Literature acquired bleeding disorder and hypercoagulable state, or

Literature defines the complex pathophysiology associated withchronic liver disease (CLD).

The liver is involved in synthetic functions suchas; 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” statewith lowered procoagulants, factor VIII and von Willebrand factor, and increasedanticoagulants, antithrombin and protein C. These four biological products arearguably the most important pieces to understanding the complex physiology of autoanticoagulationin patients with CLD to prevent an acquired bleeding disorder and hypercoagulablestate, or a venous thromboembolism (VTE). The primary aim of this drug consult isto evaluate the safety in patients by not causing a bleeding event and efficacyof 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 isa key risk factor stratification technique medical teams should use to addressthe fragile hemostasis that exists in CLD patients. The mechanism in which aVTE can happen is simplified by Virchows Tirad. It proposes that a change oralteration in blood flow, vascular endothelial injury, and(or) alterations inthe constituents of the blood (ie, inherited or acquired hypercoaguable state).In an observational study aimed to look at the incidence and attack rates ofVTE showed the incidence rates of VTE were 104 and 128 per 100,000 with lessthan half of the patients receiving prophylaxis during high risk periods priorto an attack.

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1,2 This suggests that medical teams should be lookingto identify at risk patients and carefully monitor them for improvement.   While CLD patients do exhibit a newly rebalance hemostasis,it does not make them less susceptible to any prevailing attacks frominfections, surgery, hemorrhagic, or thrombotic directions. A retrospectivestudy looking to demonstrate the risk for VTE or pulmonary embolism in patientswith cirrhosis and noncirrhosis liver found there is an increased risk forcirrhosis than noncirrhossis and there is an increased risk for themanifestation of a thromboembolism.

3  Another single-center, retrospective cohort analysis soughtout to measure the incidence of VTE in CLD hospitalized patients over a 3-yearperiod undergoing trauma, surgery of a history of VTE. With 1581hospitalization, 392 (24.7%) patients received pharmacologic VTE prophylaxis. Theincidence of VTE in the prophylaxis group was significantly lower by 1.3% from1.8% prevalence in patients not receiving prophylaxis. Additionally, bleedingrates were also lower by 8.

2% (p<0.001). Overall, VTE prophylaxis wasassociated with a decreased incidence of VTE (OR 0.34, 95% CI 0.04-0.

88).  Aforementioned studies describe there is some benefit whenproviding thromboprohylaxis. Limited data is available to support the efficacy andsafety of thromboprophylaxis in patients with CLD.

 A hospital in Spain sought out to evaluate the safety ofanticoagulation theray and efficacy regarding the rate of rethrombosis afterrestoring blood flow. When treating patients with cirrhosis with aanticoagulant from 2003 to 2010. They analyzed 55 patients with cirrhosis andportal-vein thrombosis receiving anticoagulation for an acute thrombosis (31patients) and progression of a previous PVT (24 patients).

26 patients were onanticoagulation therapy with low molecular weight heparin (LMWH) and 29 with vitaminK antagonist. 4 The clinical events during anticoagulation therapy showliver events were 27% more frequent in patients not achieving a restoration ofblood flow, yet not shown to be statistically significant (P=0.1%). Additionally,there were five bleeding episodes documented which were likely attributable tothe anticoagulation therapy.

Eleven patients were observed having a bleedingepisode with labs documented with low platelets during the use of vitamin Kantagonist therapy (VKA). It’s important to note this likely implies some safetyimplications towards patients with a low platelet count defined at <50 x 109/L.Also, their data suggests that early initiation of anticoagulation therapy wasassociated with restoration of blood flow and improves the outcome in patientsstudied with cirrhosis. The use of anticoagulation therapy was regarded as generallysafe due to the 11 bleeding episodes and zero deaths associated with treatment.In terms of pharmacotherapy, while it was not statistically significant, VKAwas associated with an increased bleed risk compared to LMWH.

The authorsconclude anticoagulation is relatively safe and effective treatment forpatients with cirrhosis and PVT.4

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