DOI: 10.1097/01.aia.0000182640.39691.dd

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PMID: 16189393

Issn Print: 0020-5907

Publication Date: 2005/10/01


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Coagulopathy in Massive Transfusion

Paul J Wojciechowski; Nancy Samol; James Walker

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Excerpt

A 27-year-old, 20 weeks pregnant woman involved in a motor vehicle crash presented emergently to the operating room (OR) with hypotension after multiple intrathoracic, intraabdominal, and orthopedic injuries. Hemoperitoneum was noted when entering the abdomen. The source of the bleeding appeared to be an avulsed aortic branch at the crus of the diaphragm that was not easily accessible from the abdomen. A left thoracotomy was performed revealing massive hemothorax. After appropriate exposure, the bleeding artery was ligated and attention returned to the abdomen for splenectomy, packing, and rapid closure. By this time, the patient had sustained prolonged hypotension and massive resuscitation, which included 6000 mL crystalloid, 35 units packed red blood cells, 20 units fresh-frozen plasma, 40 units cryoprecipitate, and 36 units of platelets. Her temperature reached a nadir at 35.2°C. This, combined with hemodilution, metabolic acidosis (lowest pH 7.21), and massive transfusion, led to the development of significant intraoperative coagulopathy that ultimately required the use of recombinant factor VIIa (rFVIIa). A significant improvement in hemostasis was noted after administration of 6000 μg rFVIIa. The patient was transferred to the surgical intensive care unit for further resuscitation and stabilization. Her postoperative course included posttraumatic acute respiratory distress syndrome (ARDS) and repeated trips to the OR for wound closure and repair of orthopedic injuries. She had no further bleeding complications but did experience an intrauterine fetal death during her initial surgery. There were no thromboembolic sequelae.
Massive hemorrhage is a formidable challenge for anesthesia care providers in the elective setting and poses even greater potential challenges in the trauma setting. In both cases, the anesthesia care providers are faced with large-volume resuscitations that typically start with crystalloid and colloid and rapidly progress to blood and blood products. These large-volume replacements may cause coagulopathy, which can be difficult to manage in the setting of ongoing blood loss.
The term “massive transfusion” has been coined for the clinical situation in which large volumes of fractionated blood products are given to maintain tissue oxygenation and hemostasis. Specifically, massive transfusion can be defined as the replacement of one blood volume in 24 hours or the replacement of 50% of the blood volume in 3 hours.1,2 In the acute clinical setting, a more practical definition of massive transfusion is helpful. Such a definition includes history of transfusion of 4 or more red cell concentrates within 1 hour when ongoing need is foreseeable.3 This type of resuscitation frequently leads to development of coagulopathy from multiple causes. Deciding what treatment strategies to implement can present a challenge to even the most experienced anesthesia provider.
The goal of this review is to provide an introduction to the pathophysiology of coagulopathy in massive transfusion; provide relevant history, physical examination, and diagnostic tests to identify coagulopathy in massive transfusion; and to provide strategies and alternatives for the treatment of coagulopathy from massive transfusion. The population of patients discussed here meets the criteria for massive transfusion and is known to be hemostatically competent before the traumatic event. Massive transfusion in patients with preexisting coagulopathies, including liver disease, is not discussed because it is beyond the scope of this review.
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