Risk Management Pitfalls, Medico Legal, Clinical, Critical Care, Shock

Diagnosing and Managing Shock

From the March 2014 issue of Emergency Medicine Practice, “Diagnosis and Management of Shock in the Emergency Department.” Reprinted with permission. To access your EMRA member benefit of free online access to all EM Practice, Pediatric EM Practice, and EM Practice Guidelines Update issues, go to www.ebmedicine.net/emra, call 1-800-249-5770, or send e-mail to ebm@ebmedicine.net.

  1. “His blood pressure is normal. He can't be in shock.”
    Focusing on blood pressure alone as an indicator of shock can lead to missing signs of occult shock. Impaired organ perfusion, as evidenced by acute renal failure, altered mental status and/or increased serum lactate concentration, is a sign of shock pathophysiology and obligates early, aggressive clinical management.
  2. “Let's get the chest CT scan before deciding whether to give antibiotics or not.”
    Failure to give antibiotics within one hour of presentation for all cases of possible septic shock may result in increased mortality. Early empiric antibiotic coverage is indicated for suspected septic shock with a target of administering (not just ordering) antibiotics within one hour of presentation.
  3. “Her ejection fraction is 30%, so let's start norepinephrine instead of giving a second liter of fluid.”
    Adequate volume resuscitation for hypovolemic patients is critical. Markers of tissue perfusion such as lactate clearance, ScvO2, pulse pressure variation with passive leg raise, and ultrasonographic measures of intravascular volume are appropriate determinants of the need for further volume resuscitation. A history of a low ejection fraction or other hypothetical concerns may lead clinicians to underresuscitate hypovolemic patients and may result in inappropriate initiation of vasopressors.
  4. “It could be a myocardial infarction, but let's wait for the troponin to come back before calling cardiology.”
    Time-to-revascularization is one of the primary determinants of survival in patients with cardiogenic shock due to acute coronary syndromes. Delaying time to catheterization and revascularization will increase patient morbidity and mortality. When cardiogenic shock is possible, early consultation with cardiology and activation of the catheterization laboratory are necessary to optimize patient outcomes.
  5. “Let's give a fifth liter of saline and see if her mean arterial pressure comes up to at least 60 mm Hg”¦”
    Starting vasopressors without adequately volume resuscitating a patient while following markers of tissue perfusion and intravascular volume status is inappropriate (see pitfall #3); however, not recognizing that vasopressors need to be started for patients who are not volume responsive is also inappropriate. Patients with a pathologically decreased systemic vascular resistance may require vasopressors to maintain mean arterial pressure even after volume resuscitation and normalization of intravascular volume status. Continuing to administer fluids and not recognizing the need for vasopressors can result in perpetuating complications of shock.
  6. “She has a fever and hypoxemia. Her hypotension is probably due to sepsis from pneumonia.”
    Failure to consider obstructive shock on the differential diagnosis can lead to inappropriate clinical management, such as treating a pulmonary embolism with antibiotics. Maintaining a broad differential diagnosis and considering obstructive pathophysiologic causes of shock, when clinically appropriate, can lead to more rapid diagnosis and treatment.
  7. “I read that a hemoglobin of 7 gm/dL is the evidence-based transfusion trigger, so let's hold off on giving this hypotensive trauma patient blood.”
    While conservative transfusion thresholds are appropriate for critically ill patients without active hemorrhage, prompt resuscitation with blood products is critically important for patients presenting with hemorrhagic shock. Furthermore, the hemoglobin concentration will not reflect the degree of blood loss early in such a patient's presentation, obligating the emergency clinician to identify possible acute hemorrhage based on the patient's clinical circumstances.
  8. “Her mean arterial pressure of 50 mmHg is probably just because she's pregnant.”
    Numerous physiologic changes occur during pregnancy, including increased cardiac output, increased heart rate, and decreased systemic vascular resistance. The decrease in systemic vascular resistance usually results in a drop in the mean arterial pressure of 5 mm Hg to 10 mm Hg from normal prepregnancy levels. Mean arterial pressures <60 mm Hg, however, should raise awareness of the possibility of pathophysiologic processes contributing to hypotension.
  9. “Let's try bilevel positive airway pressure and see if his pneumonia gets better after antibiotics.”
    Recognition of multiorgan system failure and hypotension from septic shock that requires early intubation and mechanical ventilation is critically important. Failure to intubate early in the course of care for critically ill patients in septic shock can perpetuate the cycle of impaired oxygen uptake, deficient oxygen delivery to peripheral tissues, and increased metabolic demand from increased work of breathing. Furthermore, recognizing that a patient's disease process will take days, rather than hours, to resolve prioritizes intubation above noninvasive mechanical ventilation.
  10. “I know how to treat sepsis: antibiotics, fluids, and pressors. I don't need a protocol.”
    Aggressive, protocolized, and bundled clinical management of patients in septic shock results in improved initial resuscitation and improved patient outcomes. Adherence to institutional guidelines for the initial treatment of septic shock is an important component of the acute care of severe sepsis and septic shock.