• 6 months for fingernails
• 12 months for toenails

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Complications of Tuberculous Meningitis

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MRI: Gadolinium Enhancement in TB Meningitis

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1. Hydrocephalus

• Communicating hydrocephalus - blockage of basal cisterns (most common)
• Obstructive hydrocephalus - ependymitis blocking the aqueduct or fourth ventricle (less common)
• Ventriculoperitoneal shunting is required in ~25% of patients
• Endoscopic third ventriculostomy (ETV) is an alternative, particularly in children (recent 2025 systematic review, PMID 40479834)

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2. Vasculitis and Cerebral Infarction

• Obliterative endarteritis: The arteries running through the subarachnoid space develop marked intimal thickening, leading to arterial occlusion and brain infarction
• Predominantly affects the middle cerebral artery territory and perforating branches supplying the basal ganglia
• Results in hemiplegia, movement disorders (including hemiballism), or focal deficits
• This is one of the "most serious complications" of chronic TBM - Robbins & Cotran Pathologic Basis of Disease

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3. Cranial Nerve Palsies

• CN III, IV, VI - ocular palsies (most common)
• CN VII - facial palsy
• CN VIII - sensorineural deafness
• CN II - optic involvement, papilledema

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4. Arachnoid Fibrosis (Adhesive Arachnoiditis)

• Contributes further to hydrocephalus
• Entraps spinal nerve roots when it extends to the spinal subarachnoid space
• Causes spinal radiculopathies and cord compression

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5. Tuberculomas

• Tumor-like masses of tuberculous granulation tissue, 2-12 mm in diameter, forming in the brain parenchyma
• May produce focal neurologic deficits or obstructive hydrocephalus (especially periventricular location)
• In developing countries, represent 5-30% of all intracranial mass lesions
• Paradoxical enlargement can occur during anti-TB therapy - managed with adjunctive corticosteroids
• Adams & Victor's Principles of Neurology, 12th ed.

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6. Spinal Cord Involvement (Myeloradiculitis)

• Spinal block from exudate compression
• Posterior and lateral column disease (from pia/ependyma invasion into cord parenchyma)
• Multiple spinal radiculopathies
• Pott's disease (Pott paraplegia) - tuberculous osteomyelitis of the spine leading to vertebral body collapse, kyphosis, and cord compression by an epidural abscess or granulation tissue mass

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7. Cerebral Abscess

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8. Seizures

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9. Metabolic Complications

• Hyponatremia - due to syndrome of inappropriate antidiuretic hormone (SIADH), noted at presentation
• Hypothermia - reported in some cases at time of diagnosis

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10. Long-term Neurologic Sequelae

• Cognitive impairment and intellectual disability (especially children)
• Persistent motor deficits (hemiplegia, paraplegia)
• Persistent cranial nerve deficits
• Epilepsy
• Visual loss

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Summary Table

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Clinical Case Analysis: 39-Year-Old Man with Recurrent Chest Pain

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ECG Reference: Wellens Syndrome Patterns

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Question 1: Main Diagnosis, Leading Syndrome, Concomitant Diseases, Complications, and Differential Diagnosis

Leading Syndrome

• Recurrent central chest pain at rest and with minimal exertion
• Pain not relieved by standard therapy (ranitidine ineffective)
• High-risk ECG pattern (Wellens syndrome - see Q4)
• Multiple cardiovascular risk factors

Main Diagnosis (Structured Format)

• Classification by ACS type: NSTE-ACS (unstable angina, cTnI negative x2)
• GRACE risk score: High-risk (age 39 + multiple risk factors + ECG changes + recurrent symptoms)
• Canadian Cardiovascular Society (CCS) class: Class III-IV (symptoms at minimal exertion and at rest)
• Braunwald classification of Unstable Angina: Class IIIB (rest angina, >48 hours, no precipitating cause)

1. Arterial hypertension (BP 145/80 mmHg, untreated)
2. Active smoking (20 cigarettes/day - 20 pack-year history)
3. Family history of premature CAD (father MI at age 41)
4. Likely insulin resistance / pre-diabetes (South Asian ethnicity + family history of diabetes)

• At risk for: Anterior STEMI (proximal LAD occlusion), cardiogenic shock, malignant arrhythmia, sudden cardiac death - the Wellens pattern identifies this patient as having a time-critical pre-infarction state

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Differential Diagnosis: 3 Diseases

1. Gastro-oesophageal Reflux Disease (GERD) - Already diagnosed on 2nd visit

• Ranitidine 150 mg BD gave no relief across 3 weeks
• The ECG now shows deep T-wave inversions in V2-V5 - GERD does not produce precordial T-wave changes
• High cardiovascular risk profile (South Asian, family history premature CAD, hypertension, smoking) makes cardiac ischemia statistically far more likely
• The pain is not clearly postprandial, positional, or relieved by antacids
• GERD diagnosis should never be accepted until cardiac causes are fully excluded in a high-risk patient - Fuster & Hurst's The Heart, 15th ed.

2. Pulmonary Embolism (PE)

• No pleuritic quality, no dyspnoea, no tachycardia (HR 75), O2 sat 98%
• No risk factors for VTE (no immobility, surgery, malignancy, long-haul travel)
• ECG does not show S1Q3T3 pattern or right heart strain; instead shows anterior precordial T-wave changes pointing to LAD territory ischemia
• Three-week history without haemodynamic deterioration is atypical for significant PE

3. Aortic Dissection

• Pain is NOT tearing/ripping in character, NOT sudden-onset maximal from the start
• Does NOT radiate to the back
• BP equal bilaterally (implied by single BP reading, no pulse deficit described)
• Recurrent 3-week history is incompatible with untreated aortic dissection (which is rapidly lethal if untreated)
• ECG changes are anterior ischemic, not the diffuse non-specific changes of dissection

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Question 2: Description of Typical Angina

1. Substernal pressure-like discomfort - described as squeezing, heavy, burning, or tightness in the central chest; patients often deny "pain" and use terms like "pressure," "ache," or "tightness"
2. Precipitated by exertion or emotional stress - due to increased myocardial oxygen demand exceeding supply across a fixed atherosclerotic obstruction
3. Relieved by rest or sublingual nitroglycerin within 5 minutes

• Duration typically 2-5 minutes, rarely more than 15 minutes
• May radiate to the left arm, jaw, neck, or shoulder
• Reproducible threshold - the same degree of exertion consistently triggers pain
• Worsened by cold, heavy meals, emotional upset
• Atypical presentations (nausea, diaphoresis, fatigue without chest pain) are more common in women, diabetics, and the elderly

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Question 3: ECG Findings (Fig. 4.1)

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Question 4: Differential Diagnosis of the ECG Findings and Most Likely Diagnosis

Differential Diagnosis for Anterior T-wave Inversions

Most Likely Diagnosis: Wellens Syndrome (Type B)

• Definition: Wellens syndrome is a specific ECG pattern of T-wave changes in leads V2-V3 (often extending to V4-V5) that represents critical stenosis of the proximal left anterior descending artery (LAD) during a pain-free interval between ischemic episodes
• Type A (25%): Biphasic T waves (initially positive then negative) in V2-V3
• Type B (75%): Deep, symmetric T-wave inversions in V2-V3 - this patient has Type B
• The T-wave changes occur during the pain-free interval - this is the hallmark and is exactly what is seen here (patient is "anxious but pain free" on examination)
• Troponin is typically negative or minimally elevated because these changes reflect reperfused ischemia, not completed infarction
• This ECG pattern predicts imminent anterior STEMI if the LAD occludes completely. Up to 75% of untreated Wellens patients progress to extensive anterior MI. - Rosen's Emergency Medicine

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Question 5: Most Correct Next Management Step

Immediate Actions (Emergency Management)

Step 1 - Immediate Stabilisation

Step 2 - Antiplatelet Therapy (Dual)

Step 3 - Anticoagulation

Step 4 - Anti-ischemic Therapy

Step 5 - Urgent Coronary Angiography + PCI

• Wellens syndrome mandates urgent invasive strategy - coronary angiography within 24-48 hours (or immediately if pain recurs or haemodynamic deterioration)
• Expected finding: critical proximal LAD stenosis (typically >90%)
• Treatment: Percutaneous Coronary Intervention (PCI) with drug-eluting stent (DES) to the proximal LAD
• If anatomy is unsuitable for PCI: Coronary Artery Bypass Grafting (CABG) referral

Step 6 - Other Medications

Medications to AVOID in Wellens Syndrome

• Stress testing / exercise ECG - absolutely contraindicated, can precipitate complete LAD occlusion and massive anterior MI
• Dobutamine stress echo - also contraindicated
• Discharge on medical management alone without angiography - high mortality risk

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Question 5 (Part B): Specialist Referral

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Summary: Key Clinical Pearls in This Case

1. Never accept a GI diagnosis in a high-risk chest pain patient without a normal ECG - this patient had anterior T-wave changes that signalled impending LAD occlusion
2. Wellens syndrome is a pre-infarction state - normal troponins and pain-free state make it deceptively reassuring, but it carries a very high risk of anterior STEMI
3. South Asian men have a 3-4x higher risk of premature CAD than the white European population - the age of 39 is not reassuring in this ethnicity
4. Family history of MI at 41 pushes the pre-test probability of significant CAD very high
5. Stress testing is contraindicated - the correct next step is urgent angiography, not more non-invasive testing