1. Sultan Qaboos University Hospital
Internship - Medicine Block
Gastroenterology Rotation
hepatology & Liver transplantation Division
Hemostasis in
cirrhotic patient
Ali Ahmad Al-Mashani
2. Introduction .
--12th leading cause of death in the united
states in 2002
-On average about 27,000 deaths per year
-Patients with cirrhosis are susceptible to a
variety of complications and their life
expectancy is markedly reduced
4. normal physiology of hemostasis
-Individuals with liver disease have a variety of hemostatic abnormalities, resulting
in "rebalanced" hemostasis.
- increase risks of bleeding as well as thrombosis
6. Thrombocytopenia and platelet
dysfunction
-may be normal .
-mild (100-140)75% & moderate (50-100 ) 13%
-reduced plt count? What are the causes?
-impaired platelet production, from decreased hepatic
synthesis of thrombopoietin
-bone marrow suppression, from hepatitis C virus (HCV)
infection or alcohol use, other infection
-antiviral therapy .??
-increased platelet sequestration in the spleen, in the
setting of portal hypertension and hypersplenism
7.
8. Effects Of Hepatic Dysfunction on
hemostasis
- diminished hepatic function leads to both
procoagulant and anticoagulant effects.
9. Coagulation factor defects
-The liver is the site of
production of almost all
of coagulation factors.
EXCEPT?
- hepatocytes also make
post-translational
modifications such as
glycosylation and
gamma-carboxylation of
some factors. Both
synthesis and post-
translational
modification may be
impaired in liver disease
10. Prothrombotic changes
1-the liver also produces endogenous inhibitors of
coagulation
2-ADAMTS13 :clears von Willebrand factor (VWF), which
is produced in endothelial cells. Liver disease may
contribute to a prothrombotic state because these
natural inhibitors may be reduced .
3-Reduced vascular flow also contributes to
prothrombotic tendencies. Examples include stasis in the
portal circulation and lower extremity venous stasis due
to peripheral edema.
11. IMPORTANT
-conventional tests are very poor at predicting
the risk of bleeding in individuals with liver
disease because they only reflect changes in
procoagulant factors
-While these prothrombotic changes are
increasingly appreciated, standard tests of
coagulation do not measure them.
12. Plt transfusion in cirrhotic patient
-is it necessary ?
-what is the cut point for transfusion?
-what are the indication ?
-Thrombopoietin receptor agonists ?
13. plasma products transfusion?
-not routinely administer FFP or Cryoprecipitate to
"correct" the PT/INR value prior to a procedure,
because several large reviews of available evidence
have shown no clinical benefit .
-Additional risks and disadvantages of giving FFP
include transfusion reactions, volume overload .
Administration of FFP also may create a significant
delay while awaiting ABO typing, thawing of FFP,
administration, and repeated laboratory testing of
the PT/INR .
14. Hematological complications
Since there are imbalance in hemostasis in
cirrhotic patient so the patient will develops
complications:
-portal vein thrombosis
-hepatic vein thrombosis (budd chiari syndrome)
-deep vein thrombosis
15. Hematological complications
Since there are imbalance in hemostasis in
cirrhotic patient so the patient will develops
complications:
-portal vein thrombosis
-hepatic vein thrombosis (budd chiari syndrome)
-deep vein thrombosis
16. Our Case
-Dawood , A 33 yrs old pateint follow hepatolgy
clinic at SQUH due to decompensated liver
cirrhosis
-he is diagnosed with HBV since 7 yrs but was
noncompliant
-he did not have either hepatic encephalopathy
or variceal bleeding
-he had ascites
18. Budd Chiari Syndrome
-Any process that interrupts blood outflow from
the liver: hepatic venous outflow obstruction
19. - if the patient has a separate indication for
anticoagulation, we do not consider cirrhosis to
be a contraindication for the use of an
anticoagulant, following assessment and
treatment of high-risk varices if present.
20. Signs and Symptoms
-Abdominal Pain
-Hepatomegaly
-Ascites
-N/V
-Jaundice, esp if acute-
-Venous collateralization – varices,
abdominal/flank collaterals
21. So ,what are the
causes?
FIRST THINK
-Hypercoagulable
-Polycythemia vera
-Other myeloproliferative
diseases
-Multiple causes in one
person
often see + JAK2
mutation
27. How to diagnose?
-Clinical context + imaging
-Liver U/s + doppler: first choice
-CT Abdomen
-MRA Abdomen: as for CT; can help distinguish acuity-
-Gold standard ?
28. Liver Ultrasound with Doppler Studies
normal right hepatic
vein
doppler study showing
normal expected biphasic
waveform across hepatic
vein
no hepatic vein, no venous
flow
29. Tx
●Prevent the
propagation of the
clot
●Restore
patency of
thrombosed
veins
●Decompress
the congested
live
●Prevent or
manage
complications
General Approach to the Tx
30. Management
General Approach :
●Prevent the propagation of the clot
•Anticoagulation
●Restore patency of thrombosed veins
•Thrombolysis
•Angioplasty/stenting
●Decompress the congested liver
•Transjugular intrahepatic portosystemic shunt (TIPS) placement
•Surgical shunting
●Prevent or manage complications
•Treatment of portal hypertension
•Liver transplantation
31. We recommend that nearly all patients be
started on anticoagulation at the time of
diagnosis & the risk of anticoagulation should be
considered
32.
33. •OUT OF 26 PATEINTS: Primary patency was
76.5%, and primary assisted patency was 94.1%.
-Two patients with TIPS and two with surgical
therapy maintained excellent results.
-The medical treatment remained effective only in a
limited group of 6 (21.4%) of the 28 patients.
