DISSEMINATED INTRAVASCULAR COAGULATION AND THROMBOSIS

23 DISSEMINATED INTRAVASCULAR COAGULATION AND THROMBOSIS



1 What is disseminated intravascular coagulation (DIC)?


Disseminated intravascular coagulation is the result of a primary inflammatory or tissue-damaging process. DIC is a complex syndrome involving a transition between accelerated activation of platelets, coagulation proteins, and plasmin evolving into consumption of coagulation proteins, platelets, and inhibitors of fibrinolysis. Coagulation is accelerated systemically when the following occur:


a. Blood comes into contact with tissues containing tissue thromboplastin or subendothelial collagen.

b. Significant quantities of circulating white blood cells, inflammatory mediators, or cytokines are present.

c. Significant contact occurs between coagulation proteins and phospholipids from platelets or red blood cells (RBCs).

d. Circulating tissue debris is present from RBCs, tissue necrosis, tumor tissue, or heartworms.

Uncontrolled coagulation leads to rapid consumption of platelets, consumption or degradation of coagulation proteins, and consumption or degradation of natural anticoagulants—DIC.



2 How is DIC diagnosed?


The diagnosis of DIC is based on clinical suspicion, knowledge of the pathophysiologic mechanisms responsible in associated diseases, and abnormal serial tests of hemostasis indicative of this secondary process. The clinical signs of DIC depend on the phase the patient is experiencing. The phase of DIC depends on the intensity of the underlying disease, concentration and variety of inhibitors present, and length of time the coagulation mechanisms are exposed to the initiators. An ideal hemostasis laboratory profile includes the prothrombin time (PT), activated partial thromboplastin time (aPTT), platelet count, fibrinogen concentration, fibrin-fibrinogen degradation product (FDP) concentration, and antithrombin III (AT-III) concentration. These tests should be serially evaluated to determine trends in any patient thought to have a primary disease likely to initiate DIC but with nondiagnostic test results.



3 Describe the phases of DIC.



a. Peracute (hypercoagulable) phase, characterized by no or few overt clinical signs

b. Acute (consumptive) phase, characterized by venipuncture oozing or modest hemorrhage

c. Chronic phase, characterized by no clinical signs of oozing blood


4 What are the laboratory test expectations in the peracute or hypercoagulable phase of DIC?


The PT and aPTT are within reference limits or have a shortened time (below reference limits) in the peracute phase. Platelet numbers are normal, which should increase clinical suspicion because platelet counts in most systemic inflammatory disorders are at the upper end of the reference interval or above the reference interval. Fibrinogen concentration is appropriate or modestly declining, which should also increase clinical suspicion because fibrinogen concentration in most systemic inflammatory disorders is at the upper end of the reference interval or above the reference interval. FDP and AT-III concentrations are within the reference range.



5 What are the laboratory test expectations in the acute or consumptive phase of DIC?


The laboratory findings in the acute phase are most characteristic of DIC. This includes prolongation of the PT and aPPT, decreasing platelet numbers, decreasing fibrinogen concentrations, increasing FDP concentrations, and decreasing concentrations of AT-III.



6 What are the laboratory test expectations in the chronic phase of DIC?


The PT and aPTT remain prolonged in the chronic phase. Platelet numbers remain decreased. Fibrinogen concentration is most unpredictable and may be within reference limits or severely decreased. The concentration of FDPs depends on the adequacy of the mononuclear phagocytic system (MPS). If the MPS in the liver and spleen is not overwhelmed by tissue and hemostatic debris, FDPs will remain appropriate or mildly elevated. If the MPS is fully saturated with tissue and hemostatic debris, FDPs will be notably elevated. The concentrations of AT-III may remain decreased in more fulminant clinical situations or return toward baseline or the reference interval in less fulminant situations.



7 Is the activated coagulation (aCT) time useful in the laboratory diagnosis of DIC?


Activated coagulation time (aCT) examines the intrinsic and common coagulation pathways. Therefore aCT identifies the same coagulation protein problems as aPTT. Accomplished serially, aCT will help define trends. It is much less sensitive than the aPTT; aCT requires marked deficiencies in coagulation proteins before becoming prolonged. If a process associated with DIC is suspected and the aCT result is within reference limits, aPTT should be performed. If the aCT result is prolonged, however, there is no need to perform aPTT because it also will be prolonged. Remember that there is potential for prolongation of aCT if the platelet count is greatly decreased. Marked thrombocytopenia will not cause prolongation of aPTT.



8 List clinical diseases and their initiators in DIC.



a. Systemic inflammatory response syndrome (SIRS) initiates DIC by exposure of subendothelial collagen, accelerating the immune response, release of inflammatory mediators, and in pancreatitis, release of trypsin. Uncontrolled immune-mediated cellular destruction results from circulating RBC membrane phospholipid, cellular debris, and cytokine release.

b. Trauma and burns can initiate DIC by similar mechanisms to SIRS and immune-mediated disease.

c. Metabolic acidosis and severe shock result in exposure of subendothelial collagen. Shock also accelerates the immune response and prevents clearance of activated coagulation proteins and delivery of coagulation protein inhibitors.

c. Neoplasia exposes subendothelial collagen and results in increased concentrations of intravascular tissue debris.

d. Hepatosplenic disease results in inadequate production of coagulation proteins and inadequate clearance of activated coagulation proteins and tissue debris.

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Aug 26, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on DISSEMINATED INTRAVASCULAR COAGULATION AND THROMBOSIS

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