Clinical review: Hemorrhagic shock

Guillermo Gutierrez¹ , H David Reines² and Marian E Wulf-Gutierrez³

¹Professor, Pulmonary and Critical Care Medicine Division, Department of Medicine, The George Washington University Medical Center, Washington, District of Columbia, USA

²Professor, Virginia Commonwealth University and Vice-Chairman, Department of Surgery, Inova Fairfax Hospital, Falls Church, Virginia, USA

³Associate Professor, Department of Obstetrics and Gynecology, The George Washington University, Inova Fairfax Hospital, Falls Church, Virginia, USA

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Critical Care 2004, 8:373-381doi:10.1186/cc2851


Published:	2 April 2004

See related letter, http://ccforum.com/content/8/5/396

Abstract

This review addresses the pathophysiology and treatment of hemorrhagic shock – a condition produced by rapid and significant loss of intravascular volume, which may lead sequentially to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage, and death. Hemorrhagic shock can be rapidly fatal. The primary goals are to stop the bleeding and to restore circulating blood volume. Resuscitation may well depend on the estimated severity of hemorrhage. It now appears that patients with moderate hypotension from bleeding may benefit by delaying massive fluid resuscitation until they reach a definitive care facility. On the other hand, the use of intravenous fluids, crystalloids or colloids, and blood products can be life saving in those patients who are in severe hemorrhagic shock. The optimal method of resuscitation has not been clearly established. A hemoglobin level of 7–8 g/dl appears to be an appropriate threshold for transfusion in critically ill patients with no evidence of tissue hypoxia. However, maintaining a higher hemoglobin level of 10 g/dl is a reasonable goal in actively bleeding patients, the elderly, or individuals who are at risk for myocardial infarction. Moreover, hemoglobin concentration should not be the only therapeutic guide in actively bleeding patients. Instead, therapy should be aimed at restoring intravascular volume and adequate hemodynamic parameters.