Tracheal extubation under deep sevoflurane anesthesia: A novel strategy for weaning difficulties in intensive care
A 59-year-old 60 kg male presented with an acute severe exacerbation of chronic obstructive pulmonary disease (COPD). His COPD had been diagnosed 15 years previously and had clearly been troublesome, as he was well known to the respiratory physicians. Features of his presentation suggested an infective exacerbation - core temperature of 38.5°C, white cell count (WCC) of 22 × 109 L-1, and C-reactive protein (CRP) 134 mgL-1 Apart from controlled hypertension and hypercholesterolemia, there was no other relevant past medical history. Recent pulmonary function tests indicated severe COPD with a forced expiratory volume in 1 second (FEV1) of 0.69 liters (19% of predicted), forced vital capacity (FVC) 2.95 liters (66% of predicted), FEV1/FVC 0.23 (30% of predicted), and peak expiratory flow rate (PEFR) less than 50% of predicted. These results were typical for the patient. His regular medications consisted of simvastatin 40 mg, ramipril 2.5 mg, clopidogrel 75 mg, aspirin 75 mg, and prednisolone 30 mg, all once-a-day, along with salbutamol (100 mcg metered dose inhaler) (MDI) and beclomethasone (200 mcg MDI) one puff each, 6 and 12 hourly, respectively.\nEight hours following admission, he was intubated and ventilated in the intensive care unit (ICU). Initial arterial blood gases (ABGs) showed severe respiratory acidosis (pH 7.02, pCO2 18 kPa, pO2 12.4 kPa, HCO3- 26 mmolL-1, BE 1.7). From the start, it was very difficult to ventilate him, but we were able to achieve adequate tidal volumes (VT)(= 0.5 L) following muscle relaxation with vecuronium bromide 10 mg intravenous (IV). Inspiratory pressures (Pinsp) were 32 cm H2O on pressure controlled (PCV) mode. Arterial and central venous catheterization was performed for hemodynamic management. He was commenced on cefotaxime 1 gm IV and clarithromycin 0.5 gm IV (both 12 hourly), salbutamol 5 mg and ipratropium bromide 500 mcg 6 hourly (both nebulized), hydrocortisone sodium succinate 50 mg IV 6 hourly and low molecular weight heparin (LMWH). Aminophylline was commenced at 41.6 mg/hour following a bolus dose of 300 mg IV. He required minimal vasopressor support (nor-adrenaline 0.025 mcg/kg/min) to support his blood pressure.\nSedation was maintained with propofol and alfentanil, with the requirement for each amounting to 3.3 mg/kg/hour (20 ml/hr of 1 % solution) and 5.5 mcg/kg/min (20 ml/hour of 1 mg/ml solution), respectively. It was not possible to satisfactorily ventilate the patient with lower levels of sedation with the endotracheal tube in situ. Even slight reduction in the level of sedation provoked episodes of severe bronchospasm with desaturation (SpO2 dropping to 60-70%) despite administration of 100% O2. In spite of liberal use of bronchodilators, it took an average 45 minutes to 1 hour to settle him following such episodes. Stimuli such as endotracheal suctioning and rolling of the patient triggered troublesome episodes of bronchospasm and desaturation, associated with ABG evidence of severe respiratory acidosis (pCO2 up to 12.5 kPa). All these events prompted high levels of sedation, the addition of terbutaline (0.5 mg S/C, 6 hourly) to his treatment regimen and an increase of salbutamol frequency to 4 hourly.\nBy day 4, his infective markers had improved significantly (white cell count normalized, C-reactive protein reduced to normal, and the patient was afebrile). However, there was no improvement in his brittle airway reactivity. When stable, the patient had VT of 0.6 liters at Pinsp of 26 cm H2O, PEEP of 8 cm H2O (on PCV mode) and SpO2 of 99% with a FiO2 of 0.35. (pH 7.43, PO2 12.5 kPa, PCO2 5.4 kPa, BE + 2).\nWhen heavily sedated, the patient arguably met the criteria for consideration for extubation (according to published recommendations),[] but certainly not when the sedation was reduced. Notably, he would not be able to pass the spontaneous breathing test (SBT), his compliance fell to 20 ml/cm H2O, and his PaO2/FiO2 ratio fell to as low as 40 (PaO2 in mmHg).\nThere was much discussion regarding the next move in his treatment strategy. Although no guidelines or protocols would have supported it, experience and instinct lead us to consider extubation under deep inhalational anesthesia with sevoflurane. The alternative would have been a tracheostomy and the slow wean over days or weeks typical of many COPD patients. This would risk all of the well-recognized ventilator-associated complications.\nAn anesthetic machine (Dräger Cato edition) with a sevoflurane vaporizer (Dräger Vapor 2000) was brought to ICU. Sedation was turned off, and the patient gently manually ventilated with 100% O2 and sevoflurane using a Bain’s circuit, achieving end-tidal sevoflurane concentrations of 3-4 kPa. His blood pressure (BP) was supported by a small increase in nor-adrenaline from 0.025 to 0.05 mcg/kg/min. 15 minutes following cessation of sedation, 400 mcg of naloxone was administered IV and the patient started to breathe spontaneously. At this stage, his BP was 140/70 mm Hg, heart rate (HR) 70/min, RR 9/min, and SpO2 was 98%. 15 minutes later, the trachea was extubated following gentle endotracheal suctioning in the sitting position with a nasopharyngeal airway in situ. He was oxygenated with an anesthetic mask attached to Water’s circuit for the next 30 minutes with a FiO2 of 1.0 at 10 l/min until he was responsive to verbal commands. 45 minutes following extubation, his BP and HR were 140/84 mm Hg and 70/min, respectively. Initial ABGs were encouraging in view of his previous condition: pH 7.3, pCO2 8.9 kPa, pO2 12 kPa, HCO3-26 mmolL-1, BE 4.5, FiO2 0.6.\n2 hours later, he had an episode of respiratory depression, which was treated with a further bolus of 400 mcg of naloxone IV. 2-3 minutes later, he was fully conscious with a RR of 18/min and was able to cough. Naloxone was then administered as an infusion overnight (500 mcg/hour), with no further episodes of respiratory depression. He subsequently made an uneventful recovery and was discharged from the hospital 3 days later. Hemophilus influenzae was identified as the infective cause for the exacerbation of his chest disease.