Oesophagus
Paul Ong, Rachel Skittrall in Gastrointestinal Nursing, 2017
Achalasia is a rare motility disorder of the oesophagus. It affects approximately between 0.3 and 1.63 of adults per 100,000 of the population, occurring equally in men and women (Boeckxstaens et al., 2014). The precise etiology is unknown but it is likely to be associated with a combination of genetic, immune and environmental factors. Antibodies to the myenteric plexus, inflammatory infiltrates containing T lymphocytes in the myenteric plexus and the association with autoimmune connective tissue disease, point towards an autoimmune etiology. Infectious agents such as poliomyelitis, varicella zoster, herpes simplex virus and Guillain-Barre syndrome have all preceded achalasia and may suggest a viral etiology. There is no clear hereditary or genetic pattern.
Esophageal Motility: Measures and Disorders of Esophageal Motor Function
John F. Pohl, Christopher Jolley, Daniel Gelfond in Pediatric Gastroenterology, 2014
Symptoms of achalasia primarily include dysphagia or difficulty in swallowing. The symptoms are often gradual, developing slowly over several weeks to years and increase as the disease progresses. The diagnosis of achalasia should be suspected in any patients complaining of dysphagia for solids and liquids with regurgitation of bland food and saliva. Initially the dysphagia may be primarily for solids; however, by the time of clinical presentation, nearly all patients complain of dysphagia for solids and liquids while eating and drinking, especially cold beverages. Various maneuvers, including ‘power swallows’ and carbonated beverages, both of which increase intraesophageal pressure, may be used to improve esophageal emptying. As the disease progresses, the increasing contraction of the LES on swallowing leads to regurgitation of food that has not entered the stomach and to retrosternal pain, particularly when there is extreme dilatation of the esophagus. Restricted movement of food and avoidance of food may lead to weight loss. This process can occur swiftly, but typically takes place over a longer period lasting several months or years.
Per oral endoscopic myotomy (POEM) for achalasia
Larry R. Kaiser, Sarah K. Thompson, Glyn G. Jamieson in Operative Thoracic Surgery, 2017
Achalasia patients should always have a comprehensive symptom assessment covering typical presenting symptoms including dysphagia, chest pain, regurgitation of undigested foods, weight loss, and previous interventions—all of which have been shown to affect outcomes of any treatments. The Eckardt score, a useful standardized symptom tool, can score patients to stratify disease severity and predict treatment success (see Table 42.1). Upper endoscopy with biopsies is essential to exclude pseudoachalasia related to infiltrative cancers. Upper GI barium esophagogram—preferably a timed barium swallow—serves as a roadmap for the operation, excludes significant findings like diverticula and serves as a baseline study for long-term patient follow-up. Although “heartburn” is a frequent complaint of achalasia patients, gastroesophageal reflux is physiologically extremely unlikely and thus 24-hour pH acid studies are not usually indicated.
Pneumatic dilation for esophageal achalasia: patient selection and perspectives
Published in Scandinavian Journal of Gastroenterology, 2022
Abdul Mohammed, Rajat Garg, Neethi Paranji, Aneesh V. Samineni, Prashanthi N. Thota, Madhusudhan R. Sanaka
Achalasia is an idiopathic esophageal motility disorder that occurs due to the selective loss of inhibitory neurons in the myenteric plexus of the distal esophagus and lower esophageal sphincter (LES), causing an imbalance between excitatory and inhibitory activity [1,2]. It results in esophageal aperistalsis and impaired relaxation of the lower esophageal sphincter (LES). It is a rare disease with an estimated prevalence of 10.82 and incidence of 0.3–1.63 per 100,000 adults per year [3]. Clinical manifestations of achalasia include dysphagia, regurgitation, chest pain, weight loss, and aspiration pneumonia. There is no cure for achalasia, and treatment is palliative and aimed at reducing the LES pressure so that gravity can assist in esophageal emptying. Pneumatic dilation (PD) and esophagomyotomy, either laparoscopic Heller myotomy (LHM) or per oral endoscopic myotomy (POEM), is the standard treatment modalities [4,5]. Patients failing treatment or left untreated can progress to end-stage achalasia. Standard endoscopic dilators are ineffective in disrupting the muscularis propria at LES, which is needed for symptoms relief. PD is an effective option for the treatment of achalasia. The technique has evolved from the use of standard high-compliant dilators to less compliant Rigiflex dilators (Boston Scientific, Marlborough, MA).
Application of botulinum toxin in pregnancy and its impact on female reproductive health
Published in Expert Opinion on Drug Safety, 2020
Axillary achalasia is a functional esophageal obstruction caused by loss of esophageal sphincter motor neurons. Other causes of achalasia include obstruction of the gastroesophageal junction, neuronal degeneration, viral infection, heredity, and autoimmune disease [38]. Achalasia is characterized by a loss of lower esophageal sphincter (LES) activity, and of esophageal peristalsis; the main symptoms are dysphagia, chest pain, and reflux. Achalasia is a rare disease, with an incidence rate of approximately 1–3 per 100,000 population in various age groups. The risk of achalasia increases with age, and the most common clinical symptoms occur in patients aged 50 years or older [39–45]. Some studies have suggested that the peak incidence may be between 17 and 30 years of age [41,46,47]. Therefore, achalasia appears to affect women of childbearing age.
Non-surgical treatment of esophageal perforation after pneumatic dilation for achalasia: a case series
Published in Scandinavian Journal of Gastroenterology, 2020
Renske A. B. Oude Nijhuis, Jacques J. G. H. M. Bergman, R. Bart Takkenberg, Paul Fockens, Albert J. Bredenoord
An 80-year-old female was referred to our clinic because of long-standing dysphagia. The diagnosis of achalasia type II was established by barium esophagogram and manometry. Two weeks after a first 30-mm pneumatic dilation, the patient underwent a second dilation with a 35-mm diameter balloon. Endoscopic inspection immediately after dilation showed a 4-cm linear esophageal perforation just proximal to the gastroesophageal junction. The perforation was closed endoscopically with eight endoclips. The patient was kept nil per mouth and tube-fed. The CT study performed the next day showed localized extraluminal contrast spill just proximal of the esophagogastric junction (Figure 3). Under intravenous antibiotics, symptoms resolved swiftly. A second chest CT scan 3 days later confirmed absence of extraluminal contrast and the patient was discharged 6 days post-procedure. After 12 weeks she visited our out-patient clinic and reported complete symptom remission.
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