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 76-year-old Chinese man complained of acutely worsening abdominal pain after treatment with 4,000 anti-Xa U of LMWH, q12h (low molecular weight heparin calcium injection, 0.4 ml/4000IU) as an anticoagulant for 3 days.\nThe patient was admitted to our hospital because of palpitation and shortness of breath for three days, and diagnosed with atrial fibrillation and heart failure, with cardiac function NYHA grade III at Northern Jiangsu People’s Hospital on March 21, 2018. He had a CHA2DS2-VASc score of 4, which indicated a high risk of stroke. His body mass index was 21.66 kg/m2, and renal function was normal. Therefore, he was given furosemide and spironolactone for diuretic therapy, valsartan capsules for antihypertensive treatment, and LMWH for anticoagulation therapy.\nThe patient had a prior history of hypertension well controlled by treatment with angiotensin-converting enzyme inhibitors.\nThe patient had no specific underlying disease. He had no family history of other significant diseases.\nPhysical examination showed abdomen tenderness and no signs of peritoneal irritation.\nOn March 21, laboratory results showed that N-terminal pro–B-type natriuretic peptide was 1590 pg/ml, international normalized ratio was 1.14, activated partial thromboplastin time (APTT) was 38.20 s, fibrinogen was 1.67 g/L, hemoglobin was 113 g/L, red blood cell count was 3.34 × 1012/L, creatinine was 83 μmol/L, alanine transferase was (ALT) 39.0 U/L, aspartate aminotransferase (AST) was 36.0 U/L, gamma-glutamyltransferase (GGT) was 115.0 U/L, and platelet cell count was 183 × 109/L. After anticoagulation therapy for 3 days, an emergency laboratory test showed that the red blood cell count was 2.56 × 1012/L, and hemoglobin and platelet counts decreased to 82 g/L and 102 × 109/L, respectively. Furthermore, the coagulation function test demonstrated a prolonged APTT of 49.50 s. There was no bleeding per rectum, and his fecal occult blood test was negative. Considering the patient’s symptoms of abdominal pain and the rapid drop in hemoglobin and red blood cell count, there was clinical suspicion for retroperitoneal or gastrointestinal hemorrhage.\nAbdominal computed tomography (CT) showed the thickening areas of the colon up to 110 mm × 78 mm in thickness, which was a symptom of hematoma of the colon ().