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Emergency War Surgery NATO Handbook: Part II: Response of the Body to Wounding: Chapter X: Compensatory and Pathophysiological Responses to Trauma

Hematologic and Clotting Subsystems

United States Department of Defense
Peer Review Status: Internally Peer Reviewed


Certain casualties, such as those with heart or liver wounds and those with pelvic crush injuries, require very substantial infusions of whole blood. Very often, ten units of blood will have been infused before operative control of the source of hemorrhage is controlled. In the combat zone, it is not uncommon for bank blood to be nearing its expiration date. This combination of circumstances set the stage for catastrophic cardiac arrhythmia. The elevated potassium concentration of old bank blood, when infused directly into a cardiac chamber, can precipitate fatal arrhythmias. The same complication can result from infusion of large quantities of cold blood. The blood should be warmed, and infusion directly into the right atrium should be avoided.

Another common and very serious complication in this sort of circumstance is the development of a diffuse bleeding diathesis. Some degree of coagulopathy occurs routinely after about ten units of infusion and worsens as the blood requirement increases. The diathesis can be avoided, lessened, or corrected with infusions of fresh frozen plasma and platelet packs. If these components are not available, freshly drawn blood, less than 24 hours old and procured within the facility from the walking donor pool, should be employed. If the hemorrhage or diathesis persists, requiring massive transfusion, about every fourth unit should be freshly drawn. Bank blood becomes progressively platelet- and clotting-factor-deficient from the third day on. Citrate in banked blood aggravates the situation. When available to the surgeon, therapy is based on the results of the platelet count, partial thromboplastin time, prothrombin time, and the fibrinogen level. With lesser laboratory capability, the surgeon must anticipate the diathesis and resort to empiricism.

Anemia will develop in those casualties where large volumes of asanguineous fluids were utilized to treat hemorrhagic shock. Reticuloendothelial system removal of damaged bank red cells and the excessive drawing off of blood for laboratory tests will contribute to the anemia.

Disseminated intravascular coagulation (DIC) may develop in association with shock, tissue injury, or sepsis. Consumption of clotting factors by disseminated intravascular microthrombi give rise to the consumptive coagulopathy. The casualty with DIC may present a clinical spectrum ranging from a simple hypercoagulability state to fulminant consumptive coagulopathy resulting in massive diffuse bleeding. Therapy includes correction of the shock state, appropriate wound debridement, and treatment of sepsis. In the presence of laboratory evidence of DIC and elevated levels of circulating fibrin degradation products, patients with a bleeding diathesis may be treated with repeated small doses of heparin.

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