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.
A 4-year-old boy was transferred to our pediatric intensive care unit from an outside hospital for further management of a persistent seizure disorder of unknown etiology. A right femoral triple lumen central venous line (CVL) had been placed prior to transfer. Five days after arrival, the patient began to exhibit increased swelling in his right lower extremity, and ultrasonography revealed a catheter-related, acute occlusive deep venous thrombosis in the right common femoral vein. He was started on LMWH (enoxaparin) at 1 mg/kg for a planned course of 3 months. Five days after initiating treatment, the CVL was removed. The patient had no personal or family history of thrombophilia or bleeding diathesis. His anti-Xa level, checked after the second dose, was within the therapeutic range.\nHis hospital course was complicated by multisystem organ failure in the setting of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome secondary to anticonvulsive therapy. One week after starting LMWH heparin, the patient experienced gross hematuria. The next day, the injection sites were noted to be slightly oozy, and, in the setting of his anti-Xa levels continuing to rise (0.87), LMWH heparin was held. He required continuous venovenous hemofiltration, during which time anticoagulation was switched to unfractionated heparin. After renal recovery, LMWH therapy was restarted at a lower dose (70% of original dose), but his anti-Xa levels continued to be labile and difficult to control. Eventually, a steady regimen was found with consistently stable and therapeutic anti-Xa levels ().\nOn the 15th day of this regimen, however, he developed signs of bowel obstruction with new onset of copious bilious vomiting. An abdominal ultrasound found a small amount of fluid in the pelvis. A CT of the abdomen and pelvis showed a high-grade small bowel obstruction, with 2 areas of small bowel, suspicious for intussusception (Figures and ). The patient's hemoglobin was found to have dropped from 9.9 to 6.2.\nHe was brought to the operating room for exploratory laparotomy. Intraoperatively, bloody ascites and multiple dilated loops of small bowel were found. Approximately 30 cm of the distal jejunum was found to be tense, heavy, firm, and discolored with a blue hue, with a hematoma that had dissected through the layers of the bowel (). A serosal defect was found on the antimesenteric border of the involved bowel, likely causing the bloody ascites. As the bowel was severely compromised, a resection of the involved segment was performed.\nPathologic analysis of the resected bowel showed an extensive, 35 cm submucosal hematoma causing internal bulging of the mucosa and submucosa, causing attenuation and focal pressure necrosis of the muscularis propria. The serosa was noted to be diffusely purple-red, with a small ovoid defect that was presumably caused by the hematoma. At both ends of the resected bowel, there was evidence of the mucosa and submucosa bulging into the lumen of the bowel as a result of the hematoma.\nThe patient recovered from the operation in the pediatric ICU with no further episodes of emesis or signs of bowel obstruction. He was restarted on LMWH 5 days later and completed his 3-month course without any further signs of bleeding. He was discharged from the hospital 3 weeks later with resolution of his seizures to a rehabilitation facility, without any further complications of bleeding or bowel obstruction.