Hemodialysis without Anticoagulation for a Patient with Chronic Disseminated Intravascular Coagulation
In November 2008, a 68-year-old Japanese man was admitted to our hospital for the construction of an arteriovenous fistula (AVF). Proteinuria and hematuria had been noted at the age of 18 years. Hypertension was diagnosed when he was 40 years old and a calcium channel blocker was prescribed. In 1990, chest pain occurred suddenly without any precipitating cause, and dissection of the ascending thoracic aorta (Stanford A type) was diagnosed. Surgical treatment was performed using a synthetic graft. In 2002, dissection also occurred in the descending thoracic aorta (Stanford B type) and surgical repair was done. Since then, mild thrombocytopenia with a platelet count of around 100,000/ml had been noted, but he was asymptomatic. Computed tomography (CT) was done every 6 months and revealed a new aneurysm with thrombosis in the residual aorta, adjacent to the anastomosis, in 2005 (fig. ). No further surgical treatment was performed. In August 2008, an AVF was constructed to allow dialysis for end-stage renal failure, but a transfusion was required (400 ml of red blood cells and 1,600 ml of fresh-frozen plasma) because of the massive bleeding. Thereafter, his platelet count decreased to 52,000/μl while his prothrombin time (PT) was 80.5% (normal: >75), his activated partial thromboplastin time (APTT) was 31.9 s (normal range: 27.0–40.0), fibrinogen was 128.4 mg/dl (normal range: 120–300), fibrinogen degradation products (FDP) were 119.5 μg/ml (normal range: <5), and D-dimer was 79.8 μg/l (normal range: <1). In addition, the thrombin-antithrombin complex level was 46.4 ng/ml (normal range: 3–4), the plasmin-α2 plasmin inhibitor complex was 4.9 mg/ml (normal range: <0.8), and antithrombin-3 was 69.6% (normal range: 84–122) (table ). Chronic DIC, a less active condition than acute DIC, was diagnosed based on the following findings: an underlying disease associated with DIC (aortic aneurysm), elevation of FDP, APTT, PT, and fibrinogen within the normal range and mild thrombocytopenia [, ]. CT showed no change of the aortic aneurysm. There was no evidence of other risk factors for chronic DIC, including malignancy. Therefore, his chronic DIC was considered to be secondary to the aortic aneurysm with thrombosis. Initiation of hemodialysis was required in December 2008 due to a urea nitrogen level of 120 mg/dl and a creatinine level of 7.1 mg/dl. It was considered that administration of an anticoagulant for dialysis sessions was associated with a high risk of worsening his aortic condition. Therefore, because his ACT was prolonged to 150–180 s (normal range: 90–140), hemodialysis was started without the administration of an anticoagulant and was therefore performed successfully without any complications (such as clotting inside the dialysis circuit or dialyzer). Thereafter, hemodialysis (4 h, 3 times weekly) was continued without an anticoagulant, and he is doing well as of February 2012.