluded patients who had been seen for second opinions or whose scoliosis had been managed elsewhere in the past. Patients with syndromic, neuromuscular, or congenital scoliosis were also excluded.
Medical records were checked to ascertain time from initial evaluation to decision for surgery, time from recommendation for surgery until actual procedure, and insurance status. Distance traveled was figured from patients’ home addresses. Cobb angles were calculated from initial preoperative and final preoperative posteroanterior (PA) radiographs. Curves as seen on PA, lateral, and maximal effort, supine bending thoracic and lumbar radiographs from the initial preoperative visit were classified using the system of Lenke and colleagues.10 Hospital records were queried to determine number of levels fused at surgery, number of implants placed, and length of stay. Patients were evaluated without prior screening of insurance status and without prior consultation with referring physicians. Surgical procedures were scheduled on a first-come, first-served basis without preference for insurance status.
Results
We identified 135 consecutive patients with newly diagnosed AIS treated with PSF by our group between January 2008 and December 2012 (Table 1). Sixty-one percent had private insurance; 39% had Medicaid. There was no difference in age or ASA (American Society of Anesthesiologists) score between groups. Mean (SD) Cobb angle at initial presentation was 47.5° (14.3°) (range, 18.0°-86.0°) for the private insurance group and 57.2° (15.7°) (range, 23.0°-95.0°) for the Medicaid group (P < .0001). At time of surgery, mean (SD) Cobb angles were 54.6° (11.7°) and 60.6° (13.9°) for the private insurance and Medicaid groups, respectively (P = .008). There was no difference in curve types (Lenke and colleagues10 classification) between groups (Table 2, P = .83). Medicaid patients traveled a shorter mean (SD) distance for care, 56.3 (57.0) miles, versus 73.7 (66.7) miles (P = .05). There was no statistical difference (P = .14) in mean (SD) surgical wait time from surgery recommendation to actual surgery, 103.1 (62.4) days and 128.8 (137.5) days for the private insurance and Medicaid groups, respectively. The difference between patient groups in mean (SD) number of levels fused did not reach statistical significance (P = .16), 10.3 (2.2) levels for the Medicaid group and 9.7 (2.3) levels for the private insurance group. Mean (SD) estimated blood loss was higher for Medicaid patients, 445.7 (415.9) mL versus 335.1 (271.5) mL (P = .06), though there was no difference in use of posterior column osteotomies between groups. There was no difference (P = .11) in mean (SD) length of hospital stay between Medicaid patients, 2.6 (0.8) days, and private insurance patients, 2.4 (0.5) days.
Discussion
According to an extensive body of literature, patients with government insurance have limited access to specialty care.1,11,12 Medicaid-insured children in need of orthopedic care are no exception. Sabharwal and colleagues13 examined a database of pediatric fracture cases and found that 52% of the privately insured patients and 22% of the publicly insured patients received orthopedic care (P = .013).13 When Pierce and colleagues14 called 42 orthopedic practices regarding a fictitious 14-year-old patient with an anterior cruciate ligament tear, 38 offered an appointment within 2 weeks to a privately insured patient, and 6 offered such an appointment to a publicly insured patient. Skaggs and colleagues4 surveyed 230 orthopedic practices nationally and found that Medicaid-insured children had limited access to orthopedic care; 41 practices (18%) would not see a child with Medicaid under any circumstances. Using a fictitious case of a 10-year-old boy with a forearm fracture, Iobst and colleagues3 tried making an appointment at 100 orthopedic offices. Eight gave an appointment within 1 week to a Medicaid-insured patient, and 36 gave an appointment to a privately insured patient.3
There are few data regarding insurance status and scoliosis care in children. Spinal deformity differs from simple fractures and ligamentous injuries, as timely care may result in a less invasive treatment (bracing) if the curvature is caught early. Goldstein and colleagues9 recently evaluated 642 patients who presented for scoliosis evaluation over a 10-year period. There was no difference in curve magnitudes between patients with and without Medicaid insurance. Thirty-two percent of these patients were evaluated for a second opinion, and the authors chose not to subdivide patients on the basis of curve severity and treatment needed, noting only no difference between groups. There was no discussion of the potential difference between patients with and without private insurance with respect to surgically versus nonsurgically treated curves. We wanted to focus specifically on patients who required surgical intervention, as our experience has been that many patients with government insurance present with either very mild scoliosis (10°) or very large curves that were not identified because of lack of primary care access or inadequate school screening. Although summing these 2 groups would result in a similar average, they would represent a different cohort than patients with curves along a bell curve. Furthermore, it is the group of patients who would require surgical intervention that is so critical to identify early in order to intervene.
Our data suggest a difference in presenting curves between patients with and without private insurance. The approximately 10° difference between patient groups in this study could potentially represent the difference between bracing and surgery. Furthermore, Miyanji and colleagues6 evaluated the relationship between Cobb angle and health care consumption and correlated larger curve magnitudes with more levels fused, longer surgeries, and higher rates of transfusion. Specifically, every 10° increase in curve magnitude resulted in 7.8 more minutes of operative time, 0.3 extra levels fused, and 1.5 times increased risk for requiring a blood transfusion.
Cho and Egorova15 recently evaluated insurance status with respect to surgical outcomes using a national inpatient database and found that 42.4% of surgeries for AIS in children with Medicaid had fusions involving 9 or more levels, whereas only 33.6% of privately insured patients had fusions of 9 or more levels. There was no difference in osteotomy or reoperation for pseudarthrosis between groups, but there was a slightly higher rate of infectious (1.1% vs 0.6%) and hemorrhagic (2.5% vs 1.7%) complications in the Medicaid group. Hospital stay was longer in patients with Medicaid, though complications were not different between groups.
The mean difference in the magnitude of the curves treated in our study was not more than 10° between patients with and without Medicaid, perhaps explaining the lack of a statistically significant difference in number of levels fused between groups. Although the groups were similar with respect to the percentage requiring posterior column spinal osteotomies, we noted a difference in estimated blood loss between groups, likely explained by the fact that a junior surgeon was added just before initiation of the study period, potentially skewing the estimated blood loss as this surgeon gained experience. Payer status has been correlated to length of hospital stay in children with scoliosis. Vitale and colleagues8 reviewed the effect of payer status on surgical outcomes in 3606 scoliosis patients from a statewide database in California and concluded that, compared with patients having all other payment sources, Medicaid patients had higher odds for complications and longer hospital stay. Our hospital has adopted a highly coordinated care pathway that allows for discharge on postoperative day 2, likely explaining the lack of any difference in postoperative stay.16
The disparity in curve magnitudes among patients with and without private insurance is striking and probably multifactorial. Very likely, the combination of schools with limited screening programs within urban or rural school systems,17 restricted access to pediatricians,18,19 and longer waits to see orthopedic specialists20 all contribute to this disparity. It should be noted that school screening is mandatory in our state. This discrepancy may be related to a previously established tendency in minority populations toward waiting longer to seek care and refusing surgical recommendations, though we were unable to query socioeconomic factors such as race and household income.21,22 It is clearly important to increase access to care for underinsured patients with scoliosis. A comprehensive approach, including providing better education in the schools, establishing communication with referring primary care providers, and increasing access through more physicians or physician extenders, is likely needed. Orthopedists should perhaps treat scoliosis evaluation with the same sense of urgency given to minor fractures, and primary care providers should try to ensure that appropriate referrals for scoliosis are made. Also curious was the shorter travel distance for Medicaid patients versus private insurance patients in this study. We hypothesize this is related to our urban location and its large Medicaid population.
Our study had several limitations. Our electronic medical records (EMR) system does not store data related to the time a patient calls for an initial appointment, limiting our ability to determine how long patients waited for their initial consultation. Furthermore, the decision to undergo surgery is multifactorial and cannot be simplified into time from initial recommendation to surgery, as some patients delay surgery because of school or other obligations. These data should be reasonably consistent over time, as patients seen in the early spring in both groups may delay surgery until the summer, and those diagnosed in June may prefer earlier surgery.
Summary
Children with AIS are at risk for curve progression. Therefore, delays in providing timely care may result in worsening scoliosis. Compared with private insurance patients, Medicaid patients presented with larger curve magnitudes. Further study is needed to better delineate ways to improve care access for patients with scoliosis in communities with larger Medicaid populations.
Rising health care costs have led many health insurers to limit benefits, which may be a problem for children in need of specialty care. Uninsured children have poorer access to specialty care than insured children. Children with public health coverage have better access to specialty care than uninsured children but inferior access compared with privately insured children.1,2 It is well documented that children with government insurance have limited access to orthopedic care for fractures, ligamentous knee injuries, and other injuries.1,3-5 Adolescent idiopathic scoliosis (AIS) differs from many other conditions managed by pediatric orthopedists, as it may be progressive, with management becoming increasingly more complex as the curve magnitude increases.6 The ability to access care earlier in the disease process may allow for earlier nonoperative interventions, such as bracing. For patients who require spinal fusion, earlier diagnosis and referral to a specialist could potentially result in shorter fusions and preserve distal motion segments. The ability to access the health care system in a timely fashion would therefore be of utmost importance for patients with scoliosis.
The literature on AIS is lacking in studies focused on care access based on insurance coverage and the potential impact that this may have on curve progression.7-9 We conducted a study to determine whether there is a difference between patients with and without private insurance who present to a busy urban pediatric orthopedic practice for management of scoliosis that eventually resulted in surgical treatment.
Materials and Methods
After obtaining institutional review board approval for this study, we retrospectively reviewed the medical records of patients (age, 10-18 years) who underwent posterior spinal fusion (PSF) for newly diagnosed AIS between 2008 and 2012. We excluded patients treated with growing spine instrumentation (growing rods), patients younger than 10 years or older than 18 years at presentation, and patients without adequate radiographs or clinical data, including insurance status. To focus on newly diagnosed scoliosis, we also excluded patients who had been seen for second opinions or whose scoliosis had been managed elsewhere in the past. Patients with syndromic, neuromuscular, or congenital scoliosis were also excluded.
Medical records were checked to ascertain time from initial evaluation to decision for surgery, time from recommendation for surgery until actual procedure, and insurance status. Distance traveled was figured from patients’ home addresses. Cobb angles were calculated from initial preoperative and final preoperative posteroanterior (PA) radiographs. Curves as seen on PA, lateral, and maximal effort, supine bending thoracic and lumbar radiographs from the initial preoperative visit were classified using the system of Lenke and colleagues.10 Hospital records were queried to determine number of levels fused at surgery, number of implants placed, and length of stay. Patients were evaluated without prior screening of insurance status and without prior consultation with referring physicians. Surgical procedures were scheduled on a first-come, first-served basis without preference for insurance status.
Results
We identified 135 consecutive patients with newly diagnosed AIS treated with PSF by our group between January 2008 and December 2012 (Table 1). Sixty-one percent had private insurance; 39% had Medicaid. There was no difference in age or ASA (American Society of Anesthesiologists) score between groups. Mean (SD) Cobb angle at initial presentation was 47.5° (14.3°) (range, 18.0°-86.0°) for the private insurance group and 57.2° (15.7°) (range, 23.0°-95.0°) for the Medicaid group (P < .0001). At time of surgery, mean (SD) Cobb angles were 54.6° (11.7°) and 60.6° (13.9°) for the private insurance and Medicaid groups, respectively (P = .008). There was no difference in curve types (Lenke and colleagues10 classification) between groups (Table 2, P = .83). Medicaid patients traveled a shorter mean (SD) distance for care, 56.3 (57.0) miles, versus 73.7 (66.7) miles (P = .05). There was no statistical difference (P = .14) in mean (SD) surgical wait time from surgery recommendation to actual surgery, 103.1 (62.4) days and 128.8 (137.5) days for the private insurance and Medicaid groups, respectively. The difference between patient groups in mean (SD) number of levels fused did not reach statistical significance (P = .16), 10.3 (2.2) levels for the Medicaid group and 9.7 (2.3) levels for the private insurance group. Mean (SD) estimated blood loss was higher for Medicaid patients, 445.7 (415.9) mL versus 335.1 (271.5) mL (P = .06), though there was no difference in use of posterior column osteotomies between groups. There was no difference (P = .11) in mean (SD) length of hospital stay between Medicaid patients, 2.6 (0.8) days, and private insurance patients, 2.4 (0.5) days.
Discussion
According to an extensive body of literature, patients with government insurance have limited access to specialty care.1,11,12 Medicaid-insured children in need of orthopedic care are no exception. Sabharwal and colleagues13 examined a database of pediatric fracture cases and found that 52% of the privately insured patients and 22% of the publicly insured patients received orthopedic care (P = .013).13 When Pierce and colleagues14 called 42 orthopedic practices regarding a fictitious 14-year-old patient with an anterior cruciate ligament tear, 38 offered an appointment within 2 weeks to a privately insured patient, and 6 offered such an appointment to a publicly insured patient. Skaggs and colleagues4 surveyed 230 orthopedic practices nationally and found that Medicaid-insured children had limited access to orthopedic care; 41 practices (18%) would not see a child with Medicaid under any circumstances. Using a fictitious case of a 10-year-old boy with a forearm fracture, Iobst and colleagues3 tried making an appointment at 100 orthopedic offices. Eight gave an appointment within 1 week to a Medicaid-insured patient, and 36 gave an appointment to a privately insured patient.3
There are few data regarding insurance status and scoliosis care in children. Spinal deformity differs from simple fractures and ligamentous injuries, as timely care may result in a less invasive treatment (bracing) if the curvature is caught early. Goldstein and colleagues9 recently evaluated 642 patients who presented for scoliosis evaluation over a 10-year period. There was no difference in curve magnitudes between patients with and without Medicaid insurance. Thirty-two percent of these patients were evaluated for a second opinion, and the authors chose not to subdivide patients on the basis of curve severity and treatment needed, noting only no difference between groups. There was no discussion of the potential difference between patients with and without private insurance with respect to surgically versus nonsurgically treated curves. We wanted to focus specifically on patients who required surgical intervention, as our experience has been that many patients with government insurance present with either very mild scoliosis (10°) or very large curves that were not identified because of lack of primary care access or inadequate school screening. Although summing these 2 groups would result in a similar average, they would represent a different cohort than patients with curves along a bell curve. Furthermore, it is the group of patients who would require surgical intervention that is so critical to identify early in order to intervene.
Our data suggest a difference in presenting curves between patients with and without private insurance. The approximately 10° difference between patient groups in this study could potentially represent the difference between bracing and surgery. Furthermore, Miyanji and colleagues6 evaluated the relationship between Cobb angle and health care consumption and correlated larger curve magnitudes with more levels fused, longer surgeries, and higher rates of transfusion. Specifically, every 10° increase in curve magnitude resulted in 7.8 more minutes of operative time, 0.3 extra levels fused, and 1.5 times increased risk for requiring a blood transfusion.
Cho and Egorova15 recently evaluated insurance status with respect to surgical outcomes using a national inpatient database and found that 42.4% of surgeries for AIS in children with Medicaid had fusions involving 9 or more levels, whereas only 33.6% of privately insured patients had fusions of 9 or more levels. There was no difference in osteotomy or reoperation for pseudarthrosis between groups, but there was a slightly higher rate of infectious (1.1% vs 0.6%) and hemorrhagic (2.5% vs 1.7%) complications in the Medicaid group. Hospital stay was longer in patients with Medicaid, though complications were not different between groups.
The mean difference in the magnitude of the curves treated in our study was not more than 10° between patients with and without Medicaid, perhaps explaining the lack of a statistically significant difference in number of levels fused between groups. Although the groups were similar with respect to the percentage requiring posterior column spinal osteotomies, we noted a difference in estimated blood loss between groups, likely explained by the fact that a junior surgeon was added just before initiation of the study period, potentially skewing the estimated blood loss as this surgeon gained experience. Payer status has been correlated to length of hospital stay in children with scoliosis. Vitale and colleagues8 reviewed the effect of payer status on surgical outcomes in 3606 scoliosis patients from a statewide database in California and concluded that, compared with patients having all other payment sources, Medicaid patients had higher odds for complications and longer hospital stay. Our hospital has adopted a highly coordinated care pathway that allows for discharge on postoperative day 2, likely explaining the lack of any difference in postoperative stay.16
The disparity in curve magnitudes among patients with and without private insurance is striking and probably multifactorial. Very likely, the combination of schools with limited screening programs within urban or rural school systems,17 restricted access to pediatricians,18,19 and longer waits to see orthopedic specialists20 all contribute to this disparity. It should be noted that school screening is mandatory in our state. This discrepancy may be related to a previously established tendency in minority populations toward waiting longer to seek care and refusing surgical recommendations, though we were unable to query socioeconomic factors such as race and household income.21,22 It is clearly important to increase access to care for underinsured patients with scoliosis. A comprehensive approach, including providing better education in the schools, establishing communication with referring primary care providers, and increasing access through more physicians or physician extenders, is likely needed. Orthopedists should perhaps treat scoliosis evaluation with the same sense of urgency given to minor fractures, and primary care providers should try to ensure that appropriate referrals for scoliosis are made. Also curious was the shorter travel distance for Medicaid patients versus private insurance patients in this study. We hypothesize this is related to our urban location and its large Medicaid population.
Our study had several limitations. Our electronic medical records (EMR) system does not store data related to the time a patient calls for an initial appointment, limiting our ability to determine how long patients waited for their initial consultation. Furthermore, the decision to undergo surgery is multifactorial and cannot be simplified into time from initial recommendation to surgery, as some patients delay surgery because of school or other obligations. These data should be reasonably consistent over time, as patients seen in the early spring in both groups may delay surgery until the summer, and those diagnosed in June may prefer earlier surgery.
Summary
Children with AIS are at risk for curve progression. Therefore, delays in providing timely care may result in worsening scoliosis. Compared with private insurance patients, Medicaid patients presented with larger curve magnitudes. Further study is needed to better delineate ways to improve care access for patients with scoliosis in communities with larger Medicaid populations.
1. Skaggs DL. Less access to care for children with Medicaid. Orthopedics. 2003;26(12):1184, 1186.
2. Skinner AC, Mayer ML. Effects of insurance status on children’s access to specialty care: a systematic review of the literature. BMC Health Serv Res. 2007;7:194.
3. Iobst C, King W, Baitner A, Tidwell M, Swirsky S, Skaggs DL. Access to care for children with fractures. J Pediatr Orthop. 2010;30(3):244-247.
4. Skaggs DL, Lehmann CL, Rice C, et al. Access to orthopaedic care for children with Medicaid versus private insurance: results of a national survey. J Pediatr Orthop. 2006;26(3):400-404.
5. Skaggs DL, Oda JE, Lerman L, et al. Insurance status and delay in orthotic treatment in children. J Pediatr Orthop. 2007;27(1):94-97.
6. Miyanji F, Slobogean GP, Samdani AF, et al. Is larger scoliosis curve magnitude associated with increased perioperative health-care resource utilization? A multicenter analysis of 325 adolescent idiopathic scoliosis curves. J Bone Joint Surg Am. 2012;94(9):809-813.
7. Nuno M, Drazin DG, Acosta FL Jr. Differences in treatments and outcomes for idiopathic scoliosis patients treated in the United States from 1998 to 2007: impact of socioeconomic variables and ethnicity. Spine J. 2013;13(2):116-123.
8. Vitale MA, Arons RR, Hyman JE, Skaggs DL, Roye DP, Vitale MG. The contribution of hospital volume, payer status, and other factors on the surgical outcomes of scoliosis patients: a review of 3,606 cases in the state of California. J Pediatr Orthop. 2005;25(3):393-399.
9. Goldstein RY, Joiner ER, Skaggs DL. Insurance status does not predict curve magnitude in adolescent idiopathic scoliosis at first presentation to an orthopaedic surgeon. J Pediatr Orthop. 2015;35(1):39-42.
10. Lenke LG, Betz RR, Harms J, et al. Adolescent idiopathic scoliosis: a new classification to determine extent of spinal arthrodesis. J Bone Joint Surg Am. 2001;83(8):1169-1181.
11. Alosh H, Riley LH 3rd, Skolasky RL. Insurance status, geography, race, and ethnicity as predictors of anterior cervical spine surgery rates and in-hospital mortality: an examination of United States trends from 1992 to 2005. Spine. 2009;34(18):1956-1962.
12. Newacheck PW, Hughes DC, Hung YY, Wong S, Stoddard JJ. The unmet health needs of America’s children. Pediatrics. 2000;105(4 pt 2):989-997.
13. Sabharwal S, Zhao C, McClemens E, Kaufmann A. Pediatric orthopaedic patients presenting to a university emergency department after visiting another emergency department: demographics and health insurance status. J Pediatr Orthop. 2007;27(6):690-694.
14. Pierce TR, Mehlman CT, Tamai J, Skaggs DL. Access to care for the adolescent anterior cruciate ligament patient with Medicaid versus private insurance. J Pediatr Orthop. 2012;32(3):245-248.
15. Cho SK, Egorova NN. The association between insurance status and complications, length of stay, and costs for pediatric idiopathic scoliosis. Spine. 2015;40(4):247-256.
16. Fletcher ND, Shourbaji N, Mitchell PM, Oswald TS, Devito DP, Bruce RW Jr. Clinical and economic implications of early discharge following posterior spinal fusion for adolescent idiopathic scoliosis. J Child Orthop. 2014;8(3):257-263.
17. Kasper MJ, Robbins L, Root L, Peterson MG, Allegrante JP. A musculoskeletal outreach screening, treatment, and education program for urban minority children. Arthritis Care Res. 1993;6(3):126-133.
18. Berman S, Dolins J, Tang SF, Yudkowsky B. Factors that influence the willingness of private primary care pediatricians to accept more Medicaid patients. Pediatrics. 2002;110(2 pt 1):239-248.
19. Sommers BD. Protecting low-income children’s access to care: are physician visits associated with reduced patient dropout from Medicaid and the Children’s Health Insurance Program? Pediatrics. 2006;118(1):e36-e42.
20. Bisgaier J, Polsky D, Rhodes KV. Academic medical centers and equity in specialty care access for children. Arch Pediatr Adolesc Med. 2012;166(4):304-310.
21. Sedlis SP, Fisher VJ, Tice D, Esposito R, Madmon L, Steinberg EH. Racial differences in performance of invasive cardiac procedures in a Department of Veterans Affairs medical center. J Clin Epidemiol. 1997;50(8):899-901.
22. Mitchell JB, McCormack LA. Time trends in late-stage diagnosis of cervical cancer. Differences by race/ethnicity and income. Med Care. 1997;35(12):1220-1224.
1. Skaggs DL. Less access to care for children with Medicaid. Orthopedics. 2003;26(12):1184, 1186.
2. Skinner AC, Mayer ML. Effects of insurance status on children’s access to specialty care: a systematic review of the literature. BMC Health Serv Res. 2007;7:194.
3. Iobst C, King W, Baitner A, Tidwell M, Swirsky S, Skaggs DL. Access to care for children with fractures. J Pediatr Orthop. 2010;30(3):244-247.
4. Skaggs DL, Lehmann CL, Rice C, et al. Access to orthopaedic care for children with Medicaid versus private insurance: results of a national survey. J Pediatr Orthop. 2006;26(3):400-404.
5. Skaggs DL, Oda JE, Lerman L, et al. Insurance status and delay in orthotic treatment in children. J Pediatr Orthop. 2007;27(1):94-97.
6. Miyanji F, Slobogean GP, Samdani AF, et al. Is larger scoliosis curve magnitude associated with increased perioperative health-care resource utilization? A multicenter analysis of 325 adolescent idiopathic scoliosis curves. J Bone Joint Surg Am. 2012;94(9):809-813.
7. Nuno M, Drazin DG, Acosta FL Jr. Differences in treatments and outcomes for idiopathic scoliosis patients treated in the United States from 1998 to 2007: impact of socioeconomic variables and ethnicity. Spine J. 2013;13(2):116-123.
8. Vitale MA, Arons RR, Hyman JE, Skaggs DL, Roye DP, Vitale MG. The contribution of hospital volume, payer status, and other factors on the surgical outcomes of scoliosis patients: a review of 3,606 cases in the state of California. J Pediatr Orthop. 2005;25(3):393-399.
9. Goldstein RY, Joiner ER, Skaggs DL. Insurance status does not predict curve magnitude in adolescent idiopathic scoliosis at first presentation to an orthopaedic surgeon. J Pediatr Orthop. 2015;35(1):39-42.
10. Lenke LG, Betz RR, Harms J, et al. Adolescent idiopathic scoliosis: a new classification to determine extent of spinal arthrodesis. J Bone Joint Surg Am. 2001;83(8):1169-1181.
11. Alosh H, Riley LH 3rd, Skolasky RL. Insurance status, geography, race, and ethnicity as predictors of anterior cervical spine surgery rates and in-hospital mortality: an examination of United States trends from 1992 to 2005. Spine. 2009;34(18):1956-1962.
12. Newacheck PW, Hughes DC, Hung YY, Wong S, Stoddard JJ. The unmet health needs of America’s children. Pediatrics. 2000;105(4 pt 2):989-997.
13. Sabharwal S, Zhao C, McClemens E, Kaufmann A. Pediatric orthopaedic patients presenting to a university emergency department after visiting another emergency department: demographics and health insurance status. J Pediatr Orthop. 2007;27(6):690-694.
14. Pierce TR, Mehlman CT, Tamai J, Skaggs DL. Access to care for the adolescent anterior cruciate ligament patient with Medicaid versus private insurance. J Pediatr Orthop. 2012;32(3):245-248.
15. Cho SK, Egorova NN. The association between insurance status and complications, length of stay, and costs for pediatric idiopathic scoliosis. Spine. 2015;40(4):247-256.
16. Fletcher ND, Shourbaji N, Mitchell PM, Oswald TS, Devito DP, Bruce RW Jr. Clinical and economic implications of early discharge following posterior spinal fusion for adolescent idiopathic scoliosis. J Child Orthop. 2014;8(3):257-263.
17. Kasper MJ, Robbins L, Root L, Peterson MG, Allegrante JP. A musculoskeletal outreach screening, treatment, and education program for urban minority children. Arthritis Care Res. 1993;6(3):126-133.
18. Berman S, Dolins J, Tang SF, Yudkowsky B. Factors that influence the willingness of private primary care pediatricians to accept more Medicaid patients. Pediatrics. 2002;110(2 pt 1):239-248.
19. Sommers BD. Protecting low-income children’s access to care: are physician visits associated with reduced patient dropout from Medicaid and the Children’s Health Insurance Program? Pediatrics. 2006;118(1):e36-e42.
20. Bisgaier J, Polsky D, Rhodes KV. Academic medical centers and equity in specialty care access for children. Arch Pediatr Adolesc Med. 2012;166(4):304-310.
21. Sedlis SP, Fisher VJ, Tice D, Esposito R, Madmon L, Steinberg EH. Racial differences in performance of invasive cardiac procedures in a Department of Veterans Affairs medical center. J Clin Epidemiol. 1997;50(8):899-901.
22. Mitchell JB, McCormack LA. Time trends in late-stage diagnosis of cervical cancer. Differences by race/ethnicity and income. Med Care. 1997;35(12):1220-1224.
Open Carpal Tunnel Release With Use of a Nasal Turbinate Speculum
Carpal tunnel syndrome (CTS) is a disorder characterized by entrapment of the median nerve at the wrist, which may lead to symptoms of pain, paresthesia, and, ultimately, thenar muscle atrophy. Surgical intervention is indicated with persistent or progressive symptoms despite nonoperative management. Timely surgical decompression aims to halt progression of this disorder and prevent permanent peripheral nerve injury.
Carpal tunnel release (CTR) is the most common hand and wrist surgery in the United States, with about 400,000 operations performed annually.1,2 Several methods of decompressing the carpal tunnel have been described.3 These include standard open CTR (OCTR), mini-open approaches, and various endoscopic techniques. OCTR was initially described by Sir James Learmonth in 1933,4 and it remains the gold-standard surgical treatment for patients with symptomatic CTS. Uniform excellent results with high patient satisfaction and low complication rates have been reported in several series.5-9 Common to all techniques is complete proximal-to-distal division of the transverse carpal ligament (TCL). Magnetic resonance imaging studies have shown that TCL transection and the resulting diastasis between the radial and ulnar leaflets cause a significant increase in the volume of the carpal tunnel, leading to decreased pressure.10,11
Endoscopic CTR (ECTR) techniques were developed in an effort to reduce complications, scar sensitivity, and pillar pain and facilitate more rapid return to work.12-17 Outcome studies have demonstrated that both open and endoscopic releases yield patient-reported subjective improvements over preoperative symptoms.18-22 A randomized, controlled trial by Trumble and colleagues23 in 2002 found that ECTR led to improved patient outcomes in the early postoperative period (first 3 months), though differences in outcomes were reduced at final follow-up. More recently (2007), a Cochrane review of 33 trials concluded there was no strong evidence favoring use of alternative techniques over OCTR.3 Further, OCTR has been found to be technically less demanding and associated with decreased complications and costs.24
Indications
The benefit of median nerve decompression at the wrist for CTS is clear.6,7 Indications for surgery in patients with CTS include persistent symptoms despite nonoperative treatment, objective sensory disturbance or motor weakness, and thenar atrophy. Symptomatic response to corticosteroid injection is predictive of success after carpal tunnel surgery.25 More than 87% of patients who gain symptomatic relief from corticosteroid injection have an excellent surgical outcome.
Technique
OCTR allows direct visualization of the TCL and the distal volar forearm fascia (DVFF) and evaluation for the presence of anomalous branching patterns of the median nerve. OCTR traditionally was performed through a 4- to 5-cm longitudinal incision extending from the wrist crease proximally to the Kaplan cardinal line distally. The mini-open technique is identical with the exception of incision length. We routinely use a 2.5- to 3-cm incision. Regardless of incision length, each OCTR should proceed through the same reproducible steps.
We perform OCTR under tourniquet control. Choice of anesthesia is surgeon and patient preference. We prefer local anesthesia with conscious sedation. After conscious sedation is administered, we infiltrate the carpal tunnel and surrounding subcutaneous tissue with 10 mL of a 50:50 mixture of 0.5% bupivacaine and 1% lidocaine without epinephrine.
A 2.5- to 3-cm longitudinal incision is made along the axis of the radial border of the ring finger from the Kaplan cardinal line26 and extending about 3 cm proximally toward the wrist flexion crease ulnar to the palmaris longus if present (Figure 1).
After the skin is incised longitudinally, the subcutaneous fat is mobilized and cutaneous sensory branches identified and protected. The underlying superficial palmar fascia is incised in line with the skin incision. The underlying midportion of the TCL is now visualized.
Transverse Carpal Ligament Release
Occasionally, the investing fascia along the ulnar edge of the thenar musculature is mobilized radialward (if the thenar musculature is well developed) to visualize the proximal limb of the TCL. Injury to any anomalous motor branch of the median nerve is avoided by directly visualizing and then incising the TCL (Figure 2). The TCL is incised along its ulnar border just radial to the hook of hamate from distal to proximal in line with the radial border of the ring finger. Staying near the ulnar attachment of the TCL keeps the plane of ligament division farther away from the median nerve and its recurrent motor branches. Although the ulnar neurovascular bundle typically resides ulnar to the hook of hamate in the canal of Guyon, the surgeon must be aware that it can be located radial to the hook in some instances.27,28 In the elderly, the ulnar artery may be tortuous and enter the field and require retraction. The TCL is incised distally until the sentinel fat pad, which marks the superficial palmar arterial arch, is visualized. This bed of adipose tissue marks the distal edge of the TCL.29
Proximally, subcutaneous tissues above the proximal limb of the TCL and DVFF are mobilized to about 2 cm proximal to the wrist flexion crease to create a plane for the fine long nasal turbinate speculum. The nasal turbinate speculum is then inserted into this plane above the proximal limb of the TCL and DVFF (Figure 3). Once inserted to the level of the confluence of the TCL and the DVFF, the speculum is opened.
Topside visualization is now encountered with the ulnar neurovascular bundle protected by the ulnar blade of the speculum. A long-handle scalpel is used to incise the TCL and the DVFF under direct visualization from proximal to distal in line with the previously completed distal release (Figure 4). As the nasal turbinate speculum is stretching the TCL and putting it under tension, the TCL can be heard splitting as it is being incised. Once the TCL and the DVFF are divided, the speculum is slowly closed and removed. Wide diastasis of the radial and ulnar leaflets of the TCL and the DVFF is directly visualized. Complete decompression of the median nerve from the distal forearm fascia to the superficial palmar arch is confirmed.
Adhesions between the undersurface of the radial leaflet and the flexor tendons and median nerve are mobilized. The median nerve is assessed for “hourglass” morphology or atrophy. The flexor tendons can be swept radialward with a free elevator to inspect the floor of the carpal tunnel. Flexor tenosynovectomy is not routinely performed. The incision is closed with interrupted simple sutures using 4-0 nylon.
Study Results
This study was conducted at Hand Surgery PC, Newton-Wellesley Hospital, Tufts University School of Medicine. Over a 10-month interval, 101 consecutive mini-OCTRs (63 right hands, 38 left hands) were performed with this proximal release modification in 88 patients (51 females, 37 males) by Dr. Ruchelsman and Dr. Belsky (Table). CTRs performed in the setting of wrist and/or carpal trauma were excluded. Mean age was 62.8 years. Mean follow-up was 11.3 weeks (~3 months). For isolated cases of CTR, mean tourniquet time was 16 minutes. CTS symptoms were relieved in all patients with a high degree of satisfaction as measured with history and examination findings at follow-up visits. There were no major complications (eg, infection, neural or vascular damage, severe residual pain). Four patients reported minor residual numbness in the fingers at latest follow-up but nevertheless had major improvement over preoperative baseline. These 4 patients had preoperative electromyograms or nerve conduction studies documenting the extent of their disease. There was 1 case of minor wound complication. Three weeks after surgery, the patient had a 1-cm wound opening, which closed with local wound care. The patient did not develop any drainage, infection, bleeding, or neurologic symptoms.
Discussion
Open release of the TCL—the gold standard of surgical treatment for CTS—produces reliable symptom relief in the vast majority of patients.25,30 Given that the most common complication of carpal tunnel surgery is incomplete release of the TCL,31,32 this technique, which uses a nasal turbinate speculum to better visualize the median nerve, could potentially reduce the reoperation rate. The nasal turbinate speculum allows the surgeon to see the confluence of the TCL and the DVFF. In addition, as the complete release can be visualized, there is minimal chance of injury.
The 2007 Cochrane review3 found no strong evidence supporting replacing OCTR with endoscopic techniques. Previous investigators have questioned the utility of ECTR given that it is higher in cost and more resource-intensive than OCTR1,33,34 and is associated with higher rates of certain complications.5,22,35-37 A 2004 meta-analysis of 13 randomized, controlled trials found a higher rate of reversible nerve damage with an odds ratio of 3.1 for ECTR versus OCTR.35 A more recent (2006) review of more than 80 studies found transient neurapraxias in 1.45% of ECTR cases and 0.25% of OCTR cases.5 The same study reported overall complication rates (reversible and major neurovascular structural injuries) of 0.74% for OCTR and 1.63% for ECTR (P < .005). Another limitation of ECTR is that endoscopic techniques require a higher degree of surgical skill, which makes teaching residents and fellows more challenging.
The novel nasal turbinate speculum technique presented here is easily reproducible and allows first-time surgeons to visualize all important structures. Given that this technique does not require an endoscope or an endoscope-viewing tower, it is likely more cost-effective and requires less time for turnover between cases. Patients obtain good relief of their CTS symptoms with this technique, and most return to their daily activities within weeks after operation.
1. Ono S, Clapham PJ, Chung KC. Optimal management of carpal tunnel syndrome. Int J Gen Med. 2010;3(4):255-261.
2. Concannon MJ, Brownfield ML, Puckett CL. The incidence of recurrence after endoscopic carpal tunnel release. Plast Reconstr Surg. 2000;105(5):1662-1665.
3. Scholten RJ, Mink van der Molen A, Uitdehaag BM, Bouter LM, de Vet HC. Surgical treatment options for carpal tunnel syndrome. Cochrane Database Syst Rev. 2007;(4):CD003905.
4. In memoriam Sir James Learmonth, K.C.V.O., C.B.E., hon. F.R.C.S. (1895-1967). Ann R Coll Surg Engl. 1967;41(5):438-439.
5. Benson LS, Bare AA, Nagle DJ, Harder VS, Williams CS, Visotsky JL. Complications of endoscopic and open carpal tunnel release. Arthroscopy. 2006;22(9):919-924, 924.e1-e2.
6. Jarvik JG, Comstock BA, Kliot M, et al. Surgery versus non-surgical therapy for carpal tunnel syndrome: a randomised parallel-group trial. Lancet. 2009;374(9695):1074-1081.
7. Verdugo RJ, Salinas RA, Castillo JL, et al. Surgical versus non-surgical treatment for carpal tunnel syndrome. Cochrane Database Syst Rev. 2008;(4):CD001552.
8. Garland H, Langworth EP, Taverner D, et al. Surgical treatment for the carpal tunnel syndrome. Lancet. 1964;1(7343):1129-1130.
9. Gerritsen AA, de Vet HC, Scholten RJ, et al. Splinting vs surgery in the treatment of carpal tunnel syndrome: a randomized controlled trial. JAMA. 2002;288(10):1245-1251.
10. Gelberman RH, Hergenroeder PT, Hargens AR, et al. The carpal tunnel syndrome. A study of carpal canal pressures. J Bone Joint Surg Am. 1981;63(3):380-383.
11. Sucher BM. Myofascial manipulative release of carpal tunnel syndrome: documentation with magnetic resonance imaging. J Am Osteopath Assoc. 1993;93(12):1273-1278.
12. Pereira EE, Miranda DA, Sere I, et al. Endoscopic release of the carpal tunnel: a 2-portal-modified technique. Tech Hand Up Extrem Surg. 2010;14(4):263-265.
13. Louis DS, Greene TL, Noellert RC. Complications of carpal tunnel surgery. J Neurosurg. 1985;62(3):352-356.
14. Mirza MA, King ET Jr, Tanveer S. Palmar uniportal extrabursal endoscopic carpal tunnel release. Arthroscopy. 1995;11(1):82-90.
15. Brown MG, Keyser B, Rothenberg ES. Endoscopic carpal tunnel release. J Hand Surg Am. 1992;17(6):1009-1011.
16. Agee JM, McCarroll HR Jr, Tortosa RD, et al. Endoscopic release of the carpal tunnel: a randomized prospective multicenter study. J Hand Surg Am. 1992;17(6):987-995.
17. Okutsu I, Ninomiya S, Takatori Y, et al. Endoscopic management of carpal tunnel syndrome. Arthroscopy. 1989;5(1):11-18.
18. Ghaly RF, Saban KL, Haley DA, et al. Endoscopic carpal tunnel release surgery: report of patient satisfaction. Neurol Res. 2000;22(6):551-555.
19. Lee WP, Plancher KD, Strickland JW. Carpal tunnel release with a small palmar incision. Hand Clin. 1996;12(2):271-284.
20. Biyani A, Downes EM. An open twin incision technique of carpal tunnel decompression with reduced incidence of scar tenderness. J Hand Surg Br. 1993;18(3):331-334.
21. Brown RA, Gelberman RH, Seiler JG 3rd, et al. Carpal tunnel release. A prospective, randomized assessment of open and endoscopic methods. J Bone Joint Surg Am. 1993;75(9):1265-1275.
22. Chow JC. Endoscopic release of the carpal ligament for carpal tunnel syndrome: 22-month clinical result. Arthroscopy. 1990;6(4):288-296.
23. Trumble TE, Diao E, Abrams RA, et al. Single-portal endoscopic carpal tunnel release compared with open release: a prospective, randomized trial. J Bone Joint Surg Am. 2002;84(7):1107-1115.
24. Gerritsen AA, Uitdehaag BM, van Geldere D, et al. Systematic review of randomized clinical trials of surgical treatment for carpal tunnel syndrome. Br J Surg. 2001;88(10):1285-1295.
25. Edgell SE, McCabe SJ, Breidenbach WC, et al. Predicting the outcome of carpal tunnel release. J Hand Surg Am. 2003;28(2):255-261.
26. Vella JC, Hartigan BJ, Stern PJ. Kaplan’s cardinal line. J Hand Surg Am. 2006;31(6):912-918.
27. Kwon JY, Kim JY, Hong JT, et al. Position change of the neurovascular structures around the carpal tunnel with dynamic wrist motion. J Korean Neurosurg Soc. 2011;50(4):377-380.
28. Netscher D, Polsen C, Thornby J, et al. Anatomic delineation of the ulnar nerve and ulnar artery in relation to the carpal tunnel by axial magnetic resonance imaging scanning. J Hand Surg Am. 1996;21(2):273-276.
29. Madhav TJ, To P, Stern PJ. The palmar fat pad is a reliable intraoperative landmark during carpal tunnel release. J Hand Surg Am. 2009;34(7):1204-1209.
30. Kulick MI, Gordillo G, Javidi T, et al. Long-term analysis of patients having surgical treatment for carpal tunnel syndrome. J Hand Surg Am. 1986;11(1):59-66.
31. Bland JD. Treatment of carpal tunnel syndrome. Muscle Nerve. 2007;36(2):167-171.
32. MacDonald RI, Lichtman DM, Hanlon JJ, et al. Complications of surgical release for carpal tunnel syndrome. J Hand Surg Am. 1978;3(1):70-76.
33. Atroshi I, Larsson GU, Ornstein E, Hofer M, Johnsson R, Ranstam J. Outcomes of endoscopic surgery compared with open surgery for carpal tunnel syndrome among employed patients: randomised controlled trial. BMJ. 2006;332(7556):1473.
34. Ferdinand RD, MacLean JG. Endoscopic versus open carpal tunnel release in bilateral carpal tunnel syndrome. A prospective, randomised, blinded assessment. J Bone Joint Surg Br. 2002;84(3):375-379.
35. Thoma A, Veltri K, Haines T, et al. A meta-analysis of randomized controlled trials comparing endoscopic and open carpal tunnel decompression. Plast Reconstr Surg. 2004;114(5):1137-1146.
36. Murphy RX Jr, Jennings JF, Wukich DK. Major neurovascular complications of endoscopic carpal tunnel release. J Hand Surg Am. 1994;19(1):114-118.
37. Palmer DH, Paulson JC, Lane-Larsen CL, et al. Endoscopic carpal tunnel release: a comparison of two techniques with open release. Arthroscopy. 1993;9(5):498-508.
Carpal tunnel syndrome (CTS) is a disorder characterized by entrapment of the median nerve at the wrist, which may lead to symptoms of pain, paresthesia, and, ultimately, thenar muscle atrophy. Surgical intervention is indicated with persistent or progressive symptoms despite nonoperative management. Timely surgical decompression aims to halt progression of this disorder and prevent permanent peripheral nerve injury.
Carpal tunnel release (CTR) is the most common hand and wrist surgery in the United States, with about 400,000 operations performed annually.1,2 Several methods of decompressing the carpal tunnel have been described.3 These include standard open CTR (OCTR), mini-open approaches, and various endoscopic techniques. OCTR was initially described by Sir James Learmonth in 1933,4 and it remains the gold-standard surgical treatment for patients with symptomatic CTS. Uniform excellent results with high patient satisfaction and low complication rates have been reported in several series.5-9 Common to all techniques is complete proximal-to-distal division of the transverse carpal ligament (TCL). Magnetic resonance imaging studies have shown that TCL transection and the resulting diastasis between the radial and ulnar leaflets cause a significant increase in the volume of the carpal tunnel, leading to decreased pressure.10,11
Endoscopic CTR (ECTR) techniques were developed in an effort to reduce complications, scar sensitivity, and pillar pain and facilitate more rapid return to work.12-17 Outcome studies have demonstrated that both open and endoscopic releases yield patient-reported subjective improvements over preoperative symptoms.18-22 A randomized, controlled trial by Trumble and colleagues23 in 2002 found that ECTR led to improved patient outcomes in the early postoperative period (first 3 months), though differences in outcomes were reduced at final follow-up. More recently (2007), a Cochrane review of 33 trials concluded there was no strong evidence favoring use of alternative techniques over OCTR.3 Further, OCTR has been found to be technically less demanding and associated with decreased complications and costs.24
Indications
The benefit of median nerve decompression at the wrist for CTS is clear.6,7 Indications for surgery in patients with CTS include persistent symptoms despite nonoperative treatment, objective sensory disturbance or motor weakness, and thenar atrophy. Symptomatic response to corticosteroid injection is predictive of success after carpal tunnel surgery.25 More than 87% of patients who gain symptomatic relief from corticosteroid injection have an excellent surgical outcome.
Technique
OCTR allows direct visualization of the TCL and the distal volar forearm fascia (DVFF) and evaluation for the presence of anomalous branching patterns of the median nerve. OCTR traditionally was performed through a 4- to 5-cm longitudinal incision extending from the wrist crease proximally to the Kaplan cardinal line distally. The mini-open technique is identical with the exception of incision length. We routinely use a 2.5- to 3-cm incision. Regardless of incision length, each OCTR should proceed through the same reproducible steps.
We perform OCTR under tourniquet control. Choice of anesthesia is surgeon and patient preference. We prefer local anesthesia with conscious sedation. After conscious sedation is administered, we infiltrate the carpal tunnel and surrounding subcutaneous tissue with 10 mL of a 50:50 mixture of 0.5% bupivacaine and 1% lidocaine without epinephrine.
A 2.5- to 3-cm longitudinal incision is made along the axis of the radial border of the ring finger from the Kaplan cardinal line26 and extending about 3 cm proximally toward the wrist flexion crease ulnar to the palmaris longus if present (Figure 1).
After the skin is incised longitudinally, the subcutaneous fat is mobilized and cutaneous sensory branches identified and protected. The underlying superficial palmar fascia is incised in line with the skin incision. The underlying midportion of the TCL is now visualized.
Transverse Carpal Ligament Release
Occasionally, the investing fascia along the ulnar edge of the thenar musculature is mobilized radialward (if the thenar musculature is well developed) to visualize the proximal limb of the TCL. Injury to any anomalous motor branch of the median nerve is avoided by directly visualizing and then incising the TCL (Figure 2). The TCL is incised along its ulnar border just radial to the hook of hamate from distal to proximal in line with the radial border of the ring finger. Staying near the ulnar attachment of the TCL keeps the plane of ligament division farther away from the median nerve and its recurrent motor branches. Although the ulnar neurovascular bundle typically resides ulnar to the hook of hamate in the canal of Guyon, the surgeon must be aware that it can be located radial to the hook in some instances.27,28 In the elderly, the ulnar artery may be tortuous and enter the field and require retraction. The TCL is incised distally until the sentinel fat pad, which marks the superficial palmar arterial arch, is visualized. This bed of adipose tissue marks the distal edge of the TCL.29
Proximally, subcutaneous tissues above the proximal limb of the TCL and DVFF are mobilized to about 2 cm proximal to the wrist flexion crease to create a plane for the fine long nasal turbinate speculum. The nasal turbinate speculum is then inserted into this plane above the proximal limb of the TCL and DVFF (Figure 3). Once inserted to the level of the confluence of the TCL and the DVFF, the speculum is opened.
Topside visualization is now encountered with the ulnar neurovascular bundle protected by the ulnar blade of the speculum. A long-handle scalpel is used to incise the TCL and the DVFF under direct visualization from proximal to distal in line with the previously completed distal release (Figure 4). As the nasal turbinate speculum is stretching the TCL and putting it under tension, the TCL can be heard splitting as it is being incised. Once the TCL and the DVFF are divided, the speculum is slowly closed and removed. Wide diastasis of the radial and ulnar leaflets of the TCL and the DVFF is directly visualized. Complete decompression of the median nerve from the distal forearm fascia to the superficial palmar arch is confirmed.
Adhesions between the undersurface of the radial leaflet and the flexor tendons and median nerve are mobilized. The median nerve is assessed for “hourglass” morphology or atrophy. The flexor tendons can be swept radialward with a free elevator to inspect the floor of the carpal tunnel. Flexor tenosynovectomy is not routinely performed. The incision is closed with interrupted simple sutures using 4-0 nylon.
Study Results
This study was conducted at Hand Surgery PC, Newton-Wellesley Hospital, Tufts University School of Medicine. Over a 10-month interval, 101 consecutive mini-OCTRs (63 right hands, 38 left hands) were performed with this proximal release modification in 88 patients (51 females, 37 males) by Dr. Ruchelsman and Dr. Belsky (Table). CTRs performed in the setting of wrist and/or carpal trauma were excluded. Mean age was 62.8 years. Mean follow-up was 11.3 weeks (~3 months). For isolated cases of CTR, mean tourniquet time was 16 minutes. CTS symptoms were relieved in all patients with a high degree of satisfaction as measured with history and examination findings at follow-up visits. There were no major complications (eg, infection, neural or vascular damage, severe residual pain). Four patients reported minor residual numbness in the fingers at latest follow-up but nevertheless had major improvement over preoperative baseline. These 4 patients had preoperative electromyograms or nerve conduction studies documenting the extent of their disease. There was 1 case of minor wound complication. Three weeks after surgery, the patient had a 1-cm wound opening, which closed with local wound care. The patient did not develop any drainage, infection, bleeding, or neurologic symptoms.
Discussion
Open release of the TCL—the gold standard of surgical treatment for CTS—produces reliable symptom relief in the vast majority of patients.25,30 Given that the most common complication of carpal tunnel surgery is incomplete release of the TCL,31,32 this technique, which uses a nasal turbinate speculum to better visualize the median nerve, could potentially reduce the reoperation rate. The nasal turbinate speculum allows the surgeon to see the confluence of the TCL and the DVFF. In addition, as the complete release can be visualized, there is minimal chance of injury.
The 2007 Cochrane review3 found no strong evidence supporting replacing OCTR with endoscopic techniques. Previous investigators have questioned the utility of ECTR given that it is higher in cost and more resource-intensive than OCTR1,33,34 and is associated with higher rates of certain complications.5,22,35-37 A 2004 meta-analysis of 13 randomized, controlled trials found a higher rate of reversible nerve damage with an odds ratio of 3.1 for ECTR versus OCTR.35 A more recent (2006) review of more than 80 studies found transient neurapraxias in 1.45% of ECTR cases and 0.25% of OCTR cases.5 The same study reported overall complication rates (reversible and major neurovascular structural injuries) of 0.74% for OCTR and 1.63% for ECTR (P < .005). Another limitation of ECTR is that endoscopic techniques require a higher degree of surgical skill, which makes teaching residents and fellows more challenging.
The novel nasal turbinate speculum technique presented here is easily reproducible and allows first-time surgeons to visualize all important structures. Given that this technique does not require an endoscope or an endoscope-viewing tower, it is likely more cost-effective and requires less time for turnover between cases. Patients obtain good relief of their CTS symptoms with this technique, and most return to their daily activities within weeks after operation.
Carpal tunnel syndrome (CTS) is a disorder characterized by entrapment of the median nerve at the wrist, which may lead to symptoms of pain, paresthesia, and, ultimately, thenar muscle atrophy. Surgical intervention is indicated with persistent or progressive symptoms despite nonoperative management. Timely surgical decompression aims to halt progression of this disorder and prevent permanent peripheral nerve injury.
Carpal tunnel release (CTR) is the most common hand and wrist surgery in the United States, with about 400,000 operations performed annually.1,2 Several methods of decompressing the carpal tunnel have been described.3 These include standard open CTR (OCTR), mini-open approaches, and various endoscopic techniques. OCTR was initially described by Sir James Learmonth in 1933,4 and it remains the gold-standard surgical treatment for patients with symptomatic CTS. Uniform excellent results with high patient satisfaction and low complication rates have been reported in several series.5-9 Common to all techniques is complete proximal-to-distal division of the transverse carpal ligament (TCL). Magnetic resonance imaging studies have shown that TCL transection and the resulting diastasis between the radial and ulnar leaflets cause a significant increase in the volume of the carpal tunnel, leading to decreased pressure.10,11
Endoscopic CTR (ECTR) techniques were developed in an effort to reduce complications, scar sensitivity, and pillar pain and facilitate more rapid return to work.12-17 Outcome studies have demonstrated that both open and endoscopic releases yield patient-reported subjective improvements over preoperative symptoms.18-22 A randomized, controlled trial by Trumble and colleagues23 in 2002 found that ECTR led to improved patient outcomes in the early postoperative period (first 3 months), though differences in outcomes were reduced at final follow-up. More recently (2007), a Cochrane review of 33 trials concluded there was no strong evidence favoring use of alternative techniques over OCTR.3 Further, OCTR has been found to be technically less demanding and associated with decreased complications and costs.24
Indications
The benefit of median nerve decompression at the wrist for CTS is clear.6,7 Indications for surgery in patients with CTS include persistent symptoms despite nonoperative treatment, objective sensory disturbance or motor weakness, and thenar atrophy. Symptomatic response to corticosteroid injection is predictive of success after carpal tunnel surgery.25 More than 87% of patients who gain symptomatic relief from corticosteroid injection have an excellent surgical outcome.
Technique
OCTR allows direct visualization of the TCL and the distal volar forearm fascia (DVFF) and evaluation for the presence of anomalous branching patterns of the median nerve. OCTR traditionally was performed through a 4- to 5-cm longitudinal incision extending from the wrist crease proximally to the Kaplan cardinal line distally. The mini-open technique is identical with the exception of incision length. We routinely use a 2.5- to 3-cm incision. Regardless of incision length, each OCTR should proceed through the same reproducible steps.
We perform OCTR under tourniquet control. Choice of anesthesia is surgeon and patient preference. We prefer local anesthesia with conscious sedation. After conscious sedation is administered, we infiltrate the carpal tunnel and surrounding subcutaneous tissue with 10 mL of a 50:50 mixture of 0.5% bupivacaine and 1% lidocaine without epinephrine.
A 2.5- to 3-cm longitudinal incision is made along the axis of the radial border of the ring finger from the Kaplan cardinal line26 and extending about 3 cm proximally toward the wrist flexion crease ulnar to the palmaris longus if present (Figure 1).
After the skin is incised longitudinally, the subcutaneous fat is mobilized and cutaneous sensory branches identified and protected. The underlying superficial palmar fascia is incised in line with the skin incision. The underlying midportion of the TCL is now visualized.
Transverse Carpal Ligament Release
Occasionally, the investing fascia along the ulnar edge of the thenar musculature is mobilized radialward (if the thenar musculature is well developed) to visualize the proximal limb of the TCL. Injury to any anomalous motor branch of the median nerve is avoided by directly visualizing and then incising the TCL (Figure 2). The TCL is incised along its ulnar border just radial to the hook of hamate from distal to proximal in line with the radial border of the ring finger. Staying near the ulnar attachment of the TCL keeps the plane of ligament division farther away from the median nerve and its recurrent motor branches. Although the ulnar neurovascular bundle typically resides ulnar to the hook of hamate in the canal of Guyon, the surgeon must be aware that it can be located radial to the hook in some instances.27,28 In the elderly, the ulnar artery may be tortuous and enter the field and require retraction. The TCL is incised distally until the sentinel fat pad, which marks the superficial palmar arterial arch, is visualized. This bed of adipose tissue marks the distal edge of the TCL.29
Proximally, subcutaneous tissues above the proximal limb of the TCL and DVFF are mobilized to about 2 cm proximal to the wrist flexion crease to create a plane for the fine long nasal turbinate speculum. The nasal turbinate speculum is then inserted into this plane above the proximal limb of the TCL and DVFF (Figure 3). Once inserted to the level of the confluence of the TCL and the DVFF, the speculum is opened.
Topside visualization is now encountered with the ulnar neurovascular bundle protected by the ulnar blade of the speculum. A long-handle scalpel is used to incise the TCL and the DVFF under direct visualization from proximal to distal in line with the previously completed distal release (Figure 4). As the nasal turbinate speculum is stretching the TCL and putting it under tension, the TCL can be heard splitting as it is being incised. Once the TCL and the DVFF are divided, the speculum is slowly closed and removed. Wide diastasis of the radial and ulnar leaflets of the TCL and the DVFF is directly visualized. Complete decompression of the median nerve from the distal forearm fascia to the superficial palmar arch is confirmed.
Adhesions between the undersurface of the radial leaflet and the flexor tendons and median nerve are mobilized. The median nerve is assessed for “hourglass” morphology or atrophy. The flexor tendons can be swept radialward with a free elevator to inspect the floor of the carpal tunnel. Flexor tenosynovectomy is not routinely performed. The incision is closed with interrupted simple sutures using 4-0 nylon.
Study Results
This study was conducted at Hand Surgery PC, Newton-Wellesley Hospital, Tufts University School of Medicine. Over a 10-month interval, 101 consecutive mini-OCTRs (63 right hands, 38 left hands) were performed with this proximal release modification in 88 patients (51 females, 37 males) by Dr. Ruchelsman and Dr. Belsky (Table). CTRs performed in the setting of wrist and/or carpal trauma were excluded. Mean age was 62.8 years. Mean follow-up was 11.3 weeks (~3 months). For isolated cases of CTR, mean tourniquet time was 16 minutes. CTS symptoms were relieved in all patients with a high degree of satisfaction as measured with history and examination findings at follow-up visits. There were no major complications (eg, infection, neural or vascular damage, severe residual pain). Four patients reported minor residual numbness in the fingers at latest follow-up but nevertheless had major improvement over preoperative baseline. These 4 patients had preoperative electromyograms or nerve conduction studies documenting the extent of their disease. There was 1 case of minor wound complication. Three weeks after surgery, the patient had a 1-cm wound opening, which closed with local wound care. The patient did not develop any drainage, infection, bleeding, or neurologic symptoms.
Discussion
Open release of the TCL—the gold standard of surgical treatment for CTS—produces reliable symptom relief in the vast majority of patients.25,30 Given that the most common complication of carpal tunnel surgery is incomplete release of the TCL,31,32 this technique, which uses a nasal turbinate speculum to better visualize the median nerve, could potentially reduce the reoperation rate. The nasal turbinate speculum allows the surgeon to see the confluence of the TCL and the DVFF. In addition, as the complete release can be visualized, there is minimal chance of injury.
The 2007 Cochrane review3 found no strong evidence supporting replacing OCTR with endoscopic techniques. Previous investigators have questioned the utility of ECTR given that it is higher in cost and more resource-intensive than OCTR1,33,34 and is associated with higher rates of certain complications.5,22,35-37 A 2004 meta-analysis of 13 randomized, controlled trials found a higher rate of reversible nerve damage with an odds ratio of 3.1 for ECTR versus OCTR.35 A more recent (2006) review of more than 80 studies found transient neurapraxias in 1.45% of ECTR cases and 0.25% of OCTR cases.5 The same study reported overall complication rates (reversible and major neurovascular structural injuries) of 0.74% for OCTR and 1.63% for ECTR (P < .005). Another limitation of ECTR is that endoscopic techniques require a higher degree of surgical skill, which makes teaching residents and fellows more challenging.
The novel nasal turbinate speculum technique presented here is easily reproducible and allows first-time surgeons to visualize all important structures. Given that this technique does not require an endoscope or an endoscope-viewing tower, it is likely more cost-effective and requires less time for turnover between cases. Patients obtain good relief of their CTS symptoms with this technique, and most return to their daily activities within weeks after operation.
1. Ono S, Clapham PJ, Chung KC. Optimal management of carpal tunnel syndrome. Int J Gen Med. 2010;3(4):255-261.
2. Concannon MJ, Brownfield ML, Puckett CL. The incidence of recurrence after endoscopic carpal tunnel release. Plast Reconstr Surg. 2000;105(5):1662-1665.
3. Scholten RJ, Mink van der Molen A, Uitdehaag BM, Bouter LM, de Vet HC. Surgical treatment options for carpal tunnel syndrome. Cochrane Database Syst Rev. 2007;(4):CD003905.
4. In memoriam Sir James Learmonth, K.C.V.O., C.B.E., hon. F.R.C.S. (1895-1967). Ann R Coll Surg Engl. 1967;41(5):438-439.
5. Benson LS, Bare AA, Nagle DJ, Harder VS, Williams CS, Visotsky JL. Complications of endoscopic and open carpal tunnel release. Arthroscopy. 2006;22(9):919-924, 924.e1-e2.
6. Jarvik JG, Comstock BA, Kliot M, et al. Surgery versus non-surgical therapy for carpal tunnel syndrome: a randomised parallel-group trial. Lancet. 2009;374(9695):1074-1081.
7. Verdugo RJ, Salinas RA, Castillo JL, et al. Surgical versus non-surgical treatment for carpal tunnel syndrome. Cochrane Database Syst Rev. 2008;(4):CD001552.
8. Garland H, Langworth EP, Taverner D, et al. Surgical treatment for the carpal tunnel syndrome. Lancet. 1964;1(7343):1129-1130.
9. Gerritsen AA, de Vet HC, Scholten RJ, et al. Splinting vs surgery in the treatment of carpal tunnel syndrome: a randomized controlled trial. JAMA. 2002;288(10):1245-1251.
10. Gelberman RH, Hergenroeder PT, Hargens AR, et al. The carpal tunnel syndrome. A study of carpal canal pressures. J Bone Joint Surg Am. 1981;63(3):380-383.
11. Sucher BM. Myofascial manipulative release of carpal tunnel syndrome: documentation with magnetic resonance imaging. J Am Osteopath Assoc. 1993;93(12):1273-1278.
12. Pereira EE, Miranda DA, Sere I, et al. Endoscopic release of the carpal tunnel: a 2-portal-modified technique. Tech Hand Up Extrem Surg. 2010;14(4):263-265.
13. Louis DS, Greene TL, Noellert RC. Complications of carpal tunnel surgery. J Neurosurg. 1985;62(3):352-356.
14. Mirza MA, King ET Jr, Tanveer S. Palmar uniportal extrabursal endoscopic carpal tunnel release. Arthroscopy. 1995;11(1):82-90.
15. Brown MG, Keyser B, Rothenberg ES. Endoscopic carpal tunnel release. J Hand Surg Am. 1992;17(6):1009-1011.
16. Agee JM, McCarroll HR Jr, Tortosa RD, et al. Endoscopic release of the carpal tunnel: a randomized prospective multicenter study. J Hand Surg Am. 1992;17(6):987-995.
17. Okutsu I, Ninomiya S, Takatori Y, et al. Endoscopic management of carpal tunnel syndrome. Arthroscopy. 1989;5(1):11-18.
18. Ghaly RF, Saban KL, Haley DA, et al. Endoscopic carpal tunnel release surgery: report of patient satisfaction. Neurol Res. 2000;22(6):551-555.
19. Lee WP, Plancher KD, Strickland JW. Carpal tunnel release with a small palmar incision. Hand Clin. 1996;12(2):271-284.
20. Biyani A, Downes EM. An open twin incision technique of carpal tunnel decompression with reduced incidence of scar tenderness. J Hand Surg Br. 1993;18(3):331-334.
21. Brown RA, Gelberman RH, Seiler JG 3rd, et al. Carpal tunnel release. A prospective, randomized assessment of open and endoscopic methods. J Bone Joint Surg Am. 1993;75(9):1265-1275.
22. Chow JC. Endoscopic release of the carpal ligament for carpal tunnel syndrome: 22-month clinical result. Arthroscopy. 1990;6(4):288-296.
23. Trumble TE, Diao E, Abrams RA, et al. Single-portal endoscopic carpal tunnel release compared with open release: a prospective, randomized trial. J Bone Joint Surg Am. 2002;84(7):1107-1115.
24. Gerritsen AA, Uitdehaag BM, van Geldere D, et al. Systematic review of randomized clinical trials of surgical treatment for carpal tunnel syndrome. Br J Surg. 2001;88(10):1285-1295.
25. Edgell SE, McCabe SJ, Breidenbach WC, et al. Predicting the outcome of carpal tunnel release. J Hand Surg Am. 2003;28(2):255-261.
26. Vella JC, Hartigan BJ, Stern PJ. Kaplan’s cardinal line. J Hand Surg Am. 2006;31(6):912-918.
27. Kwon JY, Kim JY, Hong JT, et al. Position change of the neurovascular structures around the carpal tunnel with dynamic wrist motion. J Korean Neurosurg Soc. 2011;50(4):377-380.
28. Netscher D, Polsen C, Thornby J, et al. Anatomic delineation of the ulnar nerve and ulnar artery in relation to the carpal tunnel by axial magnetic resonance imaging scanning. J Hand Surg Am. 1996;21(2):273-276.
29. Madhav TJ, To P, Stern PJ. The palmar fat pad is a reliable intraoperative landmark during carpal tunnel release. J Hand Surg Am. 2009;34(7):1204-1209.
30. Kulick MI, Gordillo G, Javidi T, et al. Long-term analysis of patients having surgical treatment for carpal tunnel syndrome. J Hand Surg Am. 1986;11(1):59-66.
31. Bland JD. Treatment of carpal tunnel syndrome. Muscle Nerve. 2007;36(2):167-171.
32. MacDonald RI, Lichtman DM, Hanlon JJ, et al. Complications of surgical release for carpal tunnel syndrome. J Hand Surg Am. 1978;3(1):70-76.
33. Atroshi I, Larsson GU, Ornstein E, Hofer M, Johnsson R, Ranstam J. Outcomes of endoscopic surgery compared with open surgery for carpal tunnel syndrome among employed patients: randomised controlled trial. BMJ. 2006;332(7556):1473.
34. Ferdinand RD, MacLean JG. Endoscopic versus open carpal tunnel release in bilateral carpal tunnel syndrome. A prospective, randomised, blinded assessment. J Bone Joint Surg Br. 2002;84(3):375-379.
35. Thoma A, Veltri K, Haines T, et al. A meta-analysis of randomized controlled trials comparing endoscopic and open carpal tunnel decompression. Plast Reconstr Surg. 2004;114(5):1137-1146.
36. Murphy RX Jr, Jennings JF, Wukich DK. Major neurovascular complications of endoscopic carpal tunnel release. J Hand Surg Am. 1994;19(1):114-118.
37. Palmer DH, Paulson JC, Lane-Larsen CL, et al. Endoscopic carpal tunnel release: a comparison of two techniques with open release. Arthroscopy. 1993;9(5):498-508.
1. Ono S, Clapham PJ, Chung KC. Optimal management of carpal tunnel syndrome. Int J Gen Med. 2010;3(4):255-261.
2. Concannon MJ, Brownfield ML, Puckett CL. The incidence of recurrence after endoscopic carpal tunnel release. Plast Reconstr Surg. 2000;105(5):1662-1665.
3. Scholten RJ, Mink van der Molen A, Uitdehaag BM, Bouter LM, de Vet HC. Surgical treatment options for carpal tunnel syndrome. Cochrane Database Syst Rev. 2007;(4):CD003905.
4. In memoriam Sir James Learmonth, K.C.V.O., C.B.E., hon. F.R.C.S. (1895-1967). Ann R Coll Surg Engl. 1967;41(5):438-439.
5. Benson LS, Bare AA, Nagle DJ, Harder VS, Williams CS, Visotsky JL. Complications of endoscopic and open carpal tunnel release. Arthroscopy. 2006;22(9):919-924, 924.e1-e2.
6. Jarvik JG, Comstock BA, Kliot M, et al. Surgery versus non-surgical therapy for carpal tunnel syndrome: a randomised parallel-group trial. Lancet. 2009;374(9695):1074-1081.
7. Verdugo RJ, Salinas RA, Castillo JL, et al. Surgical versus non-surgical treatment for carpal tunnel syndrome. Cochrane Database Syst Rev. 2008;(4):CD001552.
8. Garland H, Langworth EP, Taverner D, et al. Surgical treatment for the carpal tunnel syndrome. Lancet. 1964;1(7343):1129-1130.
9. Gerritsen AA, de Vet HC, Scholten RJ, et al. Splinting vs surgery in the treatment of carpal tunnel syndrome: a randomized controlled trial. JAMA. 2002;288(10):1245-1251.
10. Gelberman RH, Hergenroeder PT, Hargens AR, et al. The carpal tunnel syndrome. A study of carpal canal pressures. J Bone Joint Surg Am. 1981;63(3):380-383.
11. Sucher BM. Myofascial manipulative release of carpal tunnel syndrome: documentation with magnetic resonance imaging. J Am Osteopath Assoc. 1993;93(12):1273-1278.
12. Pereira EE, Miranda DA, Sere I, et al. Endoscopic release of the carpal tunnel: a 2-portal-modified technique. Tech Hand Up Extrem Surg. 2010;14(4):263-265.
13. Louis DS, Greene TL, Noellert RC. Complications of carpal tunnel surgery. J Neurosurg. 1985;62(3):352-356.
14. Mirza MA, King ET Jr, Tanveer S. Palmar uniportal extrabursal endoscopic carpal tunnel release. Arthroscopy. 1995;11(1):82-90.
15. Brown MG, Keyser B, Rothenberg ES. Endoscopic carpal tunnel release. J Hand Surg Am. 1992;17(6):1009-1011.
16. Agee JM, McCarroll HR Jr, Tortosa RD, et al. Endoscopic release of the carpal tunnel: a randomized prospective multicenter study. J Hand Surg Am. 1992;17(6):987-995.
17. Okutsu I, Ninomiya S, Takatori Y, et al. Endoscopic management of carpal tunnel syndrome. Arthroscopy. 1989;5(1):11-18.
18. Ghaly RF, Saban KL, Haley DA, et al. Endoscopic carpal tunnel release surgery: report of patient satisfaction. Neurol Res. 2000;22(6):551-555.
19. Lee WP, Plancher KD, Strickland JW. Carpal tunnel release with a small palmar incision. Hand Clin. 1996;12(2):271-284.
20. Biyani A, Downes EM. An open twin incision technique of carpal tunnel decompression with reduced incidence of scar tenderness. J Hand Surg Br. 1993;18(3):331-334.
21. Brown RA, Gelberman RH, Seiler JG 3rd, et al. Carpal tunnel release. A prospective, randomized assessment of open and endoscopic methods. J Bone Joint Surg Am. 1993;75(9):1265-1275.
22. Chow JC. Endoscopic release of the carpal ligament for carpal tunnel syndrome: 22-month clinical result. Arthroscopy. 1990;6(4):288-296.
23. Trumble TE, Diao E, Abrams RA, et al. Single-portal endoscopic carpal tunnel release compared with open release: a prospective, randomized trial. J Bone Joint Surg Am. 2002;84(7):1107-1115.
24. Gerritsen AA, Uitdehaag BM, van Geldere D, et al. Systematic review of randomized clinical trials of surgical treatment for carpal tunnel syndrome. Br J Surg. 2001;88(10):1285-1295.
25. Edgell SE, McCabe SJ, Breidenbach WC, et al. Predicting the outcome of carpal tunnel release. J Hand Surg Am. 2003;28(2):255-261.
26. Vella JC, Hartigan BJ, Stern PJ. Kaplan’s cardinal line. J Hand Surg Am. 2006;31(6):912-918.
27. Kwon JY, Kim JY, Hong JT, et al. Position change of the neurovascular structures around the carpal tunnel with dynamic wrist motion. J Korean Neurosurg Soc. 2011;50(4):377-380.
28. Netscher D, Polsen C, Thornby J, et al. Anatomic delineation of the ulnar nerve and ulnar artery in relation to the carpal tunnel by axial magnetic resonance imaging scanning. J Hand Surg Am. 1996;21(2):273-276.
29. Madhav TJ, To P, Stern PJ. The palmar fat pad is a reliable intraoperative landmark during carpal tunnel release. J Hand Surg Am. 2009;34(7):1204-1209.
30. Kulick MI, Gordillo G, Javidi T, et al. Long-term analysis of patients having surgical treatment for carpal tunnel syndrome. J Hand Surg Am. 1986;11(1):59-66.
31. Bland JD. Treatment of carpal tunnel syndrome. Muscle Nerve. 2007;36(2):167-171.
32. MacDonald RI, Lichtman DM, Hanlon JJ, et al. Complications of surgical release for carpal tunnel syndrome. J Hand Surg Am. 1978;3(1):70-76.
33. Atroshi I, Larsson GU, Ornstein E, Hofer M, Johnsson R, Ranstam J. Outcomes of endoscopic surgery compared with open surgery for carpal tunnel syndrome among employed patients: randomised controlled trial. BMJ. 2006;332(7556):1473.
34. Ferdinand RD, MacLean JG. Endoscopic versus open carpal tunnel release in bilateral carpal tunnel syndrome. A prospective, randomised, blinded assessment. J Bone Joint Surg Br. 2002;84(3):375-379.
35. Thoma A, Veltri K, Haines T, et al. A meta-analysis of randomized controlled trials comparing endoscopic and open carpal tunnel decompression. Plast Reconstr Surg. 2004;114(5):1137-1146.
36. Murphy RX Jr, Jennings JF, Wukich DK. Major neurovascular complications of endoscopic carpal tunnel release. J Hand Surg Am. 1994;19(1):114-118.
37. Palmer DH, Paulson JC, Lane-Larsen CL, et al. Endoscopic carpal tunnel release: a comparison of two techniques with open release. Arthroscopy. 1993;9(5):498-508.
TCT: Immobilized leaflets on bioprosthetic aortic valves trigger concern
SAN FRANCISCO – The newly discovered issue of reduced leaflet motion and possible thrombus on bioprosthetic aortic heart valves, called by one expert “an imaging observation of uncertain clinical significance,” nonetheless drew lots of attention at the Transcatheter Cardiovascular Therapeutics annual meeting. Reduced leaflet motion was the focus of the meeting’s opening session as well as a specially scheduled press conference.
Much of the attention dealt with clarifying the situation and calling for calm after patient concerns were aroused by a report on Oct. 5 that examination of detailed CT scans from small series of patients who had recently undergone aortic valve replacement showed reduced-motion or immobilized valve leaflets on some of the bioprosthetic valves. The pattern of the finding, made using four-dimensional CT imaging, indicated that reduced-motion leaflets did not occur, and possibly even resolved, when patients were on anticoagulant therapy, suggesting that leaflet immobilization involved thrombus. Also, reduced-motion leaflets appeared following both transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR), said Dr. Raj R. Makkar.
Dr. Makkar summarized his CT findings in several talks during the meeting and also in a report published a few days before the meeting (N Engl J Med. 2015 Oct 5. doi: 10.1056/NEJMoa1509233).
“We started with what we thought was an imaging artifact and established that is it real. We also established with reasonable certainty that it is related to thrombus,” said Dr. Makkar, professor at the University of California, Los Angeles, and director of the Cardiovascular Interventional Center at Cedars-Sinai Medical Center in Los Angeles. The evidence also indicates that this is a class effect that occurs with all types of TAVR systems as well as surgically placed valves.
What the evidence so far does not indicate is that patients with reduced-motion leaflets face any clinical consequence nor need for routine CT imaging of a newly-placed TAVR or SAVR valve. Also no need for routine anticoagulant therapy instead of standard treatment with dual antiplatelet therapy for several months following placement of a bioprosthetic aortic valve. “We should not make the leap that following TAVR, everyone should be on an anticoagulant” because anticoagulant treatment carries it own risks, said Dr. Makkar, who noted that roughly a quarter of TAVR patients receive anticoagulant treatment because of another indication, such as atrial fibrillation.
“The study did not show a temporal or causal relationship between the imaging findings and stroke. That needs emphasis,” commented Dr. Susheel Kodali, codirector of the Heart Valve Center at the Center for Interventional Vascular Therapy at Columbia University in New York. The possible link between leaflet immobility and strokes or other neurologic events “warrants further study,” as the data that Dr. Makkar reported involved a total of only six strokes or transient ischemic attacks. Data from all the TAVR trials and registries reported so far showed “no late signal of stroke,” said Dr. Kodali, who added that SAVR had a 30-year record of net benefit for appropriate patients.
“Is valve-leaflet thickening an important controversy or much ado about nothing?” wondered Dr. Martin B. Leon, director of the Center for Interventional Vascular Therapy of Columbia University.
“Patients should not feel at risk, and there is no need to do anything differently” for the time being in routine practice, commented Dr. Jeffrey J. Popma, professor at Harvard Medical School and director of interventional cardiology at Beth Israel Deaconess Medical Center, both in Boston.
Dr. Makkar said that in the days following the publication of his report, he had “a lot of phone calls and time spent allaying anxiety in patients and reassuring them.”
One reason why these leaflet-motion abnormalities may have shown up on CT examinations recently is that “the cameras have gotten better,” said Dr. Jonathon A. Leipsic, codirector of advanced cardiac imaging at the Providence Health Care Heart Center at St. Paul’s Hospital in Vancouver. Dr. Leipsic also highlighted that with state-of-the-art CT images, immobilized leaflets are easy to identify.
Despite that, Dr. Popma stressed that standardized imaging protocols are needed going forward to produce reliable incidence data.
The data that Dr. Makkar reported came from a review of four-dimensional CT imaging done on 187 replacement aortic valves, usually within 3 months of placement. Images for 55 aortic valves came from the device-approval trial for a new TAVR system, taken 30 days after patients underwent TAVR with any of three types of systems. The images showed reduced leaflet motion in 22 valves (40%).
CT images for another 132 valves came from a Cedar’s-Sinai registry and a second, independent registry maintained in Denmark. CT images showed that 17 (13%) of the replaced aortic valves showed a leaflet-motion abnormality, including two valves placed using SAVR. Half the registry patients had undergone CT imaging within 88 days of valve replacement. The only signal of a clinical outcome linked with reduced-motion leaflets was a small increase in the incidence of transient ischemic attacks, but Dr. Makkar cautioned that transient ischemic attacks “are hard to adjudicate.”
Dr. Makkar’s report was “a small but important study, one of the first reports of this phenomenon. You don’t want to lose sight of all the evidence of patient benefit” from aortic valve replacement, stressed Dr. Kodali at the meeting, sponsored by the Cardiovascular Research Foundation. “This needs to be investigated further, probably by a Food and Drug Administration–mandated trial with CT imaging.”
“Aortic valves are lifesaving devices. The last thing that should happen is patients not getting their aortic valves replaced” when their condition demands it, Dr. Makkar said.
The PORTICO IDE study and RESOLVE registry were funded by St. Jude. Dr. Makkar has received honoraria and research support from St. Jude, lecture fees from Edwards Lifesciences, research grants from Edwards and Medtronic, and has an equity interest in Entourage. Dr. Kodali has been a consultant to Edwards Lifesciences and Claret Medical and has an equity interest in Thubrikar Aortic Valve. Dr. Leon has been a consultant to Edwards. Dr. Popma has been a consultant to Abbott Laboratories, Boston Scientific, and St. Jude, and he has been a speaker for and received grants from Medtronic, Dr. Leipsic has been a consultant to Edwards and Heartflow and received grants from Edwards, Neovasc, and Tendyne.
On Twitter @mitchelzoler
SAN FRANCISCO – The newly discovered issue of reduced leaflet motion and possible thrombus on bioprosthetic aortic heart valves, called by one expert “an imaging observation of uncertain clinical significance,” nonetheless drew lots of attention at the Transcatheter Cardiovascular Therapeutics annual meeting. Reduced leaflet motion was the focus of the meeting’s opening session as well as a specially scheduled press conference.
Much of the attention dealt with clarifying the situation and calling for calm after patient concerns were aroused by a report on Oct. 5 that examination of detailed CT scans from small series of patients who had recently undergone aortic valve replacement showed reduced-motion or immobilized valve leaflets on some of the bioprosthetic valves. The pattern of the finding, made using four-dimensional CT imaging, indicated that reduced-motion leaflets did not occur, and possibly even resolved, when patients were on anticoagulant therapy, suggesting that leaflet immobilization involved thrombus. Also, reduced-motion leaflets appeared following both transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR), said Dr. Raj R. Makkar.
Dr. Makkar summarized his CT findings in several talks during the meeting and also in a report published a few days before the meeting (N Engl J Med. 2015 Oct 5. doi: 10.1056/NEJMoa1509233).
“We started with what we thought was an imaging artifact and established that is it real. We also established with reasonable certainty that it is related to thrombus,” said Dr. Makkar, professor at the University of California, Los Angeles, and director of the Cardiovascular Interventional Center at Cedars-Sinai Medical Center in Los Angeles. The evidence also indicates that this is a class effect that occurs with all types of TAVR systems as well as surgically placed valves.
What the evidence so far does not indicate is that patients with reduced-motion leaflets face any clinical consequence nor need for routine CT imaging of a newly-placed TAVR or SAVR valve. Also no need for routine anticoagulant therapy instead of standard treatment with dual antiplatelet therapy for several months following placement of a bioprosthetic aortic valve. “We should not make the leap that following TAVR, everyone should be on an anticoagulant” because anticoagulant treatment carries it own risks, said Dr. Makkar, who noted that roughly a quarter of TAVR patients receive anticoagulant treatment because of another indication, such as atrial fibrillation.
“The study did not show a temporal or causal relationship between the imaging findings and stroke. That needs emphasis,” commented Dr. Susheel Kodali, codirector of the Heart Valve Center at the Center for Interventional Vascular Therapy at Columbia University in New York. The possible link between leaflet immobility and strokes or other neurologic events “warrants further study,” as the data that Dr. Makkar reported involved a total of only six strokes or transient ischemic attacks. Data from all the TAVR trials and registries reported so far showed “no late signal of stroke,” said Dr. Kodali, who added that SAVR had a 30-year record of net benefit for appropriate patients.
“Is valve-leaflet thickening an important controversy or much ado about nothing?” wondered Dr. Martin B. Leon, director of the Center for Interventional Vascular Therapy of Columbia University.
“Patients should not feel at risk, and there is no need to do anything differently” for the time being in routine practice, commented Dr. Jeffrey J. Popma, professor at Harvard Medical School and director of interventional cardiology at Beth Israel Deaconess Medical Center, both in Boston.
Dr. Makkar said that in the days following the publication of his report, he had “a lot of phone calls and time spent allaying anxiety in patients and reassuring them.”
One reason why these leaflet-motion abnormalities may have shown up on CT examinations recently is that “the cameras have gotten better,” said Dr. Jonathon A. Leipsic, codirector of advanced cardiac imaging at the Providence Health Care Heart Center at St. Paul’s Hospital in Vancouver. Dr. Leipsic also highlighted that with state-of-the-art CT images, immobilized leaflets are easy to identify.
Despite that, Dr. Popma stressed that standardized imaging protocols are needed going forward to produce reliable incidence data.
The data that Dr. Makkar reported came from a review of four-dimensional CT imaging done on 187 replacement aortic valves, usually within 3 months of placement. Images for 55 aortic valves came from the device-approval trial for a new TAVR system, taken 30 days after patients underwent TAVR with any of three types of systems. The images showed reduced leaflet motion in 22 valves (40%).
CT images for another 132 valves came from a Cedar’s-Sinai registry and a second, independent registry maintained in Denmark. CT images showed that 17 (13%) of the replaced aortic valves showed a leaflet-motion abnormality, including two valves placed using SAVR. Half the registry patients had undergone CT imaging within 88 days of valve replacement. The only signal of a clinical outcome linked with reduced-motion leaflets was a small increase in the incidence of transient ischemic attacks, but Dr. Makkar cautioned that transient ischemic attacks “are hard to adjudicate.”
Dr. Makkar’s report was “a small but important study, one of the first reports of this phenomenon. You don’t want to lose sight of all the evidence of patient benefit” from aortic valve replacement, stressed Dr. Kodali at the meeting, sponsored by the Cardiovascular Research Foundation. “This needs to be investigated further, probably by a Food and Drug Administration–mandated trial with CT imaging.”
“Aortic valves are lifesaving devices. The last thing that should happen is patients not getting their aortic valves replaced” when their condition demands it, Dr. Makkar said.
The PORTICO IDE study and RESOLVE registry were funded by St. Jude. Dr. Makkar has received honoraria and research support from St. Jude, lecture fees from Edwards Lifesciences, research grants from Edwards and Medtronic, and has an equity interest in Entourage. Dr. Kodali has been a consultant to Edwards Lifesciences and Claret Medical and has an equity interest in Thubrikar Aortic Valve. Dr. Leon has been a consultant to Edwards. Dr. Popma has been a consultant to Abbott Laboratories, Boston Scientific, and St. Jude, and he has been a speaker for and received grants from Medtronic, Dr. Leipsic has been a consultant to Edwards and Heartflow and received grants from Edwards, Neovasc, and Tendyne.
On Twitter @mitchelzoler
SAN FRANCISCO – The newly discovered issue of reduced leaflet motion and possible thrombus on bioprosthetic aortic heart valves, called by one expert “an imaging observation of uncertain clinical significance,” nonetheless drew lots of attention at the Transcatheter Cardiovascular Therapeutics annual meeting. Reduced leaflet motion was the focus of the meeting’s opening session as well as a specially scheduled press conference.
Much of the attention dealt with clarifying the situation and calling for calm after patient concerns were aroused by a report on Oct. 5 that examination of detailed CT scans from small series of patients who had recently undergone aortic valve replacement showed reduced-motion or immobilized valve leaflets on some of the bioprosthetic valves. The pattern of the finding, made using four-dimensional CT imaging, indicated that reduced-motion leaflets did not occur, and possibly even resolved, when patients were on anticoagulant therapy, suggesting that leaflet immobilization involved thrombus. Also, reduced-motion leaflets appeared following both transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR), said Dr. Raj R. Makkar.
Dr. Makkar summarized his CT findings in several talks during the meeting and also in a report published a few days before the meeting (N Engl J Med. 2015 Oct 5. doi: 10.1056/NEJMoa1509233).
“We started with what we thought was an imaging artifact and established that is it real. We also established with reasonable certainty that it is related to thrombus,” said Dr. Makkar, professor at the University of California, Los Angeles, and director of the Cardiovascular Interventional Center at Cedars-Sinai Medical Center in Los Angeles. The evidence also indicates that this is a class effect that occurs with all types of TAVR systems as well as surgically placed valves.
What the evidence so far does not indicate is that patients with reduced-motion leaflets face any clinical consequence nor need for routine CT imaging of a newly-placed TAVR or SAVR valve. Also no need for routine anticoagulant therapy instead of standard treatment with dual antiplatelet therapy for several months following placement of a bioprosthetic aortic valve. “We should not make the leap that following TAVR, everyone should be on an anticoagulant” because anticoagulant treatment carries it own risks, said Dr. Makkar, who noted that roughly a quarter of TAVR patients receive anticoagulant treatment because of another indication, such as atrial fibrillation.
“The study did not show a temporal or causal relationship between the imaging findings and stroke. That needs emphasis,” commented Dr. Susheel Kodali, codirector of the Heart Valve Center at the Center for Interventional Vascular Therapy at Columbia University in New York. The possible link between leaflet immobility and strokes or other neurologic events “warrants further study,” as the data that Dr. Makkar reported involved a total of only six strokes or transient ischemic attacks. Data from all the TAVR trials and registries reported so far showed “no late signal of stroke,” said Dr. Kodali, who added that SAVR had a 30-year record of net benefit for appropriate patients.
“Is valve-leaflet thickening an important controversy or much ado about nothing?” wondered Dr. Martin B. Leon, director of the Center for Interventional Vascular Therapy of Columbia University.
“Patients should not feel at risk, and there is no need to do anything differently” for the time being in routine practice, commented Dr. Jeffrey J. Popma, professor at Harvard Medical School and director of interventional cardiology at Beth Israel Deaconess Medical Center, both in Boston.
Dr. Makkar said that in the days following the publication of his report, he had “a lot of phone calls and time spent allaying anxiety in patients and reassuring them.”
One reason why these leaflet-motion abnormalities may have shown up on CT examinations recently is that “the cameras have gotten better,” said Dr. Jonathon A. Leipsic, codirector of advanced cardiac imaging at the Providence Health Care Heart Center at St. Paul’s Hospital in Vancouver. Dr. Leipsic also highlighted that with state-of-the-art CT images, immobilized leaflets are easy to identify.
Despite that, Dr. Popma stressed that standardized imaging protocols are needed going forward to produce reliable incidence data.
The data that Dr. Makkar reported came from a review of four-dimensional CT imaging done on 187 replacement aortic valves, usually within 3 months of placement. Images for 55 aortic valves came from the device-approval trial for a new TAVR system, taken 30 days after patients underwent TAVR with any of three types of systems. The images showed reduced leaflet motion in 22 valves (40%).
CT images for another 132 valves came from a Cedar’s-Sinai registry and a second, independent registry maintained in Denmark. CT images showed that 17 (13%) of the replaced aortic valves showed a leaflet-motion abnormality, including two valves placed using SAVR. Half the registry patients had undergone CT imaging within 88 days of valve replacement. The only signal of a clinical outcome linked with reduced-motion leaflets was a small increase in the incidence of transient ischemic attacks, but Dr. Makkar cautioned that transient ischemic attacks “are hard to adjudicate.”
Dr. Makkar’s report was “a small but important study, one of the first reports of this phenomenon. You don’t want to lose sight of all the evidence of patient benefit” from aortic valve replacement, stressed Dr. Kodali at the meeting, sponsored by the Cardiovascular Research Foundation. “This needs to be investigated further, probably by a Food and Drug Administration–mandated trial with CT imaging.”
“Aortic valves are lifesaving devices. The last thing that should happen is patients not getting their aortic valves replaced” when their condition demands it, Dr. Makkar said.
The PORTICO IDE study and RESOLVE registry were funded by St. Jude. Dr. Makkar has received honoraria and research support from St. Jude, lecture fees from Edwards Lifesciences, research grants from Edwards and Medtronic, and has an equity interest in Entourage. Dr. Kodali has been a consultant to Edwards Lifesciences and Claret Medical and has an equity interest in Thubrikar Aortic Valve. Dr. Leon has been a consultant to Edwards. Dr. Popma has been a consultant to Abbott Laboratories, Boston Scientific, and St. Jude, and he has been a speaker for and received grants from Medtronic, Dr. Leipsic has been a consultant to Edwards and Heartflow and received grants from Edwards, Neovasc, and Tendyne.
On Twitter @mitchelzoler
EXPERT ANALYSIS FROM TCT 2015
Key clinical point: CT imaging of recently placed bioprosthetic aortic valves showed several cases of leaflets with reduced motion, suggesting possible clinical consequences.
Major finding: CT imaging showed reduced leaflet motion in 22 of 55 (40%) trial patients and 17 of 132 (13%) registry patients.
Data source: An observational study of CT images collected on 187 patients who had undergone aortic valve replacement from the PORTICO IDE study (55 patients), and the RESOLVE and SAVORY registries (132 total patients).
Disclosures: The PORTICO IDE study and RESOLVE registry were funded by St. Jude. Dr. Makkar has received honoraria and research support from St. Jude, lecture fees from Edwards Lifesciences, research grants from Edwards and Medtronic, and has an equity interest in Entourage.
Glutamate-based neuroimaging identifies epileptic foci
High-resolution glutamate-based neuroimaging could help identify epileptic foci in individuals with epilepsy who have been assessed as nonlesional via conventional brain MRI, a study has found.
Researchers used glutamate chemical exchange saturation transfer imaging (GluCEST) in four patients with drug-resistant epilepsy who did not show lesions on MRI, and in 11 healthy controls, according to a paper published in Science Translational Medicine.
The glutamate-based imaging showed higher concentrations of glutamate in the ipsilateral hippocampus than in the contralateral hippocampus, and two independent, blinded epilepsy specialists both accurately lateralized the seizure onset in all four patients (Sci Transl Med. 2015 Oct 14. doi: 10.1126/scitranslmed.aaa7095).
Patients with drug-resistant epilepsy currently undergo a range of presurgical imaging, including 3-T MRI and single-photon emission computed tomography (SPECT), but in many patients this still fails to identify a seizure focus, despite the fact that 87% of patients in this group have previously been found to have abnormal histopathology.
“Because it is also well established that patients with lesional epilepsy have better surgical outcomes than those with nonlesional epilepsy, new neuroimaging techniques capable of detecting subtle lesions could potentially improve patient care and increase the chance of seizure freedom after surgery,” wrote Dr. Kathryn Adamiak Davis of Penn Epilepsy Center at the Hospital of the University of Pennsylvania, Philadelphia, and her coauthors.
The National Institutes of Health and the University of Pennsylvania supported the study. There were no conflicts of interest declared.
High-resolution glutamate-based neuroimaging could help identify epileptic foci in individuals with epilepsy who have been assessed as nonlesional via conventional brain MRI, a study has found.
Researchers used glutamate chemical exchange saturation transfer imaging (GluCEST) in four patients with drug-resistant epilepsy who did not show lesions on MRI, and in 11 healthy controls, according to a paper published in Science Translational Medicine.
The glutamate-based imaging showed higher concentrations of glutamate in the ipsilateral hippocampus than in the contralateral hippocampus, and two independent, blinded epilepsy specialists both accurately lateralized the seizure onset in all four patients (Sci Transl Med. 2015 Oct 14. doi: 10.1126/scitranslmed.aaa7095).
Patients with drug-resistant epilepsy currently undergo a range of presurgical imaging, including 3-T MRI and single-photon emission computed tomography (SPECT), but in many patients this still fails to identify a seizure focus, despite the fact that 87% of patients in this group have previously been found to have abnormal histopathology.
“Because it is also well established that patients with lesional epilepsy have better surgical outcomes than those with nonlesional epilepsy, new neuroimaging techniques capable of detecting subtle lesions could potentially improve patient care and increase the chance of seizure freedom after surgery,” wrote Dr. Kathryn Adamiak Davis of Penn Epilepsy Center at the Hospital of the University of Pennsylvania, Philadelphia, and her coauthors.
The National Institutes of Health and the University of Pennsylvania supported the study. There were no conflicts of interest declared.
High-resolution glutamate-based neuroimaging could help identify epileptic foci in individuals with epilepsy who have been assessed as nonlesional via conventional brain MRI, a study has found.
Researchers used glutamate chemical exchange saturation transfer imaging (GluCEST) in four patients with drug-resistant epilepsy who did not show lesions on MRI, and in 11 healthy controls, according to a paper published in Science Translational Medicine.
The glutamate-based imaging showed higher concentrations of glutamate in the ipsilateral hippocampus than in the contralateral hippocampus, and two independent, blinded epilepsy specialists both accurately lateralized the seizure onset in all four patients (Sci Transl Med. 2015 Oct 14. doi: 10.1126/scitranslmed.aaa7095).
Patients with drug-resistant epilepsy currently undergo a range of presurgical imaging, including 3-T MRI and single-photon emission computed tomography (SPECT), but in many patients this still fails to identify a seizure focus, despite the fact that 87% of patients in this group have previously been found to have abnormal histopathology.
“Because it is also well established that patients with lesional epilepsy have better surgical outcomes than those with nonlesional epilepsy, new neuroimaging techniques capable of detecting subtle lesions could potentially improve patient care and increase the chance of seizure freedom after surgery,” wrote Dr. Kathryn Adamiak Davis of Penn Epilepsy Center at the Hospital of the University of Pennsylvania, Philadelphia, and her coauthors.
The National Institutes of Health and the University of Pennsylvania supported the study. There were no conflicts of interest declared.
FROM SCIENCE TRANSLATIONAL MEDICINE
Key clinical point:Glutamate-based neuroimaging could identify epileptic foci in epilepsy patients who are nonlesional on conventional MRI.
Major finding: Glutamate chemical exchange saturation transfer imaging enables lateralization of seizure onset in previously nonlesional patients.
Data source: Imaging study in four individuals with drug-resistant epilepsy.
Disclosures: The National Institutes of Health and the University of Pennsylvania supported the study. There were no conflicts of interest declared.