Winning Abstracts from the 2011 Medical Student Abstract Competition: Coagulopathy in Alcohol-Induced Cirrhosis: To Bleed or Not To Bleed?

Winning Abstracts from the 2011 Medical Student Abstract Competition: Coagulopathy in Alcohol-Induced Cirrhosis: To Bleed or Not To Bleed?

Author: Nils Viesturs Brolis, University of Medicine and Dentistry New Jersey, School of Osteopathic Medicine, Class of 2011

Introduction: Cirrhosis secondary to alcohol use is a condition characterized by multiple complications, including the development of coagulopathy. While a myth exists that patients with this diagnosis are always hypocoagulable, the truth is they may also become hypercoagulable. The issue is further muddied because prothrombin time (PT) and international normalized ratio (INR), tests commonly relied upon to screen for bleeding abnormalities, become unreliable in this patient population.

Case Presentation: A 44-year-old male with a history of alcohol abuse presented to the hospital with a 2 month history of abdominal distention, lower extremity swelling, intermittent nose bleeds, and jaundice. Over the past week he had increasing shortness of breath and multiple episodes of melena. He had no known medical problems and took no medications. At presentation his vital signs were stable. His exam demonstrated jaundiced skin with multiple spider angiomas, scleral icterus, a non-tender distended abdomen with a positive fluid wave test, 3+ pitting edema of both legs and scrotum, and a heme-negative rectal exam. Laboratory values included the following: hemoglobin 7.2, platelets 124,000, PT 40.3, and INR 3.5. Ultrasound of the abdomen showed abdominal ascites and an enlarged liver with irregular borders consistent with cirrhosis. Ultrasound of the liver revealed a non-occlusive thrombosis of the main portal vein. A clinical diagnosis of cirrhosis secondary to alcohol abuse was made and he was admitted. A second diagnosis of anemia with concern for a gastrointestinal bleed was also made. During his hospitalization he was given blood, raising his hemoglobin to 8 where it stabilized. An esophagogastroduodenoscopy and colonoscopy showed grade I esophageal varices and no signs of active bleeding. He was diuresed daily and received a therapeutic and diagnostic paracentesis which suggested ascites secondary to portal hypertension. The patient reported improvement in shortness in breath following the paracentesis. No intervention was taken regarding the portal vein thrombosis. His laboratory values and clinical exam remained stable over the course of several days and he was discharged from the hospital.

Discussion: This case illustrates that a patient with alcohol-induced cirrhosis with an elevated PT and INR may still be at an increased risk of clot formation, as demonstrated by the portal vein thrombosis. Portal vein thrombosis secondary to cirrhosis is believed to be partially caused by the decreased liver production of endogenous anticoagulants, including protein C, protein S, and antithrombin III. PT and INR are poor predictors of coagulopathy in this patient population because neither accounts for a loss of these anticoagulants. Increased values are merely a reflection of the poor synthesis of clotting factors. Therefore, the suspicion for thromboembolic disease must remain high in this population, even in the context of increased laboratory values and concern for active bleeding.

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