Page 211 - Critical Care Notes

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Pathophysiology
■ In cirrhosis, FVII and protein C are the first to fall → a low FVII level, resulting
in a prolonged PT. The remaining vitamin K–dependent factors decrease →
prolonged aPTT. The fibrinogen level is usually maintained until end-stage
disease. Because of impaired synthetic function → factors and fibrinogen
may be functionally abnormal.
■ In acute toxic or infectious hepatitis, impairment of coagulation correlates
with the severity of cell damage.
Unlike the situation with other types of coagulopathy → coagulation factors
and fibrinogen may be dysfunctional → because of abnormal hepatic synthet-
ic function platelets may be dysfunctional by circulating FDPs that the liver fails
to clear.
Clinical Presentation
■ Bleeding
■ Prolonged PT, activated PTT (aPTT)
■ Elevated FDPs
■ Low platelet count
Diagnostic Tests
■ PT/PTT
■ D-dimer assay
■ Fibrin degradation/split products
■ CBC
■ Liver function tests
Management
■ Administer FFP.
■ Administer platelets.
■ Administer vitamin K.
■ Administer desmopressin acetate (DDAVP) 2-4 mcg/d IV in two divided
doses IV by direct injection or SC (may improve platelet function).
Massive Transfusion
Coagulopathy can be caused by massive transfusion when the replacement of
1 or more blood volumes occurs in a 24-hr period (1 blood volume in a 70-kg
adult is about a 5-L blood loss or transfusion volume of 10 units of packed red
blood cells [PRBCs]). Common complications of massive transfusion are dilu-
tional coagulopathy, DIC and fibrinolysis, hypothermia, citrate toxicity,
hypokalemia, hyperkalemia, and infection.
Pathophysiology
Dilutional thrombocytopenia is the most common cause of bleeding after mas-
sive transfusion. If ongoing blood loss is replaced with only PRBCs →↓ in platelet
count → splenic pool mobilizing and counteracting loss during hemorrhage. If
patient’s count was high prior to transfusion → remainder may be adequate to
HEMA/
ONCO