Unilateral pulmonary oedema following general anasthesia – previous chest wall irradiation as a possible contributing factor

Unilateral pulmonary oedema (UPO) is a rare clinical entity with a number of different causes including re-expansion of a collapsed lung, unilateral pulmonary veno-occlusive disease, pulmonary contusion, cerebral autonomic dysfunction, bronchial obstruction [1] and severe ischaemic left ventricular dysfunction [2]. We describe a case following general anasthesia in which we believe that long-standing changes in the lung following radiotherapy may have played a role. A 78-year-old moderately obese woman presented for transurethral resection of a bladder tumour. Her medication comprised atenolol and bendrofluazide once daily for hypertension, GTN spray for mild exertional angina and gaviscon for acid reflux caused by a hiatus hernia. Her chest X-ray showed mild cardiomegaly and her electrocardiogram was normal. After pre-oxygenation, rapid sequence induction of anasthesia was performed. Following tracheal intubation, the lungs were ventilated with isoflurane and 60% nitrous oxide in oxygen and neuromuscular blockade was maintained with atracurium. There was a single brief episode of hypotension (75/40 mmHg) and bradycardia (35 beats.min−1) lasting less than 2.5 min, which responded rapidly to glycopyrronium 0.6 mg. Following this the patient remained cardiovascularly stable. The uncomplicated procedure lasted approximately 30 min and oxygen saturations of 99% were maintained throughout. Following reversal of neuromuscular relaxation, the trachea was extubated with the patient supine. On arrival in the recovery room the patient’s breathing was noted to be shallow and mainly diaphragmatic with partial obstruction of her upper airway. The oxygen saturation fell to 60%, the heart rate increased to 120 beats.min−1 and the blood pressure to 250/120 mmHg. With the patient still supine an oropharyngeal airway was inserted, 100% oxygen administered through a facemask and a further dose of neostigmine (2.5 mg) was given with glycopyrronium (0.6 mg). The oxygen saturation improved to 90% over the next 5 min. Crepitations were noted on the left side of the chest and furosemide 40 mg was administered. She was also given diamorphine 2.5 mg and sublingual GTN spray for retrosternal discomfort with good effect. At this point, the patient had received approximately 750 ml of intravenous fluid since the start of surgery. A 12-lead ECG taken at this time was normal, but a portable chest radiograph showed a left sided ‘white-out’ ( Fig. 2). She was then transferred to the Intensive Care Unit where her condition improved rapidly over the next 24 h with oxygen, facial CPAP and a further dose of furosemide 20 mg. A repeat chest X-ray was completely clear, cardiac enzymes were normal and an echocardiogram showed good left ventricular function. She was discharged home 3 days later. In trying to find an explanation for UPO in this case we had to consider several possible causes. There was no clinical evidence of aspiration and if this were the cause it is very unlikely that the dramatic X-ray changes would have cleared up so quickly. Whilst either peri-operative cardiac ischaemia or upper airway obstruction may have caused the pulmonary oedema, the fact that it was confined to one lung requires additional explanation. It is highly unlikely that there had been a unilateral bronchial intubation as the patient's oxygen saturation was 99% intra-operatively with an Fio2 of 0.4. The patient had remained supine following extubation so that the development of pulmonary oedema in a dependent lung could also be excluded. Significantly, 13 years previously the patient had suffered an acute episode of radiation-induced lung damage associated with radiotherapy following breast cancer surgery. Radiation-induced lung damage consists of an acute phase and a late phase which may develop several years after treatment [3-5]. Radiation-induced fibrosis is thought to result in long-term damage to the blood vessels resulting in impaired capillary permeability and an increase in pulmonary vascular resistance in the affected lung [6]. Such persistent changes may also affect the physiological function of the pulmonary vasculature so that it is less able to respond to any stress placed upon it. We believe that this long-term damage may have rendered the left lung of our patient more susceptible to the hypoxic insult induced by a combination of upper airway obstruction and myocardial ischaemia resulting in UPO.