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 Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 4  |  Issue : 1  |  Page : 28-30

Double trouble: Cerebral vein thrombosis in a young female with ulcerative colitis


1 Department of Gastroenterology, Indira Gandhi Medical College, Shimla, India
2 Department of Medicine, Dr. Rajendra Prasad Government Medical College, Tanda, Kangra, Himachal Pradesh, India
3 Department of Radiodiagnosis, Dr. Rajendra Prasad Government Medical College, Tanda, Kangra, Himachal Pradesh, India

Date of Web Publication13-Jan-2015

Correspondence Address:
Sujeet Raina
C-15, Type-V Quarters, Dr. Rajendra Prasad Government Medical College Campus, Tanda, Kangra - 176 001, Himachal Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-344X.149252

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  Abstract 

Cerebral venous thrombosis is an uncommon disorder in the general population. Venous and arterial thrombosis is a rare but well-recognized extraintestinal complication of ulcerative colitis. Venous thromboembolic events commonly involve deep peripheral veins, and cerebral venous thrombosis is less common. We report a case of cerebral vein thrombosis associated with ulcerative colitis managed successfully with anticoagulant therapy.

Keywords: Cerebral vein, inflammatory bowel disease, thrombosis, ulcerative colitis


How to cite this article:
Sharma B, Raina S, Sharma R, Chauhan NS. Double trouble: Cerebral vein thrombosis in a young female with ulcerative colitis. Int J Health Allied Sci 2015;4:28-30

How to cite this URL:
Sharma B, Raina S, Sharma R, Chauhan NS. Double trouble: Cerebral vein thrombosis in a young female with ulcerative colitis. Int J Health Allied Sci [serial online] 2015 [cited 2021 Aug 5];4:28-30. Available from: https://www.ijhas.in/text.asp?2015/4/1/28/149252


  Introduction Top


Cerebral venous thrombosis (CVT), including thrombosis of cerebral veins and major dural sinuses, is an uncommon disorder in the general population. [1] Patients with inflammatory bowel disease (IBD) have an increased risk of thrombotic complications and arterial and venous system may be involved. Thromboembolism occurs more often in the deep veins of the leg or pulmonary circulation and CVT is less common. [2] We report a case of cerebral vein thrombosis associated with ulcerative colitis managed successfully with anticoagulant therapy. In addition, CVT in ulcerative colitis has mostly been reported in the setting of active disease while our patient developed CVT when the disease was in remission. The guidelines on the anticoagulant management particularly in actively bleeding IBD patients are also discussed.


  Case report Top


A 35-year-old right-handed female was a known case of ulcerative colitis in remission on mesalamine (5-ASA) presented with focal seizure followed by altered sensorium in the form of agitation, irrelevant talk, and poor comprehension for 1 day. There was no history of any cranial nerve involvement, motor weakness, or sensory loss. There was no history of fever, vomiting, headache, head injury, jaundice, and ear discharge. Neither similar episodes were observed in past nor any recent flare-ups of the ulcerative colitis was reported. Patient was not taking any other drug other than 5-ASA. Review of other systems was normal. There was no history of drug abuse or addictions.

On examination, patient was afebrile and hemodynamically stable. She was agitated, uncooperative, and disoriented to time, place, and person. Cranial nerve examination was normal. Speech was slurred. She was moving all the four limbs spontaneously. The tone and deep tendon reflexes were normal. The plantar reflex was bilaterally extensor. The patient was responding to painful stimulus. No meningeal signs were present. Skull and spine examination was normal. Rest of the examination was normal. Laboratory investigation showed: Hemoglobin-12 gm%, total leukocyte count-8800/cmm, platelet count-2,20,000/cmm, erythrocyte sedimentation rate (ESR)-21 mm in 1 st hour. Biochemistry profile was normal.

Magnetic resonance (MR) brain followed with venogram revealed left transverse sinus thrombosis with left temporal lobe infarct [Figure 1]. Patient was treated with anticoagulants and 5-ASA was continued. Patient improved clinically. Repeat MR brain with venogram revealed partial recanalization of left transverse sinus and resolution of abnormal signals of left temporal lobe [Figure 2]. Baseline coagulation profile including prothrombin time (PT) and partial thromboplastin time (PTT) was normal. Thrombophilia profile in the form of protein C, protein S, antithrombin III, antiphospholipid antibody were negative, and homocysteine level was normal.
Figure 1: (a) T1-weighted magnetic resonance (MR) image shows hyperintense signal in left transverse sinus (arrow). An irregular hypointense area in left temporal lobe is also seen. (b) Corresponding hyperintense signal on T2-weighted image is seen in left temporal sinus (arrow) and left temporal lobe. (c) Coronal MR venogram shows non-visualized left transverse sinus, sigmoid sinus, and internal jugular vein

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Figure 2: Post treatment, (a) Flair image shows appearance of flow within left transverse sinus (arrow) with resolution of abnormal signals of left temporal lobe. (b) Similar findings on T2 axial image. (c) Coronal magnetic resonance (MR) venogram shows partial recanalization of left transverse sinus, sigmoid sinus, and internal jugular vein

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  Discussion Top


Seventy-eight year back, thromboembolic phenomenon was recognized as a distinct complication of ulcerative colitis. [3] Extra intestinal complications of inflammatory bowel disease (IBD) in the form of neurologic manifestations seem to be more common than previously estimated. [4] Neurological dysfunction in a patient with IBD can be due to dyselectolytemia, anemia, sepsis, toxic megacolon, and steroid-induced psychosis. Cerebrovascular thromboembolic disease, demyelinating disorders like multiple sclerosis and chronic inflammatory demyelinating neuropathy and vasculitis also lead to neurological dysfunction in IBD. Risk of venous thromboembolic events in subjects with IBD is now well-established, and it has also been observed that the risks of myocardial infarction (MI), stroke, and cardiovascular death significantly increased during periods of IBD activity including flares and persistent activity. [5] Moreover, 1.6% of total cerebral venous thrombotic events are associated with IBD. It is estimated that 1.3-6.4% of adults with IBD and 3.3% of children with IBD are complicated by CVT at some point of time during the course of their disease. [4] Inflammatory bowel disease as a chronic inflammatory condition is considered a prothrombotic state. [5] In a Mayo Clinic evaluation of IBD patients with deep venous thrombosis (DVT) or pulmonary embolism (PE), 80% of patients had active disease at the time of DVT/PE; however, in another large study, one-third of thromboembolic complications occurred during disease quiescence, supporting the hypothesis of an increased procoagulant tendency in IBD, independent of disease activity. [6],[7] Factors responsible for the hypercoagulable state have included abnormalities of the platelet-endothelial interaction, hyperhomocysteinemia, alterations in the coagulation cascade, impaired fibrinolysis, involvement of tissue factor-bearing microvesicles, disruption of the normal coagulation system by autoantibodies, as well as a genetic predisposition. [8]

In a retrospective review on CVT as a complication of inflammatory bowel diseases on 65 patients, the most common site observed was superior sagittal sinus (50.7%), followed by transverse sinuses (33.8%), sagittal sinus (32.3%), lateral sinuses (20%), and cortical veins (16.9%). [4]

Management with anticoagulants particularly in actively bleeding IBD patients is a clinical challenge. Administration of anticoagulants in CVT prevents thrombus propagation, recanalizes occluded sinuses and cerebral veins, and prevents deep vein thrombosis and pulmonary embolism; and on the basis of data from randomized, controlled trials and observational studies, anticoagulation is recommended as safe and effective for treatment of CVT with or without intracranial hemorrhage on presentation. [1]

Guidelines from the European Crohn's and Colitis Organization and the American College of Gastroenterologists converge that all hospitalized adult IBD patients, especially those with active disease or prolonged immobilization, should be considered for antithrombotic prophylaxis with the rationale that these patients have threefold higher risk for thromboembolic complications, which further increases in 15-fold during disease exacerbations. [9],[10]

According to European Federation of Neurological Societies (EFNS) guidelines, oral anticoagulation should be continued for 3 months if cerebral venous sinus thrombosis (CVST) was due to a transient risk factor, for 6-12 months in patients with idiopathic CVST or mild thrombophilia and infinitively in patients with recurrent episodes of CVST or severe thrombophilia. [11] While analyzing the impact of anticoagulation therapy on outcome in CVT and IBD (inflammatory bowel diseases), most of the case reports declared complete recovery (64.6%) and only few (26.1%) reported poor outcome (partial recovery of death). [4]

 
  References Top

1.
Piazza G. Cerebral venous thrombosis. Circulation 2012;125:1704-9.  Back to cited text no. 1
    
2.
Papa A, Danese S, Urgesi R, Grillo A, Guglielmo S, Roberto I, et al. Early atherosclerosis in patients with inflammatory bowel disease. Eur Rev Med Pharmacol Sci 2006;10:7-11.  Back to cited text no. 2
    
3.
Bargen JA, Barkar NW. Extensive arterial and venous thrombosis complicating chronic ulcerative colitis. Arch Intern Med 1936;58:17-31.  Back to cited text no. 3
    
4.
Katsanos AH, Katsanos KH, Kosmidou M, Giannopoulos S, Kyritsis AP, Tsianos EV. Cerebral venous thrombosis in inflammatory bowel diseases. QJM 2013;106:401-13.  Back to cited text no. 4
    
5.
Kristensen SL, Ahlehoff O, Lindhardsen J, Erichsen R, Jensen GV, Torp-Pedersen C, et al. Disease activity in inflammatory bowel disease is associated with increased risk of myocardial infarction, stroke and cardiovascular death-a Danish nationwide cohort study. PLoS One 2013;8:e56944.  Back to cited text no. 5
    
6.
Talbot RW, Heppell J, Dozois RR, Beart RW Jr. Vascular complications of inflammatory bowel disease. Mayo Clin Proc 1986;61:140-5.  Back to cited text no. 6
[PUBMED]    
7.
Solem CA, Loftus EV, Tremaine WJ, Sandborn WJ. Venous thromboembolism in inflammatory bowel disease. Am J Gastroenterol 2004;99:97-101.  Back to cited text no. 7
    
8.
Friedman S, Blumberg RS. Inflammatory bowel disease. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison′s Principles of Internal Medicine. Vol. 2. 18 th ed. New York: McGraw-Hill; 2012. p. 2489.  Back to cited text no. 8
    
9.
Van Assche G, Dignass A, Reinisch W, Van der Woude CJ, Sturm A, De Vos M, et al.; European Crohn′s and Colitis Organisation (ECCO). The second European evidence based consensus on the diagnosis and management of Crohn′s disease: Special situations. J Crohns Colitis 2010;4:63-101.  Back to cited text no. 9
[PUBMED]    
10.
Kornbluth A, Sachar DB; Practice Parameters Committee of the American College of Gastroenterology. Ulcerative colitis practice guide-lines in adults: American College of Gastroenterology, Practice Parameters Committee. Am J Gastroenterol 2010;105:501-23.  Back to cited text no. 10
    
11.
Einhaupl K, Stam J, Bousser MG, De Bruijn SF, Ferro JM, Martinelli I, et al., European Federation of Neurological Societies. EFNS guideline on the treatment of cerebral venous and sinus thrombosis in adult patients. Eur J Neurol 2010;17:1229-35.  Back to cited text no. 11
    


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