2004 OPEN FORUM Abstracts
RV-PA CONDUIT STENOSIS WITH POST-OPERATIVE RE-PERFUSION INJURY, NASAL VENTILATION, AND REFRACTORY HYPOXEMIA
E Petsinger BS, RRT, Susan Roark RRT, Angel Cuadradro MD, CICU Children’s
Healthcare of Atlanta
INTRODUCTION: A 50 Kg. 19 yo female has a surgical history of a Truncus type I repair at two months of age with a RV-PA conduit and Aortic Homograph. The initial recovery included multiple interventions as well as a Pectus Excavatum repair. The patient presented with conduit stenosis and underwent replacement and a Tricuspid Valve Annuloplasty. The initial post-operative course was marked with moderate surgical bleeding responding to intravascular clotting factors. There was a mild to moderate A-a gradient noted on 40% and +6cmH2O of PEEP. On post-operative day one the patient was extubated to a 2 LPM NC with a PaO2 of 63 torr.
CASE SUMMARY: On post-operative day two the chest film revealed questionable LLL atelectesis. She also had moderate hypoxemia on a 50% VM with a PaO2 of 52 torr. The patient’s oxygenation worsened on post-operative day three with a 100% requirement and increasing respiratory distress, with a PaO2 of 60 torr. The chest film revealed a left lung whiteout that corresponded with diminished to absent breath sounds over the left chest. The patient was then placed on Nasal Ventilation through a Petite Nasal Mask (Respironics Inc., Murrysville PA, USA) with the Drager XL ventilator (Drager Medical, Telford PA, USA) initially on 100%, +8cmH2O CPAP, and +15cmH2O PSV. Over the next several hours the CPAP was optimized to +14cmH2O and the PSV was decreased to +3cmH2O for triggering and comfort purposes. The O2 was weaned to 40% with a PaO2 > 150 torr. Six hours after the institution of CPAP, the patient was able to sit in a chair as well as nap without the previous symptoms of respiratory distress. The CPAP level was weaned to +10cmH2O and remained at this level overnight. The next twenty-four hour period revealed patient improvement characterized by progressive CPAP titration to off and tolerating a 5LPM NC without compromising the patient’s oxygenation status. On post-operative day five the patient was ambulating without difficulty and was discharged to the step-down unit on a 2LPM NC.
CONCLUSIONS: This is a classical case of refractory hypoxemia due to a reperfusion phenomenon that was not responsive to oxygen alone. The lung’s vascular bed was existing in a low flow state due to the conduit stenosis. This physiology presents when a low flow state is suddenly presented with a higher flow and pressure state. The hydrostatic pressure gradient in the alveolar-pulmonary vascular bed needs time to re-establish the gradient with the aid of an increase in intrathoracic pressure. The ability to avoid reintubation with proactive utilization of Nasal CPAP needs to be discussed as a viable procedure in the CICU’s standard of care.