In contrast to stable chronic obstructive pulmonary disease (COPD), acute exacerbations of COPD pose special management challenges and can significantly increase the risks of morbidity and death as well as the cost of care. This review from Cleveland Clinic Journal of Medicine, available at http://www.ccjm.org/topics/pulmonary/single-article-page/treating-and-preventing-acute-exacerbations-of-copd/8265d5ff355c3a17c96fa34564ea7465.html, provides the latest information on the definition and diagnosis of COPD exacerbations, disease burden and costs, etiology and pathogenesis, and management and prevention strategies.

In contrast to stable chronic obstructive pulmonary disease (COPD), acute exacerbations of COPD pose special management challenges and can significantly increase the risks of morbidity and death as well as the cost of care. This review from Cleveland Clinic Journal of Medicine, available at http://www.ccjm.org/topics/pulmonary/single-article-page/treating-and-preventing-acute-exacerbations-of-copd/8265d5ff355c3a17c96fa34564ea7465.html, provides the latest information on the definition and diagnosis of COPD exacerbations, disease burden and costs, etiology and pathogenesis, and management and prevention strategies.

In contrast to stable chronic obstructive pulmonary disease (COPD), acute exacerbations of COPD pose special management challenges and can significantly increase the risks of morbidity and death as well as the cost of care. This review from Cleveland Clinic Journal of Medicine, available at http://www.ccjm.org/topics/pulmonary/single-article-page/treating-and-preventing-acute-exacerbations-of-copd/8265d5ff355c3a17c96fa34564ea7465.html, provides the latest information on the definition and diagnosis of COPD exacerbations, disease burden and costs, etiology and pathogenesis, and management and prevention strategies.

SAN DIEGO – New research suggests histamine-2 receptor antagonists aren’t a viable alternative to proton pump inhibitors to prevent recurrence of bleeding peptic ulcers in clopidogrel users.

U.S. and European agencies have warned of interactions between proton pump inhibitors (PPIs) and clopidogrel. But a study presented at the annual Digestive Disease Week finds significant upper GI events were much more common in patients who took famotidine (Protonix), a histamine-2 receptor antagonist (H₂RA), compared with those who took pantoprazole (Pepcid), a PPI, as a preventive treatment.

“The findings will change the practice of some physicians who prescribe H₂RA to prevent UGI [upper GI] events in clopidogrel users,” said study lead author Dr. Ping-I Hsu, chief of gastroenterology at Kaohsiung Veterans General Hospital and professor of medicine at National Yang-Ming University, both in Taiwan.

Currently, Dr. Hsu said, “physicians often use PPIs to prevent ulcer complications in clopidogrel users because it is the only drug proven useful in the prevention of peptic ulcers and ulcer complications in clopidogrel users.”

But “both the U.S. Food & Drug Administration and the European Medicines Agency have posted safety warnings and discourage the use of PPIs with clopidogrel unless absolutely necessary,” he said.

Enter the prospect of H₂RA medications as an alternative. The new study, Dr. Hsu said, is the first to explore the GI protection effect and safety of H₂RAs in patients on clopidogrel monotherapy.

The randomized prospective study followed 120 patients with a history of peptic ulcer bleeding (but not at initial endoscopy) and atherosclerosis. All long-term users of ADP receptor antagonists, they were assigned to pantoprazole (40 mg daily) or famotidine (40 mg daily) for 48 weeks.

Patients were examined via endoscopy when they experienced events like severe epigastric discomfort.

The famotidine group had more significant upper GI events (13.3%) than the pantoprazole group (1.7%). Diarrhea was equal in both groups (1.7%). Pneumonia was comparable (0% and 1.7% for pantoprazole and famotidine, respectively), as was fracture (1.7% and 0%).

Wider differences were found in acute myocardial infarction (1.5% and 4.5%), and cerebral vascular accident (0% and 3.4%) for pantoprazole and famotidine, respectively.

According to Dr. Hsu, three earlier studies linked concurrent use of PPIs and clopidogrel to significant increases in cardiovascular events. But this study linked a higher cardiac risk to the H₂RA medication.

The researchers found no differences between the drugs in sequential changes of serum magnesium levels and bone mineral densities.

Dr. Hsu made this recommendation to physicians: “Please don’t use H₂RAs to prevent peptic ulcer or ulcer complications in clopidogrel users. It is ineffective to prevent UGI [upper GI] events in clopidogrel users who have a history of ulcer bleeding. PPIs can effectively prevent UGI events in clopidogrel users with a history of ulcer bleeding.”

In addition, he said, the risk of thrombotic events is lower on a PPI.

SAN DIEGO – New research suggests histamine-2 receptor antagonists aren’t a viable alternative to proton pump inhibitors to prevent recurrence of bleeding peptic ulcers in clopidogrel users.

U.S. and European agencies have warned of interactions between proton pump inhibitors (PPIs) and clopidogrel. But a study presented at the annual Digestive Disease Week finds significant upper GI events were much more common in patients who took famotidine (Protonix), a histamine-2 receptor antagonist (H₂RA), compared with those who took pantoprazole (Pepcid), a PPI, as a preventive treatment.

“The findings will change the practice of some physicians who prescribe H₂RA to prevent UGI [upper GI] events in clopidogrel users,” said study lead author Dr. Ping-I Hsu, chief of gastroenterology at Kaohsiung Veterans General Hospital and professor of medicine at National Yang-Ming University, both in Taiwan.

Currently, Dr. Hsu said, “physicians often use PPIs to prevent ulcer complications in clopidogrel users because it is the only drug proven useful in the prevention of peptic ulcers and ulcer complications in clopidogrel users.”

But “both the U.S. Food & Drug Administration and the European Medicines Agency have posted safety warnings and discourage the use of PPIs with clopidogrel unless absolutely necessary,” he said.

Enter the prospect of H₂RA medications as an alternative. The new study, Dr. Hsu said, is the first to explore the GI protection effect and safety of H₂RAs in patients on clopidogrel monotherapy.

The randomized prospective study followed 120 patients with a history of peptic ulcer bleeding (but not at initial endoscopy) and atherosclerosis. All long-term users of ADP receptor antagonists, they were assigned to pantoprazole (40 mg daily) or famotidine (40 mg daily) for 48 weeks.

Patients were examined via endoscopy when they experienced events like severe epigastric discomfort.

The famotidine group had more significant upper GI events (13.3%) than the pantoprazole group (1.7%). Diarrhea was equal in both groups (1.7%). Pneumonia was comparable (0% and 1.7% for pantoprazole and famotidine, respectively), as was fracture (1.7% and 0%).

Wider differences were found in acute myocardial infarction (1.5% and 4.5%), and cerebral vascular accident (0% and 3.4%) for pantoprazole and famotidine, respectively.

According to Dr. Hsu, three earlier studies linked concurrent use of PPIs and clopidogrel to significant increases in cardiovascular events. But this study linked a higher cardiac risk to the H₂RA medication.

The researchers found no differences between the drugs in sequential changes of serum magnesium levels and bone mineral densities.

Dr. Hsu made this recommendation to physicians: “Please don’t use H₂RAs to prevent peptic ulcer or ulcer complications in clopidogrel users. It is ineffective to prevent UGI [upper GI] events in clopidogrel users who have a history of ulcer bleeding. PPIs can effectively prevent UGI events in clopidogrel users with a history of ulcer bleeding.”

In addition, he said, the risk of thrombotic events is lower on a PPI.

SAN DIEGO – New research suggests histamine-2 receptor antagonists aren’t a viable alternative to proton pump inhibitors to prevent recurrence of bleeding peptic ulcers in clopidogrel users.

U.S. and European agencies have warned of interactions between proton pump inhibitors (PPIs) and clopidogrel. But a study presented at the annual Digestive Disease Week finds significant upper GI events were much more common in patients who took famotidine (Protonix), a histamine-2 receptor antagonist (H₂RA), compared with those who took pantoprazole (Pepcid), a PPI, as a preventive treatment.

“The findings will change the practice of some physicians who prescribe H₂RA to prevent UGI [upper GI] events in clopidogrel users,” said study lead author Dr. Ping-I Hsu, chief of gastroenterology at Kaohsiung Veterans General Hospital and professor of medicine at National Yang-Ming University, both in Taiwan.

Currently, Dr. Hsu said, “physicians often use PPIs to prevent ulcer complications in clopidogrel users because it is the only drug proven useful in the prevention of peptic ulcers and ulcer complications in clopidogrel users.”

But “both the U.S. Food & Drug Administration and the European Medicines Agency have posted safety warnings and discourage the use of PPIs with clopidogrel unless absolutely necessary,” he said.

Enter the prospect of H₂RA medications as an alternative. The new study, Dr. Hsu said, is the first to explore the GI protection effect and safety of H₂RAs in patients on clopidogrel monotherapy.

The randomized prospective study followed 120 patients with a history of peptic ulcer bleeding (but not at initial endoscopy) and atherosclerosis. All long-term users of ADP receptor antagonists, they were assigned to pantoprazole (40 mg daily) or famotidine (40 mg daily) for 48 weeks.

Patients were examined via endoscopy when they experienced events like severe epigastric discomfort.

The famotidine group had more significant upper GI events (13.3%) than the pantoprazole group (1.7%). Diarrhea was equal in both groups (1.7%). Pneumonia was comparable (0% and 1.7% for pantoprazole and famotidine, respectively), as was fracture (1.7% and 0%).

Wider differences were found in acute myocardial infarction (1.5% and 4.5%), and cerebral vascular accident (0% and 3.4%) for pantoprazole and famotidine, respectively.

According to Dr. Hsu, three earlier studies linked concurrent use of PPIs and clopidogrel to significant increases in cardiovascular events. But this study linked a higher cardiac risk to the H₂RA medication.

The researchers found no differences between the drugs in sequential changes of serum magnesium levels and bone mineral densities.

Dr. Hsu made this recommendation to physicians: “Please don’t use H₂RAs to prevent peptic ulcer or ulcer complications in clopidogrel users. It is ineffective to prevent UGI [upper GI] events in clopidogrel users who have a history of ulcer bleeding. PPIs can effectively prevent UGI events in clopidogrel users with a history of ulcer bleeding.”

In addition, he said, the risk of thrombotic events is lower on a PPI.

SAN FRANCISCO – Hospitalized patients who have a change in the medical residents responsible for their care are more likely to die, finds a retrospective cohort study of roughly a quarter million discharges from Veterans Affairs medical centers.

A monthly change in resident care was associated with 9%-20% higher adjusted odds of death during the hospital stay and after discharge, investigators reported in a poster discussion session and press briefing at an international conference of the American Thoracic Society. Analyses suggested that such transitions accounted for 718 additional deaths in the hospital alone during the 6-year study period.

“These are very strong findings,” said Dr. Joshua L. Denson, a fellow in the divisions of pulmonary sciences and critical care medicine at the University of Colorado, Aurora.

The study results represent an important initial step in bringing the problem to light, he said. “Handoffs shift to shift have been looked at, but not this end-of-month, more permanent switching, which I think is a much more substantial transition in care.”

The factors driving the increased mortality are unclear, according to Dr. Denson; however, “when you go on to a new service [as a resident] ... you are now responsible for 20 new people all of a sudden that night.” Therefore, these transitions can be a hectic time characterized by reduced communication and inefficient discharges. In addition, the incoming residents lack familiarity with their new patients’ particulars.

“The handoffs are definitely not preventable, so this is something that has to be dealt with,” he maintained. The study’s findings hint at several possible areas for improvement.

None of the 10 residency programs surveyed provided formal education for monthly resident handoffs, focusing instead on handoffs at shift changes, and most programs lacked a standard procedure, with just one requiring that the handoff be done in person. The programs also varied greatly in their staggering of handoffs – separating transitions of interns (first-year residents) and higher-level residents by at least a few days – to minimize impact.

Despite the absence of outcomes data in this area, some hospitals are forging ahead with their own interventions intended to smooth care transitions, Dr. Denson reported. “In at least two hospitals that I’ve worked in, they are implementing what is called a warm handoff,” he explained. “Basically, a resident from the prior rotation comes the next day and rounds with the new team so he can tell them, ‘Oh, this guy looks a little worse today, you may want to watch him,’ or ‘He looks a little better.’ ”

In the study, conducted while Dr. Denson was chief resident at the NYU School of Medicine, he and his colleagues analyzed data from 10 university-affiliated Veterans Affairs hospitals and internal medicine residency programs that provided their residents’ schedules. Analyses were based on a total of 230,701 discharges of adult medical patients between July 2008 and June 2014.

Hospitalized patients were categorized as having a transition in resident care if they were admitted before the date of an end-of-month house staff transition in care and were discharged in the week after it.

In unadjusted analyses, patients who had a transition of care – whether of intern only, resident only, or both – had significantly higher odds of inpatient mortality and of 30-day mortality and 90-day postdischarge mortality, compared with counterparts who did not have the corresponding transition of care.

In adjusted analyses, patients who had an intern transition still had higher odds of in-hospital mortality (odds ratio, 1.14). In addition, patients had persistently elevated odds of 30-day mortality and 90-day postdischarge mortality if they had an intern transition (odds ratios, 1.20 and 1.17, respectively), a resident transition (1.15 and 1.14), or both (1.10 and 1.09).

The findings “suggest possibly a level-of-training effect to these transitions, as it’s the most inexperienced people that have the higher rate of mortality,” noted Dr. Denson, who disclosed that he had no relevant conflicts of interest. “Interns, being the first-years, tend to carry the bulk of the work in most hospitals, which is an interesting paradigm in our organization. And that may be a good explanation for why we are seeing this.”

SAN FRANCISCO – Hospitalized patients who have a change in the medical residents responsible for their care are more likely to die, finds a retrospective cohort study of roughly a quarter million discharges from Veterans Affairs medical centers.

A monthly change in resident care was associated with 9%-20% higher adjusted odds of death during the hospital stay and after discharge, investigators reported in a poster discussion session and press briefing at an international conference of the American Thoracic Society. Analyses suggested that such transitions accounted for 718 additional deaths in the hospital alone during the 6-year study period.

“These are very strong findings,” said Dr. Joshua L. Denson, a fellow in the divisions of pulmonary sciences and critical care medicine at the University of Colorado, Aurora.

The study results represent an important initial step in bringing the problem to light, he said. “Handoffs shift to shift have been looked at, but not this end-of-month, more permanent switching, which I think is a much more substantial transition in care.”

The factors driving the increased mortality are unclear, according to Dr. Denson; however, “when you go on to a new service [as a resident] ... you are now responsible for 20 new people all of a sudden that night.” Therefore, these transitions can be a hectic time characterized by reduced communication and inefficient discharges. In addition, the incoming residents lack familiarity with their new patients’ particulars.

“The handoffs are definitely not preventable, so this is something that has to be dealt with,” he maintained. The study’s findings hint at several possible areas for improvement.

None of the 10 residency programs surveyed provided formal education for monthly resident handoffs, focusing instead on handoffs at shift changes, and most programs lacked a standard procedure, with just one requiring that the handoff be done in person. The programs also varied greatly in their staggering of handoffs – separating transitions of interns (first-year residents) and higher-level residents by at least a few days – to minimize impact.

Despite the absence of outcomes data in this area, some hospitals are forging ahead with their own interventions intended to smooth care transitions, Dr. Denson reported. “In at least two hospitals that I’ve worked in, they are implementing what is called a warm handoff,” he explained. “Basically, a resident from the prior rotation comes the next day and rounds with the new team so he can tell them, ‘Oh, this guy looks a little worse today, you may want to watch him,’ or ‘He looks a little better.’ ”

In the study, conducted while Dr. Denson was chief resident at the NYU School of Medicine, he and his colleagues analyzed data from 10 university-affiliated Veterans Affairs hospitals and internal medicine residency programs that provided their residents’ schedules. Analyses were based on a total of 230,701 discharges of adult medical patients between July 2008 and June 2014.

Hospitalized patients were categorized as having a transition in resident care if they were admitted before the date of an end-of-month house staff transition in care and were discharged in the week after it.

In unadjusted analyses, patients who had a transition of care – whether of intern only, resident only, or both – had significantly higher odds of inpatient mortality and of 30-day mortality and 90-day postdischarge mortality, compared with counterparts who did not have the corresponding transition of care.

In adjusted analyses, patients who had an intern transition still had higher odds of in-hospital mortality (odds ratio, 1.14). In addition, patients had persistently elevated odds of 30-day mortality and 90-day postdischarge mortality if they had an intern transition (odds ratios, 1.20 and 1.17, respectively), a resident transition (1.15 and 1.14), or both (1.10 and 1.09).

The findings “suggest possibly a level-of-training effect to these transitions, as it’s the most inexperienced people that have the higher rate of mortality,” noted Dr. Denson, who disclosed that he had no relevant conflicts of interest. “Interns, being the first-years, tend to carry the bulk of the work in most hospitals, which is an interesting paradigm in our organization. And that may be a good explanation for why we are seeing this.”

SAN FRANCISCO – Hospitalized patients who have a change in the medical residents responsible for their care are more likely to die, finds a retrospective cohort study of roughly a quarter million discharges from Veterans Affairs medical centers.

A monthly change in resident care was associated with 9%-20% higher adjusted odds of death during the hospital stay and after discharge, investigators reported in a poster discussion session and press briefing at an international conference of the American Thoracic Society. Analyses suggested that such transitions accounted for 718 additional deaths in the hospital alone during the 6-year study period.

“These are very strong findings,” said Dr. Joshua L. Denson, a fellow in the divisions of pulmonary sciences and critical care medicine at the University of Colorado, Aurora.

The study results represent an important initial step in bringing the problem to light, he said. “Handoffs shift to shift have been looked at, but not this end-of-month, more permanent switching, which I think is a much more substantial transition in care.”

The factors driving the increased mortality are unclear, according to Dr. Denson; however, “when you go on to a new service [as a resident] ... you are now responsible for 20 new people all of a sudden that night.” Therefore, these transitions can be a hectic time characterized by reduced communication and inefficient discharges. In addition, the incoming residents lack familiarity with their new patients’ particulars.

“The handoffs are definitely not preventable, so this is something that has to be dealt with,” he maintained. The study’s findings hint at several possible areas for improvement.

None of the 10 residency programs surveyed provided formal education for monthly resident handoffs, focusing instead on handoffs at shift changes, and most programs lacked a standard procedure, with just one requiring that the handoff be done in person. The programs also varied greatly in their staggering of handoffs – separating transitions of interns (first-year residents) and higher-level residents by at least a few days – to minimize impact.

Despite the absence of outcomes data in this area, some hospitals are forging ahead with their own interventions intended to smooth care transitions, Dr. Denson reported. “In at least two hospitals that I’ve worked in, they are implementing what is called a warm handoff,” he explained. “Basically, a resident from the prior rotation comes the next day and rounds with the new team so he can tell them, ‘Oh, this guy looks a little worse today, you may want to watch him,’ or ‘He looks a little better.’ ”

In the study, conducted while Dr. Denson was chief resident at the NYU School of Medicine, he and his colleagues analyzed data from 10 university-affiliated Veterans Affairs hospitals and internal medicine residency programs that provided their residents’ schedules. Analyses were based on a total of 230,701 discharges of adult medical patients between July 2008 and June 2014.

Hospitalized patients were categorized as having a transition in resident care if they were admitted before the date of an end-of-month house staff transition in care and were discharged in the week after it.

In unadjusted analyses, patients who had a transition of care – whether of intern only, resident only, or both – had significantly higher odds of inpatient mortality and of 30-day mortality and 90-day postdischarge mortality, compared with counterparts who did not have the corresponding transition of care.

In adjusted analyses, patients who had an intern transition still had higher odds of in-hospital mortality (odds ratio, 1.14). In addition, patients had persistently elevated odds of 30-day mortality and 90-day postdischarge mortality if they had an intern transition (odds ratios, 1.20 and 1.17, respectively), a resident transition (1.15 and 1.14), or both (1.10 and 1.09).

The findings “suggest possibly a level-of-training effect to these transitions, as it’s the most inexperienced people that have the higher rate of mortality,” noted Dr. Denson, who disclosed that he had no relevant conflicts of interest. “Interns, being the first-years, tend to carry the bulk of the work in most hospitals, which is an interesting paradigm in our organization. And that may be a good explanation for why we are seeing this.”

This edition of Vascular Specialist is being published early to coincide with the VAM. Since medical students will be attending the meeting I thought this would be a good opportunity to describe an often overlooked reason why, after all my years in practice, I still enjoy being a vascular surgeon. By doing so I hope to encourage these young people to consider a career in vascular surgery.

Some vascular surgeons, with the same goal, have volunteered to mentor these students at the VAM. I suspect most mentors would extoll vascular surgery as unique amongst surgical specialties. They will describe the variety of complex operations as well as advanced endovascular procedures that we perform. Proudly, some mentors will mention that other practitioners turn to us for help when they encounter uncontrollable hemorrhage. They will emphasize that we are the one specialty that covers the gamut of vascular interventions from open surgery and endovascular procedures to medical management. Perhaps some mentors will incorporate my mantra that vascular surgeons “Operate, Dilate, and Medicate.”

However, I suggest that the most satisfying aspect of our profession is not the procedures that we perform but rather the interaction we have with our patients. After all, most of us entered the medical profession to take care of patients, and vascular patients are very special indeed. However, sometimes we established vascular surgeons become too enthralled by technical advances to remember the more humanistic reasons for our being. Also, changes in medical practice and reimbursement have resulted in many being so overworked that we do not have time to enjoy relationships with our patients. Perhaps those who are so burdened should take heed from the stories mentors will relate to inspire these students.

Based on my personal experience I suspect the mentors will say something along the following lines: “Vascular conditions are chronic and are wont to afflict more than one part of the body. Accordingly, we are required to follow most patients for their whole lives (or ours!). Not only do we treat these patients but we also become intimately involved with their families, often treating them as well. Often our ‘treatment’ will not be procedural but rather will involve emotional support of these relatives as they deal with their recuperating or debilitated spouse, sibling, or parent. Those of us who have been in practice for many years will fondly recall patients who have become an integral part of our lives. The patient who undergoes a vascular procedure will return every 6 or 12 months to have their bypass checked or their other carotid assessed.

“We follow asymptomatic small abdominal aneurysms and claudicants. A venous ulcer often recurs and a dialysis patient may require a new intervention. Some patients come to the office so they can be made more secure that their condition has not deteriorated, and the lonely just because we are the only human they interact with on a regular basis. They bring with them their varied life stories and these vignettes become a part of our own fiction. Perhaps we will share with them our own life story. Contrast that to the general surgeon who repairs a hernia and after a few post op visits may never see the patient again.

“Vascular patients may be very young or more commonly very old and come from all walks of life. So the vascular surgeon will learn to calm the crying infant. She will provide careful optimism to allay the fears of a mother who brings in her daughter scarred by a cavernous hemangioma. He or she will reassure the young girl, mortified by embarrassing spider veins, that she will be able to wear a dress to her high school prom. Together with the obstetrician, the vascular surgeon will guide a pregnant woman with a DVT through her entire pregnancy assuring her that both she and her baby will be safe.”

The mentor will re-count how special it was to get a hug from an old lady who he operated on 25 years previously when he was a young surgeon. Or the gratification one gets when a father, after a successful limb revascularization, shows a video of himself walking down the aisle at his daughter’s wedding. Perhaps the mentor will confide her sense of dismay every time a young dialysis patient is admitted for revision of a fistula and the joy she feels when told that her patient has finally received a viable transplant. Year after year the vascular surgeon will follow a patient with early onset, widespread vascular disease whose parents died young from the ravages of familial hyperlipidemia.

He will provide encouragement to help the patient stop smoking and commiserate when a sibling dies from a heart attack. The mentor might relate how she felt when she saved the leg of a soldier injured by a land mine or how she was amazed by the 80-year-old ballroom dancer who danced a few weeks after a below knee amputation.

Mentors will also describe getting to know a patient’s daily routine so they can informatively advise a patient whether it is worth having a procedure to improve quality of life. Or the thrill we get when that patient thanks us for relieving the claudication that prevented gainful employment. We are relieved when a longstanding patient wakes up neurologically intact from an endarterectomy.

However, we are filled with remorse when we inform a family that they have lost their loved one who died from a ruptured aneurysm. Of course, our failures may be devastating but they reinforce our humility when we acknowledge that we have been defeated by a disease that resisted our every effort.

The mentor may also share that “Every Xmas you will collect cards thanking you for saving a life or, out of the blue, receive a carton of fruit from the orchard of a farmer who finally was able to walk amongst her crop. You will pass tissues to the sobbing husband whose wife always accompanied him to his yearly physical, but who recently passed from incurable cancer. You will listen to stories from veterans of past wars. You will see pictures of patients’ children and you will remark how they have grown through the years. A patient will make you look admiringly at their latest puppy or prize-winning pig. You will be given stock advice by a millionaire and you will pay for a taxi for the indigent to get home from your office. You may keep patients waiting while you hear intriguing gossip or wonder just how you can stop the little old lady rambling on about lost loves. You will be charmed by the 98-year-old who makes sure that she has her hair and makeup done prior to coming to see you, and how her face lights up when you pronounce her more beautiful than ever.

“Dear student, the technical aspects of vascular surgery are indeed demanding and exciting. We are invigorated by the knowledge that our expertise saved a life or limb, prevented a stroke or provided the nephrotic with a working fistula. Even the more simple cosmetic procedures give us pleasure. If you still need inspiration to embark on a vascular surgical career I encourage you to read the Presidential address Dr. Bruce J. Brener gave to the Society for Clinical Vascular Surgery in March 1996. His eloquent portrayal of the vascular surgical experience is unmatched (Amer J Surg, 1996; 172:97-9). However, it is our daily and often lifelong interaction with our wonderful patients that so intimately reinforces our humanity and makes this profession so uniquely satisfying.”

This edition of Vascular Specialist is being published early to coincide with the VAM. Since medical students will be attending the meeting I thought this would be a good opportunity to describe an often overlooked reason why, after all my years in practice, I still enjoy being a vascular surgeon. By doing so I hope to encourage these young people to consider a career in vascular surgery.

Some vascular surgeons, with the same goal, have volunteered to mentor these students at the VAM. I suspect most mentors would extoll vascular surgery as unique amongst surgical specialties. They will describe the variety of complex operations as well as advanced endovascular procedures that we perform. Proudly, some mentors will mention that other practitioners turn to us for help when they encounter uncontrollable hemorrhage. They will emphasize that we are the one specialty that covers the gamut of vascular interventions from open surgery and endovascular procedures to medical management. Perhaps some mentors will incorporate my mantra that vascular surgeons “Operate, Dilate, and Medicate.”

However, I suggest that the most satisfying aspect of our profession is not the procedures that we perform but rather the interaction we have with our patients. After all, most of us entered the medical profession to take care of patients, and vascular patients are very special indeed. However, sometimes we established vascular surgeons become too enthralled by technical advances to remember the more humanistic reasons for our being. Also, changes in medical practice and reimbursement have resulted in many being so overworked that we do not have time to enjoy relationships with our patients. Perhaps those who are so burdened should take heed from the stories mentors will relate to inspire these students.

Based on my personal experience I suspect the mentors will say something along the following lines: “Vascular conditions are chronic and are wont to afflict more than one part of the body. Accordingly, we are required to follow most patients for their whole lives (or ours!). Not only do we treat these patients but we also become intimately involved with their families, often treating them as well. Often our ‘treatment’ will not be procedural but rather will involve emotional support of these relatives as they deal with their recuperating or debilitated spouse, sibling, or parent. Those of us who have been in practice for many years will fondly recall patients who have become an integral part of our lives. The patient who undergoes a vascular procedure will return every 6 or 12 months to have their bypass checked or their other carotid assessed.

“We follow asymptomatic small abdominal aneurysms and claudicants. A venous ulcer often recurs and a dialysis patient may require a new intervention. Some patients come to the office so they can be made more secure that their condition has not deteriorated, and the lonely just because we are the only human they interact with on a regular basis. They bring with them their varied life stories and these vignettes become a part of our own fiction. Perhaps we will share with them our own life story. Contrast that to the general surgeon who repairs a hernia and after a few post op visits may never see the patient again.

“Vascular patients may be very young or more commonly very old and come from all walks of life. So the vascular surgeon will learn to calm the crying infant. She will provide careful optimism to allay the fears of a mother who brings in her daughter scarred by a cavernous hemangioma. He or she will reassure the young girl, mortified by embarrassing spider veins, that she will be able to wear a dress to her high school prom. Together with the obstetrician, the vascular surgeon will guide a pregnant woman with a DVT through her entire pregnancy assuring her that both she and her baby will be safe.”

The mentor will re-count how special it was to get a hug from an old lady who he operated on 25 years previously when he was a young surgeon. Or the gratification one gets when a father, after a successful limb revascularization, shows a video of himself walking down the aisle at his daughter’s wedding. Perhaps the mentor will confide her sense of dismay every time a young dialysis patient is admitted for revision of a fistula and the joy she feels when told that her patient has finally received a viable transplant. Year after year the vascular surgeon will follow a patient with early onset, widespread vascular disease whose parents died young from the ravages of familial hyperlipidemia.

He will provide encouragement to help the patient stop smoking and commiserate when a sibling dies from a heart attack. The mentor might relate how she felt when she saved the leg of a soldier injured by a land mine or how she was amazed by the 80-year-old ballroom dancer who danced a few weeks after a below knee amputation.

Mentors will also describe getting to know a patient’s daily routine so they can informatively advise a patient whether it is worth having a procedure to improve quality of life. Or the thrill we get when that patient thanks us for relieving the claudication that prevented gainful employment. We are relieved when a longstanding patient wakes up neurologically intact from an endarterectomy.

However, we are filled with remorse when we inform a family that they have lost their loved one who died from a ruptured aneurysm. Of course, our failures may be devastating but they reinforce our humility when we acknowledge that we have been defeated by a disease that resisted our every effort.

The mentor may also share that “Every Xmas you will collect cards thanking you for saving a life or, out of the blue, receive a carton of fruit from the orchard of a farmer who finally was able to walk amongst her crop. You will pass tissues to the sobbing husband whose wife always accompanied him to his yearly physical, but who recently passed from incurable cancer. You will listen to stories from veterans of past wars. You will see pictures of patients’ children and you will remark how they have grown through the years. A patient will make you look admiringly at their latest puppy or prize-winning pig. You will be given stock advice by a millionaire and you will pay for a taxi for the indigent to get home from your office. You may keep patients waiting while you hear intriguing gossip or wonder just how you can stop the little old lady rambling on about lost loves. You will be charmed by the 98-year-old who makes sure that she has her hair and makeup done prior to coming to see you, and how her face lights up when you pronounce her more beautiful than ever.

“Dear student, the technical aspects of vascular surgery are indeed demanding and exciting. We are invigorated by the knowledge that our expertise saved a life or limb, prevented a stroke or provided the nephrotic with a working fistula. Even the more simple cosmetic procedures give us pleasure. If you still need inspiration to embark on a vascular surgical career I encourage you to read the Presidential address Dr. Bruce J. Brener gave to the Society for Clinical Vascular Surgery in March 1996. His eloquent portrayal of the vascular surgical experience is unmatched (Amer J Surg, 1996; 172:97-9). However, it is our daily and often lifelong interaction with our wonderful patients that so intimately reinforces our humanity and makes this profession so uniquely satisfying.”

This edition of Vascular Specialist is being published early to coincide with the VAM. Since medical students will be attending the meeting I thought this would be a good opportunity to describe an often overlooked reason why, after all my years in practice, I still enjoy being a vascular surgeon. By doing so I hope to encourage these young people to consider a career in vascular surgery.

Some vascular surgeons, with the same goal, have volunteered to mentor these students at the VAM. I suspect most mentors would extoll vascular surgery as unique amongst surgical specialties. They will describe the variety of complex operations as well as advanced endovascular procedures that we perform. Proudly, some mentors will mention that other practitioners turn to us for help when they encounter uncontrollable hemorrhage. They will emphasize that we are the one specialty that covers the gamut of vascular interventions from open surgery and endovascular procedures to medical management. Perhaps some mentors will incorporate my mantra that vascular surgeons “Operate, Dilate, and Medicate.”

However, I suggest that the most satisfying aspect of our profession is not the procedures that we perform but rather the interaction we have with our patients. After all, most of us entered the medical profession to take care of patients, and vascular patients are very special indeed. However, sometimes we established vascular surgeons become too enthralled by technical advances to remember the more humanistic reasons for our being. Also, changes in medical practice and reimbursement have resulted in many being so overworked that we do not have time to enjoy relationships with our patients. Perhaps those who are so burdened should take heed from the stories mentors will relate to inspire these students.

Based on my personal experience I suspect the mentors will say something along the following lines: “Vascular conditions are chronic and are wont to afflict more than one part of the body. Accordingly, we are required to follow most patients for their whole lives (or ours!). Not only do we treat these patients but we also become intimately involved with their families, often treating them as well. Often our ‘treatment’ will not be procedural but rather will involve emotional support of these relatives as they deal with their recuperating or debilitated spouse, sibling, or parent. Those of us who have been in practice for many years will fondly recall patients who have become an integral part of our lives. The patient who undergoes a vascular procedure will return every 6 or 12 months to have their bypass checked or their other carotid assessed.

“We follow asymptomatic small abdominal aneurysms and claudicants. A venous ulcer often recurs and a dialysis patient may require a new intervention. Some patients come to the office so they can be made more secure that their condition has not deteriorated, and the lonely just because we are the only human they interact with on a regular basis. They bring with them their varied life stories and these vignettes become a part of our own fiction. Perhaps we will share with them our own life story. Contrast that to the general surgeon who repairs a hernia and after a few post op visits may never see the patient again.

“Vascular patients may be very young or more commonly very old and come from all walks of life. So the vascular surgeon will learn to calm the crying infant. She will provide careful optimism to allay the fears of a mother who brings in her daughter scarred by a cavernous hemangioma. He or she will reassure the young girl, mortified by embarrassing spider veins, that she will be able to wear a dress to her high school prom. Together with the obstetrician, the vascular surgeon will guide a pregnant woman with a DVT through her entire pregnancy assuring her that both she and her baby will be safe.”

The mentor will re-count how special it was to get a hug from an old lady who he operated on 25 years previously when he was a young surgeon. Or the gratification one gets when a father, after a successful limb revascularization, shows a video of himself walking down the aisle at his daughter’s wedding. Perhaps the mentor will confide her sense of dismay every time a young dialysis patient is admitted for revision of a fistula and the joy she feels when told that her patient has finally received a viable transplant. Year after year the vascular surgeon will follow a patient with early onset, widespread vascular disease whose parents died young from the ravages of familial hyperlipidemia.

He will provide encouragement to help the patient stop smoking and commiserate when a sibling dies from a heart attack. The mentor might relate how she felt when she saved the leg of a soldier injured by a land mine or how she was amazed by the 80-year-old ballroom dancer who danced a few weeks after a below knee amputation.

Mentors will also describe getting to know a patient’s daily routine so they can informatively advise a patient whether it is worth having a procedure to improve quality of life. Or the thrill we get when that patient thanks us for relieving the claudication that prevented gainful employment. We are relieved when a longstanding patient wakes up neurologically intact from an endarterectomy.

However, we are filled with remorse when we inform a family that they have lost their loved one who died from a ruptured aneurysm. Of course, our failures may be devastating but they reinforce our humility when we acknowledge that we have been defeated by a disease that resisted our every effort.

The mentor may also share that “Every Xmas you will collect cards thanking you for saving a life or, out of the blue, receive a carton of fruit from the orchard of a farmer who finally was able to walk amongst her crop. You will pass tissues to the sobbing husband whose wife always accompanied him to his yearly physical, but who recently passed from incurable cancer. You will listen to stories from veterans of past wars. You will see pictures of patients’ children and you will remark how they have grown through the years. A patient will make you look admiringly at their latest puppy or prize-winning pig. You will be given stock advice by a millionaire and you will pay for a taxi for the indigent to get home from your office. You may keep patients waiting while you hear intriguing gossip or wonder just how you can stop the little old lady rambling on about lost loves. You will be charmed by the 98-year-old who makes sure that she has her hair and makeup done prior to coming to see you, and how her face lights up when you pronounce her more beautiful than ever.

“Dear student, the technical aspects of vascular surgery are indeed demanding and exciting. We are invigorated by the knowledge that our expertise saved a life or limb, prevented a stroke or provided the nephrotic with a working fistula. Even the more simple cosmetic procedures give us pleasure. If you still need inspiration to embark on a vascular surgical career I encourage you to read the Presidential address Dr. Bruce J. Brener gave to the Society for Clinical Vascular Surgery in March 1996. His eloquent portrayal of the vascular surgical experience is unmatched (Amer J Surg, 1996; 172:97-9). However, it is our daily and often lifelong interaction with our wonderful patients that so intimately reinforces our humanity and makes this profession so uniquely satisfying.”

NEW ORLEANS – An investigational endoscopic procedure that aims to disrupt how the gut absorbs nutrients according to principles of gastric bypass surgery achieved reductions in hemoglobin A_1c levels and improvement in other key metabolic parameters in people with type 2 diabetes participating in a single-center investigational study in Santiago, Chile.

The procedure, called duodenal mucosal resurfacing (DMR), uses a balloon catheter to thermally ablate about 10 cm of the duodenal mucosa, Alan Cherrington, Ph.D., of Vanderbilt University, Nashville, Tenn., reported at the annual scientific sessions of the American Diabetes Association.

“A lot of the gastric bypass surgeries have been very effective in not only creating weight loss but in improving glucose tolerance,” Dr. Cherrington said. “The problem is, of course, they are very invasive and difficult to do, so the hope here was to try and develop a technique which in fact would be simpler but perhaps achieve some of the same effects.”

The mucosa in people with type 2 diabetes has been known to be thickened, and the endocrine cells discommuted and morphed, Dr. Cherrington explained. “So the question was, is there a way to do something about that?” The procedure, he said, was “well tolerated” and achieved significant reduction of HbA_1c after 3 months.

An international group of bariatric experts participated in the trial report. Dr. Cherrington said the procedure involves inserting a balloon-tipped catheter through the esophagus and stomach and into the duodenum, and then seating the balloon snugly in the mucosa at the ampulla of Vater. “You need a snug fit between the balloon and the mucosa,” Dr. Cherrington said.

Once the catheter is in place, it is filled with saline that inflates the balloon to fill the space. At that point, heated saline is run through the catheter for 10 seconds, creating a circumferential ablation of 300-500 mcm. When that step is completed, the balloon is moved down approximately 2 cm and the process repeated until the full 10 cm of the duodenal length from the ampulla of Vater to the ligament of Treitz is ablated.

A trained endoscopist performed the procedure with the patients under anesthesia, Dr. Cherrington said. The average HbA_1c was 9.6% at baseline, and the 39 patients were on one or more antidiabetic agents. The average fasting plasma glucose was 187 mg/dL at baseline. Average age was 54 years, and two-thirds of patients were male.

“It was not a mechanistic study,” Dr. Cherrington said. “It was a study purely to see: Can we do this? Can it be done safely? And would there be any efficacy at all?” The patients actually received DMR of two lengths: a short-segment ablation of 3.4 cm (n = 11); and a long-segment approach of 9.3 cm (n = 28).

“Patients had no difficulty tolerating an oral diet within days of the procedure,” Dr. Cherrington said. He described the adverse events as “mild,” mostly occurring immediately after the procedure. They typically involved tenderness due to anesthesia intubation or the endoscopic procedure itself, resolving in 3 days. Three patients had stenosis “very early while the device was still in its iterative development,” Dr. Cherrington said. But since the device was modified, the episodes of stenosis were mild and “resolved easily” with dilation.

The 9.3-cm ablation achieved better outcomes than did the 3.4-cm ablation, Dr. Cherrington said. Those in the long-segment group with baseline HbA_1c as high as 11% averaged 7.5% 3 months post ablation; those with HbA_1c around 9% before ablation averaged “just below 7%” afterward, he said. The patients showed some “waning effect” in HbA_1c after 6 months.

A cohort of patients who continued their medications achieved even better results. “They came to an HbA_1c of 6.5% and drifted up minimally at 6 months,” Dr. Cherrington said. “Part of the drift upward of the others was a function that they began to come off their medications.” Other reported metabolic parameters also showed improvement.

The next step, Dr. Cherrington said, is to compile 6-month results in an ongoing trial called Revita-1 in Chile and at five centers in Europe; after that, the goal is to conduct a multicenter phase II trial, Revita-2 that will include U.S. centers. “Clearly there are many, many questions that remain to be answered, and further examination of the efficacy, of the safety, of the clinical utility, and not the least of which is what is the mechanism by which this comes about, is essential,” Dr. Cherrington said.

Dr. John M. Miles of the University of Kansas Hospital in Kansas City gave a preview of some of those questions: “I would love to know whether metformin pharmacokinetics are altered by this procedure.” Dr. Miles asked for an explanation of the initial weight loss in study patients. “I would love to see self-reported calorie counts with these people,” he said.

Dr. Cherrington said the ensuing trials would aim to answer the first question, but that no information on calorie counts was available. The patients experienced an immediate weight loss after DMR but then some rebound effect after that, he said.

Dr. Cherrington disclosed relationships with Biocon, Fractyl, Merck, Metavention, NuSirt Biopharma, Sensulin, Zafgen, Eli Lilly, Silver Lake, Islet Sciences, Novo Nordisk, Profil Institute for Clinical Research, Thermalin Diabetes, Thetis Pharmaceuticals, vTv Therapeutics, ViaCyte, and Viking.

NEW ORLEANS – An investigational endoscopic procedure that aims to disrupt how the gut absorbs nutrients according to principles of gastric bypass surgery achieved reductions in hemoglobin A_1c levels and improvement in other key metabolic parameters in people with type 2 diabetes participating in a single-center investigational study in Santiago, Chile.

The procedure, called duodenal mucosal resurfacing (DMR), uses a balloon catheter to thermally ablate about 10 cm of the duodenal mucosa, Alan Cherrington, Ph.D., of Vanderbilt University, Nashville, Tenn., reported at the annual scientific sessions of the American Diabetes Association.

“A lot of the gastric bypass surgeries have been very effective in not only creating weight loss but in improving glucose tolerance,” Dr. Cherrington said. “The problem is, of course, they are very invasive and difficult to do, so the hope here was to try and develop a technique which in fact would be simpler but perhaps achieve some of the same effects.”

The mucosa in people with type 2 diabetes has been known to be thickened, and the endocrine cells discommuted and morphed, Dr. Cherrington explained. “So the question was, is there a way to do something about that?” The procedure, he said, was “well tolerated” and achieved significant reduction of HbA_1c after 3 months.

An international group of bariatric experts participated in the trial report. Dr. Cherrington said the procedure involves inserting a balloon-tipped catheter through the esophagus and stomach and into the duodenum, and then seating the balloon snugly in the mucosa at the ampulla of Vater. “You need a snug fit between the balloon and the mucosa,” Dr. Cherrington said.

Once the catheter is in place, it is filled with saline that inflates the balloon to fill the space. At that point, heated saline is run through the catheter for 10 seconds, creating a circumferential ablation of 300-500 mcm. When that step is completed, the balloon is moved down approximately 2 cm and the process repeated until the full 10 cm of the duodenal length from the ampulla of Vater to the ligament of Treitz is ablated.

A trained endoscopist performed the procedure with the patients under anesthesia, Dr. Cherrington said. The average HbA_1c was 9.6% at baseline, and the 39 patients were on one or more antidiabetic agents. The average fasting plasma glucose was 187 mg/dL at baseline. Average age was 54 years, and two-thirds of patients were male.

“It was not a mechanistic study,” Dr. Cherrington said. “It was a study purely to see: Can we do this? Can it be done safely? And would there be any efficacy at all?” The patients actually received DMR of two lengths: a short-segment ablation of 3.4 cm (n = 11); and a long-segment approach of 9.3 cm (n = 28).

“Patients had no difficulty tolerating an oral diet within days of the procedure,” Dr. Cherrington said. He described the adverse events as “mild,” mostly occurring immediately after the procedure. They typically involved tenderness due to anesthesia intubation or the endoscopic procedure itself, resolving in 3 days. Three patients had stenosis “very early while the device was still in its iterative development,” Dr. Cherrington said. But since the device was modified, the episodes of stenosis were mild and “resolved easily” with dilation.

The 9.3-cm ablation achieved better outcomes than did the 3.4-cm ablation, Dr. Cherrington said. Those in the long-segment group with baseline HbA_1c as high as 11% averaged 7.5% 3 months post ablation; those with HbA_1c around 9% before ablation averaged “just below 7%” afterward, he said. The patients showed some “waning effect” in HbA_1c after 6 months.

A cohort of patients who continued their medications achieved even better results. “They came to an HbA_1c of 6.5% and drifted up minimally at 6 months,” Dr. Cherrington said. “Part of the drift upward of the others was a function that they began to come off their medications.” Other reported metabolic parameters also showed improvement.

The next step, Dr. Cherrington said, is to compile 6-month results in an ongoing trial called Revita-1 in Chile and at five centers in Europe; after that, the goal is to conduct a multicenter phase II trial, Revita-2 that will include U.S. centers. “Clearly there are many, many questions that remain to be answered, and further examination of the efficacy, of the safety, of the clinical utility, and not the least of which is what is the mechanism by which this comes about, is essential,” Dr. Cherrington said.

Dr. John M. Miles of the University of Kansas Hospital in Kansas City gave a preview of some of those questions: “I would love to know whether metformin pharmacokinetics are altered by this procedure.” Dr. Miles asked for an explanation of the initial weight loss in study patients. “I would love to see self-reported calorie counts with these people,” he said.

Dr. Cherrington said the ensuing trials would aim to answer the first question, but that no information on calorie counts was available. The patients experienced an immediate weight loss after DMR but then some rebound effect after that, he said.

Dr. Cherrington disclosed relationships with Biocon, Fractyl, Merck, Metavention, NuSirt Biopharma, Sensulin, Zafgen, Eli Lilly, Silver Lake, Islet Sciences, Novo Nordisk, Profil Institute for Clinical Research, Thermalin Diabetes, Thetis Pharmaceuticals, vTv Therapeutics, ViaCyte, and Viking.

NEW ORLEANS – An investigational endoscopic procedure that aims to disrupt how the gut absorbs nutrients according to principles of gastric bypass surgery achieved reductions in hemoglobin A_1c levels and improvement in other key metabolic parameters in people with type 2 diabetes participating in a single-center investigational study in Santiago, Chile.

The procedure, called duodenal mucosal resurfacing (DMR), uses a balloon catheter to thermally ablate about 10 cm of the duodenal mucosa, Alan Cherrington, Ph.D., of Vanderbilt University, Nashville, Tenn., reported at the annual scientific sessions of the American Diabetes Association.

“A lot of the gastric bypass surgeries have been very effective in not only creating weight loss but in improving glucose tolerance,” Dr. Cherrington said. “The problem is, of course, they are very invasive and difficult to do, so the hope here was to try and develop a technique which in fact would be simpler but perhaps achieve some of the same effects.”

The mucosa in people with type 2 diabetes has been known to be thickened, and the endocrine cells discommuted and morphed, Dr. Cherrington explained. “So the question was, is there a way to do something about that?” The procedure, he said, was “well tolerated” and achieved significant reduction of HbA_1c after 3 months.

An international group of bariatric experts participated in the trial report. Dr. Cherrington said the procedure involves inserting a balloon-tipped catheter through the esophagus and stomach and into the duodenum, and then seating the balloon snugly in the mucosa at the ampulla of Vater. “You need a snug fit between the balloon and the mucosa,” Dr. Cherrington said.

Once the catheter is in place, it is filled with saline that inflates the balloon to fill the space. At that point, heated saline is run through the catheter for 10 seconds, creating a circumferential ablation of 300-500 mcm. When that step is completed, the balloon is moved down approximately 2 cm and the process repeated until the full 10 cm of the duodenal length from the ampulla of Vater to the ligament of Treitz is ablated.

A trained endoscopist performed the procedure with the patients under anesthesia, Dr. Cherrington said. The average HbA_1c was 9.6% at baseline, and the 39 patients were on one or more antidiabetic agents. The average fasting plasma glucose was 187 mg/dL at baseline. Average age was 54 years, and two-thirds of patients were male.

“It was not a mechanistic study,” Dr. Cherrington said. “It was a study purely to see: Can we do this? Can it be done safely? And would there be any efficacy at all?” The patients actually received DMR of two lengths: a short-segment ablation of 3.4 cm (n = 11); and a long-segment approach of 9.3 cm (n = 28).

“Patients had no difficulty tolerating an oral diet within days of the procedure,” Dr. Cherrington said. He described the adverse events as “mild,” mostly occurring immediately after the procedure. They typically involved tenderness due to anesthesia intubation or the endoscopic procedure itself, resolving in 3 days. Three patients had stenosis “very early while the device was still in its iterative development,” Dr. Cherrington said. But since the device was modified, the episodes of stenosis were mild and “resolved easily” with dilation.

The 9.3-cm ablation achieved better outcomes than did the 3.4-cm ablation, Dr. Cherrington said. Those in the long-segment group with baseline HbA_1c as high as 11% averaged 7.5% 3 months post ablation; those with HbA_1c around 9% before ablation averaged “just below 7%” afterward, he said. The patients showed some “waning effect” in HbA_1c after 6 months.

A cohort of patients who continued their medications achieved even better results. “They came to an HbA_1c of 6.5% and drifted up minimally at 6 months,” Dr. Cherrington said. “Part of the drift upward of the others was a function that they began to come off their medications.” Other reported metabolic parameters also showed improvement.

The next step, Dr. Cherrington said, is to compile 6-month results in an ongoing trial called Revita-1 in Chile and at five centers in Europe; after that, the goal is to conduct a multicenter phase II trial, Revita-2 that will include U.S. centers. “Clearly there are many, many questions that remain to be answered, and further examination of the efficacy, of the safety, of the clinical utility, and not the least of which is what is the mechanism by which this comes about, is essential,” Dr. Cherrington said.

Dr. John M. Miles of the University of Kansas Hospital in Kansas City gave a preview of some of those questions: “I would love to know whether metformin pharmacokinetics are altered by this procedure.” Dr. Miles asked for an explanation of the initial weight loss in study patients. “I would love to see self-reported calorie counts with these people,” he said.

Dr. Cherrington said the ensuing trials would aim to answer the first question, but that no information on calorie counts was available. The patients experienced an immediate weight loss after DMR but then some rebound effect after that, he said.

Dr. Cherrington disclosed relationships with Biocon, Fractyl, Merck, Metavention, NuSirt Biopharma, Sensulin, Zafgen, Eli Lilly, Silver Lake, Islet Sciences, Novo Nordisk, Profil Institute for Clinical Research, Thermalin Diabetes, Thetis Pharmaceuticals, vTv Therapeutics, ViaCyte, and Viking.

NEW YORK - Several hepatitis C virus core antigen (HCVcAg) tests accurately diagnose hepatitis C virus (HCV) infection and could replace nucleic acid testing (NAT) in settings where HCV is prevalent, according to a systematic review and meta-analysis.

"Overall, several of the tests perform very well and while they are not equal to NAT, the lower costs may improve diagnostic capacity in the appropriate setting," Dr. J. Morgan Freiman from Boston Medical Center in Massachusetts told Reuters Health by email.

The current two-step diagnostic procedure for diagnosing HCV infection -- screening for antibodies to HCV followed by NAT for those with anti-HCV antibodies -- is a major bottleneck for addressing the HCV elimination strategy proposed by the World Health Organization. Currently, there are five tests for HCVcAg commercially available.

Dr. Freiman and colleagues evaluated the accuracy of diagnosis of active HCV infection among adults and children for these five commercially available tests compared with NAT in their systematic review and meta-analysis of 44 published reports.

The pooled sensitivity and specificity were 93.4% and 98.8% for the Abbott ARCHITECT assay, 93.2% and 99.2% for the Ortho HCV Ag ELISA, and 59.5% and 82.9% for the Hunan Jynda HCV Ag ELISA. There was insufficient information for a pooled analysis of the Eiken Lumispot HCV Ag and the Fujirebio Lumipulse Ortho HCV Ag assays.

Three reports showed that the HCVcAg correlated well with RNA when levels were at least 3000 IU/mL when the Abbott ARCHITECT assay was used, according to the June 21 Annals of Internal Medicine report.

"Although even tests with the highest performance are not as sensitive as NAT, well-performing HCVcAg tests with an analytic sensitivity reaching into the femtomolar range (equal to 3000 IU/mL) could replace NAT for HCV detection, particularly if a lower cost per test allows more patients to be served," the researchers conclude. "Therefore, HCVcAg should be explored for point-of-care (POC) testing to increase the number of patients diagnosed and streamline the HCV cascade of care."

"There is much more work to be done to determine at what sensitivity threshold a POC test would be clinically useful," Dr. Freiman said. "In settings with reliable access to centralized laboratory processing and higher diagnostic capacity, a POC test may still prove to be useful as a screening tool, but would be less likely to replace confirmatory nucleic acid testing (NAT)."

"We have the technology to detect circulating HCV RNA down to 15 IU/mL - amazing -- but how clinically relevant is that threshold when access to testing is equally as important as accuracy in resource limited settings?" he wondered.

Dr. Jose-Manuel Echevarria, from Carlos III Health Institute, Madrid, Spain, who recently reported that HCV core-specific antibody may represent occult HCV infection among blood donors, told Reuters Health by email, "Physicians should conclude from the report that HCVcAg testing provides trustful diagnostic results for the characterization of their anti-HCV positive patients as viremic or non-viremic before deciding about antiviral treatment."

"I would add that HCVcAg testing is particularly useful for the purpose of transfusion centers," he said. "Chronically infected blood donors are detected by anti-HCV screening, and HCVcAg will detect efficiently almost every blood unit obtained from donors experiencing the window period of the acute HCV infection, who test negative for anti-HCV."

"At present, high-resource settings will for sure use NAT testing because of its higher sensitivity, and because automatic equipment has reduced the chance for false-positive results because sample-to-sample contamination (is kept) to a minimum," Dr. Echevarria concluded. "However, HCVcAg testing is extremely useful and convenient for low-resource settings, and also for emergency units everywhere."

The National Institutes of Health funded this research. Three coauthors reported disclosures.

SOURCE: http://bit.ly/28LpRcU Ann Intern Med 2016.

NEW YORK - Several hepatitis C virus core antigen (HCVcAg) tests accurately diagnose hepatitis C virus (HCV) infection and could replace nucleic acid testing (NAT) in settings where HCV is prevalent, according to a systematic review and meta-analysis.

"Overall, several of the tests perform very well and while they are not equal to NAT, the lower costs may improve diagnostic capacity in the appropriate setting," Dr. J. Morgan Freiman from Boston Medical Center in Massachusetts told Reuters Health by email.

The current two-step diagnostic procedure for diagnosing HCV infection -- screening for antibodies to HCV followed by NAT for those with anti-HCV antibodies -- is a major bottleneck for addressing the HCV elimination strategy proposed by the World Health Organization. Currently, there are five tests for HCVcAg commercially available.

Dr. Freiman and colleagues evaluated the accuracy of diagnosis of active HCV infection among adults and children for these five commercially available tests compared with NAT in their systematic review and meta-analysis of 44 published reports.

The pooled sensitivity and specificity were 93.4% and 98.8% for the Abbott ARCHITECT assay, 93.2% and 99.2% for the Ortho HCV Ag ELISA, and 59.5% and 82.9% for the Hunan Jynda HCV Ag ELISA. There was insufficient information for a pooled analysis of the Eiken Lumispot HCV Ag and the Fujirebio Lumipulse Ortho HCV Ag assays.

Three reports showed that the HCVcAg correlated well with RNA when levels were at least 3000 IU/mL when the Abbott ARCHITECT assay was used, according to the June 21 Annals of Internal Medicine report.

"Although even tests with the highest performance are not as sensitive as NAT, well-performing HCVcAg tests with an analytic sensitivity reaching into the femtomolar range (equal to 3000 IU/mL) could replace NAT for HCV detection, particularly if a lower cost per test allows more patients to be served," the researchers conclude. "Therefore, HCVcAg should be explored for point-of-care (POC) testing to increase the number of patients diagnosed and streamline the HCV cascade of care."

"There is much more work to be done to determine at what sensitivity threshold a POC test would be clinically useful," Dr. Freiman said. "In settings with reliable access to centralized laboratory processing and higher diagnostic capacity, a POC test may still prove to be useful as a screening tool, but would be less likely to replace confirmatory nucleic acid testing (NAT)."

"We have the technology to detect circulating HCV RNA down to 15 IU/mL - amazing -- but how clinically relevant is that threshold when access to testing is equally as important as accuracy in resource limited settings?" he wondered.

Dr. Jose-Manuel Echevarria, from Carlos III Health Institute, Madrid, Spain, who recently reported that HCV core-specific antibody may represent occult HCV infection among blood donors, told Reuters Health by email, "Physicians should conclude from the report that HCVcAg testing provides trustful diagnostic results for the characterization of their anti-HCV positive patients as viremic or non-viremic before deciding about antiviral treatment."

"I would add that HCVcAg testing is particularly useful for the purpose of transfusion centers," he said. "Chronically infected blood donors are detected by anti-HCV screening, and HCVcAg will detect efficiently almost every blood unit obtained from donors experiencing the window period of the acute HCV infection, who test negative for anti-HCV."

"At present, high-resource settings will for sure use NAT testing because of its higher sensitivity, and because automatic equipment has reduced the chance for false-positive results because sample-to-sample contamination (is kept) to a minimum," Dr. Echevarria concluded. "However, HCVcAg testing is extremely useful and convenient for low-resource settings, and also for emergency units everywhere."

The National Institutes of Health funded this research. Three coauthors reported disclosures.

SOURCE: http://bit.ly/28LpRcU Ann Intern Med 2016.

NEW YORK - Several hepatitis C virus core antigen (HCVcAg) tests accurately diagnose hepatitis C virus (HCV) infection and could replace nucleic acid testing (NAT) in settings where HCV is prevalent, according to a systematic review and meta-analysis.

"Overall, several of the tests perform very well and while they are not equal to NAT, the lower costs may improve diagnostic capacity in the appropriate setting," Dr. J. Morgan Freiman from Boston Medical Center in Massachusetts told Reuters Health by email.

The current two-step diagnostic procedure for diagnosing HCV infection -- screening for antibodies to HCV followed by NAT for those with anti-HCV antibodies -- is a major bottleneck for addressing the HCV elimination strategy proposed by the World Health Organization. Currently, there are five tests for HCVcAg commercially available.

Dr. Freiman and colleagues evaluated the accuracy of diagnosis of active HCV infection among adults and children for these five commercially available tests compared with NAT in their systematic review and meta-analysis of 44 published reports.

The pooled sensitivity and specificity were 93.4% and 98.8% for the Abbott ARCHITECT assay, 93.2% and 99.2% for the Ortho HCV Ag ELISA, and 59.5% and 82.9% for the Hunan Jynda HCV Ag ELISA. There was insufficient information for a pooled analysis of the Eiken Lumispot HCV Ag and the Fujirebio Lumipulse Ortho HCV Ag assays.

Three reports showed that the HCVcAg correlated well with RNA when levels were at least 3000 IU/mL when the Abbott ARCHITECT assay was used, according to the June 21 Annals of Internal Medicine report.

"Although even tests with the highest performance are not as sensitive as NAT, well-performing HCVcAg tests with an analytic sensitivity reaching into the femtomolar range (equal to 3000 IU/mL) could replace NAT for HCV detection, particularly if a lower cost per test allows more patients to be served," the researchers conclude. "Therefore, HCVcAg should be explored for point-of-care (POC) testing to increase the number of patients diagnosed and streamline the HCV cascade of care."

"There is much more work to be done to determine at what sensitivity threshold a POC test would be clinically useful," Dr. Freiman said. "In settings with reliable access to centralized laboratory processing and higher diagnostic capacity, a POC test may still prove to be useful as a screening tool, but would be less likely to replace confirmatory nucleic acid testing (NAT)."

"We have the technology to detect circulating HCV RNA down to 15 IU/mL - amazing -- but how clinically relevant is that threshold when access to testing is equally as important as accuracy in resource limited settings?" he wondered.

Dr. Jose-Manuel Echevarria, from Carlos III Health Institute, Madrid, Spain, who recently reported that HCV core-specific antibody may represent occult HCV infection among blood donors, told Reuters Health by email, "Physicians should conclude from the report that HCVcAg testing provides trustful diagnostic results for the characterization of their anti-HCV positive patients as viremic or non-viremic before deciding about antiviral treatment."

"I would add that HCVcAg testing is particularly useful for the purpose of transfusion centers," he said. "Chronically infected blood donors are detected by anti-HCV screening, and HCVcAg will detect efficiently almost every blood unit obtained from donors experiencing the window period of the acute HCV infection, who test negative for anti-HCV."

"At present, high-resource settings will for sure use NAT testing because of its higher sensitivity, and because automatic equipment has reduced the chance for false-positive results because sample-to-sample contamination (is kept) to a minimum," Dr. Echevarria concluded. "However, HCVcAg testing is extremely useful and convenient for low-resource settings, and also for emergency units everywhere."

The National Institutes of Health funded this research. Three coauthors reported disclosures.

SOURCE: http://bit.ly/28LpRcU Ann Intern Med 2016.

The Coding & Reimbursement for Vascular Surgeons Workshop will be held October 21-22, 2016 at the Millennium Knickerbocker Hotel in Chicago.

Vascular surgeons and their support staff need to maintain knowledge and competence for appropriate billing and coding procedures. The Coding and Reimbursement for Vascular Surgeons course is an intensive two-day program designed to address the 2016 updates including changes to endovascular stent placement outside the lower extremity and PQRS as well as coding for intravascular embolization and retrograde intrathoracic carotid stenting.

Additionally, the course will review the proposed updates for 2016 with a focus on reporting standards for interventional and open surgical procedures. The program also includes information about the global surgical package and how it impacts billing and reimbursement, along with the application of modifiers for streamlined reimbursement. This will be accomplished by using a multi-modality educational forum with didactic lectures, panel discussions, case studies, and question-answer sessions.

For further information and to sign up click here.

The Coding & Reimbursement for Vascular Surgeons Workshop will be held October 21-22, 2016 at the Millennium Knickerbocker Hotel in Chicago.

Vascular surgeons and their support staff need to maintain knowledge and competence for appropriate billing and coding procedures. The Coding and Reimbursement for Vascular Surgeons course is an intensive two-day program designed to address the 2016 updates including changes to endovascular stent placement outside the lower extremity and PQRS as well as coding for intravascular embolization and retrograde intrathoracic carotid stenting.

Additionally, the course will review the proposed updates for 2016 with a focus on reporting standards for interventional and open surgical procedures. The program also includes information about the global surgical package and how it impacts billing and reimbursement, along with the application of modifiers for streamlined reimbursement. This will be accomplished by using a multi-modality educational forum with didactic lectures, panel discussions, case studies, and question-answer sessions.

For further information and to sign up click here.

The Coding & Reimbursement for Vascular Surgeons Workshop will be held October 21-22, 2016 at the Millennium Knickerbocker Hotel in Chicago.

Vascular surgeons and their support staff need to maintain knowledge and competence for appropriate billing and coding procedures. The Coding and Reimbursement for Vascular Surgeons course is an intensive two-day program designed to address the 2016 updates including changes to endovascular stent placement outside the lower extremity and PQRS as well as coding for intravascular embolization and retrograde intrathoracic carotid stenting.

Additionally, the course will review the proposed updates for 2016 with a focus on reporting standards for interventional and open surgical procedures. The program also includes information about the global surgical package and how it impacts billing and reimbursement, along with the application of modifiers for streamlined reimbursement. This will be accomplished by using a multi-modality educational forum with didactic lectures, panel discussions, case studies, and question-answer sessions.

For further information and to sign up click here.

Neuropathic hand complaints—for which patients typically seek medical attention when the pain or paresthesia starts to interfere with their daily routine—are common and diverse. The ability to assess and accurately diagnose upper extremity compression neuropathies is critical for physicians in primary care.

Assessment starts, of course, with a thorough history of the present illness and past medical history, which helps define a broad differential diagnosis and identify comorbidities. Physical examination, including judicious use of provocative testing, allows you to objectively identify the pathologic deficit, evaluate function and coordination of multiple organ systems, and detect nerve dysfunction. The results determine whether additional tools, such as electrodiagnostic testing, are needed.

We’ve created this guide, detailed in the text, tables, and figures that follow, to help you hone your ability to accurately diagnose patients who present with compression neuropathies of the hand.

The medical history: Knowing what to ask

To clearly define a patient’s symptoms and disability, start with a thorough history of the presenting complaint.

Inquire about symptom onset and chronicity. Did the pain or paresthesia begin after an injury? Are the symptoms associated with repetitive use of the extremity? Do they occur at night?

Pinpoint the location or distribution of pain or paresthesia. It is paramount to identify the affected nerve.^1,2 Ask patients to complete a hand or upper extremity profile documenting location and/or type of numbness, tingling, or decreased sensation. A diagram of the peripheral nerves responsible for sensory innervation of the hand (FIGURE 1) is an effective way to screen individuals at high risk of carpal tunnel syndrome (CTS) or ulnar tunnel syndrome (UTS).^1,2

A patient report such as, “My whole hand is numb,” calls for a follow-up question to determine whether the little finger is affected,³ which would indicate that the ulnar nerve, rather than just the median nerve, is involved. And if a patient reports feeling as if he or she is wearing gloves or mittens, it is essential to consider the possibility of a systemic neuropathy rather than a single peripheral neuropathy.³

Gather basic patient information. Inquire about hand dominance, occupation, and baseline function, any or all of which may be critical in the assessment and initiation of treatment.^4,5

Review systemic conditions and medications

A broad range of comorbidities, such as cervical radiculopathy, diabetes, hypothyroidism, and vitamin deficiencies (TABLE 1),^6,7 may be responsible for neuropathic hand complaints, and a thorough review of systemic complaints and past medical history is critical. Include a medication history and a review of prior procedures, such as post-traumatic surgeries of the hand or upper extremity or nerve decompression surgeries, which may provide additional insight into disease etiology.

Symptoms guide physical exam, provocative testing

A physical examination, including provocative testing, follows based on reported symptoms, medical history, and suspected source of nerve compression.

Carpal tunnel syndrome

CTS is the most common peripheral neuropathy.⁸ Patients often report nocturnal pain or paresthesia in the distal median nerve distribution, comprising the palmar surface of the thumb, index, middle, and radial half of the ring finger.

Researchers have identified 6 standardized clinical criteria for the diagnosis of CTS. Two criteria—numbness mostly in median nerve territory and nocturnal numbness—can be ascertained during the history of present illness.The other 4, detailed below, will be found during the physical exam.⁹

Thenar weakness or atrophy.⁹ Begin your evaluation by inspecting the thenar musculature for atrophic changes. Motor exam of intrinsic musculature innervated by the recurrent motor branch of the median nerve includes assessment of thumb abduction strength (assessed by applying resistance to the metacarpophalangeal joint [MCPJ] base towards the palm in the position of maximal abduction) and opposition strength (assessed by applying force to the MCPJ from the ulnar aspect).¹⁰

Positive Phalen’s test.⁹ Provocative testing for CTS includes Phalen’s test (sensitivity 43%-86%, specificity 48%-67%),¹¹ which is an attempt to reproduce the numbness or tingling in the median nerve territory within 60 seconds of full wrist flexion. Ask the patient to hold his or her forearms vertically with elbows resting on the table (allowing gravity to flex the wrists),¹² and to tell you if numbness or tingling occurs.

Consider the possibility of a systemic neuropathy in patients who report that they feel as though they are wearing gloves.

Positive Tinel’s sign.⁹ Tinel’s sign (sensitivity 45%-75%, specificity 48%-67%)¹¹ is performed by lightly tapping the median nerve from the proximal to distal end over the carpal tunnel. The test is positive if paresthesia results. Provocative testing may also include Durkan’s test, also known as the carpal compression test. Durkan’s test (sensitivity 49%-89%, specificity 54%-96%)¹¹ involves placing your thumb directly over the carpal tunnel and holding light compression for 60 seconds, or until paresthesia is reported.

Positive 2-point discrimination test.⁹ To assess CTS disease severity, use 2-point discrimination to evaluate the patient’s sensation qualitatively and quantitatively. Two-point discrimination can only be tested, however, if light touch sensation is intact. It is typically performed by lightly applying 2 caliper points at fixed distances sufficient to blanch the skin, but some clinicians have used other tools, such as a modified paperclip.¹³ The smallest distance at which the patient can detect 2 distinct stimuli is then recorded.

Researchers have reported an average of 3 to 5 mm for 2-point discrimination at the fingertipand a normal 2-point discrimination of 6 to 9 mm in the volar surface of the hand (TABLE 2).^14,15

The scratch collapse test (sensitivity 64%, specificity 99%) is a supplemental exam that uses a different outcome measure to diagnose CTS.¹⁶ It involves lightly scratching the skin over the compressed carpal tunnel while the patient performs sustained resisted bilateral shoulder external rotation in an adducted position. A momentary loss of muscle resistance to external rotation indicates a positive test.

Pronator syndrome

Pronator syndrome (PS) is a proximal median neuropathy that may present in isolation or in combination with CTS as a double crush syndrome. Clinical symptoms include features of CTS and sensory paresthesias in the palm and distal forearm in the distribution of the palmar cutaneous branch of the median nerve. PS is commonly associated with volar proximal forearm pain exacerbated by repetitive activities involving pronation and supination.

PS is not easy to assess. Palpatory examination of a large supracondylar process at the distal humerus proximal to the medial epicondyle on its anteromedial aspect can be difficult, especially if the patient is overweight. And motor weakness is not a prominent feature. What’s more, power assessment of the pronator teres, flexor carpi radialis, and flexor digitorum superficialis may exacerbate symptoms.

Because the symptoms of PS and CTS may be the same, PS provocation maneuvers should be performed on patients with CTS symptoms and paresthesia involving the palm. Start by testing for Tinel’s sign over the pronator teres muscle, although this has been found to be positive in less than 50% of PS cases.¹⁷ Palpate the antecubital fossa and the proximal aspect of the pronator teres muscle to assess for discomfort or tenderness.

Pronator compression test. The pronator compression test has been found to be the most sensitive way to assess PS.^18,19 This test involves direct compression of the proximal and radial edge of the pronator teres muscle belly along the proximal volar forearm with the thumb.²⁰ It is performed bilaterally on supinated upper extremities, with the clinician applying pressure on each forearm simultaneously (FIGURE 2). If the symptoms in the hand are reproduced in ≤30 seconds, the test is positive. In a study of 10 patients with surgically confirmed PS, the pronator compression test was positive in every case.^20,21

Resistance testing. You can also evaluate the pronator teres compression site by testing the patient’s ability to resist pronation with his or her elbow extended and the forearm in neutral position. To test for compression from the bicipital aponeurosis, ask the patient to flex the elbow to approximately 120° to 130° and apply active supinated resistance.²² Likewise, resistance of the long finger proximal interphalangeal joint (IPJ) to flexion—a maneuver performed with elbow fully extended—assesses compression from the fibrous arcade of the flexor digitorum superficialis (FDS).²¹ A positive resistance test will reproduce the reported symptoms.

Ulnar tunnel syndrome

Symptoms of UTS, which is much less common than CTS, include pain in the wrist and hand that is associated with paresthesia or numbness in the small finger and ulnar half of the ring finger. Patients may report difficulty with motor tasks involving grip and pinch strength or fatigue with prolonged action of the intrinsic muscles. Many also report an exacerbation of symptoms associated with increased wrist flexion or at night.

Evaluation of UTS requires a full assessment of the upper extremity, starting with observation of hand posture and muscle bulk to identify signs of chronic nerve compression. The contralateral extremity serves as a control to the neuropathic hand. Classically, chronic ulnar nerve compression leads to intrinsic muscle atrophy, evidenced by loss of topographical soft tissue bulk in the first dorsal web space, the palmar transverse metacarpal arch, and the hypothenar area.²³ Ulnar motor nerve dysfunction is limited to the intrinsic muscles of the hand. The inverted pyramid sign, signified by atrophy of the transverse head of the adductor pollicis, is another visual aberrancy,²⁴ as is clawing of the ring finger and small finger. The clawing, which involves hyperextension of the MCPJ and flexion of the proximal and distal IPJ, is commonly known as Duchenne’s sign. FIGURE 3 demonstrates hypothenar atrophy and the loss of muscle bulk in the first dorsal web space.

When you suspect UTS, palpate the wrist and hand in an attempt to locate a mass or area of tenderness. Not all patients with a volar ganglion cyst responsible for UTS present with a palpable mass, but tenderness along the radial aspect of the pisiform or an undefined fullness in this area may be noted.²⁵ Any patient with a palpable mass should be tested for Tinel’s sign over the mass and undergo a thorough vascular assessment. Fracture of the hook of the hamate is indicated by tenderness in the region approximated by the intersection of Kaplan’s line and the proximal extension line from the ring finger.

Perform 2-point discrimination testing at the palmar distal aspect of the small finger and ulnar half of the ring finger. This tests the superficial sensory division of the ulnar nerve that travels within Guyon’s canal. Testing the dorsal ulnar cutaneous nerve involves the skin of the dorso-ulnar hand and dorsum of the long finger proximal to the IPJ. If this area is spared and the palmar distal ulnar digits are affected, compression within Guyon’s canal is likely. If both areas are affected, suspect a more proximal compression site at the cubital tunnel, as the dorsal ulnar cutaneous nerve branches proximal to Guyon’s canal.²⁶

Ulnar motor nerve dysfunction in UTS is limited to the intrinsic muscles of the hand. Assessment of intrinsic muscle function is described in TABLE 3.^27-32 It is important to become familiar with the tests and maneuvers described, but also to be aware that a comprehensive evaluation of ulnar nerve motor function requires a combination of tests.

Cubital tunnel syndrome

Cubital tunnel syndrome—the second most common peripheral neuropathy⁸—involves the proximal site of ulnar nerve compression in the upper extremity. Patients typically report symptoms similar to those of UTS, with sensory paresthesia in the ulnar digits and intrinsic weakness. To learn more about the symptoms, ask if the onset of pain or paresthesia is related to a particular elbow position, such as increased elbow flexion.

Notably, pain is usually not the initial complaint, unless the disease is advanced. This may be the reason atrophic intrinsic changes are 4 times more likely to be seen in patients with cubital tunnel syndrome than in those with CTS.³³ You’re more likely to hear about vague motor problems, including hand clumsiness and difficulty with fine coordination of the fingers.³⁴ Thus, it is important to evaluate patients for concurrent UTS and/or CTS, as well as for differentiation.

Focus on the elbow. Whenever you suspect cubital tunnel syndrome, pay special attention to the elbow. Examine the carrying angle of the elbow in relation to the contralateral extremity. Deformity may provide clues to a history of trauma. Assess the ulnar nerve during active flexion and extension to identify a subluxatable nerve at the cubital tunnel. Examine the ulno-humeral joint for crepitus, and palpate the joint line for large osteophytes and/or ganglion cysts.

Motor examination of the ulnar nerve primarily focuses on the intrinsic muscles detailed in TABLE 3,^27-32 although the flexor carpi ulnaris (FCU) and flexor digitorum profundus (FDP) to the ring finger and small finger are also innervated by the ulnar nerve. The FCU mediates the power grip, and can be tested by resisted wrist flexion and ulnar deviation. Ring finger and small finger FDP strength should be examined by resistance testing at the distal IPJ.

Provocative testing of cubital tunnel syndrome includes Tinel’s sign (performed over the cubital tunnel), the elbow flexion test (performed with elbow in maximum flexion and wrist at neutral position and held for 60 seconds), and the pressure provocation test (performed by applying pressure to the ulnar nerve just proximal to the cubital tunnel with your index and long fingers for 60 seconds while the patient’s elbow is at 20° flexion with the forearm supinated). For each test, eliciting distal paresthesia in ulnar nerve territory is a positive result. The sensitivity of these tests ranges from 70% (Tinel’s sign) to 98% (combined elbow flexion and pressure); specificity ranges from 95% to 99%.³⁵

The scratch collapse test for cubital tunnel syndrome evaluation is similar to the version used to assess for CTS; the only difference is the location of the site that is scratched, in this case the cubital tunnel. The reported sensitivity and specificity are 69% and 99%, respectively.¹¹

Wartenberg’s syndrome

When you suspect ulnar tunnel syndrome, palpate the wrist and hand in an attempt to locate a mass or area of tenderness.

When a patient reports paresthesia or pain along the radial aspect of the forearm that radiates into the dorsal thumb and index and middle fingers, consider Wartenberg’s syndrome—compression of the superficial radial nerve. The condition, also known as “cheiralgia paresthetica,” may exist anywhere along the course of the nerve in the forearm,³⁶ but the compression typically occurs 9 cm proximal to the radial styloid.

Assess the skin over the forearm and hand for evidence of prior trauma, surgical scars, or external compression sources, such as a watch.^37-39 Then use palpation to identify superficial or deep masses along the nerve.⁴⁰ Perform Tinel’s sign by lightly tapping along the nerve course from proximal to distal in the forearm. The test is positive if paresthesias are provoked distally.^41,42

Motor function of the extremity is unaffected in Wartenberg’s syndrome, unless a prior traumatic injury occurred or a comorbidity exists. Comorbidities to consider include de Quervain’s tenosynovitis, cervical radiculopathy, injury to the lateral antebrachial cutaneous nerve, and CTS.

Gross sensory testing usually is negative, but 2-point discrimination may show diminished responses. Testing distribution includes the dorsal radial wrist and hand, dorsal thumb skin proximal to the IPJ, and the dorsal surface of the index, middle, and radial half of the ring finger proximal to the IPJ.

Proceed with caution. Provocative testing with a pronated forearm and a flexed and ulnar-deviated wrist may exacerbate symptoms,^12,42 and Finkelstein’s maneuver (isolated ulnar deviation at the wrist to elicit pain over the first dorsal wrist compartment) and Phalen’s test may elicit false-positive results. Upper motor neuron exams (ie, deep tendon reflexes) and Hoffman’s sign (reflexive flexion of the terminal phalanges of the thumb and index finger induced by flicking or tapping the distal phalanx of the long finger) should be symmetric to the contralateral extremity.

In patients with more than one compression injury, Spurling’s sign (neck extension and lateral rotation towards the affected extremity) may induce paresthesia when combined with axial compression, while the shoulder abduction test (shoulder 90° abduction, with external rotation) may diminish reported paresthesia. In those for whom Wartenberg’s syndrome is their only compression injury, however, these provocative maneuvers will be negative.

Anterior interosseous nerve syndrome

A rare clinical entity that affects the anterior interosseous innervated muscles in the forearm, anterior interosseous nerve syndrome (AINS)’s etiology is unclear. But it is likely related to a spontaneous neuritis rather than a compressive etiology.⁴³ Paresis or paralysis of the flexor pollicis longus (FPL) and the flexor digitorum profundus (FDP) of the index and long finger is its hallmark, but patients may report vague forearm pain associated with weakness or absence of function.

Examination begins with a visual assessment and palpation of the forearm and hand for atrophy or a space-occupying lesion. Notably, sensory function of the hand should remain at baseline despite the motor dysfunction, as the anterior interosseous is purely a motor nerve.

Motor testing should focus on the median and anterior interosseous innervated muscles.

The FPL is tested by isolated thumb IPJ flexion and the Kiloh and Nevin sign—the inability to make an “OK” sign with the thumb and index finger.⁴⁴ Assess pinch grasp with a maximally flexed thumb IPJ and distal IPJ of the index finger. Anterior interosseous nerve dysfunction results in a flattened pinch without IPJ or distal IPJ flexion, which increases the contact of the thumb and index finger pulp.⁴⁵ In a series of 14 patients, researchers reported complete paralysis of FPL and FDP index finger in 5 patients, isolated paralysis of FPL in 7 patients, and isolated paralysis of FDP index and long fingers in 2 patients. None had isolated paralysis of the FDP long finger.⁴⁶FIGURE 4 shows complete (A) and incomplete (B) paralysis.

Pain is usually not the initial complaint with cubital tunnel syndrome. You're more likely to hear about hand clumsiness and difficulty with fine coordination of the fingers.

Evaluation of AINS also includes assessment of FPL and FDP tendon integrity with passive tenodesis. The appearance of the hand at rest should reflect the natural digital cascade. In a completely relaxed or anesthetized hand, the forearm is placed in wrist supination and extension, allowing gravity to extend the wrist and placing the thumb MCPJ at 30° flexion, the index finger MCPJ at 40°, and the small finger MCPJ at 70°. The thumb IPJ should approximate the radial fingertip pulp of the index finger. The forearm is then pronated and flexed at the wrist, straightening the thumb MCPJ and producing a mild flexion cascade at the proximal and distal IPJ of the index, long, ring, and small fingers within 20° of full extension. This dynamic exercise is used to confirm that the patient has an intact tenodesis effect, thus excluding tendon lacerations or ruptures from the differential diagnosis. In one study, in 9 of 33 cases of partial or complete isolated index finger FPL or FDP, paralysis was initially diagnosed as tendon rupture.⁴⁷

When to consider electrodiagnostic testing

Electrodiagnostic testing—a combination of electromyography and nerve conduction studies to assess the status of a peripheral nerve⁴⁸—provides objective data that can help diagnose a challenging presentation, rule out a competing diagnosis, or clarify an atypical clinical picture or vague subjective history. This type of testing is also used to localize the entrapment site, identify a patient with polyneuropathy or brachial plexopathy, and assess the severity of nerve injury or presence of a double crush syndrome.^49,50 Any patient with signs and symptoms of a compression neuropathy and supportive findings on physical exam should be referred for electrodiagnostic testing and/or to a surgeon specializing in treating these conditions.

CORRESPONDENCE
Kyle J. MacGillis, MD, University of Illinois at Chicago, Department of Orthopaedic Surgery, 835 South Wolcott Avenue, M/C 844, Chicago, IL 60612; [email protected].

Neuropathic hand complaints—for which patients typically seek medical attention when the pain or paresthesia starts to interfere with their daily routine—are common and diverse. The ability to assess and accurately diagnose upper extremity compression neuropathies is critical for physicians in primary care.

Assessment starts, of course, with a thorough history of the present illness and past medical history, which helps define a broad differential diagnosis and identify comorbidities. Physical examination, including judicious use of provocative testing, allows you to objectively identify the pathologic deficit, evaluate function and coordination of multiple organ systems, and detect nerve dysfunction. The results determine whether additional tools, such as electrodiagnostic testing, are needed.

We’ve created this guide, detailed in the text, tables, and figures that follow, to help you hone your ability to accurately diagnose patients who present with compression neuropathies of the hand.

The medical history: Knowing what to ask

To clearly define a patient’s symptoms and disability, start with a thorough history of the presenting complaint.

Inquire about symptom onset and chronicity. Did the pain or paresthesia begin after an injury? Are the symptoms associated with repetitive use of the extremity? Do they occur at night?

Pinpoint the location or distribution of pain or paresthesia. It is paramount to identify the affected nerve.^1,2 Ask patients to complete a hand or upper extremity profile documenting location and/or type of numbness, tingling, or decreased sensation. A diagram of the peripheral nerves responsible for sensory innervation of the hand (FIGURE 1) is an effective way to screen individuals at high risk of carpal tunnel syndrome (CTS) or ulnar tunnel syndrome (UTS).^1,2

A patient report such as, “My whole hand is numb,” calls for a follow-up question to determine whether the little finger is affected,³ which would indicate that the ulnar nerve, rather than just the median nerve, is involved. And if a patient reports feeling as if he or she is wearing gloves or mittens, it is essential to consider the possibility of a systemic neuropathy rather than a single peripheral neuropathy.³

Gather basic patient information. Inquire about hand dominance, occupation, and baseline function, any or all of which may be critical in the assessment and initiation of treatment.^4,5

Review systemic conditions and medications

A broad range of comorbidities, such as cervical radiculopathy, diabetes, hypothyroidism, and vitamin deficiencies (TABLE 1),^6,7 may be responsible for neuropathic hand complaints, and a thorough review of systemic complaints and past medical history is critical. Include a medication history and a review of prior procedures, such as post-traumatic surgeries of the hand or upper extremity or nerve decompression surgeries, which may provide additional insight into disease etiology.

Symptoms guide physical exam, provocative testing

A physical examination, including provocative testing, follows based on reported symptoms, medical history, and suspected source of nerve compression.

Carpal tunnel syndrome

CTS is the most common peripheral neuropathy.⁸ Patients often report nocturnal pain or paresthesia in the distal median nerve distribution, comprising the palmar surface of the thumb, index, middle, and radial half of the ring finger.

Researchers have identified 6 standardized clinical criteria for the diagnosis of CTS. Two criteria—numbness mostly in median nerve territory and nocturnal numbness—can be ascertained during the history of present illness.The other 4, detailed below, will be found during the physical exam.⁹

Thenar weakness or atrophy.⁹ Begin your evaluation by inspecting the thenar musculature for atrophic changes. Motor exam of intrinsic musculature innervated by the recurrent motor branch of the median nerve includes assessment of thumb abduction strength (assessed by applying resistance to the metacarpophalangeal joint [MCPJ] base towards the palm in the position of maximal abduction) and opposition strength (assessed by applying force to the MCPJ from the ulnar aspect).¹⁰

Positive Phalen’s test.⁹ Provocative testing for CTS includes Phalen’s test (sensitivity 43%-86%, specificity 48%-67%),¹¹ which is an attempt to reproduce the numbness or tingling in the median nerve territory within 60 seconds of full wrist flexion. Ask the patient to hold his or her forearms vertically with elbows resting on the table (allowing gravity to flex the wrists),¹² and to tell you if numbness or tingling occurs.

Consider the possibility of a systemic neuropathy in patients who report that they feel as though they are wearing gloves.

Positive Tinel’s sign.⁹ Tinel’s sign (sensitivity 45%-75%, specificity 48%-67%)¹¹ is performed by lightly tapping the median nerve from the proximal to distal end over the carpal tunnel. The test is positive if paresthesia results. Provocative testing may also include Durkan’s test, also known as the carpal compression test. Durkan’s test (sensitivity 49%-89%, specificity 54%-96%)¹¹ involves placing your thumb directly over the carpal tunnel and holding light compression for 60 seconds, or until paresthesia is reported.

Positive 2-point discrimination test.⁹ To assess CTS disease severity, use 2-point discrimination to evaluate the patient’s sensation qualitatively and quantitatively. Two-point discrimination can only be tested, however, if light touch sensation is intact. It is typically performed by lightly applying 2 caliper points at fixed distances sufficient to blanch the skin, but some clinicians have used other tools, such as a modified paperclip.¹³ The smallest distance at which the patient can detect 2 distinct stimuli is then recorded.

Researchers have reported an average of 3 to 5 mm for 2-point discrimination at the fingertipand a normal 2-point discrimination of 6 to 9 mm in the volar surface of the hand (TABLE 2).^14,15

The scratch collapse test (sensitivity 64%, specificity 99%) is a supplemental exam that uses a different outcome measure to diagnose CTS.¹⁶ It involves lightly scratching the skin over the compressed carpal tunnel while the patient performs sustained resisted bilateral shoulder external rotation in an adducted position. A momentary loss of muscle resistance to external rotation indicates a positive test.

Pronator syndrome

Pronator syndrome (PS) is a proximal median neuropathy that may present in isolation or in combination with CTS as a double crush syndrome. Clinical symptoms include features of CTS and sensory paresthesias in the palm and distal forearm in the distribution of the palmar cutaneous branch of the median nerve. PS is commonly associated with volar proximal forearm pain exacerbated by repetitive activities involving pronation and supination.

PS is not easy to assess. Palpatory examination of a large supracondylar process at the distal humerus proximal to the medial epicondyle on its anteromedial aspect can be difficult, especially if the patient is overweight. And motor weakness is not a prominent feature. What’s more, power assessment of the pronator teres, flexor carpi radialis, and flexor digitorum superficialis may exacerbate symptoms.

Because the symptoms of PS and CTS may be the same, PS provocation maneuvers should be performed on patients with CTS symptoms and paresthesia involving the palm. Start by testing for Tinel’s sign over the pronator teres muscle, although this has been found to be positive in less than 50% of PS cases.¹⁷ Palpate the antecubital fossa and the proximal aspect of the pronator teres muscle to assess for discomfort or tenderness.

Pronator compression test. The pronator compression test has been found to be the most sensitive way to assess PS.^18,19 This test involves direct compression of the proximal and radial edge of the pronator teres muscle belly along the proximal volar forearm with the thumb.²⁰ It is performed bilaterally on supinated upper extremities, with the clinician applying pressure on each forearm simultaneously (FIGURE 2). If the symptoms in the hand are reproduced in ≤30 seconds, the test is positive. In a study of 10 patients with surgically confirmed PS, the pronator compression test was positive in every case.^20,21

Resistance testing. You can also evaluate the pronator teres compression site by testing the patient’s ability to resist pronation with his or her elbow extended and the forearm in neutral position. To test for compression from the bicipital aponeurosis, ask the patient to flex the elbow to approximately 120° to 130° and apply active supinated resistance.²² Likewise, resistance of the long finger proximal interphalangeal joint (IPJ) to flexion—a maneuver performed with elbow fully extended—assesses compression from the fibrous arcade of the flexor digitorum superficialis (FDS).²¹ A positive resistance test will reproduce the reported symptoms.

Ulnar tunnel syndrome

Symptoms of UTS, which is much less common than CTS, include pain in the wrist and hand that is associated with paresthesia or numbness in the small finger and ulnar half of the ring finger. Patients may report difficulty with motor tasks involving grip and pinch strength or fatigue with prolonged action of the intrinsic muscles. Many also report an exacerbation of symptoms associated with increased wrist flexion or at night.

Evaluation of UTS requires a full assessment of the upper extremity, starting with observation of hand posture and muscle bulk to identify signs of chronic nerve compression. The contralateral extremity serves as a control to the neuropathic hand. Classically, chronic ulnar nerve compression leads to intrinsic muscle atrophy, evidenced by loss of topographical soft tissue bulk in the first dorsal web space, the palmar transverse metacarpal arch, and the hypothenar area.²³ Ulnar motor nerve dysfunction is limited to the intrinsic muscles of the hand. The inverted pyramid sign, signified by atrophy of the transverse head of the adductor pollicis, is another visual aberrancy,²⁴ as is clawing of the ring finger and small finger. The clawing, which involves hyperextension of the MCPJ and flexion of the proximal and distal IPJ, is commonly known as Duchenne’s sign. FIGURE 3 demonstrates hypothenar atrophy and the loss of muscle bulk in the first dorsal web space.

When you suspect UTS, palpate the wrist and hand in an attempt to locate a mass or area of tenderness. Not all patients with a volar ganglion cyst responsible for UTS present with a palpable mass, but tenderness along the radial aspect of the pisiform or an undefined fullness in this area may be noted.²⁵ Any patient with a palpable mass should be tested for Tinel’s sign over the mass and undergo a thorough vascular assessment. Fracture of the hook of the hamate is indicated by tenderness in the region approximated by the intersection of Kaplan’s line and the proximal extension line from the ring finger.

Perform 2-point discrimination testing at the palmar distal aspect of the small finger and ulnar half of the ring finger. This tests the superficial sensory division of the ulnar nerve that travels within Guyon’s canal. Testing the dorsal ulnar cutaneous nerve involves the skin of the dorso-ulnar hand and dorsum of the long finger proximal to the IPJ. If this area is spared and the palmar distal ulnar digits are affected, compression within Guyon’s canal is likely. If both areas are affected, suspect a more proximal compression site at the cubital tunnel, as the dorsal ulnar cutaneous nerve branches proximal to Guyon’s canal.²⁶

Ulnar motor nerve dysfunction in UTS is limited to the intrinsic muscles of the hand. Assessment of intrinsic muscle function is described in TABLE 3.^27-32 It is important to become familiar with the tests and maneuvers described, but also to be aware that a comprehensive evaluation of ulnar nerve motor function requires a combination of tests.

Cubital tunnel syndrome

Cubital tunnel syndrome—the second most common peripheral neuropathy⁸—involves the proximal site of ulnar nerve compression in the upper extremity. Patients typically report symptoms similar to those of UTS, with sensory paresthesia in the ulnar digits and intrinsic weakness. To learn more about the symptoms, ask if the onset of pain or paresthesia is related to a particular elbow position, such as increased elbow flexion.

Notably, pain is usually not the initial complaint, unless the disease is advanced. This may be the reason atrophic intrinsic changes are 4 times more likely to be seen in patients with cubital tunnel syndrome than in those with CTS.³³ You’re more likely to hear about vague motor problems, including hand clumsiness and difficulty with fine coordination of the fingers.³⁴ Thus, it is important to evaluate patients for concurrent UTS and/or CTS, as well as for differentiation.

Focus on the elbow. Whenever you suspect cubital tunnel syndrome, pay special attention to the elbow. Examine the carrying angle of the elbow in relation to the contralateral extremity. Deformity may provide clues to a history of trauma. Assess the ulnar nerve during active flexion and extension to identify a subluxatable nerve at the cubital tunnel. Examine the ulno-humeral joint for crepitus, and palpate the joint line for large osteophytes and/or ganglion cysts.

Motor examination of the ulnar nerve primarily focuses on the intrinsic muscles detailed in TABLE 3,^27-32 although the flexor carpi ulnaris (FCU) and flexor digitorum profundus (FDP) to the ring finger and small finger are also innervated by the ulnar nerve. The FCU mediates the power grip, and can be tested by resisted wrist flexion and ulnar deviation. Ring finger and small finger FDP strength should be examined by resistance testing at the distal IPJ.

Provocative testing of cubital tunnel syndrome includes Tinel’s sign (performed over the cubital tunnel), the elbow flexion test (performed with elbow in maximum flexion and wrist at neutral position and held for 60 seconds), and the pressure provocation test (performed by applying pressure to the ulnar nerve just proximal to the cubital tunnel with your index and long fingers for 60 seconds while the patient’s elbow is at 20° flexion with the forearm supinated). For each test, eliciting distal paresthesia in ulnar nerve territory is a positive result. The sensitivity of these tests ranges from 70% (Tinel’s sign) to 98% (combined elbow flexion and pressure); specificity ranges from 95% to 99%.³⁵

The scratch collapse test for cubital tunnel syndrome evaluation is similar to the version used to assess for CTS; the only difference is the location of the site that is scratched, in this case the cubital tunnel. The reported sensitivity and specificity are 69% and 99%, respectively.¹¹

Wartenberg’s syndrome

When you suspect ulnar tunnel syndrome, palpate the wrist and hand in an attempt to locate a mass or area of tenderness.

When a patient reports paresthesia or pain along the radial aspect of the forearm that radiates into the dorsal thumb and index and middle fingers, consider Wartenberg’s syndrome—compression of the superficial radial nerve. The condition, also known as “cheiralgia paresthetica,” may exist anywhere along the course of the nerve in the forearm,³⁶ but the compression typically occurs 9 cm proximal to the radial styloid.

Assess the skin over the forearm and hand for evidence of prior trauma, surgical scars, or external compression sources, such as a watch.^37-39 Then use palpation to identify superficial or deep masses along the nerve.⁴⁰ Perform Tinel’s sign by lightly tapping along the nerve course from proximal to distal in the forearm. The test is positive if paresthesias are provoked distally.^41,42

Motor function of the extremity is unaffected in Wartenberg’s syndrome, unless a prior traumatic injury occurred or a comorbidity exists. Comorbidities to consider include de Quervain’s tenosynovitis, cervical radiculopathy, injury to the lateral antebrachial cutaneous nerve, and CTS.

Gross sensory testing usually is negative, but 2-point discrimination may show diminished responses. Testing distribution includes the dorsal radial wrist and hand, dorsal thumb skin proximal to the IPJ, and the dorsal surface of the index, middle, and radial half of the ring finger proximal to the IPJ.

Proceed with caution. Provocative testing with a pronated forearm and a flexed and ulnar-deviated wrist may exacerbate symptoms,^12,42 and Finkelstein’s maneuver (isolated ulnar deviation at the wrist to elicit pain over the first dorsal wrist compartment) and Phalen’s test may elicit false-positive results. Upper motor neuron exams (ie, deep tendon reflexes) and Hoffman’s sign (reflexive flexion of the terminal phalanges of the thumb and index finger induced by flicking or tapping the distal phalanx of the long finger) should be symmetric to the contralateral extremity.

In patients with more than one compression injury, Spurling’s sign (neck extension and lateral rotation towards the affected extremity) may induce paresthesia when combined with axial compression, while the shoulder abduction test (shoulder 90° abduction, with external rotation) may diminish reported paresthesia. In those for whom Wartenberg’s syndrome is their only compression injury, however, these provocative maneuvers will be negative.

Anterior interosseous nerve syndrome

A rare clinical entity that affects the anterior interosseous innervated muscles in the forearm, anterior interosseous nerve syndrome (AINS)’s etiology is unclear. But it is likely related to a spontaneous neuritis rather than a compressive etiology.⁴³ Paresis or paralysis of the flexor pollicis longus (FPL) and the flexor digitorum profundus (FDP) of the index and long finger is its hallmark, but patients may report vague forearm pain associated with weakness or absence of function.

Examination begins with a visual assessment and palpation of the forearm and hand for atrophy or a space-occupying lesion. Notably, sensory function of the hand should remain at baseline despite the motor dysfunction, as the anterior interosseous is purely a motor nerve.

Motor testing should focus on the median and anterior interosseous innervated muscles.

The FPL is tested by isolated thumb IPJ flexion and the Kiloh and Nevin sign—the inability to make an “OK” sign with the thumb and index finger.⁴⁴ Assess pinch grasp with a maximally flexed thumb IPJ and distal IPJ of the index finger. Anterior interosseous nerve dysfunction results in a flattened pinch without IPJ or distal IPJ flexion, which increases the contact of the thumb and index finger pulp.⁴⁵ In a series of 14 patients, researchers reported complete paralysis of FPL and FDP index finger in 5 patients, isolated paralysis of FPL in 7 patients, and isolated paralysis of FDP index and long fingers in 2 patients. None had isolated paralysis of the FDP long finger.⁴⁶FIGURE 4 shows complete (A) and incomplete (B) paralysis.

Pain is usually not the initial complaint with cubital tunnel syndrome. You're more likely to hear about hand clumsiness and difficulty with fine coordination of the fingers.

Evaluation of AINS also includes assessment of FPL and FDP tendon integrity with passive tenodesis. The appearance of the hand at rest should reflect the natural digital cascade. In a completely relaxed or anesthetized hand, the forearm is placed in wrist supination and extension, allowing gravity to extend the wrist and placing the thumb MCPJ at 30° flexion, the index finger MCPJ at 40°, and the small finger MCPJ at 70°. The thumb IPJ should approximate the radial fingertip pulp of the index finger. The forearm is then pronated and flexed at the wrist, straightening the thumb MCPJ and producing a mild flexion cascade at the proximal and distal IPJ of the index, long, ring, and small fingers within 20° of full extension. This dynamic exercise is used to confirm that the patient has an intact tenodesis effect, thus excluding tendon lacerations or ruptures from the differential diagnosis. In one study, in 9 of 33 cases of partial or complete isolated index finger FPL or FDP, paralysis was initially diagnosed as tendon rupture.⁴⁷

When to consider electrodiagnostic testing

Electrodiagnostic testing—a combination of electromyography and nerve conduction studies to assess the status of a peripheral nerve⁴⁸—provides objective data that can help diagnose a challenging presentation, rule out a competing diagnosis, or clarify an atypical clinical picture or vague subjective history. This type of testing is also used to localize the entrapment site, identify a patient with polyneuropathy or brachial plexopathy, and assess the severity of nerve injury or presence of a double crush syndrome.^49,50 Any patient with signs and symptoms of a compression neuropathy and supportive findings on physical exam should be referred for electrodiagnostic testing and/or to a surgeon specializing in treating these conditions.

CORRESPONDENCE
Kyle J. MacGillis, MD, University of Illinois at Chicago, Department of Orthopaedic Surgery, 835 South Wolcott Avenue, M/C 844, Chicago, IL 60612; [email protected].

Neuropathic hand complaints—for which patients typically seek medical attention when the pain or paresthesia starts to interfere with their daily routine—are common and diverse. The ability to assess and accurately diagnose upper extremity compression neuropathies is critical for physicians in primary care.

Assessment starts, of course, with a thorough history of the present illness and past medical history, which helps define a broad differential diagnosis and identify comorbidities. Physical examination, including judicious use of provocative testing, allows you to objectively identify the pathologic deficit, evaluate function and coordination of multiple organ systems, and detect nerve dysfunction. The results determine whether additional tools, such as electrodiagnostic testing, are needed.

We’ve created this guide, detailed in the text, tables, and figures that follow, to help you hone your ability to accurately diagnose patients who present with compression neuropathies of the hand.

The medical history: Knowing what to ask

To clearly define a patient’s symptoms and disability, start with a thorough history of the presenting complaint.

Inquire about symptom onset and chronicity. Did the pain or paresthesia begin after an injury? Are the symptoms associated with repetitive use of the extremity? Do they occur at night?

Pinpoint the location or distribution of pain or paresthesia. It is paramount to identify the affected nerve.^1,2 Ask patients to complete a hand or upper extremity profile documenting location and/or type of numbness, tingling, or decreased sensation. A diagram of the peripheral nerves responsible for sensory innervation of the hand (FIGURE 1) is an effective way to screen individuals at high risk of carpal tunnel syndrome (CTS) or ulnar tunnel syndrome (UTS).^1,2

A patient report such as, “My whole hand is numb,” calls for a follow-up question to determine whether the little finger is affected,³ which would indicate that the ulnar nerve, rather than just the median nerve, is involved. And if a patient reports feeling as if he or she is wearing gloves or mittens, it is essential to consider the possibility of a systemic neuropathy rather than a single peripheral neuropathy.³

Gather basic patient information. Inquire about hand dominance, occupation, and baseline function, any or all of which may be critical in the assessment and initiation of treatment.^4,5

Review systemic conditions and medications

A broad range of comorbidities, such as cervical radiculopathy, diabetes, hypothyroidism, and vitamin deficiencies (TABLE 1),^6,7 may be responsible for neuropathic hand complaints, and a thorough review of systemic complaints and past medical history is critical. Include a medication history and a review of prior procedures, such as post-traumatic surgeries of the hand or upper extremity or nerve decompression surgeries, which may provide additional insight into disease etiology.

Symptoms guide physical exam, provocative testing

A physical examination, including provocative testing, follows based on reported symptoms, medical history, and suspected source of nerve compression.

Carpal tunnel syndrome

CTS is the most common peripheral neuropathy.⁸ Patients often report nocturnal pain or paresthesia in the distal median nerve distribution, comprising the palmar surface of the thumb, index, middle, and radial half of the ring finger.

Researchers have identified 6 standardized clinical criteria for the diagnosis of CTS. Two criteria—numbness mostly in median nerve territory and nocturnal numbness—can be ascertained during the history of present illness.The other 4, detailed below, will be found during the physical exam.⁹

Thenar weakness or atrophy.⁹ Begin your evaluation by inspecting the thenar musculature for atrophic changes. Motor exam of intrinsic musculature innervated by the recurrent motor branch of the median nerve includes assessment of thumb abduction strength (assessed by applying resistance to the metacarpophalangeal joint [MCPJ] base towards the palm in the position of maximal abduction) and opposition strength (assessed by applying force to the MCPJ from the ulnar aspect).¹⁰

Positive Phalen’s test.⁹ Provocative testing for CTS includes Phalen’s test (sensitivity 43%-86%, specificity 48%-67%),¹¹ which is an attempt to reproduce the numbness or tingling in the median nerve territory within 60 seconds of full wrist flexion. Ask the patient to hold his or her forearms vertically with elbows resting on the table (allowing gravity to flex the wrists),¹² and to tell you if numbness or tingling occurs.

Consider the possibility of a systemic neuropathy in patients who report that they feel as though they are wearing gloves.

Positive Tinel’s sign.⁹ Tinel’s sign (sensitivity 45%-75%, specificity 48%-67%)¹¹ is performed by lightly tapping the median nerve from the proximal to distal end over the carpal tunnel. The test is positive if paresthesia results. Provocative testing may also include Durkan’s test, also known as the carpal compression test. Durkan’s test (sensitivity 49%-89%, specificity 54%-96%)¹¹ involves placing your thumb directly over the carpal tunnel and holding light compression for 60 seconds, or until paresthesia is reported.

Positive 2-point discrimination test.⁹ To assess CTS disease severity, use 2-point discrimination to evaluate the patient’s sensation qualitatively and quantitatively. Two-point discrimination can only be tested, however, if light touch sensation is intact. It is typically performed by lightly applying 2 caliper points at fixed distances sufficient to blanch the skin, but some clinicians have used other tools, such as a modified paperclip.¹³ The smallest distance at which the patient can detect 2 distinct stimuli is then recorded.

Researchers have reported an average of 3 to 5 mm for 2-point discrimination at the fingertipand a normal 2-point discrimination of 6 to 9 mm in the volar surface of the hand (TABLE 2).^14,15

The scratch collapse test (sensitivity 64%, specificity 99%) is a supplemental exam that uses a different outcome measure to diagnose CTS.¹⁶ It involves lightly scratching the skin over the compressed carpal tunnel while the patient performs sustained resisted bilateral shoulder external rotation in an adducted position. A momentary loss of muscle resistance to external rotation indicates a positive test.

Pronator syndrome

Pronator syndrome (PS) is a proximal median neuropathy that may present in isolation or in combination with CTS as a double crush syndrome. Clinical symptoms include features of CTS and sensory paresthesias in the palm and distal forearm in the distribution of the palmar cutaneous branch of the median nerve. PS is commonly associated with volar proximal forearm pain exacerbated by repetitive activities involving pronation and supination.

PS is not easy to assess. Palpatory examination of a large supracondylar process at the distal humerus proximal to the medial epicondyle on its anteromedial aspect can be difficult, especially if the patient is overweight. And motor weakness is not a prominent feature. What’s more, power assessment of the pronator teres, flexor carpi radialis, and flexor digitorum superficialis may exacerbate symptoms.

Because the symptoms of PS and CTS may be the same, PS provocation maneuvers should be performed on patients with CTS symptoms and paresthesia involving the palm. Start by testing for Tinel’s sign over the pronator teres muscle, although this has been found to be positive in less than 50% of PS cases.¹⁷ Palpate the antecubital fossa and the proximal aspect of the pronator teres muscle to assess for discomfort or tenderness.

Pronator compression test. The pronator compression test has been found to be the most sensitive way to assess PS.^18,19 This test involves direct compression of the proximal and radial edge of the pronator teres muscle belly along the proximal volar forearm with the thumb.²⁰ It is performed bilaterally on supinated upper extremities, with the clinician applying pressure on each forearm simultaneously (FIGURE 2). If the symptoms in the hand are reproduced in ≤30 seconds, the test is positive. In a study of 10 patients with surgically confirmed PS, the pronator compression test was positive in every case.^20,21

Resistance testing. You can also evaluate the pronator teres compression site by testing the patient’s ability to resist pronation with his or her elbow extended and the forearm in neutral position. To test for compression from the bicipital aponeurosis, ask the patient to flex the elbow to approximately 120° to 130° and apply active supinated resistance.²² Likewise, resistance of the long finger proximal interphalangeal joint (IPJ) to flexion—a maneuver performed with elbow fully extended—assesses compression from the fibrous arcade of the flexor digitorum superficialis (FDS).²¹ A positive resistance test will reproduce the reported symptoms.

Ulnar tunnel syndrome

Symptoms of UTS, which is much less common than CTS, include pain in the wrist and hand that is associated with paresthesia or numbness in the small finger and ulnar half of the ring finger. Patients may report difficulty with motor tasks involving grip and pinch strength or fatigue with prolonged action of the intrinsic muscles. Many also report an exacerbation of symptoms associated with increased wrist flexion or at night.

Evaluation of UTS requires a full assessment of the upper extremity, starting with observation of hand posture and muscle bulk to identify signs of chronic nerve compression. The contralateral extremity serves as a control to the neuropathic hand. Classically, chronic ulnar nerve compression leads to intrinsic muscle atrophy, evidenced by loss of topographical soft tissue bulk in the first dorsal web space, the palmar transverse metacarpal arch, and the hypothenar area.²³ Ulnar motor nerve dysfunction is limited to the intrinsic muscles of the hand. The inverted pyramid sign, signified by atrophy of the transverse head of the adductor pollicis, is another visual aberrancy,²⁴ as is clawing of the ring finger and small finger. The clawing, which involves hyperextension of the MCPJ and flexion of the proximal and distal IPJ, is commonly known as Duchenne’s sign. FIGURE 3 demonstrates hypothenar atrophy and the loss of muscle bulk in the first dorsal web space.

When you suspect UTS, palpate the wrist and hand in an attempt to locate a mass or area of tenderness. Not all patients with a volar ganglion cyst responsible for UTS present with a palpable mass, but tenderness along the radial aspect of the pisiform or an undefined fullness in this area may be noted.²⁵ Any patient with a palpable mass should be tested for Tinel’s sign over the mass and undergo a thorough vascular assessment. Fracture of the hook of the hamate is indicated by tenderness in the region approximated by the intersection of Kaplan’s line and the proximal extension line from the ring finger.

Perform 2-point discrimination testing at the palmar distal aspect of the small finger and ulnar half of the ring finger. This tests the superficial sensory division of the ulnar nerve that travels within Guyon’s canal. Testing the dorsal ulnar cutaneous nerve involves the skin of the dorso-ulnar hand and dorsum of the long finger proximal to the IPJ. If this area is spared and the palmar distal ulnar digits are affected, compression within Guyon’s canal is likely. If both areas are affected, suspect a more proximal compression site at the cubital tunnel, as the dorsal ulnar cutaneous nerve branches proximal to Guyon’s canal.²⁶

Ulnar motor nerve dysfunction in UTS is limited to the intrinsic muscles of the hand. Assessment of intrinsic muscle function is described in TABLE 3.^27-32 It is important to become familiar with the tests and maneuvers described, but also to be aware that a comprehensive evaluation of ulnar nerve motor function requires a combination of tests.

Cubital tunnel syndrome

Cubital tunnel syndrome—the second most common peripheral neuropathy⁸—involves the proximal site of ulnar nerve compression in the upper extremity. Patients typically report symptoms similar to those of UTS, with sensory paresthesia in the ulnar digits and intrinsic weakness. To learn more about the symptoms, ask if the onset of pain or paresthesia is related to a particular elbow position, such as increased elbow flexion.

Notably, pain is usually not the initial complaint, unless the disease is advanced. This may be the reason atrophic intrinsic changes are 4 times more likely to be seen in patients with cubital tunnel syndrome than in those with CTS.³³ You’re more likely to hear about vague motor problems, including hand clumsiness and difficulty with fine coordination of the fingers.³⁴ Thus, it is important to evaluate patients for concurrent UTS and/or CTS, as well as for differentiation.

Focus on the elbow. Whenever you suspect cubital tunnel syndrome, pay special attention to the elbow. Examine the carrying angle of the elbow in relation to the contralateral extremity. Deformity may provide clues to a history of trauma. Assess the ulnar nerve during active flexion and extension to identify a subluxatable nerve at the cubital tunnel. Examine the ulno-humeral joint for crepitus, and palpate the joint line for large osteophytes and/or ganglion cysts.

Motor examination of the ulnar nerve primarily focuses on the intrinsic muscles detailed in TABLE 3,^27-32 although the flexor carpi ulnaris (FCU) and flexor digitorum profundus (FDP) to the ring finger and small finger are also innervated by the ulnar nerve. The FCU mediates the power grip, and can be tested by resisted wrist flexion and ulnar deviation. Ring finger and small finger FDP strength should be examined by resistance testing at the distal IPJ.

Provocative testing of cubital tunnel syndrome includes Tinel’s sign (performed over the cubital tunnel), the elbow flexion test (performed with elbow in maximum flexion and wrist at neutral position and held for 60 seconds), and the pressure provocation test (performed by applying pressure to the ulnar nerve just proximal to the cubital tunnel with your index and long fingers for 60 seconds while the patient’s elbow is at 20° flexion with the forearm supinated). For each test, eliciting distal paresthesia in ulnar nerve territory is a positive result. The sensitivity of these tests ranges from 70% (Tinel’s sign) to 98% (combined elbow flexion and pressure); specificity ranges from 95% to 99%.³⁵

The scratch collapse test for cubital tunnel syndrome evaluation is similar to the version used to assess for CTS; the only difference is the location of the site that is scratched, in this case the cubital tunnel. The reported sensitivity and specificity are 69% and 99%, respectively.¹¹

Wartenberg’s syndrome

When you suspect ulnar tunnel syndrome, palpate the wrist and hand in an attempt to locate a mass or area of tenderness.

When a patient reports paresthesia or pain along the radial aspect of the forearm that radiates into the dorsal thumb and index and middle fingers, consider Wartenberg’s syndrome—compression of the superficial radial nerve. The condition, also known as “cheiralgia paresthetica,” may exist anywhere along the course of the nerve in the forearm,³⁶ but the compression typically occurs 9 cm proximal to the radial styloid.

Assess the skin over the forearm and hand for evidence of prior trauma, surgical scars, or external compression sources, such as a watch.^37-39 Then use palpation to identify superficial or deep masses along the nerve.⁴⁰ Perform Tinel’s sign by lightly tapping along the nerve course from proximal to distal in the forearm. The test is positive if paresthesias are provoked distally.^41,42

Motor function of the extremity is unaffected in Wartenberg’s syndrome, unless a prior traumatic injury occurred or a comorbidity exists. Comorbidities to consider include de Quervain’s tenosynovitis, cervical radiculopathy, injury to the lateral antebrachial cutaneous nerve, and CTS.

Gross sensory testing usually is negative, but 2-point discrimination may show diminished responses. Testing distribution includes the dorsal radial wrist and hand, dorsal thumb skin proximal to the IPJ, and the dorsal surface of the index, middle, and radial half of the ring finger proximal to the IPJ.

Proceed with caution. Provocative testing with a pronated forearm and a flexed and ulnar-deviated wrist may exacerbate symptoms,^12,42 and Finkelstein’s maneuver (isolated ulnar deviation at the wrist to elicit pain over the first dorsal wrist compartment) and Phalen’s test may elicit false-positive results. Upper motor neuron exams (ie, deep tendon reflexes) and Hoffman’s sign (reflexive flexion of the terminal phalanges of the thumb and index finger induced by flicking or tapping the distal phalanx of the long finger) should be symmetric to the contralateral extremity.

In patients with more than one compression injury, Spurling’s sign (neck extension and lateral rotation towards the affected extremity) may induce paresthesia when combined with axial compression, while the shoulder abduction test (shoulder 90° abduction, with external rotation) may diminish reported paresthesia. In those for whom Wartenberg’s syndrome is their only compression injury, however, these provocative maneuvers will be negative.

Anterior interosseous nerve syndrome

A rare clinical entity that affects the anterior interosseous innervated muscles in the forearm, anterior interosseous nerve syndrome (AINS)’s etiology is unclear. But it is likely related to a spontaneous neuritis rather than a compressive etiology.⁴³ Paresis or paralysis of the flexor pollicis longus (FPL) and the flexor digitorum profundus (FDP) of the index and long finger is its hallmark, but patients may report vague forearm pain associated with weakness or absence of function.

Examination begins with a visual assessment and palpation of the forearm and hand for atrophy or a space-occupying lesion. Notably, sensory function of the hand should remain at baseline despite the motor dysfunction, as the anterior interosseous is purely a motor nerve.

Motor testing should focus on the median and anterior interosseous innervated muscles.

The FPL is tested by isolated thumb IPJ flexion and the Kiloh and Nevin sign—the inability to make an “OK” sign with the thumb and index finger.⁴⁴ Assess pinch grasp with a maximally flexed thumb IPJ and distal IPJ of the index finger. Anterior interosseous nerve dysfunction results in a flattened pinch without IPJ or distal IPJ flexion, which increases the contact of the thumb and index finger pulp.⁴⁵ In a series of 14 patients, researchers reported complete paralysis of FPL and FDP index finger in 5 patients, isolated paralysis of FPL in 7 patients, and isolated paralysis of FDP index and long fingers in 2 patients. None had isolated paralysis of the FDP long finger.⁴⁶FIGURE 4 shows complete (A) and incomplete (B) paralysis.

Pain is usually not the initial complaint with cubital tunnel syndrome. You're more likely to hear about hand clumsiness and difficulty with fine coordination of the fingers.

Evaluation of AINS also includes assessment of FPL and FDP tendon integrity with passive tenodesis. The appearance of the hand at rest should reflect the natural digital cascade. In a completely relaxed or anesthetized hand, the forearm is placed in wrist supination and extension, allowing gravity to extend the wrist and placing the thumb MCPJ at 30° flexion, the index finger MCPJ at 40°, and the small finger MCPJ at 70°. The thumb IPJ should approximate the radial fingertip pulp of the index finger. The forearm is then pronated and flexed at the wrist, straightening the thumb MCPJ and producing a mild flexion cascade at the proximal and distal IPJ of the index, long, ring, and small fingers within 20° of full extension. This dynamic exercise is used to confirm that the patient has an intact tenodesis effect, thus excluding tendon lacerations or ruptures from the differential diagnosis. In one study, in 9 of 33 cases of partial or complete isolated index finger FPL or FDP, paralysis was initially diagnosed as tendon rupture.⁴⁷

When to consider electrodiagnostic testing

Electrodiagnostic testing—a combination of electromyography and nerve conduction studies to assess the status of a peripheral nerve⁴⁸—provides objective data that can help diagnose a challenging presentation, rule out a competing diagnosis, or clarify an atypical clinical picture or vague subjective history. This type of testing is also used to localize the entrapment site, identify a patient with polyneuropathy or brachial plexopathy, and assess the severity of nerve injury or presence of a double crush syndrome.^49,50 Any patient with signs and symptoms of a compression neuropathy and supportive findings on physical exam should be referred for electrodiagnostic testing and/or to a surgeon specializing in treating these conditions.

CORRESPONDENCE
Kyle J. MacGillis, MD, University of Illinois at Chicago, Department of Orthopaedic Surgery, 835 South Wolcott Avenue, M/C 844, Chicago, IL 60612; [email protected].