Cerebral Venous Sinus Thrombosis in Patients with Ulcerative Colitis

Dear Editor, Venous thrombosis associated with active ulcerative colitis (UC) was first reported (1936) by Bargen and Barker and has an estimated prevalence of up to 6%; cerebral venous thromboses (CVT) are rare, but neurological consequences may be ominous.[1-8] As a whole, primary healthcare workers do not have enough awareness about this neurological condition that must be detected early and promptly and adequately treated. Therefore, the recent article by Sardana and Singh,[7] published in this journal, merits being highlighted as an effective example for enhancing the suspicion index on this issue. They reported a 25-year-old man with the diagnosis of UC and using mesalamine, who developed intense bifrontal headache, weakness in the right upper and lower limbs, right facial palsy, dysarthria, and right-sided hyperreflexia, besides a positive Babinski sign.[7] The brain imaging studies revealed a CVT sited in the superior sagittal sinus, causing a venous infarct in the left cerebral hemisphere that improved with the anticoagulation.[7] The authors emphasized the elevated risk of thromboembolic events in individuals with UC and the role of multidisciplinary management to optimize the patient’s outcomes.[7] The following comments aim to focus on new references about CVT and UC. Albakr and AlMohish[1] reviewed risk factors for CVT among 35 cases of inflammatory bowel disease (IBD), and the event occurred 3.8 times more in UC than in Crohn’s disease. More than 90% of IBDs were active, the mean time from this diagnosis and CVT was 3 years, headache was the main symptom, multiple venous sinuses were affected in nearly 60% of cases, and corticosteroid therapy was the major pro-thrombotic risk factor (57.14%).[1] Hemorrhagic complications occurred in 10% of the patients, and anemia in 42.8%, whereas the CVT risk factors other than IBDs were identified in 65.7% of participants.[1] Besides anemia, the enrolled risks of CVT included: corticosteroid therapy (57.14%), antecedent of diverse thrombotic episodes (14.2%), inherited thrombophilia (11.4%), hyperhomocysteinemia (5.7%), hormone therapy (5.7%), and postoperative status (5.7%).[1] All patients initially used heparin or low molecular weight heparin (LMWH) 3 needed endovascular treatment; LMWH was followed by warfarin administration in 58.06%.[1] Some of the patients also utilized aspirin, apixaban, or rivaroxaban; the complete recovery was confirmed in 27 patients (77.14%), and the partial recovery was obtained in 6.[1] Alomari et al.[2] compared 215 patients using corticoids (91 with short tapering and 124 with long tapering), and more cases of the second group had a longer duration of disease with moderate to severe disease activity (63.8 months vs. 25.6 months, 46.8% vs. 23.1%). During the 6-month follow-up, the rates of rehospitalizations by flares of UC were comparable between the two groups (68.3% vs. 68.5%), showing both steroid taper regimens with similar post-hospitalization results, indicating the short tapering for a standard.[2] Griffiths et al.[4] studied the thrombotic profiles of 27 acute severe ulcerative colitis (ASUC) during hospitalization and up to 12 weeks post-discharge, compared to 25 controls. Thrombin generation, rotational thromboelastometry, pro-coagulant factors, anti-coagulant factors, and fibrinolytic markers were tested for ASUC group on days 1 and 5, 4 weeks, and at 8–12 weeks; exams were performed on a single occasion for controls.[4] The determinations revealed that ASUC patients were pro-thrombotic compared to controls with quiescent colitis, and differences persisted 8–12 weeks after presentation, confirming that patients with ASUC maintain the risk of CVT after hospital discharge.[4] Hamid et al. described a 34-year-old female with antecedents of UC for 3 years and vaccination for coronavirus disease 2019 9 months ago, who presented with acute right-sided weakness. Brain images showed superior sagittal sinus thrombosis and left frontoparietal infarction successfully managed by anticoagulation, plus prednisolone and azathioprine for UC.[5] The authors stressed the CVT suspicion in cases of UC with acute neurological changes, and the maintenance of anticoagulants even after the onset of symptomatic remission.[5] Kilani et al.[6] compared data of primary venous thromboembolism (VTE) admissions of patients with and without inflammatory bowel disease (IBD) between 2016 and 2020. Deep vein thrombosis (DVT), portal vein thrombosis (PVT), Budd Chiari syndrome (BCS), renal vein thrombosis (RVT), and cerebral vein thrombosis (CVT) were included. Primary VTE-related admissions of people with IBD (n = 15,565) were compared to the control individuals without IBD (n = 1,449,164), showing that IBD increased the odds for DVT, PVT, and CVST, without a significant increase in the odds of PE, BCS, or RVT.[6] The authors highlighted the high index of suspicion role during evaluations of VTE-related manifestations among individuals with IBD, because the presence of IBD favors a higher risk of DVT, PVT, and CVST-related hospitalizations, and with longer stays.[6] Yamazaki et al.[8] reported a 48-year-old female with occasional bloody stools in previous months, before the development of paresthesia and left upper limb weakness. The brain images showed a right frontoparietal infarction complicated by hemorrhage, total occlusion of the right rolandic vein and inferior sagittal sinus, plus partial occlusion of the superior sagittal sinus, and was diagnosed as a cerebral venous sinus thrombosis.[8] She underwent a surgical hematoma evacuation immediately, and unfractionated heparin; after endoscopic diagnosis of UC, prednisolone, sulfasalazine, and mesalamine were added, and five days later, all the digestive manifestations and intestinal bleeding were resolved.[8] The corticosteroid was then tapered, and the anticoagulation was changed to warfarin. The authors highlighted the suspicion of new-onset UC after CVT, mainly in people presenting with gastrointestinal disturbances, favoring the early diagnosis and treatment; besides, the rigorous adequate maintenance therapy for UC to prevent CVT recurrence.[8] In conclusion, the authors strongly believe that even single case reports can play a favorable role by enhancing the suspicion index of healthcare workers of CVT in UC. Suspected cases should have multidisciplinary assistance, and those with confirmed diagnoses will have better outcomes. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.