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After acute airway obstruction by a foreign body, removal of the offending object generally leads to swift recovery. A rare complication is negative-pressure pulmonary oedema.
A previously healthy man aged 47 choked while eating a piece of boneless chicken breast, and a Heimlich manoeuvre was immediately performed. The apparent airway obstruction was improved but he continued to cough vigorously, producing blood-stained frothy sputum. He also reported increasing dyspnoea and retrosternal pain. On admission to hospital three hours after the incident the patient was still coughing and pulse oximetry showed an oxygen saturation of 92% on room air. On examination the trachea was central; percussion of the chest was dull over the right base and midzone with poor air entry and coarse crackles. No radio-opaque foreign body was visible on chest radiography but there was haziness in all lung fields except for the right middle lobe.
Acute airway obstruction by a foreign body was diagnosed and the patient underwent urgent bronchoscopy and rigid endoscopic assessment of the bronchial tree. No foreign body was found, but copious frothy bloody secretions were suctioned from both main bronchi. Despite the appearance of the chest X-ray, the area of the right middle lobe bronchus was endoscopically no different from the remainder of the tracheo-bronchial tree. A rigid oesophagoscopy was also performed, but again no foreign body was retrieved. Oxygen saturation remained around 90% throughout this procedure despite administration of 100% oxygen. When extubation was attempted the patient became restless and was unable to maintain oxygenation. He was reintubated and transferred to the intensive care unit for ventilation. Treatment with intravenous metronidazole and cefuroxime was started.
A CT scan of the chest did not reveal any focal lesion but over the next few days oxygenation became increasingly difficult to maintain. The patient had to be ventilated with positive end-expiratory pressure in the prone position and a tracheostomy was performed to assist with bronchial toilet. Recovery was slow, but he was eventually weaned from the ventilator and later decannulated before being discharged home.
Pulmonary oedema as a complication of upper airway obstruction in adults was originally reported by Oswalt et al. in 19771. In this series of three cases the causes were upper airway tumour, strangulation and hanging. Since then, negative-pressure pulmonary oedema has been reported mainly by anaesthetists2,3,4 as a consequence of postoperative laryngospasm. According to one estimate, negative-pressure pulmonary oedema develops in 11% of all patients requiring active intervention for acute upper airway obstruction5. Healthy middle-aged males seem especially prone to this complication2.
What is the pathophysiological mechanism of negative-pressure pulmonary oedema? A generally accepted cause is excessive negative intrapleural and transpulmonary pressure produced by forceful inspiration against a closed glottis. The negative intrathoracic pressure also increases right-sided cardiac filling, raising pulmonary arterial pressure and thereby pulmonary capillary pressure with transudation into the interstitial and alveolar spaces3,4,5. The other main factor implicated in the pathophysiology of negative-pressure pulmonary oedema is mechanical disruption of the alveolar-capillary membrane or what is termed ‘stress failure’6. Hypoxia, acidosis and a hyperadrenergic state are also thought to be important1, 7, 8. Goldenberg et al.9 point to the possible relevance of cardiac anomalies: they found that 50% of patients with negative-pressure pulmonary oedema had such abnormalities compared with 1% of the general population. In the patient reported here, an echocardiogram was not performed.
In the published reports there is much variation both in the duration of obstruction that precedes negative-pressure pulmonary oedema and in the time between obstruction and onset. Usually the condition develops within minutes but in some instances it has begun up to an hour after clearance of the upper airway obstruction. A suggested explanation for delayed onset is that forced expiration against a closed glottis creates positive intra-alveolar pressures that oppose fluid transudation—a protective effect that is lost after clearance of the blockage2.
The recovery of our patient was atypically slow. Negative-pressure pulmonary oedema usually resolves rapidly with short-term ventilatory support, the key principle of treatment being early application of positive pressure to the airway. Adjunctive treatment with steroids, diuretics and bronchodilators has been proposed but their contribution to management is unclear3.