Steven Rakita

Laparoscopic Heller Myotomy Provides Durable Relief From Achalasia and Salvages Failures After Botox or Dilation

Objective:To report outcome after laparoscopic Heller myotomy in a large number of patients. Summary Background Data:Laparoscopic Heller myotomy has been undertaken for over a decade, but most studies involve small numbers of patients with limited follow-up. Methods:Since 1992, 262 patients have undergone laparoscopic Heller myotomy and been prospectively followed. Concomitant fundoplication was undertaken for a patulous hiatus or large hiatal hernia or to buttress the repair of an esophagotomy until recently when it became routinely applied. With mean follow-up at 32months, symptoms were scored by patients on a Likert scale (frequency: 0 = Never to 10 = Every time I eat/always; severity: 0 = Not bothersome to 10 = Very bothersome). Results:Before myotomy, 79% received Botox or bag dilation: 52% had Botox, 59% underwent dilation, and 36% had both. Inadvertent esophagotomy occurred in 5%. Concomitant diverticulectomy was undertaken in 4%, and fundoplication was undertaken in 30%. Complications were infrequent. Median length of stay was 1 day. After myotomy, the frequency and severity of symptoms of achalasia and reflux significantly decreased. Eighty-eight percent of patients felt their symptoms were greatly improved or resolved, and 90% felt their outcome was satisfying or better. Ninety-three percent felt they would undergo myotomy again, if necessary. Conclusions:Laparoscopic Heller myotomy can safely and durably relieve symptoms of dysphagia while also reducing symptoms of reflux. Length of stay is short and patient satisfaction is very high with extended follow-up. Laparoscopic Heller myotomy is strongly encouraged for patients with symptomatic achalasia and is efficacious even after failures of dilation and/or Botox therapy.

Esophagotomy during laparoscopic Heller myotomy cannot be predicted by preoperative therapies and does not influence long-term outcome.

The conventional wisdom is that inadvertent esophagotomy complicates laparoscopic Heller myotomy. This study was undertaken to determine if esophagotomy at myotomy can be predicted by preoperative therapy, and if esophagotomy and/or its repair jeopardizes outcomes. Of 222 laparoscopic Heller myotomies undertaken since 1992, inadvertent esophagotomy occurred in 16 patients (7%); 60 patients who underwent myotomy without esophagotomy were utilized for comparison. Dysphagia and reflux before/ after myotomy were scored by patients on a Likert scale (0-5). The median (mean _ SD) follow-up after myotomy with esophagotomy was 38.8 months (31.6 ± 21.9 months) versus 46.3 months (51.0 ± 21.2 months) after myotomy alone. All esophagotomies were immediately recognized and repaired. Patients who experienced esophagotomy were similar to those who did not in application of Botox (56% vs. 77%) or dilation (44% vs. 65%), years of dysphagia (7.3 ± 5.4 vs. 7.4 ± 6.0), and mean preoperative dysphagia score (4.9 ± 0.4 vs. 4.8 ± 0.4). Esophagotomy led to longer hospitalizations (5.2 days ± 2.5 days vs. 1.5 days ± 0.7 days, P < 0.05) but not different postoperative dysphagia scores (1.5 ± 1.7 vs. 2.1 ± 1.4), reflux scores (1.4 ± 1.7 vs. 2.3 ± 1.3), or good or excellent outcomes (86% vs 84%). Esophagotomy during laparoscopic Heller myotomy is infrequent and cannot be predicted by preoperative therapy or duration or severity of dysphagia. Furthermore, complications after esophagotomy are infrequent and outcomes are indistinguishable from those of patients undergoing uneventful myotomy.

Roux-en-Y gastric bypass alters tumor necrosis factor-α but not adiponectin signaling in immediate postoperative period in obese rats

BACKGROUND Adiponectin has anti-inflammatory properties and is increased with weight loss. Tumor necrosis factor (TNF)-α is a pro-inflammatory cytokine that negatively regulates adiponectin. Previously, we have demonstrated that Roux-en-Y gastric bypass (RYGB) induces weight loss and improves steatosis in obese rats. We hypothesized that RYGB would alter the interplay of TNF-α and adiponectin signaling in the postoperative period. METHODS Obese Sprague-Dawley male rats that had undergone RYGB (n = 5) or sham (n = 4) were euthanatized at 9 weeks postoperatively. The adiponectin levels from serial serum samples were measured by enzyme-linked immunosorbent assay. Adiponectin, adiponectin receptor 2, and TNF-α mRNA from adipose and liver samples were quantified by reverse transcriptase-polymerase chain reaction. Data are presented as mean ± standard deviation; using a t test, P <.05 was significant. RESULTS RYGB did not change the serum adiponectin, adipose tissue adiponectin mRNA, or hepatic adiponectin receptor 2 levels compared with the levels in the sham-operated rats (P >.05). However, the TNF-α mRNA levels had decreased in the adipose tissue (P >.05) but remained unchanged in the liver compared with the sham controls (P >.05). CONCLUSION Surgically-induced weight loss in a rat model of RYGB did not increase adiponectin signaling in the immediate postoperative period but was associated with decreased pro-inflammatory signaling in the adipose tissue. During this period, pro-inflammatory signaling might play a more important role than adiponectin. Additional studies with longer follow-up are necessary to determine whether adiponectin plays a role in weight loss and improvement of steatosis after RYGB.