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.

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.

Etiology

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, hypotension occurs, which results in decreased tissue perfusion leading to local hypoxia and tissue acidosis, which further exacerbates DIC by causing tissue release of cytokines. By keeping the patient’s volume replete, DIC can often be avoided, even in the presence of profound anemia. One of the best ways to prevent this at time of cesarean delivery is to constantly inform the anesthetist/anesthesiology about ongoing blood loss.

Following placental separation after a vaginal delivery, fibrinogen is activated to become a fibrin mesh, which covers the placental site on the endometrium. This, along with uterine contraction, prevents excessive blood loss in the immediate postpartum period. The genesis of this fibrin mesh results in an immediate 10% reduction in the concentration of fibrinogen following a normal vaginal delivery. Placental abruption is a similar situation gone awry. In severe cases, before delivery, the placenta almost completely detaches from the wall of the uterus and a retroplacental clot forms. As the clot expands, it consumes coagulation factors, which continually break down because of ongoing fibrinolysis. This results in a consumptive coagulopathy. While clinical bleeding is “realtime,” the laboratory values are like a delayed “replay.” Therefore, DIC should be suspected with any significant abruption. The earliest laboratory sign of DIC is a significant fall in fibrinogen, which is being consumed as it is converted to fibrin. It is important to note that the concentration of clottable fibrinogen is usually greatly increased during a normal pregnancy. A concentration that is “labeled” as normal by your laboratory may, indeed, be abnormally low for a pregnant patient with an abruption of postpartum hemorrhage. Therefore, the clinician should not be lulled into a false sense of security when the fibrinogen concentration is normal. A “low-normal” fibrinogen concentration may actually be a significant drop for the individual patient, representing early DIC. The clinician must rely on the overall clinical picture, because a “baseline” fibrinogen concentration is usually not available.

Severe preeclampsia and HELLP (hemolysis, elevated liver transaminases, low platelets) syndrome can result in DIC, if delivery is not effected promptly. Often, these patients show isolated thrombocytopenia, which should not be confused with DIC in the absence of clinical bleeding or other coagulation abnormalities. This isolated thrombocytopenia is due to increased platelet destruction by the reticuloendothelial system or decreased platelet synthesis in the bone marrow, and is not a consumptive coagulopathy. If the mean platelet volume (MPV) is increased, this signifies that immature platelets are being released into the circulation. This is an indication that increased platelet destruction by the reticuloendothelial system is the cause of the thrombocytopenia. Clinical DIC in these cases is uncommon, unless delivery is delayed in the patient with preeclampsia/HELLP or if the associated hypertension results in a placental abruption. Laboratory evidence of subclinical DIC, nevertheless, is common in preeclamptics. This may manifest as an increased D-dimer, which is unreliable in pregnancy, as D-dimer may be elevated in normal pregnancy.

There is a common misconception that a retained dead fetus commonly results in DIC. This rarely occurs and usually takes several weeks to develop. This can rarely be seen with the demise of one fetus in a twin pair in mid-gestation, with long-term conservative management of the other twin. With effective cervical ripening agents, there is no reason to expectantly manage the intrauterine demise for extended periods. If, however, an unsuspected demise is discovered and it appears that the fetus expired some time previously, a coagulation profile is indicated, but will only rarely show evidence of DIC.

Sepsis, regardless of cause, can be associated with DIC. Obviously, any infection should be treated aggressively with broad-spectrum antibiotics. Most hospitals have a readily accessible sepsis protocol, and this should be followed. However, the antibiotic regimen may need to be altered because of pregnancy and the patient’s allergy profile.

Diagnosis of DIC

The presumptive diagnosis of DIC is usually made clinically, with confirmation made through laboratory studies. Table 4-2 shows readily available diagnostic tests. In obstetrics, a falling fibrinogen concentration is usually the hallmark of DIC. It is important to remember that the prothrombin time (PT) is affected by disorders of the vitamin K–dependent, extrinsic clotting system (factors II, VII, IX, X). The PT/INR (international normalized ratio) will often become prolonged before there is prolongation of the activated partial thromboplastin time (aPTT) in DIC. This is because the aPTT depends on the intrinsic clotting system, which includes factor VIII. Not only does factor VIII normally increase during pregnancy, but it also increases early in the course of DIC, secondary to a release of factor VIII/von Willebrand factor, from damaged endothelial cells. However, as the DIC becomes overwhelming, the aPTT will also become prolonged. Tests of fibrin degradation such as fibrin degradation products and D-dimer will also be elevated. However, in normal pregnancy, one can often find mildly elevated levels of these tests. No single test should be used in assigning a diagnosis of DIC.

Treatment

The basic treatment for DIC is to reverse the inciting event. Simultaneously, blood component therapy should also be initiated, if needed. Blood products should not be used frivolously. However, with blood bank initiatives to decrease blood component use we are often too reticent to initiate blood component therapy. DIC is more easily reversed when treated immediately. In cases of severe uterine atony, many have become enamored with the intrauterine balloon. It is a great tool to help staunch bleeding. It does not treat ongoing consumptive coagulopathy. Blood products can be lifesaving in DIC. Even in the largest hospitals, it often takes a long time to receive fresh frozen plasma (FFP), platelets, or cryoprecipitate from the blood bank. In small hospitals, these components must often be transported from the local Red Cross. If you feel that there is a possibility that you will need blood components, order them early. Time can be crucial. Therapies are outlined in Tables 4-3 and 4-4. It is crucial to realize that treatment should not be sequential, but that several forms of therapy should be occurring simultaneously. Therefore, if possible, two intravenous lines should be established and a Foley catheter should be in place. A true assessment of intake and output is essential. Aggressive fluid resuscitation can be accomplished while blood component therapy is given. Having an accurate assessment of the intake and output can potentially prevent iatrogenic pulmonary edema. In addition to the modalities listed in Table 4-4, recombinant activated factor VII can be used in life-threatening hemorrhage. A side effect is thrombotic phenomena. Therefore, it should be used only in the most refractory cases, and under the supervision of someone who is familiar with this agent. It is important to note that vitamin K and folate should be administered, as patients with DIC often develop deficiencies in these vitamins. There is some evidence that antithrombin III concentrate may promote endothelial healing and decrease fibrinolytic activity. It inactivates serine proteases. It should be used, if antithrombin III activity is low. It often takes a significant amount of time to receive the results of this testing. As previously mentioned, it is very easy to underestimate blood loss or underestimate the volume of crystalloid/blood components administered. It is crucial to keep meticulous track of this. If the patient is not given enough volume, she could develop acute renal failure making treatment and assessment even more difficult. Conversely, if an overabundance of fluid is administered, the patient can develop fluid overload and pulmonary edema.