Literature acquired bleeding disorder and hypercoagulable state, or

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Literature defines the complex pathophysiology associated with
chronic liver disease (CLD). The liver is involved in synthetic functions such
as; production of procoagulant factors (I, II, VII, X), anticoagulant factors
(antithrombin, protein C & S), and colony stimulating factor for thrombocytes
– thrombopoetin. Patients with CLD have pathology of elevated INR,
thrombocytopenia (defined as in citation), and an “auto-anticoagulation” state
with lowered procoagulants, factor VIII and von Willebrand factor, and increased
anticoagulants, antithrombin and protein C. These four biological products are
arguably the most important pieces to understanding the complex physiology of autoanticoagulation
in patients with CLD to prevent an acquired bleeding disorder and hypercoagulable
state, or a venous thromboembolism (VTE). The primary aim of this drug consult is
to evaluate the safety in patients by not causing a bleeding event and efficacy
of preventing a HA-VTE.


Being able to assess whether a patient with CLD needs VTE prophylaxes,
either mechanical or pharmacological, upon and during the hospital admission is
a key risk factor stratification technique medical teams should use to address
the fragile hemostasis that exists in CLD patients. The mechanism in which a
VTE can happen is simplified by Virchows Tirad. It proposes that a change or
alteration in blood flow, vascular endothelial injury, and(or) alterations in
the constituents of the blood (ie, inherited or acquired hypercoaguable state).

In an observational study aimed to look at the incidence and attack rates of
VTE showed the incidence rates of VTE were 104 and 128 per 100,000 with less
than half of the patients receiving prophylaxis during high risk periods prior
to an attack.1,2 This suggests that medical teams should be looking
to identify at risk patients and carefully monitor them for improvement.

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While CLD patients do exhibit a newly rebalance hemostasis,
it does not make them less susceptible to any prevailing attacks from
infections, surgery, hemorrhagic, or thrombotic directions. A retrospective
study looking to demonstrate the risk for VTE or pulmonary embolism in patients
with cirrhosis and noncirrhosis liver found there is an increased risk for
cirrhosis than noncirrhossis and there is an increased risk for the
manifestation of a thromboembolism. 3


Another single-center, retrospective cohort analysis sought
out to measure the incidence of VTE in CLD hospitalized patients over a 3-year
period undergoing trauma, surgery of a history of VTE. With 1581
hospitalization, 392 (24.7%) patients received pharmacologic VTE prophylaxis. The
incidence of VTE in the prophylaxis group was significantly lower by 1.3% from
1.8% prevalence in patients not receiving prophylaxis. Additionally, bleeding
rates were also lower by 8.2% (p<0.001). Overall, VTE prophylaxis was associated with a decreased incidence of VTE (OR 0.34, 95% CI 0.04-0.88).   Aforementioned studies describe there is some benefit when providing thromboprohylaxis. Limited data is available to support the efficacy and safety of thromboprophylaxis in patients with CLD.   A hospital in Spain sought out to evaluate the safety of anticoagulation theray and efficacy regarding the rate of rethrombosis after restoring blood flow. When treating patients with cirrhosis with a anticoagulant from 2003 to 2010. They analyzed 55 patients with cirrhosis and portal-vein thrombosis receiving anticoagulation for an acute thrombosis (31 patients) and progression of a previous PVT (24 patients). 26 patients were on anticoagulation therapy with low molecular weight heparin (LMWH) and 29 with vitamin K antagonist. 4   The clinical events during anticoagulation therapy show liver events were 27% more frequent in patients not achieving a restoration of blood flow, yet not shown to be statistically significant (P=0.1%). Additionally, there were five bleeding episodes documented which were likely attributable to the anticoagulation therapy. Eleven patients were observed having a bleeding episode with labs documented with low platelets during the use of vitamin K antagonist therapy (VKA). It's important to note this likely implies some safety implications towards patients with a low platelet count defined at <50 x 109/L.

Also, their data suggests that early initiation of anticoagulation therapy was
associated with restoration of blood flow and improves the outcome in patients
studied with cirrhosis. The use of anticoagulation therapy was regarded as generally
safe due to the 11 bleeding episodes and zero deaths associated with treatment.

In terms of pharmacotherapy, while it was not statistically significant, VKA
was associated with an increased bleed risk compared to LMWH. The authors
conclude anticoagulation is relatively safe and effective treatment for
patients with cirrhosis and PVT.4

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