Journal of the Louisiana State Medical Society
Figure 1: Transverse and sagittal views showing the presence of a large (20 cm x 10 cm) spontaneous rectus sheath hematoma.
Figure 2: Transverse and sagittal views showing the presence of a large (22 cm x 2 cm) spontaneous rectus sheath hematoma.
primary care physicianwith hemoglobin of 5.8 g/dl (normal 12.1-15.1 g/dL) and abdominal discomfort. The abdominal pain was present over three weeks and localized to the left lower quadrant. She also complained of worsening fatigue over two weeks. She denied any history of trauma or bleeding disorders. Additionally, she had a recent upper respiratory infection with non-productive cough. She had a renal biopsy confirmingWegener’s Granulomatosis andwas taking prednisone 25 mg daily and mycophenolate 1 gram twice daily. Wegener’s was originally diagnosed when she presentedwith rapidly progressive renal failure twomonths earlier. She was not on dialysis. She also had hypertension, dyslipidemia, depression, and gastroesophageal reflux disease. She was taking citalopram, famotidine, labetalol, and pravastatin. Her vital signs were stable on admission. On examination, there was visible bruising and associated tenderness over the left lower quadrant. Her hemoglobin was 5.3 mg/dl. She was started on intravenous fluid and was transfused with four units of PRBC. CT of the abdomen showed a large rectus sheath hematoma measuring 22 cm in the cranio-caudal dimension (Figure 2). Her hemoglo-
bin improved with transfusion to 10 g/dl. Her symptoms improved, and she was hemodynamically stable. She was dischargedwith close follow-up in seven days at outpatient clinic. At follow-up, her hemoglobin remained stable; her bruising and abdominal pain had improved. DISCUSSION The most common risk factor for the development of SRSH is anticoagulation and over anticoagulation increases the risk substantially. 5 Triggering factors, such as cough, are usually present in up to 70% of the patients with SRSH. 6 The first patient was anticoagulated for five days with intravenous heparin. Her aPTTwas in the therapeutic range. She was given aspirin and a loading dose of clopidogrel, the effect of which lasts for five to seven days. Although she was treated initially with bivalirudin and eptifibatide, those are less likely to have triggered the hematoma formation as they have a short half-life. Moreover, she had a mild drop in platelets (lowest count of 120/mm3) possibly related to heparin infusion in the absence of heparin-induced throm-
198 J La State Med Soc VOL 166 September/October 2014
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