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Flitting radiographic shadows: an unusual presentation of cancer in the lungs
  1. W M Edmondstone
  1. Royal Hospital Haslar, Gosport, Hampshire PO12 2AA, UK
  1. Dr W M Edmondstone.


Tumour involvement of pulmonary blood vessels occurs frequently in advanced lung cancer and occasionally may cause pulmonary infarction. A case is reported of diffuse obstruction of pulmonary arteries by cancer in which no primary tumour was found, and which presented as flitting radiographic opacities due to pulmonary infarction.

  • pulmonary infarcts
  • pulmonary arterial tumour embolism
  • cancer

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Radiographic opacities which “flit” around the lungs are characteristic of a number of conditions including allergic bronchopulmonary aspergillosis and other pulmonary eosinophilic syndromes, and cryptogenic organising pneumonia. They may follow aspiration from the upper airways or oesophagus, or occur in acute infective exacerbations of bronchiectasis or chronic bronchitis. Recurrent pulmonary emboli may cause infarcts which result in transient consolidation. Malignant disease in the lungs usually causes progressive enlargement of one or more radiographic opacities and is not associated with flitting shadows.

A case is reported where infarcts due to obstruction of pulmonary arteries by tumour occurred in the absence of an obvious primary cancer and resulted in flitting radiographic shadows.

Case report

In 1980 a 50 year old man underwent radical radiotherapy followed by a total laryngectomy for squamous cell carcinoma of the larynx.Subsequently there was no evidence of tumour recurrence and he remained well until 1996 when, aged 66, he developed right upper chest pain, breathlessness on exertion, dry cough, malaise, and weight loss. He had been a heavy smoker until his laryngectomy and he had been exposed to asbestos. He was referred after several courses of antibiotics had failed to clear an area of consolidation in the periphery of the right lung apex.

Apart from his tracheostomy, examination was unremarkable. His erythrocyte sedimentation rate was slightly elevated at 24 mm/h but otherwise blood tests and the electrocardiogram were normal or negative. A fibreoptic bronchoscopic examination was normal and washings and brushings from the right upper lobe revealed no malignant cells. A computed tomographic (CT) scan (fig 1) confirmed a peripheral opacity at the apex of the right lung with some thickening of the overlying pleura. A CT guided percutaneous biopsy specimen was non-diagnostic, showing some fibrous thickening of the pleura only.

Figure 1

Chest CT scan showing peripheral consolidation at the apex of the right lung.

During the next four months his chest radiograph improved and the right apical opacity gradually resolved. He continued to feel unwell and to lose weight, however, and his breathlessness increased. Four months after his original presentation his chest radiograph showed almost complete resolution of the apical lesion, but a new opacity had developed in the right lower lobe. A further CT scan (fig 2) showed a cavitating lesion in the periphery of the posterobasal right lower lobe. Blood tests including antineutrophil cytoplasmic antibodies were negative, bronchoscopy was again normal, and a repeat CT guided needle biopsy specimen revealed only necrotic debris.

Figure 2

Chest CT scan four months later showing a new area of consolidation with cavitation in the right lower lobe. Both the opacities proved to be pulmonary infarcts secondary to obstruction of pulmonary arteries by squamous cell carcinoma.

A ventilation-perfusion lung scan showed matching defects in the right upper and lower lobes but multiple mismatched defects elsewhere, indicating a high probability of pulmonary emboli. While being anticoagulated he developed a right hemiplegia which was shown by CT scanning to be due to a cerebral infarct. He subsequently deteriorated rapidly and died.

The necropsy showed evidence of a recent infarct in the left cerebral hemisphere. In the chest there were bilateral pleural plaques, both lungs were congested and oedematous, and there were two necrotic areas in the right upper and right lower lobes. Microscopy showed these to be infarcts which were undergoing organisation. There was no evidence of macroscopic tumour in the chest or elsewhere, but microscopic examination of sections of the right upper and lower lobes and the left upper lobe showed extensive spread of poorly differentiated squamous cell carcinoma within pulmonary arteries and fibrous septa. Although no primary tumour was found there was infiltration of the left hilar lymph nodes and an area of severely dysplastic squamous epithelium in a section of the right main bronchus.


Many cancers induce a hypercoagulable state and thrombotic pulmonary embolism is the second commonest cause of death in patients with solid tumours.1 Although it is rarely diagnosed in life, necropsy studies have demonstrated that pulmonary arterial tumour embolism occurs in 8–20% of advanced cancers, being particularly associated with carcinoma of the lung, breast, liver, pancreas, and gastrointestinal tract.2-4 Occlusion of pulmonary arteries by tumour may be compounded by thrombosis in situ and may lead to infarction. Without a lung biopsy the diagnosis, and its differentiation from thrombotic pulmonary embolism, may be difficult to make.4 Whether pulmonary infarction complicates arterial tumour embolism more frequently than thrombotic embolism remains undecided.2 ,4 In a series of 100 pneumonectomies for lung cancer there were 10 pulmonary infarcts of which two were due to tumour infiltration and thrombosis of pulmonary vessels, three resulted from vascular compression by tumour, and in the remainder no obvious cause was found.5

In this case the diagnosis of primary pulmonary or pleural malignancy was suspected initially but not supported by investigations. The appearance of a second opacity in the right lower lobe raised the possibility of aspiration of infected material from the patient’s tracheostomy. Recurrent pulmonary infarcts were also thought to be likely. This diagnosis was supported by the ventilation-perfusion lung scan which showed multiple mismatches, but these were subsequently found to be due to carcinomatous rather than thrombotic occlusion of pulmonary vessels. The possibility of this diagnosis was not considered, especially as there appeared to be no evidence of a primary tumour. Whether the extensive infiltration by squamous cell carcinoma was due to late metastasis from the patient’s previous laryngeal tumour, or whether it was due to a covert lung primary is uncertain.

Tumour involvement of pulmonary vessels is not uncommon. This diagnosis should be considered in patients with a history of previous malignancy who present with flitting lung shadows.


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