Course, Predictors of Diaphragm Recovery After Phrenic Nerve Injury During Pediatric Cardiac Surgery
ABSTRACT Hemidiaphragm paralysis from phrenic nerve injury is a known complication of congenital cardiac surgery. Return of diaphragm function has been reported; however, prior studies on this subject have been limited by small numbers, static assessment methods, or observation of plicated or non-plicated patients alone. To describe return of function, we reviewed fluoroscopy and ultrasonography in all diagnosed cases of diaphragmatic paralysis.
Surgical cases at our institution between 1991 and 2010 were identified for patients with postoperative hemidiaphragm paralysis diagnosed by chest X-ray, ultrasound, or fluoroscopy. Follow-up ultrasound and fluoroscopic studies were reviewed for return of diaphragm function.
Seventy-two cases of postoperative hemidiaphragm paralysis were identified. Forty cases were plicated prior to discharge. Plicated patients were younger at time of diagnosis (median 46 days average 3.6 months; p = 0.025) and had a larger proportion of single ventricle diagnoses (48% vs 16%) compared with non-plicated patients. Twenty-six patients with paralysis were excluded in follow-up due to lack of studies documenting diaphragm function after the diagnostic study. Of the remaining 46 cases, median follow-up was 353 days (range: 6 days to 17 years). Plicated and non-plicated patients regained function at similar frequency (60% and 54.8%, respectively). Plication status, Risk Adjustment for Congenital Heart Surgery (RACHS) 1 score, age at diagnosis, and side of paralysis did not predict failure of recovery.
In the current era, return of diaphragm function after phrenic nerve injury sustained during congenital cardiac surgery is a known occurrence; however, predicting recovery continues to be difficult.
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ABSTRACT: The diaphragm muscle (DIAm) has a large reserve capacity for force generation such that in rats, the transdiaphragmatic pressure (Pdi) generated during ventilatory behaviors is less than 50% of maximal Pdi (Pdimax) elicited by bilateral phrenic nerve stimulation. Accordingly, we hypothesized that following unilateral denervation (DNV), the ability of the contralateral DIAm to generate sufficient Pdi to accomplish ventilatory behaviors will not be compromised and normal ventilation (as determined by arterial blood gas measurements) will not be impacted, although neural drive to the DIAm increases. In contrast, we hypothesized that higher force, non-ventilatory behaviors requiring Pdi generation greater than 50% of Pdimax will be compromised following DIAm hemiparalysis i.e., increased neural drive cannot fully compensate for lack of force generating capacity. Pdi generated during ventilatory behaviors (eupnea and hypoxia (10% O2) - hypercapnia (5% CO2)) did not change after DNV and arterial blood gases were unaffected by DNV. However, neural drive to the contralateral DIAm, assessed by the rate of rise of root mean squared (RMS) EMG at 75ms after onset of inspiratory activity (RMS75), increased after DNV (p<0.05). In contrast, Pdi generated during higher force, non-ventilatory behaviors was significantly reduced after DNV (p<0.01), while RMS75 was unchanged. These findings support our hypothesis that only non-ventilatory behaviors requiring Pdi generation greater than 50% of Pdimax are impacted after DNV. Clinically, these results indicate that an evaluation of DIAm weakness requires examination of Pdi across multiple motor behaviors, not just ventilation. Copyright © 2015. Published by Elsevier B.V.Respiratory Physiology & Neurobiology 01/2015; 210. DOI:10.1016/j.resp.2015.01.013 · 1.97 Impact Factor