A 42 year old man presented with a week-long history of increasing shortness of breath, cough  (productive of purulent sputum) and fevers on a background of significant chronic lung disease. He had a ten year history of interstitial lung disease and was on the waiting list for a lung transplant. He used oxygen at a rate of 2 litres per minute at home, 24 hours a day. His usual exercise tolerance of 200 metres had been significantly reduced for the past week. His regular medications included seretide and salbutamol inhalers, lansoprazole, azathioprine, prednisolone alendronate.

On arrival in hospital, he was alert and orientated. He had a patent airway, but was tachypnoeic (rate of 50/minute) using his respiratory accessory muscles and a tracheal tug was evident. An arterial blood gas revealed type two respiratory failure (pH 7.26; pO₂ 8.14, pCO₂ 7.52 on 15 liters/min of face mask oxygen). He was hypotensive (80/40mmHg) and tachycardic (130/minute, sinus rhythm). A pyrexia of 39.2°C was recorded. Blood results showed normal renal function, a slightly elevated white cell count of 14.

The patient was admitted to the high dependency for close monitoring in view of his history and presentation. He was commenced on treatment for a presumed infection (viral or bacterial) with oseltamivir, co-amoxiclav and clarithromycin and given three “pulsed” doses (750mg) of methylprednisolone. He remained stable for the next twelve hours.

Early the next morning, he became very hypoxic (oxygen saturations less than 50%), bradycardic (<35 beats per minute) and had a brief hypoxic respiratory arrest. He received 1 cycle of cardiopulmonary resuscitation and was intubated. There was subsequently a return of spontaneous circulation.

The next 24 hours involved a period of difficulty with ventilation. His peak airway pressures were very high, despite being paralysed and a low volume/high respiratory rate strategy being employed. He was discussed with a tertiary respiratory centre and it was decided that he should be transferred for insertion of a pumpless arteriovenous interventional lung assist (for extracorporeal carbon dioxide removal) as a bridge prior to lung transplantation. He had formal ultrasound measurement of his femoral arteries. His left common femoral artery was widely patent (AP and transverse diameter of 8-9mm throughout), but the right was only 4-5mm throughout.

In the meantime, his peak airway pressures were consistently between 35 and 40cmH2O, despite tidal volumes of 230ml, 3.8ml/kg). With a rate of 32-35 breaths per minute, his pH was  initially maintained above 7.2, with a pCO₂ of 9-11kPa. Over the course of the next few hours, this became increasingly difficult to achieve. His oxygen requirements did not escalate (an FiO₂ of 0.6 provided a pO₂ of 8-9kPa). When his pCO₂ increased to 15.4kPa and his pH dropped to 7.17, further adjustments were made and the PEEP decreased to 5cmH₂O from 10cmH₂O. His noradrenaline requirements were increasing and with the aid of the cardiac output monitoring, he was cautiously given fluid with a good response.

He was transferred to the centre in which a lung transplant could be performed within hours of the referral. A Novalung device was inserted and he underwent a bilateral lobar lung transplant several days later. He was in hospital for 6 weeks and made a very good long-term recovery. At six months, he was extremely well and was undertaking his activities of daily living completely normally with stable lung function. He even managed to complete an eight mile bike ride.

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