INTRODUCTION: Ulcerative colitis (UC) is primarily a disease of the bowel but can exhibit extraintestinal manifestations in less than 10% of patients. We report a case of a relatively young patient with multiple thromboembolic events as a rare manifestation of UC.
CASE PRESENTATION:A 36-year-old female with history of untreated UC presented with expressive aphasia and syncope. She had fatigue, anorexia, and intermittent diarrhea, vomiting & hematochezia in the last 7 months. On presentation, she had fever (101.9'F), heart rate of 139, blood pressure of 145/81 & oxygen saturation of 96% on room air. Labs were remarkable for hemoglobin 3.3 g/dL, platelets 701, lactate 2.7, sodium 131, potassium 2.8, albumin 2.6, D-dimer 3.91 & INR 1.3. Head CT showed a focal area of hypodensity in the left temporal lobe. Abdominal CT showed diffuse concentric mural colonic wall thickening compatible with pancolitis, felt to reflect ulcerative colitis flare. She was given intravenous fluids, ceftriaxone & metronidazole, and subsequently transfused 3 units of pRBCs. Levetiracetam was given for seizure prophylaxis. Brain MRI showed 2.5-cm left temporal lobe hemorrhagic lesion with post-contrast enhancement and multiple small foci of diffusion restriction within the peripheral frontal lobes without enhancement. TEE showed ejection fraction of 65% with no vegetations. Brain MRV showed non-occlusive thromboses in the left transverse sinus, sigmoid sinus junction & right internal jugular vein. Brain MRA was unremarkable. Duplex ultrasound showed a non-occlusive thrombus in the left common femoral vein and saphenofemoral junction. CTPA showed acute pulmonary embolism in the right lower and upper lobe segmental arteries. Heparin drip was started with close monitoring in the ICU, given her hemorrhagic lesion. At this point, hypercoagulopathy work-up done prior to anticoagulation revealed only low protein S and antithrombin levels. Her neurologic exam continued to improve, with eventual resolution of symptoms. She was discharged with apixaban and outpatient GI follow-up.DISCUSSION: IBD poses up to 16-times higher risk of thrombosis in those with disease flare. Prevalence of thrombosis in patients with IBD is ~5.6%. Its pathogenesis is thought to be multifactorial and linked to excessive immune function, with cytokines interleukin-6 and TNF-alpha playing a potential role. However, the exact nature is still unclear. Studies [1, 2] showed up to 25% of patients had diminished proteins S & C and antithrombin in active UC, as in our patient. CONCLUSIONS: Our case of a patient with multiple thrombi, ischemic cerebrovascular accident, and severe anemia highlights the rare and potentially serious manifestations of untreated UC. Awareness is important to facilitate prompt treatment.