Incidence of Complications Associated With Lipectomy Techniques and Patient Body Mass Index: An Institutional and National Analysis Using the Tracking Operations and Outcomes for Plastic Surgeons.

INTRODUCTION: An evaluation of complication rates in different abdominal lipectomy techniques with relationship to body mass index (BMI) and other risk factors. METHODS: We identified patients who underwent an abdominal lipectomy at our institution from January 2015 to July 2020. Those with concurrent hernia repair were excluded. Patients were classified into 2 groups: (1) horizontal lipectomy with or without umbilical translocation and (2) inverted-T lipectomy with translocation. Demographics, operative details, and postoperative complications were collected for 1 year postoperatively. Bivariate analyses were conducted to determine factors associated with type of procedure and complications. Crude and stratum-specific (based on BMI) odds ratios for complications were calculated for the inverted T as compared with the horizontal group. A replicate analysis using the national Tracking Operations and Outcomes for Plastic Surgeons (TOPS) as a single cohort was performed. RESULTS: At our institution, 362 patients (group 1 = 196, group 2 = 166) were included. A total of 40.9% of patients experienced at least one complication at 1 year postoperatively with the complication rate decreasing to 28.0% when analyzed at the 30-day postoperative period. Specifically, wound disruption rates were highest in group 2 (39.8%) compared with group 1 (15.6%; P < 0.0001). The odds of experiencing a complication were greater in the inverted-T group overall and within each stratum of BMI. When dividing the cohort based on BMI class (normal weight, overweight, class I, class II, and class III obesity), the incidence of wound disruption increased as did BMI (2.6%, 22.2%, 27.2%, 48.2%, and 56.3%, respectively; P < 0.0001). The TOPS data set included 23,067 patients and showed an overall complication rate of 13.1% at 30-day postop. Overall, wound disruption rate was 4.6%. Compared with normal weight patients, the odds of experiencing a complication trended higher with each stratum of BMI. Other factors associated with complications included BMI, tobacco use, diabetes, American Society of Anesthesiology, prior massive weight loss, and LOS. CONCLUSIONS: The increasing complication rate within each BMI stratum of the large sample size of the TOPS patient cohort, in addition to our similar institutional trends, suggests that a staged procedure may be more appropriate for higher BMI patients. Surgical technique modification with limited flap undermining in patients undergoing inverted-T lipectomy to preserve flap perfusion may also decrease overall complication rates.

Extrasynaptic muscarinic acetylcholine receptors on neuronal cell bodies regulate presynaptic function in Caenorhabditis elegans.

Acetylcholine (ACh) is a potent neuromodulator in the brain, and its effects on cognition and memory formation are largely performed through muscarinic acetylcholine receptors (mAChRs). mAChRs are often preferentially distributed on specialized membrane regions in neurons, but the significance of mAChR localization in modulating neuronal function is not known. Here we show that the Caenorhabditis elegans homolog of the M1/M3/M5 family of mAChRs, gar-3, is expressed in cholinergic motor neurons, and GAR-3-GFP fusion proteins localize to cell bodies where they are enriched at extrasynaptic regions that are in contact with the basal lamina. The GAR-3 N-terminal extracellular domain is necessary and sufficient for this asymmetric distribution, and mutation of a predicted N-linked glycosylation site within the N-terminus disrupts GAR-3-GFP localization. In transgenic animals expressing GAR-3 variants that are no longer asymmetrically localized, synaptic transmission at neuromuscular junctions is impaired and there is a reduction in the abundance of the presynaptic protein sphingosine kinase at release sites. Finally, GAR-3 can be activated by endogenously produced ACh released from neurons that do not directly contact cholinergic motor neurons. Together, our results suggest that humoral activation of asymmetrically localized mAChRs by ACh is an evolutionarily conserved mechanism by which ACh modulates neuronal function.