Prolonged intubation may cause tracheal stenosis, with progressive dyspnoea and wheeze easily misdiagnosed as asthma

Tracheal obstruction may be due to trauma, infection, tumour, or aspirated foreign bodies. Despite improvements in the design of tracheal tubes, however, tracheal stenosis after intubation remains an important cause of tracheal obstruction, which may be life threatening. We describe a patient with tracheal stenosis which was initially misdiagnosed as asthma after prolonged tracheal intubation.

A 16 year old man, with a history of asthma that had needed hospital admission on several occasions, was referred to the intensive care unit with a diagnosis of acute severe asthma. Seven weeks earlier he had sustained a head injury in a road traffic accident and had been mechanically ventilated through an oral tracheal tube for 84 hours at another hospital. Subsequently he had been transferred to a neurological rehabilitation unit. Two days after admission he complained of exertional dyspnoea and wheeze. Although treatment with bronchodilators was started, his symptoms worsened progressively over the next two weeks, and he became acutely dyspnoeic at rest. He was transferred to an acute medical ward but continued to deteriorate despite receiving nebulised bronchodilators, intravenous hydrocortisone, aminophylline, and antibiotics. He became exhausted within 24 hours and was thus referred to our intensive care unit for further management.

On admission he was in extremis and had tachypnoea (respiratory rate 30/min), a virtually silent chest, and hypercarbia (partial pressure of carbon dioxide 9.3 kPa) on arterial blood gas analysis. We decided to intubate and ventilate him. After intravenous induction of anaesthesia, laryngoscopy was performed, with a good view of a normal glottis, but it was impossible to pass a tracheal tube (size 7-9 mm internal diameter) further than 2 cm beyond his vocal cords before firm resistance was felt. It was similarly impossible to pass even a flexible gum elastic bougie beyond the obstruction. We managed to ventilate him adequately with a bag, valve, and mask. We decided that instead of acute severe asthma the patient had a severe tracheal stenosis secondary to tracheal intubation after his head injury. Surgical help was sought quickly, and both emergency cricothyroidotomy and tracheostomy were considered. It was almost certain, however, that the stenosis extended beyond the level of the cricothyroid membrane and probably below the level of a surgical tracheostomy. We therefore decided to make another attempt to intubate the trachea by way of the oral route. A paediatric tracheal tube (4.5 mm internal diameter) was threaded on to a semirigid introducer, which was allowed to protrude 5 cm beyond the end of the tube. The tip of the introducer was then passed through the vocal cords until resistance was felt. The introducer was then firmly pushed with a twisting motion until a sudden give was felt as it passed through and dilated the stenosis. With some difficulty, the tracheal tube was passed, using the introducer as a guide. Once intubated, the patient was easy to ventilate without excessively high airway pressures, and there was no wheeze on auscultation of the chest. The patient was referred to the regional cardiothoracic centre for further management.  Medical Supply.