Post-TB Sequelae — Comprehensive MD Exam Answer (15 Marks)

INTRODUCTION

CLASSIFICATION (Table Format)

DETAILED DESCRIPTION OF EACH SEQUELA

1. HAEMOPTYSIS

• Rasmussen's aneurysm: Inflammation and necrosis of cavity walls → weakening → aneurysmal dilatation of pulmonary artery branches → rupture during coughing or exertion
• Direct erosion of capillaries/arteries by granulomatous inflammation or endarteritis
• Vasculitis secondary to TB antigen–antibody reaction
• TB endobronchitis — bleeding from bronchial granulomas
• Post-TB bronchiectasis and aspergilloma (secondary causes)
• Broncholith/cavernolith — calcified concretions detaching and eroding vessel walls

• Mild: bed rest, sedation, resuscitation, broad-spectrum antibiotics
• Massive (>600 mL/24 hours): blood transfusion + bronchial artery embolisation (BAE) — first-line; BAE is effective and relatively safe but re-bleeding risk is high in destroyed lung, chronic liver disease, fungal ball, elevated CRP
• Surgery (resection) — reserved for refractory cases with adequate pulmonary reserve
• Risk of re-bleeding after BAE is higher in: destroyed lung, anticoagulant use, fungal ball co-existence

2. ASPERGILLOMA (MYCETOMA / "FUNGUS BALL")

• Often asymptomatic — incidental radiological finding
• Haemoptysis — most common symptom (5%–90%)
  • Mechanisms: mechanical friction, endotoxin with haemolytic properties, Aspergillus-derived anticoagulant factor, local vasculitis, direct vascular invasion
• Chronic cough, weight loss, dyspnoea (less common)
• Mortality: 2–14%

• CXR: "Air crescent sign" — semi-circular crescentic air shadow around radio-opaque fungus ball in upper lobe cavity; fungus ball moves with position change (best seen on fluoroscopy/CT)
• Serum precipitins (IgG): Positive in ~100% of cases
• Sputum culture: Positive in ~50% only
• CT chest: Confirms position-dependent mobility of fungus ball

• Asymptomatic: Watch and wait — no treatment needed
• Systemic antifungals: Ineffective (cannot penetrate intracavitary fungi); IV amphotericin-B has no effect
• Itraconazole: Tried with varying success
• Local intracavitary instillation of amphotericin B — limited success
• BAE: Temporary measure for life-threatening haemoptysis only
• Surgery (lobectomy/pneumonectomy): Indicated for repeated severe haemoptysis with adequate lung reserve; surgical mortality 7%–23%
• Cavernostomy: Useful in complicated cases

3. POST-TB BRONCHIECTASIS

1. Caseation necrosis + granulomatous inflammation → destruction and dilatation of bronchi
2. Scarring → bronchial stenosis → mixed bacterial infection → retention of secretions → further destruction
3. Compression of bronchial lumen by enlarged TB lymph nodes (especially in children)
4. Broncholith formation — calcified lymph node penetrating airway
5. Healed TB cavities re-lined with ciliated columnar epithelium → structurally resemble bronchiectatic cavities
6. NTM (M. avium-intracellulare) colonisation in post-TB lung also contributes

• Predominantly upper lobe (most common site of TB)
• "Dry" or "sicca" bronchiectasis — effective gravitational drainage from upper lobes means less purulent sputum; presentation is more with haemoptysis or recurrent bacterial infections

• HRCT chest — investigation of choice (replaced bronchography)
• CXR findings non-specific

4. TB ENDOBRONCHITIS AND TRACHEITIS

• Occurs in ~one-third of pulmonary TB patients
• Routes of infection: direct implantation, submucosal lymphatics, haematogenous spread, from adjacent lymph nodes
• Clinical features: Cough, haemoptysis, breathlessness, sub-sternal constriction
• Sequela: Healing → bronchostenosis (permanent airway narrowing)

5. SPONTANEOUS PNEUMOTHORAX

• Incidence: 5%–15% of pulmonary TB patients
• In TB-endemic countries, TB is an important cause of pneumothorax
• Mechanism:
  • Rupture of subpleural TB cavity into pleural space → pyopneumothorax
  • Rupture of open healed cavity or bleb/bulla secondary to fibrosis and lung destruction

6. CALCIFICATION & BRONCHOLITH FORMATION

• Lung lesions of TB heal by calcification — hallmark of healed primary TB
• Calcifications are usually innocuous — discrete radio-opaque parenchymal shadows or sheet-like pleural calcifications
• Complications:
  • Calcified concretions may detach, erode through bronchial wall/blood vessel → massive haemoptysis
  • Patient coughs out calcified stones — broncholiths or pneumoliths
  • Extensive calcification → respiratory failure or chronic cor-pulmonale

7. "OPEN-NEGATIVE" SYNDROME

• Thin-walled cavities with complete epithelialisation extending from bronchioles to cavity lining
• Cavities remain open but do not collapse
• More common since the advent of chemotherapy ("isoniazid cavities")
• Clinically inactive — but histopathology may show incomplete epithelialisation with necrotic foci harboring Mtb
• Radiologically: Ring shadows with thin walls
• Hazards: Secondary infection, fungal ball formation (aspergilloma), scar carcinoma, spontaneous pneumothorax, loss of effective lung volume

8. SCAR CARCINOMA

• Development of lung cancer in TB scars is well-recognised
• In Auerbach's autopsy series: 82/1186 cases had scar carcinoma — 23.2% from TB scars
• A population cohort study found TB patients had 11-fold higher incidence of lung cancer vs non-TB subjects
• Hazard ratio for lung cancer further increased with co-existing COPD or smoking
• Presence of old TB lesion is an independent predictor of poor survival [HR 1.72] in squamous cell carcinoma
• Mechanism: Impaired lung ventilation → ↑ CO₂ → hyperplasia of pulmonary neuroendocrine cells → malignant transformation; also receptor sensitivity to O₂/CO₂ producing autocrine growth factors
• Meta-analysis (30 studies) — previous TB confers RR 1.76 for lung cancer (independent of smoking, RR 1.90)
• Most common histological type: NSCLC (especially adenocarcinoma)

9. PULMONARY FUNCTION CHANGES

• Obstructive airways disease: Diffuse airway obstruction in 30%–60% of pulmonary TB patients
• Restrictive defect: From diffuse parenchymal fibrosis, pleural effusion/thickening, and fibrothorax
• Mixed pattern: Most common in MDR-TB post-treatment sequelae
• Study from New Delhi (MDR-TB, n=130): At 24-month post-treatment follow-up — 78% had persistent respiratory symptoms; 98% had residual radiological sequelae; 96% had abnormal pulmonary function tests; 66% mixed pattern, 19% restrictive, 11% obstructive
• Study from Gujarat (n=264): 84% cough, 87% had obstructive airways disease

10. CHRONIC RESPIRATORY FAILURE

• Type I and Type II respiratory failure may complicate extensive TB
• Mechanism:
  • Extensive destruction of pulmonary parenchyma → ventilation-perfusion (V/Q) mismatch
  • Associated pleural thickening/fibrothorax → thoracic wall malfunction → pump failure
  • Atrophy/disuse of respiratory muscles → respiratory muscle pump failure
• Progressive tachypnoea, hypoxia (Type I) → hypercapnia (Type II) → death
• Destroyed lung/fibrothorax: all three components (parenchyma, bronchi, pleura) involved; lung grossly shrunken and fibrosed; mediastinum pulled to same side

11. PULMONARY HYPERTENSION AND CHRONIC COR-PULMONALE

1. Occlusion/destruction of vascular bed by lung parenchymal destruction
2. Vasculitis and endarteritis → ↓ cross-sectional area of pulmonary circulation
3. Hypoxia → hypoxic pulmonary vasoconstriction
4. Acidosis with hypercapnia
5. Increased blood viscosity from polycythaemia (less important in India due to malnutrition and anaemia)

• Distended neck veins, peripheral oedema, cyanosis
• Accentuated pulmonic component of S2 (earliest sign)
• Right ventricular S3 gallop in epigastrium
• Pulmonary regurgitation murmur, pansystolic TR murmur (accentuated on inspiration) with advanced PAH
• Raised JVP in both phases of respiration (right heart failure)

• P-pulmonale in leads II, III, aVF
• S1Q3 or S1-S2-S3 pattern
• Right axis deviation
• R:S ratio in V6 ≤ 1.0
• rSR' pattern in right precordial leads
• Dominant R or R' in V1/V3R with inverted T waves (definite sign)

12. SECONDARY (REACTIVE) AMYLOIDOSIS

• Mechanism: Chronic TB inflammation stimulates cytokines (IL-1, IL-6, TNF-α) → hepatic synthesis of serum amyloid A precursor → deposition of extracellular eosinophilic protein in organs
• Incidence of renal amyloidosis in TB: 8%–33%
• At PGIMER Chandigarh: TB most common predisposing cause of secondary amyloidosis (59.1%) → pulmonary TB leading cause (81.6%)
• Mean interval between onset of TB and amyloidosis: 6.9 years (>5 years in 67% of patients; range 6 months–43 years)
• Can occur even in adequately treated patients
• Diagnosis: Abdominal fat pad biopsy, rectal mucosal biopsy, liver/kidney biopsy — Congo red staining

13. CHRONIC EMPYEMA AND BRONCHOPLEURAL FISTULA

• Empyema: pus in pleural space, often mixed with mycobacteria and secondary bacteria
• Bronchopleural fistula (BPF): Pathological communication between bronchial tree and pleural space; may result from:
  • Active TB cavity rupture
  • Post-surgical complication
  • Chronic empyema eroding through bronchial wall
• BPF is a serious complication associated with repeated infections, protein loss, frozen shoulder, respiratory disability
• Management: Prolonged chest drainage, surgical intervention (thoracoplasty, pneumonectomy, muscle flap repair)

14. FIBROTHORAX AND DESTROYED LUNG

• "Destroyed lung" = all three compartments affected (parenchyma + bronchi + pleura)
• Lung grossly shrunken, fibrosed; mediastinum pulled to ipsilateral side
• Features: cavity, crepitations, recurrent infections, haemoptysis
• Progressive → respiratory cripple → respiratory failure → cor-pulmonale
• Surgical options: Pneumonectomy, pleuropneumonectomy (high morbidity/mortality in severely compromised patients)

15. NONTUBERCULOUS MYCOBACTERIAL (NTM) DISEASE

• Post-TB lung is a substrate for NTM colonisation and infection (especially M. avium-intracellulare)
• Distinction between colonisation and active NTM disease requires careful clinical assessment
• Important cause of ongoing respiratory disease after "cured" TB

SUMMARY TABLE FOR QUICK REVISION

CLINICAL SIGNIFICANCE

• 78% of cured MDR-TB patients have persistent respiratory symptoms at 24 months
• 98% have residual radiological changes
• 96% have abnormal pulmonary function tests (predominantly mixed pattern)
• TB survivors have significant long-term disability — the "day after TB" is a growing concern
• Early detection, pulmonary rehabilitation, and long-term follow-up are essential components of TB care beyond bacteriological cure