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INTRODUCTION

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Although uncommon, significant hemorrhage, coagulopathy, and need for transfusion are encountered by every practicing obstetrician. We often walk a fine “tight rope” trying to determine when to deliver a patient or when to wait longer. With our increasing emphasis on preventing prematurity, we are being more conservative in treating preeclampsia and patients with third trimester bleeding. The possible trade-off more abruption and HELLP (hemolysis, elevated liver enzyme levels, and low platelet levels) syndrome; hence more disseminated intravascular coagulopathy (DIC). Prevention is obviously superior to treatment. By understanding the pathophysiology and events that lead to these potentially catastrophic clinical situations, we can respond more rapidly and often prevent them from progressing to critical situations. Even with meticulous care, we cannot prevent all such cases. Rapid, decisive, and knowledgeable action on the part of the obstetrician can usually avert an adverse outcome. In this chapter, I cover the areas of clinical DIC and clinically significant thrombocytopenia. The best form of therapy is aimed at correcting the underlying pathophysiologic problem, as well as treating the acquired or inherent clotting problem. There are many ways to treat these clinical entities. This chapter outlines a practical approach to these patients with these complications.

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DISSEMINATED INTRAVASCULAR COAGULOPATHY

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Disseminated intravascular coagulopathy describes a clinical scenario that can be initiated by many pathologic processes. It is characterized by accelerated formation of fibrin clots with simultaneous dissolution of these same clots. It is, indeed, a consumptive coagulopathy. The body consumes clotting factors faster than they can be produced in the liver and endothelial cells. This cycle keeps repeating until an intervention stops the cycle or the patient succumbs to hemorrhage. Normally, our body is in a constant balance between fibrin generation and fibrinolysis. When this delicate balance is disturbed and the coagulation cascade and fibrinolytic systems go unchecked, DIC can result. DIC may arise from massive activation of the coagulation system that overwhelms endogenous control mechanisms. This is usually the result of activation of the intrinsic clotting system. DIC, however, may be initiated by exposure of blood to tissue factor, which triggers activation of the factor VII and the extrinsic clotting system. This may be the result of trauma or endotoxins damaging tissue. Also, proteolytic enzyme release may trigger DIC and can occur in events such as placental abruption. Endotoxins, from sepsis can occasionally be the initiating factor. This critical clinical picture, therefore, can have many etiologies that manifest similarly. For truly effective treatment, one must rapidly determine the etiology while initiating therapy.

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Etiology

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The most common obstetric causes of DIC are listed in Table 4-1. The most common underlying cause of mild DIC encountered by the obstetrician is probably underestimation of blood loss at the time of vaginal or cesarean delivery with inadequate replacement by crystalloid or colloid. In these cases, vasospasm occurs with resultant endothelial damage and initiation of DIC. Also, in these instances, ...

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