Collateral Damage

The patient had a history of hypothyroidism, autoimmune alopecia, and transient acantholytic dermatosis (Grover’s disease). He had been in his usual state of health, without active problems, until 1 week earlier, when he awoke with a swollen, erythematous lower left leg. He was hospitalized and diagnosed with widespread deepvein thrombosis in the left leg, including the left common femoral, superficial femoral, deep femoral, popliteal, greater saphenous, gastrocnemius, posterior tibial, and peroneal veins. His only known risk factor was an airline flight from Rome to Chicago 1 month earlier. The results of an extensive hypercoagulability workup, including tests for anticardiolipin antibodies, lupus antibodies, prothrombin gene mutation G20210, factor V Leiden, protein C, protein S, homocysteine, and antithrombin III, were normal. Anticoagulation was initiated with enoxaparin with a transition to warfarin, and he was discharged home 4 days before this admission. On presentation, he was still taking both enoxaparin and warfarin. His only other medication was levothyroxine. He awoke early in the morning with severe rightsided abdominal and flank pain. His pain had no relation to eating or body position, although it increased with movement. In the last few hours before presentation his urine had changed to a dark tea color, although there was no frank blood in the urine. He reported no nausea, vomiting, diarrhea, constipation, fever, chills, night sweats, shortness of breath, cough, easy bruising or bleeding, weight changes, or bloody stools. He reported that he did not smoke or use alcohol. He did not have any history of hypertension, hyperlipidemia, or cardiovascular disease and had no family history of gastrointestinal, cardiovascular, or thrombotic disease.