Author Archive for: Swami

Topical TXA in Epistaxis

07 Dec
December 7, 2017

Background: Epistaxis is a common Emergency Department (ED) complaint with over 450,000 visits per year and a lifetime incidence of 60% (Gifford 2008, Pallin 2005). Standard anterior epistaxis treatment consists of holding pressure, use of local vasoconstrictors, topical application of silver nitrate and placement of an anterior nasal pack. ED patients with epistaxis often fail conservative management and end up with anterior nasal packs which are uncomfortable. This is even more common in the group of patients who are taking antiplatelet agents like aspirin or clopidogrel. Recently, the use of topical tranexamic acid (TXA) has been described in patients with anterior epistaxis with shorter time to epistaxis control and shorter ED length of stay (Zahed 2013). However, prior studies have not focused specifically on patients taking antiplatelet agents. Read more →

Bacterial Endocarditis

04 Dec
December 4, 2017


  • Definition
    • Infective Endocarditis (IE) = Inflammation of the endothelium of the heart, heart valves (or both) (Osman 2013)
  • Epidemiology
    • Annual incidence = 5-7 cases per 100,000 (Fraimow 2013)
    • 40,000 to 50,000 new cases in the US per year. Average hospital charges in excess of $120,000 per patient (Bor 2013)
    • Slightly higher male predominance (1.5:1 – 2:1) (Moreillon 2010)
    • In-hospital mortality of 14–22% and 1-year mortality of 20-40% (Gomes 2017, (Habib 2006)
    • Before antibiotics and surgery it was almost universally fatal  (Aretz 2010, Osman 2013)
  • Pathophysiology (Moreillon 2010, Faza 2013, Tan 2014, Osman 2013, Kokowski 2018)
    • The normal, undamaged valve endothelium is very resistant to colonization and infection by circulating bacteria
    • Micro-trauma (caused by turbulent flow, intracardiac devices, etc) or chronic diseases (rheumatic heart disease, congenital heart disease, prosthetic valves, previous IE) can cause damage to the endothelium
    • Damage to endothelium produces a fibin and platelet sterile thrombus.  Microbes can seed that thrombus during transient episodes of bacteremia, fungemia and viremia
  • Risk factors –  (Faza 2013, Moreillon 2010).
    • Diseased/damaged heart (highest risk)
    • IV drug use (IVDU)
    • Low immune function –
    • Poor oral hygiene. (Faza 2013)
    • Nosocomial

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Spontaneous Bacterial Peritonitis

16 Nov
November 16, 2017

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%

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Acetaminophen vs. Diclofenac vs. Combo for Acute MSK Pain

02 Nov
November 2, 2017

Background: Acute, minor musculoskeletal injuries (i.e. non-fracture or dislocations) are frequently seen in the Emergency Department. Aside from ruling out a more severe injury, management often focuses on pain relief or mitigation of pain. Though many analgesic agents exist, acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for this indication. Both have important side effects or potential for adverse events that must be considered when prescribing them. Finally, it is unclear if combining the two classes of medications is beneficial. Read more →

Acute Pancreatitis

12 Oct
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%)


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


  • 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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