Reperfusion Injury After Hemorrhage: A Collective Review

G D. Rushing, MD; L D. Britt, MD, MPH


Annals of Surgery. 2008;247(6):929-937. 

In This Article

Abstract and Introduction

Objective: To review current knowledge of hemorrhagic shock and reperfusion injury.
Summary Background Data: Patients with hemorrhagic shock require optimal resuscitation and cessation of ongoing bleeding. Often our resuscitative measures, while necessary, cause a wide range of detrimental physiologic effects. Research continues to answer questions regarding measurable endpoints and optimal fluids used in resuscitation. Elucidation and understanding of the complex metabolic pathways involved in reperfusion injury are areas of intense current investigative effort.
Methods: A literature review was performed using MEDLINE and key words related to experimental and clinical studies concerning shock and reperfusion.
Results: Experimental studies have shown that resuscitation with colloid and crystalloid show no difference in outcomes in critically ill patients. Laboratory studies are showing promising results with immunomodulation of response to injury. However, no clinical trials have shown significance yet.
Conclusions: It is unlikely that a single treatment modality or magic bullet will be able to substantially block such a complex regulated process unless performed before feedback mechanisms known to be in place. Ongoing translational research will inevitably have a major impact on patient care.

Shock is one of the primary causes of morbidity and mortality in the intensive care units of today's hospitals. The body's inflammatory response is profound and, if unchecked, can lead to multiple end organ failure and death. Although sepsis is the likely source prompting an inflammatory response in critically ill patients who become hypotensive and tachycardic, hypovolemic shock is also associated with severe systemic inflammatory processes based on components of innate immunity. Although the most common etiology of hypovolemic shock is hemorrhagic, there are other pathophysiologic processes that can result in this type of shock state. The concept of shock has evolved since first being described in ancient traumatic wounds and hemorrhage. Initially, the correlation between blood loss and death was not made; treatment for shock during the time of Hippocrates (460-380 BC) was bloodletting. George James Guthrie (1785-1856) was the first to use the term shock to delineate physiologic instability.[1] Keith used dye dilution measurements to show that hypovolemia was a mechanism for shock in 1919.[2] However, in 1930, Alfred Blalock classic animal experiments proved, indisputably, that blood loss was the primary cause of traumatic shock.[3,4]

The definition of shock has progressed considerably but in its most simple terms is defined as a physiologic state where delivery of oxygen does not meet metabolic demands. Traumatic blood loss is often easy to recognize; however, volume and location of bleeding can be extremely difficult to discern. To assist the surgeon with treatment of hemorrhage, classes of shock have been devised to delineate severity ( Table 1 ). The first sign of hypovolemic shock is a decrease in pulse pressure. This phenomenon is due to an increase in diastolic blood pressure, secondary to a catecholamine surge. Compensatory responses to hypovolemia such as mild tachycardia, anxiousness, tachypnea, and decrease in urine output occur in class II shock. Sustained hypotension is seen with both class III and class IV shock.


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