DISSEMINATED INTRAVASCULAR COAGULATION

Disseminated intravascular coagulation (DIC), also termed as consumption coagulopathy, is a common and potentially life-threatening problem, characterized by disproportionately excessive activation of coagulant mechanisms, which leads to:

• Generalized microvascular thrombosis (tissue ischemia/necrosis),

• Consumption of coagulation factors (bleeding tendencies) and

• Excessive fibrinolysis (elevated levels of fibrin degradation products).

Etiopathogenesis: DIC is usually a terminal event in many serious illnesses, e.g.

While clinical presentations are primarily hemorrhagic, disseminated tissue injury is predominantly caused by extensive fibrin deposition in microvasculature and consequent tissue ischemia (Fig. 19.12). Intravascular sludging of RBCs leads to microangiopathic haemolytic anemia. Destruction of excessive formed fibrin in thrombotic process is responsible for increase in fibrin degradation products (FDPs) in these cases.

Clinical features: Most cases are seriously sick with primary disease, when they develop sudden bleeding from venipuncture sites and generalized petechiae, ecchymosis and gangrenous infarctions of skin and subcutaneous tissues.

Rapidly, these cases progress to develop systemic bleeding diathesis with GIT, urinary and pulmonary hemorrhage as terminal events. Features of precipitating event are almost always present.

Investigations: Diagnosis is largely clinical, supported by—(a) thrombocytopenia, (b) abnormal clotting tests

TABLE 19.26: Causes of DIC

• Infections: Gm -ve sepsis, meningococcemia*

• Post-hemorrhagic: Head injury, crush injuries

• Metabolic: Hypoxia, shock, hypo-#8725;hyperthermia

• Poisonings: Snake/insect bites

• Microangiopathy: Hemolytic-uremic syndrome

• Malignancies: Promyelocytic leukemia, others

• Acute hepatic failure and Reye syndrome

• Miscellaneous: Mismatched transfusions

*Purpura fulminans

( PT, aPTT, TT), (c) microangiopathic haemolytic anemia on peripheral smear (fragmented, burr and helmet-shaped erythrocytes) and (d) presence offibrin degradation products (FDPs); last being a common screening test. D-dimer assay (a FDP itself) is equally sensitive but more specific than FDP levels.

Management of DIC includes:

• Treatment of primary cause, e.g. sepsis, acidosis, hypoxia, etc.

• Pro-coagulant therapy with 12-24 hourly infusions of FFP (10-15 ml/kg) and platelet concentrates (frac12;-1 bag), to maintain platelet counts gt;50,000/mm3 and fibrinogen levels gt;75 mg/dl.

• Anti-coagulant therapy with heparin is indicated in selected cases (slow infusion of 5-10 U/kg/hr) to maintain aPTT at ~ 1.5-2.0 times of normal.

Despite clinical improvement in bleeding/thrombo- embolic manifestation and correction of laboratory parameters, heparin does not alter the course of DIC due to underlying disease process. Heparin therapy should not be used in septic shock, snake-venom poisoning, heat stroke, head injury and transfusion reactions, unless vascular thrombosis is certain. Antithrombin-III concentrates may be used with heparin in selected cases.

19.14