The role of Continuous Positive Airway Pressure (CPAP) in asthma management has been well described (1). Higher positive end expiratory pressure is required to change baseline diameter of bronchus (2 ). Avoiding hyperinflation and high peak pressures have been the mainstays of mechanical ventilation in acute asthma. We describe a case of status asthmaticus responsive APRV.
A 21-year-old Caucasian female with history of moderate asthma presented to our Emergency Department with worsening dyspnea of four hours duration coupled with nonproductive cough, myalgias, coryza and rhinorrhea of three days duration. She described increasing dyspnea with wheezing requiring multiple emergency visits managed with standard therapy of antibiotics, bronchodilators and steroids over the preceding months. On presentation to our facility her only active prescription was Albuterol. She was initially admitted to general medicine with asthma exacerbation managed with bronchodilators, steroids and antibiotics. She deteriorated clinically and blood gas revealed an Arterial-alveolar gradient greater than 500 on 100% face mask and was admitted to the Intensive Care Unit. Investigations targeting shunt physiology were negative including computed tomography (CT) angiography of the chest and echocardiography with bubble study. She remained afebrile with mild leukocytosis and plain films of the chest revealed increasing basilar densities consistent with bibasilar ground glass seen on CT. The patient remained clinically unchanged despite aggressive medical therapy and was electively intubated on Day 3 to tolerate bronchoscopy with bronchoalveolar lavage (BAL) as imaging remained discordantly benign compared to the patients oxygen debt. She was placed on continuous positive airway pressure of 10 cm H2O with pressure support of 18 cm H2O with 80% FIO2 and saturations remained in the 85–95% range despite pulse dosing of steroids and continuous bronchodilator therapy. BAL revealed only mucous plugging with all cultures and stains negative for typical and atypical organisms. She began to have more frequent and sustained bouts of severe desaturation requiring escalating FIO2 and pressure support. The patient was cycled through multiple standard modes of ventilation with all being inferior to the patient’s clinical parameters on CPAP which was then, by Day 6, also failing. At that time the patient was placed on APRV with a P high /P low of 25/0 cm H2O and T high/T low of 5/0.85s generating a mean airway pressure of 21 cm H2O. Oxygen saturation rapidly increased to >95% and stabilized. Mean airway pressure was weaned deliberately to CPAP over a 24 hour period and the patient was durably extubated on hospital day 7.
The use APRV in acute asthma has not been previously described. We document a rapid recovery in such a patient with the use of APRV. Xue et al demonstrated that hyperinflation of lungs with chronic CPAP decreases the airway responsiveness and contractile protein activation in airway smooth muscle (1). Whether or not this effect can be seen in acute settings with APRV is yet to be studied. It may be postulated that relief of air trapping with decreasing upper airway obstruction may be facilitated by the high MAP of APRV while the unique characteristics of APRV allow innocuous spontaneous respiration and, in our experience, a satiation of air hunger.
Clinical guidelines for mechanical ventilation in acute asthma remain controversial. We believe that the distinctive mode of APRV in asthma management is under utilized. It is our hope that this report provides the impetus for further study.
Naveed Hasan, No Financial Disclosure Information; No Product/Research Disclosure Information