|Year : 2022 | Volume
| Issue : 1 | Page : 44-46
Intestinal tuberculosis complicated by pulmonary embolism and deep vein thrombosis
Mansoor C Abdulla
Department of General Medicine, Nizar Hospital, Valanchery, Kerala, India
|Date of Submission||25-Mar-2022|
|Date of Acceptance||20-May-2022|
|Date of Web Publication||21-Jul-2022|
Mansoor C Abdulla
Department of General Medicine, Nizar Hospital, Valanchery, Kerala
Source of Support: None, Conflict of Interest: None
Venous thromboembolism (VTE) secondary to tuberculosis (TB) is a rare complication that can occur either at the time of presentation or later in the course of the disease. A 24-year-old woman was admitted with low-grade fever, abdominal pain, abdominal distension, and loose stools for one and half months. She was evaluated and diagnosed with abdominal TB. On the second day of admission, she had a sudden onset of the right lower limb edema with pain followed by breathlessness. Contrast-enhanced computed tomography of the thorax showed a thrombus in the left pulmonary artery. She was treated with low-molecular-weight heparin and started on anti-TB drugs. She was continued on oral anticoagulation with warfarin. We describe a patient who developed pulmonary embolism and lower limb deep vein thrombosis secondary to abdominal TB without paraaortic lymphadenopathy and a negative procoagulant workup, which was not reported previously. The mechanisms of VTE in TB are complex and may need further studies in the future, which may help the clinicians develop appropriate strategies for treatment.
Keywords: Deep vein thrombosis, intestinal tuberculosis, pulmonary embolism
|How to cite this article:|
Abdulla MC. Intestinal tuberculosis complicated by pulmonary embolism and deep vein thrombosis. Niger J Gastroenterol Hepatol 2022;14:44-6
| Introduction|| |
Tuberculosis (TB) can lead to hypercoagulability, increased venous stasis, and endothelial dysfunction, thus increasing the susceptibility to venous thromboembolism (VTE). The risk of developing VTE is considered to be increased in patients with severe disease.
| Case report|| |
A 24-year-old woman was admitted with low-grade fever, abdominal pain, abdominal distension, and loose stools for one and half months. She had a decreased appetite and significant weight loss (8 kg in one and half months). She had no history of previous medical illness and had no addictions. She denied a history of high-risk behavior and had no sick contacts. On examination, the abdomen was distended, and there was shifting dullness. The rest of the examination was unremarkable.
Hemoglobin was 8.5 g/dL, total leukocyte count was 6,750/mm3, platelet count was 179,000/µL, and erythrocyte sedimentation rate was 82 mm in 1 h. Peripheral smear showed microcytic hypochromic anemia. Blood chemistries were normal except for hypoalbuminemia. Chest x-ray was normal. The ultrasonography of the abdomen showed moderate ascites. Ascitic fluid analysis showed lymphocytic-predominant exudative effusion with a high adenosine deaminase level of 49 U/L (reference range: 8.6–20.5 U/L). Ascitic fluid gram stain, cartridge-based nucleic acid amplification test for TB, mycobacterial culture, and bacterial culture were negative. Contrast-enhanced computed tomography (CT) of the abdomen showed long-segment bowel wall thickening and moderate ascites with peritoneal wall enhancement (peritonitis) [Figure 1]. Colonoscopy showed colonic ulcers.
|Figure 1: Contrast-enhanced computed tomography of abdomen showing moderate ascites (A, arrows), long segment bowel wall thickening (B, arrows), and peritoneal wall enhancement|
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Colonoscopic biopsy from the ulcer showed necrotizing granulomatous inflammation, and cartridge-based nucleic acid amplification test of biopsy was positive without rifampicin resistance.
On the second day of admission, she had a sudden onset of the right lower limb edema with pain followed by breathlessness. Chest x-ray repeated was normal, and electrocardiogram showed sinus tachycardia. Venous Doppler showed a right iliac vein thrombus. Echocardiogram was normal. Contrast-enhanced CT of the thorax showed a thrombus in the left pulmonary artery [Figure 2]. She was diagnosed with intestinal TB (tuberculous enterocolitis), pulmonary embolism, and deep vein thrombosis. She was treated with enoxaparin 40 mg twice daily for 10 days and started on warfarin 5 mg daily (the dosage was adjusted to keep the international normalized ratio within a range of 2.0–3.0). She received anti-TB drugs (isoniazid 300 mg, rifampicin 450 mg, pyrazinamide 1 g, and ethambutol 800 mg daily for the first 2 months, and isoniazid 300 mg, rifampicin 450 mg were continued for 4 more months) under directly observed therapy for the short term.
|Figure 2: Contrast-enhanced computed tomography of thorax showing thrombus in the left pulmonary artery|
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Her blood coagulation profile was normal. The procoagulant workup showed negative IgG and IgM anti-cardiolipin antibodies, IgG and IgM beta-2 glycoprotein, and lupus anticoagulant tests. Factor V Leiden, methylenetetrahydrofolate reductase polymorphism, and prothrombin G20210A were not detected. Her serum levels of homocysteine, protein C, and protein S were normal. Following 6 months of treatment with anti-TB drugs and anticoagulants, she had a complete recovery from her illness.
| Discussion|| |
VTE secondary to TB is a rare complication that can occur either at the time of presentation or later in the course of the disease. TB is an infection having thrombogenic potential. VTE in patients with TB commonly causes pulmonary embolism and lower limb deep vein thrombosis. VTE due to TB affecting the hepatic veins and cerebral venous sinuses was also reported previously in the literature.,
VTE in TB can be due to different causes. Increased fibrinogen level, impaired fibrinolysis, decreased antithrombin III level, and reactive thrombocytosis secondary to inflammation can trigger VTE. Changes in blood viscosity due to dehydration in severe forms of TB and the use of anti-TB drugs such as rifampicin and compressive effects of enlarged lymph nodes on the blood vessels are the other mechanisms attributed to the thrombogenic potential of TB.
Paraaortic lymph nodes causing inferior vena cava obstruction resulting in bilateral deep vein thrombosis was reported previously in two patients. Gathwala et al. reported a 13-year-old girl with abdominal TB having deep vein thrombosis due to a decreased level of antithrombin III. A 13-year-old girl with abdominal TB and deep vein thrombosis was reported by Gupta et al., while a 22-year-old woman with abdominal TB complicated by reverse ileocecal intussusception and VTE has also been documented., The patient presented here had abdominal TB complicated by VTE (pulmonary embolism and lower limb deep vein thrombosis). Her procoagulant workup was negative, and she had no paraaortic lymphadenopathy.
Gastrointestinal TB is placed sixth in the order of frequency of occurrence of extrapulmonary TB in India. The proportion of patients with extrapulmonary TB is 8%–13% in India, and among these, abdominal TB accounts for 7% of the patients. Studies from India in the last three decades have shown that pain is the most common presenting symptom (80%–100% of the patients). Peritoneal involvement usually presents with abdominal distension and pain, whereas the intestinal variant presents with pain and features of subacute intestinal obstruction.
We describe a patient who developed pulmonary embolism and lower limb deep vein thrombosis secondary to abdominal TB without paraaortic lymphadenopathy and a negative procoagulant workup, which was not reported previously. The mechanisms of VTE in TB are complex and may need further studies in the future, which may help the clinicians develop appropriate strategies for treatment.
I would like to thank Dr. Asik Siddik of pathology whose comments and suggestions were immensely valuable for improving this case report.
All procedures performed in studies involving human participants were by the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
Informed signed written consent was taken from the patient involved.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]