Complications
Patients may transmit infection to close contacts. As soon as TB is suspected, the treating physician must take steps to prevent further transmission. These include isolating the patient at home or in a negative-pressure room (if hospitalised). If isolated at home, the patient must not have new contacts or come into contact with small children or immunocompromised individuals.
The conservative approach dictates that patients are considered infectious until 3 consecutive sputum acid-fast bacilli smears are negative, they have been on standard therapy for at least 2 weeks, and they show clinical improvement on TB therapy.[94]
Also known as a paradoxical response. This syndrome involves transient worsening of TB symptoms and lesions following initiation of antituberculosis therapy. This is much more common in HIV-positive patients with severe immunosuppression who are placed on antiretroviral therapy (ART).[79]
Up to 20% to 30% of HIV-infected TB patients may develop IRIS after initiation of ART (median onset 2 weeks). IRIS is also described in HIV-negative patients, where median onset of paradoxical symptoms is 8 weeks after initiation of therapy. In both groups, IRIS appears to be more common in extrapulmonary TB.
Presentation may include fever, worsening of chest x-ray, lymphadenopathy, or an increase in pleural effusions.
Other aetiologies, such as bacterial pneumonia and Pneumocystis jirovecii pneumonia, should be eliminated, as well as TB treatment failures because of undetected non-adherence to TB therapy or drug-resistant TB.[80][95][96]
Paradoxical responses are transient, and generally antituberculosis or ART therapy does not need to be discontinued. If there are significant symptoms, consider steroids (e.g., prednisone 1-2 mg/kg once daily for a few weeks then taper gradually over several weeks) while maintaining antituberculosis and ART. For severe and occasionally life-threatening IRIS, some or all therapy might need to be discontinued.
TB is an uncommon cause of respiratory failure requiring mechanical ventilation (MV). There is a stronger association between respiratory failure and miliary TB than with tuberculous pneumonia (20-fold greater risk). Mortality rate in TB requiring MV is up to 69%.[93]
Treatment is directed at respiratory support with MV and antituberculosis therapy. In these critically ill patients malabsorption may be present with resulting inadequate drug concentrations, and treatment may require use of parenteral antituberculosis medicines (e.g., isoniazid, rifampicin, levofloxacin, and amikacin).
Results from rupture into the pleural space of a peripheral cavity or of a subpleural caseous focus that has liquefied. The associated bronchopleural fistula (BPF) may seal off or persist. Large BPF may lead to empyema formation.[54] Management is with chest tube (tube thoracostomy). Persistent BPF may require surgical repair.
May be seen in primary disease but usual presentation is in the setting of extensive parenchymal disease.
Management is with chest tube (tube thoracostomy). May require surgical intervention.
May result from primary TB, distal to the site of obstruction if adenopathy causes bronchial compression. If re-activation causes parenchymal destruction, bronchiectasis may develop in the area of involvement.
Symptoms are similar to those associated with other causes of bronchiectasis, but may be minimal (dry bronchiectasis). Diagnosis is best made with high-resolution computed tomography.
Extensive pulmonary parenchymal destruction may occur in primary or re-activation TB. Pulmonary destruction is usually the result of chronic, progressive, untreated pulmonary TB. Radiological studies may show a fibrotic, contracted lung; hilar elevation, lower lobe emphysema, and bronchiectasis may also be present. An uncommon, rapidly progressive process of pulmonary destruction is known as pulmonary gangrene. Diffuse vascular thrombosis leads to infarction and necrosis.
Intermittent or persistent collapse of the RML due to compression of the RML bronchus by adjacent enlarged lymph nodes. May be seen as a result of TB or other aetiologies. May predispose to recurrent RML pneumonias. Diagnosed by bronchoscopy. Severe cases may require lobectomy.
TB accounts for <10% of cases of haemoptysis.[97][98] It may be seen in active or treated disease and is usually small in volume. Cases of massive haemoptysis because of TB may result from a Rasmussen aneurysm resulting from erosion of a TB cavity into a vessel wall. TB-related aetiologies of haemoptysis include bronchiectasis, aspergilloma, or scar carcinoma.
Evaluation for haemoptysis may include sputum studies (for TB recurrence), bronchoscopy, and chest computed tomography.
In active TB, sedation, bed rest, and antituberculosis therapy may be adequate. For more severe haemoptysis, pulmonary consultation should be obtained and treatment may involve interventional radiology (for embolisation) or thoracic surgery for resection.[54]
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