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

July 20, 2017

Background: Perichondritis is an infection of the connective tissue of the ear that covers the cartilaginous auricle or pinna, excluding the lobule (Caruso 2014). The term perichondritis is itself a misnomer, as the cartilage is almost always involved, with abscess formation and cavitation (Prasad 2007). Perichondritis can be a devastating disease, and if left improperly treated, the infection can worsen into a liquefying chondritis resulting in disfigurement and/or loss of the external ear (Noel 1989) (Martin 1976). Unfortunately, misdiagnosis and mistreatment is common. In one small retrospective review, the overwhelming majority of patients presenting to a large general hospital were prescribed antibiotics without appropriate antimicrobial coverage, resulting in a significant number of patients developing chondral deformities or “cauliflower ear” (Liu 2013).

June 8, 2017

Background: Cellulitis is a common emergency department (ED) presentation. Despite the fact that diagnosis remains relatively straight forward, complexity remains in management in terms of the causative agent and appropriate antibiotic regimen. Though beta-hemolytic Streptococci are the most common causative agents there is increasing prevalence of community acquired methicillin-resistant Staphylococcus aureus (MRSA). Cephalexin has long been used to treat uncomplicated cellulitis because of it’s activity against streptococci and methicillin-sensitive S. aureus (MSSA). Despite the current Infectious Disease Society of America (IDSA) recommendations against routine coverage of MRSA, trimethoprim-sulfamethoxazole (TMP-SMX) is often added to cephalexin (Stephens 2014). While there are other single options for coverage, they either have suboptimal MRSA coverage (i.e. clindamycin and doxycycline) or are more expensive (i.e. linezolid). Without reliable ways to determine which patients need MRSA coverage, it is unclear which patients with uncomplicated cellulitis need to be discharged with MRSA coverage and which will do fine with a single agent.

June 5, 2017

The Background: Nearly 50% of patients in the U.S. with cirrhotic liver disease develop ascites over a 10-year period of observation, placing them at risk for developing spontaneous bacterial peritonitis (SBP) (Runyon 2012). It is estimated that 12-25% of patients with ascites in the ED will have spontaneous bacterial peritonitis (SBP) but the classic triad of fever, abdominal pain, and worsening ascites is often absent (Borzio 2001)(Runyon 1988). With a mortality rate approaching 40%, rapid diagnosis and evidence-based treatment is critical in the management of patients presenting with SBP (Salerno 2013).

SBP is diagnosed via cell count and differential of ascitic fluid obtained by paracentesis demonstrating an elevated polymorphonuclear leukocyte (PMN) count ( 250 cells/mm3). Treatment focuses on appropriate antibiotic therapy. A third-generation cephalosporin is the treatment of choice as they are typically effective in covering the three most common isolates from infected ascitic fluid: Escherichia coli, Klebsiella pneumonia, and Streptococcus pneumonia (Runyon 2012). Intravenous albumin administration is often added to the management of these patients but the utility for improving morbidity and mortality is questionable. The benefit of albumin infusion in SBP is not entirely known, although multiple possible mechanisms have been identified. Albumin has been demonstrated to mitigate endotoxemia, block lipopolysaccharide-stimulated neutrophil activity, and modulate nitric oxide activity, mitigating systemic vasodilation and capillary leak (Salerno 2013).