DDSEP® 8 Quick Quiz

Q2: Answer: D

The history of weight loss, intermittent diarrhea, and bloating are suspicious for celiac disease. While lactose intolerance can explain the pain, diarrhea, and bloating, there does not appear to be any correlation with the ingestion of particular foods, nor should there be any weight loss. While inflammatory bowel disease is certainly a possible explanation for his symptoms, it would be premature to jump to upper and lower endoscopy as initial evaluations.

Tissue transglutaminase antibodies are a sensitive and specific screening test for celiac disease, with published sensitivities and specificities greater than 95%. Obtaining a total serum IgA level at the time of screening is recommended to exclude IgA deficiency, which may result in a false-negative test.  

Reference

1. Husby S., Koletzko S., Korponay-Szabo I.R., et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease. J Pediatr Gastroenterol Nutr. 2012;54:136-60.

2. Olen O., Gudjonsdottir A., Browaldh L., et al. Antibodies against deamindated gliadin peptides and tissue transglutaminase for diagnosis of pediatric celiac disease. J Pediatr Gastroenterol Nutr. 2012;55:695-700.

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Q2: Answer: D

The history of weight loss, intermittent diarrhea, and bloating are suspicious for celiac disease. While lactose intolerance can explain the pain, diarrhea, and bloating, there does not appear to be any correlation with the ingestion of particular foods, nor should there be any weight loss. While inflammatory bowel disease is certainly a possible explanation for his symptoms, it would be premature to jump to upper and lower endoscopy as initial evaluations.

Tissue transglutaminase antibodies are a sensitive and specific screening test for celiac disease, with published sensitivities and specificities greater than 95%. Obtaining a total serum IgA level at the time of screening is recommended to exclude IgA deficiency, which may result in a false-negative test.  

Reference

1. Husby S., Koletzko S., Korponay-Szabo I.R., et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease. J Pediatr Gastroenterol Nutr. 2012;54:136-60.

2. Olen O., Gudjonsdottir A., Browaldh L., et al. Antibodies against deamindated gliadin peptides and tissue transglutaminase for diagnosis of pediatric celiac disease. J Pediatr Gastroenterol Nutr. 2012;55:695-700.

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Q2: Answer: D

The history of weight loss, intermittent diarrhea, and bloating are suspicious for celiac disease. While lactose intolerance can explain the pain, diarrhea, and bloating, there does not appear to be any correlation with the ingestion of particular foods, nor should there be any weight loss. While inflammatory bowel disease is certainly a possible explanation for his symptoms, it would be premature to jump to upper and lower endoscopy as initial evaluations.

Tissue transglutaminase antibodies are a sensitive and specific screening test for celiac disease, with published sensitivities and specificities greater than 95%. Obtaining a total serum IgA level at the time of screening is recommended to exclude IgA deficiency, which may result in a false-negative test.  

Reference

1. Husby S., Koletzko S., Korponay-Szabo I.R., et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease. J Pediatr Gastroenterol Nutr. 2012;54:136-60.

2. Olen O., Gudjonsdottir A., Browaldh L., et al. Antibodies against deamindated gliadin peptides and tissue transglutaminase for diagnosis of pediatric celiac disease. J Pediatr Gastroenterol Nutr. 2012;55:695-700.

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Q2: Answer: B

This patient has chronic hepatitis E infection, as demonstrated by the positive hepatitis IgG antibody. It is recommended that HEV RNA be identified in serum or stool for diagnosis of hepatitis E. However, HEV RNA PCR is not readily available outside of research settings and therefore the Centers for Disease Control and Prevention states that the diagnosis can be confirmed only by testing for the presence of antibody against HEV or HEV RNA. Providers must be aware of the possibility of false positives and negatives for HEV serologies.

In immunocompetent individuals, hepatitis E is generally a self-limited condition, but in solid-organ transplant recipients, chronic infection can ensue. Hepatitis E infection in solid-organ transplant recipients has been linked to consumption of game meat, pork, and mussels. The infection is largely asymptomatic, but occasionally presents with jaundice. The liver test elevations are mild, with ALT levels up to 300 U/L. Approximately 60% of transplant recipients who are infected with hepatitis E develop chronic infections.

The best treatment for chronic hepatitis E in solid-organ transplant recipients is ribavirin. In one study, the sustained virologic response rate was 78% after a course of approximately 3 months of ribavirin. Pegylated interferon has been used for treatment of hepatitis E, but has less evidence to support its use and has a less favorable side effect profile. Sofosbuvir is a treatment for hepatitis C and therefore is not correct, though there are recent data suggesting that sofosbuvir inhibits hepatitis E virus replication in vitro and results in an additive effect when combined with ribavirin.

Observation is not a correct answer, as about 10% of patients with chronic hepatitis E may develop cirrhosis. Although not one of the provided answers, lowering the overall immunosuppression would be part of the treatment approach in a solid-organ transplant recipient with chronic hepatitis E.

Reference

1. Kamar N., Izopet J., Tripon S., et al. Ribavirin for chronic hepatitis E virus infection in transplant recipients. N Engl J Med. 2014 Mar 20;370(12):1111-20.

2. Dao Thi V.L., Debing Y., Wu X. Sofosbuvir inhibits hepatitis E virus replication in vitro and results in an additive effect when combined with ribavirin. Gastroenterology. 2016 Jan;150(1):82-5.

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Q2: Answer: B

This patient has chronic hepatitis E infection, as demonstrated by the positive hepatitis IgG antibody. It is recommended that HEV RNA be identified in serum or stool for diagnosis of hepatitis E. However, HEV RNA PCR is not readily available outside of research settings and therefore the Centers for Disease Control and Prevention states that the diagnosis can be confirmed only by testing for the presence of antibody against HEV or HEV RNA. Providers must be aware of the possibility of false positives and negatives for HEV serologies.

In immunocompetent individuals, hepatitis E is generally a self-limited condition, but in solid-organ transplant recipients, chronic infection can ensue. Hepatitis E infection in solid-organ transplant recipients has been linked to consumption of game meat, pork, and mussels. The infection is largely asymptomatic, but occasionally presents with jaundice. The liver test elevations are mild, with ALT levels up to 300 U/L. Approximately 60% of transplant recipients who are infected with hepatitis E develop chronic infections.

The best treatment for chronic hepatitis E in solid-organ transplant recipients is ribavirin. In one study, the sustained virologic response rate was 78% after a course of approximately 3 months of ribavirin. Pegylated interferon has been used for treatment of hepatitis E, but has less evidence to support its use and has a less favorable side effect profile. Sofosbuvir is a treatment for hepatitis C and therefore is not correct, though there are recent data suggesting that sofosbuvir inhibits hepatitis E virus replication in vitro and results in an additive effect when combined with ribavirin.

Observation is not a correct answer, as about 10% of patients with chronic hepatitis E may develop cirrhosis. Although not one of the provided answers, lowering the overall immunosuppression would be part of the treatment approach in a solid-organ transplant recipient with chronic hepatitis E.

Reference

1. Kamar N., Izopet J., Tripon S., et al. Ribavirin for chronic hepatitis E virus infection in transplant recipients. N Engl J Med. 2014 Mar 20;370(12):1111-20.

2. Dao Thi V.L., Debing Y., Wu X. Sofosbuvir inhibits hepatitis E virus replication in vitro and results in an additive effect when combined with ribavirin. Gastroenterology. 2016 Jan;150(1):82-5.

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Q2: Answer: B

This patient has chronic hepatitis E infection, as demonstrated by the positive hepatitis IgG antibody. It is recommended that HEV RNA be identified in serum or stool for diagnosis of hepatitis E. However, HEV RNA PCR is not readily available outside of research settings and therefore the Centers for Disease Control and Prevention states that the diagnosis can be confirmed only by testing for the presence of antibody against HEV or HEV RNA. Providers must be aware of the possibility of false positives and negatives for HEV serologies.

In immunocompetent individuals, hepatitis E is generally a self-limited condition, but in solid-organ transplant recipients, chronic infection can ensue. Hepatitis E infection in solid-organ transplant recipients has been linked to consumption of game meat, pork, and mussels. The infection is largely asymptomatic, but occasionally presents with jaundice. The liver test elevations are mild, with ALT levels up to 300 U/L. Approximately 60% of transplant recipients who are infected with hepatitis E develop chronic infections.

The best treatment for chronic hepatitis E in solid-organ transplant recipients is ribavirin. In one study, the sustained virologic response rate was 78% after a course of approximately 3 months of ribavirin. Pegylated interferon has been used for treatment of hepatitis E, but has less evidence to support its use and has a less favorable side effect profile. Sofosbuvir is a treatment for hepatitis C and therefore is not correct, though there are recent data suggesting that sofosbuvir inhibits hepatitis E virus replication in vitro and results in an additive effect when combined with ribavirin.

Observation is not a correct answer, as about 10% of patients with chronic hepatitis E may develop cirrhosis. Although not one of the provided answers, lowering the overall immunosuppression would be part of the treatment approach in a solid-organ transplant recipient with chronic hepatitis E.

Reference

1. Kamar N., Izopet J., Tripon S., et al. Ribavirin for chronic hepatitis E virus infection in transplant recipients. N Engl J Med. 2014 Mar 20;370(12):1111-20.

2. Dao Thi V.L., Debing Y., Wu X. Sofosbuvir inhibits hepatitis E virus replication in vitro and results in an additive effect when combined with ribavirin. Gastroenterology. 2016 Jan;150(1):82-5.

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Q2: Answer: B

Objective: Diagnose dyssynergic defecation and treat with biofeedback therapy.

Rationale: This patient has a functional defecation disorder, or dyssynergic defecation. According to Rome III guidelines, to fulfill this diagnosis, the patient must satisfy criteria for functional constipation.

In addition, they must also have at least 2 of the following: 1) Evidence of impaired evacuation on balloon expulsion test or imaging; 2) inappropriate contraction of the pelvic floor muscles or less than 20% relaxation of basal resting sphincter pressure by manometry, imaging or EEG; and 3) inadequate propulsive forces assessed by manometry or imaging.

The treatment mainstay for functional defecation disorders is pelvic floor retraining and biofeedback. Although lubiprostone and fiber supplementation are used to treat constipation, this is not the treatment of choice for dyssynergic defecation. Amitriptyline is often used for functional gastrointestinal disorders, but is not the primary therapy for dyssynergic defection, and often can worsen constipation and therefore is not appropriate for this patient.

Finally, rectal biopsy is the gold standard for diagnosis of Hirschsprung’s disease or congenital aganglionic megacolon. This is thought to be due to the failure of neural crest cells to migrate during gestation. The manometric findings with Hirschsprung’s consist of lack of relaxation of internal anal sphincter with distention of the rectum. This is a diagnosis usually made during childhood. Adults with Hirschsprung’s disease usually describe severe constipation since birth. It is therefore not the most likely diagnosis in this patient.

Reference

1. Bharucha A.E., Wald A., Enck P., Rao S. Functional anorectal disorders. Gastroenterology 2006;130:1510-8.

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Q2: Answer: B

Objective: Diagnose dyssynergic defecation and treat with biofeedback therapy.

Rationale: This patient has a functional defecation disorder, or dyssynergic defecation. According to Rome III guidelines, to fulfill this diagnosis, the patient must satisfy criteria for functional constipation.

In addition, they must also have at least 2 of the following: 1) Evidence of impaired evacuation on balloon expulsion test or imaging; 2) inappropriate contraction of the pelvic floor muscles or less than 20% relaxation of basal resting sphincter pressure by manometry, imaging or EEG; and 3) inadequate propulsive forces assessed by manometry or imaging.

The treatment mainstay for functional defecation disorders is pelvic floor retraining and biofeedback. Although lubiprostone and fiber supplementation are used to treat constipation, this is not the treatment of choice for dyssynergic defecation. Amitriptyline is often used for functional gastrointestinal disorders, but is not the primary therapy for dyssynergic defection, and often can worsen constipation and therefore is not appropriate for this patient.

Finally, rectal biopsy is the gold standard for diagnosis of Hirschsprung’s disease or congenital aganglionic megacolon. This is thought to be due to the failure of neural crest cells to migrate during gestation. The manometric findings with Hirschsprung’s consist of lack of relaxation of internal anal sphincter with distention of the rectum. This is a diagnosis usually made during childhood. Adults with Hirschsprung’s disease usually describe severe constipation since birth. It is therefore not the most likely diagnosis in this patient.

Reference

1. Bharucha A.E., Wald A., Enck P., Rao S. Functional anorectal disorders. Gastroenterology 2006;130:1510-8.

[email protected]

Q2: Answer: B

Objective: Diagnose dyssynergic defecation and treat with biofeedback therapy.

Rationale: This patient has a functional defecation disorder, or dyssynergic defecation. According to Rome III guidelines, to fulfill this diagnosis, the patient must satisfy criteria for functional constipation.

In addition, they must also have at least 2 of the following: 1) Evidence of impaired evacuation on balloon expulsion test or imaging; 2) inappropriate contraction of the pelvic floor muscles or less than 20% relaxation of basal resting sphincter pressure by manometry, imaging or EEG; and 3) inadequate propulsive forces assessed by manometry or imaging.

The treatment mainstay for functional defecation disorders is pelvic floor retraining and biofeedback. Although lubiprostone and fiber supplementation are used to treat constipation, this is not the treatment of choice for dyssynergic defecation. Amitriptyline is often used for functional gastrointestinal disorders, but is not the primary therapy for dyssynergic defection, and often can worsen constipation and therefore is not appropriate for this patient.

Finally, rectal biopsy is the gold standard for diagnosis of Hirschsprung’s disease or congenital aganglionic megacolon. This is thought to be due to the failure of neural crest cells to migrate during gestation. The manometric findings with Hirschsprung’s consist of lack of relaxation of internal anal sphincter with distention of the rectum. This is a diagnosis usually made during childhood. Adults with Hirschsprung’s disease usually describe severe constipation since birth. It is therefore not the most likely diagnosis in this patient.

Reference

1. Bharucha A.E., Wald A., Enck P., Rao S. Functional anorectal disorders. Gastroenterology 2006;130:1510-8.

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Q1: Answer: D

Objective: Understand the role of the restrictive transfusion strategy during patient stabilization and resuscitation as the initial step in the management of a variceal bleed.

Discussion: The initial therapy for acute variceal hemorrhage is resuscitation in an intensive care unit. Blood volume restitution should be undertaken promptly but with caution, with the goals of maintaining hemodynamic stability and hemoglobin around 7–8 g/dL.

Over-transfusion or volume overexpansion can precipitate variceal re-bleeding. A randomized clinical trial found that a restrictive transfusion strategy (transfusion when the hemoglobin fell below 7 g/dL) in patients with cirrhosis significantly improved survival. Endoscopic evaluation with potential variceal band ligation is appropriate only after initial resuscitation and stabilization of the patient.

Placement of a Blakemore tube and TIPS are not first-line therapy for this patient with Childs class A cirrhosis, and could be considered for recurrent bleeding that fails endoscopic therapy.

Endoscopic variceal ligation is more effective than sclerotherapy and is associated with fewer side effects. However, in patients for whom endoscopic variceal ligation is not feasible, sclerotherapy is a reasonable alternative.

References

1. Garcia-Tsao G., Sanyal A.J., Grace N.D., Carey W. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46(3):922-38.

2. Garcia-Tsao G., Bosch J.. Management of varices and variceal hemorrhage in cirrhosis. N Engl J Med. 2010;362(9):823-32.

3. Villanueva C., Colomo A., Bosch A., et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013;368(1):11-21.

4. Villanueva C., Piqueras M., Aracil C., et al. A randomized controlled trial comparing ligation and sclerotherapy as emergency endoscopic treatment added to somatostatin in acute variceal bleeding. J Hepatol. 2006;45(4):560-7.

Q1: Answer: D

Objective: Understand the role of the restrictive transfusion strategy during patient stabilization and resuscitation as the initial step in the management of a variceal bleed.

Discussion: The initial therapy for acute variceal hemorrhage is resuscitation in an intensive care unit. Blood volume restitution should be undertaken promptly but with caution, with the goals of maintaining hemodynamic stability and hemoglobin around 7–8 g/dL.

Over-transfusion or volume overexpansion can precipitate variceal re-bleeding. A randomized clinical trial found that a restrictive transfusion strategy (transfusion when the hemoglobin fell below 7 g/dL) in patients with cirrhosis significantly improved survival. Endoscopic evaluation with potential variceal band ligation is appropriate only after initial resuscitation and stabilization of the patient.

Placement of a Blakemore tube and TIPS are not first-line therapy for this patient with Childs class A cirrhosis, and could be considered for recurrent bleeding that fails endoscopic therapy.

Endoscopic variceal ligation is more effective than sclerotherapy and is associated with fewer side effects. However, in patients for whom endoscopic variceal ligation is not feasible, sclerotherapy is a reasonable alternative.

References

1. Garcia-Tsao G., Sanyal A.J., Grace N.D., Carey W. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46(3):922-38.

2. Garcia-Tsao G., Bosch J.. Management of varices and variceal hemorrhage in cirrhosis. N Engl J Med. 2010;362(9):823-32.

3. Villanueva C., Colomo A., Bosch A., et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013;368(1):11-21.

4. Villanueva C., Piqueras M., Aracil C., et al. A randomized controlled trial comparing ligation and sclerotherapy as emergency endoscopic treatment added to somatostatin in acute variceal bleeding. J Hepatol. 2006;45(4):560-7.

Q1: Answer: D

Objective: Understand the role of the restrictive transfusion strategy during patient stabilization and resuscitation as the initial step in the management of a variceal bleed.

Discussion: The initial therapy for acute variceal hemorrhage is resuscitation in an intensive care unit. Blood volume restitution should be undertaken promptly but with caution, with the goals of maintaining hemodynamic stability and hemoglobin around 7–8 g/dL.

Over-transfusion or volume overexpansion can precipitate variceal re-bleeding. A randomized clinical trial found that a restrictive transfusion strategy (transfusion when the hemoglobin fell below 7 g/dL) in patients with cirrhosis significantly improved survival. Endoscopic evaluation with potential variceal band ligation is appropriate only after initial resuscitation and stabilization of the patient.

Placement of a Blakemore tube and TIPS are not first-line therapy for this patient with Childs class A cirrhosis, and could be considered for recurrent bleeding that fails endoscopic therapy.

Endoscopic variceal ligation is more effective than sclerotherapy and is associated with fewer side effects. However, in patients for whom endoscopic variceal ligation is not feasible, sclerotherapy is a reasonable alternative.

References

1. Garcia-Tsao G., Sanyal A.J., Grace N.D., Carey W. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46(3):922-38.

2. Garcia-Tsao G., Bosch J.. Management of varices and variceal hemorrhage in cirrhosis. N Engl J Med. 2010;362(9):823-32.

3. Villanueva C., Colomo A., Bosch A., et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013;368(1):11-21.

4. Villanueva C., Piqueras M., Aracil C., et al. A randomized controlled trial comparing ligation and sclerotherapy as emergency endoscopic treatment added to somatostatin in acute variceal bleeding. J Hepatol. 2006;45(4):560-7.

Answer: E

Critique: Children with early-onset inflammatory bowel disease tend to present with colonic disease. Many of them eventually develop signs and symptoms consistent with Crohn’s disease as they get older. They are often diagnosed as “indeterminant” colitis or even ulcerative colitis but the diagnosis often changes. The colitis does not usually improve with age and these early-onset patients often follow a complicated course. This boy may eventually require enteral tube feedings or even a colectomy — however that cannot be predicted at this time. Provided his disease is well managed, he should reach his expected mid-parental height. 

References

1. Oliva-Hemker M., Hutfless S., Al Kazzi E., et al. Clinical presentation and five-year therapeutic management of very early-onset inflammatory bowel disease in a large North American cohort. J Pediatr. 2015;167:527-32.

2. Aloi M., Lionetti P., Barabino A., et al. Phenotype and disease course of early-onset pediatric inflammatory bowel disease. Inflamm Bowel Dis. 2014;20:597-605.

3. Mamula P., Markowitz J.E., Baldassano R.N. Inflammatory bowel disease in early childhood and adolescence: special considerations. Gastroenterol Clin North Am. 2003;32(3):967–95, viii.

Answer: E

Critique: Children with early-onset inflammatory bowel disease tend to present with colonic disease. Many of them eventually develop signs and symptoms consistent with Crohn’s disease as they get older. They are often diagnosed as “indeterminant” colitis or even ulcerative colitis but the diagnosis often changes. The colitis does not usually improve with age and these early-onset patients often follow a complicated course. This boy may eventually require enteral tube feedings or even a colectomy — however that cannot be predicted at this time. Provided his disease is well managed, he should reach his expected mid-parental height. 

References

1. Oliva-Hemker M., Hutfless S., Al Kazzi E., et al. Clinical presentation and five-year therapeutic management of very early-onset inflammatory bowel disease in a large North American cohort. J Pediatr. 2015;167:527-32.

2. Aloi M., Lionetti P., Barabino A., et al. Phenotype and disease course of early-onset pediatric inflammatory bowel disease. Inflamm Bowel Dis. 2014;20:597-605.

3. Mamula P., Markowitz J.E., Baldassano R.N. Inflammatory bowel disease in early childhood and adolescence: special considerations. Gastroenterol Clin North Am. 2003;32(3):967–95, viii.

Answer: E

Critique: Children with early-onset inflammatory bowel disease tend to present with colonic disease. Many of them eventually develop signs and symptoms consistent with Crohn’s disease as they get older. They are often diagnosed as “indeterminant” colitis or even ulcerative colitis but the diagnosis often changes. The colitis does not usually improve with age and these early-onset patients often follow a complicated course. This boy may eventually require enteral tube feedings or even a colectomy — however that cannot be predicted at this time. Provided his disease is well managed, he should reach his expected mid-parental height. 

References

1. Oliva-Hemker M., Hutfless S., Al Kazzi E., et al. Clinical presentation and five-year therapeutic management of very early-onset inflammatory bowel disease in a large North American cohort. J Pediatr. 2015;167:527-32.

2. Aloi M., Lionetti P., Barabino A., et al. Phenotype and disease course of early-onset pediatric inflammatory bowel disease. Inflamm Bowel Dis. 2014;20:597-605.

3. Mamula P., Markowitz J.E., Baldassano R.N. Inflammatory bowel disease in early childhood and adolescence: special considerations. Gastroenterol Clin North Am. 2003;32(3):967–95, viii.

Answer: D

Objective: Recognize that spontaneous bacterial peritonitis may present in an asymptomatic manner.

Discussion: It is important to recognize that patients with spontaneous bacterial peritonitis may present in various ways and may not exhibit classic abdominal pain or fevers. Patients may have atypical or no overt symptoms at all. With direct inoculation of ascitic fluid into culture bottles at bedside, cultures may identify bacteria in up to 40%-50% of cases.

Patients who survive an episode of SBP have a very high risk of recurrence (70%) within the first year of the index episode. It is therefore essential that patients recovering from SBP be started on prophylactic therapy prior to hospital discharge. Nonabsorbable (or poorly absorbable) antibiotics are most effective for such prophylaxis by selectively eliminating gram-negative organisms in the gut.

These agents reduce the rate of SBP recurrence to around 15–20%. Nosocomial infections respond poorly (~40% of cases) to 3rd generation cephalosporins. Those who have been in the hospital and received antibiotics within the past 90 days should receive extended-spectrum antibiotics.

References

1. Rimola A., Garcia-Tsao G., Navasa M., et al. Diagnosis, treatment and prophylaxis of spontaneous bacterial peri- tonitis: a consensus document. J Hepatol. 2000;32:142-53.

2. Tandon P., Garcia-Tsao G. Bacterial infections, sepsis, and multiorgan failure in cirrhosis. Semin Liver Dis. 2008;28(1):26-42.

Answer: D

Objective: Recognize that spontaneous bacterial peritonitis may present in an asymptomatic manner.

Discussion: It is important to recognize that patients with spontaneous bacterial peritonitis may present in various ways and may not exhibit classic abdominal pain or fevers. Patients may have atypical or no overt symptoms at all. With direct inoculation of ascitic fluid into culture bottles at bedside, cultures may identify bacteria in up to 40%-50% of cases.

Patients who survive an episode of SBP have a very high risk of recurrence (70%) within the first year of the index episode. It is therefore essential that patients recovering from SBP be started on prophylactic therapy prior to hospital discharge. Nonabsorbable (or poorly absorbable) antibiotics are most effective for such prophylaxis by selectively eliminating gram-negative organisms in the gut.

These agents reduce the rate of SBP recurrence to around 15–20%. Nosocomial infections respond poorly (~40% of cases) to 3rd generation cephalosporins. Those who have been in the hospital and received antibiotics within the past 90 days should receive extended-spectrum antibiotics.

References

1. Rimola A., Garcia-Tsao G., Navasa M., et al. Diagnosis, treatment and prophylaxis of spontaneous bacterial peri- tonitis: a consensus document. J Hepatol. 2000;32:142-53.

2. Tandon P., Garcia-Tsao G. Bacterial infections, sepsis, and multiorgan failure in cirrhosis. Semin Liver Dis. 2008;28(1):26-42.

Answer: D

Objective: Recognize that spontaneous bacterial peritonitis may present in an asymptomatic manner.

Discussion: It is important to recognize that patients with spontaneous bacterial peritonitis may present in various ways and may not exhibit classic abdominal pain or fevers. Patients may have atypical or no overt symptoms at all. With direct inoculation of ascitic fluid into culture bottles at bedside, cultures may identify bacteria in up to 40%-50% of cases.

Patients who survive an episode of SBP have a very high risk of recurrence (70%) within the first year of the index episode. It is therefore essential that patients recovering from SBP be started on prophylactic therapy prior to hospital discharge. Nonabsorbable (or poorly absorbable) antibiotics are most effective for such prophylaxis by selectively eliminating gram-negative organisms in the gut.

These agents reduce the rate of SBP recurrence to around 15–20%. Nosocomial infections respond poorly (~40% of cases) to 3rd generation cephalosporins. Those who have been in the hospital and received antibiotics within the past 90 days should receive extended-spectrum antibiotics.

References

1. Rimola A., Garcia-Tsao G., Navasa M., et al. Diagnosis, treatment and prophylaxis of spontaneous bacterial peri- tonitis: a consensus document. J Hepatol. 2000;32:142-53.

2. Tandon P., Garcia-Tsao G. Bacterial infections, sepsis, and multiorgan failure in cirrhosis. Semin Liver Dis. 2008;28(1):26-42.

Q2: Answer: B

Objective: Diagnose HELLP syndrome

Rationale: This patient’s presentation and laboratory findings are consistent with HELLP syndrome – the syndrome of hemolysis, elevated liver enzymes, and low platelets. HELLP is on the preeclampsia spectrum, which encompasses preeclampsia, eclampsia, and HELLP. Patients with HELLP will have hypertension (BP above 140/90), thrombocytopenia to less than 100,000/mm3 and aminotransferase levels above 70 U/L.

The diagnosis can be confirmed with an LDH (lactate dehydrogenase) greater than 600 U/L and microangiopathic hemolytic anemia on peripheral blood smear. On liver biopsy, HELLP is characterized by periportal or focal parenchyma necrosis with hyaline deposition of fibrin material in the sinusoids. However, liver biopsies are rarely performed in this setting as it likely will not change management (delivery of the fetus) and it exposes the mother and fetus to additional risks.

There is significant overlap between HELLP and acute fatty liver of pregnancy, although elevated prothrombin and partial thromboplastin time, severe hypoglycemia, and elevated creatinine are more common in acute fatty liver of pregnancy. Hypertension is more common in HELLP, and therefore this patient’s presentation is more consistent with HELLP.

Reference

1. Kia L, Rinella ME. Interpretation and management of hepatic abnormalities in pregnancy. Clin Gastroenterol Hepatol. 2013;11(11):1392-8.

Q2: Answer: B

Objective: Diagnose HELLP syndrome

Rationale: This patient’s presentation and laboratory findings are consistent with HELLP syndrome – the syndrome of hemolysis, elevated liver enzymes, and low platelets. HELLP is on the preeclampsia spectrum, which encompasses preeclampsia, eclampsia, and HELLP. Patients with HELLP will have hypertension (BP above 140/90), thrombocytopenia to less than 100,000/mm3 and aminotransferase levels above 70 U/L.

The diagnosis can be confirmed with an LDH (lactate dehydrogenase) greater than 600 U/L and microangiopathic hemolytic anemia on peripheral blood smear. On liver biopsy, HELLP is characterized by periportal or focal parenchyma necrosis with hyaline deposition of fibrin material in the sinusoids. However, liver biopsies are rarely performed in this setting as it likely will not change management (delivery of the fetus) and it exposes the mother and fetus to additional risks.

There is significant overlap between HELLP and acute fatty liver of pregnancy, although elevated prothrombin and partial thromboplastin time, severe hypoglycemia, and elevated creatinine are more common in acute fatty liver of pregnancy. Hypertension is more common in HELLP, and therefore this patient’s presentation is more consistent with HELLP.

Reference

1. Kia L, Rinella ME. Interpretation and management of hepatic abnormalities in pregnancy. Clin Gastroenterol Hepatol. 2013;11(11):1392-8.

Q2: Answer: B

Objective: Diagnose HELLP syndrome

Rationale: This patient’s presentation and laboratory findings are consistent with HELLP syndrome – the syndrome of hemolysis, elevated liver enzymes, and low platelets. HELLP is on the preeclampsia spectrum, which encompasses preeclampsia, eclampsia, and HELLP. Patients with HELLP will have hypertension (BP above 140/90), thrombocytopenia to less than 100,000/mm3 and aminotransferase levels above 70 U/L.

The diagnosis can be confirmed with an LDH (lactate dehydrogenase) greater than 600 U/L and microangiopathic hemolytic anemia on peripheral blood smear. On liver biopsy, HELLP is characterized by periportal or focal parenchyma necrosis with hyaline deposition of fibrin material in the sinusoids. However, liver biopsies are rarely performed in this setting as it likely will not change management (delivery of the fetus) and it exposes the mother and fetus to additional risks.

There is significant overlap between HELLP and acute fatty liver of pregnancy, although elevated prothrombin and partial thromboplastin time, severe hypoglycemia, and elevated creatinine are more common in acute fatty liver of pregnancy. Hypertension is more common in HELLP, and therefore this patient’s presentation is more consistent with HELLP.

Reference

1. Kia L, Rinella ME. Interpretation and management of hepatic abnormalities in pregnancy. Clin Gastroenterol Hepatol. 2013;11(11):1392-8.

Q1: Answer: A

The Food and Drug Administration issued a postmarketing warning about potential for interaction between sofosbuvir and amiodarone. Nine patients taking sofosbuvir (with other antiviral agents) and amiodarone developed significant bradycardia. Seven patients were on concomitant beta-blockade. One patient died of cardiac arrest while three others required pacemaker placement. Two-thirds of the events occurred within 24 hours of coadministration while the other third occurred within 12 days. Three patients had recurrence of bradycardia with rechallenge of sofosbuvir treatment while on amiodarone. The mechanism of bradycardia is not fully understood. Amiodarone is considered an absolute contraindication to the use of a sofosbuvir-containing regimen. The sofosbuvir-containing regimens listed are endorsed by the AASLD/IDSA joint guidelines for treatment of genotype 1a hepatitis C, as long as the patient is not on amiodarone, although the combination of sofosbuvir and daclatasvir is not FDA approved for genotype 1.

Reference

1. Fontaine H, Lazarus A, Pol S, et al.; Cochin Hepatology and Cardiology Group. N Engl J Med. 2015 Nov 5;373(19):1886-8.

Q1: Answer: A

The Food and Drug Administration issued a postmarketing warning about potential for interaction between sofosbuvir and amiodarone. Nine patients taking sofosbuvir (with other antiviral agents) and amiodarone developed significant bradycardia. Seven patients were on concomitant beta-blockade. One patient died of cardiac arrest while three others required pacemaker placement. Two-thirds of the events occurred within 24 hours of coadministration while the other third occurred within 12 days. Three patients had recurrence of bradycardia with rechallenge of sofosbuvir treatment while on amiodarone. The mechanism of bradycardia is not fully understood. Amiodarone is considered an absolute contraindication to the use of a sofosbuvir-containing regimen. The sofosbuvir-containing regimens listed are endorsed by the AASLD/IDSA joint guidelines for treatment of genotype 1a hepatitis C, as long as the patient is not on amiodarone, although the combination of sofosbuvir and daclatasvir is not FDA approved for genotype 1.

Reference

1. Fontaine H, Lazarus A, Pol S, et al.; Cochin Hepatology and Cardiology Group. N Engl J Med. 2015 Nov 5;373(19):1886-8.

Q1: Answer: A

The Food and Drug Administration issued a postmarketing warning about potential for interaction between sofosbuvir and amiodarone. Nine patients taking sofosbuvir (with other antiviral agents) and amiodarone developed significant bradycardia. Seven patients were on concomitant beta-blockade. One patient died of cardiac arrest while three others required pacemaker placement. Two-thirds of the events occurred within 24 hours of coadministration while the other third occurred within 12 days. Three patients had recurrence of bradycardia with rechallenge of sofosbuvir treatment while on amiodarone. The mechanism of bradycardia is not fully understood. Amiodarone is considered an absolute contraindication to the use of a sofosbuvir-containing regimen. The sofosbuvir-containing regimens listed are endorsed by the AASLD/IDSA joint guidelines for treatment of genotype 1a hepatitis C, as long as the patient is not on amiodarone, although the combination of sofosbuvir and daclatasvir is not FDA approved for genotype 1.

Reference

1. Fontaine H, Lazarus A, Pol S, et al.; Cochin Hepatology and Cardiology Group. N Engl J Med. 2015 Nov 5;373(19):1886-8.

Q2. Answer: C

Rationale: MALT lymphomas are associated with H. pylori infection in 80%-90% of cases. H. pylori triggers a B-cell clonal expansion leading to lymphoma. Detection of chronic H. pylori using histology is directly dependent on the number of mucosal biopsies. Negative H. pylori testing should prompt an alternative test for H. pylori (either breath or stool antigen test). Treatment of H. pylori is successful in achieving complete remission in up to 80% of cases. Surveillance after treatment of MALT lymphoma is indicated, though the exact protocol has not been established.

References

1. ASGE Standards of Practice Committee. The role of endoscopy in management of premalignant and malignant conditions of the stomach. Gastrointest Endosc. 2015 82(1):1-8.

2. Gisbert J.P., Calvet X. Review article: common misconceptions in the management of Helicobacter pylori-associated gastric MALT-lymphoma. Aliment Pharmacol Ther. 2011 Nov;34(9):1047-62.

Q2. Answer: C

Rationale: MALT lymphomas are associated with H. pylori infection in 80%-90% of cases. H. pylori triggers a B-cell clonal expansion leading to lymphoma. Detection of chronic H. pylori using histology is directly dependent on the number of mucosal biopsies. Negative H. pylori testing should prompt an alternative test for H. pylori (either breath or stool antigen test). Treatment of H. pylori is successful in achieving complete remission in up to 80% of cases. Surveillance after treatment of MALT lymphoma is indicated, though the exact protocol has not been established.

References

1. ASGE Standards of Practice Committee. The role of endoscopy in management of premalignant and malignant conditions of the stomach. Gastrointest Endosc. 2015 82(1):1-8.

2. Gisbert J.P., Calvet X. Review article: common misconceptions in the management of Helicobacter pylori-associated gastric MALT-lymphoma. Aliment Pharmacol Ther. 2011 Nov;34(9):1047-62.

Q2. Answer: C

Rationale: MALT lymphomas are associated with H. pylori infection in 80%-90% of cases. H. pylori triggers a B-cell clonal expansion leading to lymphoma. Detection of chronic H. pylori using histology is directly dependent on the number of mucosal biopsies. Negative H. pylori testing should prompt an alternative test for H. pylori (either breath or stool antigen test). Treatment of H. pylori is successful in achieving complete remission in up to 80% of cases. Surveillance after treatment of MALT lymphoma is indicated, though the exact protocol has not been established.

References

1. ASGE Standards of Practice Committee. The role of endoscopy in management of premalignant and malignant conditions of the stomach. Gastrointest Endosc. 2015 82(1):1-8.

2. Gisbert J.P., Calvet X. Review article: common misconceptions in the management of Helicobacter pylori-associated gastric MALT-lymphoma. Aliment Pharmacol Ther. 2011 Nov;34(9):1047-62.

Q1. Answer: A

While heartburn responds well to acid suppression with a proton pump inhibitor, regurgitation does not necessarily improve. It is well known that reflux persists despite acid suppression; in some patients, this manifests as troublesome postprandial regurgitation.  Transient LES relaxations (TLESRs) are the prime mechanism for persisting reflex, in patients both with and without hiatal hernias. 

Baclofen, a gamma amino butyric acid B (GABA-B) agonist, inhibits TLESRs and has potential to improve persisting regurgitation.  Metoclopramide has been demonstrated to have no adjunctive value in treating reflux disease. Hyoscyamine and sucralfate are similarly not of particular benefit in this setting. Cholesytramine is a bile salt binding resin that has value in the management of postcholecystectomy diarrhea.

References 

1. Kahrilas P.J., Jonsson A., Denison H., et al. Regurgitation is less responsive to acid suppression than heartburn in patients with gastroesophageal reflux disease. Clin Gastroenterol Hepatol. 2012;10(6):612-9. 

2. Vela M.F., Camacho-Lobato L., Srinivasan R., et al. Simultaneous intraesophageal impedance and pH measurement of acid and nonacid gastroesophageal reflux: effect of omeprazole. Gastroenterology. 2001 Jun;120(7):1599-606.

3. Vela M.F., Tutuian R, Katz PO, et al. Baclofen decreases acid and non-acid post-prandial gastro-oesophageal reflux measured by combined multichannel intraluminal impedance and pH. Aliment Pharmacol Ther. 2003 Jan;17(2):243-51.

Q1. Answer: A

While heartburn responds well to acid suppression with a proton pump inhibitor, regurgitation does not necessarily improve. It is well known that reflux persists despite acid suppression; in some patients, this manifests as troublesome postprandial regurgitation.  Transient LES relaxations (TLESRs) are the prime mechanism for persisting reflex, in patients both with and without hiatal hernias. 

Baclofen, a gamma amino butyric acid B (GABA-B) agonist, inhibits TLESRs and has potential to improve persisting regurgitation.  Metoclopramide has been demonstrated to have no adjunctive value in treating reflux disease. Hyoscyamine and sucralfate are similarly not of particular benefit in this setting. Cholesytramine is a bile salt binding resin that has value in the management of postcholecystectomy diarrhea.

References 

1. Kahrilas P.J., Jonsson A., Denison H., et al. Regurgitation is less responsive to acid suppression than heartburn in patients with gastroesophageal reflux disease. Clin Gastroenterol Hepatol. 2012;10(6):612-9. 

2. Vela M.F., Camacho-Lobato L., Srinivasan R., et al. Simultaneous intraesophageal impedance and pH measurement of acid and nonacid gastroesophageal reflux: effect of omeprazole. Gastroenterology. 2001 Jun;120(7):1599-606.

3. Vela M.F., Tutuian R, Katz PO, et al. Baclofen decreases acid and non-acid post-prandial gastro-oesophageal reflux measured by combined multichannel intraluminal impedance and pH. Aliment Pharmacol Ther. 2003 Jan;17(2):243-51.

Q1. Answer: A

While heartburn responds well to acid suppression with a proton pump inhibitor, regurgitation does not necessarily improve. It is well known that reflux persists despite acid suppression; in some patients, this manifests as troublesome postprandial regurgitation.  Transient LES relaxations (TLESRs) are the prime mechanism for persisting reflex, in patients both with and without hiatal hernias. 

Baclofen, a gamma amino butyric acid B (GABA-B) agonist, inhibits TLESRs and has potential to improve persisting regurgitation.  Metoclopramide has been demonstrated to have no adjunctive value in treating reflux disease. Hyoscyamine and sucralfate are similarly not of particular benefit in this setting. Cholesytramine is a bile salt binding resin that has value in the management of postcholecystectomy diarrhea.

References 

1. Kahrilas P.J., Jonsson A., Denison H., et al. Regurgitation is less responsive to acid suppression than heartburn in patients with gastroesophageal reflux disease. Clin Gastroenterol Hepatol. 2012;10(6):612-9. 

2. Vela M.F., Camacho-Lobato L., Srinivasan R., et al. Simultaneous intraesophageal impedance and pH measurement of acid and nonacid gastroesophageal reflux: effect of omeprazole. Gastroenterology. 2001 Jun;120(7):1599-606.

3. Vela M.F., Tutuian R, Katz PO, et al. Baclofen decreases acid and non-acid post-prandial gastro-oesophageal reflux measured by combined multichannel intraluminal impedance and pH. Aliment Pharmacol Ther. 2003 Jan;17(2):243-51.