Etiology, diagnosis, and treatment of failures after laparoscopic Heller myotomy for achalasia

Giovanni Zaninotto, Mario Costantini, Giuseppe Portale, Giorgio Battaglia, Daniela Molena, Alessanda Carta, Michela Costantino, Loredana Nicoletti, Ermanno Ancona, Giovanni Zaninotto, Mario Costantini, Giuseppe Portale, Giorgio Battaglia, Daniela Molena, Alessanda Carta, Michela Costantino, Loredana Nicoletti, Ermanno Ancona

Abstract

Objective: To assess the causes of failure of laparoscopic Heller myotomy and to verify whether endoscopic pneumatic dilation is a feasible treatment.

Summary background data: Laparoscopic Heller myotomy has proved an effective treatment for esophageal achalasia, with good or excellent results in 90% of patients. The treatment of failures remains controversial, however.

Methods: From 1992 to 1999, 113 patients underwent laparoscopic Heller myotomy for esophageal achalasia. Ten patients (8.7%) reported dysphagia (n = 7) or chest pain (n = 3) a median of 5 months after surgery (range 1-12) and were considered surgical failures. Pre- and postoperative radiologic, manometric, and 24-hour pH monitoring findings in patients with achalasia recurrence were compared with those of 74 asymptomatic subjects.

Results: The preoperative characteristics of the two groups were comparable. After surgery, a decrease in resting lower esophageal sphincter pressure was observed in both groups, whereas the abdominal and overall lengths were significantly shorter among the asymptomatic patients. No patients with recurrence had abnormal gastroesophageal reflux. Based on time to recurrence and manometric and fluoroscopic findings, the etiology of the recurrences was classified as incomplete myotomy upward (n = 1), incomplete myotomy or sclerosis of the myotomy downward (n = 7), or sigmoid megaesophagus (n = 1); in one patient the authors could not establish the etiology. Seven of nine patients were effectively treated with endoscopic pneumatic dilations (median 2 dilations, range 1-4); one refused to undergo further treatment. Two patients underwent redo surgery.

Conclusions: Recurrence of symptoms after myotomy is mainly related to incomplete myotomy or sclerosis of the distal site of the myotomy; it can be treated by dilations after surgery.

Figures

https://www.ncbi.nlm.nih.gov/pmc/articles/instance/1422413/bin/5FF1.jpg
Figure 1. Actuarial curve for symptom control showing probability of patients being symptom-free at 5-year follow-up. The number of patients evaluated is given in brackets. No patients were lost to follow-up; three died of unrelated causes 18, 44, and 56 months, respectively, after the Heller myotomy.
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Figure 2. Timing of recurrence and main symptom. The arrows indicate the months since surgery when patients had recurrent symptoms, the main symptoms being P (chest pain) and D (dysphagia). Four patients had early symptom recurrence (within 3 months of surgery) and six had late recurrence (4 months or more after surgery).
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Figure 3. Pre- and postoperative esophageal diameters, as measured at barium swallow. Patients with and without recurrent symptoms had a similar preoperative esophageal diameter (white column) and a significant reduction after surgery (gray column), but patients with recurrent symptoms had a larger esophageal diameter at follow-up than those without symptoms (P < .05).
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Figure 4. Timing and diameter of pneumatic dilations in nine patients agreeing to further treatment at our institution. The left X coordinate shows the patient’s main symptom (P, chest pain; D, dysphagia) and the right X coordinate shows the final outcome of dilation (G, good; F, fair; N, none). The white dots indicate the 30-mm Rigiflex dilator, the striped dots the 35-mm dilator, and the gray dots the 40-mm dilator. All patients required multiple dilations and only one remained symptomatic.
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Figure 5. Manometric characteristics of the lower esophageal sphincter (LES) before and after pneumatic dilation. Resting pressure was not modified by the dilations (A), whereas all but one patient had a decrease in LES lengths (B, C); the patient whose LES lengths further increased is one of the two symptomatic patients.

Source: PubMed

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