To the Editor: Acute neurological dysfunction in a patient with inflammatory bowel disease (IBD) can be due to various causes including electrolyte imbalance, anemia, toxic megacolon, septicemia, and steroid-induced psychosis. Rarely, IBD itself can lead to neurological dysfunction due to vasculitis, demyelination, and thrombosis in the central nervous system.1 We report 1 such unusual case of cortical venous thrombosis (CVT) in a patient with IBD. A 40-year-old woman presented with altered sensorium of 1 day duration. She was a diagnosed case of ulcerative colitis (histologically proven) since 8 years. 5-Amino salicylic acid (5-ASA) was started along with tapering dose of steroids, to which she responded. She discontinued the medications on her own for the last year. For the past 4 days, she complained of 4-6 loose stools per day, mixed with fresh blood and tenemus. Repeat sigmoidoscopy showed active colitis. She was managed with intravenous fluids and restarted on intravenous hydrocortisone and 5-ASA, to which she was responding. One day prior to admission, she developed altered sensorium and was referred to our center. She was a nonsmoker and was not on oral contraceptive pills. Examination revealed the patient to be drowsy, with a blood pressure of 138/90 mmHg, normal skin turgor and pallor. Central venous pressure was 12 cm of water. On neurological examination the patient had a Glasgow coma scale (GCS) of 8/15, right hemiplegia (power left V/V, right 0/V), brisk deep tendon reflexes, and extensor plantar on the right side. The rest of the systemic examination was unremarkable. Laboratory investigations showed hemoglobin of 9.5 g/dL, with normal total leukocyte count, platelet count, coagulogram, renal and liver function tests with an elevated erythrocyte sedimentation rate (50 mm), and C-reactive protein (12 mg/dL). Noncontrast computed tomography (NCCT) of head revealed hemorrhagic infarct involving the left frontoparietal region (Fig. 1A). Magnetic resonance venography (MRV) of the brain showed thrombosis of superior sagittal, bilateral transverse and sigmoid sinus, and left internal jugular vein (IJV). Other investigations including electrocardiogram, echocardiography, protein C, protein S antithrombin III, serum homocysteine levels, antinuclear factor (ANA), anticytoplasmic antibodies (ANCA), IgG and IgM anticardiolipin antibodies, CD 55, and CD 59 did not show any abnormality. A diagnosis of CVT with acute exacerbation of ulcerative colitis was made. She was managed with phenytoin sodium, anticerebral edema measures, intravenous hydrocortisone, 5-ASA, and ventilatory support. After a careful search of the literature, a therapeutic dose of heparin was also administered subcutaneously, without a successful outcome.
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Chauhan et al. (2007) studied this question.
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