High Frequency Oscillatory Ventilation: A Cautionary Tale

Abstract

INTRODUCTION: Systemic air emboli have been reported to occur in association with positive pressure ventilation (PPV). However, a case of systemic air emboli in an adult patient with Acute Respiratory Distress Syndrome (ARDS) treated with High-Frequency Oscillatory Ventilation (HFOV) is unique. No single pathophysiological mechanism explains systemic air emboli in patients treated with PPV. A case of H1N1 associated ARDS in 2011 receiving HFOV complicated by fatal cerebral air embolism is presented. CASE PRESENTATION: A 22 year-old woman developed ARDS from influenza A subtype H1N1. Her hypoxemia was refractory to 100% oxygen delivered at 6cc/Kg ideal body weight tidal volumes with mean airway pressures of 25-30cm of H2O despite the use of neuromuscular blockade and inhaled nitric oxide. Echocardiogram demonstrated normal cardiac function and no evidence of intracardiac shunt using a bubble study. Her hospital course was complicated by acute kidney injury requiring dialysis to control her acidemia and intra-vascular volume. A right chest tube was placed for a large right pleural effusion. Despite these interventions a mean airway pressure over 30cm of H2O with an FIO2 of 0.9 was required to obtain a pO2 of 50mm Hg. The mode of mechanical ventilation was changed to high frequency oscillatory ventilation (HFOV) with mean airway pressures of 35-40cm H2O. On the HFOV, the FIO2 was decreased to 0.60 while obtaining a pO2 of 50-60mm Hg. She was not felt to be a candidate for Extra Corporeal Membrane Oxygenation (ECMO) therapy based on her high body mass index and multi-organ system dysfunction. The day after HFOV initiation the bedside nurse noted sudden bilateral pupillary dilation in the patient. Emergent bedside CT of her head revealed diffuse cerebral edema, bi-cortical infarcts, brainstem herniation and multiple bilateral cortical air emboli (figure 1). Goals of care were changed to palliation after discussions with the patient's family. She died immediately after withdrawal of mechanical ventilation. DISCUSSION: Little is known about the mechanism of systemic air emboli in the setting of positive pressure ventilation. One possible mechanism is that the high airway pressures in acute lung injury can allow air to dissect into the bronchovascular tree and push air emboli into damaged capillaries to the pulmonary venous return. This theoretical mechanism is similar to the one proposed for systemic gas emboli associated with the bronchoscopic use of neodymium:yttrium-aluminum garnet (Nd:YAG) laser or Argon-Plasma Coagulation (APC) of endobronchial lesions (1). Capillary or venous membrane integrity is compromised and the airflow or endobronchial pressures are thought to be transiently high enough allowing for gas to enter the bronchial venous system. Alternatively, Butler and Hills demonstrated in 1985 that transpulmonary passage of gas can occur in the absence of lung injury or a right to left intracardiac shunt when the filtering capacity of the lung is “overwhelmed ” by large amounts of pulmonary arterial gas (2). Weaver and Morris published a case of venous gas emboli that presumably traveled systemically through this mechanism resulting in fatal cerebral gas emboli (3). CONCLUSIONS: Multiple mechanisms may contribute to systemic gas emboli during positive pressure ventilation and the clinician should minimize the patients risk by, staying vigilant about venous access sites, use lowest effective ventilator delivered pressures and minimize sources of lung injury in an attempt to prevent this catastrophic event.