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Study reviews literature and management guidelines for severe sepsis and septic shock


Severe sepsis and septic shock are as widespread and potentially lethal as other acute life-threatening conditions confronted daily by emergency physicians, such as heart attack, stroke and trauma. Recent studies have led to a better understanding of the pathogenic mechanisms of severe sepsis and septic shock, and to the development of new and more effective therapies that stress early and aggressive management.

An independent literature review recently published in Annals of Emergency Medicine examined the recent pathogenic, diagnostic and therapeutic advances in severe sepsis and septic shock for adults, with a particular focus on emergency department medicine. The authors identified treatments that improve outcomes, including goaldirected therapy, early treatment with antimicrobials, source control, recombinant human activated protein C, corticosteroids and low tidal volume mechanical ventilation.

High mortality/long waits for care

Severe sepsis and septic shock carry mortality rates of 30 to 50 percent. Several studies have shown a significant reduction in mortality with new or newly applied therapies. However, treatment for many severe sepsis and septic shock patients is delayed by slow transfers from emergency medicine departments to intensive care units. Some of the new approaches to treating severe sepsis and septic shock appear to be time dependent, offering emergency physicians a limited window of opportunity and increasing their importance in caring for these patients.

Terms defined

Severe sepsis: Presence of an infection with one or more organs showing dysfunction, such as acute lung injury; blood clotting abnormalities; a decrease in blood platelets; altered mental status; renal, liver or heart failure or evidence of global tissue hypoxia as reflected by an elevated arterial or central venous lactic acid level.

Septic shock: The presence of an infection with refractory hypotension, for example systolic blood pressure under 90 mm Hg, mean arterial pressure less than 65 mm Hg or a decrease of 40 mm Hg in systolic blood pressure.

Rapid diagnosis

To diagnose severe sepsis and septic shock as early as possible, it is vital to recognize historical, clinical and laboratory finding that are indicative of infection, organ dysfunction and global tissue hypoxia. Also important to diagnosis is consideration of:

  • The patient’s risk for infection, such as contact risk for meningococcemia and the presence of immunocompromising conditions and prosthetics such as intravenous lines, heart valves and urinary catheters.

  • The presence of fever, the hallmark finding of infection. However, some patients may present without a fever and develop one during evaluation. Study Recommendations The following are guidelines for the management of severe sepsis and septic shock in the emergency department. The recommendations are consistent with those provided by the Surviving Sepsis Campaign and the Society of Critical Care Medicine:

  • Early recognition and management of severe sepsis and septic shock optimizes outcome. Patients suspected of having either should be prioritized and receive timely care.

  • Initiate immediate and continuous monitoring of vital signs, pulse oximetry and urine output and initial laboratory testing to assess severity of global tissue hypoxia and organ dysfunction, including testing for lactic acidosis, renal and liver dysfunction, acute lung injury and coagulation abnormalities.

  • Seek the source of infection through clinical evaluation, urinalysis, chest X-ray and other imaging as indicated. Obtain appropriate cultures (including blood, urine and site specific) before administering antibiotics.

  • Initiate antibiotics as soon as possible. Ideally, site-specific regimens should be administered if identification of the infection site does not significantly prolong the time until antibiotic therapy is given.

  • Once severe sepsis or septic shock is recognized, early goal-directed therapy should be institute quickly with placement of a subclavian or internal jugular center venous catheter for monitoring pressure and ScvO2. Once target goals are met (central venous pressure of 8 – 12 mm Hg, mean arterial pressure 65 – 90 mm Hg and ScvO2 greater than 70 percent), serial lactate levels should be obtained to evaluate response.

  • Source control (abscess drainage, debridement and removal of infected tissues or prostheses) should be pursued aggressively, according to infection site.

  • Patients requiring mechanical ventilation should be treated with low tidal volume to maintain end-inspiratory plateau pressure of less than 30 cm H2O.

  • Patients with a high risk of death who don’t respond to early goal-directed therapy, antibiotics and source control should be considered for drotrecogin-alfa administration.

  • Patients with refractory shock or organ dysfunction who are receiving mechanical ventilation should receive an adrenocorticotropic hormone stimulation test and be given low-dose replacement corticosteroid therapy. Note, however, that a recent validation trial failed to confirm the efficacy of this therapy.

Relevant publication

Severe Sepsis and Septic Shock: Review of the Literature and Emergency Department Management Guidelines. Fredrick M. Abrahamian, Gregory J. Moran, David A. Talan (Olive View-UCLA Medical Center); H. Bryant Nguyen (Loma Linda University); Emmanuel P. Rivers (Henry Ford Hospital); Edward Abraham (University of Colorado); Stephen Trzeciak (Cooper University Hospital); David T. Huang (University of Pittsburgh); Tiffany Osborn (University of Virginia, Charlottesville); and Denis Stevens (VA Medical Center, Boise , ID) Ann Emerg Med. 2006;48:28-54

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