Status asthmaticus is an acute exacerbation of asthma that is unresponsive to initial treatment with bronchodilators and can rapidly escalate into acute ventilatory failure. The clinical picture of severe asthma include agitation, drowsiness or confusion, breathlessness at rest, tachypnea, use of accessory respiratory muscles, tachycardia, and pulsus paradoxus. Pharmacological treatments include but are not limited to beta-2-mimetics, anticholinergic agents, magnesium sulphate, steroids and aminophylline. Asthma exacerbations can be triggered by interrupting chronic treatment: in war torn areas as Sudan it is mainly due to the abrupt lack of availability of drugs.
A 58 years old 80 kg man with history of severe asthma presented to our triage complaining of severe dyspnea in the last 3 days, unresponsive to treatment with bronchodilators and systemic corticosteroids. He stopped his chronic therapy with budesonide/formeterol due to the unavailability of the drug. At the arrival he showed orthopnea, severe tachypnoea (60 breaths/min) and sinus tachicardia (130 bpm), silent chest and SpO2 86% on reservoir mask 15 l O2/min. The ABG showed pH7.27, pO2 47, pCO2 60. The chest Xray and the transthoracic echo were unremarkable. After receiving repeated nebulizers (salbutamol 5 mg + adrenaline 1 mg every 20′ for 2 h), iv hydrocortisone high dose (1 g), iv aminophylline 240 mg, iv magnesium sulphate 2 g, iv ketamine 100 mg there were neither clinical nor ABG improvement. Given the unavailability of drugs as ipratropium and sevofluorane and of treatments like V-V ECMO, a rescue trial with iv enoximone was performed, administrating 0.3 mg/kg iv bolus followed by 3 mg/kg/min continuous infusion, conbined with NIV to decrease the respiratory workload and salbutamol nebulizers. Improvement of the respiratory mechanics and of the gas exhange were immediate, leading to normal ABG, mild tachypnoea and mild chest wheezes after the administration of 200 mg of enoximone, with no cardiovascular side effects. The patient was discharged home on the 6th day, without respiratory symptoms.
Enoximone acts as an inotrope by inhibiting PDE-3 activity and increasing intracellular cAMP levels in cardiac myocytes. Increasing intracellular cAMP is also the main mechanism of β2-agonists bronchodilators, and both experimental models and clinical experience suggest that enoximone can overcome the asthma-related β-receptors downregulation, providing a therapeutic role in status asthmaticus.