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24 Pulmonary Function Test and Tuberculosis 24 Pulmonary Function Test and Tuberculosis MAJDY M. IDREEs, SIRAJ 0 WALl, ABDULLA AL-AMOUDI CONTENTS Before the availability of chemotherapy, pulmo­ nary function assessment was frequently performed 24.1 Pulmonary Function Abnormalities in patients with pulmonary tuberculosis. In 1846, in Tuberculosis 385 24.1.1 Historical Aspect 385 Hutchinson suggested a correlation between the sever­ 24.2 TB and Restrictive Lung Disease 385 ity of the reduction in vital capacity and the extent of 24.2.1 Parenchymal Lung Disease 385 the parenchymal disease. 24.2.2 Pleural Disease and Fibrothorax 386 There are no characteristic pulmonary function 24.2.3 Endobronchial Tuberculosis 386 abnormalities in patients with pulmonarytuberculosis. 24.2.4 Surgical and Collapse Procedures 386 24.3 TB and Obstructive Lung Disease 387 Restrictive, obstructive or mixed pattern can present, 24.3.1 Endobronchial Tuberculosis 387 depending on the extent, chronicity and the location of 24.3.2 Bronchiectasis 388 the disease (see below). However, in most patients with 24.4 TB and Mixed Pattern of Obstructive mild to moderate disease, the pathological abnormality and Restrictive Abnormality 389 is transient and complete recovery in pulmonary func­ 24.5 TB and Respiratory Failure/Hemodynamics 389 24.6 Preoperative Evaluation 390 tion tests takes place after completion oftherapy. 24.7 Case Illustration 391 As an infection control measure, in our lab a pul­ 24.8 Discussion 392 monary function test is not performed until three References 392 sputum samples have stained negative for acid-fast bacilli (AFB). 24.1 Pulmonary Function Abnormalities in Tuberculosis 24.2 T8 and Restrictive Lung Disease 24.1.1 Historical Aspect Both complications and therapeutic measures for controlling tuberculosis can result in restrictive lung Tuberculosis (TB) is an ancient disease. It has been disease. found in the spines ofEgyptian mummies. Drawings ofpersonswith Potts's disease have been found on the walls ofEgyptian tombs. Hippocrates (460-370 B.C.) 24.2.1 called the disease "phthisis," and Varro (116-28 B.C.) Parenchymal Lung Disease conceived the notion that organisms too small to be seen by the naked eye might be causing the disease. The pulmonary tissue response to the inhalation of Mycobacterium tuberculosis is characterized by hypersensitivity leading to necrosis that is sur­ M. M. IDREEs, MD, FRCP (C), FCCP rounded by inflammatory cells. These cells form a Head, Pulmonary Function Laboratory, Division ofPulmonary Medicine, Department of Medicine, Riyadh Armed Forces fibrotic tissue encompassing the area involved in the Hospital, ClIO, P.O. Box 7897, Riyadh 11159, Saudi Arabia inflammatory process, isolating it from the remain­ S. O. WAll, MD, FRCP (C), FCCP ing lung parenchyma. Limitation of the infection to Head, Division ofPulmonaryMedicine,Department ofMedicine, this stage has no significant effect on pulmonary King Khalid Hospital, National Guard, Jeddah, Saudi Arabia A. AL-AMOUDI, MD, FRCP (C) function or gas exchange abnormality. Deputy Head, Department of Medicine, King Faisal Specialist, Decreased static and dynamic lung volume, reduced Hospital & Research Center, Jeddah, Saudi Arabia forced expiratoryvolume in one second (FEV!) propor- M. Monir Madkour et al. (eds.), Tuberculosis © Springer-Verlag Berlin Heidelberg 2004 386 M. M. Idrees et aI. tionally to forced vital capacity (FVC) and reduction in 24.2.2 the diffusion capacity (DLco) can result from necrotiz­ Pleural Disease and Fibrothorax ing tuberculous pneumonitis. In massive pneumonia, severe hypoxemia and widening ofthe alveolar-arterial Pleural involvement is very common in tuberculous oxygen gradient (A-a 02) take place. This is related infection. It usually occurs through direct extension to the low V/Q ratio and the development of venous from a subpleural focus. Tuberculous pleural effusion admixture. In the absence of coexisting significant and residual pleural thickness may occur in up to airway obstructions, hypercapnia is rarely observed. 50% of patients (Barbas et al.I991). The exact patho­ Tuberculosis is an uncommon, but treatable, genesis behind the development of pleural thickness cause of Acute Lung Injury I Acute Respiratory is probably related to a delayed hypersensitivity reac­ Distress Syndrome ALIIARDS that might develop tion, rather than to an inflammatory response to the as a complication of tuberculous pneumonitis. The infection. The role of corticosteroids in reducing exact pathogenesis of ALIIARDS in TB is unclear. the risk of pleural thickness is controversial. Recent Massive release ofmycobacteria into pulmonarycir­ reports suggest no beneficial effect (Lee et al. 1988; culation with secondary hyperimmune and inflam­ Senderovitz and Viskum 1994). The coexistence matory reaction leading to infiltrative and oblit­ of empyema thoracis may complicate the clinical erative endarteritis, basal membrane thickness and picture, leading to grossly thickened pleura with vascular and endothelial leakage is the postulated loculated pleural fluid. Once extensive, this process mechanism. Whether partial or complete resolution can result in trapped lung syndrome and a variable of the lung function abnormalities will take place degree of volume loss leading to significant restric­ depend on the extent of scarring and fibrous tissue tive lung disease. This is manifested by low TLC and deposition after the acute injury. Most patients who a proportional reduction in both FEVI and FVC. survive the acute attack will have a mild degree DLco may also be reduced, resulting in a variable of parallel reduction in both FEVI and FVC three degree of gas exchange abnormalities. Shunting and months after hospital discharge that will continue to venous admixture may take place at the atelectatic improve during the first year. A subset of survivors lobes, leading to a significant degree of widening of might end with permanent residual abnormality A-a 02 gradient and hypoxemia. manifested by low diffusion capacity. In a group of 73 patients with cavitary disease and 27 patients with non-cavitary disease, Marcus and 24.2.3 colleagues reported an average vital capacity of 67% Endobronchial Tuberculosis and a diffusing capacity of 63% of that predicted at baseline (Marcus et al. 1963). In contrast, Malik and Endobronchial tuberculosis will be discussed in Martin reported an average arterial oxygen tension detail as a cause of obstructive lung disease (see (Pa02) of 76 mmHg at baseline in 104 patients with below). It should be noted, however, that a restrictive tuberculosis, but the number of cavities was not pattern is not uncommon in patients with endobron­ specified (Malik and Martin 1969). chial TB. Post obstructive pneumonitis, atelectasis or More recently, Long and coworkers reported coexisting parenchymal or pleural disease are likely milder changes in pulmonary function in these causes for restrictive lung disease in this patient patients. They prospectively studied 25 patients with population. pulmonary tuberculosis. Pulmonary function tests were performed at baseline, 1 and 6 month intervals. Patients with non-cavitary disease (15 cases) had 24.2.4 virtually normal lung function, while those with Surgical and Collapse Procedures cavitary disease (10 cases) had very mild restrictive changes (vital capacity and diffusing capacity aver­ The need for collapse procedures such as thora­ aging 88 and 85%, respectively, ofthat predicted) and coplasty, pneumothorax, pneumoperitoneum and trivial hypoxemia with Pa02 averaging 85 mmHg. In phrenic nerve crush has been virtually eliminated by the same study, some correlation of lung function the great success of anti-TB chemotherapy. However, with structure (number of cavities) was found (Long excisional surgery can still be called upon to deal et al. 1998). This may explain why patients in earlier with complications, such as bronchopleural fistula, studies had inferior values, i.e. they had more disease persistent empyema, significant hemoptysis from or pre-existing lung function abnormalities. bronchiectasis or aspergilloma or excision of a lobe Pulmonary Function Test and Tuberculosis 387 or segment infected by multi-drug resistant organ­ Obstructive lung disease might be due to tuberculous isms. These "volume reduction" procedures result in involvement ofthe bronchial tree. Sub-mucosal tuber­ a variable degree of restriction. In addition, a mixed culous involvement and nonspecific inflammation are obstructive-restrictive pattern has been observed. frequently observed in resected specimens of bronchi The obstructive element in these patients may be from tuberculous patients (Thompson and Kent 1958). related to the development of compensatory hyper­ Bronchial obstruction and dilatation can complicate inflation of the lung postoperatively. It has also been lymph node involvement of the primary infection. In suggested that airway obstruction may be related chronic post primary tuberculosis, severe bronchiec­ to the alteration of the bronchial caliber, coexist­ tasis may result from the involvement of the tuber­ ing cigarette smoking or endobronchial location of culous lesion in specific segments of the bronchial specific inflammation (Marino and Giuliano 1998). tree (see below). Chronic bronchitis, emphysema and DLco may be normal when compared to residual bronchial asthma may develop as purely coincidental alveolar volume. The net effect on gas exchange and phenomena, especially in patients with atopy or a his­ pulmonary circulation hemodynamics depend upon tory ofheavy
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