Hemorrhagic Shock in Emergency Medicine Treatment & Management

Updated: May 06, 2016
  • Author: William P Bozeman, MD; Chief Editor: Trevor John Mills, MD, MPH  more...
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Prehospital Care

The standard care consists of rapid assessment and expeditious transport to an appropriate center for evaluation and definitive care.

Intravenous access and fluid resuscitation are standard. However, this practice has become controversial. For many years, aggressive fluid administration has been advocated to normalize hypotension associated with severe hemorrhagic shock. Recent studies of urban patients with penetrating trauma have shown that mortality increases with these interventions; these findings call these practices into question. [5, 6, 7]

Resuscitation with crystalloid solutions has been shown to put patients with hemorrhagic shock at risk for marked acidosis and iatrogenically worsen the lethal triad of coagulopathy, hypothermia, and acidosis. Lactated Ringer’s resuscitation elevated lactate levels, and normal saline negatively affected the base deficit. [8, 6, 7, 9, 10, 11]

Reversal of hypotension prior to the achievement of hemostasis may increase hemorrhage, dislodge partially formed clots, and dilute existing clotting factors. Findings from animal studies of uncontrolled hemorrhage support these postulates. These provocative results raise the possibility that moderate hypotension may be physiologically protective and should be permitted, if present, until hemorrhage is controlled. These findings should not yet be clinically extrapolated to other settings or etiologies of hemorrhage. The ramifications of permissive hypotension in humans remain speculative, and safety limits have not been established yet.

In a study of patients who received 7.5% NaCl (HS), 7.5% NaCl/6% Dextran 70 (HSD), or 0.9% NaCl (normal saline [NS]) in the prehospital setting, treatment with HS/HSD led to higher admission systolic blood pressure, sodium, chloride, and osmolarity, whereas lactate, base deficit, fluid requirement, and hemoglobin levels were similar in all groups. The HSD-resuscitated patients had higher admission international normalized ratio values and more hypocoagulable patients. Prothrombotic tissue factor was elevated in shock treated with NS but depressed in both HS and HSD groups. The HSD patients had the worst imbalance between procoagulation/anticoagulation and profibrinolysis/antifibrinolysis, resulting in more hypocoagulability and hyperfibrinolysis. [7]


Emergency Department Care

Management of hemorrhagic shock should be directed toward optimizing perfusion of and oxygen delivery to vital organs.

Diagnosis and treatment of the underlying hemorrhage must be performed rapidly and concurrently with management of shock.

Supportive therapy, including oxygen administration, monitoring, and establishment of intravenous access (eg, 2 large-bore catheters in peripheral lines, central venous access), should be initiated. Intravascular volume and oxygen-carrying capacity should be optimized. In addition to crystalloids, some colloid solutions, hypertonic solutions, and oxygen-carrying solutions (eg, hemoglobin-based and perfluorocarbon emulsions) are used or being investigated for use in hemorrhagic shock.

Blood products are often required in severe hemorrhagic shock. Replacement of lost components using red blood cells (RBCs), fresh frozen plasma (FFP), and platelets may be essential. The ideal ratio of RBCs to FFP remains undetermined. Recent combat experience has suggested that aggressive use of FFP may reduce coagulopathies and improve outcomes. [15, 9]

Determination of the site and etiology of hemorrhage is critical to guide further interventions and definitive care.

Control of hemorrhage may be achieved in the ED, or control may require consultations and special interventions.

In an Australian study of the long-term outcomes of major-trauma patients who received massive transfusions, massive transfusion was independently associated with unfavorable outcomes. In massively transfused patients, the authors found no significant change in measured outcomes over the study period, with a persistent 23% mortality in hospital, a 52% unfavorable GOSE (Glasgow Outcome Score - extended) at 6 months, and a 44% unfavorable GOSE at 12 months. [8]



Consult a general or specialized surgeon, gastroenterologist, obstetrician-gynecologist, interventional radiologist, and others as required.