Chiefs’ Inquiry Corner – 9/28/2021

September 28, 2021

Chief residents of the NYU Langone Internal Medicine Residency give quick-and-easy, evidence-based answers to interesting questions posed by house staff, both in their clinics and on the wards.

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 According to the American Association for the Study of Liver Diseases (AASLD), a follow-up analysis of the ascitic fluid is not required or recommended in the majority of patients being treated for SBP. In patients with advanced cirrhosis, fluid studies in a typical presentation will show a low protein level(<1 g/dL) and single organism. In these cases, patients will have a marked clinical response with initiation of appropriate antibiotics. In patients with atypical findings, such as a polymicrobial infection or delayed clinical improvement, a repeat paracentesis may reveal a secondary peritonitis which would prompt surgical consultation. If on follow-up paracentesis the PMNs haven’t decreased by at least 25% after two days of antibiotic therapy, you may need to broaden therapy or consider secondary causes. One small study of 16 patients with cirrhosis secondary to alcohol use disorder actually followed patients who obtained serial paracentesis with the goal of determining optimal antibiotic therapy; they found that patients whose PMNs decreased to <250 had a lower rate of recurrence. However, the data supporting its use routinely is lacking and thus, the AASLD does not recommend routine follow-up taps.

References: The value of ascitic fluid polymorphonuclear cell count determination during therapy of spontaneous bacterial peritonitis in patients with liver cirrhosis.
  Calprotectin is a protein that binds calcium and zinc, and it is thought to be largely neutrophil specific. In acute inflammation, neutrophils disintegrate and release a number of factors, including calprotectin. It is highly resistant to degradation and can actually remain stable in a stool sample for up to a week. However, this test is inflammation-specific and not necessarily disease-specific; elevated levels may be present in NSAID-related inflammation or alcohol-associated inflammation, in addition to inflammatory bowel disease. The test may be particularly useful in young patients presenting with abdominal symptoms, in whom a physician is considering inflammatory bowel disease vs irritable bowel syndrome (IBS). IBS has a prevalence of 10-15% within the adult population, so these symptoms are common in the clinic. While the diagnostic range has been less clear due to variations in the testing assays, a value over 200 μg/mg has a higher positive predictive value; values over 500 are associated with a very high likelihood of pathologic findings. One study out of London examined about 600 patients presenting with symptoms concerning for either IBS or organic inflammatory bowel disease. They obtained fecal calprotectin as well as characterized patients by the ROME criteria, after which they all underwent endoscopic evaluation. Fecal calprotectin had about 89% sensitivity and 79% specificity for IBD in this study. You may thus find utility in this test as a screening test; however, it is not recommended as a replacement for diagnostic colonoscopy in patients who have a consistent clinical history and risk factors. 

References: Fecal calprotectin in inflammatory bowel disease.
 BRASH syndrome (bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia) involves the synergistic effect of AV nodal blockade and hyperkalemia resulting in severe bradycardia. The resulting reduction in cardiac output, in turn, leads to poor renal perfusion, therefore, worsening the acute kidney injury as well as the degree of hyperkalemia. While severe hyperkalemia alone can cause bradycardia, in BRASH syndrome profound bradycardia can occur even in the setting of mild hyperkalemia due to the synergistic effect. Renally cleared AV nodal blockers, such as metoprolol and amlodipine, impose a greater risk as the concentration in the renal tubules inversely increases as the GFR decreases. If undiagnosed, this can progress to multisystem organ failure requiring transvenous pacing and hemodialysis. This vicious cycle is often initiated by a recent illness or medication changes. One of the most common causes is hypovolemia resulting from dehydration and a subsequent pre-renal acute kidney injury. Other common triggers include up-titration of medications that alter the cardiac output or renal perfusion, and the initiation of nephrotoxic agents or potassium-sparing diuretics. While estimates of this syndrome’s prevalence are unclear, it is likely under-recognized in general so it may be something to consider in such cases. 

References: BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia