CHAPTER 89 MANAGEMENT OF COAGULATION DISORDERS IN THE SURGICAL INTENSIVE CARE UNIT
Surgeons commonly encounter coagulation disorders in the course of caring for patients, especially those with serious injury and those undergoing or recovering from surgery. Whereas bleeding is a condition well known to man since the beginnings of time, understanding the pathophysiology of bleeding and coagulation and developing effective therapies for them have come relatively recently and continue to undergo change as more is learned about the complex mechanism of blood coagulation and fibrinolysis. The ability to treat hemorrhage effectively had to await the discovery of blood types A, B, and O by Karl Landsteiner in 1900 and the AB blood type by Alfred Decastello and Adriano Sturli in 1902.
INCIDENCE
Congenital Bleeding Disorders
Von Willebrand Disease
1-deamino-8-D-arginine vasopressin (DDAVP) may be used to stimulate production of vWf and increase factor VIII levels in type 1 and type 2a disease. It is ineffective in type 3, however, and contraindicated in type 2b due to risk of thrombocytopenia and increased bleeding. Concentrates of factor VIII vWf are virus inactivated and are used commonly in types 2 and 3, but also in type 1 that is unresponsive to DDAVP. Cryoprecipitate contains vWf and factor VIII, and may be used in all types of vWD. However, it is pooled and not virus inactivated. It is only recommended as a third-line therapy. Antifibrinolytic amino acids, such as aminocaproic acid and tranexamic acid, are used as adjuvant therapy in all types of vWD along with the previously cited treatments.
Acquired Bleeding Disorders
Acidosis
Metabolic acidosis has long been recognized as a consequence of, and contributor to, coagulopathy. However, the specific pathways whereby acidosis impairs coagulation have yet to be clearly defined. Animal data suggest that hypothermia induces a delayed onset of thrombin formation, whereas acidosis decreases the overall thrombin generation rate. The association of severe acidosis (pH < 7.1) with hypotension and hypothermia in severely injured patients virtually guarantees life-threatening coagulopathy. Therapy is again directed at the cause of acidosis and not merely the correction of the pH. While simultaneously addressing the inciting events, lactic acidosis is treated with fluid resuscitation to optimize tissue perfusion. It can be guided by following the trend in base deficit or lactate level. Sodium bicarbonate administration is ineffective and potentially harmful in lactic acidosis, and is not recommended.