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FACP. Colegio de médicos de Tarragona Nº 4305520 / fgcapriles@gmail.com




Wednesday, December 2, 2015

Imitadores de Sepsis

emDocs - December 1, 2015 - Author: Long B // Edited by: Koyfman A & Bright J.
SIRS and sepsis are common clinical entities. A wide range of estimates for prevalence exists, with 300 to 1000 cases per 100,000 persons per year. Once a septic patient is admitted, more than half will require at least step down unit care or greater. Sepsis syndromes consist of a continuum, with varying definitions. The definition of SIRS includes: HR > 90 bpm, RR > 20 or PaCO2 < 32, temperature < 36oC or > 38oC, and a WBC count < 4 x 109 cells/L or > than 12 x 109 cells/L or > 10% bands. Two or more of these equals SIRS, and two or more with a source of infection equals sepsis.1,2 Unfortunately these criteria are non-specific, and the criteria alone do not provide a diagnosis or predict outcome. However, associated organ dysfunction does predict worse outcome.
A great deal of literature exists on sepsis and providing state of the art care in the ED. As EM physicians, we pride ourselves on resuscitating sick patients, and we are well aware that septic patients can rapidly decline clinically. Finding the source and providing appropriate antibiotics, adequate preload with IV fluids, and vasopressors if necessary are key components. The SIRS criteria are our first line of defense in the early identification of sepsis. But, it is important to recognize that just because a patient has multiple SIRS criteria, they may not actually be septic.
Many conditions mimic sepsis by meeting criteria for SIRS. If these conditions are not considered, there is potential for increased mortality and morbidity. These conditions include: pulmonary embolism (PE), adrenal insufficiency, diabetic ketoacidosis (DKA), pancreatitis, anaphylaxis, bowel obstruction, hypovolemia, colitis, vasculitis, toxin ingestion/overdose/withdrawal, and medication effect. These mimics are a common cause of misdiagnosis in the ED. All of these clinical conditions produce symptoms and signs that meet SIRS (fever, elevated WBC, tachypnea, decreased distal perfusion, low urine output, confusion, end-organ malfunction).
Why do these conditions mimic sepsis? It all comes down to the pathophysiology. Sepsis ultimately results from a complex interaction of pro-inflammatory, anti-inflammatory, activated complement system, and coagulation mediators that in association with detector and signaling markers, trigger a host response. Initiators (microbes, trauma, hypoxia, ischemia, toxins) cause local tissue damage, which release local pro- and anti-inflammatory markers. Proinflammatory signalers include TNF, IL-1, and IL-6, while anti-inflammatory markers include IL-4, IL-10, IL-11 and soluble TNF receptors. These are designed to function and contain at a local level. If the initiators overwhelm the local response, the mediators affect multiple systems in the body: dermal, cardiovascular, gastrointestinal, renal, neurologic, hematologic/coagulopathic, pulmonary, and endocrine.3,4All of these mimics have a similar endgame: triggering a systemic reaction that looks just like sepsis.
This post will take a step-by-step approach on how to avoid misdiagnosis and catch these mimics."