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A 75-year-old former boiler repairman presented with breathlessness. He had undergone coronary artery bypass grafting (CABG) 20 years previously, with diffuse pleural thickening (DPT) identified preoperatively (fig 1). At repeat CABG 10 years later phrenic nerve damage occurred, with resultant diaphragmatic weakness necessitating prolonged mechanical ventilator support. Post weaning, arterial blood gases on room air showed pH 7.39, partial CO2 7.31 kPa, partial O2 6.52 kPa. A sleep study on current hospital admission confirmed hypoxaemia with hypercapnia, and pulmonary function tests confirmed a restrictive defect (forced expiratory volume in 1 s (FEV1/)/forced expiratory vital capacity (FVC) =104%; KCO =1.73 mmol/min/kPa/litre =115% predicted). Nocturnal non-invasive positive pressure ventilation (NPPV) was given, as a result of these investigations, with resolution of symptoms.
The chest radiograph showed DPT of up to 10 mm and an elevated left hemidiaphragm (fig 1).
A CT scan confirmed symmetrical thickening with calcified diaphragmatic pleural plaques and an area of rounded atelectasis (Blesovsky sign; fig 2).
Diffuse pleural thickening (DPT) has been reported in 5% to 14% of asbestos-exposed individuals1 and results from thickened, fibrotic visceral pleura fusing with parietal pleura, secondary to an exudative pleural effusion.2 It differs from pleural plaques, as it is associated with chest pain and a decrease in lung function.
Phrenic nerve damage during cardiac surgery may be related to cold-induced injury from myocardial protection strategies or mechanical injury during internal mammary artery harvesting. Recovery is variable.3
Careful surveillance of patients with combined intrathoracic and extrathoracic restriction is required as incipient respiratory failure may be successfully treated with non-invasive positive pressure ventilation (NPPV).
Competing interests: None.
Patient consent: Patient/guardian consent was obtained for publication.
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