Physiologic mechanism and preoperative prediction of new-onset dysphagia after laparoscopic Nissen fundoplication

The aim of this study was to determine whether preoperative physiologic factors can account for and be used to predict the development of postoperative dysphagia after laparoscopic Nissen fundoplication. One hundred sixty-three patients with gastroesophageal reflux disease underwent laparoscopic Nissen fundoplication with a median follow-up of 14 months (range 6 to 81 months). Preoperative dysphagia was present in 37% (60 of 163) and was relieved in all but five patients (92%). Female sex (P = 0.01) and the presence of a stricture (P = 0.02) were the only preoperative variables associated with the presence of preoperative dysphagia. Eight percent (8 of 103) of patients without preoperative dysphagia developed new-onset dysphagia, and of these 63% (5 of 8) had a normal lower esophageal sphincter (LES) (pressure >6 mm Hg; length >2 cm; abdominal length >1 cm). New-onset dysphagia was significantly more common in patients with a normal LES (22% [5 of 23] vs. 4% [3 of 80], P = 001). Patients with a normal LES had almost a sixfold increase in the risk of developing dysphagia as those with an abnormal LES (relative risk = 5.8). Only a preoperative normal LES (P = 0.02) or mean LES pressures (P = 0.04) were positively associated with the development of postoperative dysphagia. The severity of this dysphagia also showed a strong positive trend of increasing with mean preoperative LES pressures (P = 0.07). Finally, preoperative LES pressure significantly correlated with postoperative LES pressure (r = 0.48, P = 0.01) and with mean residual LES (nadir) pressure (r = 0.33, P = 0.05) offering insight into the mechanism of this dysphagia. In conclusion, preoperative LES parameters play a role in the development of dysphagia after laparoscopic Nissen fundoplication. Patients with a normal LES or high mean LES pressures are at increased risk for developing this complication and should be informed of this before laparoscopic Nissen fundoplication. Presented at the Forty-Second Annual Meeting of The Society for Surgery of the Alimentary Tract, Atlanta, Ga., May 20–23, 2001.     

The Cotton osteotomy: indications and techniques

Stage II posterior tibial tendon dysfunction (PTTD) is characterized by an incompetent posterior tibial tendon that results in a flexible pes planovalgus deformity. As the hindfoot drifts into valgus, compensatory varus develops in the forefoot. Alternatively, in some cases medial column instability can result in primary forefoot varus that drives the hindfoot into valgus. Recently, there has been increasing awareness of the importance of forefoot varus in PTTD.     

The evolving risk of sudden cardiac death after heart transplant. An analysis of the ISHLT Thoracic Transplant Registry

Sudden cardiac death (SCD) is responsible for ~10% of post‐heart transplant deaths. We conducted a retrospective analysis of the ISHLT registry evaluating the risk of post‐transplant SCD. Adult heart transplant recipients (2004‐2014) surviving the first year were included. We used multivariable multistate competing risk survival analysis to evaluate the impact of history of treated rejection and cardiac allograft vasculopathy (CAV) on SCD risk. We used a probabilistic analytical model and Monte Carlo simulation to estimate the impact of CAV severity and graft dysfunction on SCD. We included 25 242 recipients. During a median follow‐up of 4.7 (2.3‐7.0) years, 582 patients died suddenly. Treated rejection (HR 1.76, 95% CI 1.36‐2.31) and CAV (HR 3.32, 95% CI 2.73‐4.03) were important risk factors for SCD. The estimated SCD risk in patients with severe CAV without and with graft dysfunction was 3.2% (95% CI 2.0‐4.6) and 5.4% (95% CI 3.8‐7.0), respectively, at 2 years from the CAV diagnosis, and 4.9% (95% CI 3.4‐6.5) and 8.0% (95% CI 6.1‐10.0), respectively, in those who also had treated rejection. These results provide evidence that recipients with severe CAV and graft dysfunction or treated rejection are at clinically significant increased SCD risk. The benefit of ICD post‐transplant remains uncertain.     

Sexual activity and function in women with and without pelvic floor disorders

Introduction and hypothesis

We describe differences in sexual activity and function in women with and without pelvic floor disorders (PFDs).

Methods

Heterosexual women ≥40 years of age who presented to either urogynecology or general gynecology clinics at 11 clinical sites were recruited. Women were asked if they were sexually active with a male partner. Validated questionnaires and Pelvic Organ Prolapse Quantification (POP-Q) examinations assessed urinary incontinence (UI), fecal incontinence (FI), and/or pelvic organ prolapse (POP). Sexual activity and function was measured by the Female Sexual Function Index (FSFI). Student’s t test was used to assess continuous variables; categorical variables were assessed with Fisher’s exact test and logistic regression. Univariate and multivariate analyses were used to assess the impact of pelvic floor disorders (PFDs) on FSFI total and domain scores.

Results

Five hundred and five women met eligibility requirements and gave consent for participation. Women with and without PFDs did not differ in race, body mass index (BMI), comorbid medical conditions, or hormone use. Women with PFDs were slightly older than women without PFDs (55.6?+?10.8 vs. 51.6?+?8.3 years, P <0.001); all analyses were controlled for age. Women with PFDs were as likely to be sexually active as women without PFDs (61.6 vs. 75.5 %, P?=?0.09). There was no difference in total FSFI scores between cohorts (23.2?+?8.5 vs. 24.4?+?9.2, P?=?0.23) or FSFI domain scores (all P?=?NS).

Conclusion

Rates of sexual activity and function are not different between women with and without PFDs.     

Transumbilical single-port sleeve gastrectomy: initial experience and comparative study

Background  

Sleeve gastrectomy is gaining relevance in the surgical armamentarium against obesity. The transumbilical single port has proved to be an attractive and safe alternative for a variety of minimally invasive abdominal surgeries. The purpose of this study is to evaluate the initial results of a group of patients operated by single-port sleeve gastrectomy compared with a group operated by conventional laparoscopic technique.     

Reimplantation of the aortic valve at 20 years

Objective

To provide additional information on clinical and echocardiographic outcomes after reimplantation of the aortic valve (RAV) in patients with aortic root aneurysm.

Vitamin D, parathyroid hormone levels and bone mineral density in community-dwelling older women: The Rancho Bernardo Study

Vitamin D (25(OH)D) increases the efficiency of intestinal calcium absorption. Low levels of serum calcium stimulate the secretion of parathyroid hormone (PTH), which maintains serum calcium levels at the expense of increased bone turnover, bone loss and increased risk of fractures. We studied the association between 25(OH)D and PTH levels, and their associations with bone mineral density (BMD), bone loss, and prevalence of hip fractures in 615 community-dwelling postmenopausal aged 50–97 years. Mean level of 25(OH)D and PTH were 102.0 nmol/l±35.0 nmol/l and 49.4 ng/l±23.2 nmol/l, respectively; 49% of women were current hormone therapy users. The overall prevalence of vitamin D insufficiency (25(OH)D<50 nmol/l) was 2%, and prevalence of high PTH levels (>65 ng/l) was 17.4%. In multiple linear regression analyses hip BMD was negatively and independently associated with PTH levels ( p =0.04), and positively and independently associated with 25(OH)D levels ( p =0.03). There were only 23 women (3.7%) who experienced a hip fracture. In age-adjusted analyses there were no significant differences of 25(OH)D and PTH levels by hip fracture status. Across the entire range of values, the overall correlation between 25(OH)D and PTH was moderate ( r =–0.20). However, after the threshold vitamin D level of 120 nmol/l, all PTH values were below 65 ng/l. Further studies are necessary to identify the optimal vitamin D levels necessary to prevent secondary hyperparathyroidism.