A Case Study of Achalasia of Cardia

Introduction: Achalasia is a benign idiopathic disorder caused by progressive neuronal degeneration in the mesenteric plexus of Auerbach, which causing non-relaxing, hypertensive lower esophageal sphincter (LES) and aperistalsis of the esophageal body. This functional damage is irreversible and the treatment of esophageal achalasia is mainly palliative. Case Report: Our patient is a 55 years old lady presents with progressive dysphagia, regurgitation, chest pain and weight loss. After clinical examination and relevant investigations, she was diagnosed as a case of achalasia of cardia of oesophagus. Discussion: She was prepared for Heller’s myotomy with antireflux procedure. Operative procedure was done under general anaesthesia. Conclusion: Postoperative recovery was good. The patient is asymptomatic, general condition improved and found healthy on follow up after one year. Medicine Today 2019 Vol.31(2): 128-130

Focal Achalasia – Case Report and Review of the Literature

Esophageal achalasia is a primary smooth muscle motility disorder specified by aperistalsis of the tubular esophagus in combination with a poorly relaxing and occasionally hypertensive lower esophageal sphincter (LES). These changes occur secondary to the destruction of the neural network coordinating esophageal peristalsis and LES relaxation (plexus myentericus). There are limited data on segmental involvement of the esophagus in adults.We report on the case of a 54-year-old man who presented initially with complete aperistalsis limited to the distal esophagus. After a primary good response to BoTox-infiltration of the distal esophagus the patient relapsed two years later. The manometric recordings documented now a progression of the disease with a poorly relaxing hypertensive lower esophageal sphincter and complete aperistalsis of the tubular esophagus (type III achalasia according to the Chicago 3.0 classification system).This paper also reviews diagnostic findings (including high resolution manometry, CT scan, barium esophagram, upper endoscopy and upper endoscopic ultrasound data) in patients with achalasia and summarizes the therapeutic options (including pneumatic balloon dilatation, botulinum toxin injection, surgical or endoscopic myotomy).

A gastrooesophagealis refluxbetegség nyelőcsőszövődményei: következmények vagy védekezőreakciók?

Gastroesophageal reflux disease affects more than 10% of the adult population. Most patients can be effectively treated with lifestyle changes and adequate acid-reducing therapy. However, about 10% of the patients remain symptomatic despite treatment and severe complications may develop. Interestingly, some of these complications seem to be a sort of defensive mechanism that may either alleviate the patient’s symptoms or prevent developing further complications. In Barrett’s esophagus, which can be unambigously considered as a complication of gastroesophageal reflux disease, reflux symptoms ruining the quality of life may significantly improve, since the metaplastic Barrett epithelium is much more resistent to gastric acid, than the normal epithelial lining of the esophagus. Furthermore, the motility disorders (hypertensive lower esophageal sphincter, achalasia, cricopharyngeal achalasia) and structural changes (Schatzki’s ring, esophageal stricture, subglottic trachea stenosis), which develop as a complication of reflux may help to prevent aspiration that can cause new complaints and may lead to further complications. Orv Hetil. 2017; 158(20): 763–769.

Large epiphrenic diverticula: a rare case presentation

A 70-year old female was admitted to hospital with heartburn and chronic halitosis since 5 years. She was on proton pump inhibitors for the same. Her complaints worsened during the last one-year. Workup comprising of esophagogastro- duodenoscopy, esophageal manometry, 3D computed tomography scan showed rightsided epiphrenic diverticula measuring 10x10 cm with wide mouth about 5 cm with hypertensive lower esophageal sphincter. Patient underwent a video assisted thoracoscopic surgery for esophageal diverticulectomy using two 45 mm staplers. On day 5, the patient developed leak, which was managed by a covered esophageal stent placement. Patient started on oral feeds from day 3 and the esophageal leak healed completely within 2 weeks. Literature suggests that esophageal leaks treated conservatively took approximately 30-40 days on an average for healing. Literature search did not reveal esophageal leak managed by stent with faster recovery (2 weeks). This is one of the largest epiphrenic diverticuli reported in literature.