East Carolina University/Vidant Medical Center Greenville, NC
MaryKate Kratzer, MD1, Durga Pemmaraju, MD2, William Leland, MD2; 1East Carolina University/Vidant Medical Center, Greenville, NC; 2East Carolina University, Greenville, NC
Introduction: Inflammatory bowel disease (IBD) is associated with a myriad of systemic complications, including thrombosis; in fact, patients with IBD are up to three times more likely to develop deep vein thrombosis or pulmonary embolism. Less frequently, thrombosis can occur in the cerebral circulation. We discuss a case of cerebral sinus thrombosis in the setting of newly diagnosed Ulcerative Colitis (UC).
Methods: A 30 year-old African American female complained of 2 weeks of odynophagia, fever, and watery, nonbloody diarrhea with no prior history of similar complaints. Physical exam was remarkable only for fever of 101.5F, sinus tachycardia, and oral thrush. Initial labs showed mild leukocytosis, microcytic anemia, and hypokalemia. The patient later developed sharp, diffuse, abdominal pain followed by multiple bloody, mucous-containing stools. Imaging revealed colonic wall thickening, consistent with moderate to severe colitis, as well as thrombosis of the right sigmoid sinus and upper aspect of the right internal jugular vein. Her only neurological symptom was a dull right-sided headache. The patient was treated conservatively for suspected infectious colitis and anticoagulated with heparin drip. Due to persistent gastrointestinal symptoms, colonoscopy was performed. It revealed diffuse areas of moderately to severely erythematous, hemorrhagic, pseudopolypoid and ulcerated mucosa with rectal involvement to the proximal transverse colon. Biopsies were consistent with idiopathic ulcerative colitis. Discussion: The most common sites of cerebral thrombosis in IBD are the sagittal and lateral venous sinuses. Presenting symptoms typically include diffuse headache, nausea, and vomiting, and less commonly seizures. Many theories exist as to the etiology of increased incidence of thrombotic events in IBD, the most common being chronic inflammation; however, when studied against rheumatoid arthritis (RA) and Celiac disease (CD), the odds ratio for thrombotic events was significantly increased in IBD and decreased in RA and CD. Other potential causes include altered platelet activity and decreased anti-clotting factors in IBD, as well as chronic dehydration. Extent of bowel involvement may also correlate with higher risk of thrombosis. Management of cerebral venous thrombosis is similar to DVT, with 3 to 6 months of anticoagulation. It is questionable whether lifelong anticoagulation improves overall mortality.
Disclosures: MaryKate Kratzer indicated no relevant financial relationships. Durga Pemmaraju indicated no relevant financial relationships. William Leland indicated no relevant financial relationships.