Coagulopathy in Liver Disease - Raghda Marzaban
-
Upload
mohammad-fadel-satriansyah -
Category
Documents
-
view
244 -
download
1
description
Transcript of Coagulopathy in Liver Disease - Raghda Marzaban
-
Hemostatic Disorder in Hepatic DiseaseDr. Tjatur Winarsanto SpPDRS CiremaiCirebon 2011
-
Coagulopathy is a medical term for a defect in the body's mechanism for blood clotting There are several possible causes that generally result in excessive bleeding and a lack of clotting.
-
Causes of coagulopathy:Inherited: - Deficiency of coagulation factor e.g Haemophilia (A/B), vonWillibrand disease, etc - Platelet disorder e.g Glanzmann thromboasthenia, platelel granule disorder, etc - Fibrinolytic disorder e.g plasminogen activator inhibitor-1 deficiency, etc
-
- Vascular e.g haemorrhagic telangiectasia.
- Connective tissue disorder e.g Ehlers- Danlos syndrome
-
Acquired: - Drugs; anticoagulants e.g warfarin, antiplatelet agents, myelosuppressents, haematotoxin venoms e.g certain species of snakes eg Bothrops, rattlesnakes and other species of viper, antithrombins, etc...
- Haematologic disorder e.g acute leukaemia, myelodysplasia, monoclonal gammopathy, etc
-
- Dissimination intravascular coagulopathy (DIC);acute e.g sepsis, trauma, obstetric, etc chronic e.g malignancies, giant haemangioma, etc
- Thrombocytopenia e.g autoimmune, hypersplenism, hypoplasia, etc
- Acquired antibodies to coagulation factors e.g antiphospholipid syndrome, etc
-
- Vitamin K deficiency e.g malabsorption, prolonged antibiotics, prolonged biliary obstruction, etc - Vascular e.g scurvy, Henoch-schnlein, vasculitis, etc - Renal failure.
- Liver disease.
-
Role of liver in coagulation: Synthesis of coagulation factors I, II, V, VII, IX & X [Vitamin K dependent factors are II, VII, IX and X ]
-
[ All coagulation factors are produced in the liver except for von Willebrand's factor which is produced in endothelial cells. Von Willebrand's factor is a major source of factor VIII however the spleen is also a source for factor VIII]
-
Inhibition of fibrinolysis / coagulation; the liver is responsible for synthesizing plasma anticoagulant proteins e.g. protein C, protein S and antithrombin III. Absorption of vitamin K
-
Clearance of activated coagulation factors; fibrin and tissue plasminogen activator (tPA) are removed from the circulation by the liver's reticuloendothelial system
-
Accordingly - The liver has a pivotal role in the coagulation process so it is not surprising that clotting abnormalities are a prominent feature of acute and chronic liver disease. - Liver disease can cause both quantitative and qualitative abnormalities in clotting factors.
-
The clinical presentation of hepatic coagulopathy depends on the severity and nature of the underlying disease A coagulation defect is suggested by:- Bleeding at any site; spontaneous or traumatic.- Acute viral / toxic hepatitis present with coagulopathy in only fulminant cases.
-
Factors that contribute to defective hemostasis in patients with liver disease
- Dysfibrinogenaemia. - Thrombocytopenia (autoimmune, folate deficiency, sequestrated in splenomegaly) - Qualitative platelet defects - Myelosuppression of thrombopoiesis (eg, by alcohol, hepatitis virus infection) - DIC
-
Laboratory Findings:
Prolonged Prothrombin time (PT) Fibrinogen levels are usually normal. Its synthesis is affected only in severe disease.
-
Factor V is affected first in disease.
Factor VII is the earliest of all to decline because of its short half-life (6 hours).
Factor VIII may be normal or even increased in liver disease except in the presence of DIC.
-
Platelet counts are normal unless spleen is also enlarged or the person recently drank alcohol
- Platelet function may also be affected i.e adhesion and aggregation. Hence, prolongation of bleeding time.
-
Liver function tests abnormal, depending on the type of liver disease (in end-stage liver disease, liver tests may become "normalized" because so much of the liver is now non-functioning.)
-
Treatment:Fresh frozen plasma infusion: - to replace deficient coagulation factors. - Administered=10-15 ml/kg, q12h; assess coagulation values after each infusion. - Plasma exchange may be considered if repeated infusions of fresh frozen plasma are required and there is evidence of volume overload.
-
in Vitamin K deficiency; - Vitamin K supplementation: Administer 10 mg subcutaneously; repeat parenterally in 24 hr.
- Prothrombin complex concentrate: may be used but it does not contain factor V and may result in thrombosis.
-
Platelet transfusion: in thrombocytopenia but may be ineffective in splenomegaly.
Cryoprecipitate infusion: administer if fibrinogen value
-
Heparin administration: may be considered if there is evidence of DIC; role is not well defined but not recommended for routine use
Antifibrinolytic agents: are adminstered prior to certain procedures like dental extraction provided that DIC is ruled out as they may enhance thrombosis.