ICU Rounds Report - Dec 16th, 2010

Auto-Anticoagulation of Cirrhosis? Patients with liver failure commonly present with elevated INRs and low platelet counts. Liver dysfunction alters synthesis and production of both the pro- and anti-coagulants produced by the liver. In addition, numerous other effects alter normal coagulation in the cirrhotic patient: low platelets, platelet dysfunction, altered endothelial function (including elevated levels of prothrombotic vWF and tFVIII), elevated levels of nitric oxide, etc. Further confusing things: liver failure can dramatically increase rates of fibrinolysis. What does it all mean?

In other words: Does a liver failure patient with an INR of 2.3 needs DVT prophylaxis?

It depends on who you ask. The recent medical literature suggests that cirrhosis offers little, or no protection.  Now, in the first study of its kind, researchers at the University of Missouri looked at the relationship between pathologic INR elevations and DVT. They retrospectively evaluated 190 hospitalized patients with varying degrees of chronic liver disease and found rates of DVT of 6.3% overall (by comparison, rates of DVT in high risk surgical inpatients without prophylaxis is between 4 - 8%).  Interestingly, higher elevations in INR were associated with greater DVT risk. Lastly, the study found that receiving DVT prophylaxis didn't protect against DVT, although the study was underpowered to detect a statistical difference and only 25% of liver failure patients received some kind of prophylaxis. Sadly, there is no data available for surgical patients.

What everyone can agree on is that current panel of test used to diagnosis coagulation abnormalities in liver failure (plt count, PT, aPTT) are worthless because the balance of pro/anticoagulant factors is not considered by these tests (which tend to measure simple deficiencies of anticoagulants). Abnormal hemostatic tests have never been shown to correlate to bleeding tendencies in liver failure. Further, it is clear from liver transplantation surgery that preemptive "correction" of the abnormal values does not reduce, and probably promotes, bleeding. With this shift in thinking, many centers are now reporting the ability to keep liver transplantation "bloodless" (no transfusions needed) greater than half the time. To accurately diagnosis whether a liver failure patient is pro- anti- or euthrombotic requires much more sensitive testing, such as TEG,  which is not widely available.

So we're left where we started, which is were every good paper ends: more research is needed! Do liver patients needs SCDs/heparin? Anyone's guess. How can we even measure coagulation in liver failure? Not really possible. Does prophylaxis even work in the setting of liver failure? No one has a clue. Is working in an ICU awesome anyway? Yes, very! 
Dabbagh, O, et al. Coagulopathy does not protect against venous thromboembolism in hospitalized patients with chronic liver disease. Chest 2010; 137:1145.
Lisman, T, Porte, RJ. Rebalanced hemostasis in patients with liver disease: evidence and clinical consequences. Blood 2010; 116:878.
Gulley D et Al.  Deep vein thrombosis and pulmonary embolism in cirrhosis patients. Dig Dis Sci . 2008; 53( 11): 3012- 3017.
Northup PG, et al. Coagulopathy does not fully protect hospitalized cirrhosis patients from peripheral venous thromboembolism. Am J Gastroenterol 2006 ;101(7):1524-1528.

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