A 71-year-old gentleman was referred by his general practitioner with tachycardia. He reported a 2-day history of nausea, abdominal discomfort, and bloating with three episodes of bilious vomiting. He denied any pain, change in bowel habits or infective symptoms. He passed a normal bowel motion on the day of presentation and had no evidence of upper or lower gastrointestinal bleeding. His comorbid medical conditions were hypertension, hypercholesterolaemia and metallic aortic valve replacement. His regular medications included eplerenone, bisoprolol, fenofibrate and warfarin. The patient admitted taking a double dose of warfarin (4 mg daily) for the past 30 days. On arrival in the Emergency Department, his heart rate was 140 b.p.m., however, other haemodynamic parameters were normal. His abdomen was distended but soft and non-tender with active bowel sounds and no peritonism. Other system examinations were unremarkable and he had no stigmata of active bleeding. Electrocardiogram indicated rapid atrial fibrillation, which was managed with intravenous magnesium sulphate and beta blockade followed by an amiodarone infusion. Laboratory results showed a leukocytosis (white cell count 21 × 109/l), normal haemoglobin 152 g/l, elevated C-reactive protein 77 mg/l, lactate 4.6 mmol/l and supratherapeutic international normalized ratio (INR) of 9.9. The patient received urgent surgical review, fluid resuscitation and INR reversal with intravenous vitamin K, prothrombinex and two units of fresh frozen plasma. Bedside abdominal ultrasound indicated intra-abdominal free fluid which was further investigated with a computed tomography (CT) mesenteric angiogram. This showed circumferential, hyperdense bowel wall thickening involving a long segment of small bowel up to the mid-ileum (Fig. ). The bowel wall density was 50–60 Hounsfield units, consistent with an intramural haematoma. The duodenum and the stomach were dilated with no associated transition point and the distal ileum and the colon were decompressed. Haemoperitoneum was noted adjacent to the liver and spleen (Fig. ). Normal contrast enhancement was demonstrated in the major abdominal vasculature. The patient was admitted to the intensive care unit (ICU) for monitoring and non-operative management with bowel rest, nasogastric decompression and intravenous fluids. Warfarin was withheld and no venous thromboembolism prophylaxis administered due to his high bleeding risk. Repeat INR 5 hours after presentation was 1.5. The patient remained haemodynamically stable in ICU with no evidence of active bleeding. He reverted to sinus rhythm after 2 days of amiodarone infusion and did not require surgical intervention or blood transfusion. Diet was progressed and he was transferred to the ward on Day 3. Cardiology advised that the patient was unsuitable for NOAC (new oral anticoagulant) therapy and he was recommenced on warfarin at 1 mg daily. He was discharged on Day 6 with plan for outpatient warfarin titration. On discharge, the patient was asymptomatic, opening his bowels and tolerating full diet with INR 1.2 and stable haemoglobin of 102 g/l.
The patient is a 52-year-old incarcerated male with a past medical history of diabetes mellitus, chronic pancreatitis, and remote history of open cholecystectomy who was transferred to the hospital for complaint of abdominal pain. He reported three days of worsening epigastric and periumbilical abdominal pain with associated nausea and obstipation. He also reported two days of hematuria without dysuria or frequency. Four days prior, he was awakened by another prisoner who was kicking him in the abdomen.\nOn presentation, he was tachycardic but normotensive. His abdomen was distended and diffusely tender. Initial lab work was notable for leukocytosis of 17 and significant coagulopathy with an unmeasurable international normalized ratio (INR), partial thromboplastin time (PTT) > 200, and prothrombin time (PT) > 120. Repeat labs confirmed the coagulopathy. He denied any ingestions or known exposures. He was given two units of fresh-frozen plasma (FFP) as well as vitamin K and his coagulopathy began to correct.\nA CT scan of the abdomen/pelvis revealed significant bowel dilatation with mural edema and thickened loops of jejunum (Figure ). There was fecalization of the proximal small bowel consistent with high-grade small bowel obstruction. Given his tachycardia, obstructive symptoms, diffuse abdominal pain and CT findings, there was concern for intestinal ischemia and the decision was made to perform an exploratory laparotomy. On inspection, the mid-small bowel was dilated with about 30 centimeters of thickened small bowel with circumferential hematoma. The entirety of the small bowel was examined and the point of obstruction appeared to be the extensive small bowel hematoma. This portion was resected and primarily anastomosed. The abdomen was closed and the patient was brought to the recovery room.\nHis post-operative labs were notable for a normalizing INR of 1.4 and PTT of 30. Given the unclear etiology for his extreme coagulopathy, Hematology was consulted. He had no family history of coagulopathies or hematologic disorders. He reported no history of bleeding symptoms prior to this episode. Coagulation studies were consistent with a deficiency of vitamin K dependent clotting factors that corrected with mixing studies. Differential diagnosis included common pathway factor deficiency, inhibitor exposure, or false result. Disseminated intravascular coagulation (DIC) and liver failure were ruled out. As his coagulopathy quickly corrected with FFP and vitamin K, the most likely etiology was exposure to overdose of a warfarin-based substance. He received additional vitamin K and recovery was otherwise unremarkable. Hematuria had resolved with correction of the coagulopathy. He was discharged on the seventh post-operative day to the prison infirmary. The final pathology was notable for portion of small intestine with transmural hemorrhage with clear resection margins.