New guidelines for managing patients with nonvalvular atrial fibrillation recommend dabigatran, rivaroxaban, and apixaban, as well as warfarin, and call on physicians to use a more comprehensive stroke risk calculator.

"I think physicians are still learning how to use the newer anticoagulants, and this is something that will require time," said Dr. Craig T. January, chair of the AF guidelines committee, assembled by the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society.

The guidelines, published in Circulation and in the Journal of the American College of Cardiology, focus on nonvalvular AF and feature a detailed dosing chart organized by anticoagulant type and renal function, which is impaired in up to 20% of those with AF.

"The goal was to create a straightforward chart on how to use these drugs," said Dr. January, a clinician/scientist with the University of Wisconsin School of Medicine and Public Health, Madison.

© Graça Victoria/Thinkstockphotos.com

Dabigatran (Pradaxa) and rivaroxaban (Xarelto) are not recommended for AF patients with nonvalvular disease and end-stage kidney disease, either on or off dialysis, because of a lack of evidence from clinical trials regarding the balance of risks and benefits.

No recommendation was made for apixaban (Eliquis) in patients with severe or end-stage renal impairment, because of a lack of published data, although a recent secondary analysis of the ARISTOTLE (Apixaban for the Prevention of Stroke in Subjects With Atrial Fibrillation) trial suggests the direct factor Xa inhibitor provides the greatest reduction in major bleeding in patients with impaired renal function compared with warfarin (Eur. Heart J. 2012;33:2821-30).

The guidelines advise clinicians to evaluate renal function prior to initiating any of the direct thrombin or factor Xa inhibitors, and to reevaluate at least annually and when clinically indicated.

Previously, warfarin (Coumadin) was the only recommended anticoagulant in the 2006 guidelines. It’s admittedly cheaper, but the guidelines note that the novel anticoagulants eliminate dietary limitations and the need for repeated international normalized ratio (INR) monitoring, and have more predictable pharmacological profiles and fewer drug-drug interactions.

The oral agents have revolutionized the treatment of AF since entering the market in the past few years, but by no means replace warfarin.

For patients with nonvalvular AF who are well controlled and satisfied with warfarin therapy, the guidelines say, "It is not necessary to change to one of the newer agents," Dr. January observed.

Warfarin should also be used for valvular AF to manage patients with a mechanical heart valve or hemodynamically significant mitral stenosis because these populations were excluded from all three major trials – RE-LY (Randomized Evaluation of Long Term Anticoagulant Therapy With Dabigatran Etexilate), ROCKET-AF (An Efficacy and Safety Study of Rivaroxaban With Warfarin for the Prevention of Stroke and Non-Central Nervous System Systemic Embolism in Patients With Non-Valvular Atrial Fibrillation), and ARISTOTLE – that led to the approval of the newer anticoagulants.

Dabigatran is specifically not recommended for patients with a mechanical valve because of the potential for harm, which was recently recognized by the Food and Drug Administration.

The document includes a section on dose interruption and bridging therapy, which in part reflects the fact that the new oral agents carry a black box warning from the FDA because discontinuation can increase the risk of thromboembolism. In addition, reversal agents are in development, but they are not currently available should immediate reversal be needed.

The new recommendations will elicit discussion, but are not expected to be controversial like the updated cholesterol management guidelines recently released by the American College of Cardiology and the American Heart Association, Dr. January said.

Another noteworthy change is the diminished use of aspirin in preventing stroke. "Most of the published data have shown that aspirin is not as effective as full anticoagulation and that aspirin itself in many trials has little benefit. This was a point of a lot of discussion in the committee," he said.

To calculate stroke risk, the guidelines recommend that clinicians use the CHA₂DS₂-VASc (Congestive heart failure, Hypertension, Age 75 or older (doubled), Diabetes mellitus, Prior Stroke or TIA or thromboembolism (doubled), Vascular disease, Age 65 to 74 years, Sex category female) calculator because it has a broader score range (0 to 9) and includes a larger number of risk factors than the older CHADS₂ score.

"What the CHA₂DS₂-VASc provides is better discrimination for patients at the lower end of risk," Dr. January said. "I think there was uniform agreement in the committee that the CHA₂DS₂-VASc was the preferred risk calculator and that we should move on from the CHADS₂ score.

"The CHA₂DS₂-VASc score is an interesting score because, depending on how you implement it, women can never have a score of zero," he added. "In fact, there are data out of Europe in the last year that the risk of stroke in women [with AF] is really quite low for those under 65."

As with the 2006 guidelines, the new document emphasizes an increased role for using radiofrequency ablation in the treatment of AF. This reflects the continued evolution of the technology as an AF therapy, Dr. January said. As a result, RF ablation will be increasingly used for AF treatment, particularly in symptomatic patients.

The work of the writing committee was supported exclusively by the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society without commercial support. Dr. January and his coauthors reported no relevant industry relationships.

[email protected]

New guidelines for managing patients with nonvalvular atrial fibrillation recommend dabigatran, rivaroxaban, and apixaban, as well as warfarin, and call on physicians to use a more comprehensive stroke risk calculator.

"I think physicians are still learning how to use the newer anticoagulants, and this is something that will require time," said Dr. Craig T. January, chair of the AF guidelines committee, assembled by the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society.

The guidelines, published in Circulation and in the Journal of the American College of Cardiology, focus on nonvalvular AF and feature a detailed dosing chart organized by anticoagulant type and renal function, which is impaired in up to 20% of those with AF.

"The goal was to create a straightforward chart on how to use these drugs," said Dr. January, a clinician/scientist with the University of Wisconsin School of Medicine and Public Health, Madison.

© Graça Victoria/Thinkstockphotos.com

Dabigatran (Pradaxa) and rivaroxaban (Xarelto) are not recommended for AF patients with nonvalvular disease and end-stage kidney disease, either on or off dialysis, because of a lack of evidence from clinical trials regarding the balance of risks and benefits.

No recommendation was made for apixaban (Eliquis) in patients with severe or end-stage renal impairment, because of a lack of published data, although a recent secondary analysis of the ARISTOTLE (Apixaban for the Prevention of Stroke in Subjects With Atrial Fibrillation) trial suggests the direct factor Xa inhibitor provides the greatest reduction in major bleeding in patients with impaired renal function compared with warfarin (Eur. Heart J. 2012;33:2821-30).

The guidelines advise clinicians to evaluate renal function prior to initiating any of the direct thrombin or factor Xa inhibitors, and to reevaluate at least annually and when clinically indicated.

Previously, warfarin (Coumadin) was the only recommended anticoagulant in the 2006 guidelines. It’s admittedly cheaper, but the guidelines note that the novel anticoagulants eliminate dietary limitations and the need for repeated international normalized ratio (INR) monitoring, and have more predictable pharmacological profiles and fewer drug-drug interactions.

The oral agents have revolutionized the treatment of AF since entering the market in the past few years, but by no means replace warfarin.

For patients with nonvalvular AF who are well controlled and satisfied with warfarin therapy, the guidelines say, "It is not necessary to change to one of the newer agents," Dr. January observed.

Warfarin should also be used for valvular AF to manage patients with a mechanical heart valve or hemodynamically significant mitral stenosis because these populations were excluded from all three major trials – RE-LY (Randomized Evaluation of Long Term Anticoagulant Therapy With Dabigatran Etexilate), ROCKET-AF (An Efficacy and Safety Study of Rivaroxaban With Warfarin for the Prevention of Stroke and Non-Central Nervous System Systemic Embolism in Patients With Non-Valvular Atrial Fibrillation), and ARISTOTLE – that led to the approval of the newer anticoagulants.

Dabigatran is specifically not recommended for patients with a mechanical valve because of the potential for harm, which was recently recognized by the Food and Drug Administration.

The document includes a section on dose interruption and bridging therapy, which in part reflects the fact that the new oral agents carry a black box warning from the FDA because discontinuation can increase the risk of thromboembolism. In addition, reversal agents are in development, but they are not currently available should immediate reversal be needed.

The new recommendations will elicit discussion, but are not expected to be controversial like the updated cholesterol management guidelines recently released by the American College of Cardiology and the American Heart Association, Dr. January said.

Another noteworthy change is the diminished use of aspirin in preventing stroke. "Most of the published data have shown that aspirin is not as effective as full anticoagulation and that aspirin itself in many trials has little benefit. This was a point of a lot of discussion in the committee," he said.

To calculate stroke risk, the guidelines recommend that clinicians use the CHA₂DS₂-VASc (Congestive heart failure, Hypertension, Age 75 or older (doubled), Diabetes mellitus, Prior Stroke or TIA or thromboembolism (doubled), Vascular disease, Age 65 to 74 years, Sex category female) calculator because it has a broader score range (0 to 9) and includes a larger number of risk factors than the older CHADS₂ score.

"What the CHA₂DS₂-VASc provides is better discrimination for patients at the lower end of risk," Dr. January said. "I think there was uniform agreement in the committee that the CHA₂DS₂-VASc was the preferred risk calculator and that we should move on from the CHADS₂ score.

"The CHA₂DS₂-VASc score is an interesting score because, depending on how you implement it, women can never have a score of zero," he added. "In fact, there are data out of Europe in the last year that the risk of stroke in women [with AF] is really quite low for those under 65."

As with the 2006 guidelines, the new document emphasizes an increased role for using radiofrequency ablation in the treatment of AF. This reflects the continued evolution of the technology as an AF therapy, Dr. January said. As a result, RF ablation will be increasingly used for AF treatment, particularly in symptomatic patients.

The work of the writing committee was supported exclusively by the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society without commercial support. Dr. January and his coauthors reported no relevant industry relationships.

[email protected]

New guidelines for managing patients with nonvalvular atrial fibrillation recommend dabigatran, rivaroxaban, and apixaban, as well as warfarin, and call on physicians to use a more comprehensive stroke risk calculator.

"I think physicians are still learning how to use the newer anticoagulants, and this is something that will require time," said Dr. Craig T. January, chair of the AF guidelines committee, assembled by the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society.

The guidelines, published in Circulation and in the Journal of the American College of Cardiology, focus on nonvalvular AF and feature a detailed dosing chart organized by anticoagulant type and renal function, which is impaired in up to 20% of those with AF.

"The goal was to create a straightforward chart on how to use these drugs," said Dr. January, a clinician/scientist with the University of Wisconsin School of Medicine and Public Health, Madison.

© Graça Victoria/Thinkstockphotos.com

Dabigatran (Pradaxa) and rivaroxaban (Xarelto) are not recommended for AF patients with nonvalvular disease and end-stage kidney disease, either on or off dialysis, because of a lack of evidence from clinical trials regarding the balance of risks and benefits.

No recommendation was made for apixaban (Eliquis) in patients with severe or end-stage renal impairment, because of a lack of published data, although a recent secondary analysis of the ARISTOTLE (Apixaban for the Prevention of Stroke in Subjects With Atrial Fibrillation) trial suggests the direct factor Xa inhibitor provides the greatest reduction in major bleeding in patients with impaired renal function compared with warfarin (Eur. Heart J. 2012;33:2821-30).

The guidelines advise clinicians to evaluate renal function prior to initiating any of the direct thrombin or factor Xa inhibitors, and to reevaluate at least annually and when clinically indicated.

Previously, warfarin (Coumadin) was the only recommended anticoagulant in the 2006 guidelines. It’s admittedly cheaper, but the guidelines note that the novel anticoagulants eliminate dietary limitations and the need for repeated international normalized ratio (INR) monitoring, and have more predictable pharmacological profiles and fewer drug-drug interactions.

The oral agents have revolutionized the treatment of AF since entering the market in the past few years, but by no means replace warfarin.

For patients with nonvalvular AF who are well controlled and satisfied with warfarin therapy, the guidelines say, "It is not necessary to change to one of the newer agents," Dr. January observed.

Warfarin should also be used for valvular AF to manage patients with a mechanical heart valve or hemodynamically significant mitral stenosis because these populations were excluded from all three major trials – RE-LY (Randomized Evaluation of Long Term Anticoagulant Therapy With Dabigatran Etexilate), ROCKET-AF (An Efficacy and Safety Study of Rivaroxaban With Warfarin for the Prevention of Stroke and Non-Central Nervous System Systemic Embolism in Patients With Non-Valvular Atrial Fibrillation), and ARISTOTLE – that led to the approval of the newer anticoagulants.

Dabigatran is specifically not recommended for patients with a mechanical valve because of the potential for harm, which was recently recognized by the Food and Drug Administration.

The document includes a section on dose interruption and bridging therapy, which in part reflects the fact that the new oral agents carry a black box warning from the FDA because discontinuation can increase the risk of thromboembolism. In addition, reversal agents are in development, but they are not currently available should immediate reversal be needed.

The new recommendations will elicit discussion, but are not expected to be controversial like the updated cholesterol management guidelines recently released by the American College of Cardiology and the American Heart Association, Dr. January said.

Another noteworthy change is the diminished use of aspirin in preventing stroke. "Most of the published data have shown that aspirin is not as effective as full anticoagulation and that aspirin itself in many trials has little benefit. This was a point of a lot of discussion in the committee," he said.

To calculate stroke risk, the guidelines recommend that clinicians use the CHA₂DS₂-VASc (Congestive heart failure, Hypertension, Age 75 or older (doubled), Diabetes mellitus, Prior Stroke or TIA or thromboembolism (doubled), Vascular disease, Age 65 to 74 years, Sex category female) calculator because it has a broader score range (0 to 9) and includes a larger number of risk factors than the older CHADS₂ score.

"What the CHA₂DS₂-VASc provides is better discrimination for patients at the lower end of risk," Dr. January said. "I think there was uniform agreement in the committee that the CHA₂DS₂-VASc was the preferred risk calculator and that we should move on from the CHADS₂ score.

"The CHA₂DS₂-VASc score is an interesting score because, depending on how you implement it, women can never have a score of zero," he added. "In fact, there are data out of Europe in the last year that the risk of stroke in women [with AF] is really quite low for those under 65."

As with the 2006 guidelines, the new document emphasizes an increased role for using radiofrequency ablation in the treatment of AF. This reflects the continued evolution of the technology as an AF therapy, Dr. January said. As a result, RF ablation will be increasingly used for AF treatment, particularly in symptomatic patients.

The work of the writing committee was supported exclusively by the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society without commercial support. Dr. January and his coauthors reported no relevant industry relationships.

[email protected]

CASE: OBESE PATIENT REQUESTS TOTAL LAPAROSCOPIC HYSTERECTOMY
A 45-year-old woman (G2P2), who delivered both children by cesarean section, schedules an office visit for a complaint of abnormal uterine bleeding. She is obese, with a body mass index (BMI) of 35 kg/m², and has an enlarged uterus of approximately 14 weeks’ size with minimal descensus. An earlier trial of hormone therapy failed to provide relief. After you counsel her extensively about her treatment options, she elects to undergo total laparoscopic hysterectomy.

What anatomy would you review to help ensure the procedure’s success?

Although the vaginal route is preferred for hysterectomy, total laparoscopic hysterectomy is another minimally invasive option that offers lower morbidity and a shorter hospital stay than the abdominal approach.¹ Perhaps more than any other variable, the key to safe, efficient, and effective laparoscopic surgery is a comprehensive knowledge of anatomy. For example, a thorough understanding of the anatomy of the anterior abdominal wall is critical to laparoscopic entry.^2,3 Also, pelvic anatomy visualized two-dimensionally under magnification during traditional laparoscopy can look very different than it does during conventional surgery, due to the effects of the pneumoperitoneum, steep Trendelenburg position, and/or the use of uterine manipulators.³

The abdominal cavity is traditionally divided into nine regions. Regardless of the quadrants chosen for laparoscopic access, thorough knowledge of the relevant surface anatomy increases patient safety during surgery (FIGURE 1).

PRIMARY PORT PLACEMENT
Primary port placement, including insertion of the Veress needle, accounts for approximately 40% of laparoscopic complications.⁴ To help minimize complications, surgeons should ensure that the operating table remains level during placement. As the patient is moved into the Trendelenburg position, the great vessels are more in line with the 45-degree angle that most surgeons use when placing their Veress needle and primary trocar, which can lead to an increased risk of injury. Thus, proper positioning in relationship to anatomy is critical to successful laparoscopic surgery.

Veress or closed technique
Most gynecologists employ the closed method or Veress needle approach to establish pneumoperitoneum.^5,6 an initial intraperitoneal pressure below 10 mm Hg, regardless of a woman’s body habitus, height, or age, indicates correct placement of the Veress needle.^7,8 Vilos and colleagues demonstrated that Veress intraperitoneal pressure correlates positively with a woman’s weight and BMI and correlates negatively with her parity.⁸

Hasson or open technique
During the Hasson or open technique, many surgeons use the umbilical ring to gain entry into the abdominal cavity.⁹ Many view the umbilical ring as a window into the anterior abdominal wall, through which access to the peritoneal cavity can be achieved, but it can also be a site of hernia development.¹⁰ The shape of the umbilical ring can vary, appearing round or oval, but it also can be obliterated, slitted, or covered completely by a connecting band, which can result in more difficult laparoscopic entry.¹⁰

Palmer’s point
In the 1940s, the French gynecologist Raoul Palmer advocated placing the laparoscope at a point in the left midclavicular line, approximately 3 cm caudal to the costal margin, because visceral-parietal adhesions rarely were found there. Gynecologists still favor this entry site when intra-abdominal adhesions are likely, especially in patients with a history of significant adhesions or multiple previous pelvic surgeries.¹¹ In a study published by Agarwala and colleagues, which included 504 patients with intra-abdominal adhesions, left upper quadrant entry was found to be safe with a complication rate as low as 0.39%.¹²

If supraumbilical or left upper quadrant port sites are used, the surface anatomy of the spleen and stomach become relevant. The portion of the stomach that is in contact with the abdominal wall is represented roughly by a triangular area extending between the tip of the 10th left costal cartilage, the tip of the ninth right cartilage, and the end of the eighth left costal cartilage.¹³ The size and shape of the stomach differs by position. Some authors recommend emptying the stomach using a nasogastric or oral gastric tube prior to port insertion to avoid injury.¹²

The spleen can be mapped using the 10th rib as representing its long axis; vertically, the spleen is situated between the upper border of the ninth and lower border of the 11th ribs.¹³ In patients without splenic enlargement, the spleen should not be found below the rib cage.

Related article: Tips and techniques for robot-assisted laparoscopic myomectomy Arnold P. Advincula, MD, and Bich-Van Tran, MD (Surgical Technique, August 2013)

CASE CONTINUED
On the day of surgery, your patient is brought to the operating room. you use the Veress needle for insufflation. Your opening pressure is 5 mm Hg. You know that an opening pressure of less than 10 mm Hg indicates proper placement, so you continue on to place a 10-mm port. After inserting the primary umbilical port through the umbilicus, you decide to insert secondary ports through lower quadrants. Upon insertion, you note active bleeding at one of the secondary port sites.

How do you proceed?

VASCULAR ANATOMY OF THE ANTERIOR ABDOMINAL WALL
Understanding anterior abdominal wall anatomy and the course of the deep inferior and superficial epigastric vessels is essential to the safe placement of secondary laparoscopic ports. epigastric vessels are the most commonly injured vessels during laparoscopic surgery.^14,15 The inferior epigastric vessels originate at the external iliac, immediately above the inguinal ligament. They course medially to the round ligament and travel beneath the lateral third of the rectus abdominis muscle. Using anterior abdominal wall landmarks, the inferior epigastric artery can be identified midway between the anterior superior iliac spine and the pubic symphysis as it travels toward the umbilicus. The inferior epigastric artery also serves as the lateral boundary of Hesselbach’s triangle; the other two boundaries are the lateral edge of the rectus abdominis and the medial aspect of the inguinal ligament (FIGURE 2).¹³

As the inferior epigastric vessels course cranially, the distance from the midline
decreases. the average distance from the midline at the pubis is approximately
7.5 cm. At the umbilicus, it is approximately 4.6 cm.^16,17 The most efficient way to identify laparoscopically the inferior epigastric vessel is to first identify the round ligament. This can be done using a uterine manipulator to deviate the uterus to the contralateral side. Then observe the course of the inferior epigastric vessel just medial to the entry of the round ligament into the inguinal canal. The laparoscopic surgeon can then follow the course of the inferior epigastric vessels to determine the safest location for placement of secondary ports. Transillumination can identify the superficial epigastric vessels, which course within the subcutaneous tissue of the anterior abdominal wall, although it doesn’t identify the deep inferior epigastric vessels that are beneath the lateral third of the rectus muscle. The superficial epigastric vessels follow a course similar to that of the deep inferior epigastric vessels, however, and can serve as a surrogate to guide safe placement of accessory ports.¹⁷

Landmarks of the anterior abdominal wall during laparoscopic visualization can also guide placement of secondary ports. The median umbilical fold, which is the peritoneal covering of the umbilical ligament/urachus, travels between the bladder and umbilicus in the midline anterior abdominal wall. Immediately lateral is the medial umbilical fold, which is the peritoneal covering of the obliterated umbilical artery, a branch of the superior vesical artery that comes off the anterior trunk of the internal iliac artery.² The lateral umbilical folds are lateral to the medial umbilical fold and are the peritoneal covering of the deep inferior epigastric vessels. Identification of these anterior abdominal wall landmarks can assist the surgeon in placing lateral ports so as to avoid injury to these vessels.

Related article: How to avoid major vessel injury during gynecologic laparoscopy Michael Baggish, MD (Surgical Technique, August 2012)

MAJOR RETROPERITONEAL VESSELS
Although major retroperitoneal vessel injury is uncommon, occurring in only 0.3% to 1.0% of laparoscopic surgeries, it has the potential to be catastrophic.¹⁸ Therefore, an understanding of the surface anatomy of the major vessels is essential for midline port placement.

The abdominal aorta begins about 4 cm above the transpyloric line and extends to
2 cm inferior and to the left of the umbilicus, or, more accurately, to a point 2 cm left of the middle line on a line that passes through the highest points of the iliac crests. The point of termination of the abdominal aorta corresponds to the level of the fourth lumbar vertebra; a line drawn from it to a point midway between the anterior superior iliac spine and the symphysis pubis indicates the common and external iliac arteries. The common iliac is represented by the upper third of this line and the external iliac, by the remaining two-thirds.¹³

Related article: How to avoid intestinal and urinary tract injuries during gynecologic laparoscopy Michael Baggish, MD (Surgical Technique, October 2012)

OBESITY AND LAPAROSCOPIC SURGERY
Over two-thirds of the US adult population is now classified as overweight or obese.¹⁹ Research has shown that, compared with abdominal hysterectomy, laparoscopic surgery entails a shorter hospital stay, less blood loss, and fewer abdominal wall and wound infections, which are important advantages for this particular population.²⁰

Laparoscopic entry can be particularly challenging in the obese patient. A study by Hurd and colleagues showed that the mean umbilical location was 2.4 cm caudal to the bifurcation of the aorta in the overweight population and 2.9 cm caudal in the obese population.²¹ Because the bifurcation of the aorta is more cephalad to the umbilicus in overweight and obese patients, the laparoscopic surgeon can introduce the Veress needle at a steeper angle and more perpendicular to the abdominal wall than for a thinner patient (FIGURE 3).

RELEVANT NERVES OF THE ANTERIOR ABDOMINAL WALL
The iliohypogastric and ilioinguinal nerves are also at risk for injury with laterally placed trocars through direct trauma or nerve entrapment. These nerves emerge from the T12 to L1 and L1 to L2 regions, respectively, and course through the muscles of the anterior abdominal wall. Specifically, the iliohypogastric nerve penetrates the fascia of the internal oblique muscle, and the ilioinguinal nerve penetrates the fascia of the transverse abdominus muscle.²² Fascial closure at lateral port sites can also increase the risk of injury to those nerves (FIGURE 4).²³

CASE CONTINUED
As you continue your case, you have had to replace your right lower quadrant port several times. During the last insertion, you notice that you have an enlarging abdominal wall hematoma. You suspect that you have injured the inferior epigastric vessel.

How should it be repaired?

HOW TO PREVENT AND REPAIR INJURED DEEP INFERIOR EPIGASTRIC VESSELS
A thorough knowledge of anatomy is the most effective way to prevent these types of injuries. The use of bladeless radially expanding trocars and smooth conical-tip trocars that push the vessels away may result in fewer port-site bleeding complications and injuries than large pyramidal or cutting trocars.^24–26 It is important to inspect all ports sites at the end of any laparoscopic procedure because the port itself can tamponade an injured anterior abdominal wall vessel and obscure an injury.

If an injury occurs, leave the trocars in place until a plan for repair is devised. First, start by compressing the bleeding point by moving the cannula against it. Because there are two bleeding ends, the vessels must be sutured cephalad and caudad to the site of injury. The use of electrosurgical desiccation is usually less successful.²⁵ In obese patients we prefer to suture-ligate the bleeder intracorporeally or use a laparoscopic port closure device. In thin and pediatric patients, percutaneous suture ligation can be done easily.

Another option to control bleeding at the cannula site is placement of a Foley catheter to tamponade the vessel using a large balloon placed on tension.²⁷ If abdominal loop sutures are used to control bleeding, the sutures typically are left intact for 8 hours prior to removal.²⁵ If identification of the bleeding point is difficult, percutaneous placement of a suture ligature over a roll of gauze or using a Foley catheter to tamponade the bleeder can be helpful.

CASE RESOLVED
A laparoscopic port closure device is used to suture ligate the bleeding vessel. Hemostasis is achieved and the laparoscopic hysterectomy is completed without further complications.

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CASE: OBESE PATIENT REQUESTS TOTAL LAPAROSCOPIC HYSTERECTOMY
A 45-year-old woman (G2P2), who delivered both children by cesarean section, schedules an office visit for a complaint of abnormal uterine bleeding. She is obese, with a body mass index (BMI) of 35 kg/m², and has an enlarged uterus of approximately 14 weeks’ size with minimal descensus. An earlier trial of hormone therapy failed to provide relief. After you counsel her extensively about her treatment options, she elects to undergo total laparoscopic hysterectomy.

What anatomy would you review to help ensure the procedure’s success?

Although the vaginal route is preferred for hysterectomy, total laparoscopic hysterectomy is another minimally invasive option that offers lower morbidity and a shorter hospital stay than the abdominal approach.¹ Perhaps more than any other variable, the key to safe, efficient, and effective laparoscopic surgery is a comprehensive knowledge of anatomy. For example, a thorough understanding of the anatomy of the anterior abdominal wall is critical to laparoscopic entry.^2,3 Also, pelvic anatomy visualized two-dimensionally under magnification during traditional laparoscopy can look very different than it does during conventional surgery, due to the effects of the pneumoperitoneum, steep Trendelenburg position, and/or the use of uterine manipulators.³

The abdominal cavity is traditionally divided into nine regions. Regardless of the quadrants chosen for laparoscopic access, thorough knowledge of the relevant surface anatomy increases patient safety during surgery (FIGURE 1).

PRIMARY PORT PLACEMENT
Primary port placement, including insertion of the Veress needle, accounts for approximately 40% of laparoscopic complications.⁴ To help minimize complications, surgeons should ensure that the operating table remains level during placement. As the patient is moved into the Trendelenburg position, the great vessels are more in line with the 45-degree angle that most surgeons use when placing their Veress needle and primary trocar, which can lead to an increased risk of injury. Thus, proper positioning in relationship to anatomy is critical to successful laparoscopic surgery.

Veress or closed technique
Most gynecologists employ the closed method or Veress needle approach to establish pneumoperitoneum.^5,6 an initial intraperitoneal pressure below 10 mm Hg, regardless of a woman’s body habitus, height, or age, indicates correct placement of the Veress needle.^7,8 Vilos and colleagues demonstrated that Veress intraperitoneal pressure correlates positively with a woman’s weight and BMI and correlates negatively with her parity.⁸

Hasson or open technique
During the Hasson or open technique, many surgeons use the umbilical ring to gain entry into the abdominal cavity.⁹ Many view the umbilical ring as a window into the anterior abdominal wall, through which access to the peritoneal cavity can be achieved, but it can also be a site of hernia development.¹⁰ The shape of the umbilical ring can vary, appearing round or oval, but it also can be obliterated, slitted, or covered completely by a connecting band, which can result in more difficult laparoscopic entry.¹⁰

Palmer’s point
In the 1940s, the French gynecologist Raoul Palmer advocated placing the laparoscope at a point in the left midclavicular line, approximately 3 cm caudal to the costal margin, because visceral-parietal adhesions rarely were found there. Gynecologists still favor this entry site when intra-abdominal adhesions are likely, especially in patients with a history of significant adhesions or multiple previous pelvic surgeries.¹¹ In a study published by Agarwala and colleagues, which included 504 patients with intra-abdominal adhesions, left upper quadrant entry was found to be safe with a complication rate as low as 0.39%.¹²

If supraumbilical or left upper quadrant port sites are used, the surface anatomy of the spleen and stomach become relevant. The portion of the stomach that is in contact with the abdominal wall is represented roughly by a triangular area extending between the tip of the 10th left costal cartilage, the tip of the ninth right cartilage, and the end of the eighth left costal cartilage.¹³ The size and shape of the stomach differs by position. Some authors recommend emptying the stomach using a nasogastric or oral gastric tube prior to port insertion to avoid injury.¹²

The spleen can be mapped using the 10th rib as representing its long axis; vertically, the spleen is situated between the upper border of the ninth and lower border of the 11th ribs.¹³ In patients without splenic enlargement, the spleen should not be found below the rib cage.

Related article: Tips and techniques for robot-assisted laparoscopic myomectomy Arnold P. Advincula, MD, and Bich-Van Tran, MD (Surgical Technique, August 2013)

CASE CONTINUED
On the day of surgery, your patient is brought to the operating room. you use the Veress needle for insufflation. Your opening pressure is 5 mm Hg. You know that an opening pressure of less than 10 mm Hg indicates proper placement, so you continue on to place a 10-mm port. After inserting the primary umbilical port through the umbilicus, you decide to insert secondary ports through lower quadrants. Upon insertion, you note active bleeding at one of the secondary port sites.

How do you proceed?

VASCULAR ANATOMY OF THE ANTERIOR ABDOMINAL WALL
Understanding anterior abdominal wall anatomy and the course of the deep inferior and superficial epigastric vessels is essential to the safe placement of secondary laparoscopic ports. epigastric vessels are the most commonly injured vessels during laparoscopic surgery.^14,15 The inferior epigastric vessels originate at the external iliac, immediately above the inguinal ligament. They course medially to the round ligament and travel beneath the lateral third of the rectus abdominis muscle. Using anterior abdominal wall landmarks, the inferior epigastric artery can be identified midway between the anterior superior iliac spine and the pubic symphysis as it travels toward the umbilicus. The inferior epigastric artery also serves as the lateral boundary of Hesselbach’s triangle; the other two boundaries are the lateral edge of the rectus abdominis and the medial aspect of the inguinal ligament (FIGURE 2).¹³

As the inferior epigastric vessels course cranially, the distance from the midline
decreases. the average distance from the midline at the pubis is approximately
7.5 cm. At the umbilicus, it is approximately 4.6 cm.^16,17 The most efficient way to identify laparoscopically the inferior epigastric vessel is to first identify the round ligament. This can be done using a uterine manipulator to deviate the uterus to the contralateral side. Then observe the course of the inferior epigastric vessel just medial to the entry of the round ligament into the inguinal canal. The laparoscopic surgeon can then follow the course of the inferior epigastric vessels to determine the safest location for placement of secondary ports. Transillumination can identify the superficial epigastric vessels, which course within the subcutaneous tissue of the anterior abdominal wall, although it doesn’t identify the deep inferior epigastric vessels that are beneath the lateral third of the rectus muscle. The superficial epigastric vessels follow a course similar to that of the deep inferior epigastric vessels, however, and can serve as a surrogate to guide safe placement of accessory ports.¹⁷

Landmarks of the anterior abdominal wall during laparoscopic visualization can also guide placement of secondary ports. The median umbilical fold, which is the peritoneal covering of the umbilical ligament/urachus, travels between the bladder and umbilicus in the midline anterior abdominal wall. Immediately lateral is the medial umbilical fold, which is the peritoneal covering of the obliterated umbilical artery, a branch of the superior vesical artery that comes off the anterior trunk of the internal iliac artery.² The lateral umbilical folds are lateral to the medial umbilical fold and are the peritoneal covering of the deep inferior epigastric vessels. Identification of these anterior abdominal wall landmarks can assist the surgeon in placing lateral ports so as to avoid injury to these vessels.

Related article: How to avoid major vessel injury during gynecologic laparoscopy Michael Baggish, MD (Surgical Technique, August 2012)

MAJOR RETROPERITONEAL VESSELS
Although major retroperitoneal vessel injury is uncommon, occurring in only 0.3% to 1.0% of laparoscopic surgeries, it has the potential to be catastrophic.¹⁸ Therefore, an understanding of the surface anatomy of the major vessels is essential for midline port placement.

The abdominal aorta begins about 4 cm above the transpyloric line and extends to
2 cm inferior and to the left of the umbilicus, or, more accurately, to a point 2 cm left of the middle line on a line that passes through the highest points of the iliac crests. The point of termination of the abdominal aorta corresponds to the level of the fourth lumbar vertebra; a line drawn from it to a point midway between the anterior superior iliac spine and the symphysis pubis indicates the common and external iliac arteries. The common iliac is represented by the upper third of this line and the external iliac, by the remaining two-thirds.¹³

Related article: How to avoid intestinal and urinary tract injuries during gynecologic laparoscopy Michael Baggish, MD (Surgical Technique, October 2012)

OBESITY AND LAPAROSCOPIC SURGERY
Over two-thirds of the US adult population is now classified as overweight or obese.¹⁹ Research has shown that, compared with abdominal hysterectomy, laparoscopic surgery entails a shorter hospital stay, less blood loss, and fewer abdominal wall and wound infections, which are important advantages for this particular population.²⁰

Laparoscopic entry can be particularly challenging in the obese patient. A study by Hurd and colleagues showed that the mean umbilical location was 2.4 cm caudal to the bifurcation of the aorta in the overweight population and 2.9 cm caudal in the obese population.²¹ Because the bifurcation of the aorta is more cephalad to the umbilicus in overweight and obese patients, the laparoscopic surgeon can introduce the Veress needle at a steeper angle and more perpendicular to the abdominal wall than for a thinner patient (FIGURE 3).

RELEVANT NERVES OF THE ANTERIOR ABDOMINAL WALL
The iliohypogastric and ilioinguinal nerves are also at risk for injury with laterally placed trocars through direct trauma or nerve entrapment. These nerves emerge from the T12 to L1 and L1 to L2 regions, respectively, and course through the muscles of the anterior abdominal wall. Specifically, the iliohypogastric nerve penetrates the fascia of the internal oblique muscle, and the ilioinguinal nerve penetrates the fascia of the transverse abdominus muscle.²² Fascial closure at lateral port sites can also increase the risk of injury to those nerves (FIGURE 4).²³

CASE CONTINUED
As you continue your case, you have had to replace your right lower quadrant port several times. During the last insertion, you notice that you have an enlarging abdominal wall hematoma. You suspect that you have injured the inferior epigastric vessel.

How should it be repaired?

HOW TO PREVENT AND REPAIR INJURED DEEP INFERIOR EPIGASTRIC VESSELS
A thorough knowledge of anatomy is the most effective way to prevent these types of injuries. The use of bladeless radially expanding trocars and smooth conical-tip trocars that push the vessels away may result in fewer port-site bleeding complications and injuries than large pyramidal or cutting trocars.^24–26 It is important to inspect all ports sites at the end of any laparoscopic procedure because the port itself can tamponade an injured anterior abdominal wall vessel and obscure an injury.

If an injury occurs, leave the trocars in place until a plan for repair is devised. First, start by compressing the bleeding point by moving the cannula against it. Because there are two bleeding ends, the vessels must be sutured cephalad and caudad to the site of injury. The use of electrosurgical desiccation is usually less successful.²⁵ In obese patients we prefer to suture-ligate the bleeder intracorporeally or use a laparoscopic port closure device. In thin and pediatric patients, percutaneous suture ligation can be done easily.

Another option to control bleeding at the cannula site is placement of a Foley catheter to tamponade the vessel using a large balloon placed on tension.²⁷ If abdominal loop sutures are used to control bleeding, the sutures typically are left intact for 8 hours prior to removal.²⁵ If identification of the bleeding point is difficult, percutaneous placement of a suture ligature over a roll of gauze or using a Foley catheter to tamponade the bleeder can be helpful.

CASE RESOLVED
A laparoscopic port closure device is used to suture ligate the bleeding vessel. Hemostasis is achieved and the laparoscopic hysterectomy is completed without further complications.

Tell us what you think!
Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Share your thoughts by sending a letter to [email protected]. Please include the city and state in which you practice. Stay in touch! Your feedback is important to us!

CASE: OBESE PATIENT REQUESTS TOTAL LAPAROSCOPIC HYSTERECTOMY
A 45-year-old woman (G2P2), who delivered both children by cesarean section, schedules an office visit for a complaint of abnormal uterine bleeding. She is obese, with a body mass index (BMI) of 35 kg/m², and has an enlarged uterus of approximately 14 weeks’ size with minimal descensus. An earlier trial of hormone therapy failed to provide relief. After you counsel her extensively about her treatment options, she elects to undergo total laparoscopic hysterectomy.

What anatomy would you review to help ensure the procedure’s success?

Although the vaginal route is preferred for hysterectomy, total laparoscopic hysterectomy is another minimally invasive option that offers lower morbidity and a shorter hospital stay than the abdominal approach.¹ Perhaps more than any other variable, the key to safe, efficient, and effective laparoscopic surgery is a comprehensive knowledge of anatomy. For example, a thorough understanding of the anatomy of the anterior abdominal wall is critical to laparoscopic entry.^2,3 Also, pelvic anatomy visualized two-dimensionally under magnification during traditional laparoscopy can look very different than it does during conventional surgery, due to the effects of the pneumoperitoneum, steep Trendelenburg position, and/or the use of uterine manipulators.³

The abdominal cavity is traditionally divided into nine regions. Regardless of the quadrants chosen for laparoscopic access, thorough knowledge of the relevant surface anatomy increases patient safety during surgery (FIGURE 1).

PRIMARY PORT PLACEMENT
Primary port placement, including insertion of the Veress needle, accounts for approximately 40% of laparoscopic complications.⁴ To help minimize complications, surgeons should ensure that the operating table remains level during placement. As the patient is moved into the Trendelenburg position, the great vessels are more in line with the 45-degree angle that most surgeons use when placing their Veress needle and primary trocar, which can lead to an increased risk of injury. Thus, proper positioning in relationship to anatomy is critical to successful laparoscopic surgery.

Veress or closed technique
Most gynecologists employ the closed method or Veress needle approach to establish pneumoperitoneum.^5,6 an initial intraperitoneal pressure below 10 mm Hg, regardless of a woman’s body habitus, height, or age, indicates correct placement of the Veress needle.^7,8 Vilos and colleagues demonstrated that Veress intraperitoneal pressure correlates positively with a woman’s weight and BMI and correlates negatively with her parity.⁸

Hasson or open technique
During the Hasson or open technique, many surgeons use the umbilical ring to gain entry into the abdominal cavity.⁹ Many view the umbilical ring as a window into the anterior abdominal wall, through which access to the peritoneal cavity can be achieved, but it can also be a site of hernia development.¹⁰ The shape of the umbilical ring can vary, appearing round or oval, but it also can be obliterated, slitted, or covered completely by a connecting band, which can result in more difficult laparoscopic entry.¹⁰

Palmer’s point
In the 1940s, the French gynecologist Raoul Palmer advocated placing the laparoscope at a point in the left midclavicular line, approximately 3 cm caudal to the costal margin, because visceral-parietal adhesions rarely were found there. Gynecologists still favor this entry site when intra-abdominal adhesions are likely, especially in patients with a history of significant adhesions or multiple previous pelvic surgeries.¹¹ In a study published by Agarwala and colleagues, which included 504 patients with intra-abdominal adhesions, left upper quadrant entry was found to be safe with a complication rate as low as 0.39%.¹²

If supraumbilical or left upper quadrant port sites are used, the surface anatomy of the spleen and stomach become relevant. The portion of the stomach that is in contact with the abdominal wall is represented roughly by a triangular area extending between the tip of the 10th left costal cartilage, the tip of the ninth right cartilage, and the end of the eighth left costal cartilage.¹³ The size and shape of the stomach differs by position. Some authors recommend emptying the stomach using a nasogastric or oral gastric tube prior to port insertion to avoid injury.¹²

The spleen can be mapped using the 10th rib as representing its long axis; vertically, the spleen is situated between the upper border of the ninth and lower border of the 11th ribs.¹³ In patients without splenic enlargement, the spleen should not be found below the rib cage.

Related article: Tips and techniques for robot-assisted laparoscopic myomectomy Arnold P. Advincula, MD, and Bich-Van Tran, MD (Surgical Technique, August 2013)

CASE CONTINUED
On the day of surgery, your patient is brought to the operating room. you use the Veress needle for insufflation. Your opening pressure is 5 mm Hg. You know that an opening pressure of less than 10 mm Hg indicates proper placement, so you continue on to place a 10-mm port. After inserting the primary umbilical port through the umbilicus, you decide to insert secondary ports through lower quadrants. Upon insertion, you note active bleeding at one of the secondary port sites.

How do you proceed?

VASCULAR ANATOMY OF THE ANTERIOR ABDOMINAL WALL
Understanding anterior abdominal wall anatomy and the course of the deep inferior and superficial epigastric vessels is essential to the safe placement of secondary laparoscopic ports. epigastric vessels are the most commonly injured vessels during laparoscopic surgery.^14,15 The inferior epigastric vessels originate at the external iliac, immediately above the inguinal ligament. They course medially to the round ligament and travel beneath the lateral third of the rectus abdominis muscle. Using anterior abdominal wall landmarks, the inferior epigastric artery can be identified midway between the anterior superior iliac spine and the pubic symphysis as it travels toward the umbilicus. The inferior epigastric artery also serves as the lateral boundary of Hesselbach’s triangle; the other two boundaries are the lateral edge of the rectus abdominis and the medial aspect of the inguinal ligament (FIGURE 2).¹³

As the inferior epigastric vessels course cranially, the distance from the midline
decreases. the average distance from the midline at the pubis is approximately
7.5 cm. At the umbilicus, it is approximately 4.6 cm.^16,17 The most efficient way to identify laparoscopically the inferior epigastric vessel is to first identify the round ligament. This can be done using a uterine manipulator to deviate the uterus to the contralateral side. Then observe the course of the inferior epigastric vessel just medial to the entry of the round ligament into the inguinal canal. The laparoscopic surgeon can then follow the course of the inferior epigastric vessels to determine the safest location for placement of secondary ports. Transillumination can identify the superficial epigastric vessels, which course within the subcutaneous tissue of the anterior abdominal wall, although it doesn’t identify the deep inferior epigastric vessels that are beneath the lateral third of the rectus muscle. The superficial epigastric vessels follow a course similar to that of the deep inferior epigastric vessels, however, and can serve as a surrogate to guide safe placement of accessory ports.¹⁷

Landmarks of the anterior abdominal wall during laparoscopic visualization can also guide placement of secondary ports. The median umbilical fold, which is the peritoneal covering of the umbilical ligament/urachus, travels between the bladder and umbilicus in the midline anterior abdominal wall. Immediately lateral is the medial umbilical fold, which is the peritoneal covering of the obliterated umbilical artery, a branch of the superior vesical artery that comes off the anterior trunk of the internal iliac artery.² The lateral umbilical folds are lateral to the medial umbilical fold and are the peritoneal covering of the deep inferior epigastric vessels. Identification of these anterior abdominal wall landmarks can assist the surgeon in placing lateral ports so as to avoid injury to these vessels.

Related article: How to avoid major vessel injury during gynecologic laparoscopy Michael Baggish, MD (Surgical Technique, August 2012)

MAJOR RETROPERITONEAL VESSELS
Although major retroperitoneal vessel injury is uncommon, occurring in only 0.3% to 1.0% of laparoscopic surgeries, it has the potential to be catastrophic.¹⁸ Therefore, an understanding of the surface anatomy of the major vessels is essential for midline port placement.

The abdominal aorta begins about 4 cm above the transpyloric line and extends to
2 cm inferior and to the left of the umbilicus, or, more accurately, to a point 2 cm left of the middle line on a line that passes through the highest points of the iliac crests. The point of termination of the abdominal aorta corresponds to the level of the fourth lumbar vertebra; a line drawn from it to a point midway between the anterior superior iliac spine and the symphysis pubis indicates the common and external iliac arteries. The common iliac is represented by the upper third of this line and the external iliac, by the remaining two-thirds.¹³

Related article: How to avoid intestinal and urinary tract injuries during gynecologic laparoscopy Michael Baggish, MD (Surgical Technique, October 2012)

OBESITY AND LAPAROSCOPIC SURGERY
Over two-thirds of the US adult population is now classified as overweight or obese.¹⁹ Research has shown that, compared with abdominal hysterectomy, laparoscopic surgery entails a shorter hospital stay, less blood loss, and fewer abdominal wall and wound infections, which are important advantages for this particular population.²⁰

Laparoscopic entry can be particularly challenging in the obese patient. A study by Hurd and colleagues showed that the mean umbilical location was 2.4 cm caudal to the bifurcation of the aorta in the overweight population and 2.9 cm caudal in the obese population.²¹ Because the bifurcation of the aorta is more cephalad to the umbilicus in overweight and obese patients, the laparoscopic surgeon can introduce the Veress needle at a steeper angle and more perpendicular to the abdominal wall than for a thinner patient (FIGURE 3).

RELEVANT NERVES OF THE ANTERIOR ABDOMINAL WALL
The iliohypogastric and ilioinguinal nerves are also at risk for injury with laterally placed trocars through direct trauma or nerve entrapment. These nerves emerge from the T12 to L1 and L1 to L2 regions, respectively, and course through the muscles of the anterior abdominal wall. Specifically, the iliohypogastric nerve penetrates the fascia of the internal oblique muscle, and the ilioinguinal nerve penetrates the fascia of the transverse abdominus muscle.²² Fascial closure at lateral port sites can also increase the risk of injury to those nerves (FIGURE 4).²³

CASE CONTINUED
As you continue your case, you have had to replace your right lower quadrant port several times. During the last insertion, you notice that you have an enlarging abdominal wall hematoma. You suspect that you have injured the inferior epigastric vessel.

How should it be repaired?

HOW TO PREVENT AND REPAIR INJURED DEEP INFERIOR EPIGASTRIC VESSELS
A thorough knowledge of anatomy is the most effective way to prevent these types of injuries. The use of bladeless radially expanding trocars and smooth conical-tip trocars that push the vessels away may result in fewer port-site bleeding complications and injuries than large pyramidal or cutting trocars.^24–26 It is important to inspect all ports sites at the end of any laparoscopic procedure because the port itself can tamponade an injured anterior abdominal wall vessel and obscure an injury.

If an injury occurs, leave the trocars in place until a plan for repair is devised. First, start by compressing the bleeding point by moving the cannula against it. Because there are two bleeding ends, the vessels must be sutured cephalad and caudad to the site of injury. The use of electrosurgical desiccation is usually less successful.²⁵ In obese patients we prefer to suture-ligate the bleeder intracorporeally or use a laparoscopic port closure device. In thin and pediatric patients, percutaneous suture ligation can be done easily.

Another option to control bleeding at the cannula site is placement of a Foley catheter to tamponade the vessel using a large balloon placed on tension.²⁷ If abdominal loop sutures are used to control bleeding, the sutures typically are left intact for 8 hours prior to removal.²⁵ If identification of the bleeding point is difficult, percutaneous placement of a suture ligature over a roll of gauze or using a Foley catheter to tamponade the bleeder can be helpful.

CASE RESOLVED
A laparoscopic port closure device is used to suture ligate the bleeding vessel. Hemostasis is achieved and the laparoscopic hysterectomy is completed without further complications.

Tell us what you think!
Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Share your thoughts by sending a letter to [email protected]. Please include the city and state in which you practice. Stay in touch! Your feedback is important to us!

ANSWER

The radiograph shows the lungs overall to be clear. There are some slight increased markings, perhaps suggestive of mild congestion, but no infiltrate or consolidation.

Of note is a small nodule within the middle portion of the left upper lobe that requires monitoring and further workup. Also, although it is incompletely imaged, there appears to be a fracture of the right humeral neck.

Additional imaging confirmed the fracture. Orthopedic consultation was obtained.

ANSWER

The radiograph shows the lungs overall to be clear. There are some slight increased markings, perhaps suggestive of mild congestion, but no infiltrate or consolidation.

Of note is a small nodule within the middle portion of the left upper lobe that requires monitoring and further workup. Also, although it is incompletely imaged, there appears to be a fracture of the right humeral neck.

Additional imaging confirmed the fracture. Orthopedic consultation was obtained.

ANSWER

The radiograph shows the lungs overall to be clear. There are some slight increased markings, perhaps suggestive of mild congestion, but no infiltrate or consolidation.

Of note is a small nodule within the middle portion of the left upper lobe that requires monitoring and further workup. Also, although it is incompletely imaged, there appears to be a fracture of the right humeral neck.

Additional imaging confirmed the fracture. Orthopedic consultation was obtained.

A 45-year-old man, RT, with a six-month history of poorly controlled type 2 diabetes presents for evaluation of increased weakness and pain in the left lower extremity. The symptoms developed in the past three weeks. Previously able to ambulate without assistance, he purchased a cane yesterday due to concerns about falling.

RT reports poor adherence to his diabetes medications. His fingerstick blood sugars have ranged from 200 to 380 mg/dL over the past month. His weight has been stable; his BMI is 34. Review of other systems is negative. Vital signs include a blood pressure of 125/82 mm Hg; pulse, 74 beats/min; and respiratory rate, 16 breaths/min.

Physical examination is notable for muscle atrophy and tenderness to compression in the left quadriceps. Straight leg raise does not elicit pain bilaterally. Muscle strength is 4-/5 in the left hip with pain elicited on hip flexion, 4-/5 in the left knee, and 5/5 in the left ankle. Muscle strength is 4+/5 in the right hip, 5/5 in the right knee, and 5/5 in the right ankle. Muscle strength in both upper extremities is 5/5. Patellar deep tendon reflexes (DTRs) and ankle DTRs are absent bilaterally. Biceps and triceps DTRs are each 2+ bilaterally. Gait is slow and unsteady with use of the cane. Cranial nerves I-XII are intact. Sensation to sharp and dull testing is normal in both the upper and lower extremities.

Labwork reveals an A1C of 10.8%. The patient’s thyroid function studies, creatine kinase, and vitamin B₁₂ level are all in normal range. The serum creatinine is 1.2 mg/dL, and eGFR (estimated glomerular filtration rate) is 58 mL/min/1.73 m². Liver enzymes are normal, and complete blood count and other chemistry panels are unremarkable.

RT is referred to neurology. MRI of the thoracic and lumbar spine shows no mass lesions or disc disease. Electromyography reveals findings consistent with denervation and axonal damage in the proximal muscles in both lower extremities (left > right).

RT is diagnosed with diabetic amyotrophy and begins physical therapy three days a week. He achieves aggressive improvement in blood sugar control, and after three months, his A1C has improved to 7%.  Although still using a cane, he reports improved muscle strength in the lower extremities and better gait stability.

Continued on next page >>

PREVALENCE AND TYPES OF DIABETIC PERIPHERAL NEUROPATHY

According to the CDC, 25.8 million children and adults in the United States (8.3% of the population) have diabetes. Approximately 60% to 70% of them have mild to severe neuropathy.¹

Distal symmetric neuropathy is the most common form of diabetic peripheral neuropathy, accounting for more than 50% of cases. It is characterized by distal onset, predominately sensory polyneuropathy, and slow proximal progression.²

In contrast, diabetic amyotrophy is very rare, accounting for only 1% of all cases of neuropathy in diabetes. Prevalence is higher in those with type 2 versus type 1 diabetes (1.1% and 0.3%, respectively).^3,4 The most commonly misdiagnosed of the asymmetric diabetic neuropathies, diabetic amyotrophy is characterized by acute, progressive, asymmetrical weakness and pain in the muscles of the proximal lower extremities.⁵ It is also been referred to as proximal diabetic neuropathy, ischemic mononeuropathy multiplex, diabetic femoral neuropathy, Bruns-Garland syndrome, and diabetic lumbosacral polyradiculopathy.⁵

LOCALIZATION AND PATHOGENESIS

The site of the lesion in diabetic amyotrophy remains controversial; it is theorized that diabetic amyotrophy may result from involvement of multiple sites, such as lumbosacral anterior horn cells, motor roots, plexus, or motor axons to the muscles of the proximal lower limbs.⁴

The pathogenesis remains unknown. One theory is that hyperglycemia may cause metabolic derangements in nerve conduction. Another is that there is ischemic damage followed by axonal degeneration. Immune-mediated inflammatory processes, such as microvasculitis, have also been proposed as causes.^4,6

CLINICAL FEATURES

Diabetic amyotrophy is characterized by relatively rapid, progressive asymmetrical weakness and pain in the muscles in the proximal lower extremities; it develops over weeks to months and may continue for more than one year.^2,6 It typically begins unilaterally and can progress bilaterally—normally without impairment in sensation. Patients commonly experience pain in the hip, buttock, or thigh, as well as difficulty walking, standing, or climbing stairs. Occasionally, the condition is painless and can be associated with weight loss. It causes significant acute disability, with the degree of recovery variable.^2,4

Diabetic amyotrophy often presents either at diagnosis of diabetes or shortly thereafter. It most commonly affects men ages 40 to 50 and older, with higher incidence in type 2 diabetes.^2,5

Physical exam findings include proximal muscle weakness and atrophy in the quadriceps, hamstring, gluteal, hip adductors/abductors, and iliopsoas muscles.^4,5 Typically, there is no sensory impairment; however, mild sensory loss may be observed in patients with coexisting chronic distal sensorimotor polyneuropathy.^2,4 The patellar tendon reflexes are typically diminished or absent, and the ankle reflexes may be normal or diminished.⁴

Continued on next page >>

DIAGNOSTIC WORK-UP AND DIFFERENTIAL DIAGNOSIS

Although the diagnosis of diabetic amyotrophy is made primarily through detailed history taking and neurologic examination, other studies—electromyography, nerve conduction, imaging and labs, and nerve biopsy—may provide confirmation. Referral to neurology should also be considered.

The differential diagnosis is ­extensive and includes myopathies, muscular dystrophies, intervertebral disc disease, spinal stenosis, polyradiculopathies due to porphyria, amyloid, heavy metal poisoning, anterior horn cell diseases  (eg, poliomyelitis), neoplasms, chronic inflammatory demyelinating polyneuropathy, Guillain-Barré syndrome, monoclonal gammopathy, inflammatory vasculitis, hypothyroidism, vitamin B₆ or B₁₂ deficiencies, syphilis, AIDS, Lyme disease, and Charcot-Marie-Tooth disease.^2,5-7 Diabetic neuropathic cachexia should also be considered in the differential, as it presents with weight loss and lower limb pain but no weakness.⁵

Lab evaluation should begin with analysis of fasting plasma glucose, complete blood count, comprehensive metabolic profile, A1C, erythrocyte sedimentation rate (ESR), creatine kinase, vitamin B₁₂, and thyroid-stimulating hormone levels.⁷ Elevations in ESR and positive rheumatoid factor and antinuclear antibody can occur in patients with diabetic amyotrophy and are suggestive of a coexisting autoimmune disorder.⁶ Serum creatine kinase and thyroid function studies are normal.⁴ Additional lab tests, if clinically indicated, include paraneoplastic panel to evaluate for occult malignancy, antimyelin-associated glycoprotein antibodies, antiganglioside antibodies, cryoglobulins, cerebrospinal fluid analysis, porphyrin titers, and testing for heavy metals.⁷

Electrodiagnostic studies are recommended if the diagnosis of diabetic amyotrophy remains unclear following history taking, physical examination, and preliminary testing. Electromyography and nerve conduction studies typically reveal findings consistent with denervation and axonal damage in proximal muscles of the lower extremities.⁴ If demyelination is observed, a diagnosis of chronic demyelinating polyneuropathy should be considered.⁵

Nerve biopsy is considered if the diagnosis remains unclear after laboratory and electrodiagnostic testing or when confirmation of the diagnosis is needed before starting aggressive treatment. The sural and superficial peroneal nerves are preferred for biopsy. In cases of diabetic amyotrophy, sural nerve biopsy reveals significant fiber loss in an asymmetric fashion, resembling focal ischemia.⁵

MRI or CT scan of the lumbosacral spine is employed to exclude mass lesions and structural disorders such as spinal stenosis and disc disease.⁴ Cerebrospinal fluid is typically acellular, with a mildly elevated protein level of 60 to 100 mg/dL (but occasionally as high as 400 mg/dL).⁵

Continued on next page >>

PROGNOSIS AND MANAGEMENT

The course of diabetic amyo­trophy is variable. There is often gradual but incomplete restoration in muscle strength in correlation with aggressive glycemic control and physical therapy.² The majority of patients have residual muscle weakness, absent patellar and/or ankle DTRs, exercise-related pain, stiffness, and difficulty walking or climbing stairs. Full recovery of strength only occurs in 10% to 20% of patients.⁶

Treatment with IV immunoglobulin or other immuno­suppressive drugs is controversial. According to a Cochrane review of immunotherapy for diabetic amyotrophy, only one completed controlled trial using IV methylprednisolone was found. There is currently no evidence to support use of immunoglobulins to halt progression and improve symptoms.⁸

Neuropathic pain may be ­difficult to control. The severe pain associated with diabetic amyotrophy begins to diminish several months after onset, but residual pain may persist for several years. Pregabalin, duloxetine, tricyclic antidepressants, antiepileptic drugs, and narcotic analgesics can be helpful.^2,4 High doses of corticosteroids may lead to improvement of severe pain in some patients with diabetic amyotrophy.⁵

References >>

REFERENCES

1. CDC. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, 2011.

2. Nagsayi S, Somasekhar C, James CM. Diagnosis and management of diabetic amyotrophy. Geriatric Med. 2010;40:327-329.

3. Pasnoor M, Dimachkie MM, Kluding P, Barohn RJ. Diabetic neuropathy part 1: overview and symmetric phenotypes. Neurol Clin. 2013;31(2):425-445.

4. Sander HW, Chokroverty S. Diabetic amyotrophy: current concepts. Semin Neurol. 1996;16(2):173-177.

5. Pasnoor M, Dimachkie MM, Barohn RJ. Diabetic neuropathy part 2: proximal and asymmetric phenotypes. Neurol Clin. 2013;31(2): 447-462.

6. Idiculla J, Shirazi N, Opacka-Juffry J, Ganapathi. Diabetic amyotrophy: a brief review. Natl Med J India. 2004;17(4):
200-202.

7. Azhary H, Farooq M, Bhanushali M, Majid A. Peripheral neuropathy: differential diagnosis and management. Am Fam Physician. 2010;81(7):887-892.

8. Chan YC, Lo YL, Chan ES. Immunotherapy for diabetic amyotrophy. Cochrane Database Syst Rev. 2012;13(6):2-6.

A 45-year-old man, RT, with a six-month history of poorly controlled type 2 diabetes presents for evaluation of increased weakness and pain in the left lower extremity. The symptoms developed in the past three weeks. Previously able to ambulate without assistance, he purchased a cane yesterday due to concerns about falling.

RT reports poor adherence to his diabetes medications. His fingerstick blood sugars have ranged from 200 to 380 mg/dL over the past month. His weight has been stable; his BMI is 34. Review of other systems is negative. Vital signs include a blood pressure of 125/82 mm Hg; pulse, 74 beats/min; and respiratory rate, 16 breaths/min.

Physical examination is notable for muscle atrophy and tenderness to compression in the left quadriceps. Straight leg raise does not elicit pain bilaterally. Muscle strength is 4-/5 in the left hip with pain elicited on hip flexion, 4-/5 in the left knee, and 5/5 in the left ankle. Muscle strength is 4+/5 in the right hip, 5/5 in the right knee, and 5/5 in the right ankle. Muscle strength in both upper extremities is 5/5. Patellar deep tendon reflexes (DTRs) and ankle DTRs are absent bilaterally. Biceps and triceps DTRs are each 2+ bilaterally. Gait is slow and unsteady with use of the cane. Cranial nerves I-XII are intact. Sensation to sharp and dull testing is normal in both the upper and lower extremities.

Labwork reveals an A1C of 10.8%. The patient’s thyroid function studies, creatine kinase, and vitamin B₁₂ level are all in normal range. The serum creatinine is 1.2 mg/dL, and eGFR (estimated glomerular filtration rate) is 58 mL/min/1.73 m². Liver enzymes are normal, and complete blood count and other chemistry panels are unremarkable.

RT is referred to neurology. MRI of the thoracic and lumbar spine shows no mass lesions or disc disease. Electromyography reveals findings consistent with denervation and axonal damage in the proximal muscles in both lower extremities (left > right).

RT is diagnosed with diabetic amyotrophy and begins physical therapy three days a week. He achieves aggressive improvement in blood sugar control, and after three months, his A1C has improved to 7%.  Although still using a cane, he reports improved muscle strength in the lower extremities and better gait stability.

Continued on next page >>

PREVALENCE AND TYPES OF DIABETIC PERIPHERAL NEUROPATHY

According to the CDC, 25.8 million children and adults in the United States (8.3% of the population) have diabetes. Approximately 60% to 70% of them have mild to severe neuropathy.¹

Distal symmetric neuropathy is the most common form of diabetic peripheral neuropathy, accounting for more than 50% of cases. It is characterized by distal onset, predominately sensory polyneuropathy, and slow proximal progression.²

In contrast, diabetic amyotrophy is very rare, accounting for only 1% of all cases of neuropathy in diabetes. Prevalence is higher in those with type 2 versus type 1 diabetes (1.1% and 0.3%, respectively).^3,4 The most commonly misdiagnosed of the asymmetric diabetic neuropathies, diabetic amyotrophy is characterized by acute, progressive, asymmetrical weakness and pain in the muscles of the proximal lower extremities.⁵ It is also been referred to as proximal diabetic neuropathy, ischemic mononeuropathy multiplex, diabetic femoral neuropathy, Bruns-Garland syndrome, and diabetic lumbosacral polyradiculopathy.⁵

LOCALIZATION AND PATHOGENESIS

The site of the lesion in diabetic amyotrophy remains controversial; it is theorized that diabetic amyotrophy may result from involvement of multiple sites, such as lumbosacral anterior horn cells, motor roots, plexus, or motor axons to the muscles of the proximal lower limbs.⁴

The pathogenesis remains unknown. One theory is that hyperglycemia may cause metabolic derangements in nerve conduction. Another is that there is ischemic damage followed by axonal degeneration. Immune-mediated inflammatory processes, such as microvasculitis, have also been proposed as causes.^4,6

CLINICAL FEATURES

Diabetic amyotrophy is characterized by relatively rapid, progressive asymmetrical weakness and pain in the muscles in the proximal lower extremities; it develops over weeks to months and may continue for more than one year.^2,6 It typically begins unilaterally and can progress bilaterally—normally without impairment in sensation. Patients commonly experience pain in the hip, buttock, or thigh, as well as difficulty walking, standing, or climbing stairs. Occasionally, the condition is painless and can be associated with weight loss. It causes significant acute disability, with the degree of recovery variable.^2,4

Diabetic amyotrophy often presents either at diagnosis of diabetes or shortly thereafter. It most commonly affects men ages 40 to 50 and older, with higher incidence in type 2 diabetes.^2,5

Physical exam findings include proximal muscle weakness and atrophy in the quadriceps, hamstring, gluteal, hip adductors/abductors, and iliopsoas muscles.^4,5 Typically, there is no sensory impairment; however, mild sensory loss may be observed in patients with coexisting chronic distal sensorimotor polyneuropathy.^2,4 The patellar tendon reflexes are typically diminished or absent, and the ankle reflexes may be normal or diminished.⁴

Continued on next page >>

DIAGNOSTIC WORK-UP AND DIFFERENTIAL DIAGNOSIS

Although the diagnosis of diabetic amyotrophy is made primarily through detailed history taking and neurologic examination, other studies—electromyography, nerve conduction, imaging and labs, and nerve biopsy—may provide confirmation. Referral to neurology should also be considered.

The differential diagnosis is ­extensive and includes myopathies, muscular dystrophies, intervertebral disc disease, spinal stenosis, polyradiculopathies due to porphyria, amyloid, heavy metal poisoning, anterior horn cell diseases  (eg, poliomyelitis), neoplasms, chronic inflammatory demyelinating polyneuropathy, Guillain-Barré syndrome, monoclonal gammopathy, inflammatory vasculitis, hypothyroidism, vitamin B₆ or B₁₂ deficiencies, syphilis, AIDS, Lyme disease, and Charcot-Marie-Tooth disease.^2,5-7 Diabetic neuropathic cachexia should also be considered in the differential, as it presents with weight loss and lower limb pain but no weakness.⁵

Lab evaluation should begin with analysis of fasting plasma glucose, complete blood count, comprehensive metabolic profile, A1C, erythrocyte sedimentation rate (ESR), creatine kinase, vitamin B₁₂, and thyroid-stimulating hormone levels.⁷ Elevations in ESR and positive rheumatoid factor and antinuclear antibody can occur in patients with diabetic amyotrophy and are suggestive of a coexisting autoimmune disorder.⁶ Serum creatine kinase and thyroid function studies are normal.⁴ Additional lab tests, if clinically indicated, include paraneoplastic panel to evaluate for occult malignancy, antimyelin-associated glycoprotein antibodies, antiganglioside antibodies, cryoglobulins, cerebrospinal fluid analysis, porphyrin titers, and testing for heavy metals.⁷

Electrodiagnostic studies are recommended if the diagnosis of diabetic amyotrophy remains unclear following history taking, physical examination, and preliminary testing. Electromyography and nerve conduction studies typically reveal findings consistent with denervation and axonal damage in proximal muscles of the lower extremities.⁴ If demyelination is observed, a diagnosis of chronic demyelinating polyneuropathy should be considered.⁵

Nerve biopsy is considered if the diagnosis remains unclear after laboratory and electrodiagnostic testing or when confirmation of the diagnosis is needed before starting aggressive treatment. The sural and superficial peroneal nerves are preferred for biopsy. In cases of diabetic amyotrophy, sural nerve biopsy reveals significant fiber loss in an asymmetric fashion, resembling focal ischemia.⁵

MRI or CT scan of the lumbosacral spine is employed to exclude mass lesions and structural disorders such as spinal stenosis and disc disease.⁴ Cerebrospinal fluid is typically acellular, with a mildly elevated protein level of 60 to 100 mg/dL (but occasionally as high as 400 mg/dL).⁵

Continued on next page >>

PROGNOSIS AND MANAGEMENT

The course of diabetic amyo­trophy is variable. There is often gradual but incomplete restoration in muscle strength in correlation with aggressive glycemic control and physical therapy.² The majority of patients have residual muscle weakness, absent patellar and/or ankle DTRs, exercise-related pain, stiffness, and difficulty walking or climbing stairs. Full recovery of strength only occurs in 10% to 20% of patients.⁶

Treatment with IV immunoglobulin or other immuno­suppressive drugs is controversial. According to a Cochrane review of immunotherapy for diabetic amyotrophy, only one completed controlled trial using IV methylprednisolone was found. There is currently no evidence to support use of immunoglobulins to halt progression and improve symptoms.⁸

Neuropathic pain may be ­difficult to control. The severe pain associated with diabetic amyotrophy begins to diminish several months after onset, but residual pain may persist for several years. Pregabalin, duloxetine, tricyclic antidepressants, antiepileptic drugs, and narcotic analgesics can be helpful.^2,4 High doses of corticosteroids may lead to improvement of severe pain in some patients with diabetic amyotrophy.⁵

References >>

REFERENCES

1. CDC. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, 2011.

2. Nagsayi S, Somasekhar C, James CM. Diagnosis and management of diabetic amyotrophy. Geriatric Med. 2010;40:327-329.

3. Pasnoor M, Dimachkie MM, Kluding P, Barohn RJ. Diabetic neuropathy part 1: overview and symmetric phenotypes. Neurol Clin. 2013;31(2):425-445.

4. Sander HW, Chokroverty S. Diabetic amyotrophy: current concepts. Semin Neurol. 1996;16(2):173-177.

5. Pasnoor M, Dimachkie MM, Barohn RJ. Diabetic neuropathy part 2: proximal and asymmetric phenotypes. Neurol Clin. 2013;31(2): 447-462.

6. Idiculla J, Shirazi N, Opacka-Juffry J, Ganapathi. Diabetic amyotrophy: a brief review. Natl Med J India. 2004;17(4):
200-202.

7. Azhary H, Farooq M, Bhanushali M, Majid A. Peripheral neuropathy: differential diagnosis and management. Am Fam Physician. 2010;81(7):887-892.

8. Chan YC, Lo YL, Chan ES. Immunotherapy for diabetic amyotrophy. Cochrane Database Syst Rev. 2012;13(6):2-6.

A 45-year-old man, RT, with a six-month history of poorly controlled type 2 diabetes presents for evaluation of increased weakness and pain in the left lower extremity. The symptoms developed in the past three weeks. Previously able to ambulate without assistance, he purchased a cane yesterday due to concerns about falling.

RT reports poor adherence to his diabetes medications. His fingerstick blood sugars have ranged from 200 to 380 mg/dL over the past month. His weight has been stable; his BMI is 34. Review of other systems is negative. Vital signs include a blood pressure of 125/82 mm Hg; pulse, 74 beats/min; and respiratory rate, 16 breaths/min.

Physical examination is notable for muscle atrophy and tenderness to compression in the left quadriceps. Straight leg raise does not elicit pain bilaterally. Muscle strength is 4-/5 in the left hip with pain elicited on hip flexion, 4-/5 in the left knee, and 5/5 in the left ankle. Muscle strength is 4+/5 in the right hip, 5/5 in the right knee, and 5/5 in the right ankle. Muscle strength in both upper extremities is 5/5. Patellar deep tendon reflexes (DTRs) and ankle DTRs are absent bilaterally. Biceps and triceps DTRs are each 2+ bilaterally. Gait is slow and unsteady with use of the cane. Cranial nerves I-XII are intact. Sensation to sharp and dull testing is normal in both the upper and lower extremities.

Labwork reveals an A1C of 10.8%. The patient’s thyroid function studies, creatine kinase, and vitamin B₁₂ level are all in normal range. The serum creatinine is 1.2 mg/dL, and eGFR (estimated glomerular filtration rate) is 58 mL/min/1.73 m². Liver enzymes are normal, and complete blood count and other chemistry panels are unremarkable.

RT is referred to neurology. MRI of the thoracic and lumbar spine shows no mass lesions or disc disease. Electromyography reveals findings consistent with denervation and axonal damage in the proximal muscles in both lower extremities (left > right).

RT is diagnosed with diabetic amyotrophy and begins physical therapy three days a week. He achieves aggressive improvement in blood sugar control, and after three months, his A1C has improved to 7%.  Although still using a cane, he reports improved muscle strength in the lower extremities and better gait stability.

Continued on next page >>

PREVALENCE AND TYPES OF DIABETIC PERIPHERAL NEUROPATHY

According to the CDC, 25.8 million children and adults in the United States (8.3% of the population) have diabetes. Approximately 60% to 70% of them have mild to severe neuropathy.¹

Distal symmetric neuropathy is the most common form of diabetic peripheral neuropathy, accounting for more than 50% of cases. It is characterized by distal onset, predominately sensory polyneuropathy, and slow proximal progression.²

In contrast, diabetic amyotrophy is very rare, accounting for only 1% of all cases of neuropathy in diabetes. Prevalence is higher in those with type 2 versus type 1 diabetes (1.1% and 0.3%, respectively).^3,4 The most commonly misdiagnosed of the asymmetric diabetic neuropathies, diabetic amyotrophy is characterized by acute, progressive, asymmetrical weakness and pain in the muscles of the proximal lower extremities.⁵ It is also been referred to as proximal diabetic neuropathy, ischemic mononeuropathy multiplex, diabetic femoral neuropathy, Bruns-Garland syndrome, and diabetic lumbosacral polyradiculopathy.⁵

LOCALIZATION AND PATHOGENESIS

The site of the lesion in diabetic amyotrophy remains controversial; it is theorized that diabetic amyotrophy may result from involvement of multiple sites, such as lumbosacral anterior horn cells, motor roots, plexus, or motor axons to the muscles of the proximal lower limbs.⁴

The pathogenesis remains unknown. One theory is that hyperglycemia may cause metabolic derangements in nerve conduction. Another is that there is ischemic damage followed by axonal degeneration. Immune-mediated inflammatory processes, such as microvasculitis, have also been proposed as causes.^4,6

CLINICAL FEATURES

Diabetic amyotrophy is characterized by relatively rapid, progressive asymmetrical weakness and pain in the muscles in the proximal lower extremities; it develops over weeks to months and may continue for more than one year.^2,6 It typically begins unilaterally and can progress bilaterally—normally without impairment in sensation. Patients commonly experience pain in the hip, buttock, or thigh, as well as difficulty walking, standing, or climbing stairs. Occasionally, the condition is painless and can be associated with weight loss. It causes significant acute disability, with the degree of recovery variable.^2,4

Diabetic amyotrophy often presents either at diagnosis of diabetes or shortly thereafter. It most commonly affects men ages 40 to 50 and older, with higher incidence in type 2 diabetes.^2,5

Physical exam findings include proximal muscle weakness and atrophy in the quadriceps, hamstring, gluteal, hip adductors/abductors, and iliopsoas muscles.^4,5 Typically, there is no sensory impairment; however, mild sensory loss may be observed in patients with coexisting chronic distal sensorimotor polyneuropathy.^2,4 The patellar tendon reflexes are typically diminished or absent, and the ankle reflexes may be normal or diminished.⁴

Continued on next page >>

DIAGNOSTIC WORK-UP AND DIFFERENTIAL DIAGNOSIS

Although the diagnosis of diabetic amyotrophy is made primarily through detailed history taking and neurologic examination, other studies—electromyography, nerve conduction, imaging and labs, and nerve biopsy—may provide confirmation. Referral to neurology should also be considered.

The differential diagnosis is ­extensive and includes myopathies, muscular dystrophies, intervertebral disc disease, spinal stenosis, polyradiculopathies due to porphyria, amyloid, heavy metal poisoning, anterior horn cell diseases  (eg, poliomyelitis), neoplasms, chronic inflammatory demyelinating polyneuropathy, Guillain-Barré syndrome, monoclonal gammopathy, inflammatory vasculitis, hypothyroidism, vitamin B₆ or B₁₂ deficiencies, syphilis, AIDS, Lyme disease, and Charcot-Marie-Tooth disease.^2,5-7 Diabetic neuropathic cachexia should also be considered in the differential, as it presents with weight loss and lower limb pain but no weakness.⁵

Lab evaluation should begin with analysis of fasting plasma glucose, complete blood count, comprehensive metabolic profile, A1C, erythrocyte sedimentation rate (ESR), creatine kinase, vitamin B₁₂, and thyroid-stimulating hormone levels.⁷ Elevations in ESR and positive rheumatoid factor and antinuclear antibody can occur in patients with diabetic amyotrophy and are suggestive of a coexisting autoimmune disorder.⁶ Serum creatine kinase and thyroid function studies are normal.⁴ Additional lab tests, if clinically indicated, include paraneoplastic panel to evaluate for occult malignancy, antimyelin-associated glycoprotein antibodies, antiganglioside antibodies, cryoglobulins, cerebrospinal fluid analysis, porphyrin titers, and testing for heavy metals.⁷

Electrodiagnostic studies are recommended if the diagnosis of diabetic amyotrophy remains unclear following history taking, physical examination, and preliminary testing. Electromyography and nerve conduction studies typically reveal findings consistent with denervation and axonal damage in proximal muscles of the lower extremities.⁴ If demyelination is observed, a diagnosis of chronic demyelinating polyneuropathy should be considered.⁵

Nerve biopsy is considered if the diagnosis remains unclear after laboratory and electrodiagnostic testing or when confirmation of the diagnosis is needed before starting aggressive treatment. The sural and superficial peroneal nerves are preferred for biopsy. In cases of diabetic amyotrophy, sural nerve biopsy reveals significant fiber loss in an asymmetric fashion, resembling focal ischemia.⁵

MRI or CT scan of the lumbosacral spine is employed to exclude mass lesions and structural disorders such as spinal stenosis and disc disease.⁴ Cerebrospinal fluid is typically acellular, with a mildly elevated protein level of 60 to 100 mg/dL (but occasionally as high as 400 mg/dL).⁵

Continued on next page >>

PROGNOSIS AND MANAGEMENT

The course of diabetic amyo­trophy is variable. There is often gradual but incomplete restoration in muscle strength in correlation with aggressive glycemic control and physical therapy.² The majority of patients have residual muscle weakness, absent patellar and/or ankle DTRs, exercise-related pain, stiffness, and difficulty walking or climbing stairs. Full recovery of strength only occurs in 10% to 20% of patients.⁶

Treatment with IV immunoglobulin or other immuno­suppressive drugs is controversial. According to a Cochrane review of immunotherapy for diabetic amyotrophy, only one completed controlled trial using IV methylprednisolone was found. There is currently no evidence to support use of immunoglobulins to halt progression and improve symptoms.⁸

Neuropathic pain may be ­difficult to control. The severe pain associated with diabetic amyotrophy begins to diminish several months after onset, but residual pain may persist for several years. Pregabalin, duloxetine, tricyclic antidepressants, antiepileptic drugs, and narcotic analgesics can be helpful.^2,4 High doses of corticosteroids may lead to improvement of severe pain in some patients with diabetic amyotrophy.⁵

References >>

REFERENCES

1. CDC. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, 2011.

2. Nagsayi S, Somasekhar C, James CM. Diagnosis and management of diabetic amyotrophy. Geriatric Med. 2010;40:327-329.

3. Pasnoor M, Dimachkie MM, Kluding P, Barohn RJ. Diabetic neuropathy part 1: overview and symmetric phenotypes. Neurol Clin. 2013;31(2):425-445.

4. Sander HW, Chokroverty S. Diabetic amyotrophy: current concepts. Semin Neurol. 1996;16(2):173-177.

5. Pasnoor M, Dimachkie MM, Barohn RJ. Diabetic neuropathy part 2: proximal and asymmetric phenotypes. Neurol Clin. 2013;31(2): 447-462.

6. Idiculla J, Shirazi N, Opacka-Juffry J, Ganapathi. Diabetic amyotrophy: a brief review. Natl Med J India. 2004;17(4):
200-202.

7. Azhary H, Farooq M, Bhanushali M, Majid A. Peripheral neuropathy: differential diagnosis and management. Am Fam Physician. 2010;81(7):887-892.

8. Chan YC, Lo YL, Chan ES. Immunotherapy for diabetic amyotrophy. Cochrane Database Syst Rev. 2012;13(6):2-6.

ANSWER

Findings on this ECG include sinus rhythm at a rate of 60 beats/min, evidence of a second-degree atrioventricular (AV) block (Mobitz I), and a right bundle branch block (RBBB).

To understand the rhythm, it is best to focus on the rhythm strip, particularly lead I at the bottom of the ECG. If you measure the P-to-P interval, you will notice that it is consistent and constant at a rate of 60 beats/min, regardless of the QRS complex. If you look at the PR interval from the second to the sixth QRS complex, you will notice that it is regular until the QRS is dropped after the P wave that follows the sixth QRS complex. Following the pause, the PR interval on the seventh, eighth, and ninth QRS complexes gradually prolongs. Although this is not a classic example of Mobitz I block, it is indicative of an AV node with a conduction abnormality.

Subsequent rhythm strips documented multiple blocked PR intervals that corresponded to the patient’s dizziness. The RBBB is evident by the RSR’ pattern seen in lead V₁ with a QRS duration ≥ 120 ms.

ANSWER

Findings on this ECG include sinus rhythm at a rate of 60 beats/min, evidence of a second-degree atrioventricular (AV) block (Mobitz I), and a right bundle branch block (RBBB).

To understand the rhythm, it is best to focus on the rhythm strip, particularly lead I at the bottom of the ECG. If you measure the P-to-P interval, you will notice that it is consistent and constant at a rate of 60 beats/min, regardless of the QRS complex. If you look at the PR interval from the second to the sixth QRS complex, you will notice that it is regular until the QRS is dropped after the P wave that follows the sixth QRS complex. Following the pause, the PR interval on the seventh, eighth, and ninth QRS complexes gradually prolongs. Although this is not a classic example of Mobitz I block, it is indicative of an AV node with a conduction abnormality.

Subsequent rhythm strips documented multiple blocked PR intervals that corresponded to the patient’s dizziness. The RBBB is evident by the RSR’ pattern seen in lead V₁ with a QRS duration ≥ 120 ms.

ANSWER

Findings on this ECG include sinus rhythm at a rate of 60 beats/min, evidence of a second-degree atrioventricular (AV) block (Mobitz I), and a right bundle branch block (RBBB).

To understand the rhythm, it is best to focus on the rhythm strip, particularly lead I at the bottom of the ECG. If you measure the P-to-P interval, you will notice that it is consistent and constant at a rate of 60 beats/min, regardless of the QRS complex. If you look at the PR interval from the second to the sixth QRS complex, you will notice that it is regular until the QRS is dropped after the P wave that follows the sixth QRS complex. Following the pause, the PR interval on the seventh, eighth, and ninth QRS complexes gradually prolongs. Although this is not a classic example of Mobitz I block, it is indicative of an AV node with a conduction abnormality.

Subsequent rhythm strips documented multiple blocked PR intervals that corresponded to the patient’s dizziness. The RBBB is evident by the RSR’ pattern seen in lead V₁ with a QRS duration ≥ 120 ms.

While not a new phenomenon, antimicrobial resistance is an alarming and, arguably, still underappreciated public health problem. A mere 70 years after the introduction of antibiotics, we face the distinct possibility of a future without effective antibiotics for some infections. Such a reality will render select surgical operations, cancer chemotherapy, and organ transplants exceedingly dangerous.

The scarcity of new antimicrobial agents and the paucity of new agents in the drug development pipeline limit treatment options, particularly for patients with infections caused by multidrug-resistant organisms. Annually, multidrug resistant organisms cause an estimated 25,000 deaths in Europe and 12,000 deaths in the United States. In response to this threat, the Transatlantic Taskforce on Antimicrobial Resistance (TATFAR) was established and published their report with 17 recommendations.

Respiratory tract infections are one of the most common symptoms presenting to primary care. Overprescribing in this setting is rampant, driven largely by patient expectations and clinician need for expediency and desire to receive "high marks" for satisfaction. Available evidence has suggested that delayed antibiotic prescribing is effective. But what is the best method to delay antibiotic prescribing?

Researchers in the United Kingdom evaluated the comparative effectiveness of four different strategies of delayed antibiotic prescribing for patients not needing antibiotics right away:

• Recontact: Patients were asked to contact the office and leave a message for a clinician to prescribe an antibiotic.

• Postdated prescription: The prescription could be filled only after a certain date.

• Wait/Request: Patients were instructed to wait but could request an antibiotic from the front office.

• Delayed use: Patients received antibiotics but were asked to wait to use them.

A "no prescription" arm was added later in the trial. The primary outcome was symptom severity measured at the end of each day during days 2-4 of a two-week symptom diary. Secondary outcomes included antibiotic use and side effects.

No differences were observed between the four strategies with respect to symptom control. Antibiotic use did not differ significantly between strategies and the lowest use was reported in the no prescription arm. No significant differences were observed between groups in patient satisfaction. Complications were slightly higher in the no antibiotic group (2.5%), compared with the delayed groups (1.4%).

Delayed prescribing is associated with less than 40% of patients using an antibiotic. Given the current crisis with multidrug resistance, we should feel obligated to try one of the proposed strategies for delayed antibiotic prescription if patients do not need one right away.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.

While not a new phenomenon, antimicrobial resistance is an alarming and, arguably, still underappreciated public health problem. A mere 70 years after the introduction of antibiotics, we face the distinct possibility of a future without effective antibiotics for some infections. Such a reality will render select surgical operations, cancer chemotherapy, and organ transplants exceedingly dangerous.

The scarcity of new antimicrobial agents and the paucity of new agents in the drug development pipeline limit treatment options, particularly for patients with infections caused by multidrug-resistant organisms. Annually, multidrug resistant organisms cause an estimated 25,000 deaths in Europe and 12,000 deaths in the United States. In response to this threat, the Transatlantic Taskforce on Antimicrobial Resistance (TATFAR) was established and published their report with 17 recommendations.

Respiratory tract infections are one of the most common symptoms presenting to primary care. Overprescribing in this setting is rampant, driven largely by patient expectations and clinician need for expediency and desire to receive "high marks" for satisfaction. Available evidence has suggested that delayed antibiotic prescribing is effective. But what is the best method to delay antibiotic prescribing?

Researchers in the United Kingdom evaluated the comparative effectiveness of four different strategies of delayed antibiotic prescribing for patients not needing antibiotics right away:

• Recontact: Patients were asked to contact the office and leave a message for a clinician to prescribe an antibiotic.

• Postdated prescription: The prescription could be filled only after a certain date.

• Wait/Request: Patients were instructed to wait but could request an antibiotic from the front office.

• Delayed use: Patients received antibiotics but were asked to wait to use them.

A "no prescription" arm was added later in the trial. The primary outcome was symptom severity measured at the end of each day during days 2-4 of a two-week symptom diary. Secondary outcomes included antibiotic use and side effects.

No differences were observed between the four strategies with respect to symptom control. Antibiotic use did not differ significantly between strategies and the lowest use was reported in the no prescription arm. No significant differences were observed between groups in patient satisfaction. Complications were slightly higher in the no antibiotic group (2.5%), compared with the delayed groups (1.4%).

Delayed prescribing is associated with less than 40% of patients using an antibiotic. Given the current crisis with multidrug resistance, we should feel obligated to try one of the proposed strategies for delayed antibiotic prescription if patients do not need one right away.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.

While not a new phenomenon, antimicrobial resistance is an alarming and, arguably, still underappreciated public health problem. A mere 70 years after the introduction of antibiotics, we face the distinct possibility of a future without effective antibiotics for some infections. Such a reality will render select surgical operations, cancer chemotherapy, and organ transplants exceedingly dangerous.

The scarcity of new antimicrobial agents and the paucity of new agents in the drug development pipeline limit treatment options, particularly for patients with infections caused by multidrug-resistant organisms. Annually, multidrug resistant organisms cause an estimated 25,000 deaths in Europe and 12,000 deaths in the United States. In response to this threat, the Transatlantic Taskforce on Antimicrobial Resistance (TATFAR) was established and published their report with 17 recommendations.

Respiratory tract infections are one of the most common symptoms presenting to primary care. Overprescribing in this setting is rampant, driven largely by patient expectations and clinician need for expediency and desire to receive "high marks" for satisfaction. Available evidence has suggested that delayed antibiotic prescribing is effective. But what is the best method to delay antibiotic prescribing?

Researchers in the United Kingdom evaluated the comparative effectiveness of four different strategies of delayed antibiotic prescribing for patients not needing antibiotics right away:

• Recontact: Patients were asked to contact the office and leave a message for a clinician to prescribe an antibiotic.

• Postdated prescription: The prescription could be filled only after a certain date.

• Wait/Request: Patients were instructed to wait but could request an antibiotic from the front office.

• Delayed use: Patients received antibiotics but were asked to wait to use them.

A "no prescription" arm was added later in the trial. The primary outcome was symptom severity measured at the end of each day during days 2-4 of a two-week symptom diary. Secondary outcomes included antibiotic use and side effects.

No differences were observed between the four strategies with respect to symptom control. Antibiotic use did not differ significantly between strategies and the lowest use was reported in the no prescription arm. No significant differences were observed between groups in patient satisfaction. Complications were slightly higher in the no antibiotic group (2.5%), compared with the delayed groups (1.4%).

Delayed prescribing is associated with less than 40% of patients using an antibiotic. Given the current crisis with multidrug resistance, we should feel obligated to try one of the proposed strategies for delayed antibiotic prescription if patients do not need one right away.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.

ANSWER

The correct answer is seborrheic dermatitis (choice “d”), a common cause of penile rashes that typically manifests initially as chronic dandruff or in some other form on the head or neck.

Herpes simplex (choice “a”) is certainly common, but it likely would have presented with grouped vesicles on an erythematous base. Furthermore, each episode would have been limited to about two weeks, and the eruption would have produced noticeable symptoms and responded to the valacyclovir.

Yeast infection (choice “b”), while often diagnosed, is in reality unusual, especially in the circumcised and otherwise healthy male. Nystatin, although far from the ideal treatment, should have had some effect.

Fixed drug eruption (FDE; choice “c”) could have been a suspect, had there been a drug to blame. FDE usually presents as a brownish red, shiny round macule that appears and reappears in the same area with repeated exposure to the same drug. The penile shaft is a favorite area for it. Drugs known to trigger FDE include NSAIDs, sulfa, tetracycline, penicillin, pseudoephedrine, and aspirin.

DISCUSSION

Seborrheic dermatitis (SD), also known as seborrhea, is an extremely common chronic papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk. Although not directly caused by the highly lipophilic commensal yeast Malassezia furfur, it does appear to be related to increases in the number of those organisms, as well as to immunologic abnormalities and increased production of sebum. It can range from a mild scaly rash to whole-body erythroderma and can affect an astonishing range of areas, including the genitals.

SD almost always manifests with dandruff (or “cradle cap” in the infant), followed by faint scaling in and around the ears or on the face (eg, nasolabial folds, brows, and glabella), mid chest, axillae, periumbilical region, and genitals. Below the head and neck, SD often mystifies the nondermatology provider, who tends to call it “fungal infection” or, when it’s seen in moist intertriginous skin, “yeast infection.”

SD, especially in this case, represents the perfect example of the need to “look elsewhere” for clues when confronted with a mysterious rash. Patients can certainly have more than one dermatologic diagnosis at a time, but a single explanation is considerably more likely and should therefore be sought. In this case, corroboration for the diagnosis of SD was readily found by looking for it in its known locations.

SD can take on different looks, including a distinctly annular morphology, especially in patients with darker skin. It can occasionally be severe in patients with Parkinson’s disease, multiple sclerosis, or a history of stroke. This case mirrors my experience in that I see increased stress as a major precipitating factor in the worsening of pre-existing SD.

In addition to the items already mentioned, the differential for penile rashes includes lichen planus. However, the lesions of lichen planus tend to have a distinctly purple appearance and well-defined margins, and on the penis, they tend to spill over onto the penile corona and glans.

TREATMENT/PROGNOSIS

In this case, treatment comprised a combination of oxiconazole lotion and 2.5% hydrocortisone cream. Many other combinations have been used successfully, including pimecrolimus or tacrolimus combined with ketoconazole cream.

Whatever is used, a cure will not be forthcoming, since the condition is almost always chronic. The main value of an accurate diagnosis in such a case lies in easing the patient’s mind regarding the terrible diseases he doesn’t have. 

ANSWER

The correct answer is seborrheic dermatitis (choice “d”), a common cause of penile rashes that typically manifests initially as chronic dandruff or in some other form on the head or neck.

Herpes simplex (choice “a”) is certainly common, but it likely would have presented with grouped vesicles on an erythematous base. Furthermore, each episode would have been limited to about two weeks, and the eruption would have produced noticeable symptoms and responded to the valacyclovir.

Yeast infection (choice “b”), while often diagnosed, is in reality unusual, especially in the circumcised and otherwise healthy male. Nystatin, although far from the ideal treatment, should have had some effect.

Fixed drug eruption (FDE; choice “c”) could have been a suspect, had there been a drug to blame. FDE usually presents as a brownish red, shiny round macule that appears and reappears in the same area with repeated exposure to the same drug. The penile shaft is a favorite area for it. Drugs known to trigger FDE include NSAIDs, sulfa, tetracycline, penicillin, pseudoephedrine, and aspirin.

DISCUSSION

Seborrheic dermatitis (SD), also known as seborrhea, is an extremely common chronic papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk. Although not directly caused by the highly lipophilic commensal yeast Malassezia furfur, it does appear to be related to increases in the number of those organisms, as well as to immunologic abnormalities and increased production of sebum. It can range from a mild scaly rash to whole-body erythroderma and can affect an astonishing range of areas, including the genitals.

SD almost always manifests with dandruff (or “cradle cap” in the infant), followed by faint scaling in and around the ears or on the face (eg, nasolabial folds, brows, and glabella), mid chest, axillae, periumbilical region, and genitals. Below the head and neck, SD often mystifies the nondermatology provider, who tends to call it “fungal infection” or, when it’s seen in moist intertriginous skin, “yeast infection.”

SD, especially in this case, represents the perfect example of the need to “look elsewhere” for clues when confronted with a mysterious rash. Patients can certainly have more than one dermatologic diagnosis at a time, but a single explanation is considerably more likely and should therefore be sought. In this case, corroboration for the diagnosis of SD was readily found by looking for it in its known locations.

SD can take on different looks, including a distinctly annular morphology, especially in patients with darker skin. It can occasionally be severe in patients with Parkinson’s disease, multiple sclerosis, or a history of stroke. This case mirrors my experience in that I see increased stress as a major precipitating factor in the worsening of pre-existing SD.

In addition to the items already mentioned, the differential for penile rashes includes lichen planus. However, the lesions of lichen planus tend to have a distinctly purple appearance and well-defined margins, and on the penis, they tend to spill over onto the penile corona and glans.

TREATMENT/PROGNOSIS

In this case, treatment comprised a combination of oxiconazole lotion and 2.5% hydrocortisone cream. Many other combinations have been used successfully, including pimecrolimus or tacrolimus combined with ketoconazole cream.

Whatever is used, a cure will not be forthcoming, since the condition is almost always chronic. The main value of an accurate diagnosis in such a case lies in easing the patient’s mind regarding the terrible diseases he doesn’t have. 

ANSWER

The correct answer is seborrheic dermatitis (choice “d”), a common cause of penile rashes that typically manifests initially as chronic dandruff or in some other form on the head or neck.

Herpes simplex (choice “a”) is certainly common, but it likely would have presented with grouped vesicles on an erythematous base. Furthermore, each episode would have been limited to about two weeks, and the eruption would have produced noticeable symptoms and responded to the valacyclovir.

Yeast infection (choice “b”), while often diagnosed, is in reality unusual, especially in the circumcised and otherwise healthy male. Nystatin, although far from the ideal treatment, should have had some effect.

Fixed drug eruption (FDE; choice “c”) could have been a suspect, had there been a drug to blame. FDE usually presents as a brownish red, shiny round macule that appears and reappears in the same area with repeated exposure to the same drug. The penile shaft is a favorite area for it. Drugs known to trigger FDE include NSAIDs, sulfa, tetracycline, penicillin, pseudoephedrine, and aspirin.

DISCUSSION

Seborrheic dermatitis (SD), also known as seborrhea, is an extremely common chronic papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk. Although not directly caused by the highly lipophilic commensal yeast Malassezia furfur, it does appear to be related to increases in the number of those organisms, as well as to immunologic abnormalities and increased production of sebum. It can range from a mild scaly rash to whole-body erythroderma and can affect an astonishing range of areas, including the genitals.

SD almost always manifests with dandruff (or “cradle cap” in the infant), followed by faint scaling in and around the ears or on the face (eg, nasolabial folds, brows, and glabella), mid chest, axillae, periumbilical region, and genitals. Below the head and neck, SD often mystifies the nondermatology provider, who tends to call it “fungal infection” or, when it’s seen in moist intertriginous skin, “yeast infection.”

SD, especially in this case, represents the perfect example of the need to “look elsewhere” for clues when confronted with a mysterious rash. Patients can certainly have more than one dermatologic diagnosis at a time, but a single explanation is considerably more likely and should therefore be sought. In this case, corroboration for the diagnosis of SD was readily found by looking for it in its known locations.

SD can take on different looks, including a distinctly annular morphology, especially in patients with darker skin. It can occasionally be severe in patients with Parkinson’s disease, multiple sclerosis, or a history of stroke. This case mirrors my experience in that I see increased stress as a major precipitating factor in the worsening of pre-existing SD.

In addition to the items already mentioned, the differential for penile rashes includes lichen planus. However, the lesions of lichen planus tend to have a distinctly purple appearance and well-defined margins, and on the penis, they tend to spill over onto the penile corona and glans.

TREATMENT/PROGNOSIS

In this case, treatment comprised a combination of oxiconazole lotion and 2.5% hydrocortisone cream. Many other combinations have been used successfully, including pimecrolimus or tacrolimus combined with ketoconazole cream.

Whatever is used, a cure will not be forthcoming, since the condition is almost always chronic. The main value of an accurate diagnosis in such a case lies in easing the patient’s mind regarding the terrible diseases he doesn’t have. 

PATIENT’S CLAIM The hemorrhage was caused when enoxaparin was given at 1.5 times the proper dosage because the patient’s weight was overestimated by 50%. Excessive blood, plasma, and fluids caused her weight to double after resuscitation. Her intestines were forced out of her abdominal cavity by the hemorrhage. A permanent hernia, visible underneath her skin, causes pain.

DEFENDANTS’ DEFENSE The patient’s preexisting diabetes, heart condition, high cholesterol levels, and orthopedic issues impacted her condition. She was not compliant in managing her diabetes, causing many of the current problems.

VERDICT A $9.3 million Connecticut verdict was returned.

Related article: Update: Pelvic floor dysfunction Autumn L. Edenfield, MD, and Cindy L. Amundsen, MD (October 2012)

CESAREAN DELAYED UNNECESSARILY
At 37 weeks’ gestation, a mother reported decreased fetal movement. When the biophysical profile test scored 8/8 and the fetal heart rate was reassuring, the attending ObGyn discharged the patient. However, it was the middle of the night, and the nurse kept the mother in the emergency department (ED). At 8:30 am, the fetus began to show signs of fetal distress. Three ObGyns agreed to monitor labor, although one physician wanted delivery to occur that morning.

The next morning, a second biophysical profile scored 2/8, but the on-call ObGyn misunderstood the score as 6/8 and scheduled cesarean delivery for noon. Two hours after the second biophysical profile, the fetal heart rate crashed. A nurse called the ObGyn, who began an emergency cesarean 15 minutes later. The baby, born lifeless, was resuscitated. The child suffered permanent brain damage, and has cerebral palsy, severe cognitive deficits and speech deficits, and walks with an abnormal gait.

PARENTS’ CLAIM A physician did not see the patient for 24 hours, once the decision was made to monitor the mother, even though the fetal heart rate continued to decline. A biophysical profile test score of 2/8 indicates the need for immediate delivery. An earlier cesarean delivery could have reduced the child’s injuries.

DEFENDANTS’ DEFENSE After a settlement was reached with the hospital, the trial continued against the delivering ObGyn. He claimed that decreased fetal movement indicated that the brain injury had occurred 1 to 4 days before the mother came to the ED. The technician had manipulated the mother’s abdomen to wake the fetus before starting the first biophysical profile, which invalidated the score. The nurse miscommunicated the score of the second biophysical profile.

VERDICT A gross $29.8 million Illinois verdict was returned that included a $1.65 million settlement with the hospital.

WAS FACILITY ADEQUATELY STAFFED AFTER HURRICANE IKE?
A mother was admitted to a hospital for induction of labor in September 2008. After birth, the child was found to have cerebral palsy.

PARENTS’ CLAIM The mother should have been sent to another facility before delivery was induced because the hospital was short-staffed and low on resources due to Hurricane Ike. Too much oxytocin was used to induce contractions, which led to a lack of oxygen for the fetus. All prenatal testing had shown a healthy fetus. A cesarean delivery should have occurred when fetal distress was noted.

DEFENDANTS’ DEFENSE The mother had gastric bypass surgery 8 months before she became pregnant, and smoked during pregnancy, which accounted for the infant’s injuries. Treatment during labor and delivery was appropriate. Hospital staffing and resources were adequate.

VERDICT A $6.5 million Texas settlement was reached. 

PLACENTA ACCRETA; MOTHER DIES
A 33-year-old woman became pregnant with her second child. A variety of conditions caused this to be high-risk pregnancy, so she saw a maternal-fetal medicine (MFM) specialist 2 months before delivery. The MFM reported that his examination and the ultrasonography (US) results were normal.

The ObGyn who provided prenatal care and delivered her first child scheduled cesarean delivery. During the procedure, the ObGyn noticed a 3- to 4-inch lesion where the placenta had penetrated the uterus. When the placenta was removed, the patient began to hemorrhage and a hysterectomy was performed. The hemorrhage created blood clots that led to gangrene in the patient’s extremities. She died 5 days after giving birth.

ESTATE’S CLAIM Both the MFM and the ObGyn failed to recognize placenta accreta on US prior to delivery. The ObGyn should have performed US prior to beginning cesarean delivery. The hospital’s protocols were not followed: the ObGyn should have stopped the procedure and called for extra surgical assistance and additional blood when he encountered placenta accreta, and again when the patient began to hemorrhage. Placenta accreta does not have to be fatal if detected and managed properly.

DEFENDANTS’ DEFENSE There was no negligence; the patient was treated properly.

VERDICT A $15.5 million Illinois verdict was returned against both physicians and the medical center. 

Related article: Is the risk of placenta accreta in a subsequent pregnancy higher after emergent primary cesarean or after elective primary cesarean? Yinka Oyelese, MD (Examining the Evidence, December 2013)

ANTICONVULSANT AND MIGRAINE MEDS TAKEN DURING PREGNANCY
A woman was prescribed topiramate (Topamax) for migraine headaches and hand tremors during the first trimester of her pregnancy in 2007. With a history of seizures, she also took several anticonvulsants throughout her pregnancy. Her child was diagnosed with right unilateral cleft lip (cheiloschisis) in utero. The condition had not been surgically corrected at the time of trial.

PARENTS’ CLAIM The use of topiramate caused the child’s cleft lip. Janssen Pharmaceuticals, the manufacturer of Topamax, knew about the risk of birth defects associated with the drug in 2007, but failed to provide adequate warnings.

DEFENDANTS’ DEFENSE The mother received at least two warnings from her physician regarding the potential risks of anticonvulsant and antiepileptic drugs and the importance of not becoming pregnant while taking the medications. An action against the physician was barred by the applicable statute of limitations. The mother had taken topiramate prescribed to her mother for a time; such actions should release Janssen from liability.

VERDICT A $11 million Pennsylvania verdict was returned.

PID MASKS ECTOPIC PREGNANCY
A woman in her 40s became pregnant. On the first two prenatal diagnostic imaging studies, the ObGyn saw an intrauterine pregnancy. He later realized that the pregnancy was ectopic after beta human chorionic gonadotrophin (beta-hCG) blood levels were abnormal. During surgery to terminate the pregnancy, he found he had to perform a total hysterectomy because the patient had extensive pelvic inflammatory disease (PID) caused by a long history of sexually transmitted disease.

PATIENT’S CLAIM If the ectopic pregnancy had been diagnosed earlier, one of her ovaries could have been preserved, saving her from the symptoms of surgical menopause.

PHYSICIAN’S DEFENSE PID had caused the ovaries, numerous fibroid tumors, and the uterus to fuse into one mass. That was why the first two imaging studies appeared to show an intrauterine pregnancy. It was not possible to diagnose the extent of the problem until surgery. The patient did not have a true ectopic pregnancy.

The patient’s difficulties occurred during a 2-week time period in which she had one visit with him and another visit to an ED where two other physicians examined her and missed the diagnosis.

VERDICT A Michigan defense verdict was returned. 

ILIAC ARTERY INJURED DURING LAPAROSCOPIC SURGERY; PATIENT DIES
A 40-year-old woman underwent laparoscopic gynecologic surgery performed by her ObGyn. During the procedure, the patient’s left internal iliac artery was punctured, but the injury was not recognized at the time. She was discharged the same day. The next morning, she went into hypovolemic shock due to internal bleeding. She was taken to the ED, where she died.

ESTATE’S CLAIM The ObGyn, anesthesiologist, and hospital staff were negligent in their postoperative care. The anesthesiologist prescribed pain medication that masked the injury; the patient was discharged from the postanesthesia unit too early and without proper examination. The nursing staff did not react to the patient’s reports of abdominal pain, nor did they properly assess her condition prior to discharge. The ObGyn failed to return a phone call the evening after the procedure.

DEFENDANTS’ DEFENSE The ObGyn settled before trial. The anesthesiologist and hospital denied negligence: care was proper and followed all protocols.

VERDICT A confidential California settlement was reached with the ObGyn. A defense verdict was returned for the anesthesiologist and hospital. 

Related article: Anatomy for the laparoscopic surgeon Emad Mikhail, MD; Lauren Scott, MD; Stuart Hart, MD, MS (April 2014)

GENETIC TESTING MISSED A KEY DIAGNOSIS
A 40-year-old woman underwent genetic testing after she became pregnant. She was assured that there were no abnormalities that would impact her child.

The baby was born with Wolf-Hirschhorn syndrome, characterized by facial deformities, intellectual disabilities, delayed growth, and seizures. The child is nonverbal, deaf, and blind. She uses a feeding tube and requires 24-hour care.

PARENTS’ CLAIM The genetic testing was improperly conducted. The mother would have had an abortion if she’d known that the child was so disabled.

DEFENDANTS’ DEFENSE Settlements were mediated.

VERDICT A $6.15 million New Jersey settlement was reached on behalf of the hospital and two laboratory technicians, and a $1 million settlement was reached with the director of the genetic laboratory. 

HEAT INJURY TO COLON: ABSCESSES, PERITONITIS
A 43-year-old patient had a history of symptomatic uterine fibroids and infertility. Her ObGyn performed a hysteroscopy because he suspected endometriosis, but found none. He then successfully removed a large uterine fibroid during laparoscopic myomectomy. The patient was discharged the same day.

Two days later, the patient developed abdominal pain, nausea, and fever. She went to the ED and was taken into emergency surgery after a CT scan showed free air and fluid in her abdomen. She suffered multiple abscesses and peritonitis.

PATIENT’S CLAIM The ObGyn was negligent in performing the surgery: the sigmoid colon sustained a thermal injury, which caused the abscesses and peritonitis.

PHYSICIAN’S DEFENSE There was no evidence of thermal injury during the original operation; heat damage can and does occur in the absence of negligence. The patient’s previously unknown diverticulitis contributed to the development of the recurrent abscesses and peritonitis.

VERDICT A Florida defense verdict was returned.

RUPTURED UTERUS IS UNDETECTED
During labor and delivery, a declining fetal heart rate was observed, but there was an hour’s delay before cesarean delivery was started. The child suffered a hypoxic brain injury. He has spastic quadriplegia, cannot speak, and requires a respirator and feeding tube.

PARENTS’ CLAIM The mother suffered a ruptured uterus during labor that was not recognized by the ObGyn or nursing staff.

DEFENDANTS’ DEFENSE A settlement was reached during trial.

VERDICT A $7.5 million New Jersey settlement was reached.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Tell us what you think!
Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected] Please include your name, city and state.
Stay in touch! Your feedback is important to us!

PATIENT’S CLAIM The hemorrhage was caused when enoxaparin was given at 1.5 times the proper dosage because the patient’s weight was overestimated by 50%. Excessive blood, plasma, and fluids caused her weight to double after resuscitation. Her intestines were forced out of her abdominal cavity by the hemorrhage. A permanent hernia, visible underneath her skin, causes pain.

DEFENDANTS’ DEFENSE The patient’s preexisting diabetes, heart condition, high cholesterol levels, and orthopedic issues impacted her condition. She was not compliant in managing her diabetes, causing many of the current problems.

VERDICT A $9.3 million Connecticut verdict was returned.

Related article: Update: Pelvic floor dysfunction Autumn L. Edenfield, MD, and Cindy L. Amundsen, MD (October 2012)

CESAREAN DELAYED UNNECESSARILY
At 37 weeks’ gestation, a mother reported decreased fetal movement. When the biophysical profile test scored 8/8 and the fetal heart rate was reassuring, the attending ObGyn discharged the patient. However, it was the middle of the night, and the nurse kept the mother in the emergency department (ED). At 8:30 am, the fetus began to show signs of fetal distress. Three ObGyns agreed to monitor labor, although one physician wanted delivery to occur that morning.

The next morning, a second biophysical profile scored 2/8, but the on-call ObGyn misunderstood the score as 6/8 and scheduled cesarean delivery for noon. Two hours after the second biophysical profile, the fetal heart rate crashed. A nurse called the ObGyn, who began an emergency cesarean 15 minutes later. The baby, born lifeless, was resuscitated. The child suffered permanent brain damage, and has cerebral palsy, severe cognitive deficits and speech deficits, and walks with an abnormal gait.

PARENTS’ CLAIM A physician did not see the patient for 24 hours, once the decision was made to monitor the mother, even though the fetal heart rate continued to decline. A biophysical profile test score of 2/8 indicates the need for immediate delivery. An earlier cesarean delivery could have reduced the child’s injuries.

DEFENDANTS’ DEFENSE After a settlement was reached with the hospital, the trial continued against the delivering ObGyn. He claimed that decreased fetal movement indicated that the brain injury had occurred 1 to 4 days before the mother came to the ED. The technician had manipulated the mother’s abdomen to wake the fetus before starting the first biophysical profile, which invalidated the score. The nurse miscommunicated the score of the second biophysical profile.

VERDICT A gross $29.8 million Illinois verdict was returned that included a $1.65 million settlement with the hospital.

WAS FACILITY ADEQUATELY STAFFED AFTER HURRICANE IKE?
A mother was admitted to a hospital for induction of labor in September 2008. After birth, the child was found to have cerebral palsy.

PARENTS’ CLAIM The mother should have been sent to another facility before delivery was induced because the hospital was short-staffed and low on resources due to Hurricane Ike. Too much oxytocin was used to induce contractions, which led to a lack of oxygen for the fetus. All prenatal testing had shown a healthy fetus. A cesarean delivery should have occurred when fetal distress was noted.

DEFENDANTS’ DEFENSE The mother had gastric bypass surgery 8 months before she became pregnant, and smoked during pregnancy, which accounted for the infant’s injuries. Treatment during labor and delivery was appropriate. Hospital staffing and resources were adequate.

VERDICT A $6.5 million Texas settlement was reached. 

PLACENTA ACCRETA; MOTHER DIES
A 33-year-old woman became pregnant with her second child. A variety of conditions caused this to be high-risk pregnancy, so she saw a maternal-fetal medicine (MFM) specialist 2 months before delivery. The MFM reported that his examination and the ultrasonography (US) results were normal.

The ObGyn who provided prenatal care and delivered her first child scheduled cesarean delivery. During the procedure, the ObGyn noticed a 3- to 4-inch lesion where the placenta had penetrated the uterus. When the placenta was removed, the patient began to hemorrhage and a hysterectomy was performed. The hemorrhage created blood clots that led to gangrene in the patient’s extremities. She died 5 days after giving birth.

ESTATE’S CLAIM Both the MFM and the ObGyn failed to recognize placenta accreta on US prior to delivery. The ObGyn should have performed US prior to beginning cesarean delivery. The hospital’s protocols were not followed: the ObGyn should have stopped the procedure and called for extra surgical assistance and additional blood when he encountered placenta accreta, and again when the patient began to hemorrhage. Placenta accreta does not have to be fatal if detected and managed properly.

DEFENDANTS’ DEFENSE There was no negligence; the patient was treated properly.

VERDICT A $15.5 million Illinois verdict was returned against both physicians and the medical center. 

Related article: Is the risk of placenta accreta in a subsequent pregnancy higher after emergent primary cesarean or after elective primary cesarean? Yinka Oyelese, MD (Examining the Evidence, December 2013)

ANTICONVULSANT AND MIGRAINE MEDS TAKEN DURING PREGNANCY
A woman was prescribed topiramate (Topamax) for migraine headaches and hand tremors during the first trimester of her pregnancy in 2007. With a history of seizures, she also took several anticonvulsants throughout her pregnancy. Her child was diagnosed with right unilateral cleft lip (cheiloschisis) in utero. The condition had not been surgically corrected at the time of trial.

PARENTS’ CLAIM The use of topiramate caused the child’s cleft lip. Janssen Pharmaceuticals, the manufacturer of Topamax, knew about the risk of birth defects associated with the drug in 2007, but failed to provide adequate warnings.

DEFENDANTS’ DEFENSE The mother received at least two warnings from her physician regarding the potential risks of anticonvulsant and antiepileptic drugs and the importance of not becoming pregnant while taking the medications. An action against the physician was barred by the applicable statute of limitations. The mother had taken topiramate prescribed to her mother for a time; such actions should release Janssen from liability.

VERDICT A $11 million Pennsylvania verdict was returned.

PID MASKS ECTOPIC PREGNANCY
A woman in her 40s became pregnant. On the first two prenatal diagnostic imaging studies, the ObGyn saw an intrauterine pregnancy. He later realized that the pregnancy was ectopic after beta human chorionic gonadotrophin (beta-hCG) blood levels were abnormal. During surgery to terminate the pregnancy, he found he had to perform a total hysterectomy because the patient had extensive pelvic inflammatory disease (PID) caused by a long history of sexually transmitted disease.

PATIENT’S CLAIM If the ectopic pregnancy had been diagnosed earlier, one of her ovaries could have been preserved, saving her from the symptoms of surgical menopause.

PHYSICIAN’S DEFENSE PID had caused the ovaries, numerous fibroid tumors, and the uterus to fuse into one mass. That was why the first two imaging studies appeared to show an intrauterine pregnancy. It was not possible to diagnose the extent of the problem until surgery. The patient did not have a true ectopic pregnancy.

The patient’s difficulties occurred during a 2-week time period in which she had one visit with him and another visit to an ED where two other physicians examined her and missed the diagnosis.

VERDICT A Michigan defense verdict was returned. 

ILIAC ARTERY INJURED DURING LAPAROSCOPIC SURGERY; PATIENT DIES
A 40-year-old woman underwent laparoscopic gynecologic surgery performed by her ObGyn. During the procedure, the patient’s left internal iliac artery was punctured, but the injury was not recognized at the time. She was discharged the same day. The next morning, she went into hypovolemic shock due to internal bleeding. She was taken to the ED, where she died.

ESTATE’S CLAIM The ObGyn, anesthesiologist, and hospital staff were negligent in their postoperative care. The anesthesiologist prescribed pain medication that masked the injury; the patient was discharged from the postanesthesia unit too early and without proper examination. The nursing staff did not react to the patient’s reports of abdominal pain, nor did they properly assess her condition prior to discharge. The ObGyn failed to return a phone call the evening after the procedure.

DEFENDANTS’ DEFENSE The ObGyn settled before trial. The anesthesiologist and hospital denied negligence: care was proper and followed all protocols.

VERDICT A confidential California settlement was reached with the ObGyn. A defense verdict was returned for the anesthesiologist and hospital. 

Related article: Anatomy for the laparoscopic surgeon Emad Mikhail, MD; Lauren Scott, MD; Stuart Hart, MD, MS (April 2014)

GENETIC TESTING MISSED A KEY DIAGNOSIS
A 40-year-old woman underwent genetic testing after she became pregnant. She was assured that there were no abnormalities that would impact her child.

The baby was born with Wolf-Hirschhorn syndrome, characterized by facial deformities, intellectual disabilities, delayed growth, and seizures. The child is nonverbal, deaf, and blind. She uses a feeding tube and requires 24-hour care.

PARENTS’ CLAIM The genetic testing was improperly conducted. The mother would have had an abortion if she’d known that the child was so disabled.

DEFENDANTS’ DEFENSE Settlements were mediated.

VERDICT A $6.15 million New Jersey settlement was reached on behalf of the hospital and two laboratory technicians, and a $1 million settlement was reached with the director of the genetic laboratory. 

HEAT INJURY TO COLON: ABSCESSES, PERITONITIS
A 43-year-old patient had a history of symptomatic uterine fibroids and infertility. Her ObGyn performed a hysteroscopy because he suspected endometriosis, but found none. He then successfully removed a large uterine fibroid during laparoscopic myomectomy. The patient was discharged the same day.

Two days later, the patient developed abdominal pain, nausea, and fever. She went to the ED and was taken into emergency surgery after a CT scan showed free air and fluid in her abdomen. She suffered multiple abscesses and peritonitis.

PATIENT’S CLAIM The ObGyn was negligent in performing the surgery: the sigmoid colon sustained a thermal injury, which caused the abscesses and peritonitis.

PHYSICIAN’S DEFENSE There was no evidence of thermal injury during the original operation; heat damage can and does occur in the absence of negligence. The patient’s previously unknown diverticulitis contributed to the development of the recurrent abscesses and peritonitis.

VERDICT A Florida defense verdict was returned.

RUPTURED UTERUS IS UNDETECTED
During labor and delivery, a declining fetal heart rate was observed, but there was an hour’s delay before cesarean delivery was started. The child suffered a hypoxic brain injury. He has spastic quadriplegia, cannot speak, and requires a respirator and feeding tube.

PARENTS’ CLAIM The mother suffered a ruptured uterus during labor that was not recognized by the ObGyn or nursing staff.

DEFENDANTS’ DEFENSE A settlement was reached during trial.

VERDICT A $7.5 million New Jersey settlement was reached.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Tell us what you think!
Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected] Please include your name, city and state.
Stay in touch! Your feedback is important to us!

PATIENT’S CLAIM The hemorrhage was caused when enoxaparin was given at 1.5 times the proper dosage because the patient’s weight was overestimated by 50%. Excessive blood, plasma, and fluids caused her weight to double after resuscitation. Her intestines were forced out of her abdominal cavity by the hemorrhage. A permanent hernia, visible underneath her skin, causes pain.

DEFENDANTS’ DEFENSE The patient’s preexisting diabetes, heart condition, high cholesterol levels, and orthopedic issues impacted her condition. She was not compliant in managing her diabetes, causing many of the current problems.

VERDICT A $9.3 million Connecticut verdict was returned.

Related article: Update: Pelvic floor dysfunction Autumn L. Edenfield, MD, and Cindy L. Amundsen, MD (October 2012)

CESAREAN DELAYED UNNECESSARILY
At 37 weeks’ gestation, a mother reported decreased fetal movement. When the biophysical profile test scored 8/8 and the fetal heart rate was reassuring, the attending ObGyn discharged the patient. However, it was the middle of the night, and the nurse kept the mother in the emergency department (ED). At 8:30 am, the fetus began to show signs of fetal distress. Three ObGyns agreed to monitor labor, although one physician wanted delivery to occur that morning.

The next morning, a second biophysical profile scored 2/8, but the on-call ObGyn misunderstood the score as 6/8 and scheduled cesarean delivery for noon. Two hours after the second biophysical profile, the fetal heart rate crashed. A nurse called the ObGyn, who began an emergency cesarean 15 minutes later. The baby, born lifeless, was resuscitated. The child suffered permanent brain damage, and has cerebral palsy, severe cognitive deficits and speech deficits, and walks with an abnormal gait.

PARENTS’ CLAIM A physician did not see the patient for 24 hours, once the decision was made to monitor the mother, even though the fetal heart rate continued to decline. A biophysical profile test score of 2/8 indicates the need for immediate delivery. An earlier cesarean delivery could have reduced the child’s injuries.

DEFENDANTS’ DEFENSE After a settlement was reached with the hospital, the trial continued against the delivering ObGyn. He claimed that decreased fetal movement indicated that the brain injury had occurred 1 to 4 days before the mother came to the ED. The technician had manipulated the mother’s abdomen to wake the fetus before starting the first biophysical profile, which invalidated the score. The nurse miscommunicated the score of the second biophysical profile.

VERDICT A gross $29.8 million Illinois verdict was returned that included a $1.65 million settlement with the hospital.

WAS FACILITY ADEQUATELY STAFFED AFTER HURRICANE IKE?
A mother was admitted to a hospital for induction of labor in September 2008. After birth, the child was found to have cerebral palsy.

PARENTS’ CLAIM The mother should have been sent to another facility before delivery was induced because the hospital was short-staffed and low on resources due to Hurricane Ike. Too much oxytocin was used to induce contractions, which led to a lack of oxygen for the fetus. All prenatal testing had shown a healthy fetus. A cesarean delivery should have occurred when fetal distress was noted.

DEFENDANTS’ DEFENSE The mother had gastric bypass surgery 8 months before she became pregnant, and smoked during pregnancy, which accounted for the infant’s injuries. Treatment during labor and delivery was appropriate. Hospital staffing and resources were adequate.

VERDICT A $6.5 million Texas settlement was reached. 

PLACENTA ACCRETA; MOTHER DIES
A 33-year-old woman became pregnant with her second child. A variety of conditions caused this to be high-risk pregnancy, so she saw a maternal-fetal medicine (MFM) specialist 2 months before delivery. The MFM reported that his examination and the ultrasonography (US) results were normal.

The ObGyn who provided prenatal care and delivered her first child scheduled cesarean delivery. During the procedure, the ObGyn noticed a 3- to 4-inch lesion where the placenta had penetrated the uterus. When the placenta was removed, the patient began to hemorrhage and a hysterectomy was performed. The hemorrhage created blood clots that led to gangrene in the patient’s extremities. She died 5 days after giving birth.

ESTATE’S CLAIM Both the MFM and the ObGyn failed to recognize placenta accreta on US prior to delivery. The ObGyn should have performed US prior to beginning cesarean delivery. The hospital’s protocols were not followed: the ObGyn should have stopped the procedure and called for extra surgical assistance and additional blood when he encountered placenta accreta, and again when the patient began to hemorrhage. Placenta accreta does not have to be fatal if detected and managed properly.

DEFENDANTS’ DEFENSE There was no negligence; the patient was treated properly.

VERDICT A $15.5 million Illinois verdict was returned against both physicians and the medical center. 

Related article: Is the risk of placenta accreta in a subsequent pregnancy higher after emergent primary cesarean or after elective primary cesarean? Yinka Oyelese, MD (Examining the Evidence, December 2013)

ANTICONVULSANT AND MIGRAINE MEDS TAKEN DURING PREGNANCY
A woman was prescribed topiramate (Topamax) for migraine headaches and hand tremors during the first trimester of her pregnancy in 2007. With a history of seizures, she also took several anticonvulsants throughout her pregnancy. Her child was diagnosed with right unilateral cleft lip (cheiloschisis) in utero. The condition had not been surgically corrected at the time of trial.

PARENTS’ CLAIM The use of topiramate caused the child’s cleft lip. Janssen Pharmaceuticals, the manufacturer of Topamax, knew about the risk of birth defects associated with the drug in 2007, but failed to provide adequate warnings.

DEFENDANTS’ DEFENSE The mother received at least two warnings from her physician regarding the potential risks of anticonvulsant and antiepileptic drugs and the importance of not becoming pregnant while taking the medications. An action against the physician was barred by the applicable statute of limitations. The mother had taken topiramate prescribed to her mother for a time; such actions should release Janssen from liability.

VERDICT A $11 million Pennsylvania verdict was returned.

PID MASKS ECTOPIC PREGNANCY
A woman in her 40s became pregnant. On the first two prenatal diagnostic imaging studies, the ObGyn saw an intrauterine pregnancy. He later realized that the pregnancy was ectopic after beta human chorionic gonadotrophin (beta-hCG) blood levels were abnormal. During surgery to terminate the pregnancy, he found he had to perform a total hysterectomy because the patient had extensive pelvic inflammatory disease (PID) caused by a long history of sexually transmitted disease.

PATIENT’S CLAIM If the ectopic pregnancy had been diagnosed earlier, one of her ovaries could have been preserved, saving her from the symptoms of surgical menopause.

PHYSICIAN’S DEFENSE PID had caused the ovaries, numerous fibroid tumors, and the uterus to fuse into one mass. That was why the first two imaging studies appeared to show an intrauterine pregnancy. It was not possible to diagnose the extent of the problem until surgery. The patient did not have a true ectopic pregnancy.

The patient’s difficulties occurred during a 2-week time period in which she had one visit with him and another visit to an ED where two other physicians examined her and missed the diagnosis.

VERDICT A Michigan defense verdict was returned. 

ILIAC ARTERY INJURED DURING LAPAROSCOPIC SURGERY; PATIENT DIES
A 40-year-old woman underwent laparoscopic gynecologic surgery performed by her ObGyn. During the procedure, the patient’s left internal iliac artery was punctured, but the injury was not recognized at the time. She was discharged the same day. The next morning, she went into hypovolemic shock due to internal bleeding. She was taken to the ED, where she died.

ESTATE’S CLAIM The ObGyn, anesthesiologist, and hospital staff were negligent in their postoperative care. The anesthesiologist prescribed pain medication that masked the injury; the patient was discharged from the postanesthesia unit too early and without proper examination. The nursing staff did not react to the patient’s reports of abdominal pain, nor did they properly assess her condition prior to discharge. The ObGyn failed to return a phone call the evening after the procedure.

DEFENDANTS’ DEFENSE The ObGyn settled before trial. The anesthesiologist and hospital denied negligence: care was proper and followed all protocols.

VERDICT A confidential California settlement was reached with the ObGyn. A defense verdict was returned for the anesthesiologist and hospital. 

Related article: Anatomy for the laparoscopic surgeon Emad Mikhail, MD; Lauren Scott, MD; Stuart Hart, MD, MS (April 2014)

GENETIC TESTING MISSED A KEY DIAGNOSIS
A 40-year-old woman underwent genetic testing after she became pregnant. She was assured that there were no abnormalities that would impact her child.

The baby was born with Wolf-Hirschhorn syndrome, characterized by facial deformities, intellectual disabilities, delayed growth, and seizures. The child is nonverbal, deaf, and blind. She uses a feeding tube and requires 24-hour care.

PARENTS’ CLAIM The genetic testing was improperly conducted. The mother would have had an abortion if she’d known that the child was so disabled.

DEFENDANTS’ DEFENSE Settlements were mediated.

VERDICT A $6.15 million New Jersey settlement was reached on behalf of the hospital and two laboratory technicians, and a $1 million settlement was reached with the director of the genetic laboratory. 

HEAT INJURY TO COLON: ABSCESSES, PERITONITIS
A 43-year-old patient had a history of symptomatic uterine fibroids and infertility. Her ObGyn performed a hysteroscopy because he suspected endometriosis, but found none. He then successfully removed a large uterine fibroid during laparoscopic myomectomy. The patient was discharged the same day.

Two days later, the patient developed abdominal pain, nausea, and fever. She went to the ED and was taken into emergency surgery after a CT scan showed free air and fluid in her abdomen. She suffered multiple abscesses and peritonitis.

PATIENT’S CLAIM The ObGyn was negligent in performing the surgery: the sigmoid colon sustained a thermal injury, which caused the abscesses and peritonitis.

PHYSICIAN’S DEFENSE There was no evidence of thermal injury during the original operation; heat damage can and does occur in the absence of negligence. The patient’s previously unknown diverticulitis contributed to the development of the recurrent abscesses and peritonitis.

VERDICT A Florida defense verdict was returned.

RUPTURED UTERUS IS UNDETECTED
During labor and delivery, a declining fetal heart rate was observed, but there was an hour’s delay before cesarean delivery was started. The child suffered a hypoxic brain injury. He has spastic quadriplegia, cannot speak, and requires a respirator and feeding tube.

PARENTS’ CLAIM The mother suffered a ruptured uterus during labor that was not recognized by the ObGyn or nursing staff.

DEFENDANTS’ DEFENSE A settlement was reached during trial.

VERDICT A $7.5 million New Jersey settlement was reached.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

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Nurse treating cancer patient

Credit: Rhoda Baer

A new report shows the rate of invasive cancer among US men and women dropped slightly from 2009 to 2010, and the most common cancers were solid tumor malignancies.

However, non-Hodgkin lymphoma (NHL) consistently rated among the top 10 most common cancers, regardless of patient gender or race.

The report was prepared by the Centers for Disease Control and Prevention (CDC) and appears in the current Morbidity and Mortality Weekly Report.

Researchers analyzed new cases of invasive cancers diagnosed in 2010 and reported to the CDC’s National Program of Cancer Registries and the National Cancer Institute’s Surveillance, Epidemiology and Results Program.

Data from all states (except Arkansas and Minnesota) and the District of Columbia were included in the analysis, which covered 97% of the US population.

The researchers found the rates of invasive cancer cases dropped from 459 per 100,000 people in 2009 to 446 per 100,000 in 2010.

Cancer rates were higher among men (503 per 100,000) than women (405 per 100,000). In all, there were 745,383 cases reported among men and 711,113 among women in 2010.

The highest rates were for cancers of the prostate (126 per 100,000), female breast (119 per 100,000), lung and bronchus (62 per 100,000), and colon and rectum (40 per 100,000). Together, these accounted for half of all cancer cases in the US.

However, hematologic malignancies were fairly common as well. NHL was the 6th most common cancer for men of all races/ethnicities except Hispanic. For this group, NHL was the 4th most common cancer.

NHL was the 7th most common cancer for black and white women and 6th for the remaining groups, which included American Indian/Alaskan native, Asian/Pacific Islander, and Hispanic women.

Leukemia and myeloma were also among the top 10 most common invasive cancers for certain patients.

Leukemia was the 9th most common cancer for Hispanic and white men and the 10th for American Indian/Alaskan Native women. Myeloma was the 8th most common cancer for black women.

Overall, cancer rates were highest among black patients (455 per 100,000), followed by whites (445 per 100,000), Hispanics (344 per 100,000), Asian/Pacific Islanders (289 per 100,000), and American Indians/Alaskan Natives (270 per 100,000).

Nurse treating cancer patient

Credit: Rhoda Baer

A new report shows the rate of invasive cancer among US men and women dropped slightly from 2009 to 2010, and the most common cancers were solid tumor malignancies.

However, non-Hodgkin lymphoma (NHL) consistently rated among the top 10 most common cancers, regardless of patient gender or race.

The report was prepared by the Centers for Disease Control and Prevention (CDC) and appears in the current Morbidity and Mortality Weekly Report.

Researchers analyzed new cases of invasive cancers diagnosed in 2010 and reported to the CDC’s National Program of Cancer Registries and the National Cancer Institute’s Surveillance, Epidemiology and Results Program.

Data from all states (except Arkansas and Minnesota) and the District of Columbia were included in the analysis, which covered 97% of the US population.

The researchers found the rates of invasive cancer cases dropped from 459 per 100,000 people in 2009 to 446 per 100,000 in 2010.

Cancer rates were higher among men (503 per 100,000) than women (405 per 100,000). In all, there were 745,383 cases reported among men and 711,113 among women in 2010.

The highest rates were for cancers of the prostate (126 per 100,000), female breast (119 per 100,000), lung and bronchus (62 per 100,000), and colon and rectum (40 per 100,000). Together, these accounted for half of all cancer cases in the US.

However, hematologic malignancies were fairly common as well. NHL was the 6th most common cancer for men of all races/ethnicities except Hispanic. For this group, NHL was the 4th most common cancer.

NHL was the 7th most common cancer for black and white women and 6th for the remaining groups, which included American Indian/Alaskan native, Asian/Pacific Islander, and Hispanic women.

Leukemia and myeloma were also among the top 10 most common invasive cancers for certain patients.

Leukemia was the 9th most common cancer for Hispanic and white men and the 10th for American Indian/Alaskan Native women. Myeloma was the 8th most common cancer for black women.

Overall, cancer rates were highest among black patients (455 per 100,000), followed by whites (445 per 100,000), Hispanics (344 per 100,000), Asian/Pacific Islanders (289 per 100,000), and American Indians/Alaskan Natives (270 per 100,000).

Nurse treating cancer patient

Credit: Rhoda Baer

A new report shows the rate of invasive cancer among US men and women dropped slightly from 2009 to 2010, and the most common cancers were solid tumor malignancies.

However, non-Hodgkin lymphoma (NHL) consistently rated among the top 10 most common cancers, regardless of patient gender or race.

The report was prepared by the Centers for Disease Control and Prevention (CDC) and appears in the current Morbidity and Mortality Weekly Report.

Researchers analyzed new cases of invasive cancers diagnosed in 2010 and reported to the CDC’s National Program of Cancer Registries and the National Cancer Institute’s Surveillance, Epidemiology and Results Program.

Data from all states (except Arkansas and Minnesota) and the District of Columbia were included in the analysis, which covered 97% of the US population.

The researchers found the rates of invasive cancer cases dropped from 459 per 100,000 people in 2009 to 446 per 100,000 in 2010.

Cancer rates were higher among men (503 per 100,000) than women (405 per 100,000). In all, there were 745,383 cases reported among men and 711,113 among women in 2010.

The highest rates were for cancers of the prostate (126 per 100,000), female breast (119 per 100,000), lung and bronchus (62 per 100,000), and colon and rectum (40 per 100,000). Together, these accounted for half of all cancer cases in the US.

However, hematologic malignancies were fairly common as well. NHL was the 6th most common cancer for men of all races/ethnicities except Hispanic. For this group, NHL was the 4th most common cancer.

NHL was the 7th most common cancer for black and white women and 6th for the remaining groups, which included American Indian/Alaskan native, Asian/Pacific Islander, and Hispanic women.

Leukemia and myeloma were also among the top 10 most common invasive cancers for certain patients.

Leukemia was the 9th most common cancer for Hispanic and white men and the 10th for American Indian/Alaskan Native women. Myeloma was the 8th most common cancer for black women.

Overall, cancer rates were highest among black patients (455 per 100,000), followed by whites (445 per 100,000), Hispanics (344 per 100,000), Asian/Pacific Islanders (289 per 100,000), and American Indians/Alaskan Natives (270 per 100,000).

Red blood cells

Credit: NHLBI

Results of preclinical research could aid the development of new treatments for hemolysis, which may have implications for patients with sickle cell anemia and those who receive blood transfusions.

The researchers were investigating the possibility of using haptoglobin to prevent the chemical reactions triggered by hemoglobin after hemolysis.

Haptoglobin is known to bind acellular adult hemoglobin dimers and facilitate their clearance after hemolysis.

But haptoglobin exists in different forms. The 3 main phenotypes—Hp1-1, Hp2-1, and Hp2-2—have diverse structural configurations, and previous research suggested they have different biological activities.

With the current study, however, the researchers showed the different forms of haptoglobin actually exhibit similar activity.

Todd L. Mollan, PhD, of the Center for Biologics Evaluation and Research at the Food and Drug Administration in Bethesda, Maryland, and his colleagues presented these findings in Free Radical Biology and Medicine.

The researchers studied hemoglobin dimers in complex with unfractionated haptoglobin (a mixture of Hp1-1, Hp2-1, and Hp2-2); fractionated, dimeric haptoglobin (Hp1-1); and fractionated, polymeric haptoglobin (predominantly Hp2-2, with minor amounts of Hp2-1).

The team also complexed ferrous and ferric hemoglobins with unfractionated haptoglobin and its fractionated forms.

Experiments revealed no significant differences among the different complexes with regard to hemoglobin-haptoglobin binding kinetics, hydrogen-peroxide-driven oxidative transitions of the heme iron, radical formation, heme loss, or intrinsic redox potential.

The researchers said these results should be taken into account when designing phenotype-specific haptoglobin therapies.

Red blood cells

Credit: NHLBI

Results of preclinical research could aid the development of new treatments for hemolysis, which may have implications for patients with sickle cell anemia and those who receive blood transfusions.

The researchers were investigating the possibility of using haptoglobin to prevent the chemical reactions triggered by hemoglobin after hemolysis.

Haptoglobin is known to bind acellular adult hemoglobin dimers and facilitate their clearance after hemolysis.

But haptoglobin exists in different forms. The 3 main phenotypes—Hp1-1, Hp2-1, and Hp2-2—have diverse structural configurations, and previous research suggested they have different biological activities.

With the current study, however, the researchers showed the different forms of haptoglobin actually exhibit similar activity.

Todd L. Mollan, PhD, of the Center for Biologics Evaluation and Research at the Food and Drug Administration in Bethesda, Maryland, and his colleagues presented these findings in Free Radical Biology and Medicine.

The researchers studied hemoglobin dimers in complex with unfractionated haptoglobin (a mixture of Hp1-1, Hp2-1, and Hp2-2); fractionated, dimeric haptoglobin (Hp1-1); and fractionated, polymeric haptoglobin (predominantly Hp2-2, with minor amounts of Hp2-1).

The team also complexed ferrous and ferric hemoglobins with unfractionated haptoglobin and its fractionated forms.

Experiments revealed no significant differences among the different complexes with regard to hemoglobin-haptoglobin binding kinetics, hydrogen-peroxide-driven oxidative transitions of the heme iron, radical formation, heme loss, or intrinsic redox potential.

The researchers said these results should be taken into account when designing phenotype-specific haptoglobin therapies.

Red blood cells

Credit: NHLBI

Results of preclinical research could aid the development of new treatments for hemolysis, which may have implications for patients with sickle cell anemia and those who receive blood transfusions.

The researchers were investigating the possibility of using haptoglobin to prevent the chemical reactions triggered by hemoglobin after hemolysis.

Haptoglobin is known to bind acellular adult hemoglobin dimers and facilitate their clearance after hemolysis.

But haptoglobin exists in different forms. The 3 main phenotypes—Hp1-1, Hp2-1, and Hp2-2—have diverse structural configurations, and previous research suggested they have different biological activities.

With the current study, however, the researchers showed the different forms of haptoglobin actually exhibit similar activity.

Todd L. Mollan, PhD, of the Center for Biologics Evaluation and Research at the Food and Drug Administration in Bethesda, Maryland, and his colleagues presented these findings in Free Radical Biology and Medicine.

The researchers studied hemoglobin dimers in complex with unfractionated haptoglobin (a mixture of Hp1-1, Hp2-1, and Hp2-2); fractionated, dimeric haptoglobin (Hp1-1); and fractionated, polymeric haptoglobin (predominantly Hp2-2, with minor amounts of Hp2-1).

The team also complexed ferrous and ferric hemoglobins with unfractionated haptoglobin and its fractionated forms.

Experiments revealed no significant differences among the different complexes with regard to hemoglobin-haptoglobin binding kinetics, hydrogen-peroxide-driven oxidative transitions of the heme iron, radical formation, heme loss, or intrinsic redox potential.

The researchers said these results should be taken into account when designing phenotype-specific haptoglobin therapies.