P030: STATUS ASTHMATICUS - WHEN ECMO FAILS
Joseph LaGrew II, MD, Kevin Olsen, MD, Amanda Frantz, MD; University of Florida College of Medicine
Introduction: Inhaled volatile anesthetic (VA) agents have been reported as treatments of severe, refractory asthma, or status asthmaticus (SA), as early as the 1930s as a rescue management when other more common medical management failed. These are postulated to work via direct relaxation of bronchial smooth muscle, inhibition of the release of inflammatory mediators, b-adrenergic receptor stimulation, reduction of vagal tone and vagal mediated reflexes, and antagonism of the effects of histamine and methacholine. Animal models also suggest sevoflurane functions in immune modulation to inhibit leukotriene induced inflammation, downregulating TNF-a, TGF-b and VEGF, increasing Nrf2 protective antioxidant response, and dampening sirt-1, catalase and GPx expression. To our knowledge, there have been no prior reports of implementation of volatile agent treatment for status asthmaticus after respiratory failure requiring veno-venous (V-V) ECMO. Here we describe utilization of isoflurane therapy after V-V ECMO cannulation for acute respiratory failure from status asthmaticus.
Case: A 37-year-old male presented with severe asthma exacerbation from rhinovirus infection resulting in respiratory failure, unresponsive to standard medical management, and requiring endotracheal intubation. Sedation and paralytics were started without improvement in PaO2, PaCO2, or peak airway pressures (PAP’s), ultimately requiring initiation of veno-venous extracorporeal membrane oxygenation (V-V ECMO). Despite this, he continued to have elevated PAP’s, inadequate tidal volumes and was started on isoflurane with significant improvement. ECMO decannulation occurred five days after initiation of volatile anesthetic. He was weaned from mechanical ventilation via tracheostomy and ultimately transferred to a step-down unit on room air.
Discussion: It is unclear what proportion VAs effect is due to their direct action on bronchiole smooth muscle compared to systemic uptake, but prior studies have demonstrated efficacious sedative effect from relatively modest concentrations (0.4-0.7%) of isoflurane even in the presence of severely impaired pulmonary function, indicating that both mechanisms should contribute to therapeutic benefit for our patient. In the case presented here, the patient remained with elevated peak pressures and hypercarbia days after initiation of ECMO which carried risks of significant adverse events. In this setting, VA therapy was able to minimize the total ECMO time in addition to treating the refractory SA. VAs have also been studied for ICU sedation with good results including faster weaning with better wake ups and less pain for patients ready to extubate compared to IV sedation. VAs have immune modulatory and anti-inflammatory actions as well. These potential benefits were unrealized in this patient and treatment for SA was delayed because of the inherent limitations to of volatile anesthesia supplied by a vaporizer including incompatibility with ICU ventilators, lack of scavenging capabilities in the ICU and inexperience of non-anesthesia providers with its use. These shortcomings make VA delivery inefficient and costly at least and may be barriers to delivery of care in the worst case scenario.
Conclusion: Typically given to avoid respiratory failure, isoflurane was utilized in this case as a rescue treatment for status asthmaticus in a patient failing standard medical management for acidosis and acute on chronic respiratory insufficiency requiring V-V ECMO support.