24 Pulmonary Function Test and

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 Disease 385 ity of the reduction in and the extent of 24.2.1 Parenchymal Lung Disease 385 the parenchymal disease. 24.2.2 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 387 Restrictive, obstructive or mixed pattern can present, 24.3.1 Endobronchial Tuberculosis 387 depending on the extent, chronicity and the location of 24.3.2 388 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 /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 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 . In massive , 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 admixture. In the absence of coexisting significant and residual pleural thickness may occur in up to airway obstructions, 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 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, 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, , 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 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 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 , emphysema and DLco may be normal when compared to residual bronchial 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 smoking. the integrity of the residual pulmonary tissues. The specific pathological entities involved in pulmo­ nary tuberculosis presenting with obstructive pulmo­ nary insufficiency will be discussed in detail below.

24.3 18 and Obstructive Lung Disease 24.3.1 Endobronchial Tuberculosis Obstructive airway disease came to be recognized as a complication of advanced pulmonary tuberculosis Endobronchial tuberculosis (EBTB) is most often a within a few years after the advent of effective che­ complication of primary pulmonary tuberculosis in motherapy.Anno and Tomaschefskyin 1955 reported children, although it may also occur in adults. The pulmonary function studies in 25 selected patients prevalence of EBTB varies among studies, ranging with proven pulmonary tuberculosis. They dem­ from 10-50%, probably reflecting the heterogeneity onstrated that airway obstruction and pulmonary of the studies' population and design. In the authors' hyperinflation were more common in far advanced experience of 98 adults with proven pulmonary TB, than in less advanced disease (Anno and Tomaschef­ 12 (12%) were found to have endobronchial disease sky 1955). Hallet and Martin (1961) reported on 710 (unpublished data); 10 (10%) of them had submu­ patients with pulmonary tuberculosis admitted to cosal infiltration and hyperemia and 2 (2%) had a the Firland Sanitarium. The obstructive pattern was polypoid tumor. found in 34% of these patients and occurred more Bronchoscopically, EBTB may present as an endo­ frequently in men than in women, although the bronchial mass lesion (either polypoid or ulcerative difference was not statistically significant. The inci­ granuloma), submucosal infiltration, hyperemia with dence of the obstructive abnormality increased with edema and fibrostenosis. In one study, 50 EBTB cases advanced age. The duration of smoking appeared to were diagnosed by bronchial biopsy, bronchial fine influence the incidence of obstructive disease; how­ needle aspiration and washing. Mass lesions were ever, when the age factor was controlled, the smok­ found in 31 cases (62%),21 of which were ulcerous ing relationship was no longer significant (Hallet and granulomas and 10 polypoid masses, while 11 cases Martin 1961; Martin and Hallet 1961). (22%) were ofsubmucosal infiltrative, 16 (32%) fibro­ The failure to show a very strong association stenosis and 5 (10%) hyperemia and edema (Altin et between smoking and airway obstruction in patients al.1997). with pulmonary tuberculosis is an interesting obser­ The pathogenesis of EBTB is not yet completely vation that is difficult to explain. It may be related to understood, and the course of EBTB differs accord­ the predominant effect of tuberculosis on the air­ ing to the type. The pathogenesis, presentation, treat­ ways and the subsequent damage, irrespective of the ment and prognosis of EBTB are discussed in detail smoking status of the patient. However, current data in the chapter on Endobronchial TB. The prognosis suggest an additive effect ofsmoking with tuberculo­ of the actively caseating and edematous-hyperemic sis in producing airway obstruction. types is poor, resulting in fibrostenosis in two-thirds The mechanisms of airway obstruction in pul­ of patients. Granular and non-specific bronchitic monary tuberculosis remain largely speculative. types have a more favorable prognosis (Shim 1996). 388 M. M. Idrees et al.

Clinically,,mostlynonproductive,is invariably FIoWI~J FNex present and usually persistent. General symptoms,such as fever, anorexia and weight loss, usually predominate over specific pulmonary symptoms. However, dyspnea, wheeze and strider may be the prominent features and mimic other conditions such as asthma. A variety of lung function abnormality patterns 6 8 are recognized by PFT in patients with EBTB. They include: iP Pure, restrictive defect as manifested by a propor­ 10 tional reduction of FVC and FEV1, with normal FEVlIFVC % ratio. (Post obstructive pneumonitis, atelectasis or coexisting parenchymal or pleural Fig. 24.I. FIV loop: variable extrathoracic obstruction disease are likely causes for restrictive lung dis­ ease in EBTB.) AawIVa) FNex lIIil Pure obstructive pattern defined as FEV1/FVC % ratio is less than 70%, with a low FEVI value. 10 (This is usually caused by the generalized spread of the disease endobronchially to large and small airways.)

(I Possible increased airway hyperresponsiveness. One study, however, looked at this particular issue by comparing the provocation concentrations 5 of histamine required to reduce FEVI by 20% (PC 20) of the pre-challenge baseline between 10

patients with EBTB, symptomatic asthmatics and FN~ normal healthy controls. PC 20 in EBTB patients Fig. 24.2. FIV loop: fixed obstruction and normal controls was significantly higher than in asthmatics. Furthermore, PC 20 was not affected by disease location within the bronchial tree and did not correlate with FEVI or FVC (Park 24.3.2 et al. 1995). Bronchiectasis .. Abnormal inspiratory curve of the flow volume loop, indicating a variable upper airway (Le. extra­ The pathogenesis ofbronchiectasis in tuberculosis is thoracic) obstruction (Fig. 24.1) leading to inspira­ multifactorial. Bronchial stenosis secondary to EBTB tory flow reduction. This might occur secondary to can result in post obstructive pneumonitis with a sec­ the involvement of the extrathoracic upper airway, ondary bacterial infection. Exogenous compression typically found in extensive laryngeal tuberculosis of the bronchial lumen by enlarged lymph node pro­ (LTB). LTB can result from the direct spread of duces results similar to endobronchial obstruction. contaminated sputum to the , or it can be a In both situations, the inflammatory destruction of secondary manifestation of hematological spread. the bronchial lumen and the subsequent dilatation .. Fixed large airway obstruction, characterized by of the bronchi is mainly caused by a mixed bacterial equally reduced inspiratory and expiratory flow infection and purulent bacterial secretion, with an (Fig.24.2). This can be a direct result of large exaggerated local immune reaction, rather than by airway stenosis secondary to EBTB. Hoheisel and the local spread of M. tuberculosis. coworkers found that 7% of their patients had Pulmonary function abnormalities in this situ­ a total occlusion of their airways secondary to ation can show pure obstruction, pure restriction EBTB, 13% had less than total, 13% had signifi­ or a combination of both abnormalities, depending cant,45% minor and 22% had no residual stenosis on the type and extent of the involvement and the (Hoheisel et al. 1994). degree of residual damage. In extensive disease, both DLco and lung compliance are reduced, indicating a significant degree of gas exchange abnormality, with venous admixture and increased lung stiffness. The Pulmonary Function Test and Tuberculosis 389

A-a 02 gradient is widened, and, at a more advanced 13 patients with pulmonary tuberculosis requiring stage, chronic hypoxemia and respiratory failure . Seven patients had miliary can develop. Chronic corpulmonale may develop tuberculosis and six had tuberculosis pneumonia. secondarily to a persistent increase in pulmonary Eight had ARDS and another two had probable artery pressure. The physical destruction of the ARDS. The mortality rate of these patients was 69%, pulmonary vessels by the inflammatory process may which is almost twice that of the hospital mortality play an important role in the development of pul­ for non-tuberculosis pneumonia requiring mechani­ monary hypertension, but this is unlikely to be the cal ventilation (36%) (Penner et al. 1995). major cause. Hypoxemia, active immune modulators Circulatory disturbance characterized by septic and cytokines release are more likely to be the most shock is a rare syndrome which has been reported important factors in the development of full-blown in patients with disseminated tuberculosis (Gachot and corpulmonale. et al. 1990; Piqueras et al. 1987; Sandoval et al. 1991). In recent years, the occurrence of extra-pulmonary and disseminated tuberculosis has been increasing, especially among HIV patients and intravenous drug 24.4 users, and the incidence ofseptic shock complicating T8 and Mixed Pattern of Obstructive disseminated tuberculosis is expected to be on the and Restrictive Abnormality rise as well. Pulmonary hypertension (PHT) is a known sequela In miliary TB, the reported physiological changes are of complicated pulmonary tuberculosis. The exact ofan obstructive-restrictive pattern. In a group of33 pathophysiologyfor PHT is not clear. However, various patients with miliary TB, pulmonary function test­ mechanisms have been attributed to the development ing was performed in 31 patients and arterial blood of PHT and corpulmonale in tuberculosis, including gases were analyzed in 13 patients (Shama et al.1992). chronic hypoxia and a reduced pulmonary capillary The physiologic abnormalities observed suggested a bed, caused either by the disease itself or as a result mild to moderate restrictive defect (vital capacity of surgical therapy (Ershov et al. 1996). Sandoval and of 56% of that predicted, ±14), with impairment of colleagues studied the hemodynamic behavior ofpul­ pulmonary diffusing capacity (68±2l) and arterial monary circulation in both anatomical and functional hypoxemia (Pa02 of 75 mmHg ±12), and widening settings. Six patients with miliary tuberculosis were of the A-a 02 gradient. In addition, there was a mild studied. Cardiac catheterization, with subsequent reduction in the flow rates, based on reduced mid­ hemodynamic measurements, was performed at rest expiratory flow and increased residual volume-to­ and during exercise. The mean values of the baseline total lung capacity. This suggests peripheral airway pulmonary function testing, expressed as percentage involvement and subsequent gas trapping. These ofthe predicted value, showed a vital capacity of 62%, changes are consistent with the diagnosis of inter­ FEVI of 50%, FEVlIFVC 76% and TLC of 79.5%. The stitial lung disease and peripheral airway dysfunc­ resting pulmonary artery pressure, cardiac index, tion. With treatment, however, there was significant pulmonary vascular resistance and the PAd-PWP improvement in gas exchange (mean Pa02 increased (pulmonary diastolic minus pulmonary wedge pres­ significantly, P value of <0.03), but no change in pul­ sure) were all within normal limits. As a group, the monary function abnormality (Shama et al. 1992). hemodynamic response to exercise was characterized Other pathological entities causing mixed obstruc­ by an increase in both the mean pulmonary artery tive-restrictive abnormalities are EBTB and post pressure and cardiac index, while pulmonary vascular resectional surgeries (see above). resistance remained within the normal range. At rest, hypoxemia (Pa02 59±3 mmHg) without hypercapnia and normal pH were found in the group as a whole. The alveolar arterial oxygen gradient and the dead 24.5 space (VDIVT) ratio increased. During exercise, no T8 and Respiratory Failure/Hemodynamics significant changes occurred in the gas exchange vari­ ables, except for oxygen consumption, respiratory rate Tuberculosis is an uncommon primary cause of and minute ventilation (Sandoval et al.199l). respiratory failure requiring mechanical ventila­ The correlation between survival and pulmonary tion. In a retrospective study that extended over a hypertension in patients with sequelae ofpulmonary lO-year period, Penner and colleagues reported only tuberculosis was also studied. Twenty-one patients 390 M. M. Idrees et aI.

with a past history of treated pulmonary tubercu­ 6 patients deemed inoperable by pulmonary artery losis and a mean Pa02 of 59 mmHg and PaC02 of pressure and perfusion scan-predicted FEVI mea­ 51 mmHg were included in the study. Spirometry surement had MVV less than 50% of the predicted showed a mean vital capacity of 44% of that pre­ outcome, whereas only 2 out of 23 patients who were dicted and a FEVI of 66%. Twenty patients had an deemed operable had low MVV. mPAP greater than 30 mmHg, and 18 received home FEV 1is also frequently measured to assess the risk oxygen therapy. Among those patients who required ofresection surgery for multi-drug resistant tubercu­ home oxygen therapy, blood gases and pulmonary losis or other indications, such as lung . Preop­ hemodynamics did not vary significantly between erative FEVI has been used in conjunction with per­ those who died within 2 years (short-term survivors) fusion lung scan to estimate postresectional FEVl. and those who lived for more than 5 years (long-term Based on data extrapolated from COPD patients, survivors). However, lung function parameters (FVC estimated postoperative FEVI (FEVI-PPO) less than and FEV!) were significantly lower in the short-term 0.8 I, or 30% of the predicted, has been considered vs.long-term survivors, suggesting that the principle the threshold below which resection is considered prognostic determinant for long-term survival in prohibitive. When this criterion was used to deter­ patients with post tuberculosis sequelae is the degree mine operability in high-risk lung resection patients, of restrictive pulmonary abnormality, and not PHT denying surgery to patients with an FEVI-PPO less or the severity ofgas exchange abnormalities (Sasaki than 0.81 defined a group having a 20% postoperative et a1.1998). mortality rate (Olsen et aI, 1975). More recently, Melendez and Fischer divided the preoperative tests into three predictive value groups:

lljl Spirometry, blood gas analysis and stair climbing 24.6 tolerance are helpful for screening but not very Preoperative Evaluation discriminating. This group had a poor outcome predictive value. Preoperative pulmonary function testing emerged " An intermediate predictive value was achieved in the 1950s as an appealing approach for predicting using diffusion capacity, exercise-induced decrease complications after thoracotomy. in oxygen saturation and exercise pulmonary vas­ The goals of preoperative evaluation are to: cular resistance. • Identify patients at risk G Ahigh predictive value was achieved by the full car­ • Assess the degree of risk for post operative com­ diopulmonary exercise test for the measurement of plications the oxygen consumption (V02) at 40 watts of exer­ • Identify factors associated with increased risk cise, or V02 max (Melendez and Fischer 1997). • Keep both morbidity and mortality low Richter and coworkers also evaluated the best pre­ In a retrospective analysis of 454 patients who dictor of postoperative morbidity and mortality for underwent thoracic surgery, age (greater than 65 thoracic resection surgery. In all, they prospectively years), obesity and hypocapnia (PaC02 less than evaluated 97 patients. All patients had preoperative 31 mm Hg) were found to be associated with increased maximal exercise testing and dynamic spirometry. morbidity and mortality (Beaufils et al. 1992). Logistic regression showed maximum preoperative In patients undergoing lung resection for pul­ workload to be the only predictor of cardiopulmo­ monary tuberculosis, mortality was as high as 40% nary complications. Maximum oxygen consumption among those with maximum voluntary ventilation (V02 max) was predictive of cardiopulmonary death. (MVV) less than 50% of the predicted and FVC less V02 max ofless than 50% of the predicted value was than 70%. Other parameters associated with poor associated with a high risk of death from cardio­ outcome included age older than 70 and FEVI less pulmonary causes. However, both FEV 1 and V02 than 21 (Gaensler et aI.1995). max were predictive of postoperative complications. More recent studies confirmed the correlation Finally, V02 max was correlated with long-term sur­ between MVV and poor postoperative outcome. vival, while spirometric variables were not (Richter Olsen and coworkers (1975) reported that 5 out of et al. 1997). Pulmonary Function Test and Tuberculosis 391

Recently, the role of cardiopulmonary exercise monary illness and no contact with sick people. She testing in the preoperative evaluation for thoracic has no pets, nor had she recently traveled. resection surgery has become the subject of great She was given a three-day course of azithromycin interest. It has been recommended that patients by her GP with no significant response. Clinically, she with FEV 1-PPO ofless than 40% of predicted values looked ill and mildly distressed. Temperature was should be exercised to assess oxygen transport and 37.8 0c. She had very audible wheezes all over the consumption. Patients with FEVI-PPO greater than lung fields. Chest-x-ray showed mild degree hyperin­ 30% of predicted values and peak exercise V02 flation, but was otherwise unremarkable. greater than 15 mllkg/min should be offered surgery with the goal of resecting the smallest volume of tissue that would be compatible with a cure (Gilbreth and Weisman 1994).

24.7 Case Illustration

N.S.S is a 54-year-old woman, with no previous ill­ ness aside from mild . She presented with a 3-week history of low-grade fever, cough, and wheeze. FNa She is a non-smoker and had no family history of atopy. There was no occupational risk factor for pul-

Pulmonary Function Test ------R tot 0.30 1.11 371.2 RIN 1.00 4 REX 1.34 [fl'0 2 SR tot 0.96 4.20 436.6

TLC 4.44 4.67 105.1 ITGV 2.54 3.42 134.8 1IIIe(IJ RV 1.88 2.97 158.4 RVO/OTLC 41.74 63.71 152.6 0 1 2 3 4 5 7 I ITGVO/O 55.82 73.33 131.4 •

FVC 2.23 1.76 78.5 1.62 -7.9 FEV 1 1.85 1.26 68.0 1.56 24.0 FEVI0/0F 71.57 96.35 34.6 IC 1.67 1.60 95.8 1.62 0.7 2 FET 2.65 1.26 -52.3 PEF 5.41 3.02 55.9 3.39 12.1 7- 1 FEF 25 4.92 1.66 33.7 2.39 44.1 /' FEF 50 3.28 0.86 26.3 1.34 55.2 1 FEF 75 1.06 0.39 36.2 0.56 45.5 VCIN 2.34 1.87 80.0 1.84 -1.3 -1 PIF 1.74 1.85 6.3

FIF 50 1.74 1.85 6.3 ~ FE%FIF 49.66 72.53 46.1 ...... 392 M. M. Idrees et al.

Arterial blood gases on room air were: Ershov AL, Evstaf'ev IuA, Sobkin AL et al (1996) The signifi­ cance of exacerbations of lung diseases in the development iii PH 7.41 ofchronic corpulmonale and their treatment. Probl Tuberk PaC02 5.40 kPa 4:14-16 Richter LK, Svendsen UG, Milman N et al (1997) Exercise I'll P02 8.64 kPa testing in the preoperative evaluation of patients with HC03 25.2 mmolll bronchogenic carcinoma. Eur Respir J 10:1559 Gachot B, Wolff M, Clair B (1990) Severe tuberculosis in • 02 Sat 91 % patients with human immunodeficiency virus infection. Intensive Care Med 16:491-493 Gaensler EA, Cugell DW, Lindgren I et al (1995) The role of pulmonary insufficiency in mortality and invalidism following surgery for pulmonary tuberculosis. J Thorac 24.8 Cardiovasc Surg 29:163 Discussion Gilbreth EM, Weisman 1M (1994) Role ofexercise stress testing in preoperative evaluation of patients for lung resection. Clin Chest Med 15:389 Pulmonary function testing showed a moderate Hallet WY, Martin q (1961) The diffuse obstructive pulmo­ degree of obstruction. The borderline FEVl/FVC nary syndrome in a tuberculosis sanatorium. Etiological ratio was related to incomplete exhalation and under­ factors. Ann Intern Med 54: 1146 estimation of FVC. Total lung capacity was normal, Hoheisel G, Chan BK, Chan CH et al (1994) Endobronchial tuberculosis: diagnostic features and therapeutic outcome. but both residual volume (RV) and RV% TLC were Respir Med 88:593-597 high, indicating gas trapping. There was a significant Lee CH, Wang WJ, Lan RS et al (1988) Corticosteroids in the response to bronchodilator. treatment of tuberculous : a double blind, placebo­ Arterial blood gases showed a mild degree of controlled, randomized study. Chest 94:1256-1259 hypoxemia and widening ofthe A-a 02 gradient. Long R, Maycher B, Dhar A et al (1998) Pulmonary tubercu­ losis treated with directly observed therapy. Chest 113: The patient was treated initially as a case of bron­ 933-943 chial asthma/bronchitis. Steroids,bronchodilator and Malik SK, Martin q (1969) Tuberculosis, therapy, antibiotics were started with partial initial response and pulmonary function. Am Rev Respir Dis 100:13-18 followed by deterioration. Three sputum samples for Marcus H, Yoo OH,Akyol T et al (1963) A randomized study of AFB were negative. the effect ofcorticosteroid therapy on healing ofpulmonary tuberculosis as judged by clinical, roentgenographic and Bronchoscopy was done and an endobronchial physiologic measurements. Am Rev Respir Dis 88:55-64 mass lesion in the left main stem was Marino de Rosa, Giuliano C (1998) Respiratory function found. This was associated with generalized airway impairment in pulmonary tuberculosis. Rays 23:87-92 hyperemia. Anti-TB chemotherapy was started and Martin q, Hallet WY (1961) The diffuse obstructive pulmo­ the patient subsequently improved. nary syndrome in a tuberculosis sanatorium. Incidence and symptoms. Ann Intern Med (Chic) 54:1156 Melendez JA, Fischer ME (1997) Preoperative pulmonary evaluation of the thoracic surgical patient. Chest Surg Clin North Am 7:641 References Olsen GN, BlockAJ, Swenson EW et al (1975) Pulmonary func­ tion evaluation of the lung resection candidate: a prospec­ Altin S, Cikrikcioglu S, Morgul M et al (1997) 50 endobronchial tive study. Am Rev Respir Dis 111:379 tuberculosis cases based on bronchoscopic diagnosis. Res­ Park CS, Kim KU, Lee SM et al (1995) Bronchial hyperreac­ piration 64:162-164 tivity in patients with endobronchial tuberculosis. Respir Anno H, Tomaschefsky JF (1955) Studies on the impairment Med 89:419-422 of respiratory function in pulmonary tuberculosis. Am Rev Penner C, Robert D, Kunimoto D et al (1995) Tuberculosis as a Tuberc 71:333 primary cause of respiratory failure requiring mechanical Barbas CSV, Cukier A, de Varvalho CRR et al (1991) The ventilation. AJRCCM 151:867-872 relationship between pleural fluid finding and the devel­ Piqueras AR, Marrueces L, Artugas A (1987) Miliary tuber­ opment thickening in patients with pleural tuberculosis. culosis and adult respiratory distress syndrome. Intensive Chest 100:1264-1267 Care Med 13:175-182 Beaufils LC, Brachet A, Manuelian M et al (1992) Preoperative Sandoval J, Cicero R, Seoane M et al (199l) Behavior of the evaluation of respiratory function in thoracic surgery. Do pulmonary circulation at rest and during exercise in mili­ reliable predictive criteria exists in that type of surgery. ary tuberculosis. Chest 99:152-154 Agressologie 33:15 Sasaki Y, Yamagishi F, Suzuki K et al (1998) Survival and Pulmonary Function Test and Tuberculosis 393

pulmonary hemodynamics in patients with sequelae of tion and immunologic abnormalities in miliary tuberculo­ pulmonary tuberculosis who received anti-tuberculosis sis. Am Rev Respir Dis 145:1167-1171 chemotherapy and home oxygen therapy. Nihon Kokyuki Shim YS (1996) Endobronchial tuberculosis. Respirology 1: Gakkai Zasshi 36:934-938 95-106 Senderovitz T, Viskum K (1994) Corticosteroids and tubercu­ Thompson JR, Kent G (1958) Occult tuberculous endobronchi­ losis. Respir Med 88:561-565 tis in surgically resected lung specimens. Am Rev Tuberc Shama SK, Pande JN, Singh YN et al (1992) Pulmonary func- 77:931