INTRACRANIAL BLEED AND CEREBRAL VENOUS SINUS THROMBOSIS IN A 35-YEAR-OLD FEMALE: A RARE PRESENTATION OF TUBERCULAR MENINGITIS

Biradar S, Suryawanshi H, Thakur MB. Intracranial bleed and cerebral venous sinus thrombosis in a 35-year-old female: a rare presentation of tubercular meningitis. International Journal of Infection. 2025;9(1):22-24.

S. Biradar, H. Suryawanshi and M.B. Thakur^*

Department of Internal Medicine, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India.

*Correspondence to:
Dr. Manisha Bais Thakur, MD, FICP,
Department of Internal Medicine,
Vardhman Mahavir Medical College and Safdarjung Hospital,
New Delhi, India.
e-mail: hodmedicine2015@gmail.com

ABSTRACT

Tubercular meningitis (TBM) is a life-threatening manifestation of Mycobacterium tuberculosis infection of the central nervous system. Complications such as cerebral venous sinus thrombosis (CVST) and intracranial haemorrhage (ICH) are rare but catastrophic consequences of TBM. We present a case of a 35-year-old immunocompetent female with confirmed TBM who developed CVST complicated by a frontal lobe intracerebral haemorrhage. Neuroimaging revealed Focus of late subacute bleed in right superior frontal region with mild surrounding oedema, multiple thrombi in superior sagittal sinus and transverse sinuses and diffuse prominence of bilateral sulci-gyral pattern, prominent ventricular and extraventricular CSF spaces. She was managed with antitubercular therapy, corticosteroids, antiepileptics and anticoagulation following neurosurgical consultation. This case highlights the importance of recognising rare vascular complications of TBM and instituting timely interventions to improve neurological outcomes..

KEYWORDS: Tubercular meningitis, cerebral venous sinus thrombosis, intracranial haemorrhage, hydrocephalus, TBM complication

INTRODUCTION

Tubercular meningitis (TBM), the most severe form of extrapulmonary tuberculosis, often presents subacutely and is associated with significant morbidity and mortality. The pathogenesis involves hematogenous spread of Mycobacterium tuberculosis to the meninges, causing basal exudates, inflammation, and vasculopathy (1). While hydrocephalus and infarction are known complications, cerebral venous sinus thrombosis (CVST) and intracranial haemorrhage (ICH) remain under-recognised. CVST results from thrombosis of dural sinuses, leading to impaired venous drainage, raised intracranial pressure, and hemorrhagic infarcts. ICH in TBM is rare and often results from vasculitic rupture or venous infarction with hemorrhagic transformation (2). This report presents an unusual case of TBM complicated by CVST and ICH in an immunocompetent adult, emphasising the need for early neuroimaging and comprehensive management.

CLINICAL PRESENTATION

A 35-year-old previously healthy female with no known family or personal history of tuberculosis presented with a seven-day history of fever, headache, vomiting, and loss of appetite, followed by altered sensorium for one day. There was no history of seizures, visual disturbances, trauma, or immunosuppressive conditions. The patient was initially evaluated at a nearby hospital and subsequently referred to our tertiary care centre for further evaluation and management.

On admission, the patient was drowsy but arousable, with a Glasgow Coma Scale (GCS) of E4V1M4. She was afebrile, with stable vital signs: pulse 88/min, blood pressure 124/80 mmHg, respiratory rate 18/min, and SpO₂ 98% on room air. Neurological examination revealed bilateral papilledema, neck stiffness and bilateral extensor plantar reflexes.

INVESTIGATIONS

Initial blood work showed hemoglobin 9.5g/dL, leukocyte count 10300/mm³, and platelet count 2,24,000/mm³. Liver and renal function tests were within normal limits. Serum sodium 133mEq/L, serum potassium 3.5mEq/L, serum calcium: 8.9 mg/dL, serum magnesium: 2.56 mg/dL, serum phosphorus: 4.9 mg/dL. Blood sugar was 104 mg/dL. Tests for malaria, dengue, enteric fever, rickettsial diseases, HIV, hepatitis B, and C were negative.

Cerebrospinal Fluid (CSF) Analysis revealed Total leukocyte count: 10 cells/mm³ (90% mononuclear, 10% polymorphs), protein: 500 mg/dL, glucose: 105 mg/dL (serum glucose ~170 mg/dL), ADA: 11.1 U/L, CBNAAT: Positive for Mycobacterium tuberculosis, rifampicin-sensitive, Fungal culture: Negative, Gram stain: Negative, TB culture: Awaited at time of admission

MRI of the brain with contrast revealed Focus of late subacute bleed in right superior frontal region with mild surrounding edema. Multiple thrombi in superior sagittal sinus and transverse sinuses, Diffuse prominence of bilateral sulci-gyral pattern, prominent ventricular and extraventricular CSF spaces.

TREATMENT AND OUTCOME

On the second day of admission, her sensorium deteriorated (GCS E2V1M2), necessitating endotracheal intubation. She was transferred to the intensive care unit (ICU) for ventilatory support. During the ICU stay, she experienced multiple episodes of generalised tonic-clonic seizures, which were managed effectively with optimisation of antiseizure medications. Electrolyte imbalances and serum metabolic parameters were monitored closely and corrected as required. She was started on standard four-drug antitubercular therapy (Isoniazid, Rifampicin, Pyrazinamide and Ethambutol) and intravenous dexamethasone. Neuroimaging findings consistent with cerebral venous sinus thrombosis (CVST) and subacute intracerebral haemorrhage were reviewed with the neurology and neurosurgery teams, and the patient started on anticoagulation with low molecular weight heparin (LMWH), and antiepileptics were initiated under close neurosurgical and neurological supervision. After 5days, she was transitioned to oral Warfarin. The patient was maintained on mechanical ventilation for a period of seven days, during which supportive care, including fluid management, nutritional support, and prevention of ICU-related complications, was ensured.

By the end of the first week, her sensorium began to improve, and she was successfully extubated. Oxygen supplementation was continued via face mask and gradually tapered down as her respiratory effort normalized. Over the course of her hospital stay, there was progressive neurological recovery, with GCS improving to E4V5M6. She became fully conscious, oriented to time, place, and person, and began oral intake. She was discharged on ATT, oral anticoagulation, tapering steroids and antiepileptic drugs with outpatient follow-up scheduled.

DISCUSSION

This case represents a rare but important complication of TBM—cerebral venous sinus thrombosis with intracerebral haemorrhage. TBM-related CVST is believed to result from a hypercoagulable state due to inflammation, endothelial injury, and sluggish cerebral venous flow caused by basal exudates. Additionally, vasculitis and direct invasion of the venous sinus by mycobacteria can contribute to thrombus formation (3).

Hemorrhagic infarction is often the first radiological clue in TBM patients with altered mental status or focal deficits. In one case series, CVST was reported in 3–4% of TBM cases, with a significant number developing venous infarcts or ICH (4). Recognition is difficult due to overlapping features with hydrocephalus or vasculitic infarcts.

Anticoagulation in TBM-associated CVST is controversial due to the risk of bleeding, especially in the presence of infarcts. However, most guidelines suggest that benefits outweigh the risks in cases with confirmed thrombosis and stable hemorrhagic lesions (5). In our patient, early anticoagulation was associated with neurological recovery and no worsening of the haemorrhage.

Hydrocephalus is the most common complication of TBM, present in up to 80% of cases. In communicating hydrocephalus without significant mass effect or decline in consciousness, medical management with serial monitoring may suffice (6).

This case highlights the need for multimodal imaging including CEMRI Brain/MRV in TBM patients with atypical neurological signs, and for a multidisciplinary approach incorporating ATT, steroids, and anticoagulation where indicated.

CONCLUSIONS

Intracranial haemorrhage and cerebral venous sinus thrombosis are rare but serious complications of tubercular meningitis. High clinical suspicion and early neuroimaging, particularly with MRI Brain/MRV, are essential for diagnosis. A combined approach of ATT, corticosteroids, and cautious anticoagulation can lead to favourable outcomes in selected patients. Clinicians should be vigilant for vascular complications in TBM, especially when patients exhibit sudden neurological deterioration.

Conflict of interest

The authors declare that they have no conflict of interest.

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