Complications of Tuberculosis

Introduction

1. Pulmonary (local) complications
2. Extrapulmonary complications
3. Systemic/multisystem complications

A. PULMONARY COMPLICATIONS

1. Hemoptysis

• Minor hemoptysis is common — results from destruction of lung parenchyma and rupture of blood vessels.
• Massive hemoptysis can be life-threatening. Key mechanisms:
  • Rasmussen aneurysm: Erosion of a tuberculous cavity into a pulmonary artery, forming a pseudoaneurysm — potentially fatal.
  • Aspergilloma (fungus ball) in healed cavities can erode bronchial/pulmonary vessels → massive fatal hemorrhage.
  • Superinfection of cavities by invasive organisms.
• Management: Emergency surgical resection or selective bronchial artery embolization.

2. Pneumothorax

• Occurs in <5% of patients with severe cavitary disease.
• Mechanism: Rupture of a tuberculous cavity → bronchopleural fistula, or rupture of a subpleural bleb into the pleural space.
• Delayed treatment → progressive infection and fibrosis → trapped air in pleural space (pyopneumothorax).
• Management: Tube thoracostomy with suction.

3. Pleural Effusion (Tuberculous Pleurisy)

• May occur early after primary infection (pleurisy with effusion) or late in post-primary cavitary disease.
• Often asymptomatic and may resolve spontaneously; however, 65% relapse rate if untreated — active pulmonary or extrapulmonary TB within 5 years.
• Pleural fluid characteristics: Exudate; WBC 500–2500/mL (predominantly lymphocytes); protein >50% of serum protein; glucose normal to low; AFB smear rarely positive; cultures positive in only 25–30%.
• Pleural biopsy: Most reliable for diagnosis (granulomas seen).

4. Empyema Thoracis

• Characterized by extensive, progressive parenchymal disease and cavitation.
• More common late in the disease in debilitated patients.
• Rupture of a cavity into pleural space is often catastrophic, associated with bronchopleural fistula formation.
• Untreated: Spontaneous pleuro-cutaneous fistula, chest wall mass, rib and vertebral destruction.

5. Airway Tuberculosis (Endobronchial TB)

• When a cavity drains infectious material into the bronchial tree → endobronchial TB.
• Bronchiectasis commonly complicates endobronchial TB.
• Bronchial stenosis: From extensive endobronchial damage or direct extension from tuberculous adenitis/lymphatic spread → presents as persistent segmental/lobar collapse, lobar hyperinflation, or obstructive pneumonia.
• Laryngeal TB: Most infectious form; results from proximal extension, pooling of infected secretions, or haematogenous spread. Usually coexists with active pulmonary disease.

6. Superinfection with Fungi (Aspergilloma)

• Healed open cavities and areas of bronchiectasis are susceptible to fungal superinfection.
• Most common organism: Aspergillus fumigatus → aspergilloma (fungus ball).
• Characteristic CXR finding: Opacity with air-crescent sign within a cavity.
• Clinically significant: May cause massive, fatal hemoptysis.

7. Cor Pulmonale

• Extensive pulmonary fibrosis and destruction → pulmonary hypertension → right ventricular failure (cor pulmonale).
• Results from chronic progressive disease with significant lung tissue destruction.

B. EXTRAPULMONARY COMPLICATIONS

8. Tuberculous Lymphadenitis (Scrofula)

• Most common form of extrapulmonary TB.
• More common in young women and children.
• Presentation: Enlarging, painless, firm, rubbery mass — most often in the anterior/posterior cervical chain or supraclavicular fossa.
• Progression: Nodes become matted → overlying skin inflamed → fluctuance → sinus tract (collar-stud abscess).
• Diagnosis: Fine-needle aspiration (FNA) — sensitivity 77%, specificity 93%; AFB smear positive in only ~20%.
• Do NOT incise and drain — permanent sinus tracts result.
• Treatment: Anti-TB drugs ± surgical excision if medical therapy fails.

9. Bone and Joint TB (Pott's Disease)

• Spinal TB (Pott disease): Accounts for 50–70% of skeletal TB cases.
• Hip/knee: 15–20%; other joints: 15–20%.
• Pathogenesis: Reactivation of dormant foci originally seeded haematogenously; OR contiguous spread from paravertebral lymph nodes.
• Clinical: Back pain/stiffness; loss of vertebral endplate "white stripe" on X-ray.
• Paraspinal cold abscess: Occurs in ≥50% → can spread forming "skip lesions."
• Main complication of Pott's disease: Spinal cord compression (Pott's paraplegia).
• Imaging: CT and MRI superior to plain X-ray.

10. Renal TB

• Kidney is highly vascular → haematogenous seeding → granulomas → scarring → obstruction along urinary tract (calyces, renal pelvis, ureters, bladder).
• Classic finding: Sterile pyuria (pyuria in acidic urine with no organisms on culture).
• Urinalysis: Pyuria, haematuria, albuminuria.
• Complications:
  • Nephrolithiasis
  • Ureteral obstruction or reflux
  • Hypertension
  • Papillary necrosis
  • Renal insufficiency
  • Autonephrectomy (putty kidney — dystrophic calcification of the entire kidney)
  • Rarely: Transitional cell carcinoma

11. Genital TB

• Males: Usually associated with renal TB; spreads to prostate, seminal vesicles, epididymides, testes. → Painless scrotal mass; epididymal/prostatic calcifications. → Infertility (seminal vesicle involvement).
• Females: Begins with haematogenous focus in fallopian tubes → spreads to endometrium (50%), ovaries (30%), cervix (5–15%), vagina (1%). → Infertility, menstrual irregularities, pelvic pain, ascites. → TB is an important cause of female infertility in endemic regions.

12. Tuberculous Pericarditis

• Results from: Direct extension from tracheobronchial tree, mediastinal/hilar lymph nodes, sternum, or spine; OR haematogenous spread in miliary TB.
• Leading cause of pericarditis in HIV-infected patients.
• Symptoms: Cough, chest pain, dyspnea.
• Signs: Cardiomegaly, pericardial rub, fever, tachycardia.
• Complications:
  • Pericardial effusion (cardiac tamponade)
  • Constrictive pericarditis — fibrous thickening and calcification of pericardium → impaired cardiac filling → clinical triad of raised JVP, ascites, and peripheral edema.

13. Tuberculous Peritonitis

• Presents with abdominal pain, fever, ascites.
• Ascites is an exudate; may mimic ovarian/endometrial cancer or Meigs syndrome.
• Laparoscopic biopsy with culture is confirmatory.

C. MULTISYSTEM/SYSTEMIC COMPLICATIONS

14. Miliary Tuberculosis

• Massive haematogenous dissemination to multiple organs — lesions resemble millet seeds (1–2 mm diameter).
• Pathogenesis: Host unable to contain primary or reactivated TB infection → haematogenous seeding of liver, spleen, lungs, kidneys, meninges, bone marrow, adrenals.
• Risk groups: Young children after primary infection; older adults; immunocompromised (HIV, corticosteroids, anti-TNF therapy); alcohol use disorder; cirrhosis; malignancy.
• Clinical: Insidious onset; fever, night sweats, weight loss, anorexia, hepatosplenomegaly.
• CXR: Classic miliary pattern (snowstorm appearance) — but absent in ~50% of cases.
• Laboratory: Hyponatraemia (SIADH — commonly associated with meningitis); pancytopaenia from bone marrow involvement.
• Cultures: Sputum, urine, draining lesions, blood.
• Mortality: ~21% (high due to diagnostic delay).
• Fulminant miliary TB: Can cause ARDS and DIC — most life-threatening presentation.

15. Tuberculous Meningitis (CNS TB)

• Accounts for ~6% of all extrapulmonary TB; gravest consequence.
• Peak incidence: Newborns to 4-year-old children.
• Mechanism: Rupture of a subependymal tubercle into the subarachnoid space.
• Clinical features: Fever, headache, meningism; cranial nerve palsies (CN III, VI, VII); altered sensorium.
• CSF: Lymphocytic pleocytosis, elevated protein, low glucose, rarely AFB positive on smear.
• Often coexists with miliary TB (~50% of TBM cases have pulmonary disease).
• Complications: Hydrocephalus, cranial nerve palsies, stroke (vasculitis), cerebral tuberculoma, SIADH, death.
• CNS tuberculoma: Slow-growing, space-occupying lesion; contrast-enhancing ring lesion on MRI.

16. Adrenal TB (Addison's Disease)

• Bilateral adrenal gland destruction by haematogenous TB → primary adrenal insufficiency (Addison's disease).
• TB is a classic cause of Addison's disease worldwide.
• Adrenal calcification on CT is a clue.

17. Secondary (Reactive) Amyloidosis (AA Amyloidosis)

• Chronic TB is a classical cause of secondary (AA) amyloidosis.
• Prolonged inflammation → sustained production of serum amyloid A (SAA) → amyloid deposition in kidneys (nephrotic syndrome), liver, spleen.
• Presents as nephrotic syndrome; can progress to renal failure.

D. COMPLICATIONS DUE TO TREATMENT (Drug-Related)

Summary Table