Gastrointestinal · PANCE / PANRE

Achalasia

Primary esophageal motility disorder with impaired LES relaxation and absent peristalsis.

Also known as: achalasia, esophageal achalasia, cardiospasm

Overview

Primary esophageal motility disorder characterized by failure of the lower esophageal sphincter (LES) to relax with swallowing and absent peristalsis in the esophageal body, resulting in functional obstruction at the gastroesophageal junction.

Epidemiology

Incidence 1 per 100,000 per year; equal sex distribution; peak presentation between ages 30-60. Often diagnosed years after symptom onset.

🔒 Free preview limit reached

Keep reading — start your free trial

You've read your 2 free diagnosis previews. Create your free account to unlock the full Achalasia outline — plus all 514 diagnoses, 3,500+ board-style questions, flashcards, and an AI tutor. Your 7-day free trial includes everything, and there's no credit card required.

Free to start · No credit card · Cancel anytime

Risk factors

  • Idiopathic in the vast majority
  • Pseudoachalasia: malignancy at GEJ (gastric/esophageal adenocarcinoma) — must exclude
  • Chagas disease (Trypanosoma cruzi) — Latin America
  • Familial cases and association with autoimmune disorders (Allgrove/triple A syndrome)

Pathophysiology

Selective degeneration of inhibitory neurons (nitric oxide, VIP) in the myenteric (Auerbach) plexus of the distal esophagus and LES. Loss of inhibition leaves unopposed excitatory cholinergic activity → failure of LES relaxation. Loss of coordinated peristalsis → dilation and stasis. Etiology unknown; autoimmune and viral triggers (HSV-1) proposed.

Clinical presentation

Symptoms

  • Gradual, progressive dysphagia to BOTH solids and liquids (hallmark — distinguishes from mechanical obstruction)
  • Regurgitation of undigested food and saliva, worse supine
  • Chest pain (especially in early/spastic achalasia)
  • Weight loss
  • Nocturnal cough or aspiration
  • Heartburn (paradoxical; from food fermentation, not acid reflux)

Signs / physical exam

  • Often normal exam
  • Weight loss, cachexia in advanced disease
  • Halitosis from retained food

Classic findings

Dysphagia to solids AND liquids from onset; patient must drink water to push food down or maneuver the body to facilitate emptying.

Differential diagnosis

  • Pseudoachalasia (malignancy at GEJ) — Short symptom duration, marked weight loss, age >55, rapid progression; EGD and EUS critical to exclude
  • Distal esophageal spasm — Chest pain dominant, intermittent dysphagia; manometry with premature contractions and normal LES relaxation
  • Jackhammer esophagus — Hypercontractile peristalsis with elevated DCI on manometry; chest pain and dysphagia
  • Eosinophilic esophagitis — Solid-food dysphagia, food impaction, atopy; biopsy with ≥15 eos/HPF
  • Scleroderma esophagus — GERD, dysphagia; manometry with absent peristalsis but HYPOTENSIVE LES (opposite of achalasia)
  • Peptic stricture — Long-standing GERD, solid-food dysphagia; focal narrowing on EGD/esophagram
  • Chagas disease — Latin American origin; megaesophagus plus megacolon and cardiomyopathy

Diagnostic workup

Diagnostic criteria

Chicago Classification v4.0 (manometry): elevated median IRP + absent peristalsis. Three subtypes by contractile pattern: Type I (classic, no contractility), Type II (panesophageal pressurization in ≥20% of swallows — best treatment response), Type III (spastic, premature contractions — worst response, may need POEM).

Labs

  • No specific labs; CBC/BMP/albumin to assess nutritional status

Imaging

  • Barium esophagram — 'bird's beak' tapering at GEJ, dilated esophagus with air-fluid level, loss of peristalsis; timed barium swallow quantifies emptying
  • Upper endoscopy — REQUIRED to exclude pseudoachalasia/malignancy; may show retained food/saliva, dilated esophagus, puckered or tight LES that pops open with gentle pressure
  • High-resolution esophageal manometry — GOLD STANDARD; integrated relaxation pressure (IRP) >15 mmHg + 100% failed peristalsis

Diagnostic algorithm

SubtypeManometryTreatment Response
Type I (Classic)Absent peristalsis, no pressurization, elevated IRPGood — PD, Heller, POEM all effective
Type IIPanesophageal pressurization in ≥20% swallows, elevated IRPBEST response — preferred for PD
Type III (Spastic)Premature contractions ≥20% swallows, elevated IRPWorst response — POEM preferred (long myotomy)
Chicago Classification v4.0 achalasia subtypes — guide therapeutic selection.

Treatment

First-line

  • Pneumatic balloon dilation — graded dilation of LES; 70-90% short-term success; risk of perforation ~2%
  • Laparoscopic Heller myotomy with partial fundoplication (Dor or Toupet) — durable; 90% long-term success
  • Peroral endoscopic myotomy (POEM) — endoscopic submucosal myotomy; first-line for Type III achalasia; high efficacy but increased post-procedure GERD

Type I or II (Chicago Classification)

  • Pneumatic dilation, Heller myotomy, or POEM — comparable outcomes per European Achalasia Trial
  • Choice depends on age, comorbidities, expertise, and patient preference

Type III (spastic)

  • POEM preferred — longer myotomy can address spastic segment
  • Heller myotomy less effective; pneumatic dilation worst response

Second-line / adjunct

  • Botulinum toxin injection to LES — 50-100 units divided into 4 quadrants; effect lasts 6-12 months; reserved for poor surgical candidates
  • Pharmacologic therapy (nitrates, calcium channel blockers — nifedipine, isosorbide dinitrate) — modest efficacy, frequent side effects; reserved for patients unfit for other therapies
  • Esophagectomy — end-stage achalasia with megaesophagus or sigmoid esophagus failing definitive therapy

Complications

  • Aspiration pneumonia
  • Megaesophagus and sigmoid esophagus
  • Esophageal squamous cell carcinoma (10-30× increased risk; long-standing disease)
  • Malnutrition and weight loss
  • Post-treatment GERD (highest after POEM; lower after Heller with fundoplication)
  • Esophageal perforation (during dilation or surgery)

PANCE pearls

  • ALWAYS perform EGD before treating — pseudoachalasia from malignancy at GEJ mimics achalasia perfectly; suspect when symptoms <6 months, weight loss out of proportion, age >55.
  • Manometry is the gold standard — barium esophagram and EGD support the diagnosis but cannot replace it.
  • Chicago Classification subtype guides therapy — Type II has the best treatment response; Type III often requires POEM.
  • Surveillance for squamous cell carcinoma in long-standing disease is controversial — high-risk groups may benefit from periodic EGD.
  • Pharmacologic therapy is rarely effective and is reserved for patients who cannot undergo definitive therapy.
  • Post-POEM GERD is common (up to 50%) — counsel about lifelong PPI; Heller with fundoplication has lower GERD rates.

References

  • ACG 2020 — Vaezi MF et al. ACG Clinical Guidelines: Diagnosis and Management of Achalasia. Am J Gastroenterol 2020;115:1393-1411
  • Chicago Classification v4.0 — Yadlapati R et al. Esophageal motility disorders on high-resolution manometry: Chicago classification version 4.0. Neurogastroenterol Motil 2021;33:e14058
  • European Achalasia Trial — Boeckxstaens GE et al. Pneumatic Dilation versus Laparoscopic Heller's Myotomy for Idiopathic Achalasia. NEJM 2011;364:1807-1816

Practice Gastrointestinal questions on FirstPassPA

Turn this outline into retention. 3,500+ board-style questions with an AI tutor that explains every answer — free to start, no card required.

Start studying free → Browse all 514 diagnoses

Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants.