This current study demonstrates factors associated with extubation failure in neonatal patients with hypoplastic left heart syndrome post-Norwood procedure. Vocal cord anomaly (p = 0.022), higher respiratory rates at pre-extubation baseline (p = 0.029), lower partial pressure of O2 at 10 minutes post-extubation (p = 0.022), lower cerebral NIRS at 10 minutes post-extubation (p < 0.001), lower renal NIRS at pre-extubation baseline (p = 0.001), lower renal NIRS at post-extubation steady-state (p = 0.017), and lower end-tidal CO2 at pre-extubation baseline (p < 0.001) were all associated with increased risk of extubation failure. Mechanical ventilation parameters and the presence or absence of CPAP trial were not associated with the failed extubation events.
Failed extubation is associated with increased length of stay and increased risk of inpatient mortality (10–12, 15). Extubation failure is most frequently defined in published data as needing reintubation within 24 or 48 hours (16–18). Using these definitions, extubation failure ranged from 5–24% (16, 17, 19). Previous studies identified many factors associated with extubation failure, including the presence of an airway and genetic anomalies in pediatric patients with and without congenital heart disease (18, 20–23). Similarly, we found vocal cord anomaly as a factor associated with failed extubation in the present study. When studies looked at children after the Norwood operation, specifically, the following have been demonstrated to be associated with extubation failure: the need for nitric oxide, longer duration of mechanical ventilation, presence of chylothorax, and higher cumulative midazolam dose (10–12).
The decrease in NIRS demonstrates an insufficiency in meeting the oxygen demand in the brain and kidneys (1–3, 6, 7, 13, 14, 24–28). When applied to parallel circulation physiology, these findings seem consistent with lower oxygen delivery possibly triggered by lower cardiac output or complex hemodynamic interaction due to the systemic-to-pulmonary interplay in single ventricle neonates status post-Norwood procedure (1–3, 6, 7, 14, 24–26, 29–31). The same cardiovascular construct can cause lower arterial oxygenation 10 minutes post-extubation (1–3, 6, 7, 14, 24–26, 30, 31). Other studies also found a reduction in renal NIRS during an extubation readiness trial and an increase in cerebral NIRS from baseline to extubation in congenital heart patients at risk of extubation failure (24, 25). However, those studies did not assess specifically the Norwood population.
Our institution does not have a standardized extubation readiness trial for this patient population (24, 32). Some clinicians perform the CPAT trial as an extubation readiness assessment, but it is not done universally. The presence or absence of a CPAP trial was not associated with the incidence of failed extubation events.
Also, a lower ETCO2 at baseline could be caused by increased respiratory rate due to abnormal cardiac and pulmonary interaction, reflecting vulnerable cardiac output and alteration in the balance of pulmonary-to-systemic blood flow ratio in single ventricle neonates with parallel circulation (1–3, 6, 7, 14, 24–26). Previous studies also found a rapid shallow breathing pattern before extubation in pediatric cardiac patients as a factor associated with failed extubation (32, 33).
The present study utilizes high-fidelity continuous monitoring data to determine hemodynamic indices before, immediately after, and a few hours following extubation. This is important as such data can help guide clinical decision-making. Specifically, identifying those patients at risk for extubation failure shortly after the procedure allows the clinician to adjust the inotropic support and provide selectively noninvasive respiratory support to avoid the failed extubation events (34, 35). As failed extubations have been demonstrated to be associated with increased length of stay and increased mortality, preventing failed extubations can help avoid these outcomes (10, 15–20, 23, 36). After extubation, the hemodynamic state must be monitored closely immediately after extubation to help minimize morbidity and mortality (34, 35).
This study is novel because it is one of the few studies to use high-fidelity streaming data from continuous monitoring to complement other clinical information about the patient to characterize extubation failure. Other pediatric studies have investigated factors associated with extubation failure but have not done so with such a high-fidelity focus on hemodynamics and oximetry. Additionally, this is one of few studies to focus on extubation failure in those with parallel circulation. Our findings can be directly applied in the clinical care of children with parallel circulation.
While this study has its strengths and is additive to the existing literature, it is not without limitations. As a single-center study, there may be institution-based practices that are not captured here that may impact extubation success. Thus, some findings may not be reproducible at other centers. As this study focused on characterizing the patient’s hemodynamics and oximetric dynamics rather than specific interventions, it should help maximize generalizability.