Use of Linear Tomography to Confirm the Diagnosis of Allergic Bronchopulmonary Aspergillosis

Use of Linear Tomography to Confirm the Diagnosis of Allergic Bronchopulmonary Aspergillosis

Use of Linear Tomography to Confirm the Diagnosis of Allergic Bronchopulmonary Aspergillosi~* Madeleine R. Fisher, M.D.;t Ellen B. Mendelson, M.D.;t R...

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Use of Linear Tomography to Confirm the Diagnosis of Allergic Bronchopulmonary Aspergillosi~* Madeleine R. Fisher, M.D.;t Ellen B. Mendelson, M.D.;t Richard A Mintzer, M.D., F.C.C ..P.;t Anthony]. Ricketti, M.D.;* and Paul A Greenberger, M.D.*

Allergic bronchopulmonary aspergillosis (ABPA) has been recognized increasingly in the past few years. In minimal disease, plain chest mms may be insensitive. Early detection of pulmonary involvement may help prevent irreversible damage to the lungs and bronchi. Bronchography, while both sensitive and specific, is not without hazard,

particularly to the asthmatic patient. We evaluated the usefulness of linear tomography in con6rming ABPA prior to initiation of corticosteroid therapy. We find that tomography is a simple, noninvasive instrument for detecting the presence ofor proving the absence of the earliest manifestations of ABPA.

Jt.er'!).c bronchopulmonary aspergillosis (ABPA) is an unusual complication of asthma that has been recognized with increasing frequency in the past 30 years. 1-e The clinical diagnostic features of ABPA are well known, 7-& as are the radiolo'!).c findings ('Iable l),lO,U Advanced disease usually poses no diagnostic difficulty. The disease, howeve~ may present with extremely subtle clinical and radiolo'!).c findings, even with a normal chest roentgenogram.lll Steroid therapy, which is important to administer early in the course of the disease, since it may prevent progression, 13-!5 is begun when there is radiolo'!).c evidence of ABPA. When the chest roentgenogram is normal or equivocal, additional imaging studies are required. In the past, we used bronchography to establish or confirm the diagnosis of ABPA. The airways of asthmatic patients are frequently reactive to environmental stimuli, and bronchography is not without risk. Several patients had severe asthmatic attacks following the study. In addition, endobronchial dissemination of tuberculosis is a dreadful complication of bronchography. To minimize such risks to the patient, we now utilize the noninvasive technique of tomography in establishing the radiolo'!).c findings of ABPA.

evaluating the presence or absence of the disease or in defining its extent. Fourteen of these 25 patients had ABPA. The tomographic studies of these proved ABPA patients furm the basis of this report. There were nine males and five females, whose ages ranged from seven to 60 years. 'lbmography was perfOrmed by one of several methods depending on the original radiologic findings on PA and lateral chest roentgenograms. In the presence of equivocal unilateral findings, tomographic sections were confined to the suspicious areas. In the presence of a normal chest roentgenogram or bilateral changes, a whole-lung tomographic technique of the hiJar areas was utilized. In two patients, SSO posterior oblique hiJar tomography was perfOrmed. All tomographic examinations were obtained on a Siemens optiplanomat, utilizing either a 30" or 40" linear arc. Linear tomography is utilized fur all chest examinations in our institution because of the decreased exposure time required fur this technique compared to more complex motions. Kilovoltage was kept relatively constant (ie, 66 to 75 kVp) fur all examinations.

MATERIALS AND METHODS

During the past 16 years, the Allergy-Immunology sections at our institution have evaluated well over 100 patients with suspected ABPA. Sixty-two patients were round to have the disease. Included in these patients' allergy work-up, when appropriate, were various radiologic procedures. In 25 patients, tomography w8s utilized in *From Northwestern University Medical School, Chicago. tDepartment of Radiology. *Section of Allergy-Immunology, Department of Medicine. Su~rted by USPHS grant Alll403, the Ernest S. Bazley Grant, and the Chicago Lung Association. Manuscript received July 15; revision accepted October 23 ~nt requests: Dr. Greenberger, 320 East Superior (Rm 465), CliicGgo 6f16n

RESUI.XS

Plain films and tomograms were evaluated using the radiographic criteria for diagnosis of ABPA ('Iable 2). The roentgenograms of these asthmatic patients suspected of having ABPA were interpreted independently of immunolo'!).c findings. Three groups of patients were identified. Group A patients had normal conventional chest roentgenograms. The chest roentgenograms of those in group B showed subtle or minimal manifestations of ABPA. Advanced or classic changes of ABPA were seen iri the chest roentgenograms of group C patients. In group A, those with normal chest roentgenograms, there were four patients. The tomograms of one patient demonstrated manifestations of ABPA, which led to institution of appropriate therapy (Fig 1). The remaining three were normal, and oral corticosteroid treatment was considered unnecessary at that time. Six patients were included in group B. Radiolo'!).c plain film criteria for assignment to this group consisted of transient or subtle findings, including toothCHEST I 87 I 4 I APRIL, 1985

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FIGURE 1. The PA roentgenogram (a, left) of this 32-year-old known asthmatic demonstrates peribronchial cuffing compatible with asthma. An AP tomogram (b, right) demonstrates a parallel-line shadow (arrow) involving a right upper lobe bronchus which was not seen on the conventional chest roentgenogram. With this finding, in addition to the precipitating antibodies and other positive tests in the immunologic profile against Aspergillus fumigatus, the diagnosis of ABPA was established.

paste shadows (inspissated mucus), tramline shadows, and perihilar infiltrates simulating adenopathy (Fig 2).

All of the plain film examinations were diagnostic of asthma complicated by ABPA. In one patient plain film

FIGURE 2. PA chest roentgenogram (a, left) in this 41-year-old asthmatic patient demonstrates ring and parallel-line shadows representing the permanent changes of ABPA. The extent of disease is suspected but not adequately shown on the conventional roentgenogram. AP tomograms of the right (b, center) and left (c, right) upper lobes delineate the disease process better, clearly showing proximal dilatation of the upper lobe bronchi (arrow) and a previously unseen tramline (arrowhead) .

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LJnear Tomography In Diagnosis ol ABA (Fiaher et Ill)

FIGURE 3. A 62-yeaM>ld long-tenn asthmatic patient had classic manifestations of asthma and ABPA. A close-up PA view of the left chest (a, left) demonstrates residuum of multiple previous mucoid impactions but no evidence of an acute mucoid impaction. A tomogram (b, right) through the level of the left hilum, in AP projection, con6nns that all the abnonnal Unear densities on the plain film are related to dilated bronchi.

findings were suggestive of tuberculosis as well as ABPA. All tomographic evaluations were confirmatory. In one patient, tomography helped to establish superimposed mycobacterial infection. In group C, fuur patients demonstrated moderateto-advanced pulmonary changes on plain films, such as parallel-line shadows and ring shadows indicative of proximal bronchiectasis. All fuur of these patients underwent tomography. In three of these patients with advanced disease, the tomograms defined the destructive changes more clearly than plain films. In one patient, initial plain film findings were classic. After long-tetm steroid therapy had reversed the plain film findings, tomography was often utilized to assess the presence of subtle residual abnormalities (Fig 3). DISCUSSION

Early recognition of ABPA in asthmatic patients is a difficult but extremely important task. There is significant overlap of clinical, immunologic, and of several of the radiologic findings in ABPA and uncomplicated asthma. Asthma, by definition, is a reversible airway disease while the sine qua non of ABPA is proximal bronchiectasis, a permanent alteration. 16 ABPA untreated may result in further permanent pulmonary damage (ie, blebs, cavities, and eventually pulmonary

fibrosis). In addition, the treatment of uncomplicated asthma with low-dose corticosteroids may mask the recognition of ABPA, allowing progressive destruction to occur. 17 Higher doses of corticosteroids given fur longer durations are required in the therapy of ABPA. The need to diagnose ABPA while excluding other lesions prompted us to assess the efficacy of tomography. Comprehensive examinations of bronchi and lung parenchyma were obtained using an AP tomographic technique with a trough filter. The tomograms, which included both hilar regions and the central and upper lung fields, detected changes related to ABPA with sensitivity and definition greater than that of plain films. We find that linear tomography is valuable in documenting central bronchiectasis, the definite radiologic manifestation of ABPA. When tomography did not reveal evidence of ABPA, as in three patients in group A, bronchography was not perfOrmed because of some previous adverse reactions in ABPA patients. Thus, we cannot exclude the possibility of areas of bronchiectasis detectable by bronchography but not by tomography. We utilize tomography as a prime diagnostic modality and as additional basis for instituting oral corticosteroid therapy. In the presence of a normal tomographic examination, corticosteroids may be withheld pending future radiologic CHEST I 87 I 4 I APRIL, 1985

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Primary Asthma Blood eosinophilia Immediate skin reactivity Aspergillus fumigatvs Precipitating antibodies against A fumigatvs Elevated serum IgE levels Central bronchiectasis History of pulmonary infiltrates Elevated serum IgG and IgE antibodies to A fumigatvs Secondary Mycelia of Aspergillus in sputum Expectoration of brown plugs or Becks in sputum Late skin reactivity (Arthus reactivity) to Aspergillus antigen

infiltrates, or unless they are required fur management of asthma. CoNCLUSIONS

'The diagnosis of ABPA is made by combined application of clinic8l, immunologic, and radiologic criteria ('Iables 1 and 2). In the appropriate clinical setting, when the chest roentgenogram demonstrates findings of ABPA, treatment should be begun without further investigation. When the diagnosis is suspected but the normal roentgenogram provides no supporting evidence, the clinician is hesitant to administer high-dose corticosteroid treatment. In the past, bronchography was relied on to provide visualization of the subtle manifestations of ABPA unseen on the chest roentgenogram. Bronchography is both sensitive and specific fur detection of early bronchiectasis. While reliable, bronchography is invasive. It requires topical anesthesia and iodinated contrast media. In our early experience with 25 patients with ABPA, reactions to the topical anesthesia occurred in two patients, and acute asthmatic attacks were precipitated in fOur paTable 2-Btuliograplaic Finding•, ABPA Nonspecific Manifestations namli.nes: 2 parallel, hairline shadows extending from hili toward the bronchi, width of lucent zone between the lines is that of a normal bronchus lbothpaste shadows: bandlike shadows, 2-3 em long and 5-8 em wide, secondary to mucoid impactions Massive consolidation: in some cases may be due to mucoid impaction Perihilar infiltrates simulating adenopathy Pulmonary infiltrates De&nitive radiologic criterion: Central bronchiectasis, upper lobe predilection, manifested by: Air-8uid levels in dilated, partially obstructed bronchi Gloved-finger shadows: distally occluded bronchi 6lled with secretions Ring shadows: dilated bronchi en face: 1-2 em in diameter Parallel-line shadows: dilated tramlines, the result of bronchiectasis

tients. Additionally, a patient with ABPA and atypical mycobacterial infection had dissemination of the infection by.' bronchography performed at another institution. We find that tomography is a simple, noninvasive instrument fur detecting presence of or documenting absence of the earliest manifestations of ABPA. When the plain chest film suggests ABPA and additional radiologic studies are required, linear tomography is the current modality of choice. REFERENCES

1 Hinson KFw, Moon AJ, Plummer NS. Bronchopulmonary aspergillosis. Thorax 1952; 7:317-33 2 Pepys J. Hypenensitivity diseases of the lungs due to fungi and organic dusts. Karger monographs in allergy, wl 4. Basel: S Karger AG, 1969 3 Henderson AH, English MP, Vecht RJ. Pulmonary aspergillosis: a survey of its occurrence in patients with chronic lung disease and a discussion of the signi8cance of diagnostic tests. Thorax 1968; 23:513-23 4 Patterson R, Goldberg F. Hypersensitivity disease of the lung. Univ Michigan Med Center J 1968; 34:8-11 5 Hoehne JH, Reed CE, Dickie HA. Allergic bronchopulmonary aspergillosis is not rare. Chest 1973; 63:177-81 6 Rosenberg M, Patterson R. Allergic bronchopulmonary aspergillosis, an emerging disease. J Chron Dis 1976; 30:1-3 7 Rosenberg M, Patterson R, Mintzer R, Cooper BJ, Roberts M, Harris ICE. Clinical and immunologic criteria for the diagnosis of allergic bronchopulmonary aspergillosis. Am Intern Med 1977; 86:405-14 8 Wang JLF, Patterson R, Rosenberg M, Roberts M, Cooper BJ. Serum IgE and IgG antibody activity against Aapergalu. fumigatvs as a diagnostic aid in allergic bronchopulmonary aspergillosis. Ann Rev Respir Dis 1978; 117:917-27 9 Ricketti AJ, Greenberger PA, Mintzer RA, Patterson R. Allergic bronchopulmonary aspergillosis. Arch Intern Med 1983; 43:1553-7 10 Mintzer RA, Rogen LF, Kruglik GD, Rosenberg M, Neiman HL, Patterson R. The spectrum of radiologic findings in allergic bronchopulmonary aspergillosis. Radiology 1978; 127:301-7 11 McCarthy DS, Simon G, Hargreave FE. The radiological appearances in allergic bronchopulmonary aspergillosis. Clin Radiol1970; 21:366-75 12 Rosenberg M, Mintzer R, Aaronson D, Patterson R. Allergic bronchopulmonary aspergillosis in three patients with normal chest x-ray films. Chest 1977; 72:597-600 13 Rosenberg M, Patterson R, Roberts M, Wang J. The assessment of immunologic and clinical changes occurring during corticosteroid therapy for allergic bronchopulmonary aspergillosis. Am J Med 1978; 64:559-606 14 Nichols D, Dopico GA, Braun S, Imbeau S, Peten ME, Rankin J. Acute and chronic pulmonary function changes in allergic bronchopulmonary aspergillosis. Am J Med 1979; 67:631-7 15 Safirstein BH, D'Souza MF, Simon G, 'Illi EH-C, Pepys J. Five year follow-up of allergic bronchopulmonary aspergillosis. Am Rev Respir Dis 1973; 108:450-9 16 ScaddingJG. The bronchi in allergic aspergillosis. Scand J Respir Dis 1967; 48:372-7 17 Greenberger PA, Patterson R, Ghory A, Arkins JA, Walsh 'I; Graves 'I; et al. Late sequelae of allergic bronchopulmonary aspergillosis in corticosteroid-dependent asthmatics. J Allergy Clin Immunol1980; 66:327-35