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Coagulopathy


Definition

Coagulopathy is defined as a condition in which the blood’s ability to clot is impaired. Sometimes the term is used to represent both hypocoagulability and hypercoagulability. In this chapter we will be limiting our discussion primarily to hypocoagulability.

Causes

The normal coagulation cascade at a localized site seals any breach in vascular continuity and limits blood loss. Failure of this process to advance places the patient at risk of bleeding. The main concern is bleeding in a closed compartment, such as intracranial or intraspinal, which may result in hazardous consequences. The major causes of coagulopathy in a neurosurgical patient are listed in Table 1 . Patients with a history of venous thromboembolism, stroke, coronary artery stents, prosthetic heart valves, and intracardiac thrombus are usually on anticoagulant therapy and antiplatelet drugs. They may present for some elective neurosurgical procedure or for emergency surgery secondary to development of an intracranial hemorrhage requiring urgent reversal of coagulopathy. The decision regarding cessation of drug therapy has to be taken in consultation with cardiologist, hematologist, and neurosurgeon. Patient and his family should be explained clearly about the risk of development of thromboembolism with cessation of drugs or occurrence of bleeding in case they are continued ( Table 2 ).

Table 1
List of Various Causes of Coagulopathy

  • Congenital

  • Hemophilia

  • Von Villebrands disease

  • Factor V, factor VIII, protein C, antithrombin III deficiency

  • Afibrinogenemia

  • Acquired

  • Massive blood loss

  • Dilution of coagulation factors and platelets by fluid resuscitation and blood transfusion

  • Disseminated intravascular coagulopathy

  • Sepsis

  • Drugs

  • antiplatelet agents—aspirin and other NSAIDS

    • Clopidogrel, ticlopidine

    • Glycoprotein IIb/IIa receptor antagonist (tirofiban, eptifibatide)

  • anticoagulants (warfarin, heparin, enoxaparin, dalteparin)

  • fibrinolytics (streptokinase, urokinase, alteplase, reteplase)

  • Severe liver disease

  • Vitamin K deficiency

  • Thrombocytopenic purpura

  • Hypothermia

  • Citrate toxicity

NSAIDS, Nonsteroidal antiinflammatory drugs.

Table 2
Work Up for Diagnosis of Coagulopathy

  • Complete Medical History (Present and Past)

  • Past surgical history

  • History of trauma

  • Drug history

  • Family history

  • Physical examination

  • Laboratory tests for

  • enzymatic coagulation

    • Prothrombin time/international normalized ratio, Activated Partial thromboplastin time, thrombin time, thrombin–antithrombin III complex,

    • prothrombin cleavage fragments, thromboelastography, rotational thromboelastometry.

  • fibrinolyis

    • d-dimer, fibrinogen degradation product, plasminogen activator inhibitor-1,

    • throboelastography, rotational thromboelastometry.

  • platelets

  • Platelet count, bleeding time, platelet function analyzer, rapid platelet function assay.

  • Whole-blood impedence aggregometry, thromboelastography, rotational thromboelastometry.

Brain Tumors

Brain tumors are known to cause coagulation abnormalities resulting in either hypercoagulability or less commonly hypocoagulability. Patients with benign tumors were found to have reduced coagulant property while those with malignant tumors had increased fibrinolytic activity. This hemostatic abnormality is due to hyperfibrinolysis either primary or secondary to disseminated intravascular coagulopathy (DIC). Tissue plasminogen activator released from tumor cells or from brain parenchyma during surgery may lead to development of DIC. This consumptive coagulopathy thus results in hyperfibrinolysis raising the risk of bleeding.

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