Complications Of Secondary Pulmonary Tuberculosis

Complications Of Secondary Pulmonary Tuberculosis

Fate of Secondary Pulmonary Tuberculosis:

Subapical tuberculous lesions in the lungs can develop following outcomes:

1. The lesions may heal with fibrous scarring and calcification.
2. The lesions may coalesce together to form larger area of tuberculous pneumonia and produce progressive secondary pulmonary tuberculosis with the following pulmonary and extrapulmonary involvements:

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• • Fibrocaseous tuberculosis
  • Tuberculous caseous pneumonia
  • Miliary tuberculosis
  • Tuberculous empyema
  • These lesions are briefly described below.

Fibrocaseous Tuberculosis:

The original area of tuberculous pneumonia undergoes peripheral healing and massive central caseation necrosis which may:

• Either break into a bronchus from the cavity (cavitary or open fibrocaseous tuberculosis), or
• Remain, as a soft caseous lesion without drainage into a bronchus or bronchiole to produce a non-cavitary lesion (chronic fibrocaseous tuberculosis).

The cavity provides favourable environment for the proliferation of tubercle bacilli due to high oxygen tension. The cavity may communicate with bronchial tree and becomes the source of spread of infection; this is called open tuberculosis.

Complication Of Tuberculosis

The open case of secondary tuberculosis may implant tuberculous lesion on the mucosal lining of air passages producing endobronchial and endotracheal tuberculosis.

Ingestion of sputum-containing tubercle bacilli from endogenous pulmonary lesions may produce laryngeal and intestinal tuberculosis.

• Grossly: Tuberculous cavity is spherical with thick fibrous wall, lined by yellowish, caseous, necrotic material and the lumen may be traversed by thrombosed blood vessels. Around the wall of cavity are seen foci of consolidation. The overlying pleura may also be thickened
• Microscopically: The wall and lumen of the cavity shows eosinophilic, granular, caseous material which may show foci of dystrophic calcification. Widespread coalesced tuberculous granulomas composed of epithelioid cells, Langhans’ giant cells and peripheral mantle of lymphocytes and having central caseation necrosis are seen. The outer wall of cavity shows fibrosis.

Complication Of Tuberculosis

Cavitary secondary tuberculosis may develop the following complications:

• Aneurysms of patent arteries crossing the cavity produce haemoptysis.
• Extension into pleura-producing bronchopleural fistula.
• Tuberculous empyema from deposition of caseous material on the pleural surface.
• Thickened pleura (pleurisy) from adhesions of parietal pleura.

Tuberculous Caseous Pneumonia:

Caseous material from a case of secondary tuberculosis in an individual with high degree of hypersensitivity may spread to rest of the lung producing caseous pneumonia.

Microscopically, the lesions show exudative reaction with oedema, fibrin, polymorphs and macrophages. Numerous tubercle bacilli can be demonstrated in the exudates.

Complication Of Tuberculosis – Miliary Tuberculosis:

This is lymphohaematogenous spread of tuberculous infection from primary focus or later stages of tuberculosis. The spread may occur to systemic organs or isolated organs. The spread is either by the entry of infection into pulmonary vein producingdisseminated or isolated organ lesion in different extra-pulmonary sites (for example, Liver, spleen, kidney, brain, meninges, genitourinary tract and bone marrow), or into the pulmonary artery restricting the development of miliary lesions within the lung

• Grossly: Miliary lesions are millet seed-sized (1 mm diameter), yellowish, firm areas without grossly visible caseation necrosis.
• Microscopically: The lesions show the structure of tubercles with minute areas of caseous necrosis.

Pleurisy And Tuberculous Empyema:

Caseating pulmonary lesions of tuberculosis may be associated with pleurisy (pleuritis, pleural effusion) as a reaction and is expressed as a serous or fibrinous exudates.

Pleural effusion may heal by fibrosis and obliterate the pleural space (thickened pleura by chronic pleuritis). Occasionally, pleural cavity may contain caseous material and develop into tuberculous empyema. Depicts various pulmonary and pleural lesions in tuberculosis

Clinical Features And Diagnosis of Tuberculosis:

Clinical manifestations in tuberculosis may be variable depending upon the location, extent and type of lesions. However, in secondary pulmonary tuberculosis which is the common type,

The usual clinical features are as under:

• Referable to lungs: Such as productive cough (may be with haemoptysis), pleural effusion, dyspnoea,orthopnoea etc. Chest X-ray may show typical apical changes like pleural effusion, nodularity, and miliary or diffuse infiltrates in the lung parenchyma.
• Systemic features: — such as fever, night sweats, fatigue, loss of weight and appetite. Longstanding and untreated cases of tuberculosis may develop systemic secondary amyloidosis.

Diagnosis of tuberculosis in a suspected case can be made by following tests:

• AFB microscopy of diagnostic specimen such as sputum, and aspirated material.
• Mycobacterial culture (traditional method on LJ medium for 4-8 weeks, newer rapid method by HPLC of mycolic acid with result in 2-3 weeks).

• Molecular methods such as PCR.
• Complete haemogram (lymphocytosis and raised ESR).
• Radiographic procedures for example, Chest X-ray showing characteristic hilar nodules and other
  parenchymal changes).
• Tuberculin skin test (TST, Mantoux test).
• Interferon gamma release assay (IGRA) (for example, Quantiferon-TB-gold, elispot) is a measure of cytokine released in the blood and is advocated as a substitute to the tuberculin skin test.
• However, serologic tests based on detection of antibodies are not useful although these are being used some developing countries but are not recommended by the WHO for the diagnosis of tuberculosis.
• Fine needle aspiration cytology of an enlarged peripheral lymph node is quite useful and easy way for confirmation of diagnosis and has largely replaced the biopsy diagnosis of tuberculosis (see Appendix I).
• Causes of death in pulmonary tuberculosis are usually pulmonary insufficiency, pulmonary haemorrhage, sepsis due to disseminated miliary tuberculosis, cor pulmonale or secondary amyloidosis.

Tuberculosis:

• In tuberculosis, tissue response to the causative organism, Mycobacterium tuberculosis, (a strict aerobe) is a classic example of caseating granulomatous inflammation associated with Langhans’ and foreign body giant cells.
• The organism is acid-fast bacillus (AFB) which can be demonstrated by Ziehl-Neelsen staining.
• Tubercle bacilli contain glycoside cord factor essential for the growth of the organism and glycolipids in the bacterial cell wall.
• Tuberculosis is worldwide in distribution, more common in developing countries. Other factors include malnutrition, poverty and chronic debilitating diseases and immunocompromised states like AIDS.
• The infection is commonly transmitted by inhalation of cough droplets from an infected individual and self-ingestion of infected sputum. The disease may spread locally, and by lymphohaematogenous route.
• Primary tuberculosis is infection of an individual who has not been previously infected, also called childhood tuberculosis or Ghon’s complex.
• It affects lung most commonly and the tissue response is by the formation of a small area of consolidation in the lung, and granulomatous involvement of lymphatic vessel and hilar lymph nodes.
• Secondary pulmonary tuberculosis includes fibrocaseous (cavitary) type, tuberculous caseous pneumonia, military spread to various organs and tuberculous pleurisy.
• Common methods of diagnosis of pulmonary tuberculosis are demonstration of the organism in the sputum, haematologic tests (raised ESR), positive Mantoux skin test, and X-ray chest.
• Fine needle aspiration of enlarged lymph nodes is a convenient method of confirmation of diagnosis.