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Tuesday, April 29, 2014

Weekly blog - DVT prophylaxis in cirrhotics

Two short snappers from our guest blogger EGM:

On DVT prophylaxis in liver cirrhosis: this topic has never been WELL studied.  There are about 7 retrospective studies that have looked at this topic and all of them had MAJOR limitations.

What do we know?

Patients with cirrhosis and an increased INR CANNOT be considered to be autoanticoagulated.
Thrombotic complications can be observed in patients with cirrhosis, despite standard coagulation laboratory tests revealing a prolonged PT/INR. They can have a prolonged PT but normal thrombin generation, as anticoagulant factors are also deficient in these patients.

The bottom line from the available literature:
-the INR is not predictive of the risk for DVT/PE in liver disease
-Decreased albumin may be associated with increased risk of DVT/PE in liver disease
-Patients with liver disease have at least the same degree of risk as patients with other chronic diseases and possibly more risk for DVT/PE.
-The perceived coagulopathy in patients with liver disease, as reflected in prolonged INR values, does not protect liver disease patients against venous thrombosis.

-It is better established that patients with liver resection, hepatocellular carcinoma or cholestatic liver disease appear to have increased risks for PE/DVT compared to other patients with chronic diseases.

References:

(TCL's notes)
Any choice for DVT prophylaxis must take into account the perceived benefits (DVT/PE prevention) vs. risks (bleeding) and needs to be individualized to the clinical context; though in general, is recommended for most acutely ill medical patients in the first 14 days of illness

The 2012 ACP guidelines on DVT prevention are here

What is the risk of DVT -- can I predict it? 
Score more than 4 = High risk = Consider prophylaxis based on risk

"VTE occurred in 11.0% of high-risk patients who did not receive prophylaxis vs 0.3% of low-risk patients"

Score below 4; low risk 

For acutely ill hospitalized medical patients at low risk of thrombosis (Table 2), we recommend against the use of pharmacologic prophylaxis or mechanical prophylaxis (Grade 1B).




With respect to risk of bleeding:
"the panel considered patients to have an excessive risk of bleeding if they had multiple risk factors or had one of the three risk factors with the strongest association with bleeding (OR > 3.0): active gastroduodenal ulcer, bleeding in 3 months before admission, and platelet count < 50 × 109/L"



With respect to continuing prophylaxis beyond 14 days:

" In terms of absolute effects, extended-duration enoxaparin prevented six fewer symptomatic proximal DVT per 1,000 (95% CI, from three fewer to seven fewer) at a cost of five more major bleeding events per 1,000 (95% CI, from one more to 14 more) (Table 9, Tables S10, S11). In addition to the bleeding risk, extended prophylaxis also entails the burden and cost of daily injection."



Also:
How to convert between Dabigatran and Warfarin (should you wish to do so...)
When converting patients from warfarin therapy to Dabigatran, discontinue warfarin and start Dabigatran when the INR is below 2.0.
When converting from Dabigatran to warfarin, adjust the starting time of warfarin based on creatinine clearance as follows:
• For CrCl >50 mL/min, start warfarin 3 days before discontinuing Dabigatran.
• For CrCl 31-50 mL/min, start warfarin 2 days before discontinuing Dabigatran.
• For CrCl 15-30 mL/min, start warfarin 1 day before discontinuing Dabigatran.
• For CrCl <15 mL/min: you shouldn’t be using Dabigatran.
Dabigatran can contribute to an elevated INR so the INR will better reflect warfarin’s effect after Dabigatran has been stopped for at least 2 days.
Reference: Dabigatran guidelines


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