2004 OPEN FORUM Abstracts
RV-PA CONDUIT STENOSIS WITH POST-OPERATIVE RE-PERFUSION INJURY, NASAL VENTILATION, AND REFRACTORY HYPOXEMIA
Douglas
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.