Colon cancer screening comes too late

AFTER 14 YEARS OF TREATMENT by her physician, a 73-year-old woman with a medical history that included chronic obstructive pulmonary disease and major depression underwent her first colonoscopy. It revealed colon cancer. The patient died about a year and a half later.

PLAINTIFF’S CLAIM No information about the plaintiff’s claim is available.

THE DEFENSE The physician claimed that the patient had declined his recommendations for colon cancer screening many times and that she had failed to return stool samples from a home test kit he had given her. The physician’s medical records, which began in 2001, didn’t reflect his screening recommendations. Earlier records had been destroyed in 2007 in accordance with office policy.

VERDICT $500,000 Massachusetts settlement.

COMMENT Do you routinely document refusal of preventive services by your patients? If not, you, too, may fall victim to a plaintiff’s attorney!

A drug reaction with lasting consequences

AN ALLERGIC REACTION to trimethoprim/ sulfamethoxazole caused skin changes in a 44-year-old woman. Nevertheless, her physician prescribed another regimen of the drug 4 years later. This time, the patient had a full-blown allergic reaction, characterized by red, scaly, weepy skin and elevated liver enzymes, among other symptoms.

After several emergency department visits and a hospital admission, the patient was transferred to the burn unit of a regional medical center, with a presumed diagnosis of Stevens-Johnson syndrome (SJS). After evaluating the patient, however, the director of the burn unit concluded that her symptoms were not severe enough to be SJS; he attributed them to a simple drug reaction and had the patient moved to a medical/surgical floor.

At some point, she developed peripheral sensory neuropathy in her hands and feet. The parties involved disagreed about when the neuropathy began and what caused it.

PLAINTIFF’S CLAIM The patient should not have been transferred to the medical/surgical unit; the higher level of care provided on the burn unit would have prevented the peripheral neuropathy. The patient received inadequate nutrition, which contributed to her injuries.

THE DEFENSE Because the patient didn’t actually have SJS, the medical/surgical floor was the appropriate place to treat her. The patient received proper skin care and nutrition. The patient had complained of numbness and tingling in her hands and feet before she was hospitalized, indicating that the drug-related neuropathy had existed before admission to the regional facility.

VERDICT Defense verdict following confidential settlement with the physician who prescribed trimethoprim/sulfamethoxazole.

COMMENT When prescribing any antibiotic, always confirm that the patient isn’t allergic to it. Have your nurses and medical assistants help you maintain accurate medication and allergy lists in your office chart or electronic medical record.

A colonoscopy, then hepatitis C

AFTER UNDERGOING A COLONOSCOPY, a 44-year-old man was diagnosed with hepatitis C. He claimed that the infection had been transmitted by the anesthetic used during the procedure.

PLAINTIFF’S CLAIM The anesthesiologist drew the anesthetic from a multiple-dose vial that had been used during previous procedures; proper sterile techniques weren’t followed.

THE DEFENSE No information about the defense is available.

VERDICT $675,000 New York settlement.

COMMENT I thought this practice had stopped 20 years ago. Review your office procedures and make sure it doesn’t happen. Don’t use single-dose, single-use vials for more than one patient—ever.

Colon cancer screening comes too late

AFTER 14 YEARS OF TREATMENT by her physician, a 73-year-old woman with a medical history that included chronic obstructive pulmonary disease and major depression underwent her first colonoscopy. It revealed colon cancer. The patient died about a year and a half later.

PLAINTIFF’S CLAIM No information about the plaintiff’s claim is available.

THE DEFENSE The physician claimed that the patient had declined his recommendations for colon cancer screening many times and that she had failed to return stool samples from a home test kit he had given her. The physician’s medical records, which began in 2001, didn’t reflect his screening recommendations. Earlier records had been destroyed in 2007 in accordance with office policy.

VERDICT $500,000 Massachusetts settlement.

COMMENT Do you routinely document refusal of preventive services by your patients? If not, you, too, may fall victim to a plaintiff’s attorney!

A drug reaction with lasting consequences

AN ALLERGIC REACTION to trimethoprim/ sulfamethoxazole caused skin changes in a 44-year-old woman. Nevertheless, her physician prescribed another regimen of the drug 4 years later. This time, the patient had a full-blown allergic reaction, characterized by red, scaly, weepy skin and elevated liver enzymes, among other symptoms.

After several emergency department visits and a hospital admission, the patient was transferred to the burn unit of a regional medical center, with a presumed diagnosis of Stevens-Johnson syndrome (SJS). After evaluating the patient, however, the director of the burn unit concluded that her symptoms were not severe enough to be SJS; he attributed them to a simple drug reaction and had the patient moved to a medical/surgical floor.

At some point, she developed peripheral sensory neuropathy in her hands and feet. The parties involved disagreed about when the neuropathy began and what caused it.

PLAINTIFF’S CLAIM The patient should not have been transferred to the medical/surgical unit; the higher level of care provided on the burn unit would have prevented the peripheral neuropathy. The patient received inadequate nutrition, which contributed to her injuries.

THE DEFENSE Because the patient didn’t actually have SJS, the medical/surgical floor was the appropriate place to treat her. The patient received proper skin care and nutrition. The patient had complained of numbness and tingling in her hands and feet before she was hospitalized, indicating that the drug-related neuropathy had existed before admission to the regional facility.

VERDICT Defense verdict following confidential settlement with the physician who prescribed trimethoprim/sulfamethoxazole.

COMMENT When prescribing any antibiotic, always confirm that the patient isn’t allergic to it. Have your nurses and medical assistants help you maintain accurate medication and allergy lists in your office chart or electronic medical record.

A colonoscopy, then hepatitis C

AFTER UNDERGOING A COLONOSCOPY, a 44-year-old man was diagnosed with hepatitis C. He claimed that the infection had been transmitted by the anesthetic used during the procedure.

PLAINTIFF’S CLAIM The anesthesiologist drew the anesthetic from a multiple-dose vial that had been used during previous procedures; proper sterile techniques weren’t followed.

THE DEFENSE No information about the defense is available.

VERDICT $675,000 New York settlement.

COMMENT I thought this practice had stopped 20 years ago. Review your office procedures and make sure it doesn’t happen. Don’t use single-dose, single-use vials for more than one patient—ever.

Colon cancer screening comes too late

AFTER 14 YEARS OF TREATMENT by her physician, a 73-year-old woman with a medical history that included chronic obstructive pulmonary disease and major depression underwent her first colonoscopy. It revealed colon cancer. The patient died about a year and a half later.

PLAINTIFF’S CLAIM No information about the plaintiff’s claim is available.

THE DEFENSE The physician claimed that the patient had declined his recommendations for colon cancer screening many times and that she had failed to return stool samples from a home test kit he had given her. The physician’s medical records, which began in 2001, didn’t reflect his screening recommendations. Earlier records had been destroyed in 2007 in accordance with office policy.

VERDICT $500,000 Massachusetts settlement.

COMMENT Do you routinely document refusal of preventive services by your patients? If not, you, too, may fall victim to a plaintiff’s attorney!

A drug reaction with lasting consequences

AN ALLERGIC REACTION to trimethoprim/ sulfamethoxazole caused skin changes in a 44-year-old woman. Nevertheless, her physician prescribed another regimen of the drug 4 years later. This time, the patient had a full-blown allergic reaction, characterized by red, scaly, weepy skin and elevated liver enzymes, among other symptoms.

After several emergency department visits and a hospital admission, the patient was transferred to the burn unit of a regional medical center, with a presumed diagnosis of Stevens-Johnson syndrome (SJS). After evaluating the patient, however, the director of the burn unit concluded that her symptoms were not severe enough to be SJS; he attributed them to a simple drug reaction and had the patient moved to a medical/surgical floor.

At some point, she developed peripheral sensory neuropathy in her hands and feet. The parties involved disagreed about when the neuropathy began and what caused it.

PLAINTIFF’S CLAIM The patient should not have been transferred to the medical/surgical unit; the higher level of care provided on the burn unit would have prevented the peripheral neuropathy. The patient received inadequate nutrition, which contributed to her injuries.

THE DEFENSE Because the patient didn’t actually have SJS, the medical/surgical floor was the appropriate place to treat her. The patient received proper skin care and nutrition. The patient had complained of numbness and tingling in her hands and feet before she was hospitalized, indicating that the drug-related neuropathy had existed before admission to the regional facility.

VERDICT Defense verdict following confidential settlement with the physician who prescribed trimethoprim/sulfamethoxazole.

COMMENT When prescribing any antibiotic, always confirm that the patient isn’t allergic to it. Have your nurses and medical assistants help you maintain accurate medication and allergy lists in your office chart or electronic medical record.

A colonoscopy, then hepatitis C

AFTER UNDERGOING A COLONOSCOPY, a 44-year-old man was diagnosed with hepatitis C. He claimed that the infection had been transmitted by the anesthetic used during the procedure.

PLAINTIFF’S CLAIM The anesthesiologist drew the anesthetic from a multiple-dose vial that had been used during previous procedures; proper sterile techniques weren’t followed.

THE DEFENSE No information about the defense is available.

VERDICT $675,000 New York settlement.

COMMENT I thought this practice had stopped 20 years ago. Review your office procedures and make sure it doesn’t happen. Don’t use single-dose, single-use vials for more than one patient—ever.

ILLUSTRATIVE CASE

When you prescribe an antibiotic for a 45-year-old patient with Helicobacter pylori, he worries that the medication will cause diarrhea. Should you recommend that he take probiotics?

More than a third of patients taking antibiotics develop AAD,² and in 17% of cases, AAD is fatal.^3,4 Although the diarrhea may be the result of increased gastrointestinal (GI) motility in some cases, a disruption of the GI flora that normally acts as a barrier to infection and aids in the digestion of carbohydrates is a far more common cause.

Morbidity and mortality are high
AAD is associated with several pathogens, including Clostridium difficile, Clostridium perfringens, Klebsiella oxytoca, and Staphylococcus aureus,² and varies widely in severity. Pseudomembranous colitis secondary to C difficile is the main cause of AAD-related mortality, which more than doubled from 2002 to 2009.^3,4 C difficile infections cost the US health care system up to $1.3 billion annually.⁵ With such high rates of morbidity and mortality and high health care costs associated with AAD, even a small reduction in the number of cases would have a big impact.

Probiotics replenish the natural GI flora with nonpathogenic organisms. A 2006 meta-analysis of 31 randomized controlled trials (RCTs) assessing the efficacy of probiotics for both the prevention of AAD and treatment of C difficile found a pooled relative risk of 0.43 for AAD in the patients taking probiotics.⁶ However, many of the studies included in that meta-analysis were small. As a result, in 2010, the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA) recommended against the use of probiotics for the prevention of primary C difficile infection, citing a lack of high-quality evidence.⁷

Nonetheless, that same year, 98% of gastroenterologists surveyed expressed a belief that probiotics had a role in the treatment of GI illness.⁸ And in 2011, the 3rd Yale Working Group on Probiotic Use published recommendations for probiotic use based on expert opinion.⁹ The meta-analysis detailed in this PURL, which included more than 30 trials published since the 2006 meta-analysis, addressed the efficacy of probiotics for prevention and treatment of AAD.

STUDY SUMMARY: Probiotics significantly reduce AAD

Hempel et al reviewed 82 studies and pooled data from 63 RCTs (N=11,811) to identify the relative risk (RR) of AAD among patients who received probiotics during antibiotic treatment compared with those who received no probiotics or were given a placebo.¹ The studies encompassed a variety of antibiotics, taken alone or in combination, and several probiotics, including Lactobacillus, Bifidobacterium, Saccharomyces, and some combinations.

The outcome: The pooled RR for AAD in the probiotics groups was 0.58 (95% confidence interval, 0.50-0.68; P<.001), with a number needed to treat of 13. Although the authors reported that the overall quality of the included trials was poor, a sensitivity analysis of the higher quality studies yielded similar results.

Subgroup analyses by type of probiotic and duration of antibiotic treatment were also consistent with the overall pooled RR. In subgroup analysis by age, a similar decrease in AAD was found among the youngest patients (0-17 years) and those between the ages of 17 and 65 years. Among patients older than 65 years—for whom there were just 3 studies—a non-significant decrease in risk was found. Twenty-three of the studies assessed adverse outcomes, and none was found.

WHAT’S NEW: A reason to pair antibiotics and probiotics

This meta-analysis reached a similar conclusion as the 2006 meta-analysis: Probiotics appear to be effective in preventing and treating AAD in children and adults receiving a wide variety of antibiotics for a number of conditions. The results were also consistent with those of a new meta-analysis that looked specifically at one pathogen—and found a reduction of 66% in C difficile-associated diarrhea in patients taking probiotics with their antibiotics.¹⁰

CAVEATS: Limited data on the safety of probiotics exist

There was some heterogeneity among the studies in the meta-analysis by Hempel et al, and some of the studies were of poor quality. Because of this, the authors used subgroup and sensitivity analysis, which supported their initial conclusion.

Probiotics have generally been considered safe; however, there have been rare reports of sepsis and fungemia associated with probiotic use, especially in immunosuppressed patients.¹ Fifty-nine of the included studies did not assess adverse events, which limited the ability of this meta-analysis to assess safety.¹ Patients taking probiotics should be monitored for adverse effects.

CHALLENGES TO IMPLEMENTATION: Lack of guidance on dosing and duration

Since probiotics are considered food supplements, health insurance will not cover the cost (which will likely be more than $20 per month; www.walgreens.com). No single probiotic strain has high-quality evidence; however, most of the RCTs included in the meta-analysis used combinations of Lactobacillus species, which are usually found in over-the-counter antidiarrheal probiotic supplements. No standard dose exists, but dose ranges in RCTs are 10⁷ to 10¹⁰ colony-forming units per capsule (taken one to 3 times daily);¹ however, product labels have variable accuracy.¹¹ The duration of treatment ranges from one to 3 weeks—or as long as the patient continues to take antibiotics.

Acknowledgement

The PURLs Surveillance System was developed with support from Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

When you prescribe an antibiotic for a 45-year-old patient with Helicobacter pylori, he worries that the medication will cause diarrhea. Should you recommend that he take probiotics?

More than a third of patients taking antibiotics develop AAD,² and in 17% of cases, AAD is fatal.^3,4 Although the diarrhea may be the result of increased gastrointestinal (GI) motility in some cases, a disruption of the GI flora that normally acts as a barrier to infection and aids in the digestion of carbohydrates is a far more common cause.

Morbidity and mortality are high
AAD is associated with several pathogens, including Clostridium difficile, Clostridium perfringens, Klebsiella oxytoca, and Staphylococcus aureus,² and varies widely in severity. Pseudomembranous colitis secondary to C difficile is the main cause of AAD-related mortality, which more than doubled from 2002 to 2009.^3,4 C difficile infections cost the US health care system up to $1.3 billion annually.⁵ With such high rates of morbidity and mortality and high health care costs associated with AAD, even a small reduction in the number of cases would have a big impact.

Probiotics replenish the natural GI flora with nonpathogenic organisms. A 2006 meta-analysis of 31 randomized controlled trials (RCTs) assessing the efficacy of probiotics for both the prevention of AAD and treatment of C difficile found a pooled relative risk of 0.43 for AAD in the patients taking probiotics.⁶ However, many of the studies included in that meta-analysis were small. As a result, in 2010, the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA) recommended against the use of probiotics for the prevention of primary C difficile infection, citing a lack of high-quality evidence.⁷

Nonetheless, that same year, 98% of gastroenterologists surveyed expressed a belief that probiotics had a role in the treatment of GI illness.⁸ And in 2011, the 3rd Yale Working Group on Probiotic Use published recommendations for probiotic use based on expert opinion.⁹ The meta-analysis detailed in this PURL, which included more than 30 trials published since the 2006 meta-analysis, addressed the efficacy of probiotics for prevention and treatment of AAD.

STUDY SUMMARY: Probiotics significantly reduce AAD

Hempel et al reviewed 82 studies and pooled data from 63 RCTs (N=11,811) to identify the relative risk (RR) of AAD among patients who received probiotics during antibiotic treatment compared with those who received no probiotics or were given a placebo.¹ The studies encompassed a variety of antibiotics, taken alone or in combination, and several probiotics, including Lactobacillus, Bifidobacterium, Saccharomyces, and some combinations.

The outcome: The pooled RR for AAD in the probiotics groups was 0.58 (95% confidence interval, 0.50-0.68; P<.001), with a number needed to treat of 13. Although the authors reported that the overall quality of the included trials was poor, a sensitivity analysis of the higher quality studies yielded similar results.

Subgroup analyses by type of probiotic and duration of antibiotic treatment were also consistent with the overall pooled RR. In subgroup analysis by age, a similar decrease in AAD was found among the youngest patients (0-17 years) and those between the ages of 17 and 65 years. Among patients older than 65 years—for whom there were just 3 studies—a non-significant decrease in risk was found. Twenty-three of the studies assessed adverse outcomes, and none was found.

WHAT’S NEW: A reason to pair antibiotics and probiotics

This meta-analysis reached a similar conclusion as the 2006 meta-analysis: Probiotics appear to be effective in preventing and treating AAD in children and adults receiving a wide variety of antibiotics for a number of conditions. The results were also consistent with those of a new meta-analysis that looked specifically at one pathogen—and found a reduction of 66% in C difficile-associated diarrhea in patients taking probiotics with their antibiotics.¹⁰

CAVEATS: Limited data on the safety of probiotics exist

There was some heterogeneity among the studies in the meta-analysis by Hempel et al, and some of the studies were of poor quality. Because of this, the authors used subgroup and sensitivity analysis, which supported their initial conclusion.

Probiotics have generally been considered safe; however, there have been rare reports of sepsis and fungemia associated with probiotic use, especially in immunosuppressed patients.¹ Fifty-nine of the included studies did not assess adverse events, which limited the ability of this meta-analysis to assess safety.¹ Patients taking probiotics should be monitored for adverse effects.

CHALLENGES TO IMPLEMENTATION: Lack of guidance on dosing and duration

Since probiotics are considered food supplements, health insurance will not cover the cost (which will likely be more than $20 per month; www.walgreens.com). No single probiotic strain has high-quality evidence; however, most of the RCTs included in the meta-analysis used combinations of Lactobacillus species, which are usually found in over-the-counter antidiarrheal probiotic supplements. No standard dose exists, but dose ranges in RCTs are 10⁷ to 10¹⁰ colony-forming units per capsule (taken one to 3 times daily);¹ however, product labels have variable accuracy.¹¹ The duration of treatment ranges from one to 3 weeks—or as long as the patient continues to take antibiotics.

Acknowledgement

The PURLs Surveillance System was developed with support from Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

When you prescribe an antibiotic for a 45-year-old patient with Helicobacter pylori, he worries that the medication will cause diarrhea. Should you recommend that he take probiotics?

More than a third of patients taking antibiotics develop AAD,² and in 17% of cases, AAD is fatal.^3,4 Although the diarrhea may be the result of increased gastrointestinal (GI) motility in some cases, a disruption of the GI flora that normally acts as a barrier to infection and aids in the digestion of carbohydrates is a far more common cause.

Morbidity and mortality are high
AAD is associated with several pathogens, including Clostridium difficile, Clostridium perfringens, Klebsiella oxytoca, and Staphylococcus aureus,² and varies widely in severity. Pseudomembranous colitis secondary to C difficile is the main cause of AAD-related mortality, which more than doubled from 2002 to 2009.^3,4 C difficile infections cost the US health care system up to $1.3 billion annually.⁵ With such high rates of morbidity and mortality and high health care costs associated with AAD, even a small reduction in the number of cases would have a big impact.

Probiotics replenish the natural GI flora with nonpathogenic organisms. A 2006 meta-analysis of 31 randomized controlled trials (RCTs) assessing the efficacy of probiotics for both the prevention of AAD and treatment of C difficile found a pooled relative risk of 0.43 for AAD in the patients taking probiotics.⁶ However, many of the studies included in that meta-analysis were small. As a result, in 2010, the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA) recommended against the use of probiotics for the prevention of primary C difficile infection, citing a lack of high-quality evidence.⁷

Nonetheless, that same year, 98% of gastroenterologists surveyed expressed a belief that probiotics had a role in the treatment of GI illness.⁸ And in 2011, the 3rd Yale Working Group on Probiotic Use published recommendations for probiotic use based on expert opinion.⁹ The meta-analysis detailed in this PURL, which included more than 30 trials published since the 2006 meta-analysis, addressed the efficacy of probiotics for prevention and treatment of AAD.

STUDY SUMMARY: Probiotics significantly reduce AAD

Hempel et al reviewed 82 studies and pooled data from 63 RCTs (N=11,811) to identify the relative risk (RR) of AAD among patients who received probiotics during antibiotic treatment compared with those who received no probiotics or were given a placebo.¹ The studies encompassed a variety of antibiotics, taken alone or in combination, and several probiotics, including Lactobacillus, Bifidobacterium, Saccharomyces, and some combinations.

The outcome: The pooled RR for AAD in the probiotics groups was 0.58 (95% confidence interval, 0.50-0.68; P<.001), with a number needed to treat of 13. Although the authors reported that the overall quality of the included trials was poor, a sensitivity analysis of the higher quality studies yielded similar results.

Subgroup analyses by type of probiotic and duration of antibiotic treatment were also consistent with the overall pooled RR. In subgroup analysis by age, a similar decrease in AAD was found among the youngest patients (0-17 years) and those between the ages of 17 and 65 years. Among patients older than 65 years—for whom there were just 3 studies—a non-significant decrease in risk was found. Twenty-three of the studies assessed adverse outcomes, and none was found.

WHAT’S NEW: A reason to pair antibiotics and probiotics

This meta-analysis reached a similar conclusion as the 2006 meta-analysis: Probiotics appear to be effective in preventing and treating AAD in children and adults receiving a wide variety of antibiotics for a number of conditions. The results were also consistent with those of a new meta-analysis that looked specifically at one pathogen—and found a reduction of 66% in C difficile-associated diarrhea in patients taking probiotics with their antibiotics.¹⁰

CAVEATS: Limited data on the safety of probiotics exist

There was some heterogeneity among the studies in the meta-analysis by Hempel et al, and some of the studies were of poor quality. Because of this, the authors used subgroup and sensitivity analysis, which supported their initial conclusion.

Probiotics have generally been considered safe; however, there have been rare reports of sepsis and fungemia associated with probiotic use, especially in immunosuppressed patients.¹ Fifty-nine of the included studies did not assess adverse events, which limited the ability of this meta-analysis to assess safety.¹ Patients taking probiotics should be monitored for adverse effects.

CHALLENGES TO IMPLEMENTATION: Lack of guidance on dosing and duration

Since probiotics are considered food supplements, health insurance will not cover the cost (which will likely be more than $20 per month; www.walgreens.com). No single probiotic strain has high-quality evidence; however, most of the RCTs included in the meta-analysis used combinations of Lactobacillus species, which are usually found in over-the-counter antidiarrheal probiotic supplements. No standard dose exists, but dose ranges in RCTs are 10⁷ to 10¹⁰ colony-forming units per capsule (taken one to 3 times daily);¹ however, product labels have variable accuracy.¹¹ The duration of treatment ranges from one to 3 weeks—or as long as the patient continues to take antibiotics.

Acknowledgement

The PURLs Surveillance System was developed with support from Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.

The 2013 immunization schedules have been published by the Centers for Disease Control and Prevention (CDC)’s Advisory Committee on Immunization Practices (ACIP).^1,2 Perhaps the most noticeable change is a single schedule for infants, children, and adolescents, instead of the previous 2 schedules (for those ages 0-6 years, and for those ages 7-18 years). Other major new recommendations include the following:

• tetanus-diphtheria-pertussis (Tdap) vaccine for individuals ≥65 years of age
• Tdap for pregnant women during every pregnancy
• meningococcal conjugate vaccine for high-risk infants and children
• pneumococcal conjugate vaccine for high-risk adults.

There are also minor changes in recommendations for the use of measles, mumps, and rubella (MMR) vaccine among those with human immunodeficiency virus (HIV) infection. The new immunization schedules can be found on the CDC’s immunization Web site, at http://www.cdc.gov/vaccines/schedules/index.html.

Previous Practice Alerts have reported on recommendation changes made throughout 2012, including removal of egg allergy as a contraindication for influenza vaccine for those who experience only hives after eating eggs,³ the addition of a simplified algorithm for deciding whether children younger than 9 years need one or 2 doses of influenza vaccine,³ and the addition of human papillomavirus vaccine as a routine recommendation for males ages 11 to 21 years.⁴

Tdap: Some recommendations are off label

Given the continuing elevated rates of pertussis in the United States and our understanding about the duration of protection and safety of the Tdap vaccine, ACIP has made new recommendations for the use of Tdap, including some off-label uses. Two Tdap products are available: Boostrix, approved for individuals ≥10 years, and Adacel, approved for individuals 11 to 64 years (TABLE 1).⁵ ACIP states that those ≥65 years may be vaccinated with Tdap, and that an opportunity for vaccination should not be missed; Adacel can be substituted if it is the only product available. To control the spread of pertussis to the most vulnerable, it is especially important to immunize grandparents, childcare providers, and those who are around infants.

TABLE 1
Available tetanus-diphtheria-pertussis vaccines⁵

Wound management. If a tetanus booster is indicated for wound management in an individual ≥19 years who has never received Tdap, this product is preferred to Td.⁵ There is now no suggested minimum time interval for administering Tdap after Td. Currently only one dose of Tdap is recommended for adults (except for pregnant women, as described in the next section). But this may change as time passes and we learn more about the duration of protection from the acellular pertussis antigen in the vaccine.

Pregnancy. ACIP first recommended the use of Tdap during pregnancy in October 2011, in an attempt to provide protection for newborns through the transfer of maternal antibodies to the fetus.⁶ Recent evidence indicates that the duration of protective antibody levels wanes between pregnancies and may not be high enough to protect a newborn in subsequent pregnancies.⁷ ACIP voted in October 2012 to recommend Tdap for pregnant women during each pregnancy, at the gestational age of 27 through 36 weeks. If a mother does not receive Tdap during pregnancy and has never received it, she should be vaccinated soon after delivery.

The safety data for serial vaccination with Tdap in pregnant women is sparse, and ACIP considered this concern. In the opinion of ACIP, the potential benefits to the newborn, coupled with the high rate of pertussis, outweigh this concern, and efforts will be made to monitor for safety issues. If the rate of pertussis declines, ACIP will likely revisit this recommendation.

Meningococcal vaccine: No routine immunization for infants

A previous Practice Alert described 3 new products to protect infants and children against meningococcal disease, and identified issues that make recommendations about their use difficult at a time when rates of meningococcal disease in this age group are very low.⁸ At its October 2012 meeting, ACIP considered one of these products, HibMenCY (MenHibrix), which contains antigens against meningococcal serogroups C and Y and Haemophilus influenzae B (Hib).

ACIP voted not to recommend routine immunization against meningococcal disease in infants. However, HibMenCY was recommended for high-risk infants, and it was noted that it can be used as an Hib vaccine. The details of the recommendation appear in “When should you use HibMenCY in infants?”.⁹ The current recommendation also includes vaccinating high-risk infants ages 9 through 23 months with 2 doses of MenACWY-D (Menactra) with at least 8 weeks between doses. Only one of these products should be used, and ACIP does not cite a preference between them.

Pneumococcal conjugate vaccine recommended for high-risk adults

There are now 2 products that provide protection for adults against pneumococcal disease: a 23-valent polysaccharide product (PPSV23) and a 13-valent conjugate product (PCV13). PPSV23 is recommended for all adults ≥65 years and for those <65 who are at high risk for pneumococcal disease or complications from pneumococcal disease. While PCV13 is approved by the FDA for all adults ≥50 years, ACIP recommends it only for those at higher risk for pneumococcal disease.¹⁰

ACIP also recommends that those at risk should receive both PCV13 and PPSV23. Give PCV13 first, followed by PPSV23 2 months later.¹⁰ However, if PPSV23 is given first, administer PCV13 12 months later. To complicate matters, for some risk categories it is recommended that patients receive a second dose of PPSV23 5 years after the first one. No more than 2 doses of PPSV23 should be given prior to age 65. This complicated set of recommendations is summarized in TABLE 2.¹⁰

TABLE 2
Indications for using pneumococcal vaccines in adults ≥19 years*¹⁰

MMR for those with HIV and use of IG for measles prevention

The last set of significant changes to the schedules are updated recommendations for the use of MMR vaccine in those who have HIV infection, and the use of immune globulin to prevent measles in those previously unvaccinated who are exposed to the disease. Details of these recommendations can be found at http://www.cdc.gov/vaccines/recs/provisional/downloads/mmr-Oct-2012.pdf.

The 2013 immunization schedules have been published by the Centers for Disease Control and Prevention (CDC)’s Advisory Committee on Immunization Practices (ACIP).^1,2 Perhaps the most noticeable change is a single schedule for infants, children, and adolescents, instead of the previous 2 schedules (for those ages 0-6 years, and for those ages 7-18 years). Other major new recommendations include the following:

• tetanus-diphtheria-pertussis (Tdap) vaccine for individuals ≥65 years of age
• Tdap for pregnant women during every pregnancy
• meningococcal conjugate vaccine for high-risk infants and children
• pneumococcal conjugate vaccine for high-risk adults.

There are also minor changes in recommendations for the use of measles, mumps, and rubella (MMR) vaccine among those with human immunodeficiency virus (HIV) infection. The new immunization schedules can be found on the CDC’s immunization Web site, at http://www.cdc.gov/vaccines/schedules/index.html.

Previous Practice Alerts have reported on recommendation changes made throughout 2012, including removal of egg allergy as a contraindication for influenza vaccine for those who experience only hives after eating eggs,³ the addition of a simplified algorithm for deciding whether children younger than 9 years need one or 2 doses of influenza vaccine,³ and the addition of human papillomavirus vaccine as a routine recommendation for males ages 11 to 21 years.⁴

Tdap: Some recommendations are off label

Given the continuing elevated rates of pertussis in the United States and our understanding about the duration of protection and safety of the Tdap vaccine, ACIP has made new recommendations for the use of Tdap, including some off-label uses. Two Tdap products are available: Boostrix, approved for individuals ≥10 years, and Adacel, approved for individuals 11 to 64 years (TABLE 1).⁵ ACIP states that those ≥65 years may be vaccinated with Tdap, and that an opportunity for vaccination should not be missed; Adacel can be substituted if it is the only product available. To control the spread of pertussis to the most vulnerable, it is especially important to immunize grandparents, childcare providers, and those who are around infants.

TABLE 1
Available tetanus-diphtheria-pertussis vaccines⁵

Wound management. If a tetanus booster is indicated for wound management in an individual ≥19 years who has never received Tdap, this product is preferred to Td.⁵ There is now no suggested minimum time interval for administering Tdap after Td. Currently only one dose of Tdap is recommended for adults (except for pregnant women, as described in the next section). But this may change as time passes and we learn more about the duration of protection from the acellular pertussis antigen in the vaccine.

Pregnancy. ACIP first recommended the use of Tdap during pregnancy in October 2011, in an attempt to provide protection for newborns through the transfer of maternal antibodies to the fetus.⁶ Recent evidence indicates that the duration of protective antibody levels wanes between pregnancies and may not be high enough to protect a newborn in subsequent pregnancies.⁷ ACIP voted in October 2012 to recommend Tdap for pregnant women during each pregnancy, at the gestational age of 27 through 36 weeks. If a mother does not receive Tdap during pregnancy and has never received it, she should be vaccinated soon after delivery.

The safety data for serial vaccination with Tdap in pregnant women is sparse, and ACIP considered this concern. In the opinion of ACIP, the potential benefits to the newborn, coupled with the high rate of pertussis, outweigh this concern, and efforts will be made to monitor for safety issues. If the rate of pertussis declines, ACIP will likely revisit this recommendation.

Meningococcal vaccine: No routine immunization for infants

A previous Practice Alert described 3 new products to protect infants and children against meningococcal disease, and identified issues that make recommendations about their use difficult at a time when rates of meningococcal disease in this age group are very low.⁸ At its October 2012 meeting, ACIP considered one of these products, HibMenCY (MenHibrix), which contains antigens against meningococcal serogroups C and Y and Haemophilus influenzae B (Hib).

ACIP voted not to recommend routine immunization against meningococcal disease in infants. However, HibMenCY was recommended for high-risk infants, and it was noted that it can be used as an Hib vaccine. The details of the recommendation appear in “When should you use HibMenCY in infants?”.⁹ The current recommendation also includes vaccinating high-risk infants ages 9 through 23 months with 2 doses of MenACWY-D (Menactra) with at least 8 weeks between doses. Only one of these products should be used, and ACIP does not cite a preference between them.

Pneumococcal conjugate vaccine recommended for high-risk adults

There are now 2 products that provide protection for adults against pneumococcal disease: a 23-valent polysaccharide product (PPSV23) and a 13-valent conjugate product (PCV13). PPSV23 is recommended for all adults ≥65 years and for those <65 who are at high risk for pneumococcal disease or complications from pneumococcal disease. While PCV13 is approved by the FDA for all adults ≥50 years, ACIP recommends it only for those at higher risk for pneumococcal disease.¹⁰

ACIP also recommends that those at risk should receive both PCV13 and PPSV23. Give PCV13 first, followed by PPSV23 2 months later.¹⁰ However, if PPSV23 is given first, administer PCV13 12 months later. To complicate matters, for some risk categories it is recommended that patients receive a second dose of PPSV23 5 years after the first one. No more than 2 doses of PPSV23 should be given prior to age 65. This complicated set of recommendations is summarized in TABLE 2.¹⁰

TABLE 2
Indications for using pneumococcal vaccines in adults ≥19 years*¹⁰

MMR for those with HIV and use of IG for measles prevention

The last set of significant changes to the schedules are updated recommendations for the use of MMR vaccine in those who have HIV infection, and the use of immune globulin to prevent measles in those previously unvaccinated who are exposed to the disease. Details of these recommendations can be found at http://www.cdc.gov/vaccines/recs/provisional/downloads/mmr-Oct-2012.pdf.

The 2013 immunization schedules have been published by the Centers for Disease Control and Prevention (CDC)’s Advisory Committee on Immunization Practices (ACIP).^1,2 Perhaps the most noticeable change is a single schedule for infants, children, and adolescents, instead of the previous 2 schedules (for those ages 0-6 years, and for those ages 7-18 years). Other major new recommendations include the following:

• tetanus-diphtheria-pertussis (Tdap) vaccine for individuals ≥65 years of age
• Tdap for pregnant women during every pregnancy
• meningococcal conjugate vaccine for high-risk infants and children
• pneumococcal conjugate vaccine for high-risk adults.

There are also minor changes in recommendations for the use of measles, mumps, and rubella (MMR) vaccine among those with human immunodeficiency virus (HIV) infection. The new immunization schedules can be found on the CDC’s immunization Web site, at http://www.cdc.gov/vaccines/schedules/index.html.

Previous Practice Alerts have reported on recommendation changes made throughout 2012, including removal of egg allergy as a contraindication for influenza vaccine for those who experience only hives after eating eggs,³ the addition of a simplified algorithm for deciding whether children younger than 9 years need one or 2 doses of influenza vaccine,³ and the addition of human papillomavirus vaccine as a routine recommendation for males ages 11 to 21 years.⁴

Tdap: Some recommendations are off label

Given the continuing elevated rates of pertussis in the United States and our understanding about the duration of protection and safety of the Tdap vaccine, ACIP has made new recommendations for the use of Tdap, including some off-label uses. Two Tdap products are available: Boostrix, approved for individuals ≥10 years, and Adacel, approved for individuals 11 to 64 years (TABLE 1).⁵ ACIP states that those ≥65 years may be vaccinated with Tdap, and that an opportunity for vaccination should not be missed; Adacel can be substituted if it is the only product available. To control the spread of pertussis to the most vulnerable, it is especially important to immunize grandparents, childcare providers, and those who are around infants.

TABLE 1
Available tetanus-diphtheria-pertussis vaccines⁵

Wound management. If a tetanus booster is indicated for wound management in an individual ≥19 years who has never received Tdap, this product is preferred to Td.⁵ There is now no suggested minimum time interval for administering Tdap after Td. Currently only one dose of Tdap is recommended for adults (except for pregnant women, as described in the next section). But this may change as time passes and we learn more about the duration of protection from the acellular pertussis antigen in the vaccine.

Pregnancy. ACIP first recommended the use of Tdap during pregnancy in October 2011, in an attempt to provide protection for newborns through the transfer of maternal antibodies to the fetus.⁶ Recent evidence indicates that the duration of protective antibody levels wanes between pregnancies and may not be high enough to protect a newborn in subsequent pregnancies.⁷ ACIP voted in October 2012 to recommend Tdap for pregnant women during each pregnancy, at the gestational age of 27 through 36 weeks. If a mother does not receive Tdap during pregnancy and has never received it, she should be vaccinated soon after delivery.

The safety data for serial vaccination with Tdap in pregnant women is sparse, and ACIP considered this concern. In the opinion of ACIP, the potential benefits to the newborn, coupled with the high rate of pertussis, outweigh this concern, and efforts will be made to monitor for safety issues. If the rate of pertussis declines, ACIP will likely revisit this recommendation.

Meningococcal vaccine: No routine immunization for infants

A previous Practice Alert described 3 new products to protect infants and children against meningococcal disease, and identified issues that make recommendations about their use difficult at a time when rates of meningococcal disease in this age group are very low.⁸ At its October 2012 meeting, ACIP considered one of these products, HibMenCY (MenHibrix), which contains antigens against meningococcal serogroups C and Y and Haemophilus influenzae B (Hib).

ACIP voted not to recommend routine immunization against meningococcal disease in infants. However, HibMenCY was recommended for high-risk infants, and it was noted that it can be used as an Hib vaccine. The details of the recommendation appear in “When should you use HibMenCY in infants?”.⁹ The current recommendation also includes vaccinating high-risk infants ages 9 through 23 months with 2 doses of MenACWY-D (Menactra) with at least 8 weeks between doses. Only one of these products should be used, and ACIP does not cite a preference between them.

Pneumococcal conjugate vaccine recommended for high-risk adults

There are now 2 products that provide protection for adults against pneumococcal disease: a 23-valent polysaccharide product (PPSV23) and a 13-valent conjugate product (PCV13). PPSV23 is recommended for all adults ≥65 years and for those <65 who are at high risk for pneumococcal disease or complications from pneumococcal disease. While PCV13 is approved by the FDA for all adults ≥50 years, ACIP recommends it only for those at higher risk for pneumococcal disease.¹⁰

ACIP also recommends that those at risk should receive both PCV13 and PPSV23. Give PCV13 first, followed by PPSV23 2 months later.¹⁰ However, if PPSV23 is given first, administer PCV13 12 months later. To complicate matters, for some risk categories it is recommended that patients receive a second dose of PPSV23 5 years after the first one. No more than 2 doses of PPSV23 should be given prior to age 65. This complicated set of recommendations is summarized in TABLE 2.¹⁰

TABLE 2
Indications for using pneumococcal vaccines in adults ≥19 years*¹⁰

MMR for those with HIV and use of IG for measles prevention

The last set of significant changes to the schedules are updated recommendations for the use of MMR vaccine in those who have HIV infection, and the use of immune globulin to prevent measles in those previously unvaccinated who are exposed to the disease. Details of these recommendations can be found at http://www.cdc.gov/vaccines/recs/provisional/downloads/mmr-Oct-2012.pdf.

CASE Mr. A, a 59-year-old high school science teacher, came into our medical clinic with severe pain (7/10) in his left shoulder and arm and weakness on flexion of his left elbow. A week earlier, he felt a “pop” and experienced sharp pain and immediate “swelling” of the left biceps after throwing a heavy trash bag away while at work. He went to the school nurse for evaluation and was referred to a physician.

Mr. A was healthy, had no chronic diseases, and reported no previous injuries or trauma. He denied smoking, drinking alcohol, using illegal drugs, or taking steroids or other medications. He had worked as a high school teacher for the last 10 years at the time of his clinic visit.

Imaging, physical exam tell the tale. The patient’s physical exam was normal, with one outstanding exception: a “Popeye” deformity in his left biceps (FIGURE), accompanied by severe pain and tenderness to palpation over the proximal aspect of the left biceps. Both active and passive range of motion of the elbow were full and symmetrical, but the patient had prominent pain and weakness on elbow flexion and supination. However, he had good rotator cuff strength without pain and no impingement signs or acromioclavicular joint pain. He had no atrophy or scapular dyskinesia. Similarly, a neurovascular exam of the distal aspect of the extremity was normal.

FIGURE
“Popeye” deformity in left biceps

The magnetic resonance imaging report revealed a complete tendon rupture of the long head of the biceps brachii muscle. The long head muscle was intact and there was a posttraumatic hemorrhage in the region of the tear in the upper arm. The remaining muscle, ligaments, and tendon were intact. There was no evidence of a fracture.

A 3-pronged approach. Once the diagnosis of acute complete rupture of the left long head tendon biceps brachii was reached, we laid out a 3-pronged treatment approach:

• nonsteroidal anti-inflammatory agents and muscle relaxants such as cyclobenzaprine, tizanidine, or metaxalone
• physical therapy (2-3 times per week) and daily home exercise
• modified activities—specifically, no overhead work or lifting of anything >10 lb with the affected arm.

Before we proceeded with this plan, we referred the patient to a specialist for evaluation and a second opinion.

Biceps tendon rupture usually follows a traumatic event

Long head biceps tendon ruptures often involve people between 40 and 60 years of age, with men affected significantly more often than women.^1,2 Tennis players and ballplayers are also affected, as a result of frequent swinging motions.³ As you might expect, a person’s dominant arm is more often affected.³

Excessive weightlifting or rapid stress upon the tendon can cause an acute tendon rupture. As a rule, biceps tendon ruptures are caused by a single traumatic event that typically involves lifting a heavy object while the elbow is bent at a 90-degree angle. Weight lifters who use anabolic steroids are at an increased risk of sustaining a rupture at the tendon, and clinicians may also see such ruptures among patients who have fallen forcefully onto an outstretched arm.^2,3

Keep in mind, however, that rupture can also occur in the absence of a traumatic event. This usually happens in elderly individuals with advanced tendon degeneration.⁴ Smoking, rheumatoid arthritis, steroid medications,^2,5 fluoroquinolones,⁶ and statin therapy⁷ can affect this tendon and increase the risk of spontaneous rupture, as well.

“Popeye” biceps—a telltale sign. Understanding the function of the biceps brachii helps explain at least one of the telltale signs of long head tendon rupture. The biceps muscle enables supination of the forearm and flexion of the elbow. With long head tendon rupture, however, the muscle belly retracts, causing prominent fullness and bulging of the upper arm—what’s called “Popeye” biceps. Because the rupture involves only the long head tendon of the biceps and not the short head tendon, the biceps still functions.⁸

Surgical repair vs conservative management

Whether to pursue surgery or conservative management when caring for a patient with a biceps rupture remains a subject of debate in the medical literature. There are no studies that demonstrate the superiority of one approach over the other.^2,5,9,10

Surgery. The serious complications associated with surgery have led some experts to question whether the risks of surgery outweigh the benefits.¹¹ Equally important is the patient’s individual circumstances. Clinicians need to consider each patient’s occupation, lifestyle, and age when recommending a course of action.

Published clinical guidelines usually recommend surgical repair for young athletes who require maximum supination strength in daily activities. Although the size of the Popeye deformity does diminish after conservative treatment, surgery is often recommended for patients who are unwilling to accept the cosmetic defect seen after the tendon ruptures. And finally, operative treatment is indicated for middle-aged carpenters and manual laborers whose occupations require full supination and arm strength.^2,12-14

The surgical procedure, called tenodesis, involves reattaching the torn section of the tendon to the bone.^5,15 A recent study involving 5 professional wrestlers injured while performing noted that tenodesis restored full biceps function, gave excellent cosmetic results, and allowed all of the young men to return to wrestling.¹⁵

Conservative treatment. A conservative approach is appropriate for older patients when their profession and lifestyle do not demand a high degree of supination and upper arm strength.^5,8,13,14 In addition, the more conservative approach is very well tolerated, which reduces the risk of serious complications and the cost of surgery.¹¹ Avoiding surgery also permits patients to return to work much sooner.

Patients may, however, lose up to 20% of their supination strength with conservative treatment.¹⁴ But this approach does not cause weakness in grip, pronation, or elbow extension. Nor does it affect patients’ activities of daily living,¹⁴ which may explain why more patients are treated conservatively than with surgery.^5,11 Additionally, some experts recommend nonoperative treatment of distal biceps tendon ruptures for people who are wary of surgery or present late with the injury.¹¹

CASE Two orthopedic surgeons examined our patient and both supported our recommendation to pursue conservative treatment for Mr. A.

Over the next 4 to 6 weeks, he received physical therapy 2 to 3 times per week. With the help of the physiotherapist, Mr. A performed joint mobilization and flexibility exercises to improve the range of motion in his shoulder. The therapist also helped him with strengthening and stretching exercises to restore the strength of his biceps and elbow muscle.

At home, our patient’s regimen included elbow bend and straighten movements, elbow supination and pronation movements, and static biceps contractions.

Over time, his pain diminished and the strength in his left arm improved. Mr. A was able to return to work with modified duty, 2 to 3 weeks after his injury. By Week 8, he had full range of motion in his left arm and normal strength. He was able to do his job as a high school science teacher without any restrictions, but continued to have the Popeye deformity.

Our experience treating Mr. A serves as a reminder to physicians that complete long head biceps tendon rupture can be successfully treated conservatively. Patients working in sedentary occupations usually do not need a high degree of supination or physical strength in their upper extremities, making this a worthwhile treatment option for them.

CORRESPONDENCE 
Sofya Pugach, MD, PhD, MPH, Complete Med Care, 8989 Forest Lane, Dallas, TX 75243; Drpugach@yahoo.com

CASE Mr. A, a 59-year-old high school science teacher, came into our medical clinic with severe pain (7/10) in his left shoulder and arm and weakness on flexion of his left elbow. A week earlier, he felt a “pop” and experienced sharp pain and immediate “swelling” of the left biceps after throwing a heavy trash bag away while at work. He went to the school nurse for evaluation and was referred to a physician.

Mr. A was healthy, had no chronic diseases, and reported no previous injuries or trauma. He denied smoking, drinking alcohol, using illegal drugs, or taking steroids or other medications. He had worked as a high school teacher for the last 10 years at the time of his clinic visit.

Imaging, physical exam tell the tale. The patient’s physical exam was normal, with one outstanding exception: a “Popeye” deformity in his left biceps (FIGURE), accompanied by severe pain and tenderness to palpation over the proximal aspect of the left biceps. Both active and passive range of motion of the elbow were full and symmetrical, but the patient had prominent pain and weakness on elbow flexion and supination. However, he had good rotator cuff strength without pain and no impingement signs or acromioclavicular joint pain. He had no atrophy or scapular dyskinesia. Similarly, a neurovascular exam of the distal aspect of the extremity was normal.

FIGURE
“Popeye” deformity in left biceps

The magnetic resonance imaging report revealed a complete tendon rupture of the long head of the biceps brachii muscle. The long head muscle was intact and there was a posttraumatic hemorrhage in the region of the tear in the upper arm. The remaining muscle, ligaments, and tendon were intact. There was no evidence of a fracture.

A 3-pronged approach. Once the diagnosis of acute complete rupture of the left long head tendon biceps brachii was reached, we laid out a 3-pronged treatment approach:

• nonsteroidal anti-inflammatory agents and muscle relaxants such as cyclobenzaprine, tizanidine, or metaxalone
• physical therapy (2-3 times per week) and daily home exercise
• modified activities—specifically, no overhead work or lifting of anything >10 lb with the affected arm.

Before we proceeded with this plan, we referred the patient to a specialist for evaluation and a second opinion.

Biceps tendon rupture usually follows a traumatic event

Long head biceps tendon ruptures often involve people between 40 and 60 years of age, with men affected significantly more often than women.^1,2 Tennis players and ballplayers are also affected, as a result of frequent swinging motions.³ As you might expect, a person’s dominant arm is more often affected.³

Excessive weightlifting or rapid stress upon the tendon can cause an acute tendon rupture. As a rule, biceps tendon ruptures are caused by a single traumatic event that typically involves lifting a heavy object while the elbow is bent at a 90-degree angle. Weight lifters who use anabolic steroids are at an increased risk of sustaining a rupture at the tendon, and clinicians may also see such ruptures among patients who have fallen forcefully onto an outstretched arm.^2,3

Keep in mind, however, that rupture can also occur in the absence of a traumatic event. This usually happens in elderly individuals with advanced tendon degeneration.⁴ Smoking, rheumatoid arthritis, steroid medications,^2,5 fluoroquinolones,⁶ and statin therapy⁷ can affect this tendon and increase the risk of spontaneous rupture, as well.

“Popeye” biceps—a telltale sign. Understanding the function of the biceps brachii helps explain at least one of the telltale signs of long head tendon rupture. The biceps muscle enables supination of the forearm and flexion of the elbow. With long head tendon rupture, however, the muscle belly retracts, causing prominent fullness and bulging of the upper arm—what’s called “Popeye” biceps. Because the rupture involves only the long head tendon of the biceps and not the short head tendon, the biceps still functions.⁸

Surgical repair vs conservative management

Whether to pursue surgery or conservative management when caring for a patient with a biceps rupture remains a subject of debate in the medical literature. There are no studies that demonstrate the superiority of one approach over the other.^2,5,9,10

Surgery. The serious complications associated with surgery have led some experts to question whether the risks of surgery outweigh the benefits.¹¹ Equally important is the patient’s individual circumstances. Clinicians need to consider each patient’s occupation, lifestyle, and age when recommending a course of action.

Published clinical guidelines usually recommend surgical repair for young athletes who require maximum supination strength in daily activities. Although the size of the Popeye deformity does diminish after conservative treatment, surgery is often recommended for patients who are unwilling to accept the cosmetic defect seen after the tendon ruptures. And finally, operative treatment is indicated for middle-aged carpenters and manual laborers whose occupations require full supination and arm strength.^2,12-14

The surgical procedure, called tenodesis, involves reattaching the torn section of the tendon to the bone.^5,15 A recent study involving 5 professional wrestlers injured while performing noted that tenodesis restored full biceps function, gave excellent cosmetic results, and allowed all of the young men to return to wrestling.¹⁵

Conservative treatment. A conservative approach is appropriate for older patients when their profession and lifestyle do not demand a high degree of supination and upper arm strength.^5,8,13,14 In addition, the more conservative approach is very well tolerated, which reduces the risk of serious complications and the cost of surgery.¹¹ Avoiding surgery also permits patients to return to work much sooner.

Patients may, however, lose up to 20% of their supination strength with conservative treatment.¹⁴ But this approach does not cause weakness in grip, pronation, or elbow extension. Nor does it affect patients’ activities of daily living,¹⁴ which may explain why more patients are treated conservatively than with surgery.^5,11 Additionally, some experts recommend nonoperative treatment of distal biceps tendon ruptures for people who are wary of surgery or present late with the injury.¹¹

CASE Two orthopedic surgeons examined our patient and both supported our recommendation to pursue conservative treatment for Mr. A.

Over the next 4 to 6 weeks, he received physical therapy 2 to 3 times per week. With the help of the physiotherapist, Mr. A performed joint mobilization and flexibility exercises to improve the range of motion in his shoulder. The therapist also helped him with strengthening and stretching exercises to restore the strength of his biceps and elbow muscle.

At home, our patient’s regimen included elbow bend and straighten movements, elbow supination and pronation movements, and static biceps contractions.

Over time, his pain diminished and the strength in his left arm improved. Mr. A was able to return to work with modified duty, 2 to 3 weeks after his injury. By Week 8, he had full range of motion in his left arm and normal strength. He was able to do his job as a high school science teacher without any restrictions, but continued to have the Popeye deformity.

Our experience treating Mr. A serves as a reminder to physicians that complete long head biceps tendon rupture can be successfully treated conservatively. Patients working in sedentary occupations usually do not need a high degree of supination or physical strength in their upper extremities, making this a worthwhile treatment option for them.

CORRESPONDENCE 
Sofya Pugach, MD, PhD, MPH, Complete Med Care, 8989 Forest Lane, Dallas, TX 75243; Drpugach@yahoo.com

CASE Mr. A, a 59-year-old high school science teacher, came into our medical clinic with severe pain (7/10) in his left shoulder and arm and weakness on flexion of his left elbow. A week earlier, he felt a “pop” and experienced sharp pain and immediate “swelling” of the left biceps after throwing a heavy trash bag away while at work. He went to the school nurse for evaluation and was referred to a physician.

Mr. A was healthy, had no chronic diseases, and reported no previous injuries or trauma. He denied smoking, drinking alcohol, using illegal drugs, or taking steroids or other medications. He had worked as a high school teacher for the last 10 years at the time of his clinic visit.

Imaging, physical exam tell the tale. The patient’s physical exam was normal, with one outstanding exception: a “Popeye” deformity in his left biceps (FIGURE), accompanied by severe pain and tenderness to palpation over the proximal aspect of the left biceps. Both active and passive range of motion of the elbow were full and symmetrical, but the patient had prominent pain and weakness on elbow flexion and supination. However, he had good rotator cuff strength without pain and no impingement signs or acromioclavicular joint pain. He had no atrophy or scapular dyskinesia. Similarly, a neurovascular exam of the distal aspect of the extremity was normal.

FIGURE
“Popeye” deformity in left biceps

The magnetic resonance imaging report revealed a complete tendon rupture of the long head of the biceps brachii muscle. The long head muscle was intact and there was a posttraumatic hemorrhage in the region of the tear in the upper arm. The remaining muscle, ligaments, and tendon were intact. There was no evidence of a fracture.

A 3-pronged approach. Once the diagnosis of acute complete rupture of the left long head tendon biceps brachii was reached, we laid out a 3-pronged treatment approach:

• nonsteroidal anti-inflammatory agents and muscle relaxants such as cyclobenzaprine, tizanidine, or metaxalone
• physical therapy (2-3 times per week) and daily home exercise
• modified activities—specifically, no overhead work or lifting of anything >10 lb with the affected arm.

Before we proceeded with this plan, we referred the patient to a specialist for evaluation and a second opinion.

Biceps tendon rupture usually follows a traumatic event

Long head biceps tendon ruptures often involve people between 40 and 60 years of age, with men affected significantly more often than women.^1,2 Tennis players and ballplayers are also affected, as a result of frequent swinging motions.³ As you might expect, a person’s dominant arm is more often affected.³

Excessive weightlifting or rapid stress upon the tendon can cause an acute tendon rupture. As a rule, biceps tendon ruptures are caused by a single traumatic event that typically involves lifting a heavy object while the elbow is bent at a 90-degree angle. Weight lifters who use anabolic steroids are at an increased risk of sustaining a rupture at the tendon, and clinicians may also see such ruptures among patients who have fallen forcefully onto an outstretched arm.^2,3

Keep in mind, however, that rupture can also occur in the absence of a traumatic event. This usually happens in elderly individuals with advanced tendon degeneration.⁴ Smoking, rheumatoid arthritis, steroid medications,^2,5 fluoroquinolones,⁶ and statin therapy⁷ can affect this tendon and increase the risk of spontaneous rupture, as well.

“Popeye” biceps—a telltale sign. Understanding the function of the biceps brachii helps explain at least one of the telltale signs of long head tendon rupture. The biceps muscle enables supination of the forearm and flexion of the elbow. With long head tendon rupture, however, the muscle belly retracts, causing prominent fullness and bulging of the upper arm—what’s called “Popeye” biceps. Because the rupture involves only the long head tendon of the biceps and not the short head tendon, the biceps still functions.⁸

Surgical repair vs conservative management

Whether to pursue surgery or conservative management when caring for a patient with a biceps rupture remains a subject of debate in the medical literature. There are no studies that demonstrate the superiority of one approach over the other.^2,5,9,10

Surgery. The serious complications associated with surgery have led some experts to question whether the risks of surgery outweigh the benefits.¹¹ Equally important is the patient’s individual circumstances. Clinicians need to consider each patient’s occupation, lifestyle, and age when recommending a course of action.

Published clinical guidelines usually recommend surgical repair for young athletes who require maximum supination strength in daily activities. Although the size of the Popeye deformity does diminish after conservative treatment, surgery is often recommended for patients who are unwilling to accept the cosmetic defect seen after the tendon ruptures. And finally, operative treatment is indicated for middle-aged carpenters and manual laborers whose occupations require full supination and arm strength.^2,12-14

The surgical procedure, called tenodesis, involves reattaching the torn section of the tendon to the bone.^5,15 A recent study involving 5 professional wrestlers injured while performing noted that tenodesis restored full biceps function, gave excellent cosmetic results, and allowed all of the young men to return to wrestling.¹⁵

Conservative treatment. A conservative approach is appropriate for older patients when their profession and lifestyle do not demand a high degree of supination and upper arm strength.^5,8,13,14 In addition, the more conservative approach is very well tolerated, which reduces the risk of serious complications and the cost of surgery.¹¹ Avoiding surgery also permits patients to return to work much sooner.

Patients may, however, lose up to 20% of their supination strength with conservative treatment.¹⁴ But this approach does not cause weakness in grip, pronation, or elbow extension. Nor does it affect patients’ activities of daily living,¹⁴ which may explain why more patients are treated conservatively than with surgery.^5,11 Additionally, some experts recommend nonoperative treatment of distal biceps tendon ruptures for people who are wary of surgery or present late with the injury.¹¹

CASE Two orthopedic surgeons examined our patient and both supported our recommendation to pursue conservative treatment for Mr. A.

Over the next 4 to 6 weeks, he received physical therapy 2 to 3 times per week. With the help of the physiotherapist, Mr. A performed joint mobilization and flexibility exercises to improve the range of motion in his shoulder. The therapist also helped him with strengthening and stretching exercises to restore the strength of his biceps and elbow muscle.

At home, our patient’s regimen included elbow bend and straighten movements, elbow supination and pronation movements, and static biceps contractions.

Over time, his pain diminished and the strength in his left arm improved. Mr. A was able to return to work with modified duty, 2 to 3 weeks after his injury. By Week 8, he had full range of motion in his left arm and normal strength. He was able to do his job as a high school science teacher without any restrictions, but continued to have the Popeye deformity.

Our experience treating Mr. A serves as a reminder to physicians that complete long head biceps tendon rupture can be successfully treated conservatively. Patients working in sedentary occupations usually do not need a high degree of supination or physical strength in their upper extremities, making this a worthwhile treatment option for them.

CORRESPONDENCE 
Sofya Pugach, MD, PhD, MPH, Complete Med Care, 8989 Forest Lane, Dallas, TX 75243; Drpugach@yahoo.com

CASE A 29-year-old veteran (whom we’ll call Jane Doe) served as a medical corpsman in Iraq and has been pursuing a nursing degree since her honorable discharge a year ago. She comes in for a visit and reports a 3-month history of depression without suicidal ideation. In addition, Ms. Doe says, she has had abdominal pain that waxes and wanes for the past month. The pain is diffuse and nonfocal and appears to be unaffected by eating or bowel movements. She is unable to identify a particular pattern.

The patient has no significant medical or psychiatric history, and a physical examination is unremarkable. You advise her to follow a simplified dietary regimen, avoiding spicy foods and limiting dairy intake, and schedule a follow-up visit in 2 weeks.

Since 2002, some 2.4 million US troops have served in Iraq and Afghanistan,¹ creating a new generation of veterans who need broad-based support to recover from the physical and psychological wounds of war. All too often, those wounds include sexual assault or harassment, collectively known as military sexual trauma (MST).

MST is a growing concern for the Veterans Administration (VA) for a number of reasons—an increase in women on the front lines and greater media coverage of patterns of sexual assault in the military among them.² The official lifting of the ban on women in combat announced by the Pentagon in January brought the issue to the forefront, as well.³

In fact, MST should be a concern not only for clinicians within the VA, but also for civilian physicians. There are nearly 22 million American veterans, and the vast majority (>95%) get at least some of their medical care outside of the VA system⁴—often in outpatient facilities like yours.⁵ Family physicians need to be aware of the problem and able to give veterans who have suffered from sexual trauma the sensitive care they require.

The scope of the problem? No one is sure

How widespread is MST? That question is not easily answered. The prevalence rate among female service members is 20% to 43%,⁶ according to internal reports, while studies outside the military have reported rates that range from 3% to as high as 71%.⁵ In a recent anonymous survey of women in combat zones, led by a VA researcher—widely reported but still undergoing final review—half of those surveyed reported sexual harassment and nearly one in 4 reported sexual assault.⁷

There are far less data on rates of MST among male service members. The documented prevalence rate for men is 1.1%, with a range of 0.03% to 12.4%, but these figures are based on internal reports of sexual harassment and assault.⁸

Military culture and personal history are key factors
While the rate at which MST is reported has increased over the past 30 years,⁸ many reasons for not reporting it—stigma, fear of blame, accusations of homosexuality or promiscuity, and the threat of charges of fraternization among them—still remain.^8,9 Military culture is still male-dominated, with an emphasis on self-sufficiency that often leaves victims of MST feeling as though they have nowhere to turn.

There are also circumstances military members face that can aggravate the effects of sexual trauma. Soldiers on deployment are typically isolated from their normal support systems, under significant pressure, and unable to leave their post, which often means they have ongoing exposure to the abuser.

A history of childhood sexual abuse (CSA). As many as 50% of female service members (and about 17% of military men) have reported CSA,¹⁰ compared with 25% to 27% of women and 16% of men outside of the military.^5,11 That finding may be partially explained by data showing that nearly half of women in the military cited escaping from their home environment as a primary reason for enlisting.¹²

Women in the military who have a history of CSA, however, face a significantly higher risk for MST than servicewomen who were not sexually assaulted as children.⁸ Among female Navy recruits, for example, those who reported CSA were 4.8 times more likely to be raped than those who had no history of CSA.¹³

Combat-related trauma further complicates the picture. Evidence suggests that exposure to childhood physical and sexual abuse was associated with increased risk for combat-related posttraumatic stress disorder (PTSD) among men who served in Vietnam¹⁴ and women who served in Operation Desert Storm.¹⁵

Broaching the subject should be routine

Primary care physicians can play an important role in helping veterans transition back to their civilian lives and local communities, starting with a holistic medical assessment. When you see a patient whose return is relatively recent, inquire about his or her experiences during deployment. It is important to ask specifically about traumatic experiences, and to routinely screen for MST.

CASE When Ms. Doe returns. you begin by asking about her mood, using open-ended, nondirective questions. She responds by admitting that she had left important information off of the intake form she filled out on her last visit—most notably, a history of CSA. You gently ask about her experiences in the military, particularly during the year she spent in Iraq—and whether anything happened there that you should know.

Haltingly and with much emotion, the patient tells of her experience with another soldier. She worked with him every day, she says, and had grown close to him. One evening things went further than she expected. At first, it was only kissing, but then he forced himself on her sexually. She has not told anyone else about this event, Ms. Doe confides, because she wasn’t sure whether she precipitated it and felt embarrassed and humiliated by her choice to trust this man.

She did not feel that her supervising officers would listen or understand, as romantic attachments are best avoided in a combat zone and daily injuries are the norm. She says that her role as a medic kept her focused on the pain of others and enabled her to avoid looking at her own situation.

Evidence has shown that, like Ms. Doe, most survivors of trauma do not volunteer such information, but will often respond to direct and empathic questions from their physician.¹⁶ Routine screening of all veterans for MST, which the VA recommends, has been shown to increase their use of mental health resources.^17,18 This can be easily incorporated into a medical history or an intake questionnaire, using this simple 2-question tool:^17,18

While you were in the military:

• Did you receive uninvited and unwanted sexual attention, such as touching, cornering, pressure for sexual favors, or verbal remarks?
• Did anyone ever use force or the threat of force to have sexual contact with you against your will?

Screen for PTSD, and consider other psychiatric disorders
MST has been found to confer a 9-fold risk for PTSD. Indeed, more than 4 in 10 (42%) women with a history of MST have a PTSD diagnosis.¹⁹ Thus, if the screen for MST is positive—as indicated by a Yes answer to either question—follow up with the 4-question Primary Care PTSD screen (TABLE 1) is recommended.²⁰

Veterans with a history of MST are twice as likely as other veterans to receive a mental health diagnosis;¹⁷ they’re also more likely to have 3 or more comorbid psychiatric conditions.²¹ Women appear to be more likely than men to suffer from depression, eating disorders, substance abuse,²² anxiety disorders,²¹ dissociative disorders, and personality disorders.¹⁷

Research on the mental health consequences of sexual assault in men (in any setting) is limited, however, and data on male survivors of MST are particularly sparse. What is known is that men who have experienced sexual trauma have higher rates of alcohol abuse²³ and self-harm²⁴ than women with a history of sexual trauma, and that MST has a greater association with bipolar disorder, schizophrenia, and psychosis in men.¹⁷

TABLE 1
Primary care PTSD screen (PC-PTSD)

Multiple physical symptoms are often trauma-related

Veterans with a history of MST are also more likely to report physical symptoms²⁵ and to have a lower health-related quality of life,²⁶ poorer health status, and more outpatient visits¹² than vets who were not exposed to MST. And, while pelvic pain is widely believed to be associated with female sexual abuse, survivors often present with a wide range of physical problems. The most common symptoms, similar to those affecting civilian rape survivors, include headache, gastrointestinal (GI) problems, chronic fatigue, severe menopause symptoms, and urological problems, as well as pelvic pain and sexual problems.²⁷ Cardiac and respiratory disorders are also common (TABLE 2).^17,25

Compared with their unaffected counterparts, women with a history of MST are more likely to be obese and sedentary, to smoke and drink, and to have had a hysterectomy before the age of 40 years.²⁸ They are also more than twice as likely as other female veterans to say that they were treated for a heart attack within the past year.²⁵ Data on the physical symptoms of male survivors of MST are extremely limited, but one study found an association with pulmonary and liver disease and human immunodeficiency virus and acquired immune deficiency syndrome.¹⁷

TABLE 2
Common physical symptoms reported by female MST survivors*^17,25

A cluster of nonspecific findings?
Patients with a history of MST often present with complex and nonspecific signs and symptoms, making it difficult for a primary care physician to arrive at a diagnosis. MST and combat-related trauma should be considered in such cases, as well as in veterans who present with complaints involving multiple organ systems.^21,25

Refer, treat—or do both

Once you have evidence that a patient is a survivor of MST, you need to consider a mental health referral or consultation and address physical symptoms. All honorably discharged veterans are eligible to receive VA treatment for MST, regardless of their disability rating or eligibility for other services. If a veteran indicates that he or she would like to seek psychotherapy or see a specialist outside of the VA system, it will fall to you to help the patient find the most appropriate treatment. (You’ll find links to VA and nonmilitary resources in the box.) Either way, patient acuity is a guide to the optimal approach.

Inpatient treatment will likely be needed for a patient who reveals thoughts of self-harm or harming others. If the patient is safe and stable enough for outpatient treatment, a therapist or psychiatrist with experience in treating sexual trauma is a good first step. Cognitive behavioral therapy and trauma-focused therapy have both been shown to have good outcomes in patients with sexual trauma and PTSD.²⁹ Depending on the individual’s key presenting issues, a consultation with a substance abuse specialist, gynecologist, or other specialist may be helpful, as well.

As a family physician, you are in a position to build a long-term, trusting relationship with such a patient, which may be therapeutic in itself.⁹ In building such a relationship, keep in mind that the experience of serving in the military could make a patient particularly sensitive, or resistant, to your advice; you’ll need to strive for a collaborative approach.

CASE You tell Ms. Doe that the incident she described was indeed sexual violence—and specifically known as military sexual trauma. Her feelings about it are likely surfacing now due to the time away from the military—and by the fact that she’s beginning to date. In addition to spending some time listening to her story, you advise Ms. Doe to start seeing a therapist. You suggest she consider VA treatment services, and direct her to its MST web site (www.mentalhealth.va.gov/msthome.asp). Before she leaves, you make it clear that you will continue to see and support her through this difficult time, and you schedule a follow-up visit.

CORRESPONDENCE 
Niranjan S. Karnik, MD, PhD, FAPA, University of Chicago, Pritzker School of Medicine, 5841 South Maryland, MC 3077, Chicago, IL 60637; nkarnik@bsd.uchicago.edu

CASE A 29-year-old veteran (whom we’ll call Jane Doe) served as a medical corpsman in Iraq and has been pursuing a nursing degree since her honorable discharge a year ago. She comes in for a visit and reports a 3-month history of depression without suicidal ideation. In addition, Ms. Doe says, she has had abdominal pain that waxes and wanes for the past month. The pain is diffuse and nonfocal and appears to be unaffected by eating or bowel movements. She is unable to identify a particular pattern.

The patient has no significant medical or psychiatric history, and a physical examination is unremarkable. You advise her to follow a simplified dietary regimen, avoiding spicy foods and limiting dairy intake, and schedule a follow-up visit in 2 weeks.

Since 2002, some 2.4 million US troops have served in Iraq and Afghanistan,¹ creating a new generation of veterans who need broad-based support to recover from the physical and psychological wounds of war. All too often, those wounds include sexual assault or harassment, collectively known as military sexual trauma (MST).

MST is a growing concern for the Veterans Administration (VA) for a number of reasons—an increase in women on the front lines and greater media coverage of patterns of sexual assault in the military among them.² The official lifting of the ban on women in combat announced by the Pentagon in January brought the issue to the forefront, as well.³

In fact, MST should be a concern not only for clinicians within the VA, but also for civilian physicians. There are nearly 22 million American veterans, and the vast majority (>95%) get at least some of their medical care outside of the VA system⁴—often in outpatient facilities like yours.⁵ Family physicians need to be aware of the problem and able to give veterans who have suffered from sexual trauma the sensitive care they require.

The scope of the problem? No one is sure

How widespread is MST? That question is not easily answered. The prevalence rate among female service members is 20% to 43%,⁶ according to internal reports, while studies outside the military have reported rates that range from 3% to as high as 71%.⁵ In a recent anonymous survey of women in combat zones, led by a VA researcher—widely reported but still undergoing final review—half of those surveyed reported sexual harassment and nearly one in 4 reported sexual assault.⁷

There are far less data on rates of MST among male service members. The documented prevalence rate for men is 1.1%, with a range of 0.03% to 12.4%, but these figures are based on internal reports of sexual harassment and assault.⁸

Military culture and personal history are key factors
While the rate at which MST is reported has increased over the past 30 years,⁸ many reasons for not reporting it—stigma, fear of blame, accusations of homosexuality or promiscuity, and the threat of charges of fraternization among them—still remain.^8,9 Military culture is still male-dominated, with an emphasis on self-sufficiency that often leaves victims of MST feeling as though they have nowhere to turn.

There are also circumstances military members face that can aggravate the effects of sexual trauma. Soldiers on deployment are typically isolated from their normal support systems, under significant pressure, and unable to leave their post, which often means they have ongoing exposure to the abuser.

A history of childhood sexual abuse (CSA). As many as 50% of female service members (and about 17% of military men) have reported CSA,¹⁰ compared with 25% to 27% of women and 16% of men outside of the military.^5,11 That finding may be partially explained by data showing that nearly half of women in the military cited escaping from their home environment as a primary reason for enlisting.¹²

Women in the military who have a history of CSA, however, face a significantly higher risk for MST than servicewomen who were not sexually assaulted as children.⁸ Among female Navy recruits, for example, those who reported CSA were 4.8 times more likely to be raped than those who had no history of CSA.¹³

Combat-related trauma further complicates the picture. Evidence suggests that exposure to childhood physical and sexual abuse was associated with increased risk for combat-related posttraumatic stress disorder (PTSD) among men who served in Vietnam¹⁴ and women who served in Operation Desert Storm.¹⁵

Broaching the subject should be routine

Primary care physicians can play an important role in helping veterans transition back to their civilian lives and local communities, starting with a holistic medical assessment. When you see a patient whose return is relatively recent, inquire about his or her experiences during deployment. It is important to ask specifically about traumatic experiences, and to routinely screen for MST.

CASE When Ms. Doe returns. you begin by asking about her mood, using open-ended, nondirective questions. She responds by admitting that she had left important information off of the intake form she filled out on her last visit—most notably, a history of CSA. You gently ask about her experiences in the military, particularly during the year she spent in Iraq—and whether anything happened there that you should know.

Haltingly and with much emotion, the patient tells of her experience with another soldier. She worked with him every day, she says, and had grown close to him. One evening things went further than she expected. At first, it was only kissing, but then he forced himself on her sexually. She has not told anyone else about this event, Ms. Doe confides, because she wasn’t sure whether she precipitated it and felt embarrassed and humiliated by her choice to trust this man.

She did not feel that her supervising officers would listen or understand, as romantic attachments are best avoided in a combat zone and daily injuries are the norm. She says that her role as a medic kept her focused on the pain of others and enabled her to avoid looking at her own situation.

Evidence has shown that, like Ms. Doe, most survivors of trauma do not volunteer such information, but will often respond to direct and empathic questions from their physician.¹⁶ Routine screening of all veterans for MST, which the VA recommends, has been shown to increase their use of mental health resources.^17,18 This can be easily incorporated into a medical history or an intake questionnaire, using this simple 2-question tool:^17,18

While you were in the military:

• Did you receive uninvited and unwanted sexual attention, such as touching, cornering, pressure for sexual favors, or verbal remarks?
• Did anyone ever use force or the threat of force to have sexual contact with you against your will?

Screen for PTSD, and consider other psychiatric disorders
MST has been found to confer a 9-fold risk for PTSD. Indeed, more than 4 in 10 (42%) women with a history of MST have a PTSD diagnosis.¹⁹ Thus, if the screen for MST is positive—as indicated by a Yes answer to either question—follow up with the 4-question Primary Care PTSD screen (TABLE 1) is recommended.²⁰

Veterans with a history of MST are twice as likely as other veterans to receive a mental health diagnosis;¹⁷ they’re also more likely to have 3 or more comorbid psychiatric conditions.²¹ Women appear to be more likely than men to suffer from depression, eating disorders, substance abuse,²² anxiety disorders,²¹ dissociative disorders, and personality disorders.¹⁷

Research on the mental health consequences of sexual assault in men (in any setting) is limited, however, and data on male survivors of MST are particularly sparse. What is known is that men who have experienced sexual trauma have higher rates of alcohol abuse²³ and self-harm²⁴ than women with a history of sexual trauma, and that MST has a greater association with bipolar disorder, schizophrenia, and psychosis in men.¹⁷

TABLE 1
Primary care PTSD screen (PC-PTSD)

Multiple physical symptoms are often trauma-related

Veterans with a history of MST are also more likely to report physical symptoms²⁵ and to have a lower health-related quality of life,²⁶ poorer health status, and more outpatient visits¹² than vets who were not exposed to MST. And, while pelvic pain is widely believed to be associated with female sexual abuse, survivors often present with a wide range of physical problems. The most common symptoms, similar to those affecting civilian rape survivors, include headache, gastrointestinal (GI) problems, chronic fatigue, severe menopause symptoms, and urological problems, as well as pelvic pain and sexual problems.²⁷ Cardiac and respiratory disorders are also common (TABLE 2).^17,25

Compared with their unaffected counterparts, women with a history of MST are more likely to be obese and sedentary, to smoke and drink, and to have had a hysterectomy before the age of 40 years.²⁸ They are also more than twice as likely as other female veterans to say that they were treated for a heart attack within the past year.²⁵ Data on the physical symptoms of male survivors of MST are extremely limited, but one study found an association with pulmonary and liver disease and human immunodeficiency virus and acquired immune deficiency syndrome.¹⁷

TABLE 2
Common physical symptoms reported by female MST survivors*^17,25

A cluster of nonspecific findings?
Patients with a history of MST often present with complex and nonspecific signs and symptoms, making it difficult for a primary care physician to arrive at a diagnosis. MST and combat-related trauma should be considered in such cases, as well as in veterans who present with complaints involving multiple organ systems.^21,25

Refer, treat—or do both

Once you have evidence that a patient is a survivor of MST, you need to consider a mental health referral or consultation and address physical symptoms. All honorably discharged veterans are eligible to receive VA treatment for MST, regardless of their disability rating or eligibility for other services. If a veteran indicates that he or she would like to seek psychotherapy or see a specialist outside of the VA system, it will fall to you to help the patient find the most appropriate treatment. (You’ll find links to VA and nonmilitary resources in the box.) Either way, patient acuity is a guide to the optimal approach.

Inpatient treatment will likely be needed for a patient who reveals thoughts of self-harm or harming others. If the patient is safe and stable enough for outpatient treatment, a therapist or psychiatrist with experience in treating sexual trauma is a good first step. Cognitive behavioral therapy and trauma-focused therapy have both been shown to have good outcomes in patients with sexual trauma and PTSD.²⁹ Depending on the individual’s key presenting issues, a consultation with a substance abuse specialist, gynecologist, or other specialist may be helpful, as well.

As a family physician, you are in a position to build a long-term, trusting relationship with such a patient, which may be therapeutic in itself.⁹ In building such a relationship, keep in mind that the experience of serving in the military could make a patient particularly sensitive, or resistant, to your advice; you’ll need to strive for a collaborative approach.

CASE You tell Ms. Doe that the incident she described was indeed sexual violence—and specifically known as military sexual trauma. Her feelings about it are likely surfacing now due to the time away from the military—and by the fact that she’s beginning to date. In addition to spending some time listening to her story, you advise Ms. Doe to start seeing a therapist. You suggest she consider VA treatment services, and direct her to its MST web site (www.mentalhealth.va.gov/msthome.asp). Before she leaves, you make it clear that you will continue to see and support her through this difficult time, and you schedule a follow-up visit.

CORRESPONDENCE 
Niranjan S. Karnik, MD, PhD, FAPA, University of Chicago, Pritzker School of Medicine, 5841 South Maryland, MC 3077, Chicago, IL 60637; nkarnik@bsd.uchicago.edu

CASE A 29-year-old veteran (whom we’ll call Jane Doe) served as a medical corpsman in Iraq and has been pursuing a nursing degree since her honorable discharge a year ago. She comes in for a visit and reports a 3-month history of depression without suicidal ideation. In addition, Ms. Doe says, she has had abdominal pain that waxes and wanes for the past month. The pain is diffuse and nonfocal and appears to be unaffected by eating or bowel movements. She is unable to identify a particular pattern.

The patient has no significant medical or psychiatric history, and a physical examination is unremarkable. You advise her to follow a simplified dietary regimen, avoiding spicy foods and limiting dairy intake, and schedule a follow-up visit in 2 weeks.

Since 2002, some 2.4 million US troops have served in Iraq and Afghanistan,¹ creating a new generation of veterans who need broad-based support to recover from the physical and psychological wounds of war. All too often, those wounds include sexual assault or harassment, collectively known as military sexual trauma (MST).

MST is a growing concern for the Veterans Administration (VA) for a number of reasons—an increase in women on the front lines and greater media coverage of patterns of sexual assault in the military among them.² The official lifting of the ban on women in combat announced by the Pentagon in January brought the issue to the forefront, as well.³

In fact, MST should be a concern not only for clinicians within the VA, but also for civilian physicians. There are nearly 22 million American veterans, and the vast majority (>95%) get at least some of their medical care outside of the VA system⁴—often in outpatient facilities like yours.⁵ Family physicians need to be aware of the problem and able to give veterans who have suffered from sexual trauma the sensitive care they require.

The scope of the problem? No one is sure

How widespread is MST? That question is not easily answered. The prevalence rate among female service members is 20% to 43%,⁶ according to internal reports, while studies outside the military have reported rates that range from 3% to as high as 71%.⁵ In a recent anonymous survey of women in combat zones, led by a VA researcher—widely reported but still undergoing final review—half of those surveyed reported sexual harassment and nearly one in 4 reported sexual assault.⁷

There are far less data on rates of MST among male service members. The documented prevalence rate for men is 1.1%, with a range of 0.03% to 12.4%, but these figures are based on internal reports of sexual harassment and assault.⁸

Military culture and personal history are key factors
While the rate at which MST is reported has increased over the past 30 years,⁸ many reasons for not reporting it—stigma, fear of blame, accusations of homosexuality or promiscuity, and the threat of charges of fraternization among them—still remain.^8,9 Military culture is still male-dominated, with an emphasis on self-sufficiency that often leaves victims of MST feeling as though they have nowhere to turn.

There are also circumstances military members face that can aggravate the effects of sexual trauma. Soldiers on deployment are typically isolated from their normal support systems, under significant pressure, and unable to leave their post, which often means they have ongoing exposure to the abuser.

A history of childhood sexual abuse (CSA). As many as 50% of female service members (and about 17% of military men) have reported CSA,¹⁰ compared with 25% to 27% of women and 16% of men outside of the military.^5,11 That finding may be partially explained by data showing that nearly half of women in the military cited escaping from their home environment as a primary reason for enlisting.¹²

Women in the military who have a history of CSA, however, face a significantly higher risk for MST than servicewomen who were not sexually assaulted as children.⁸ Among female Navy recruits, for example, those who reported CSA were 4.8 times more likely to be raped than those who had no history of CSA.¹³

Combat-related trauma further complicates the picture. Evidence suggests that exposure to childhood physical and sexual abuse was associated with increased risk for combat-related posttraumatic stress disorder (PTSD) among men who served in Vietnam¹⁴ and women who served in Operation Desert Storm.¹⁵

Broaching the subject should be routine

Primary care physicians can play an important role in helping veterans transition back to their civilian lives and local communities, starting with a holistic medical assessment. When you see a patient whose return is relatively recent, inquire about his or her experiences during deployment. It is important to ask specifically about traumatic experiences, and to routinely screen for MST.

CASE When Ms. Doe returns. you begin by asking about her mood, using open-ended, nondirective questions. She responds by admitting that she had left important information off of the intake form she filled out on her last visit—most notably, a history of CSA. You gently ask about her experiences in the military, particularly during the year she spent in Iraq—and whether anything happened there that you should know.

Haltingly and with much emotion, the patient tells of her experience with another soldier. She worked with him every day, she says, and had grown close to him. One evening things went further than she expected. At first, it was only kissing, but then he forced himself on her sexually. She has not told anyone else about this event, Ms. Doe confides, because she wasn’t sure whether she precipitated it and felt embarrassed and humiliated by her choice to trust this man.

She did not feel that her supervising officers would listen or understand, as romantic attachments are best avoided in a combat zone and daily injuries are the norm. She says that her role as a medic kept her focused on the pain of others and enabled her to avoid looking at her own situation.

Evidence has shown that, like Ms. Doe, most survivors of trauma do not volunteer such information, but will often respond to direct and empathic questions from their physician.¹⁶ Routine screening of all veterans for MST, which the VA recommends, has been shown to increase their use of mental health resources.^17,18 This can be easily incorporated into a medical history or an intake questionnaire, using this simple 2-question tool:^17,18

While you were in the military:

• Did you receive uninvited and unwanted sexual attention, such as touching, cornering, pressure for sexual favors, or verbal remarks?
• Did anyone ever use force or the threat of force to have sexual contact with you against your will?

Screen for PTSD, and consider other psychiatric disorders
MST has been found to confer a 9-fold risk for PTSD. Indeed, more than 4 in 10 (42%) women with a history of MST have a PTSD diagnosis.¹⁹ Thus, if the screen for MST is positive—as indicated by a Yes answer to either question—follow up with the 4-question Primary Care PTSD screen (TABLE 1) is recommended.²⁰

Veterans with a history of MST are twice as likely as other veterans to receive a mental health diagnosis;¹⁷ they’re also more likely to have 3 or more comorbid psychiatric conditions.²¹ Women appear to be more likely than men to suffer from depression, eating disorders, substance abuse,²² anxiety disorders,²¹ dissociative disorders, and personality disorders.¹⁷

Research on the mental health consequences of sexual assault in men (in any setting) is limited, however, and data on male survivors of MST are particularly sparse. What is known is that men who have experienced sexual trauma have higher rates of alcohol abuse²³ and self-harm²⁴ than women with a history of sexual trauma, and that MST has a greater association with bipolar disorder, schizophrenia, and psychosis in men.¹⁷

TABLE 1
Primary care PTSD screen (PC-PTSD)

Multiple physical symptoms are often trauma-related

Veterans with a history of MST are also more likely to report physical symptoms²⁵ and to have a lower health-related quality of life,²⁶ poorer health status, and more outpatient visits¹² than vets who were not exposed to MST. And, while pelvic pain is widely believed to be associated with female sexual abuse, survivors often present with a wide range of physical problems. The most common symptoms, similar to those affecting civilian rape survivors, include headache, gastrointestinal (GI) problems, chronic fatigue, severe menopause symptoms, and urological problems, as well as pelvic pain and sexual problems.²⁷ Cardiac and respiratory disorders are also common (TABLE 2).^17,25

Compared with their unaffected counterparts, women with a history of MST are more likely to be obese and sedentary, to smoke and drink, and to have had a hysterectomy before the age of 40 years.²⁸ They are also more than twice as likely as other female veterans to say that they were treated for a heart attack within the past year.²⁵ Data on the physical symptoms of male survivors of MST are extremely limited, but one study found an association with pulmonary and liver disease and human immunodeficiency virus and acquired immune deficiency syndrome.¹⁷

TABLE 2
Common physical symptoms reported by female MST survivors*^17,25

A cluster of nonspecific findings?
Patients with a history of MST often present with complex and nonspecific signs and symptoms, making it difficult for a primary care physician to arrive at a diagnosis. MST and combat-related trauma should be considered in such cases, as well as in veterans who present with complaints involving multiple organ systems.^21,25

Refer, treat—or do both

Once you have evidence that a patient is a survivor of MST, you need to consider a mental health referral or consultation and address physical symptoms. All honorably discharged veterans are eligible to receive VA treatment for MST, regardless of their disability rating or eligibility for other services. If a veteran indicates that he or she would like to seek psychotherapy or see a specialist outside of the VA system, it will fall to you to help the patient find the most appropriate treatment. (You’ll find links to VA and nonmilitary resources in the box.) Either way, patient acuity is a guide to the optimal approach.

Inpatient treatment will likely be needed for a patient who reveals thoughts of self-harm or harming others. If the patient is safe and stable enough for outpatient treatment, a therapist or psychiatrist with experience in treating sexual trauma is a good first step. Cognitive behavioral therapy and trauma-focused therapy have both been shown to have good outcomes in patients with sexual trauma and PTSD.²⁹ Depending on the individual’s key presenting issues, a consultation with a substance abuse specialist, gynecologist, or other specialist may be helpful, as well.

As a family physician, you are in a position to build a long-term, trusting relationship with such a patient, which may be therapeutic in itself.⁹ In building such a relationship, keep in mind that the experience of serving in the military could make a patient particularly sensitive, or resistant, to your advice; you’ll need to strive for a collaborative approach.

CASE You tell Ms. Doe that the incident she described was indeed sexual violence—and specifically known as military sexual trauma. Her feelings about it are likely surfacing now due to the time away from the military—and by the fact that she’s beginning to date. In addition to spending some time listening to her story, you advise Ms. Doe to start seeing a therapist. You suggest she consider VA treatment services, and direct her to its MST web site (www.mentalhealth.va.gov/msthome.asp). Before she leaves, you make it clear that you will continue to see and support her through this difficult time, and you schedule a follow-up visit.

CORRESPONDENCE 
Niranjan S. Karnik, MD, PhD, FAPA, University of Chicago, Pritzker School of Medicine, 5841 South Maryland, MC 3077, Chicago, IL 60637; nkarnik@bsd.uchicago.edu

Obese mother gains another 60 lb before delivery

AN OBESE WOMAN with a family history of diabetes had previously given birth to a large baby. Even though she expressed her concern that this fetus would also be macrosomic, the ObGyn planned for spontaneous vaginal delivery. At 39 weeks’ gestation, after gaining 60 lb, she went to the hospital requesting induction of labor; the ObGyn reluctantly agreed. Labor was lengthy, forceps-assisted delivery was performed, and a shoulder dystocia was encountered. The baby was born with respiratory distress, a brachial plexus injury, bruises on his right cheek and both ears, and multiple rib fractures. After transfer to a children’s hospital, surgical exploration revealed avulsion of the C6 root nerve from the spinal cord and damage to C5, C7, and C8 nerve roots. Several surgical repairs and physical therapy have led to some improvement, but the child is permanently injured. His right arm is shorter than the left, his right hand is smaller, and he has less strength and range of motion in the right arm. He also has excessive tearing in the right eye and his right eyelid droops.

PARENTS’ CLAIM The ObGyn failed to recognize the risk of delivering a macrosomic baby and did not consider cesarean delivery. The brachial plexus injury was due to downward traction applied during delivery.

PHYSICIAN’S DEFENSE There was no negligence. The brachial plexus injury was not caused by downward traction.

VERDICT A $4.1 million Indiana verdict was returned, but was reduced to the state cap of $1.25 million.

Failure to follow-up on mass: $1.97M verdict

AFTER STAGE II OVARIAN CANCER was found in 1999, a woman underwent surgery and chemotherapy, and was told she was cancer-free. She had regular visits between 2000 and 2008 with another surgical oncologist after her first surgeon moved. In 2004, the oncologist documented finding a round fullness during a pelvic exam. A CT scan confirmed a mass in the pelvic cul-de-sac.

In August 2008, the patient was treated for deep venous thrombosis in her leg. The attending physician saw the pelvic mass on imaging, and a biopsy indicated a recurrence of ovarian cancer. After chemotherapy, the patient underwent surgery, but the tumor was unresectable. In early 2011, testing revealed metastasis to the spine, sternum, pelvic bone, arm, and lung.

PATIENT’S CLAIM The surgeon did not properly investigate the mass resulting in a delayed diagnosis of cancer recurrence. The patient alleged that the surgical oncologist repeatedly stated that the mass had not changed and was most likely fluid; it was nothing to worry about. Radiology reports indicated a suspicion of cancer.

DEFENDANTS’ DEFENSE The oncologist repeatedly told the patient that the mass should be biopsied, but the patient refused because she was dealing with other medical issues. The radiologist argued that reports to the oncologist included everything needed to diagnose the cancer.

VERDICT A Pennsylvania jury found the surgical oncologist fully at fault and returned a $1,971,455 verdict.

Incomplete tubal ligation

BEFORE DELIVERY OF HER THIRD CHILD, a 26-year-old woman requested sterilization using tubal ligation. After delivery, the ObGyn performed a bilateral tubal ligation. The pathologist’s report indicated that the ligation was incomplete: the left fallopian tube had not been fully removed. The ObGyn failed to note the report’s results in the patient’s record, nor did he advise the patient. Two years later, the patient delivered a fourth child.

PATIENT’S CLAIM The patient alleged wrongful birth against both the ObGyn and pathologist. The ObGyn was negligent for not reacting to the pathologist’s report of incomplete tubal ligation, and for not informing the patient. The pathologist should have verbally confirmed receipt of the report with the ObGyn.

PHYSICIANS’ DEFENSE The ObGyn settled before trial. The pathologist claimed he had properly interpreted the specimen and reported the results.

VERDICT A Louisiana jury found the ObGyn fully at fault and assessed additional damages of $56,252 to the $100,000 settlement.

Where did this foreign body come from?

A WOMAN SUFFERED FROM PELVIC PAIN caused by adhesions following two cesarean deliveries and a hysterectomy. In January 2003, her ObGyn performed laparotomy to reduce adhesions from prior surgeries and place Gore-Tex mesh to prevent future adhesions. In October 2010, the patient reported epigastric pain, and went to a different surgeon (her insurance changed). A CT scan identified a foreign body encapsulated in scar tissue in the patient’s lower abdomen/pelvis. The surgeon removed the foreign body.

PATIENT’S CLAIM The ObGyn and hospital were negligent in conducting the 2003 procedure; the foreign object was a retained surgical sponge.

DEFENDANTS’ DEFENSE The foreign body removed in 2010 was the Gore-Tex mesh placed in 2003. The mesh became encapsulated in scar tissue due to the patient’s propensity to develop adhesions, and then moved within the patient’s body. Surgical sponges have embedded radiopaque tracers; CT scans in 2003 and 2010 did not detect any radiopaque tracers.

VERDICT A California defense verdict was returned.

Massive bleed during sacrocolpopexy

AFTER A 72-YEAR-OLD WOMAN developed pelvic organ prolapse, her urologist performed an abdominal sacrocolpopexy. As the urologist attempted to gain access to the sacral prominence, a tear in the median sacral vein expanded to involve the inferior vena cava and left iliac vein. Massive bleeding occurred and multiple units of blood were transfused. A general surgeon successfully repaired the vascular injuries. The patient was hospitalized for 16 days, received home healthcare, and fully recovered.

PATIENT’S CLAIM The urologist was negligent in overaggressive manipulation of the median sacral vein, causing it to avulse.

PHYSICIAN’S DEFENSE Bleeds of this type are a known complication of the procedure.

VERDICT A Michigan defense verdict was returned.

Was it hypoxia or autism?

AFTER SEVERAL HOURS IN LABOR, a fetal heart-rate monitor indicated decreasing fetal heart rate that led to terminal bradycardia. The ObGyn was called and performed an emergency cesarean delivery. The child was diagnosed with brain damage at 2 years of age.

PARENTS’ CLAIM A cesarean delivery should have been planned because of the fetal weight (8 lb 11 oz). A hypoxic event occurred during labor. Ultrasonography would have shown that the fetus was inverted and that the baby’s face was covered by one of its hands. Delivery was not properly managed, and fetal distress was not reported to the ObGyn in a timely manner.

DEFENDANTS’ DEFENSE The infant’s weight was not sufficient to warrant a cesarean delivery. The infant did not suffer hypoxia. The child’s abnormalities only emerged in the second year of life. An MRI at that time did not indicate brain damage. The child’s development with subsequent regression suggests autism.

VERDICT A New York defense verdict was returned.

Should mammography have been diagnostic?

A 46-YEAR-OLD WOMAN with a family history of breast cancer had regular annual screenings. In December 2006, the patient reported pain, hardness, and burning in her left breast to her gynecologist. A radiologist interpreted the mammography as normal. In May 2007, the patient found a lump in her left breast. Testing indicated she had stage IV breast cancer. She died 2 months after the trial concluded.

PATIENT’S CLAIM The 2006 mammogram was performed as a screening mammography, but should have been diagnostic, considering her family history and reported symptoms. The radiologist improperly interpreted the films.

DEFENDANTS’ DEFENSE The hospital staff testified that the patient did not report pain, hardness, and burning in her left breast when she presented for the 2006 mammography. The radiologist claimed his screening and interpretation were appropriate.

VERDICT The Louisiana court granted the patient’s motion for judgment, and awarded $558,000 in medical costs and $1.3 million in noneconomic damages, totalling $1.808 million. This was reduced to the $500,000 statutory cap.

Obese mother gains another 60 lb before delivery

AN OBESE WOMAN with a family history of diabetes had previously given birth to a large baby. Even though she expressed her concern that this fetus would also be macrosomic, the ObGyn planned for spontaneous vaginal delivery. At 39 weeks’ gestation, after gaining 60 lb, she went to the hospital requesting induction of labor; the ObGyn reluctantly agreed. Labor was lengthy, forceps-assisted delivery was performed, and a shoulder dystocia was encountered. The baby was born with respiratory distress, a brachial plexus injury, bruises on his right cheek and both ears, and multiple rib fractures. After transfer to a children’s hospital, surgical exploration revealed avulsion of the C6 root nerve from the spinal cord and damage to C5, C7, and C8 nerve roots. Several surgical repairs and physical therapy have led to some improvement, but the child is permanently injured. His right arm is shorter than the left, his right hand is smaller, and he has less strength and range of motion in the right arm. He also has excessive tearing in the right eye and his right eyelid droops.

PARENTS’ CLAIM The ObGyn failed to recognize the risk of delivering a macrosomic baby and did not consider cesarean delivery. The brachial plexus injury was due to downward traction applied during delivery.

PHYSICIAN’S DEFENSE There was no negligence. The brachial plexus injury was not caused by downward traction.

VERDICT A $4.1 million Indiana verdict was returned, but was reduced to the state cap of $1.25 million.

Failure to follow-up on mass: $1.97M verdict

AFTER STAGE II OVARIAN CANCER was found in 1999, a woman underwent surgery and chemotherapy, and was told she was cancer-free. She had regular visits between 2000 and 2008 with another surgical oncologist after her first surgeon moved. In 2004, the oncologist documented finding a round fullness during a pelvic exam. A CT scan confirmed a mass in the pelvic cul-de-sac.

In August 2008, the patient was treated for deep venous thrombosis in her leg. The attending physician saw the pelvic mass on imaging, and a biopsy indicated a recurrence of ovarian cancer. After chemotherapy, the patient underwent surgery, but the tumor was unresectable. In early 2011, testing revealed metastasis to the spine, sternum, pelvic bone, arm, and lung.

PATIENT’S CLAIM The surgeon did not properly investigate the mass resulting in a delayed diagnosis of cancer recurrence. The patient alleged that the surgical oncologist repeatedly stated that the mass had not changed and was most likely fluid; it was nothing to worry about. Radiology reports indicated a suspicion of cancer.

DEFENDANTS’ DEFENSE The oncologist repeatedly told the patient that the mass should be biopsied, but the patient refused because she was dealing with other medical issues. The radiologist argued that reports to the oncologist included everything needed to diagnose the cancer.

VERDICT A Pennsylvania jury found the surgical oncologist fully at fault and returned a $1,971,455 verdict.

Incomplete tubal ligation

BEFORE DELIVERY OF HER THIRD CHILD, a 26-year-old woman requested sterilization using tubal ligation. After delivery, the ObGyn performed a bilateral tubal ligation. The pathologist’s report indicated that the ligation was incomplete: the left fallopian tube had not been fully removed. The ObGyn failed to note the report’s results in the patient’s record, nor did he advise the patient. Two years later, the patient delivered a fourth child.

PATIENT’S CLAIM The patient alleged wrongful birth against both the ObGyn and pathologist. The ObGyn was negligent for not reacting to the pathologist’s report of incomplete tubal ligation, and for not informing the patient. The pathologist should have verbally confirmed receipt of the report with the ObGyn.

PHYSICIANS’ DEFENSE The ObGyn settled before trial. The pathologist claimed he had properly interpreted the specimen and reported the results.

VERDICT A Louisiana jury found the ObGyn fully at fault and assessed additional damages of $56,252 to the $100,000 settlement.

Where did this foreign body come from?

A WOMAN SUFFERED FROM PELVIC PAIN caused by adhesions following two cesarean deliveries and a hysterectomy. In January 2003, her ObGyn performed laparotomy to reduce adhesions from prior surgeries and place Gore-Tex mesh to prevent future adhesions. In October 2010, the patient reported epigastric pain, and went to a different surgeon (her insurance changed). A CT scan identified a foreign body encapsulated in scar tissue in the patient’s lower abdomen/pelvis. The surgeon removed the foreign body.

PATIENT’S CLAIM The ObGyn and hospital were negligent in conducting the 2003 procedure; the foreign object was a retained surgical sponge.

DEFENDANTS’ DEFENSE The foreign body removed in 2010 was the Gore-Tex mesh placed in 2003. The mesh became encapsulated in scar tissue due to the patient’s propensity to develop adhesions, and then moved within the patient’s body. Surgical sponges have embedded radiopaque tracers; CT scans in 2003 and 2010 did not detect any radiopaque tracers.

VERDICT A California defense verdict was returned.

Massive bleed during sacrocolpopexy

AFTER A 72-YEAR-OLD WOMAN developed pelvic organ prolapse, her urologist performed an abdominal sacrocolpopexy. As the urologist attempted to gain access to the sacral prominence, a tear in the median sacral vein expanded to involve the inferior vena cava and left iliac vein. Massive bleeding occurred and multiple units of blood were transfused. A general surgeon successfully repaired the vascular injuries. The patient was hospitalized for 16 days, received home healthcare, and fully recovered.

PATIENT’S CLAIM The urologist was negligent in overaggressive manipulation of the median sacral vein, causing it to avulse.

PHYSICIAN’S DEFENSE Bleeds of this type are a known complication of the procedure.

VERDICT A Michigan defense verdict was returned.

Was it hypoxia or autism?

AFTER SEVERAL HOURS IN LABOR, a fetal heart-rate monitor indicated decreasing fetal heart rate that led to terminal bradycardia. The ObGyn was called and performed an emergency cesarean delivery. The child was diagnosed with brain damage at 2 years of age.

PARENTS’ CLAIM A cesarean delivery should have been planned because of the fetal weight (8 lb 11 oz). A hypoxic event occurred during labor. Ultrasonography would have shown that the fetus was inverted and that the baby’s face was covered by one of its hands. Delivery was not properly managed, and fetal distress was not reported to the ObGyn in a timely manner.

DEFENDANTS’ DEFENSE The infant’s weight was not sufficient to warrant a cesarean delivery. The infant did not suffer hypoxia. The child’s abnormalities only emerged in the second year of life. An MRI at that time did not indicate brain damage. The child’s development with subsequent regression suggests autism.

VERDICT A New York defense verdict was returned.

Should mammography have been diagnostic?

A 46-YEAR-OLD WOMAN with a family history of breast cancer had regular annual screenings. In December 2006, the patient reported pain, hardness, and burning in her left breast to her gynecologist. A radiologist interpreted the mammography as normal. In May 2007, the patient found a lump in her left breast. Testing indicated she had stage IV breast cancer. She died 2 months after the trial concluded.

PATIENT’S CLAIM The 2006 mammogram was performed as a screening mammography, but should have been diagnostic, considering her family history and reported symptoms. The radiologist improperly interpreted the films.

DEFENDANTS’ DEFENSE The hospital staff testified that the patient did not report pain, hardness, and burning in her left breast when she presented for the 2006 mammography. The radiologist claimed his screening and interpretation were appropriate.

VERDICT The Louisiana court granted the patient’s motion for judgment, and awarded $558,000 in medical costs and $1.3 million in noneconomic damages, totalling $1.808 million. This was reduced to the $500,000 statutory cap.

Obese mother gains another 60 lb before delivery

AN OBESE WOMAN with a family history of diabetes had previously given birth to a large baby. Even though she expressed her concern that this fetus would also be macrosomic, the ObGyn planned for spontaneous vaginal delivery. At 39 weeks’ gestation, after gaining 60 lb, she went to the hospital requesting induction of labor; the ObGyn reluctantly agreed. Labor was lengthy, forceps-assisted delivery was performed, and a shoulder dystocia was encountered. The baby was born with respiratory distress, a brachial plexus injury, bruises on his right cheek and both ears, and multiple rib fractures. After transfer to a children’s hospital, surgical exploration revealed avulsion of the C6 root nerve from the spinal cord and damage to C5, C7, and C8 nerve roots. Several surgical repairs and physical therapy have led to some improvement, but the child is permanently injured. His right arm is shorter than the left, his right hand is smaller, and he has less strength and range of motion in the right arm. He also has excessive tearing in the right eye and his right eyelid droops.

PARENTS’ CLAIM The ObGyn failed to recognize the risk of delivering a macrosomic baby and did not consider cesarean delivery. The brachial plexus injury was due to downward traction applied during delivery.

PHYSICIAN’S DEFENSE There was no negligence. The brachial plexus injury was not caused by downward traction.

VERDICT A $4.1 million Indiana verdict was returned, but was reduced to the state cap of $1.25 million.

Failure to follow-up on mass: $1.97M verdict

AFTER STAGE II OVARIAN CANCER was found in 1999, a woman underwent surgery and chemotherapy, and was told she was cancer-free. She had regular visits between 2000 and 2008 with another surgical oncologist after her first surgeon moved. In 2004, the oncologist documented finding a round fullness during a pelvic exam. A CT scan confirmed a mass in the pelvic cul-de-sac.

In August 2008, the patient was treated for deep venous thrombosis in her leg. The attending physician saw the pelvic mass on imaging, and a biopsy indicated a recurrence of ovarian cancer. After chemotherapy, the patient underwent surgery, but the tumor was unresectable. In early 2011, testing revealed metastasis to the spine, sternum, pelvic bone, arm, and lung.

PATIENT’S CLAIM The surgeon did not properly investigate the mass resulting in a delayed diagnosis of cancer recurrence. The patient alleged that the surgical oncologist repeatedly stated that the mass had not changed and was most likely fluid; it was nothing to worry about. Radiology reports indicated a suspicion of cancer.

DEFENDANTS’ DEFENSE The oncologist repeatedly told the patient that the mass should be biopsied, but the patient refused because she was dealing with other medical issues. The radiologist argued that reports to the oncologist included everything needed to diagnose the cancer.

VERDICT A Pennsylvania jury found the surgical oncologist fully at fault and returned a $1,971,455 verdict.

Incomplete tubal ligation

BEFORE DELIVERY OF HER THIRD CHILD, a 26-year-old woman requested sterilization using tubal ligation. After delivery, the ObGyn performed a bilateral tubal ligation. The pathologist’s report indicated that the ligation was incomplete: the left fallopian tube had not been fully removed. The ObGyn failed to note the report’s results in the patient’s record, nor did he advise the patient. Two years later, the patient delivered a fourth child.

PATIENT’S CLAIM The patient alleged wrongful birth against both the ObGyn and pathologist. The ObGyn was negligent for not reacting to the pathologist’s report of incomplete tubal ligation, and for not informing the patient. The pathologist should have verbally confirmed receipt of the report with the ObGyn.

PHYSICIANS’ DEFENSE The ObGyn settled before trial. The pathologist claimed he had properly interpreted the specimen and reported the results.

VERDICT A Louisiana jury found the ObGyn fully at fault and assessed additional damages of $56,252 to the $100,000 settlement.

Where did this foreign body come from?

A WOMAN SUFFERED FROM PELVIC PAIN caused by adhesions following two cesarean deliveries and a hysterectomy. In January 2003, her ObGyn performed laparotomy to reduce adhesions from prior surgeries and place Gore-Tex mesh to prevent future adhesions. In October 2010, the patient reported epigastric pain, and went to a different surgeon (her insurance changed). A CT scan identified a foreign body encapsulated in scar tissue in the patient’s lower abdomen/pelvis. The surgeon removed the foreign body.

PATIENT’S CLAIM The ObGyn and hospital were negligent in conducting the 2003 procedure; the foreign object was a retained surgical sponge.

DEFENDANTS’ DEFENSE The foreign body removed in 2010 was the Gore-Tex mesh placed in 2003. The mesh became encapsulated in scar tissue due to the patient’s propensity to develop adhesions, and then moved within the patient’s body. Surgical sponges have embedded radiopaque tracers; CT scans in 2003 and 2010 did not detect any radiopaque tracers.

VERDICT A California defense verdict was returned.

Massive bleed during sacrocolpopexy

AFTER A 72-YEAR-OLD WOMAN developed pelvic organ prolapse, her urologist performed an abdominal sacrocolpopexy. As the urologist attempted to gain access to the sacral prominence, a tear in the median sacral vein expanded to involve the inferior vena cava and left iliac vein. Massive bleeding occurred and multiple units of blood were transfused. A general surgeon successfully repaired the vascular injuries. The patient was hospitalized for 16 days, received home healthcare, and fully recovered.

PATIENT’S CLAIM The urologist was negligent in overaggressive manipulation of the median sacral vein, causing it to avulse.

PHYSICIAN’S DEFENSE Bleeds of this type are a known complication of the procedure.

VERDICT A Michigan defense verdict was returned.

Was it hypoxia or autism?

AFTER SEVERAL HOURS IN LABOR, a fetal heart-rate monitor indicated decreasing fetal heart rate that led to terminal bradycardia. The ObGyn was called and performed an emergency cesarean delivery. The child was diagnosed with brain damage at 2 years of age.

PARENTS’ CLAIM A cesarean delivery should have been planned because of the fetal weight (8 lb 11 oz). A hypoxic event occurred during labor. Ultrasonography would have shown that the fetus was inverted and that the baby’s face was covered by one of its hands. Delivery was not properly managed, and fetal distress was not reported to the ObGyn in a timely manner.

DEFENDANTS’ DEFENSE The infant’s weight was not sufficient to warrant a cesarean delivery. The infant did not suffer hypoxia. The child’s abnormalities only emerged in the second year of life. An MRI at that time did not indicate brain damage. The child’s development with subsequent regression suggests autism.

VERDICT A New York defense verdict was returned.

Should mammography have been diagnostic?

A 46-YEAR-OLD WOMAN with a family history of breast cancer had regular annual screenings. In December 2006, the patient reported pain, hardness, and burning in her left breast to her gynecologist. A radiologist interpreted the mammography as normal. In May 2007, the patient found a lump in her left breast. Testing indicated she had stage IV breast cancer. She died 2 months after the trial concluded.

PATIENT’S CLAIM The 2006 mammogram was performed as a screening mammography, but should have been diagnostic, considering her family history and reported symptoms. The radiologist improperly interpreted the films.

DEFENDANTS’ DEFENSE The hospital staff testified that the patient did not report pain, hardness, and burning in her left breast when she presented for the 2006 mammography. The radiologist claimed his screening and interpretation were appropriate.

VERDICT The Louisiana court granted the patient’s motion for judgment, and awarded $558,000 in medical costs and $1.3 million in noneconomic damages, totalling $1.808 million. This was reduced to the $500,000 statutory cap.

CASE: Pelvic organ prolapse or Pouch of Douglas hernia?

A 42-year-old G3P2 woman is referred to you by her primary care provider for pelvic organ prolapse. Her medical history reveals that she has been bothered by a sense of pelvic pressure and bulge progressing over several years, and she has noticed that her symptoms are particularly worse during and after bowel movements. She reports some improved bowel evacuation with external splinting of her perineum. Upon closer questioning, the patient reports a history of chronic constipation since childhood associated with straining and a sense of incomplete emptying. She reports spending up to 30 minutes three to four times per day on the commode to completely empty her bowels.

Physical examination reveals an overweight woman with a soft, nontender abdomen remarkable for laparoscopic incision scars from a previous tubal ligation. Inspection of the external genitalia at rest is normal. Cough stress test is negative. At maximum Valsalva, however, there is significant perineal ballooning present.

Speculum examination demonstrates grade 1 uterine prolapse, grade 1 cystocele, and grade 2 rectocele. There is no evidence of pelvic floor tension myalgia. She has weak pelvic muscle strength. Visualization of the anus at maximum Valsalva reveals there is some asymmetric rectal prolapse of the anterior rectal wall. Digital rectal exam is unremarkable.

Are these patient’s symptoms due to pelvic organ prolapse or Pouch of Douglas hernia?

Pelvic organ prolapse: A common problem

Pelvic organ prolapse has an estimated prevalence of 55% in women aged 50 to 59 years.¹ More than 200,000 pelvic organ prolapse surgeries are performed annually in the United States.² Typically, patients report:

• vaginal bulge causing discomfort
• pelvic pressure or heaviness, or
• rubbing of the vaginal bulge on undergarments.

In more advanced pelvic organ prolapse, patients may report voiding dysfunction or stool trapping that requires manual splinting of the prolapse to assist in bladder and bowel evacuation.

Pouch of Douglas hernia: A lesser-known
(recognized) phenomenon

Similar to pelvic organ prolapse, Pouch of Douglas hernia also can present with symptoms of:

• pelvic pressure
• vague perineal aching
• defecatory dysfunction.

The phenomenon has been variably referred to in the literature as enterocele, descending perineum syndrome, peritoneocele, or Pouch of Douglas hernia. The concept was first introduced in 1966³ and describes descent of the entire pelvic floor and small bowel through a hernia in the Pouch of Douglas (FIGURE 1).

FIGURE 1: Pouch of Douglas hernia. The pelvic floor and small bowel descend into the Pouch of Douglas.

How does it occur? The pathophysiology is thought to be related to excessive abdominal straining in individuals with chronic constipation. This results in diminished pelvic floor muscle tone. Eventually, the whole pelvic floor descends, becoming funnel shaped due to stretching of the puborectalis muscle. Thus, stool is expelled by force, mostly through forces on the anterior rectal wall (which tends to prolapse after stool evacuation, with accompanied mucus secretion, soreness, and irritation).

Clinical pearl: Given the rectal wall prolapse that occurs after stool evacuation in Pouch of Douglas hernia, some patients will describe a rectal lump that bleeds after a bowel movement. The sensation of the rectal lump from the anterior rectal wall prolapse causes further straining.

Your patient reports pelvic pressure and bulge.
How do you proceed?

Physical examination

Look for perineal ballooning. Physical examination should start with inspection of the external genitalia. This inspection will identify any pelvic organ prolapse at or beyond the introitus. However, a Pouch of Douglas hernia will be missed if the patient is not examined during Valsalva or maximal strain. This maneuver will demonstrate the classic finding of perineal ballooning and is crucial to a final diagnosis of Pouch of Douglas hernia. Normally, the perineum will descend 1 cm to 2 cm during maximal strain; in Pouch of Douglas hernias, the perineum can descend up to 4 cm to 8 cm.⁴

Clinical pearl: It should be noted that, often, patients will not have a great deal of vaginal prolapse accompanying the perineal ballooning. In our opinion, this finding distinguishes Pouch of Douglas hernia from a vaginal vault prolapse caused by an enterocele.

Is rectal prolapse present? Beyond perineal ballooning, the presence of rectal prolapse should be evaluated. A rectocele of some degree is usually present. Asymmetric rectal prolapse affecting the anterior aspect of the rectal wall is consistent with a Pouch of Douglas hernia. This anatomic finding should be distinguished from true circumferential rectal prolapse, which remains in the differential diagnosis.

Basing the diagnosis of Pouch of Douglas hernia on physical examination alone can be difficult. Therefore, imaging studies are essential for accurate diagnosis.

Imaging investigations

Several imaging modalities can be used to diagnose such disorders of the pelvic floor as Pouch of Douglas hernia. These include:

• dynamic colpocystoproctography⁵
• defecography with oral barium⁶
• dynamic pelvic magnetic resonance imaging (MRI).⁷

In our experience, dynamic pelvic MRI has a high accuracy rate for diagnosing Pouch of Douglas hernia. FIGURE 2 illustrates the large Pouch of Douglas hernia filled with loops of small bowel. Perineal descent of the anorectal junction more than 3 cm below the pubococcygeal line during maximal straining is a diagnostic finding on imaging.⁷

FIGURE 2: MRI
Sagittal MRI during maximal Valsalva straining, demonstrating Pouch of Douglas hernia filled with small bowel.

What are your patient’s treatment options?

Reduce straining during bowel movements. The primary goal of treatment for Pouch of Douglas hernia should be relief of bothersome symptoms. Therefore, further damage can be prevented by eliminating straining during defecation. This can be accomplished with a bowel regimen that combines an irritant suppository (glycerin or bisacodyl) with a fiber supplement (the latter to increase bulk of the stool). Oral laxatives have limited use as many patients have lax anal sphincters and liquid stool could cause fecal incontinence.

Pelvic floor strengthening. The importance of pelvic floor physical therapy should be stressed. Patients can benefit from the use of modalities such as biofeedback to learn appropriate pelvic floor muscle relaxation techniques during defecation.⁸ While there is limited published evidence supporting the use of pelvic floor physical therapy, our anecdotal experience suggests that patients can gain considerable benefit with such conservative therapy.

Surgical therapy

Surgical repair of Pouch of Douglas hernia requires obliteration of the deep cul-de-sac (to prevent the small bowel from filling this space) and simultaneous pelvic floor reconstruction of the vaginal apex and any other compartments that are prolapsing (if pelvic organ prolapse is present). In our experience, these patients typically have derived greatest benefit from an abdominal approach. This usually can be accomplished with a sacrocolpopexy (if vaginal vault prolapse exists) with a Moschowitz or Halban procedure,⁹ uterosacral ligament plication, or a modified sacrocolpopexy with mesh augmentation to the sidewalls of the pelvis.¹⁰ There are currently no studies supporting one particular approach over another, but the most important feature of a surgical intervention is obliteration of the cul-de-sac (FIGURES 3, 4, and 5).

FIGURE 3: Open cul-de-sac. Open cul-de-sac after a prior abdominal sacrocolpopexy in a patient with a Pouch of Douglas hernia.

FIGURE 4: Obliterated cul-de-sac. Obliteration of the cul-de-sac with uterosacral ligament plication. Care is taken to prevent obstruction of the rectum at this level.

FIGURE 5: Cul-de-sac obliteration. Schematic diagram of obliteration of the cul-de-sac with uterosacral ligament plication sutures.

Final takeaways

Pouch of Douglas hernia is an important but often unrecognized cause of pelvic pressure and defecatory dysfunction. Perineal ballooning during maximal straining is highly suggestive of the diagnosis, with final diagnosis confirmed with various functional imaging studies of the pelvic floor. Management should include both conservative and surgical interventions to alleviate and prevent recurrence of symptoms.

ACKNOWLEDGMENT. The authors would like to thank Mr. John Hagen, Medical Illustrator, Mayo Clinic, for producing the illustrations in Figures 1 and 5.

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CASE: Pelvic organ prolapse or Pouch of Douglas hernia?

A 42-year-old G3P2 woman is referred to you by her primary care provider for pelvic organ prolapse. Her medical history reveals that she has been bothered by a sense of pelvic pressure and bulge progressing over several years, and she has noticed that her symptoms are particularly worse during and after bowel movements. She reports some improved bowel evacuation with external splinting of her perineum. Upon closer questioning, the patient reports a history of chronic constipation since childhood associated with straining and a sense of incomplete emptying. She reports spending up to 30 minutes three to four times per day on the commode to completely empty her bowels.

Physical examination reveals an overweight woman with a soft, nontender abdomen remarkable for laparoscopic incision scars from a previous tubal ligation. Inspection of the external genitalia at rest is normal. Cough stress test is negative. At maximum Valsalva, however, there is significant perineal ballooning present.

Speculum examination demonstrates grade 1 uterine prolapse, grade 1 cystocele, and grade 2 rectocele. There is no evidence of pelvic floor tension myalgia. She has weak pelvic muscle strength. Visualization of the anus at maximum Valsalva reveals there is some asymmetric rectal prolapse of the anterior rectal wall. Digital rectal exam is unremarkable.

Are these patient’s symptoms due to pelvic organ prolapse or Pouch of Douglas hernia?

Pelvic organ prolapse: A common problem

Pelvic organ prolapse has an estimated prevalence of 55% in women aged 50 to 59 years.¹ More than 200,000 pelvic organ prolapse surgeries are performed annually in the United States.² Typically, patients report:

• vaginal bulge causing discomfort
• pelvic pressure or heaviness, or
• rubbing of the vaginal bulge on undergarments.

In more advanced pelvic organ prolapse, patients may report voiding dysfunction or stool trapping that requires manual splinting of the prolapse to assist in bladder and bowel evacuation.

Pouch of Douglas hernia: A lesser-known
(recognized) phenomenon

Similar to pelvic organ prolapse, Pouch of Douglas hernia also can present with symptoms of:

• pelvic pressure
• vague perineal aching
• defecatory dysfunction.

The phenomenon has been variably referred to in the literature as enterocele, descending perineum syndrome, peritoneocele, or Pouch of Douglas hernia. The concept was first introduced in 1966³ and describes descent of the entire pelvic floor and small bowel through a hernia in the Pouch of Douglas (FIGURE 1).

FIGURE 1: Pouch of Douglas hernia. The pelvic floor and small bowel descend into the Pouch of Douglas.

How does it occur? The pathophysiology is thought to be related to excessive abdominal straining in individuals with chronic constipation. This results in diminished pelvic floor muscle tone. Eventually, the whole pelvic floor descends, becoming funnel shaped due to stretching of the puborectalis muscle. Thus, stool is expelled by force, mostly through forces on the anterior rectal wall (which tends to prolapse after stool evacuation, with accompanied mucus secretion, soreness, and irritation).

Clinical pearl: Given the rectal wall prolapse that occurs after stool evacuation in Pouch of Douglas hernia, some patients will describe a rectal lump that bleeds after a bowel movement. The sensation of the rectal lump from the anterior rectal wall prolapse causes further straining.

Your patient reports pelvic pressure and bulge.
How do you proceed?

Physical examination

Look for perineal ballooning. Physical examination should start with inspection of the external genitalia. This inspection will identify any pelvic organ prolapse at or beyond the introitus. However, a Pouch of Douglas hernia will be missed if the patient is not examined during Valsalva or maximal strain. This maneuver will demonstrate the classic finding of perineal ballooning and is crucial to a final diagnosis of Pouch of Douglas hernia. Normally, the perineum will descend 1 cm to 2 cm during maximal strain; in Pouch of Douglas hernias, the perineum can descend up to 4 cm to 8 cm.⁴

Clinical pearl: It should be noted that, often, patients will not have a great deal of vaginal prolapse accompanying the perineal ballooning. In our opinion, this finding distinguishes Pouch of Douglas hernia from a vaginal vault prolapse caused by an enterocele.

Is rectal prolapse present? Beyond perineal ballooning, the presence of rectal prolapse should be evaluated. A rectocele of some degree is usually present. Asymmetric rectal prolapse affecting the anterior aspect of the rectal wall is consistent with a Pouch of Douglas hernia. This anatomic finding should be distinguished from true circumferential rectal prolapse, which remains in the differential diagnosis.

Basing the diagnosis of Pouch of Douglas hernia on physical examination alone can be difficult. Therefore, imaging studies are essential for accurate diagnosis.

Imaging investigations

Several imaging modalities can be used to diagnose such disorders of the pelvic floor as Pouch of Douglas hernia. These include:

• dynamic colpocystoproctography⁵
• defecography with oral barium⁶
• dynamic pelvic magnetic resonance imaging (MRI).⁷

In our experience, dynamic pelvic MRI has a high accuracy rate for diagnosing Pouch of Douglas hernia. FIGURE 2 illustrates the large Pouch of Douglas hernia filled with loops of small bowel. Perineal descent of the anorectal junction more than 3 cm below the pubococcygeal line during maximal straining is a diagnostic finding on imaging.⁷

FIGURE 2: MRI
Sagittal MRI during maximal Valsalva straining, demonstrating Pouch of Douglas hernia filled with small bowel.

What are your patient’s treatment options?

Reduce straining during bowel movements. The primary goal of treatment for Pouch of Douglas hernia should be relief of bothersome symptoms. Therefore, further damage can be prevented by eliminating straining during defecation. This can be accomplished with a bowel regimen that combines an irritant suppository (glycerin or bisacodyl) with a fiber supplement (the latter to increase bulk of the stool). Oral laxatives have limited use as many patients have lax anal sphincters and liquid stool could cause fecal incontinence.

Pelvic floor strengthening. The importance of pelvic floor physical therapy should be stressed. Patients can benefit from the use of modalities such as biofeedback to learn appropriate pelvic floor muscle relaxation techniques during defecation.⁸ While there is limited published evidence supporting the use of pelvic floor physical therapy, our anecdotal experience suggests that patients can gain considerable benefit with such conservative therapy.

Surgical therapy

Surgical repair of Pouch of Douglas hernia requires obliteration of the deep cul-de-sac (to prevent the small bowel from filling this space) and simultaneous pelvic floor reconstruction of the vaginal apex and any other compartments that are prolapsing (if pelvic organ prolapse is present). In our experience, these patients typically have derived greatest benefit from an abdominal approach. This usually can be accomplished with a sacrocolpopexy (if vaginal vault prolapse exists) with a Moschowitz or Halban procedure,⁹ uterosacral ligament plication, or a modified sacrocolpopexy with mesh augmentation to the sidewalls of the pelvis.¹⁰ There are currently no studies supporting one particular approach over another, but the most important feature of a surgical intervention is obliteration of the cul-de-sac (FIGURES 3, 4, and 5).

FIGURE 3: Open cul-de-sac. Open cul-de-sac after a prior abdominal sacrocolpopexy in a patient with a Pouch of Douglas hernia.

FIGURE 4: Obliterated cul-de-sac. Obliteration of the cul-de-sac with uterosacral ligament plication. Care is taken to prevent obstruction of the rectum at this level.

FIGURE 5: Cul-de-sac obliteration. Schematic diagram of obliteration of the cul-de-sac with uterosacral ligament plication sutures.

Final takeaways

Pouch of Douglas hernia is an important but often unrecognized cause of pelvic pressure and defecatory dysfunction. Perineal ballooning during maximal straining is highly suggestive of the diagnosis, with final diagnosis confirmed with various functional imaging studies of the pelvic floor. Management should include both conservative and surgical interventions to alleviate and prevent recurrence of symptoms.

ACKNOWLEDGMENT. The authors would like to thank Mr. John Hagen, Medical Illustrator, Mayo Clinic, for producing the illustrations in Figures 1 and 5.

We want to hear from you! Tell us what you think.

CASE: Pelvic organ prolapse or Pouch of Douglas hernia?

A 42-year-old G3P2 woman is referred to you by her primary care provider for pelvic organ prolapse. Her medical history reveals that she has been bothered by a sense of pelvic pressure and bulge progressing over several years, and she has noticed that her symptoms are particularly worse during and after bowel movements. She reports some improved bowel evacuation with external splinting of her perineum. Upon closer questioning, the patient reports a history of chronic constipation since childhood associated with straining and a sense of incomplete emptying. She reports spending up to 30 minutes three to four times per day on the commode to completely empty her bowels.

Physical examination reveals an overweight woman with a soft, nontender abdomen remarkable for laparoscopic incision scars from a previous tubal ligation. Inspection of the external genitalia at rest is normal. Cough stress test is negative. At maximum Valsalva, however, there is significant perineal ballooning present.

Speculum examination demonstrates grade 1 uterine prolapse, grade 1 cystocele, and grade 2 rectocele. There is no evidence of pelvic floor tension myalgia. She has weak pelvic muscle strength. Visualization of the anus at maximum Valsalva reveals there is some asymmetric rectal prolapse of the anterior rectal wall. Digital rectal exam is unremarkable.

Are these patient’s symptoms due to pelvic organ prolapse or Pouch of Douglas hernia?

Pelvic organ prolapse: A common problem

Pelvic organ prolapse has an estimated prevalence of 55% in women aged 50 to 59 years.¹ More than 200,000 pelvic organ prolapse surgeries are performed annually in the United States.² Typically, patients report:

• vaginal bulge causing discomfort
• pelvic pressure or heaviness, or
• rubbing of the vaginal bulge on undergarments.

In more advanced pelvic organ prolapse, patients may report voiding dysfunction or stool trapping that requires manual splinting of the prolapse to assist in bladder and bowel evacuation.

Pouch of Douglas hernia: A lesser-known
(recognized) phenomenon

Similar to pelvic organ prolapse, Pouch of Douglas hernia also can present with symptoms of:

• pelvic pressure
• vague perineal aching
• defecatory dysfunction.

The phenomenon has been variably referred to in the literature as enterocele, descending perineum syndrome, peritoneocele, or Pouch of Douglas hernia. The concept was first introduced in 1966³ and describes descent of the entire pelvic floor and small bowel through a hernia in the Pouch of Douglas (FIGURE 1).

FIGURE 1: Pouch of Douglas hernia. The pelvic floor and small bowel descend into the Pouch of Douglas.

How does it occur? The pathophysiology is thought to be related to excessive abdominal straining in individuals with chronic constipation. This results in diminished pelvic floor muscle tone. Eventually, the whole pelvic floor descends, becoming funnel shaped due to stretching of the puborectalis muscle. Thus, stool is expelled by force, mostly through forces on the anterior rectal wall (which tends to prolapse after stool evacuation, with accompanied mucus secretion, soreness, and irritation).

Clinical pearl: Given the rectal wall prolapse that occurs after stool evacuation in Pouch of Douglas hernia, some patients will describe a rectal lump that bleeds after a bowel movement. The sensation of the rectal lump from the anterior rectal wall prolapse causes further straining.

Your patient reports pelvic pressure and bulge.
How do you proceed?

Physical examination

Look for perineal ballooning. Physical examination should start with inspection of the external genitalia. This inspection will identify any pelvic organ prolapse at or beyond the introitus. However, a Pouch of Douglas hernia will be missed if the patient is not examined during Valsalva or maximal strain. This maneuver will demonstrate the classic finding of perineal ballooning and is crucial to a final diagnosis of Pouch of Douglas hernia. Normally, the perineum will descend 1 cm to 2 cm during maximal strain; in Pouch of Douglas hernias, the perineum can descend up to 4 cm to 8 cm.⁴

Clinical pearl: It should be noted that, often, patients will not have a great deal of vaginal prolapse accompanying the perineal ballooning. In our opinion, this finding distinguishes Pouch of Douglas hernia from a vaginal vault prolapse caused by an enterocele.

Is rectal prolapse present? Beyond perineal ballooning, the presence of rectal prolapse should be evaluated. A rectocele of some degree is usually present. Asymmetric rectal prolapse affecting the anterior aspect of the rectal wall is consistent with a Pouch of Douglas hernia. This anatomic finding should be distinguished from true circumferential rectal prolapse, which remains in the differential diagnosis.

Basing the diagnosis of Pouch of Douglas hernia on physical examination alone can be difficult. Therefore, imaging studies are essential for accurate diagnosis.

Imaging investigations

Several imaging modalities can be used to diagnose such disorders of the pelvic floor as Pouch of Douglas hernia. These include:

• dynamic colpocystoproctography⁵
• defecography with oral barium⁶
• dynamic pelvic magnetic resonance imaging (MRI).⁷

In our experience, dynamic pelvic MRI has a high accuracy rate for diagnosing Pouch of Douglas hernia. FIGURE 2 illustrates the large Pouch of Douglas hernia filled with loops of small bowel. Perineal descent of the anorectal junction more than 3 cm below the pubococcygeal line during maximal straining is a diagnostic finding on imaging.⁷

FIGURE 2: MRI
Sagittal MRI during maximal Valsalva straining, demonstrating Pouch of Douglas hernia filled with small bowel.

What are your patient’s treatment options?

Reduce straining during bowel movements. The primary goal of treatment for Pouch of Douglas hernia should be relief of bothersome symptoms. Therefore, further damage can be prevented by eliminating straining during defecation. This can be accomplished with a bowel regimen that combines an irritant suppository (glycerin or bisacodyl) with a fiber supplement (the latter to increase bulk of the stool). Oral laxatives have limited use as many patients have lax anal sphincters and liquid stool could cause fecal incontinence.

Pelvic floor strengthening. The importance of pelvic floor physical therapy should be stressed. Patients can benefit from the use of modalities such as biofeedback to learn appropriate pelvic floor muscle relaxation techniques during defecation.⁸ While there is limited published evidence supporting the use of pelvic floor physical therapy, our anecdotal experience suggests that patients can gain considerable benefit with such conservative therapy.

Surgical therapy

Surgical repair of Pouch of Douglas hernia requires obliteration of the deep cul-de-sac (to prevent the small bowel from filling this space) and simultaneous pelvic floor reconstruction of the vaginal apex and any other compartments that are prolapsing (if pelvic organ prolapse is present). In our experience, these patients typically have derived greatest benefit from an abdominal approach. This usually can be accomplished with a sacrocolpopexy (if vaginal vault prolapse exists) with a Moschowitz or Halban procedure,⁹ uterosacral ligament plication, or a modified sacrocolpopexy with mesh augmentation to the sidewalls of the pelvis.¹⁰ There are currently no studies supporting one particular approach over another, but the most important feature of a surgical intervention is obliteration of the cul-de-sac (FIGURES 3, 4, and 5).

FIGURE 3: Open cul-de-sac. Open cul-de-sac after a prior abdominal sacrocolpopexy in a patient with a Pouch of Douglas hernia.

FIGURE 4: Obliterated cul-de-sac. Obliteration of the cul-de-sac with uterosacral ligament plication. Care is taken to prevent obstruction of the rectum at this level.

FIGURE 5: Cul-de-sac obliteration. Schematic diagram of obliteration of the cul-de-sac with uterosacral ligament plication sutures.

Final takeaways

Pouch of Douglas hernia is an important but often unrecognized cause of pelvic pressure and defecatory dysfunction. Perineal ballooning during maximal straining is highly suggestive of the diagnosis, with final diagnosis confirmed with various functional imaging studies of the pelvic floor. Management should include both conservative and surgical interventions to alleviate and prevent recurrence of symptoms.

ACKNOWLEDGMENT. The authors would like to thank Mr. John Hagen, Medical Illustrator, Mayo Clinic, for producing the illustrations in Figures 1 and 5.

We want to hear from you! Tell us what you think.

Discuss this article at www.facebook.com/CurrentPsychiatry

In addition to increasing patients’ risk for cardiovascular disease, stroke, and cancer, obesity and metabolic disturbance contribute to age-related cognitive decline and dementia. In particular, insulin resistance and hyperinsulinemia promote neurocognitive dysfunction and neurodegenerative changes during the extended, preclinical phase of Alzheimer’s disease (AD). However, with dietary modification it may be possible to resensitize insulin receptors, correct hyperinsulinemia, and improve memory function.

Metabolic disturbance and neurodegeneration

In the United States, 5.4 million people have AD, and there will be an estimated 16 million cases by 2050.¹ Simultaneously we are experiencing an epidemic of metabolic disturbance and obesity. Approximately, 64% of adults in the United States are overweight (body mass index [BMI]: 25.0 to 29.9 kg/m²) and 34% are obese (BMI: ≥30 kg/m²).² By 2030, 86% of adults will be overweight and 51% will be obese.³ This confluence of epidemics is not coincidental but instead reflects the fact that metabolic disturbance is a fundamental factor contributing to cognitive decline and neurodegeneration.⁴

Ninety-six percent of AD cases are classified as late onset, sporadic AD, occurring after age 64.¹ Mild cognitive impairment (MCI) is a clinical construct that entails greater than expected memory impairment for the patient’s age and identifies older adults who are at increased risk for dementia. MCI represents the first clinical manifestation of neurodegeneration for a subset of patients who will progress to AD.^5,6 MCI is distinguished from age-associated memory impairment (AAMI), which originally was conceptualized as normal or benign memory decline with aging.^7,8 Recent data indicate that Alzheimer’s-type neuropathologic changes are the basis for subjective memory complaints and objectively assessed age-related cognitive decline,⁹ and early neurodegeneration is present in many patients with AAMI or MCI.¹⁰ This is consistent with the idea that an extended preclinical phase precedes AD onset. The preclinical phase can persist for a decade or more and precedes MCI and overt functional decline. However, neuropathologic changes accumulate during the preclinical phase of AD¹¹ and during the preclinical phase of type 2 diabetes mellitus (T2DM).

Hyperinsulinemia and dementia

Insulin resistance and hyperinsulinemia occur in >40% of individuals age ≥60 and prevalence increases with age.^4,12 Hyperinsulinemia develops to compensate for insulin resistance to overcome receptor insensitivity and maintain glucose homeostasis. Insulin receptors are densely expressed in brain regions vulnerable to neurodegeneration, including the medial temporal lobe and prefrontal cortex, which mediate long-term memory and working memory. However, insulin must be transported into the CNS from the periphery because little is synthesized in the brain. Paradoxically, peripheral compensatory hyperinsulinemia resulting from insulin resistance is associated with central (brain) hypoinsulinemia because of insensitivity and saturation of the receptor-mediated blood-brain barrier transport mechanism.^13-15

Hyperinsulinemia is the precursor to T2DM. However, hyperinsulinemia is not well recognized in clinical contexts and generally is not a treatment target. Nonetheless, it contributes to several health problems, and insulin resistance in middle age is associated with age-related diseases such as hypertension, coronary artery disease, stroke, and cancer, while insulin sensitivity protects against such disorders.¹⁶

Chronic insulin resistance may contribute more to dementia development than T2DM because of the extended period of hyperinsulinemia that precedes T2DM onset. In population studies,¹⁷ insulin resistance syndrome increases risk for developing AD independent of apolipoprotein E (APOE e4) allele status, and in a longitudinal study,¹⁸ the risk for AD solely attributable to peripheral hyperinsulinemia was up to 39%. Being overweight in midlife increases risk for dementia in late life, and APOE e4 allele status does not contribute additional risk after accounting for BMI.¹⁹ Middle-aged individuals with hyperinsulinemia show memory decline, and obesity in middle age was associated with greater cognitive impairment after 6-year follow-up.²⁰ Even in older adults who seem cognitively unimpaired, BMI and fasting insulin are positively correlated with atrophy in frontal, temporal, and subcortical brain regions, and obesity is an independent risk for atrophy in several brain regions, including the hippocampus.²¹

Compared with healthy older adults, individuals with AD have lower ratios of cerebrospinal fluid to plasma insulin.²² This lower ratio reflects the peripheral-to-central gradient of insulin levels in AD and suggests an etiological role for such metabolic disturbance. Insulin resistance has downstream effects that potentiate neurodegenerative factors, and central hypoinsulinemia can accelerate neurodegenerative processes and cognitive decline.^4,23 Brain insulin plays a direct role in regulating proinflammatory cytokines and neurotrophic and neuroplastic factors essential for memory function. Insulin degrading enzyme, which varies with insulin levels,²⁴ regulates the generation and clearance of amyloid β (Aβ) from the brain.²⁵

Hyperinsulinemia typically is evident in increasing waist circumference and body weight.²⁶ Waist circumference of ≥100 cm (39 inches) is a sensitive, specific, and independent predictor of hyperinsulinemia for men and women and a stronger predictor than BMI, waist-to-hip ratio, and other measures of body fat.²⁷ Unpublished data derived from our clinical research with MCI subjects supports the association of metabolic disturbance with age-related cognitive decline. Our subjects are recruited from the community on the basis of mild memory decline and—other than excluding those with diabetes—weight and metabolic status are not considered in evaluating individuals for enrollment. The Table contains data on waist circumference and metabolic function in 122 older adults (age ≥68) with MCI. On average, these individuals exhibited fasting insulin values in the hyperinsulinemia range and elevated fasting glucose levels that indicated borderline diabetes. Waist circumference also was high, indicating excessive visceral fat deposition. We also observed a relationship between waist circumference and insulin, a consistent observation in older adults with memory decline. These data would not be surprising in any sample of older adults because of the population base rates for these conditions. However, we also found that waist circumference was a significant predictor of memory performance in patients with MCI. Abdominal adiposity is highly correlated with intrahepatic fat.²⁸ Given this and recent indications that Alzheimer’s-type neuropathologic factors are generated in the liver,^29,30 the predictive value of waist circumference to memory performance may reflect the fact that it is a proxy for downstream actions of liver fat.

Table

Waist circumference and metabolic factors in 122 older adults with MCI^a

Dietary interventions

There is no cure for dementia, and it is not clear when effective therapy might be developed. Prevention and risk mitigation represent the best means of reducing the impact of this public health problem. Researchers have proposed that interventions initiated when individuals have predementia conditions such as AAMI and MCI might stall progression of cognitive decline, and MCI may be the last point when interventions might be effective because of the self-reinforcing neuropathologic cascades of AD.³¹ Because central hypoinsulinemia may promote central inflammation, Aβ generation, and reduced neuroplasticity, approaches aimed at improving metabolic function (and in particular correcting hyperinsulinemia) could influence fundamental neurodegenerative processes. Dietary approaches to preventing dementia are effective, low-risk, yet underutilized interventions. Reducing insulin by restricting calories³² or maintaining a ketogenic diet³³ has been associated with improved memory function in middle-aged and older adults.

Carbohydrate consumption is the principal determinant of insulin secretion. Eliminating high-glycemic foods, including processed carbohydrates and sweets, would sensitize insulin receptors and correct hyperinsulinemia. In addition, replacing high glycemic foods with fruits and vegetables would increase polyphenol intake. Epidemiologic evidence supports the idea that greater consumption of polyphenol-containing vegetables and fruits mitigates risk for neurocognitive decline and dementia.^34,35 Preclinical evidence suggests that such protection may be related to neuronal signaling effects and anti- inflammatory and antioxidant actions.³⁶ In addition, certain polyphenol compounds, such as those found in berries, enhance metabolic function.^37,38 In a 12-week pilot trial, older adults with early memory changes (N=9, mean age 76) who drank supplemental blueberry juice showed enhanced memory and improved metabolic parameters.³⁹

Dietary changes that preserve insulin receptor sensitivity can help ensure general health with aging and substantially mitigate risk for neurodegeneration. The Western diet is particularly insulinogenic and dietary habits are difficult to change. However, the substantial benefits, absence of adverse effects, and low cost make dietary intervention the optimal means of protecting against neurodegeneration and other age-related diseases. Embarking on such a program early in life would be best, although late-life intervention can be effective.

Related Resources

• Craft S, Watson GS. Insulin and neurodegenerative disease: shared and specific mechanisms. Lancet Neurol. 2004;3(3):169-178.
• Luchsinger JA, Tang MX, Shea S, et al. Hyperinsulinemia and risk of Alzheimer’s disease. Neurology. 2004; 63(7):1187-1192.
• Krikorian R, Shidler MD, Dangelo K, et al. Dietary ketosis enhances memory in mild cognitive impairment. Neurbiol Aging. 2012;33(2):425.e19-e27.

Disclosure

Dr. Krikorian receives grant support from the National Institutes of Health, 1R01AG034617-01.

Discuss this article at www.facebook.com/CurrentPsychiatry

In addition to increasing patients’ risk for cardiovascular disease, stroke, and cancer, obesity and metabolic disturbance contribute to age-related cognitive decline and dementia. In particular, insulin resistance and hyperinsulinemia promote neurocognitive dysfunction and neurodegenerative changes during the extended, preclinical phase of Alzheimer’s disease (AD). However, with dietary modification it may be possible to resensitize insulin receptors, correct hyperinsulinemia, and improve memory function.

Metabolic disturbance and neurodegeneration

In the United States, 5.4 million people have AD, and there will be an estimated 16 million cases by 2050.¹ Simultaneously we are experiencing an epidemic of metabolic disturbance and obesity. Approximately, 64% of adults in the United States are overweight (body mass index [BMI]: 25.0 to 29.9 kg/m²) and 34% are obese (BMI: ≥30 kg/m²).² By 2030, 86% of adults will be overweight and 51% will be obese.³ This confluence of epidemics is not coincidental but instead reflects the fact that metabolic disturbance is a fundamental factor contributing to cognitive decline and neurodegeneration.⁴

Ninety-six percent of AD cases are classified as late onset, sporadic AD, occurring after age 64.¹ Mild cognitive impairment (MCI) is a clinical construct that entails greater than expected memory impairment for the patient’s age and identifies older adults who are at increased risk for dementia. MCI represents the first clinical manifestation of neurodegeneration for a subset of patients who will progress to AD.^5,6 MCI is distinguished from age-associated memory impairment (AAMI), which originally was conceptualized as normal or benign memory decline with aging.^7,8 Recent data indicate that Alzheimer’s-type neuropathologic changes are the basis for subjective memory complaints and objectively assessed age-related cognitive decline,⁹ and early neurodegeneration is present in many patients with AAMI or MCI.¹⁰ This is consistent with the idea that an extended preclinical phase precedes AD onset. The preclinical phase can persist for a decade or more and precedes MCI and overt functional decline. However, neuropathologic changes accumulate during the preclinical phase of AD¹¹ and during the preclinical phase of type 2 diabetes mellitus (T2DM).

Hyperinsulinemia and dementia

Insulin resistance and hyperinsulinemia occur in >40% of individuals age ≥60 and prevalence increases with age.^4,12 Hyperinsulinemia develops to compensate for insulin resistance to overcome receptor insensitivity and maintain glucose homeostasis. Insulin receptors are densely expressed in brain regions vulnerable to neurodegeneration, including the medial temporal lobe and prefrontal cortex, which mediate long-term memory and working memory. However, insulin must be transported into the CNS from the periphery because little is synthesized in the brain. Paradoxically, peripheral compensatory hyperinsulinemia resulting from insulin resistance is associated with central (brain) hypoinsulinemia because of insensitivity and saturation of the receptor-mediated blood-brain barrier transport mechanism.^13-15

Hyperinsulinemia is the precursor to T2DM. However, hyperinsulinemia is not well recognized in clinical contexts and generally is not a treatment target. Nonetheless, it contributes to several health problems, and insulin resistance in middle age is associated with age-related diseases such as hypertension, coronary artery disease, stroke, and cancer, while insulin sensitivity protects against such disorders.¹⁶

Chronic insulin resistance may contribute more to dementia development than T2DM because of the extended period of hyperinsulinemia that precedes T2DM onset. In population studies,¹⁷ insulin resistance syndrome increases risk for developing AD independent of apolipoprotein E (APOE e4) allele status, and in a longitudinal study,¹⁸ the risk for AD solely attributable to peripheral hyperinsulinemia was up to 39%. Being overweight in midlife increases risk for dementia in late life, and APOE e4 allele status does not contribute additional risk after accounting for BMI.¹⁹ Middle-aged individuals with hyperinsulinemia show memory decline, and obesity in middle age was associated with greater cognitive impairment after 6-year follow-up.²⁰ Even in older adults who seem cognitively unimpaired, BMI and fasting insulin are positively correlated with atrophy in frontal, temporal, and subcortical brain regions, and obesity is an independent risk for atrophy in several brain regions, including the hippocampus.²¹

Compared with healthy older adults, individuals with AD have lower ratios of cerebrospinal fluid to plasma insulin.²² This lower ratio reflects the peripheral-to-central gradient of insulin levels in AD and suggests an etiological role for such metabolic disturbance. Insulin resistance has downstream effects that potentiate neurodegenerative factors, and central hypoinsulinemia can accelerate neurodegenerative processes and cognitive decline.^4,23 Brain insulin plays a direct role in regulating proinflammatory cytokines and neurotrophic and neuroplastic factors essential for memory function. Insulin degrading enzyme, which varies with insulin levels,²⁴ regulates the generation and clearance of amyloid β (Aβ) from the brain.²⁵

Hyperinsulinemia typically is evident in increasing waist circumference and body weight.²⁶ Waist circumference of ≥100 cm (39 inches) is a sensitive, specific, and independent predictor of hyperinsulinemia for men and women and a stronger predictor than BMI, waist-to-hip ratio, and other measures of body fat.²⁷ Unpublished data derived from our clinical research with MCI subjects supports the association of metabolic disturbance with age-related cognitive decline. Our subjects are recruited from the community on the basis of mild memory decline and—other than excluding those with diabetes—weight and metabolic status are not considered in evaluating individuals for enrollment. The Table contains data on waist circumference and metabolic function in 122 older adults (age ≥68) with MCI. On average, these individuals exhibited fasting insulin values in the hyperinsulinemia range and elevated fasting glucose levels that indicated borderline diabetes. Waist circumference also was high, indicating excessive visceral fat deposition. We also observed a relationship between waist circumference and insulin, a consistent observation in older adults with memory decline. These data would not be surprising in any sample of older adults because of the population base rates for these conditions. However, we also found that waist circumference was a significant predictor of memory performance in patients with MCI. Abdominal adiposity is highly correlated with intrahepatic fat.²⁸ Given this and recent indications that Alzheimer’s-type neuropathologic factors are generated in the liver,^29,30 the predictive value of waist circumference to memory performance may reflect the fact that it is a proxy for downstream actions of liver fat.

Table

Waist circumference and metabolic factors in 122 older adults with MCI^a

Dietary interventions

There is no cure for dementia, and it is not clear when effective therapy might be developed. Prevention and risk mitigation represent the best means of reducing the impact of this public health problem. Researchers have proposed that interventions initiated when individuals have predementia conditions such as AAMI and MCI might stall progression of cognitive decline, and MCI may be the last point when interventions might be effective because of the self-reinforcing neuropathologic cascades of AD.³¹ Because central hypoinsulinemia may promote central inflammation, Aβ generation, and reduced neuroplasticity, approaches aimed at improving metabolic function (and in particular correcting hyperinsulinemia) could influence fundamental neurodegenerative processes. Dietary approaches to preventing dementia are effective, low-risk, yet underutilized interventions. Reducing insulin by restricting calories³² or maintaining a ketogenic diet³³ has been associated with improved memory function in middle-aged and older adults.

Carbohydrate consumption is the principal determinant of insulin secretion. Eliminating high-glycemic foods, including processed carbohydrates and sweets, would sensitize insulin receptors and correct hyperinsulinemia. In addition, replacing high glycemic foods with fruits and vegetables would increase polyphenol intake. Epidemiologic evidence supports the idea that greater consumption of polyphenol-containing vegetables and fruits mitigates risk for neurocognitive decline and dementia.^34,35 Preclinical evidence suggests that such protection may be related to neuronal signaling effects and anti- inflammatory and antioxidant actions.³⁶ In addition, certain polyphenol compounds, such as those found in berries, enhance metabolic function.^37,38 In a 12-week pilot trial, older adults with early memory changes (N=9, mean age 76) who drank supplemental blueberry juice showed enhanced memory and improved metabolic parameters.³⁹

Dietary changes that preserve insulin receptor sensitivity can help ensure general health with aging and substantially mitigate risk for neurodegeneration. The Western diet is particularly insulinogenic and dietary habits are difficult to change. However, the substantial benefits, absence of adverse effects, and low cost make dietary intervention the optimal means of protecting against neurodegeneration and other age-related diseases. Embarking on such a program early in life would be best, although late-life intervention can be effective.

Related Resources

• Craft S, Watson GS. Insulin and neurodegenerative disease: shared and specific mechanisms. Lancet Neurol. 2004;3(3):169-178.
• Luchsinger JA, Tang MX, Shea S, et al. Hyperinsulinemia and risk of Alzheimer’s disease. Neurology. 2004; 63(7):1187-1192.
• Krikorian R, Shidler MD, Dangelo K, et al. Dietary ketosis enhances memory in mild cognitive impairment. Neurbiol Aging. 2012;33(2):425.e19-e27.

Disclosure

Dr. Krikorian receives grant support from the National Institutes of Health, 1R01AG034617-01.

Discuss this article at www.facebook.com/CurrentPsychiatry

In addition to increasing patients’ risk for cardiovascular disease, stroke, and cancer, obesity and metabolic disturbance contribute to age-related cognitive decline and dementia. In particular, insulin resistance and hyperinsulinemia promote neurocognitive dysfunction and neurodegenerative changes during the extended, preclinical phase of Alzheimer’s disease (AD). However, with dietary modification it may be possible to resensitize insulin receptors, correct hyperinsulinemia, and improve memory function.

Metabolic disturbance and neurodegeneration

In the United States, 5.4 million people have AD, and there will be an estimated 16 million cases by 2050.¹ Simultaneously we are experiencing an epidemic of metabolic disturbance and obesity. Approximately, 64% of adults in the United States are overweight (body mass index [BMI]: 25.0 to 29.9 kg/m²) and 34% are obese (BMI: ≥30 kg/m²).² By 2030, 86% of adults will be overweight and 51% will be obese.³ This confluence of epidemics is not coincidental but instead reflects the fact that metabolic disturbance is a fundamental factor contributing to cognitive decline and neurodegeneration.⁴

Ninety-six percent of AD cases are classified as late onset, sporadic AD, occurring after age 64.¹ Mild cognitive impairment (MCI) is a clinical construct that entails greater than expected memory impairment for the patient’s age and identifies older adults who are at increased risk for dementia. MCI represents the first clinical manifestation of neurodegeneration for a subset of patients who will progress to AD.^5,6 MCI is distinguished from age-associated memory impairment (AAMI), which originally was conceptualized as normal or benign memory decline with aging.^7,8 Recent data indicate that Alzheimer’s-type neuropathologic changes are the basis for subjective memory complaints and objectively assessed age-related cognitive decline,⁹ and early neurodegeneration is present in many patients with AAMI or MCI.¹⁰ This is consistent with the idea that an extended preclinical phase precedes AD onset. The preclinical phase can persist for a decade or more and precedes MCI and overt functional decline. However, neuropathologic changes accumulate during the preclinical phase of AD¹¹ and during the preclinical phase of type 2 diabetes mellitus (T2DM).

Hyperinsulinemia and dementia

Insulin resistance and hyperinsulinemia occur in >40% of individuals age ≥60 and prevalence increases with age.^4,12 Hyperinsulinemia develops to compensate for insulin resistance to overcome receptor insensitivity and maintain glucose homeostasis. Insulin receptors are densely expressed in brain regions vulnerable to neurodegeneration, including the medial temporal lobe and prefrontal cortex, which mediate long-term memory and working memory. However, insulin must be transported into the CNS from the periphery because little is synthesized in the brain. Paradoxically, peripheral compensatory hyperinsulinemia resulting from insulin resistance is associated with central (brain) hypoinsulinemia because of insensitivity and saturation of the receptor-mediated blood-brain barrier transport mechanism.^13-15

Hyperinsulinemia is the precursor to T2DM. However, hyperinsulinemia is not well recognized in clinical contexts and generally is not a treatment target. Nonetheless, it contributes to several health problems, and insulin resistance in middle age is associated with age-related diseases such as hypertension, coronary artery disease, stroke, and cancer, while insulin sensitivity protects against such disorders.¹⁶

Chronic insulin resistance may contribute more to dementia development than T2DM because of the extended period of hyperinsulinemia that precedes T2DM onset. In population studies,¹⁷ insulin resistance syndrome increases risk for developing AD independent of apolipoprotein E (APOE e4) allele status, and in a longitudinal study,¹⁸ the risk for AD solely attributable to peripheral hyperinsulinemia was up to 39%. Being overweight in midlife increases risk for dementia in late life, and APOE e4 allele status does not contribute additional risk after accounting for BMI.¹⁹ Middle-aged individuals with hyperinsulinemia show memory decline, and obesity in middle age was associated with greater cognitive impairment after 6-year follow-up.²⁰ Even in older adults who seem cognitively unimpaired, BMI and fasting insulin are positively correlated with atrophy in frontal, temporal, and subcortical brain regions, and obesity is an independent risk for atrophy in several brain regions, including the hippocampus.²¹

Compared with healthy older adults, individuals with AD have lower ratios of cerebrospinal fluid to plasma insulin.²² This lower ratio reflects the peripheral-to-central gradient of insulin levels in AD and suggests an etiological role for such metabolic disturbance. Insulin resistance has downstream effects that potentiate neurodegenerative factors, and central hypoinsulinemia can accelerate neurodegenerative processes and cognitive decline.^4,23 Brain insulin plays a direct role in regulating proinflammatory cytokines and neurotrophic and neuroplastic factors essential for memory function. Insulin degrading enzyme, which varies with insulin levels,²⁴ regulates the generation and clearance of amyloid β (Aβ) from the brain.²⁵

Hyperinsulinemia typically is evident in increasing waist circumference and body weight.²⁶ Waist circumference of ≥100 cm (39 inches) is a sensitive, specific, and independent predictor of hyperinsulinemia for men and women and a stronger predictor than BMI, waist-to-hip ratio, and other measures of body fat.²⁷ Unpublished data derived from our clinical research with MCI subjects supports the association of metabolic disturbance with age-related cognitive decline. Our subjects are recruited from the community on the basis of mild memory decline and—other than excluding those with diabetes—weight and metabolic status are not considered in evaluating individuals for enrollment. The Table contains data on waist circumference and metabolic function in 122 older adults (age ≥68) with MCI. On average, these individuals exhibited fasting insulin values in the hyperinsulinemia range and elevated fasting glucose levels that indicated borderline diabetes. Waist circumference also was high, indicating excessive visceral fat deposition. We also observed a relationship between waist circumference and insulin, a consistent observation in older adults with memory decline. These data would not be surprising in any sample of older adults because of the population base rates for these conditions. However, we also found that waist circumference was a significant predictor of memory performance in patients with MCI. Abdominal adiposity is highly correlated with intrahepatic fat.²⁸ Given this and recent indications that Alzheimer’s-type neuropathologic factors are generated in the liver,^29,30 the predictive value of waist circumference to memory performance may reflect the fact that it is a proxy for downstream actions of liver fat.

Table

Waist circumference and metabolic factors in 122 older adults with MCI^a

Dietary interventions

There is no cure for dementia, and it is not clear when effective therapy might be developed. Prevention and risk mitigation represent the best means of reducing the impact of this public health problem. Researchers have proposed that interventions initiated when individuals have predementia conditions such as AAMI and MCI might stall progression of cognitive decline, and MCI may be the last point when interventions might be effective because of the self-reinforcing neuropathologic cascades of AD.³¹ Because central hypoinsulinemia may promote central inflammation, Aβ generation, and reduced neuroplasticity, approaches aimed at improving metabolic function (and in particular correcting hyperinsulinemia) could influence fundamental neurodegenerative processes. Dietary approaches to preventing dementia are effective, low-risk, yet underutilized interventions. Reducing insulin by restricting calories³² or maintaining a ketogenic diet³³ has been associated with improved memory function in middle-aged and older adults.

Carbohydrate consumption is the principal determinant of insulin secretion. Eliminating high-glycemic foods, including processed carbohydrates and sweets, would sensitize insulin receptors and correct hyperinsulinemia. In addition, replacing high glycemic foods with fruits and vegetables would increase polyphenol intake. Epidemiologic evidence supports the idea that greater consumption of polyphenol-containing vegetables and fruits mitigates risk for neurocognitive decline and dementia.^34,35 Preclinical evidence suggests that such protection may be related to neuronal signaling effects and anti- inflammatory and antioxidant actions.³⁶ In addition, certain polyphenol compounds, such as those found in berries, enhance metabolic function.^37,38 In a 12-week pilot trial, older adults with early memory changes (N=9, mean age 76) who drank supplemental blueberry juice showed enhanced memory and improved metabolic parameters.³⁹

Dietary changes that preserve insulin receptor sensitivity can help ensure general health with aging and substantially mitigate risk for neurodegeneration. The Western diet is particularly insulinogenic and dietary habits are difficult to change. However, the substantial benefits, absence of adverse effects, and low cost make dietary intervention the optimal means of protecting against neurodegeneration and other age-related diseases. Embarking on such a program early in life would be best, although late-life intervention can be effective.

Related Resources

• Craft S, Watson GS. Insulin and neurodegenerative disease: shared and specific mechanisms. Lancet Neurol. 2004;3(3):169-178.
• Luchsinger JA, Tang MX, Shea S, et al. Hyperinsulinemia and risk of Alzheimer’s disease. Neurology. 2004; 63(7):1187-1192.
• Krikorian R, Shidler MD, Dangelo K, et al. Dietary ketosis enhances memory in mild cognitive impairment. Neurbiol Aging. 2012;33(2):425.e19-e27.

Disclosure

Dr. Krikorian receives grant support from the National Institutes of Health, 1R01AG034617-01.

Re-experiencing a previous life-threatening stress through nightmares or recurrent memories is a hallmark of posttraumatic stress disorder (PTSD). In the United States, the lifetime risk of PTSD is 10.1% and the 12-month prevalence is 3.7%.¹ The selective serotonin reuptake inhibitors (SSRIs) sertraline and paroxetine are FDA-approved for treating PTSD; clinicians commonly use any SSRI for this disorder. Although SSRIs can alleviate many PTSD symptoms, at times patients experience only a partial response, which necessitates other interventions.

Rationale for using topiramate

The anticonvulsant topiramate blocks voltage-sensitive sodium channels, augments γ-aminobutyric acid type A, antagonizes the glutamate receptor, and inhibits carbonic anhydrase. Researchers have hypothesized that limbic nuclei become sensitized and “kindled” after exposure to a traumatic event. Anticonvulsants such as topiramate may help mitigate stress-activated kindling in PTSD.^2,3

What does the evidence say?

Although less compelling than double-blind, placebo-controlled trials, small open-label studies and some case reports indicate a potential role for topiramate in PTSD for specific populations.^4,5 In an 8-week open- label study, Alderman et al⁶ found adjunctive topiramate led to a statistically significant reduction in Clinician-Administered PTSD Scale (CAPS) scores and nightmares in 43 male veterans with combat-related PTSD. There was a nonsignificant decrease in high-risk alcohol use.

In a 2002 retrospective case series, Berlant et al⁷ found topiramate as monotherapy or adjunctive therapy reduced nightmares in 35 patients with chronic, non-combat PTSD. Nightmares decreased in 79% of patients and flashbacks decreased in 86%, with symptom improvement in a median of 4 days. Limitations of this study included lack of placebo control, a low number of participants, and a high dropout rate (9/35).

Two years later, Berlant⁸ used the PTSD Checklist-Civilian version (PCL-C) to assess response to topiramate in an open-label study of 33 patients with chronic, non-hallucinatory PTSD. Twenty-eight patients used topiramate as add-on therapy. PCL-C scores decreased by ≥30% in 77% of patients in 4 weeks, with a median dose of 50 mg/d and a median response time of 9 days.

In a double-blind, placebo-controlled trial, Tucker et al⁹ assessed 38 civilian patients who took topiramate monotherapy for PTSD. Using the CAPS, researchers concluded that topiramate reduced re-experiencing symptoms, but the effect was not statistically significant.⁹

Lindley et al¹⁰ conducted a randomized, double-blind, placebo-controlled trial to study the effect of add-on topiramate in 40 patients with chronic, combat-related PTSD. Because many patients in this study had a history of depression and substance use disorders, topiramate was added to antidepressants; no anticonvulsants, antipsychotics, or benzodiazepines were used. Similar to previous studies, researchers found no statistically significant effect on PTSD symptom severity or global symptom improvement. However, the small number of participants and a high dropout rate limited this study.¹⁰

In a 12-week, double-blind, placebo-controlled study of 35 men and women age 18 to 62 with PTSD, Yeh et al¹¹ found that topiramate (mean dose: 102.94 mg/d) lead to a statistically significant overall CAPS score reduction, with significant improvements in re-experiencing symptoms, such as nightmares.

Our opinion

FDA-approved treatments such as SSRIs should be the first pharmacologic intervention for PTSD. If a patient’s response is partial or inadequate, consider additional treatment options. For patients with persistent re-experiencing symptoms, evidence and experience with prazosin and trazodone are more robust than that for topiramate.¹²

Using topiramate to reduce re-experiencing symptoms such as nightmares in PTSD is not supported by statistically significant evidence from double-blind, placebo- controlled trials. However, numerous open-label studies and case reports suggest that there may be a role for topiramate in PTSD patients who do not respond to other treatments. Data indicate that topiramate may be helpful for PTSD patients who have high-risk alcohol use⁶ or migraine headaches.¹³ Because some patients who take topiramate lose weight, the medication may be useful for PTSD patients who are overweight.¹³

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Related Resource

• U.S. Department of Veterans Affairs. Nightmares and PTSD. www.ptsd.va.gov/public/pages/nightmares.asp.

Drug Brand Names

• Paroxetine • Paxil
• Sertraline • Zoloft
• Prazosin • Minipress
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro

Re-experiencing a previous life-threatening stress through nightmares or recurrent memories is a hallmark of posttraumatic stress disorder (PTSD). In the United States, the lifetime risk of PTSD is 10.1% and the 12-month prevalence is 3.7%.¹ The selective serotonin reuptake inhibitors (SSRIs) sertraline and paroxetine are FDA-approved for treating PTSD; clinicians commonly use any SSRI for this disorder. Although SSRIs can alleviate many PTSD symptoms, at times patients experience only a partial response, which necessitates other interventions.

Rationale for using topiramate

The anticonvulsant topiramate blocks voltage-sensitive sodium channels, augments γ-aminobutyric acid type A, antagonizes the glutamate receptor, and inhibits carbonic anhydrase. Researchers have hypothesized that limbic nuclei become sensitized and “kindled” after exposure to a traumatic event. Anticonvulsants such as topiramate may help mitigate stress-activated kindling in PTSD.^2,3

What does the evidence say?

Although less compelling than double-blind, placebo-controlled trials, small open-label studies and some case reports indicate a potential role for topiramate in PTSD for specific populations.^4,5 In an 8-week open- label study, Alderman et al⁶ found adjunctive topiramate led to a statistically significant reduction in Clinician-Administered PTSD Scale (CAPS) scores and nightmares in 43 male veterans with combat-related PTSD. There was a nonsignificant decrease in high-risk alcohol use.

In a 2002 retrospective case series, Berlant et al⁷ found topiramate as monotherapy or adjunctive therapy reduced nightmares in 35 patients with chronic, non-combat PTSD. Nightmares decreased in 79% of patients and flashbacks decreased in 86%, with symptom improvement in a median of 4 days. Limitations of this study included lack of placebo control, a low number of participants, and a high dropout rate (9/35).

Two years later, Berlant⁸ used the PTSD Checklist-Civilian version (PCL-C) to assess response to topiramate in an open-label study of 33 patients with chronic, non-hallucinatory PTSD. Twenty-eight patients used topiramate as add-on therapy. PCL-C scores decreased by ≥30% in 77% of patients in 4 weeks, with a median dose of 50 mg/d and a median response time of 9 days.

In a double-blind, placebo-controlled trial, Tucker et al⁹ assessed 38 civilian patients who took topiramate monotherapy for PTSD. Using the CAPS, researchers concluded that topiramate reduced re-experiencing symptoms, but the effect was not statistically significant.⁹

Lindley et al¹⁰ conducted a randomized, double-blind, placebo-controlled trial to study the effect of add-on topiramate in 40 patients with chronic, combat-related PTSD. Because many patients in this study had a history of depression and substance use disorders, topiramate was added to antidepressants; no anticonvulsants, antipsychotics, or benzodiazepines were used. Similar to previous studies, researchers found no statistically significant effect on PTSD symptom severity or global symptom improvement. However, the small number of participants and a high dropout rate limited this study.¹⁰

In a 12-week, double-blind, placebo-controlled study of 35 men and women age 18 to 62 with PTSD, Yeh et al¹¹ found that topiramate (mean dose: 102.94 mg/d) lead to a statistically significant overall CAPS score reduction, with significant improvements in re-experiencing symptoms, such as nightmares.

Our opinion

FDA-approved treatments such as SSRIs should be the first pharmacologic intervention for PTSD. If a patient’s response is partial or inadequate, consider additional treatment options. For patients with persistent re-experiencing symptoms, evidence and experience with prazosin and trazodone are more robust than that for topiramate.¹²

Using topiramate to reduce re-experiencing symptoms such as nightmares in PTSD is not supported by statistically significant evidence from double-blind, placebo- controlled trials. However, numerous open-label studies and case reports suggest that there may be a role for topiramate in PTSD patients who do not respond to other treatments. Data indicate that topiramate may be helpful for PTSD patients who have high-risk alcohol use⁶ or migraine headaches.¹³ Because some patients who take topiramate lose weight, the medication may be useful for PTSD patients who are overweight.¹³

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Related Resource

• U.S. Department of Veterans Affairs. Nightmares and PTSD. www.ptsd.va.gov/public/pages/nightmares.asp.

Drug Brand Names

• Paroxetine • Paxil
• Sertraline • Zoloft
• Prazosin • Minipress
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro

Re-experiencing a previous life-threatening stress through nightmares or recurrent memories is a hallmark of posttraumatic stress disorder (PTSD). In the United States, the lifetime risk of PTSD is 10.1% and the 12-month prevalence is 3.7%.¹ The selective serotonin reuptake inhibitors (SSRIs) sertraline and paroxetine are FDA-approved for treating PTSD; clinicians commonly use any SSRI for this disorder. Although SSRIs can alleviate many PTSD symptoms, at times patients experience only a partial response, which necessitates other interventions.

Rationale for using topiramate

The anticonvulsant topiramate blocks voltage-sensitive sodium channels, augments γ-aminobutyric acid type A, antagonizes the glutamate receptor, and inhibits carbonic anhydrase. Researchers have hypothesized that limbic nuclei become sensitized and “kindled” after exposure to a traumatic event. Anticonvulsants such as topiramate may help mitigate stress-activated kindling in PTSD.^2,3

What does the evidence say?

Although less compelling than double-blind, placebo-controlled trials, small open-label studies and some case reports indicate a potential role for topiramate in PTSD for specific populations.^4,5 In an 8-week open- label study, Alderman et al⁶ found adjunctive topiramate led to a statistically significant reduction in Clinician-Administered PTSD Scale (CAPS) scores and nightmares in 43 male veterans with combat-related PTSD. There was a nonsignificant decrease in high-risk alcohol use.

In a 2002 retrospective case series, Berlant et al⁷ found topiramate as monotherapy or adjunctive therapy reduced nightmares in 35 patients with chronic, non-combat PTSD. Nightmares decreased in 79% of patients and flashbacks decreased in 86%, with symptom improvement in a median of 4 days. Limitations of this study included lack of placebo control, a low number of participants, and a high dropout rate (9/35).

Two years later, Berlant⁸ used the PTSD Checklist-Civilian version (PCL-C) to assess response to topiramate in an open-label study of 33 patients with chronic, non-hallucinatory PTSD. Twenty-eight patients used topiramate as add-on therapy. PCL-C scores decreased by ≥30% in 77% of patients in 4 weeks, with a median dose of 50 mg/d and a median response time of 9 days.

In a double-blind, placebo-controlled trial, Tucker et al⁹ assessed 38 civilian patients who took topiramate monotherapy for PTSD. Using the CAPS, researchers concluded that topiramate reduced re-experiencing symptoms, but the effect was not statistically significant.⁹

Lindley et al¹⁰ conducted a randomized, double-blind, placebo-controlled trial to study the effect of add-on topiramate in 40 patients with chronic, combat-related PTSD. Because many patients in this study had a history of depression and substance use disorders, topiramate was added to antidepressants; no anticonvulsants, antipsychotics, or benzodiazepines were used. Similar to previous studies, researchers found no statistically significant effect on PTSD symptom severity or global symptom improvement. However, the small number of participants and a high dropout rate limited this study.¹⁰

In a 12-week, double-blind, placebo-controlled study of 35 men and women age 18 to 62 with PTSD, Yeh et al¹¹ found that topiramate (mean dose: 102.94 mg/d) lead to a statistically significant overall CAPS score reduction, with significant improvements in re-experiencing symptoms, such as nightmares.

Our opinion

FDA-approved treatments such as SSRIs should be the first pharmacologic intervention for PTSD. If a patient’s response is partial or inadequate, consider additional treatment options. For patients with persistent re-experiencing symptoms, evidence and experience with prazosin and trazodone are more robust than that for topiramate.¹²

Using topiramate to reduce re-experiencing symptoms such as nightmares in PTSD is not supported by statistically significant evidence from double-blind, placebo- controlled trials. However, numerous open-label studies and case reports suggest that there may be a role for topiramate in PTSD patients who do not respond to other treatments. Data indicate that topiramate may be helpful for PTSD patients who have high-risk alcohol use⁶ or migraine headaches.¹³ Because some patients who take topiramate lose weight, the medication may be useful for PTSD patients who are overweight.¹³

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Related Resource

• U.S. Department of Veterans Affairs. Nightmares and PTSD. www.ptsd.va.gov/public/pages/nightmares.asp.

Drug Brand Names

• Paroxetine • Paxil
• Sertraline • Zoloft
• Prazosin • Minipress
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro