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.
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 ().