January 20, 2020

Definition: Acute infection of the ascitic fluid in a patient with liver disease without another source of infection

Epidemiology: (Runyon 1988, Runyon 1988, Borzio 2001)

  • Incidence
    • 10-25% risk of at least one episode per year
    • 20% risk in those with ascites admitted to the hospital
  • Historically, mortality ~ 50%

Pathophysiology:

  • Not completely understood
  • Increased portal systemic hypertension
    • Causes mucosal edema of the bowel wall
    • Increases transmural migration of enteric organisms into the ascitic fluid
  • Impaired phagocytic function in the liver
  • Impaired immunologic activity in ascitic fluid

REBEL Review 92: Identification & Treatment of Spontaneous Bacterial Peritonitis

Created December 26, 2019 | Abdominal and Gastroinstestinal | DOWNLOAD

November 27, 2019

Take Home Points   
  • End stage liver disease patients have fragile baseline physiology. Minor insults can have profound effects
  • Always start with the basics - large bore IV lines
  • SBP give 3rd generation cephalosporin + albumin in severe disease
  • Upper GI bleed give appropriate blood products + ceftriaxone
 

April 13, 2018

Recently I was asked to speak at the Texas College of Emergency Physicians (TCEP) conference April 2018.  The particulars of this session were, five, 10 minute lectures on new indications for old drugs.  My topic was the use of octreotide and somatostatin for undifferentiated upper gastrointestinal bleeding.  This is a particular topic I have been getting more and more requests for, but didn’t really know the evidence behind why I was doing it.  Does it help my patients or just another expensive medication, that takes up an IV with no clear patient oriented outcome?

October 12, 2017

Acute Pancreatitis Background:

Definition: Acute inflammatory process of the pancreas; a retroperitoneal organ with endocrine and exocrine function.

Epidimiology (Rosen’s 2018)

  • US Incidence: 5 - 40/100,000
  • Mortality: 4-7%
  • Progression to severe disease: 10-15% of cases (mortality in this subset 20-50%)

Etiology:

  • Alcohol (~ 35% of cases)
  • Gallstones (~ 45% of cases)
  • Medications/toxins
  • Hypertriglyceridemia
  • Non-gallstone Obstruction (i.e. strictures, masses)
  • Trauma
  • Infectious

Pathophysiology:

  • Phase 1: Local inflammation
    • Results from obstruction of the pancreatic or bile ducts or direct toxicity to pancreatic cells
    • Inflammation results in pancreatic enzyme activation within the pancreas and ducts
    • Premature enzyme activation leads to pancreatic autodigestion
  • Phase 2
    • Enzyme digestion leads to necrosis of the pancreas
    • Erosion into vascular structures can occur as well leading to hemorrhage
  • Phase 3
    • Release of systemic inflammatory mediators
    • systemic immune response syndrome and multisystem organ dysfunction (i.e. acute renal failure, cardiac dysfunction, ARDS, disseminated intravascular coagulation)
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