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Editor,—Although the in-hospital mortality from refractory status asthmaticus is low, the treatment strategies used in the management of these patients may cause significant morbidity.1-3 Those children who require ventilation either for resuscitation or impending respiratory collapse often require the addition of “unconventional” adjuvant bronchodilator treatments, such as intravenous β2agonists,4 ketamine,5 or magnesium,6 aimed at reduction of ventilator induced volutrauma.
Inhaled anaesthetic gases are known to produce sustained bronchodilatation in refractory status asthmaticus, possibly mediated by airway reflex blockade and a direct effect on smooth muscle.7-9 We wish to highlight the use of inhaled isoflurane in two children with severe life threatening asthma, and in particular, the importance of guiding treatment by continuous intra-arterial blood gas analysis (Paratrend 7, Biomedical Sensors, High Wycombe).10
Patient A, a 4 year old boy with multiple hospital admissions for asthma, presented “in extremis” (oxygen saturation 60%) with a six hour history of increasing dyspnoea, and required emergency intubation. Arterial blood gas showed pH 7.1, carbon dioxide pressure (Pco2 ) 9.8 kPa, and oxygen pressure (Po2 ) 35 kPa. He was treated with intravenous salbutamol at 3 μg/kg/min, aminophylline at 1 mg/kg/hour after a loading dose, magnesium sulphate 25 mg/kg, ketamine 2 mg/kg bolus, morphine 20 μg/kg/hour, vecuronium 100 μg/kg/hour, and transferred to the paediatric intensive care unit.
However he continued to deteriorate (pH 6.9,Pco2 17.2 kPa, and Po2 42 kPa) on settings of: pressure control 44/2 cm H2O, rate 9, fractional inspired oxygen (Fio2 ) 0.6. Sequential Pco2 results are given in fig 1. Two hours after admission he was unable to be ventilated and became bradycardic (pH 6.8, Pco2 23.9 kPa), requiring disconnection from the ventilator and manual chest compression to achieve forced expiration. Isoflurane was administered at one minimum alveolar concentration via a Boyle’s machine and the inspiratory port of the ventilator. In order to monitor the effects of this treatment, a Paratrend sensor was inserted via a femoral arterial line documenting the rapid improvement. The isoflurane was stopped after 7 hours, he was extubated at 36 hours and discharged to the ward on day 3.
Patient B was a 23 month old boy who presented in status asthmaticus with a two day history of increasing dyspnoea. Arterial blood gas showed pH 7.27, Pco2 6.5 kPa, andPo2 44 kPa in 15 L of face mask oxygen. He received nebulised salbutamol 5 mg (×2), atrovent 250 μg, intravenous hydrocortisone 50 mg, aminophylline loading dose plus infusion at 0.9 mg/kg/hour, and salbutamol infusion at 2 μg/kg/min. After clinical improvement he was transferred self ventilating to the paediatric intensive care unit.
He was treated additionally with intravenous magnesium sulphate 25 mg/kg and salbutamol 5 μg/kg/min, but became progressively more exhausted and was electively intubated, with morphine 20 μg/kg/hour and vecuronium 100 μg/kg/hour. The response to intubation was rapid deterioration (pH 6.9 and Pco2 17.9 kPa) at initial ventilation settings of: pressure control 39/4 cm H2O, rate 11, Fio2 0.6. Passive expiratory time was 8–10 seconds. Isoflurane was administered as described above, with rapid improvement (see fig 1), although he later developed segmental atelectasis requiring five days of continued ventilation for hypoxia.
These two cases illustrate that intubation and ventilation of severe asthmatics, even in the setting of impending respiratory collapse, may result in significant deterioration despite appropriate ventilatory strategies.2 3 Early administration of isoflurane is beneficial in those children who fail to improve despite aggressive conventional and adjunctive treatment while the close temporal relationship between isoflurane administration and both clinical and biochemical improvement, suggests a rapid bronchodilatory response. Management of these patients is considerably facilitated by continuous intra-arterial blood gas analysis.