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Gastroenterology
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Achalasia

High EvidenceUpdated: 2025-12-23

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Red Flags

  • Pseudoachalasia (malignancy at GOJ) - rapid symptom onset, weight loss, older age
  • Aspiration pneumonia
  • Severe weight loss/malnutrition
  • Respiratory symptoms (nocturnal cough, recurrent chest infections)
Overview

Achalasia

1. Clinical Overview

Summary

Achalasia is a primary oesophageal motility disorder characterised by failure of Lower Oesophageal Sphincter (LOS) relaxation combined with aperistalsis of the oesophageal body. The underlying pathology involves degeneration of inhibitory neurons (nitric oxide and VIP-releasing) in the myenteric plexus. It affects approximately 1 per 100,000 population annually and presents classically with dysphagia to both solids AND liquids from onset, distinguishing it from mechanical obstruction. Diagnosis is confirmed by high-resolution manometry, and treatment focuses on reducing LOS pressure via endoscopic or surgical myotomy.

Key Facts

  • Definition: Primary oesophageal motility disorder with absent LOS relaxation and aperistalsis
  • Prevalence: 1 in 100,000 per year, equal male-to-female ratio
  • Mortality/Morbidity: Low mortality but significant quality of life impact; increased oesophageal cancer risk (squamous cell carcinoma 3-5%)
  • Key Management: Heller's myotomy or POEM for definitive treatment; pneumatic dilatation as alternative
  • Critical Finding: Dysphagia to BOTH solids AND liquids from onset (vs. mechanical = solids first)
  • Key Investigation: High-resolution oesophageal manometry (Gold Standard)

Clinical Pearls

"Solid AND Liquid" Rule: Unlike mechanical obstruction (where solids precede liquids), achalasia causes equal difficulty with both from the start due to failed peristalsis.

Pseudoachalasia Alert: Malignancy at the gastro-oesophageal junction can mimic achalasia. Suspect if: age >55, rapid symptom onset (<6 months), >6kg weight loss, or difficulty passing endoscope.

Bird's Beak Sign: Classic barium swallow appearance showing smooth tapering at the GOJ with proximal oesophageal dilatation — pathognomonic for achalasia.

Why This Matters Clinically

Untreated achalasia leads to progressive oesophageal dilatation, food retention, aspiration pneumonia, and malnutrition. Early diagnosis prevents irreversible megaoesophagus. Additionally, there is a 25-fold increased risk of developing oesophageal squamous cell carcinoma requiring surveillance consideration.


2. Epidemiology

Incidence & Prevalence

  • Incidence: 1.0-1.6 per 100,000 per year
  • Prevalence: 10 per 100,000 population
  • Trend: Stable; increased detection due to better diagnostics

Demographics

FactorDetails
AgeTypically 25-60 years; can occur at any age; bimodal peaks (30-40 and 60-70)
SexMale = Female (1:1 ratio)
EthnicityNo significant variation; equal across all groups
GeographySimilar incidence worldwide; no geographic predilection

Risk Factors

Non-Modifiable:

  • Genetic factors (rare familial cases, HLA-DQw1 association)
  • Age (peak 30-60 years)
  • Possible viral triggers (HSV-1, varicella-zoster implicated in some studies)

Modifiable:

Risk FactorRelative Risk
None well-establishedN/A
(Achalasia is considered idiopathic in most cases)—

Conditions Associated with Secondary Achalasia (Pseudoachalasia):

CauseNotes
Malignancy at GOJAdenocarcinoma, squamous cell carcinoma
Chagas diseaseEndemic in South America (Trypanosoma cruzi)
AmyloidosisRare
SarcoidosisVery rare
Post-fundoplicationTight wrap causing obstruction

3. Pathophysiology

Mechanism

Step 1: Loss of Inhibitory Neurons

  • Selective destruction of inhibitory neurons in the myenteric (Auerbach's) plexus
  • These neurons normally release nitric oxide (NO) and vasoactive intestinal peptide (VIP)
  • Loss is selective for inhibitory neurons; excitatory cholinergic neurons initially preserved
  • Cause unknown — possible autoimmune, infective (viral), or inflammatory trigger

Step 2: Imbalance of Oesophageal Tone

  • Loss of inhibitory input leads to unopposed excitatory (cholinergic) activity
  • Results in:
    • Failure of LOS relaxation (tonic contraction)
    • Aperistalsis (no coordinated propulsion)
  • Elevated resting LOS pressure in some cases

Step 3: Clinical Consequences

  • Food bolus cannot pass through non-relaxing LOS
  • Oesophageal body cannot propel food due to absent peristalsis
  • Progressive oesophageal dilatation (megaoesophagus over years)
  • Food stasis → regurgitation, aspiration, weight loss, malnutrition
  • Chronic inflammation → increased squamous cell carcinoma risk (3-5%)

Classification

Type (Chicago v4.0)Manometric DefinitionClinical FeaturesTreatment Response
Type I (Classic)Failed LOS relaxation (IRP ≥15 mmHg) + 100% failed peristalsis with minimal pressurisationMost common; dysphagia, regurgitationGood response to all treatments
Type II (with pressurisation)Failed LOS relaxation + pan-oesophageal pressurisation (>0 mmHg) in ≥20% swallowsSimilar symptoms; may have chest painBEST treatment outcomes (>0% with myotomy)
Type III (Spastic)Failed LOS relaxation + premature (spastic) contractions with DL <4.5s in ≥20% swallowsChest pain more prominent; dysphagiaWorst response; POEM may be better than Heller's

Anatomical/Physiological Considerations

The lower oesophageal sphincter is a 3-4 cm high-pressure zone located at the gastro-oesophageal junction. Normal swallowing triggers a coordinated peristaltic wave down the oesophageal body with reflex LOS relaxation mediated by inhibitory neurons. In achalasia, the LOS remains contracted and the oesophageal body has no effective peristalsis, creating a functional obstruction. Over time, the oesophagus proximal to the LOS dilates progressively, eventually forming a sigmoid-shaped "megaoesophagus" in late-stage disease.


4. Clinical Presentation

Symptoms

Typical Presentation:

Atypical Presentations:

Signs

Red Flags

[!CAUTION] Red Flags — Urgent investigation for Pseudoachalasia (malignancy) if:

  • Age >55 years at symptom onset
  • Symptom duration <6 months (rapid onset)
  • Weight loss >6 kg
  • Cannot pass endoscope through LOS (high resistance)
  • CT evidence of mass at GOJ or mediastinal lymphadenopathy
  • Dysphagia progressing despite treatment

Dysphagia to solids AND liquids (95% of patients) — key discriminator from mechanical obstruction
Common presentation.
Regurgitation of undigested food (75%) — often worse when lying down, may cause nocturnal cough
Common presentation.
Weight loss (60%) — gradual, progressive
Common presentation.
Chest pain (40%) — retrosternal, may mimic cardiac pain
Common presentation.
Heartburn (40%) — paradoxically; due to fermentation of retained food, not acid reflux
Common presentation.
5. Clinical Examination

Structured Approach

General:

  • Assess nutritional status (BMI, cachexia, muscle wasting)
  • Vital signs (fever may suggest aspiration pneumonia)
  • Hydration status

Specific System Examination:

  • ENT: Oral hygiene, halitosis
  • Respiratory: Auscultate for crackles (aspiration)
  • Abdominal: Usually normal; no specific findings
  • Neck: No masses (rule out extrinsic compression)

Special Tests

TestTechniquePositive FindingSensitivity/Specificity
Water swallow testGive water, observe for regurgitation or delayImmediate regurgitation, coughing, prolonged swallowing timeLow sensitivity; screening only
Timed barium swallowMeasure oesophageal emptying at 1, 2, 5 minutesRetained barium at 5 minutes, "Bird's Beak" appearance~90% sensitive for achalasia
High-resolution manometryMeasures LOS pressure and peristalsisIRP ≥15 mmHg, absent peristalsis98%/96% (Gold Standard)

6. Investigations

First-Line (Bedside)

  • Basic observations — exclude aspiration (fever, tachycardia)
  • CXR — may show air-fluid level behind heart, dilated oesophagus, aspiration changes

Laboratory Tests

TestExpected FindingPurpose
FBCMay show anaemia (chronic malnutrition)Assess nutritional impact
U&Es, LFTsUsually normalBaseline; dehydration assessment
AlbuminMay be low in malnutritionNutritional status
CRPElevated if aspiration pneumoniaInfection marker
Chagas serologyPositive in endemic areasRule out secondary achalasia (Chagas)

Imaging

ModalityFindingsIndication
Barium swallow"Bird's Beak" sign (smooth tapering at GOJ); Dilated, aperistaltic oesophagus; Delayed contrast passageInitial investigation; screening
OGD (Mandatory)Dilated oesophagus with retained food; Resistance at LOS (but passable); Rules out malignancyExclude pseudoachalasia; biopsy if suspicious
CT chest/abdomenDilated oesophagus; May detect GOJ mass in pseudoachalasiaIf pseudoachalasia suspected
High-resolution manometryIRP ≥15 mmHg; Type I/II/III classificationGOLD STANDARD for diagnosis
Endoscopic ultrasound (EUS)Excludes submucosa/extrinsic massIf pseudoachalasia suspected

Diagnostic Criteria

Chicago Classification v4.0 Diagnostic Criteria for Achalasia:

CriterionRequirement
Integrated Relaxation Pressure (IRP)≥15 mmHg (abnormal relaxation)
Peristalsis100% failed or premature contractions
OGDNo mechanical obstruction

Subtype Classification:

  • Type I: No oesophageal pressurisation
  • Type II: Pan-oesophageal pressurisation ≥30 mmHg in ≥20% swallows
  • Type III: Premature contractions (DL <4.5s) in ≥20% swallows

7. Management

Management Algorithm

Acute/Emergency Management (if applicable)

Immediate Actions (for severe aspiration or dehydration):

  1. NBM if aspiration risk
  2. IV fluids for dehydration/electrolyte replacement
  3. Treat aspiration pneumonia (antibiotics covering oral flora)
  4. NGT insertion if severe food impaction (rare)

Conservative Management

  • Dietary modification: Soft diet, small meals, upright position during and after eating
  • Avoid eating within 3 hours of bedtime
  • Elevate head of bed (reduce nocturnal regurgitation)
  • Adequate hydration with meals

Medical Management

Drug ClassDrugDoseDuration
Calcium Channel BlockersNifedipine10-30 mg sublingual/PO 30 minutes before mealsShort-term; primary role is symptom relief pre-definitive therapy
NitratesIsosorbide Dinitrate5 mg sublingual pre-mealsShort-term; limited efficacy
PDE5 InhibitorsSildenafil50 mg before mealsLimited evidence; rarely used

Note: Pharmacological therapy has limited long-term efficacy (<50% symptom relief) and is reserved for patients unfit for endoscopic/surgical intervention.

Endoscopic/Interventional Management

InterventionTechniqueEfficacyRisks
Botulinum toxin injection100 units injected into LOS during OGD70-80% initial relief; 50% relapse at 1 yearLow risk; temporary; fibrosis may complicate later myotomy
Pneumatic dilation (PD)Graded balloon (30-40mm) dilation of LOS70-90% initial; 30-40% need repeat at 5 yearsPerforation 1-3%; GORD
POEM (Per-Oral Endoscopic Myotomy)Endoscopic submucosal tunnel + myotomy>0% success at 2 yearsReflux post-POEM higher than Heller's; preferred for Type III

Surgical Management

Indications:

  • Failed or inadequate response to endoscopic therapy
  • Patient preference for definitive treatment
  • Type III achalasia (POEM or extended myotomy)
  • Young patients (preferring single definitive procedure)

Procedure:

  • Laparoscopic Heller's Myotomy + Partial Fundoplication (Dor or Toupet):
    • Myotomy: 6-8 cm on oesophagus + 2-3 cm onto stomach
    • Fundoplication (anterior Dor or posterior Toupet) to prevent GORD
    • >90% long-term symptom relief
    • Reflux rates ~10-15% with fundoplication

Disposition

  • Admit if: Severe dehydration, aspiration pneumonia, malnutrition, emergency endoscopy needed
  • Discharge if: Stable, able to maintain oral intake, planned outpatient workup/treatment
  • Follow-up: Post-procedure review at 4-6 weeks; long-term surveillance considering cancer risk (OGD every 3-5 years in long-standing disease)

8. Complications

Immediate (Minutes-Hours)

ComplicationIncidencePresentationManagement
Oesophageal perforation (post-dilatation/POEM)1-3% (PD); <1% (POEM)Chest pain, subcutaneous emphysema, feverCT; conservative if contained; surgery if large
AspirationVariableCough, desaturation during procedureSuction; supportive care
Bleeding<1%Haematemesis, melaenaEndoscopic haemostasis

Early (Days)

  • Dysphagia recurrence: Inadequate myotomy or fibrosis (repeat therapy may be needed)
  • Infection: Rare; mucosal breach
  • Reflux symptoms: Especially post-POEM (no anti-reflux procedure)

Late (Weeks-Months)

  • Gastro-oesophageal reflux disease (GORD): 20-40% post-POEM; 10-15% post-Heller's with fundoplication
  • Treatment failure/recurrence: 10-20% at 5 years
  • Megaoesophagus: End-stage with sigmoid deformity (may require oesophagectomy)
  • Oesophageal squamous cell carcinoma: 3-5% lifetime risk (25x general population); surveillance recommended

9. Prognosis & Outcomes

Natural History

Untreated achalasia leads to progressive oesophageal dilatation over years. Patients develop worsening dysphagia, malnutrition, weight loss, and recurrent aspiration. Eventually, the oesophagus becomes massively dilated and sigmoid-shaped (end-stage megaoesophagus), at which point myotomy is less effective and oesophagectomy may be the only option. Untreated patients have significantly impaired quality of life.

Outcomes with Treatment

VariableOutcome
MortalityLow (<0.5% procedure-related); disease rarely directly fatal
MorbiditySignificant if untreated; moderate post-treatment (reflux, recurrence)
Recurrence10-20% at 5 years; Type II has best outcomes
Long-term symptom reliefPOEM/Heller's: >0% at 2 years; PD: 70-80% at 2 years

Prognostic Factors

Good Prognosis:

  • Type II achalasia (best response to treatment)
  • Younger age at treatment
  • Shorter symptom duration before treatment
  • Non-dilated oesophagus (<6 cm)

Poor Prognosis:

  • Type III achalasia (worst treatment response)
  • End-stage megaoesophagus (sigmoid oesophagus)
  • Elderly patients with comorbidities
  • Failed prior interventions (revision surgery less effective)

10. Evidence & Guidelines

Key Guidelines

  1. ACG Clinical Guideline: Diagnosis and Management of Achalasia (2020) — Recommends high-resolution manometry for diagnosis; POEM or Heller's myotomy for definitive treatment; graded pneumatic dilation as alternative. American College of Gastroenterology
  2. ESGE/UEG Guideline on Motility Disorders (2020) — Endorses POEM as effective alternative to Heller's for Type I/II; recommends surveillance for oesophageal cancer. European Society of Gastrointestinal Endoscopy

Landmark Trials

POEM vs Laparoscopic Heller Myotomy RCT (Werner et al., 2019) — First major RCT comparing POEM to laparoscopic Heller's myotomy.

  • 221 patients randomised
  • Key finding: POEM non-inferior to Heller's at 2 years (83% vs 82% treatment success); POEM had higher GORD rates (57% vs 20%)
  • Clinical Impact: Established POEM as a valid first-line option; highlighted need for PPI post-POEM

European Achalasia Trial (Boeckxstaens et al., 2011) — RCT comparing pneumatic dilation to laparoscopic Heller's myotomy.

  • 201 patients randomised
  • Key finding: Similar efficacy at 2 and 5 years (PD: 86%, Heller's: 90%)
  • Clinical Impact: Validated pneumatic dilation as reasonable first-line, especially where surgical expertise is limited

Evidence Strength

InterventionLevelKey Evidence
POEM for Type I/II achalasia1bWerner et al. RCT 2019; NEJM
Laparoscopic Heller's myotomy + fundoplication1aMultiple RCTs; Cochrane review
Pneumatic dilation1bEuropean Achalasia Trial 2011
Botulinum toxin injection1bMultiple RCTs; short-term benefit only
Pharmacotherapy (CCB, nitrates)2bLimited efficacy; poor long-term data

11. Patient/Layperson Explanation

What is Achalasia?

Achalasia is a swallowing disorder caused by damage to the nerves in your food pipe (oesophagus). Normally, when you swallow, a valve at the bottom of the food pipe relaxes to let food into the stomach. In achalasia, this valve doesn't relax properly, and the muscles in the food pipe don't work together to push food down. Think of it like a door that won't open — food gets stuck and builds up.

Why does it matter?

If left untreated, achalasia can cause:

  • Difficulty eating: Food gets stuck, causing discomfort and weight loss
  • Food coming back up: Especially at night, which can cause choking or lung infections
  • Stretched food pipe: Over years, the food pipe can become very wide and floppy
  • Slightly higher risk of food pipe cancer: Regular check-ups may be recommended

How is it treated?

  1. Keyhole surgery (Heller's myotomy): A small operation to cut the tight valve muscle, usually with a procedure to prevent acid reflux. Very effective long-term.
  2. POEM (camera treatment): A newer technique done through a camera swallowed into the food pipe, cutting the muscle from the inside. No scars, quick recovery.
  3. Balloon stretching: A balloon is inflated to stretch the valve. May need to be repeated.
  4. Botox injection: A temporary treatment where Botox is injected to relax the valve. Effects wear off after months.

What to expect

  • Treatment is usually very effective (more than 90% of people have significant improvement)
  • You may need to take acid-reducing tablets after treatment
  • Some people may need follow-up treatments if symptoms return
  • Recovery from keyhole surgery or POEM is usually 1-2 weeks

When to seek help

  • Urgent: Choking episodes, breathing difficulties, severe chest pain, high fever (may indicate food pipe perforation or lung infection)
  • Soon: Worsening difficulty swallowing, significant weight loss, food getting stuck more often

12. References

Primary Guidelines

  1. Vaezi MF, et al. ACG Clinical Guideline: Diagnosis and Management of Achalasia. Am J Gastroenterol. 2020;115(9):1393-1411. PMID: 32773454
  2. Kahrilas PJ, et al. Chicago Classification v4.0. Neurogastroenterology & Motility. 2021;33(1):e14058. PMID: 33373111

Key Trials

  1. Werner YB, et al. Endoscopic or Surgical Myotomy in Patients with Idiopathic Achalasia. N Engl J Med. 2019;381(23):2219-2229. PMID: 31800987
  2. Boeckxstaens GE, et al. Pneumatic Dilation versus Laparoscopic Heller's Myotomy for Idiopathic Achalasia. N Engl J Med. 2011;364(19):1807-1816. PMID: 21561346

Further Resources

  • UpToDate: Achalasia Overview
  • Radiopaedia: Achalasia Imaging
  • BSG Guidelines: British Society of Gastroenterology


Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists. This content does not constitute medical advice for individual patients.

Last updated: 2025-12-23

At a Glance

EvidenceHigh
Last Updated2025-12-23

Red Flags

  • Pseudoachalasia (malignancy at GOJ) - rapid symptom onset, weight loss, older age
  • Aspiration pneumonia
  • Severe weight loss/malnutrition
  • Respiratory symptoms (nocturnal cough, recurrent chest infections)

Clinical Pearls

  • **"Solid AND Liquid" Rule**: Unlike mechanical obstruction (where solids precede liquids), achalasia causes equal difficulty with both from the start due to failed peristalsis.
  • **Bird's Beak Sign**: Classic barium swallow appearance showing smooth tapering at the GOJ with proximal oesophageal dilatation — pathognomonic for achalasia.
  • **Red Flags — Urgent investigation for Pseudoachalasia (malignancy) if:**
  • - Age &gt;55 years at symptom onset
  • - Symptom duration &lt;6 months (rapid onset)

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines