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)

April 17, 2017

Background: Upper gastrointestinal hemorrhage (UGIH) is a commonly seen complaint in the ED.  Currently, endoscopy is the standard therapy shown to not only help with diagnosis, but also risk stratify patients and potentially offer effective hemostatic treatment of acute nonvariceal UGIH.  What is frequently an area of debate, is the optimal timing of endoscopy. Even more frustrating is the different definitions of early endoscopy ranging anywhere from 1hr up to 24hrs after initial presentation. Now on one hand, earlier timing of endoscopy could be associated with suboptimal resuscitation and potential hemodynamic instability.  On the other hand, delayed endoscopy delays hemostasis from endoscopic therapy and increases the risk of rebleeding and need for surgery.  I think we all agree that we should resuscitate our patients before endoscopy (or as I like to say resuscitate before you endoscopate), but is there a population of patients with UGIH that require sooner than later endoscopy? To talk about this topic we have a special guest Rory Spiegel.  You can find Rory on twitter as @EMNerd_ or on the EMCrit blog where he discusses methodological issues with studies

February 23, 2017

Upper gastrointestinal bleeding remains a common reason for emergency department visits and is a major cause of morbidity, mortality, and medical care costs. Often when these patients arrive, the classic IV-O2-Monitor is initiated and hemodynamic stability is assessed. One of the next steps often performed includes the initiation of proton pump inhibitors (PPIs). The ultimate question however is does initiation of PPIs reduce clinically relevant outcomes (i.e. mortality, rebleeding, need for surgical intervention) in upper gastrointestinal bleeds (UGIB)?
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