Extracorporeal CO2 removal

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.

What is the rationale for extracorporeal lung assist?
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High Frequency Oscillatory Ventilation in ARDS

High Frequency Oscillatory Ventilation in ARDS

A 45 year old female presented to A&E with a 5 day history of worsening SOB, cough productive of green sputum, lethargy, anorexia, fever and rigors. She had no co- morbidities and was active and independent with a good exercise tolerance. On examination she looked unwell, clammy and drowsy. Her respiratory rate was 35 breaths per minute and SpO2 of 84% on 15 Litres of oxygen via a non-rebreathing mask. Her blood pressure was 88/40 mmHg with a heart rate of 140 per minute despite having received 3 litres of fluid. Arterial blood gas showed PaO2 6.0kPa, pH 7.28, PaCO2 7.1 kPa, Bicarbonate 14 mmol/l, BE -11 and Lactate 8.6 mmol/l. Chest radiograph demonstrated significant bilateral consolidation with infiltrates consistent with ARDS. PaO2:FiO2 was calculated as 15 indicating severe ARDS presumed secondary to CAP.

She was managed as per sepsis guidelines. Oxygen therapy was continued and CPAP was initiated due to the hypoxia whilst an ICU bed was being prepared for admission. Noradrenaline was commenced at 0.2mcg/kg/min which continued to increase. Repeat arterial blood gases confirmed worsening type 2 respiratory failure and the patient was clinically exhausted. A modified rapid sequence induction was performed and IPPV commenced. Her oxygenation remained a problem and despite a FiO2 of 1.0 and PEEP of 20 his SpO2 remained 85% and PaO2 6kPa. The patients’ sedation was deepened and muscle relaxant administered. Lung protective ventilation was continued however arterial blood gases continued to worsen. The decision was made to convert the patient from conventional ventilation (CV) to High-Frequency Oscillator Ventilation (HFOV). The initial ABGs after an hour of HFOV showed an improvement as did subsequent numbers. This mode of ventilation was continued for a further 48 hours and then converted to CV. Gas exchange continued to improve. Over the course of the following 4 weeks the patient had a tracheostomy performed to aid weaning. She subsequently developed a Ventilator Associated Pneumonia and worsening ARDS required a further period of HFOV. Improvement continued and the patient was successfully decannulated and discharged from ICU.

What is the evidence base for high frequency oscillatory ventilation in ARDS?

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ECMO for Respiratory Failure

ECMO for Respiratory Failure

A 40 year old lady was admitted under the medical team with pneumonia. She was normally well with no history of respiratory illnesses. On day two of her hospital admission she became more hypoxic necessitating continuous-positive-airway-pressure. Her condition rapidly worsened and her chest x-ray showed diffuse bilateral infiltrates. An echocardiogram demonstrated normal systolic function. She was intubated and ventilated. Despite sedation, ARDSnet ventilation, paralysis and then proning her, she remained severely hypoxaemic. A therapeutic bronchoscopy was performed prior to proning but did not improve her condition.

Should she be referred for consideration of ECMO and was is this evidence to support it’s use?

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Use of PEEP in ARDS

Use of PEEP in ARDS

A young woman was admitted with respiratory failure requiring invasive ventilation. She had bilateral lobar consolidation and positive urinary pneumococcal antigen. She was ventilated with protective lung strategies but required FiO2 of between 0.8-1.0. A PEEP of 18 was set. She was ventilated for over 2 weeks, and was tracheostomised but was discharged from the ICU after 3 weeks.

How is PEEP utilised in the ventilatory strategies in the management of Adult Respiratory Distress Syndrome?Read More »

Proning for Refractory Hypoxaemia

Proning for Refractory Hypoxaemia

A 60 yr old woman was admitted to the ICU with a severe community acquired pneumonia and septic shock. She was invasively ventilated with a lung protective strategy, optimised PEEP and recruitment manouvres as needed. Her refractory hypoxia persisted and so she was probed for 16 hours a day for the first 5 days of her admission. She made slow but steady improvements and was discharged from the ICU 10 days later.

What is the current evidence for proning as a rescue therapy for refractory hypoxia?Read More »

ECMO for Severe Refractory Hypoxaemia

ECMO for Severe Refractory Hypoxaemia

An 60 year old woman developed ARDS secondary to pneumococcal meningitis. Despite optimal ventilatory management and restrictive fluid intake her oxygenation remained severely impaired. She was referred to the regional respiratory failure unit who established her on mobile ECMO for retrieval. She remained on ECMO for five days, weaned off the ventilator after three further days and made a full neurological recovery leaving hospital two weeks later.

Is there sufficient evidence to promote the use of Extracorporeal Membrane Oxygenation (ECMO) for the management of severe refractory hypoxia in the United Kingdom?Read More »

The Role of ECMO in ARDS

The Role of ECMO in ARDS

A middle aged man with acute pancreatitis developed multiorgan failure and was admitted to the ICU and required ventilation and noradrenaline. He became progressively more hypoxic despite lung protective ventilation, paralysis, inverse ratios and a restrictive fluid regime. He developed bilateral pneumothoraces requiring chest drains. He was retrieved to the nearest refractory hypoxia centre and established on VV ECMO. On the third day of ECMO therapy he developed lateralising signs and was found to have had a large intracranial haemorrhage. Treatment was subsequently withdrawn.

Do patients with ARDS benefit from ECMO?Read More »

Nitric Oxide for Refractory Hypoxaemia in ARDS

Nitric Oxide for Refractory Hypoxaemia in ARDS

A 65 year old woman developed a hospital acquired pneumonia 24 hours after a multilevel spinal fixation. She became progressively more hypoxic and required intubation. She remained profoundly hypoxic despite FiO2 1.0, paralysis, lung protective ventilation and inverse ratios. She was established on inhaled nitric oxide therapy as anticoagulation for ECMO was felt to be contraindicated. This resulted in an rapid but modest increase in SpO2. Over the next days, her recovery was complicated by pneumothoraces requiring chest drains, but she remained on iNO for several days, and weaned off the ventilator at around day 10.

Does nitric oxide have a role to play in hypoxemia secondary to ARDS?Read More »

prone ventilation in ARDS

Prone Ventilation in ARDS

An 63 year old woman with a history of bronchiectasis required intubation for a community acquired pneumonia. Several days into her ICU admission she developed a rapid worsening in her oxygenation and new bilateral pulmonary infiltrates. She also required increasing vasopressor support and began to develop multiorgan failure. She was paralysed and ventilated with inverse ratios but remained profoundly hypoxic. She was proned with no effect on oxygenation. She was commenced on inhaled nitric oxide with no effect. She continued to rapidly deteriorate and died shortly after.

Does prone ventilation in ARDS improve mortality?

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