Tb meningitis–associated CNS vasculitis and stroke in HIV and diabetes: Highlighting multidisciplinary management

Priya*

Staff Nurse, Kauvery Hospital, Hosur, Tamil Nadu

*Correspondence

Abstract

Tuberculous meningitis (TBM) remains a major cause of morbidity and mortality, particularly in immunocompromised individuals. Central nervous system (CNS) vasculitis is a recognized complication, often leading to ischemic stroke, especially in the posterior circulation. We report a case of a 51-year-old male with newly diagnosed HIV infection and Type II diabetes mellitus who presented with subacute headache, fever, diplopia, and gait incoordination. Neuroimaging revealed multiple posterior circulation infarcts suggestive of vasculitis. Cerebrospinal fluid (CSF) analysis and PCR confirmed tuberculous meningitis. The patient was managed with antitubercular therapy and corticosteroids, with deferral of antiretroviral therapy due to high risk of immune reconstitution inflammatory syndrome (IRIS). This case highlights the importance of early recognition of TBM-associated vasculitis in immunocompromised patients.

Key words: Tuberculous meningitis (TBM); Immune reconstitution inflammatory syndrome (IRIS); Central nervous system (CNS)

Introduction

Tuberculous meningitis is the most severe form of extrapulmonary tuberculosis. It is particularly prevalent among immunocompromised individuals, including persons living with HIV/AIDS (PLHA). Stroke occurs in approximately 15–57% of TBM cases and is commonly attributed to inflammatory vasculitis affecting perforating vessels, particularly in the basal and posterior circulation regions. This case illustrates the interplay between TBM, HIV-associated immunosuppression, diabetes mellitus, and secondary CNS vasculitis leading to ischemic stroke.

Case presentation

A 51-year-old male with a known history of Type II diabetes mellitus presented with a 1-month history of progressive holocranial headache, which worsened during the evenings, accompanied by intermittent fever for 20 days. Over the preceding 10 days, he developed horizontal diplopia, particularly noticeable during near vision tasks. The patient also reported vomiting, reduced oral intake, and gait imbalance, requiring support for ambulation. No gastrointestinal complaints were noted.

Examination

Upon admission, the patient was conscious, alert, and oriented, but appeared lethargic. Neck stiffness was present, suggestive of meningeal irritation. Mild limb and gait incoordination was observed, although no new focal neurological deficits or nystagmus were detected. Extraocular movements were full.

Vital Signs

BP	140/80 mmHg
PR	80/min
RR	20/min
SpO₂	99% on room air
GRBS	290 mg/dL

Investigations

Lab Test	Results
Hb	13.2g/dl
TC	7100 cells/mm³
Platelets	2.91 lakh/mm³
ESR	28 mm/hr
Sodium	125 mmol/L
Potassium	5.4 mmol/L
HbA1c	11%
CD4 count	67 cells/µL
HIV 1 & 2 (P24 Ag & Ab)	Reactive

CSF Analysis

Clear, colourless.
Glucose: 118 mg/dL.
Protein: 345 mg/dL (elevated).
Cell count: 66 cells/µL.
Lymphocytes: 80%.
RBCs: Not seen.
Gram stain: No organisms.
CSF MTB PCR: Positive.
Cryptococcal antigen: Negative.
CSF culture: No growth.

Neuroimaging

MRI Brain

Acute non-haemorrhagic lacunar infarcts in:
Right anterior cerebellum.
Superior vermis.
Right hemipons.
Suggestive of posterior circulation infarcts. No mass lesion. No abnormal meningeal enhancement.
Findings were consistent with secondary vasculitis due to tuberculous meningitis.

Final diagnosis

Tuberculous meningitis.
Posterior circulation ischemic stroke secondary to CNS vasculitis.
PLHA (newly diagnosed HIV infection).
Hypovolemic hyponatremia.
Type II diabetes mellitus.

Nursing management:

Neurological assessment

Monitored level of consciousness (GCS), orientation, and behaviour changes.
Assessed cranial nerves—especially for diplopia, nystagmus, facial asymmetry, and limb coordination.
Observed for signs of raised intracranial pressure (ICP): headache, vomiting, bradycardia, altered sensorium.
Monitored limb strength, coordination, and gait regularly.

Care related to antitubercular therapy (AKURIT-4)

Ensured timely administration of ATT as prescribed.
Monitored the patient for adverse drug reactions such as hepatotoxicity, GI upset, and hypersensitivity.
Assessed liver function tests periodically and report abnormalities to the physician.
Educated the patient on the importance of strict drug adherence to prevent treatment failure or resistance.

Care related to corticosteroid therapy (Dexamethasone)

Monitored blood glucose levels frequently due to steroid-induced hyperglycemia.
Observed for signs of infection, as steroids suppress immunity.
Monitored for gastric irritation; administer medications with food if indicated.
Assessed for reduction in neurological symptoms and improvement in headache or nuchal rigidity.

Management of cerebral edema (Mannitol)

Monitored neurological status (GCS, pupil reaction, orientation) every 2–4 hours.
Recorded intake–output strictly to detect osmotic diuresis.
Monitored serum electrolytes and osmolality for early detection of imbalances.
Maintained head of bed at 30 degrees to promote venous drainage and reduce ICP.

Antiplatelet therapy (Aspirin)

Monitored for bleeding tendencies such as gum bleeding, bruising, or black stools.
Assessed neurological status for recurrent stroke symptoms.
Ensured patient takes aspirin after food to reduce gastric irritation.

Correction of electrolyte imbalance

Monitored serum sodium and potassium levels regularly, especially in hyponatremia.
Maintained a strict fluid balance chart and monitor for dehydration.
Administered IV fluids as prescribed and observe for improvement in sensorium and vital signs.
Assessed for symptoms of electrolyte disturbances (weakness, confusion, seizures).

Glycemic control with oral hypoglycemics

Monitored capillary blood glucose frequently, especially with concurrent steroid therapy.
Educated the patient on diabetic diet and the importance of maintaining stable glucose levels.
Ensured adherence to prescribed diabetic medications.

ART management and IRIS prevention

Provided education on why ART initiation is currently deferred in TBM (to prevent IRIS).
Monitored for any new neurological symptoms that may suggest inflammatory worsening.
Offered psychological support due to the new HIV diagnosis and changes in ART plan.
Prepared the patient for ART re-initiation during follow-up as advised.

Ophthalmology evaluation for retinitis

Assisted in coordinating ophthalmology consultations.
Monitored for complaints of visual disturbances, photophobia, or diplopia.
Educated the patient on reporting any sudden changes in vision.
Documented findings and follow recommendations from ophthalmology.

Nutritional and glycemic Support

Provided high-protein, diabetic-appropriate diet.
Monitored for nausea/vomiting and provide antiemetics.
Ensured adequate hydration.

Psychosocial and educational support

Provided emotional support following new HIV diagnosis.
Explained disease condition, prognosis, and importance of ATT adherence.
Educated about timing of ART initiation to avoid IRIS.
Involved family members in care discussions and discharge planning.

Outcome

During the course of hospitalization, the patient demonstrated gradual clinical improvement with timely initiation of antitubercular therapy, corticosteroids, and supportive management. His headache and fever reduced significantly, and there was stabilization of neurological symptoms. Although mild gait and limb incoordination persisted, no new focal deficits or deterioration were noted.

Electrolyte disturbances, particularly hyponatremia, were effectively corrected with appropriate fluid management. Glycemic levels improved with adjusted oral hypoglycemic therapy. ART, which was initially started, was withheld after confirmation of tuberculous meningitis due to the high risk of precipitating immune reconstitution inflammatory syndrome (IRIS). By the time of discharge, the patient was conscious, oriented, and hemodynamically stable, with residual but non-progressive cerebellar signs. Neck stiffness had reduced to terminal limitation. The patient and caregivers were educated regarding medication adherence, infection precautions, and warning signs requiring urgent medical attention.

Discussion – medical aspects

Tuberculous meningitis represents the most severe form of tuberculosis and is associated with serious complications such as cranial nerve palsy, cerebral edema, vasculitis, and ischemic stroke. In this patient, posterior circulation infarcts involving the cerebellum, vermis, and pons were attributed to inflammatory vasculitis caused by the basal meningeal exudates typical of TBM. Early MRI findings were crucial to identifying these lesions before irreversible neurological deficits occurred. HIV co-infection with a CD4 count of 67 cells/µL further amplified susceptibility to TBM and complicated the clinical course. Severe immunosuppression often leads to atypical presentations, delayed diagnosis, and increased risk of neurological sequelae. The management required balancing urgent antitubercular therapy with careful timing of antiretroviral therapy to prevent immune reconstitution inflammatory syndrome (IRIS), which can worsen CNS inflammation and increase mortality in TBM. Hyponatremia in this case was likely multifactorial, with hypovolemia being the primary contributor, although SIADH and cerebral salt wasting are also well-recognized complications of TBM. Correction of sodium imbalance played a key role in stabilizing sensorium and preventing seizures.

Diabetes mellitus (HbA1c 11%) added an additional layer of complexity, worsening immune function and delaying recovery. Steroid therapy, while essential for reducing inflammation and cerebral edema, further impacted glycemic control and required close monitoring. Medical management included ATT (AKURIT-4), corticosteroids, mannitol for cerebral edema, antiplatelet therapy for stroke prevention, electrolyte correction, and glycemic control. ART was intentionally deferred to reduce IRIS risk. This multidisciplinary approach was essential for stabilizing the patient’s neurological and systemic health.

Discussion – Nursing aspects

Nursing care played a fundamental role in early detection of complications, continuous monitoring, medication safety, and patient education. Neurological assessment focusing on GCS, cranial nerve evaluation, coordination, and signs of raised intracranial pressure helped track the progression and response to therapy. Frequent monitoring allowed timely intervention in case of worsening edema, stroke, or altered sensorium. Nurses ensured safe administration of antitubercular drugs, monitored for hepatotoxicity, and reinforced treatment adherence crucial factors in preventing drug resistance. Steroid therapy required vigilant monitoring of blood glucose levels, infection prevention measures, and awareness of gastrointestinal side effects. Because the patient had significant electrolyte imbalance, strict fluid balance charting, serial sodium monitoring, and assessment for signs of dehydration or seizures were essential nursing responsibilities. Mannitol administration mandated careful monitoring of urine output, osmolality, and ICP-related symptoms. Mobility support, gait assistance, and fall precautions were vital due to cerebellar involvement and the risk of further injury. Nutritional support addressed both diabetic needs and poor intake secondary to vomiting. Nurses also coordinated ophthalmology consultations to rule out HIV-related retinitis and monitored for visual disturbances. Psychosocial support was an important nursing focus, especially after the new diagnosis of HIV. Nurses educated the patient and family regarding TBM, medication regimens, ART deferral, infection control practices, and follow-up requirements. This holistic approach enhanced patient understanding, improved compliance, and supported emotional well-being. Nursing management contributed significantly to stabilizing neurological status, preventing complications, improving safety, and facilitating recovery. Effective communication, continuous assessment, and multidisciplinary coordination were key components of nursing care in this complex case.

Conclusion

Tuberculous meningitis should be considered in immunocompromised patients presenting with prolonged fever, headache, and neurological symptoms. CNS vasculitis leading to posterior circulation infarcts is a serious complication requiring early imaging and prompt treatment. Integrated medical therapy combined with vigilant nursing monitoring, patient education, and coordinated multidisciplinary care is essential for improving prognosis in TBM, particularly in patients with HIV and diabetes. Early diagnosis, prompt initiation of ATT and steroids, and careful timing of ART are crucial to improving outcomes.

Tb meningitis–associated CNS vasculitis and stroke in HIV and diabetes: Highlighting multidisciplinary management

Tb meningitis–associated CNS vasculitis and stroke in HIV and diabetes: Highlighting multidisciplinary management

Priya*

Nightingale Journals