Achalasia
Videos
Overview
Achalasia is an uncommon but well-defined disorder of the esophageal smooth muscle, characterized by two linked defects: impaired relaxation of the lower esophageal sphincter (LES) and absent or abnormal peristalsis in the body of the esophagus (Savarino et al., Nature Reviews Disease Primers, 2022). The underlying problem is a progressive loss of the inhibitory nerve cells in the myenteric plexus of the esophageal wall — the neurons that normally signal the LES to open and coordinate the downward wave of swallowing (Scaffidi et al., Cochrane Database of Systematic Reviews, 2025). Without those signals, the sphincter stays closed and food backs up above it.
Achalasia is rare, with a reported prevalence of roughly 10 to 27 per 100,000 people and an incidence of about 0.5 to 2 per 100,000 per year; it affects men and women about equally, with no racial predilection, and most commonly presents between ages 30 and 60 (Vaezi et al., ACG Clinical Guidelines, 2020; Harvey et al., Gut, 2019). Because its hallmark symptom — trouble swallowing that is often accompanied by heartburn and regurgitation — overlaps heavily with gastroesophageal reflux disease, achalasia is frequently mistaken for GERD and treated with acid-suppressing medication for months or years before the correct diagnosis is made (Vaezi et al., ACG Clinical Guidelines, 2020). (See our acid reflux (GERD) page for how the two conditions are distinguished.) Achalasia is a chronic condition that cannot be cured, but durable, life-changing symptom relief is achievable with the right procedure, most commonly a laparoscopic Heller myotomy (see our Heller myotomy page) (Patel et al., Gastroenterology, 2022).
Achalasia at a Glance
In achalasia, the nerves of the esophagus are damaged so that the lower esophageal sphincter fails to relax and the esophagus loses its normal wave-like contractions (Vaezi et al., ACG Clinical Guideline, American Journal of Gastroenterology, 2020). Food and liquid collect in the esophagus instead of passing into the stomach. Because achalasia is uncommon, many patients are first treated for reflux or anxiety for years before the correct diagnosis is made, and choosing the right treatment benefits from a surgeon experienced in all of the options.
The Three Types of Achalasia
High-resolution manometry classifies achalasia into three subtypes using the Chicago Classification, and the subtype helps predict which treatment will work best (Yadlapati et al., Chicago Classification v4.0, Neurogastroenterology & Motility, 2021):
- Type I (classic): no meaningful contractions in the esophagus; responds well to myotomy or dilation.
- Type II: the whole esophagus pressurizes at once; generally has the best response to any treatment.
- Type III (spastic): premature, forceful spasms in the lower esophagus; often responds best to POEM, which allows a longer muscle cut tailored to the spastic segment (Vaezi et al., ACG Clinical Guideline, American Journal of Gastroenterology, 2020).
Causes
The primary (idiopathic) form has no single identified cause. The leading explanation is an autoimmune process: in a genetically predisposed person, an environmental trigger — possibly a viral infection such as herpes simplex or varicella zoster — is thought to set off an immune attack on the esophageal myenteric nerves, leading to chronic inflammation (myenteric plexitis) and the gradual destruction of inhibitory neurons (Savarino et al., Nature Reviews Disease Primers, 2022). As these neurons are lost, excitatory signaling goes unopposed, the LES stays contracted, and coordinated peristalsis disappears (Patel et al., Gastroenterology, 2022).
Secondary achalasia (a clinically identical picture caused by another disease) is far less common. The most important causes are Chagas disease (infection with Trypanosoma cruzi, relevant in patients from endemic regions of Latin America) and malignancy at or near the gastroesophageal junction, which can mimic achalasia — a presentation termed pseudoachalasia that must always be excluded (Scaffidi et al., Cochrane Database of Systematic Reviews, 2025).
Risk Factors
- Age 30–60, though achalasia can occur at any age (Vaezi et al., ACG Clinical Guidelines, 2020).
- Genetic predisposition, including certain HLA class II alleles and rare familial/syndromic forms (Savarino et al., Nature Reviews Disease Primers, 2022).
- Autoimmune conditions, reflecting the proposed immune-mediated mechanism (Scaffidi et al., Cochrane Database of Systematic Reviews, 2025).
- Chagas disease exposure in patients from endemic areas (secondary achalasia) (Scaffidi et al., Cochrane Database of Systematic Reviews, 2025).
- A history of chronic reflux disease. Some evidence and clinical observation suggest long-standing GERD may, in a subset of patients, precede and possibly contribute to the development of achalasia, though this remains a hypothesis (Vereczkei et al., Therapeutics and Clinical Risk Management, 2018).
How Achalasia Affects the Body
Achalasia disrupts normal swallowing and esophageal emptying:
- Food and liquids remain trapped in the esophagus
- The esophagus dilates over time
- Pressure builds behind the LES
- Regurgitation occurs, especially at night
- Chronic stasis leads to inflammation and aspiration
Advanced achalasia can cause:
- Megaesophagus
- Severe malnutrition
- Aspiration pneumonia
- Esophageal ulceration
- Increased risk of esophageal cancer
Complications
- Progressive esophageal dilation
- Esophagitis
- Aspiration pneumonia
- Weight loss
- Malnutrition
- Chest pain
- Nighttime regurgitation
- Megaesophagus
- Increased risk of squamous cell carcinoma
Symptoms and Signs
Achalasia symptoms are often mistaken for GERD or anxiety:
- Difficulty swallowing solids and liquids
- Regurgitation of undigested food
- Chest discomfort or pressure
- Sensation of food “sticking”
- Coughing at night
- Waking up choking
- Unintentional weight loss
- Heartburn‑like symptoms
- Recurrent respiratory infections
- Hiccups
- Early satiety
- Bloating
Patients often adapt by:
- Eating slowly
- Drinking water with meals
- Avoiding certain foods
- Standing or walking after eating
- Sleeping upright
Achalasia is one of several causes of swallowing difficulty; see dysphagia (difficulty swallowing) for how the causes are told apart.
Diagnosis
Achalasia requires specialized testing:
1. High‑Resolution Esophageal Manometry (Gold Standard)
Shows LES non‑relaxation and absent peristalsis.
Rules out strictures, tumors, inflammation, or pseudoachalasia.
3. Barium Swallow / Upper GI Series
Shows classic “bird‑beak” narrowing and esophageal dilation.
4. CT Scan
Used when anatomy or obstruction is suspected.
5. pH Monitoring
Helps differentiate achalasia from severe reflux.
Key Tests for Achalasia
- High-resolution esophageal manometry: the gold standard, confirming failed relaxation of the lower sphincter and determining the subtype (Yadlapati et al., Chicago Classification v4.0, Neurogastroenterology & Motility, 2021)
- Timed barium esophagram: shows the classic "bird's beak" narrowing and measures how much barium remains after one and five minutes, a useful way to track treatment results
- Upper endoscopy: excludes cancer or other causes of narrowing (pseudoachalasia)
- Functional luminal imaging (EndoFLIP): measures how distensible the junction is, helpful when manometry is inconclusive and during surgery to tailor the myotomy
Differential Diagnosis
- GERD
- Esophageal stricture
- Esophageal cancer
- EGJOO (Esophagogastric Junction Outflow Obstruction)
- Diffuse esophageal spasm
- Jackhammer esophagus
- Functional dysphagia
- Hiatal hernia
- Eosinophilic esophagitis
- Pseudoachalasia (tumor‑related)
Lifestyle Modifications
Lifestyle changes do not cure achalasia but may reduce symptoms:
- Eat slowly
- Chew thoroughly
- Drink water with meals
- Avoid very dry foods
- Avoid lying down after eating
- Sleep with head elevated
- Smaller, more frequent meals
- Avoid carbonated beverages
- Avoid alcohol
- Maintain hydration
Treatment Options
Treatment does not cure achalasia; it relieves the obstruction by reducing LES pressure so the esophagus can empty (Patel et al., Gastroenterology, 2022). Options fall into two groups.
For patients who are candidates for a procedure, three durable, first-line therapies exist (Scaffidi et al., Cochrane Database of Systematic Reviews, 2025):
- Laparoscopic Heller myotomy (LHM) — a minimally invasive operation that divides the muscle fibers of the LES, almost always combined with a partial fundoplication (Dor or Toupet) to limit postoperative reflux. It offers excellent, durable relief and is a preferred definitive treatment for good surgical candidates (see our Heller Myotomy page for technique, recovery, and outcomes) (Patel et al., Gastroenterology, 2022).
- Peroral endoscopic myotomy (POEM) — an incisionless, endoscopic myotomy with success rates above 90%; it is the preferred option for type III (spastic) achalasia because the myotomy length can be extended, but it carries a higher rate of postoperative reflux than LHM because it includes no antireflux wrap (Kahrilas et al., AGA Clinical Practice Update, 2017; Patel et al., Gastroenterology, 2022).
- Pneumatic dilation (PD) — graded balloon dilation of the LES; effective but often requires repeat sessions, with a perforation risk of about 1% (Patel et al., Gastroenterology, 2022).
For patients who are not candidates for surgery or endoscopic myotomy, temporizing measures include endoscopic botulinum toxin injection into the LES (effect lasts months and is useful as a bridge) and pharmacologic agents such as calcium channel blockers or nitrates, which are limited by modest efficacy and side effects (Scaffidi et al., Cochrane Database of Systematic Reviews, 2025).
Because every effective therapy disrupts the antireflux barrier, post-treatment GERD is common and may require acid suppression or, in selected cases, further management — which is why structured follow-up matters (see our acid reflux (GERD) page) (Patel et al., Gastroenterology, 2022). When symptoms persist or recur after a prior myotomy (10%–20% of LHM patients), rescue options include POEM, pneumatic dilation, revisional myotomy, and, as a last resort for end-stage disease, esophagectomy (Saleh et al., Gastroenterology, 2023).
What the Evidence Shows
- POEM vs. Heller myotomy: in a randomized trial, POEM was non-inferior to laparoscopic Heller myotomy with Dor fundoplication, with clinical success in about 83% versus 82% at two years; reflux esophagitis was more common after POEM (44% vs. 29%) (Werner et al., New England Journal of Medicine, 2019).
- POEM vs. pneumatic dilation: in treatment-naive patients, POEM succeeded in about 92% versus 54% for dilation at two years (Ponds et al., JAMA, 2019).
- Pneumatic dilation vs. Heller myotomy: both produced high success rates in a European trial, though dilation often needs to be repeated (Boeckxstaens et al., New England Journal of Medicine, 2011).
Choosing the Right Treatment
Guidelines recommend that the choice among POEM, Heller myotomy and pneumatic dilation be based on achalasia subtype, patient preference, reflux risk and local expertise (Vaezi et al., ACG Clinical Guideline, American Journal of Gastroenterology, 2020). Heller myotomy with a partial fundoplication may be preferred for patients concerned about reflux or with a hiatal hernia; POEM is favored for type III achalasia, for patients who have had prior abdominal surgery, and for failed previous treatments. See POEM, Heller myotomy and Dor fundoplication.
When Previous Treatment Has Failed
Symptoms can return after any achalasia treatment, from incomplete myotomy, scarring, reflux-related narrowing or progression to a dilated, sigmoid-shaped esophagus. Options include redo POEM, redo Heller myotomy, dilation and, for end-stage disease, esophagectomy (Vaezi et al., ACG Clinical Guideline, American Journal of Gastroenterology, 2020). Evaluation by a surgeon experienced in revisional foregut surgery is essential.
When to See a Doctor
Seek medical evaluation if you experience progressive difficulty swallowing, regurgitation, chest pain, weight loss, or nighttime coughing.
When to Seek Treatment
Seek evaluation if:
- You have difficulty swallowing
- You regurgitate undigested food
- You wake up choking
- You have chest discomfort after eating
- You have weight loss
- You have recurrent pneumonia
- You have symptoms despite reflux treatment
- You have nighttime coughing or aspiration
- You have long‑standing dysphagia
Long‑Term Outlook
With definitive therapy, most patients:
- Eat normally
- Avoid regurgitation
- Prevent esophageal dilation
- Improve quality of life
- Reduce aspiration risk
- Maintain long‑term esophageal health
Patients require periodic follow‑up to monitor esophageal function and anatomy.
Related Reading and Videos
Read more in our articles GERD vs. Heartburn vs. Acid Reflux: What's the Difference (and When It's Serious) and When Does Acid Reflux Need Surgery? A Guide to Your Options (Nissen, Toupet, LINX, and TIF). Watch The Reflux Talk Every Patient Needs: Hiatal Hernias, Warning Signs & What Doctors Don’t Explain on our video library. Related conditions include Jackhammer Esophagus. Treatments that may be involved include POEM (Peroral Endoscopic Myotomy), Laparoscopic Heller Myotomy (Heller-Dor Surgery for Achalasia), Dor Fundoplication (Anterior 180°–200° Partial Wrap) for Reflux and After Heller Myotomy and Esophageal Dilation (Endoscopic Balloon & Bougie Dilation for Strictures & Dysphagia).
More Foregut and Reflux Conditions
Explore related topics in our foregut patient library: EGJ Outflow Obstruction, Jackhammer Esophagus, Diffuse Esophageal Spasm, Esophageal Cancer, Erosive Esophagitis and Barrett’s Esophagus. For an overview of surgical options, see anti-reflux surgery and hiatal and paraesophageal hernia repair.
Prognosis
Achalasia is chronic but highly treatable. Most patients achieve excellent long‑term symptom control with POEM or Heller myotomy. Early treatment prevents esophageal dilation, aspiration, and malnutrition.
Why Choose Dr. de la Cruz‑Muñoz
Achalasia is commonly misdiagnosed as reflux, and choosing the correct operation depends on precise, subtype-specific diagnosis and reflux-conscious surgical technique. Dr. Nestor de la Cruz-Muñoz, MD, FACS, DABOM, is a board-certified surgeon specializing in minimally invasive foregut and bariatric surgery in Miami who directed a bariatric surgery fellowship for 10 years, training 13–14 fellows who also gained experience in foregut surgery. He has extensive experience in laparoscopic Heller myotomy with partial fundoplication and the full spectrum of foregut motility and reflux surgery. His practice emphasizes complete esophageal evaluation — high-resolution manometry, timed barium esophagram, and endoscopy — before any intervention, so that achalasia is never mistaken for GERD and the procedure is matched to the achalasia subtype. Patients benefit from an integrated foregut program that manages both the swallowing disorder and any post-treatment reflux, with structured long-term follow-up.
Achalasia surgery is foregut surgery, and foregut surgery is a cornerstone of Dr. de la Cruz-Muñoz's work. Across over 25 years in practice he has completed over 15,000 minimally invasive procedures, including complex foregut, hernia, gallbladder and abdominal operations and bariatric surgery.
Featured Procedures
FAQ
Both are excellent first-line treatments with very high, comparable success rates — roughly 90% or better symptom relief — and modern guidelines consider both appropriate first-line options (Vaezi et al., ACG Clinical Guidelines, 2020; Kahrilas et al., AGA Clinical Practice Update, 2017). The practical difference comes down to two things: achalasia subtype and reflux. For type III (spastic) achalasia, POEM is generally preferred because the myotomy can be extended higher to cover the spastic segment, with superior response rates compared with Heller myotomy (Patel et al., Gastroenterology, 2022). For types I and II, either works well, and the main trade-off is that POEM — which does not include an antireflux wrap — carries a meaningfully higher rate of post-procedure acid reflux than a laparoscopic Heller myotomy paired with a partial fundoplication. A meta-analysis of nearly 7,800 patients found POEM slightly more effective at relieving swallowing symptoms short-term but associated with far more erosive esophagitis (odds ratio ~9 for erosive esophagitis), and a 2026 systematic review restricted to the highest-quality trials confirmed the same reflux signal (Schlottmann et al., Annals of Surgery, 2018; Mirza et al., Surgical Endoscopy, 2026). Because up to roughly half of POEM patients develop reflux — sometimes without symptoms — many will need long-term acid-suppression and endoscopic monitoring (Kahrilas et al., AGA Clinical Practice Update, 2017). The right choice is individualized to your subtype, your reflux risk, and your surgeon's expertise (Blonski et al., Dysphagia, 2023). (See our Heller Myotomy page and our GERD / Acid Reflux page.)
For the vast majority of patients, achalasia is not inherited and will not be passed to your children. It is overwhelmingly a sporadic, idiopathic disorder thought to arise when an environmental trigger provokes an autoimmune attack on the esophageal nerves in a genetically susceptible person (Savarino et al., Nature Reviews Disease Primers, 2022). While certain immune-system gene variants (HLA class II alleles) are associated with achalasia, familial clustering is genuinely rare — one survey of over 1,000 first-degree relatives of achalasia patients identified no affected relatives (Pandolfino et al., Yamada's Textbook of Gastroenterology, 2022). True inherited achalasia is confined to a few uncommon genetic syndromes, most notably Allgrove (triple-A) syndrome — a childhood-onset autosomal recessive disorder of achalasia, alacrima (absent tears), and adrenal insufficiency caused by AAAS gene mutations — and it can also occur in Down syndrome (Pandolfino & Gawron, JAMA, 2015). These syndromic forms are far more likely to be identified in children with achalasia than in adults (Savarino et al., Nature Reviews Disease Primers, 2022). Outside of research settings, genetic testing has no role in routine management of typical adult achalasia (Pandolfino & Gawron, JAMA, 2015).
Diet does not treat achalasia, but how you eat can meaningfully reduce symptoms while you await treatment and afterward. Helpful habits include eating slowly, taking small bites and chewing thoroughly, drinking plenty of water with meals to help wash food through the tight junction, avoiding eating within 2–3 hours of lying down, and elevating the head of the bed to let gravity assist emptying (Cappell et al., Digestive Diseases and Sciences, 2020). During symptomatic periods, softer foods — and chopping, mincing, or pureeing solids — ease passage through the lower esophageal sphincter; some patients also find carbonated or very cold beverages worsen symptoms (Cappell et al., Digestive Diseases and Sciences, 2020). If swallowing becomes so limited that weight loss or aspiration risk develops, temporary tube feeding may be needed until definitive treatment (Cappell et al., Digestive Diseases and Sciences, 2020). After a successful myotomy, most patients return to a near-normal, regular diet. The transition is gradual: typically clear liquids for the first day or two after confirming no leak, advancing to soft or pureed foods over about a week, then a regular diet over the following month (Santes et al., Surgical Endoscopy, 2021). Because treatment can cause reflux, long-term dietary and positional reflux precautions remain worthwhile (see our GERD / Acid Reflux page) (Blonski et al., Dysphagia, 2023).
Cutting the lower esophageal sphincter to relieve achalasia (the Heller myotomy) predictably allows new acid reflux, because the valve that normally prevents reflux has been deliberately weakened. Adding a Dor fundoplication dramatically reduces this: in a double-blind randomized trial, abnormal esophageal acid exposure fell from 47% after myotomy alone to 9% after myotomy plus a Dor wrap (relative risk 0.11), and the benefit persists long term (Vaezi et al., American College of Gastroenterology, 2020). A partial wrap like Dor is preferred over a complete Nissen wrap after myotomy because a full wrap can obstruct an esophagus that no longer has normal muscle contractions (Midya et al., Cochrane Database of Systematic Reviews, 2022). The anterior Dor also physically covers and protects the exposed myotomy (Tassi et al., Annals of Surgery, 2023).
Diagnosis usually starts with an upper endoscopy to rule out narrowing, tumors or inflammation. The key test is high-resolution esophageal manometry, which measures the pressure and coordination of the esophageal muscle with each swallow and classifies disorders such as achalasia, EGJ outflow obstruction, diffuse esophageal spasm and jackhammer esophagus (Yadlapati et al., Neurogastroenterology & Motility, 2021). A timed barium esophagram shows how well the esophagus empties, and pH testing checks for reflux.
Esophageal motility disorders are conditions in which the muscles of the esophagus or the valve at its lower end do not work normally, so food is not pushed smoothly into the stomach. They include achalasia, EGJ outflow obstruction, diffuse esophageal spasm, jackhammer esophagus and ineffective esophageal motility. Symptoms include difficulty swallowing both solids and liquids, chest pain, regurgitation and weight loss. Treatment ranges from medications and botulinum toxin to dilation, POEM or Heller myotomy.
POEM (peroral endoscopic myotomy) is used mainly for achalasia — particularly type III (spastic) achalasia, where a longer myotomy is helpful — and for selected patients with other spastic esophageal disorders, such as jackhammer esophagus or diffuse esophageal spasm, when symptoms are severe despite medical treatment. It is also an option after a failed Heller myotomy. Because POEM does not include an anti-reflux wrap, patients at high risk of reflux may be better served by Heller myotomy with partial fundoplication.
POEM, or peroral endoscopic myotomy, is an incisionless procedure performed through the mouth with a flexible endoscope. The endoscopist creates a tunnel inside the wall of the esophagus and divides the tight or spastic muscle, allowing food to pass into the stomach. It treats achalasia and selected spastic esophageal disorders and relieves swallowing symptoms in most patients. Because no anti-reflux wrap is added, post-procedure reflux is common and may require medication and monitoring.
Most esophageal diverticula form because of increased pressure inside the esophagus, often from a muscle that does not relax properly. At the top of the esophagus, a tight cricopharyngeus muscle leads to Zenker's diverticulum. Just above the stomach, epiphrenic diverticula are often linked to motility disorders such as achalasia. Mid-esophageal diverticula may result from inflammation or scarring that pulls on the wall. This is why manometry is part of the evaluation.
