Intranasal Salbutamol Instillation in Asthma Attack NATAN WEKSLER, MD, S BRILL, MD, A TARNAPOLSKI, MD, GM GURMAN, MD Beta-two sympathomimetic drugs are the treatment of choice for asth- matic attack. Their main effect is to dilate the bronchi by a direct action on beta-two adrenoreceptors on the smooth muscle, and also by mediator release inhibition from mast cells. Salbutamol is widely used in the treatment of bronchial asthma, and is usually administered either by inhalation, orally, or parenterally. The nasal route seems to afford an effective way to administer medications, since the nasal mucosa has a relatively large surface area, and there is no gastrointestinal-hepatic first pass-effect, thus avoiding extensive loss of the administered drug. We describe herein the use of nasal salbutamol in 3 patients with severe asthma attacks who were refractory to conventional therapy, with favor- able responses and without significant undesirable effects. (Am J Emerg i e d 1999;17:686-688. Copyright © 1999 by W.B. Saunders Company) The pathophysiological features of an asthmatic episode in the tracheobronchial tree include smooth muscle spasm, mucosal edema, and bronchial plugging with thick secre- tions. 1 Similarly, thickening of basal membrane, vascular, and lymphatic engorgement aggravate the bronchial obstruc- tion, leading to air trapping and hyperinflation of the lungs. These changes are clinically manifested by cough, pro- longed expiration, and wheezing. When obstruction be- comes more severe, there is insufficient expiratory flow, and wheezing may not be audible on auscultation. 2 Beta-sympathomimetic amines are the drugs of choice in treatment of asthma attacks, acting by a two-fold mecha- nism. The first and main effect is to dilate the bronchi by a direct action on beta-two adrenoreceptors, and the second one is through the inhibition of mediators' release from mast cells.3,4 Salbutamol is still the "first-choice" drug for treatment of bronchoconstriction, 3,5 and is administered by inhalation, orally, or parenterally. 5,6 There is no clinical report related to intranasal instillation of salbutamol. We report herein 3 patients with acute severe asthma who have responded to nasal administration of salbutamol after failure of the conventional therapy to improve their clinical status. From the Division of Anesthesiology, Soroka University Medical Center, Faculty of Medical Sciences, Ben Gurion University of the Negev, Beer Sheva 84101, Israel. Manuscript received August 11, 1998, returned September 10, 1998; revision received November 9, 1998, accepted November 27, 1998. Address reprint requests to Dr Natan Weksler, Division of Anesthe- siology, Soroka University Medical Center, PO Box 151, Beer-Sheva 84101, Israel. Key Words:Asthma, salbutamol, nasal route. Copyright © 1999 by W.B. Saunders Company 0735-6757/99/1707-0015510.00/0 686 CASE REPORTS Patient 1 A 30-year-old man was admitted to the GICU from the emergency room with a severe asthma attack. His medical history was remarkable for mild bronchial asthma treatment by salbutamol during acute episodes. Before being transferred to the hospital he received 3 consecutive salbutamol inhalations, with a time lapse of about 10 to 15 minutes between them (100 lag per inhalation) without any improvement. In the emergency room he was treated with 2 salbutamol inhalations of 5 mg each, intravenous injection of hydrocortisone, and aminophylline. Despite the treatment, his clinical condition continued to deteriorate rapidly, he became lethargic, and on chest auscultation, no respiratory sounds were detected. Endotracheal intubation was performed after administra- tion of ketamine 2mg/kg, midazolam 0.07 mg/kg, and pancuro- nium 0.1 mg/kg. Mechanical ventilation was started with a tidal volume of 10 mL/kg and a respiratory rate of 12 breaths/rain generating a peak inspiratory pressure above 70 cm H20. Decreasing the tidal volume to 5 mL/min with a respiratory rate of 20 breaths/min caused evident incomplete expiratory phase, with a peak inspiratory pressure of 60 cm H20. Arterial blood gas examination showed mixed (metabolic-respiratory) acidosis: pH 7.1, PaCO2 60 mm Hg, PaO2 80 mm Hg (on a FIO2 of 1), and bicarbonate of 18 mEq/L. Additional doses of ketamine, hydrocortisone, pancuronium, and inhalations of salbutamol did not improve the respiratory condi- tion. Similarly, the blood pressure decreased from 140/80 to 90/50 mm Hg, and the pulse rate increased from 120 to 160 beats/min. Ten milligrams of salbutamol were then intranasally administered. Fifteen minutes later the peak inspiratory pressure decreased to 45 cm H20, mad lung inflation was clearly heard, with evident expiratory wheezing that gradually decreased. A second nasal instillation of salbutamol was followed by a complete wheezing relief and clean inspiration. Sixty minutes later the patient was comfortable, breathing spontaneously, and fully conscious. A T-piece trial did not cause further deterioration, and was followed after 40 minutes by a successful extubation. Patient 2 A 32-year-old, five-months'--pregnant woman arrived in the emergency room complaining of an increasing shortness of breath. In the ananmesis, she denied previous history of asthma, chronic bronchitis, or any other disease. On admission, she was in frank respiratory distress, with tachypnea (28 breaths/rain) and using the respiratory accessory muscles. On auscultation, intense expiratory wheezing and prolonged expiration were noticed. Blood pressure was 125/70 mm Hg, pulse rate 130 beats/rain, and body tempera- ture 30°C. She was treated with 3 consecutive nebulizations of 5 mg each, salbutamol, and intravenous methylprednisolone. A second and third inhaled dose of salbutamol of 100 lag each did not relieve the symptoms. Intranasal administration of 10 mg of salbutamol, after a delay of 30 minutes, was followed by a progressive relief of the symptoms, and 20 minutes later only a few wheezes were heard. A second intranasal instillation of salbutamol