Coagulopathy in the critically injured patient

A. Mayo, U. Martinowitz, Y. Kluger

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

Trauma is an increasingly common cause of death of modern society. Death caused by trauma is rapidly surpassing the number of deaths due to stroke or cardiovascular disease. Uncontrolled bleeding is the leading cause of early in-hospital mortality (within 48 h of admission) and the second leading cause of pre-hospital death, accounting for 40% and 45% of the fatalities, respectively [1]. Massive hemorrhage after traumatic injury is frequently a combination of surgical and coagulopathic bleeding. Coagulopathic bleeding results from impairments in platelet function, fibrin formation, or enhanced degradation, or combinations of all these mechanisms. Understanding the exact etiology is crucial for successful management of this pathology. Early coagulopathy post-injury is observed in 25 to 36% of trauma victims upon admission to the emergency department [2, 3] and correlates with the severity of trauma. It is associated with an increased risk of mortality beyond the expected figures from the severity of the injury [3]. Coagulopathy can develop during, and be the result of the 'traditional aggressive' fluid resuscitation of hemorrhagic shock. It can also develop late, due to surgical complications such as sepsis or multiple organ failure (MOF). This chapter describes the pathophysiology of coagulopathy in various phases of trauma and discusses the mechanisms that can contribute to it.

Original languageEnglish
Title of host publicationIntensive Care Medicine
Subtitle of host publicationAnnual Update 2006
PublisherSpringer New York
Pages232-243
Number of pages12
ISBN (Print)0387301569, 9780387301563
DOIs
StatePublished - 2007
Externally publishedYes

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