Implementation of a Modified Enhanced Recovery Protocol in Cleft Palate Repairs.

AIMS: Enhanced Recovery after Surgery (ERAS) protocols have been shown to improve patient outcomes in numerous adult surgical populations, but there are few known standards for their use in pediatric patients. To assess the effectiveness in pediatric craniofacial surgery, we present our results following the application of a modified ERAS protocol for patients undergoing primary palatoplasty. METHODS: A modified ERAS program was developed and implemented in a multidisciplinary manner. The primary components of the protocol included: (1) administration of gabapentinoids, (2) minimal perioperative narcotic use, and (3) post-operative pain control using nonnarcotic first-line agents. Fifty patients were collected prospectively, assigned to the modified ERAS protocol and compared to historic controls. We reviewed patient demographics, narcotic use, length of stay (LOS), oral intake, and complication rates. RESULTS: Between April 2017 and June 2018, 50 patients underwent palatoplasty under the modified ERAS protocol. The mean age (control: 9.7 ±â€Š2.3 months; ERAS: 9.9 ±â€Š1.6 months), weight (8.8 ±â€Š1.3 kg; 8.6 ±â€Š1.3 kg), and comorbidities did not vary between the groups. ERAS patients evidenced an increase in oral intake normalized per LOS (22.3 mL/h vs 15.4 mL/h). Total narcotic usage (morphine equivalents) during each phase of care was greater in the controls compared with ERAS (Intraop: 3.71 mg vs 0.12 mg; PACU: 0.51 mg vs 0.05 mg; Postop: 2.6 mg vs 0.07 mg). The implementation of this protocol led to a 36.6% decrease in LOS (1.83 days vs 1.16 days) without an increase in perioperative complications. CONCLUSIONS: Implementation of a modified ERAS protocol provided effective perioperative pain control allowing narcotic minimization, increased post-operative oral intake, and a shorter LOS without an increased complication rate.

Vascular rarefaction in peripheral skeletal muscle after experimental heart failure.

A decrease in vascular density in peripheral skeletal muscle has been associated with exercise intolerance in humans with congestive heart failure (CHF). The purpose of this study was to determine whether CHF results in a reduction in vascular density in peripheral skeletal muscle. In this established model, CHF was induced by coronary artery ligation in New Zealand White rabbits and sham rabbits that underwent an identical surgical procedure without ligation of the coronary artery. At study termination, rabbits underwent hemodynamic testing and skeletal muscle analysis. The first series of rabbits was divided into sham (n = 6) and CHF (n = 6) 21 days postoperatively. Ten CHF rabbits were then examined 3 (n = 3), 7 (n = 3), and 14 days (n = 4) postoperatively. Vascular density in sham tibialis anterior muscle was 347 +/- 41 capillaries/mm2 or 1.20 +/- 0.11 capillaries/muscle fiber. In 21-day CHF rabbits, the capillary density was significantly lower, 236 +/- 14 capillaries/mm2 or 0.84 +/- 0.04 capillaries/muscle fiber (both P < 0.00001 vs. sham); PECAM protein was 2-fold lower (P < 0.0001) in muscle protein lysates; the fraction of apoptotic cells was greater, 3.8 +/- 2.2 vs. 0.69 +/- 0.56 (P < 0.02 vs. sham) with many TdT-mediated dUTP-biotin nick-end labeling-positive endothelial cells; and Bax protein was 2.8-fold greater (P < 0.0001). By regression analysis, vascular density tended to decrease over time (r2 = 0.572, P < 0.0001). Vascular rarefaction and endothelial apoptosis develop after experimental CHF and may contribute to the skeletal muscle abnormalities in this disease. Modulating vascular density may provide new approaches to treat exercise intolerance in CHF.