Indian Journal of Radiology and Imaging Indian Journal of Radiology and Imaging

: 2006  |  Volume : 16  |  Issue : 4  |  Page : 989--91

Radiological quiz - chest

J Kumar, A Kumar 
 Department Of Radiodiagnosis, All India Institute Of Medical Sciences, New Delhi, India

Correspondence Address:
A Kumar
175, Minakshi Garden,, P.O. Tilak Nagar, New Delhi - 110018

How to cite this article:
Kumar J, Kumar A. Radiological quiz - chest.Indian J Radiol Imaging 2006;16:989-91

How to cite this URL:
Kumar J, Kumar A. Radiological quiz - chest. Indian J Radiol Imaging [serial online] 2006 [cited 2020 Jan 29 ];16:989-91
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Full Text

An eighteen year old man presented with cough and expectoration with fever for 3 months. His medical history included asthma and type II diabetes mellitus. He was a non smoker. Imaging of the chest was undertaken, initially with plain radiographs [Figure 1] and subsequently with computed tomography [Figure 2][FIgure 3]. What is the diagnosis?

 Radiological Diagnosis


 Radiologic and Immunologic Findings

A PA chest radiograph [Figure 1] demonstrated thick tubular branching opacities in left middle and lower zone radiating outwards from the prominent left hilum. Selected images from a computed tomographic scan revealed tubular branching opacities giving the typical 'finger in glove' appearance. [Figure 2][Figure 3]. Relevant serology revealed a markedly elevated total serum IgE (3649 ng/ml). Aspergillus specific IgE and IgG in serum were positive. There was immediate type cutaneous reactivity to aspergillus fumigatus antigen. Blood workup revealed eosinophilia (1200 cells/ l).


ABPA represents a type I and type III (IgE and IgG mediated) hypersensitivity reaction to the endobronchial growth of aspergillus species[1]. It is seen predominantly in patients with asthma but also occurs in patients with cystic fibrosis. These two groups of patients account for the majority of ABPA cases. However ABPA uncommonly occurs in the absence of these conditions[2].

In ABPA there is eosinophilic infiltration and mucus plugging of the airway. The aspergillus does not invade the bronchial wall or surrounding lung[2].

The disorder is characterised by chest X ray infiltrates, specific serological status and cutaneous sensitivity to A. fumigatus. ABPA may be subdivided into following 2 groups: patients with or without central bronchiectasis. The essential criteria for diagnosis of the group with ABPA and central bronchiectasis are asthma, immediate skin reactivity to Aspergillus antigens, serum IgE level > 1000 ng/ml, and central bronchiectasis. Patients without central bronchiectasis are labelled ABPA-seropositive, and the minimal criteria for diagnosis are asthma, immediate skin reactivity to aspergillus, serum IgE level > 1000 ng/ml, history of pulmonary infiltrates, and elevated levels of serum IgE and IgG antibodies to A fumigatus. A positive sputum culture for A fumigatus is not essential for diagnosis[3].

There is a range of CT findings in patients with ABPA. Central bronchiectasis is a common finding. The bronchiectasis is usually varicose or cystic in appearance, and the frequent formation of mucus plugs containing fungus and inflammatory cells results in a characteristic pattern of mucoid impaction, atelectasis or consolidation. Bronchial wall thickening is frequent, and air-fluid levels may be detected in dilated, cystic airways. Ancilliary findings include evidence of peripheral airway disease, with mucus impaction in bronchioles resulting in a tree-in-bud pattern, or mosaic attenuation because of bronchiolar obstruction with resulting air trapping. High CT attenuation numbers have been measured in the central impacted mucus. Presumably representing the presence of calcium or metallic ions within viscous mucus, the prevelance of this finding has been noted to be as high as 28% in one series, and when present should be considered characteristic[1]. High resolution CT in asthmatic patients showing bronchiectasis affecting 3 or more lobes, centrilobular nodules and mucoid impaction is also considered highly suggestive of ABPA[4]. Although ABPA has classically been associated with central bronchiectasis, this finding is neither sensitive nor specific for ABPA[5],[6]. Other described imaging appearances of ABPA in the literature include pleural thickening/effusions and emphysematous bullae (indication of underlying airway obstruction)[2].

Ward et al retrospectively assessed the accuracy of CT in the diagnosis of ABPA in asthmatic patients. Comparing the CT findings in 44 patients with ABPA with 36 asthmatic controls, these authors noted a clear distinction in the frequency of a number of CT findings in patients with ABPA, including bronchiectasis in 95% of cases versus 29% of asthmatics, centrilobular nodules in 93% of cases versus 28% of asthmatics, and mucoid impaction in 67% of cases versus 4% of asthmatics. Additionally, patients with ABPA consistently had more severe and extensive disease compared with asthmatics[7].

As the clinical features of ABPA significantly overlap those of asthmatics without complicating ABPA, including eosinophilia, bronchiestasis, serum precipitins, and positive skin tests for A fumigatus in most cases, imaging by CT plays a crucial role in establishing the diagnosis[7].

Paterson et al divided this syndrome into 5 identifiable stages that guide the management of disease: acute stage, remission stage, exacerbation stage, corticosteroid dependent stage and fibrotic stage[8].

The mainstay of treatment for ABPA is oral corticosteroids to suppress the immunologic response to aspergillus antigen and the secondary inflammatory reaction. Treatment with corticosteroids leads to the relief of bronchospasm, clearing of pulmonary infiltrates and a decrease in IgE level and peripheral eosinophils[3].


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