A summary of the most recent ACG (American College of Gastroenterology) guidelines for the diagnosis and management of achalasia


Achalasia is a primary esophageal motor disorder of unknown etiology characterized manometrically by insufficient relaxation of the lower esophageal sphincter (LES) and loss of esophageal peristalsis; radiographically by aperistalsis, esophageal dilation, with minimal LES opening, “ bird-beak ” appearance, poor emptying of barium; and endoscopically by dilated esophagus with retained saliva, liquid, and undigested food particles in the absence of mucosal stricturing or tumor.

  • The diagnosis of achalasia is supported by esophagram findings including dilation of the esophagus, a narrow esophagogastric junction with “bird-beak” appearance, aperistalsis, and poor emptying of barium (strong recommendation, moderate-quality evidence).
  • All patients with suspected achalasia who do not have evidence of a mechanical obstruction on endoscopy or esophagram should undergo esophageal motility testing before a diagnosis of achalasia can be confirmed (strong recommendation, low-quality evidence).
  • Endoscopic assessment of the gastroesophageal junction and gastric cardia is recommended in all patients with achalasia to rule out pseudoachalasia (strong recommendation, moderate-quality evidence).
  • Either graded pneumatic dilation (PD) or laparoscopic surgical myotomy with a partial fundoplication are recommended as initial therapy for the treatment of achalasia in those fit and willing to undergo surgery (strong recommendation, moderate-quality evidence).
  • Botulinum toxin therapy is recommended in patients who are not good candidates for more definitive therapy with PD or surgical myotomy (strong recommendation, moderatequality evidence).
  • Pharmacologic therapy for achalasia is recommended for patients who are unwilling or cannot undergo definitive treatment with either PD or surgical myotomy and have failed botulinum toxin therapy (strong recommendation, low-quality evidence).
  • Patient follow-up aft er therapy may include assessment of both symptom relief and esophageal emptying by barium
    esophagram (strong recommendation, low-quality evidence).
  • Surveillance endoscopy for esophageal cancer is not recommended (strong recommendation, low-quality evidence).

Achalasia Algo

Am J Gastroenterol 2013; 108:1238–1249; doi:10.1038/ajg.2013.196; published online 23 July 2013

H. Pylori, when to test and treat

If you haven’t already noticed by our posts, this week we start the GI block of our curriculum. This morning in MR, we reviewed a board question related to H pylori and MALT lymphoma. Here are some highlights, answers to questions posed in MR and a great review article from NEJM.

Our case was a 48 yo with sx of dyspepsia for 6 months with no weight loss, fever or night sweats, no medications and normal labs.

What is dyspepsia?

  • Non specific term that refers to recurrent upper abdominal pain and discomfort and includes:
    • Epigastric fullness, belching, bloating, gnawing pain, heartburn
  • Most often non severe and pts remain functional

What is the differential diagnosis?

  • Peptic ulcer disease, gastritis, biliary colic, gastroparesis, pancreatitis, GI malignancy

What work up needs to be done?

  • Take a full H&P looking for etiologies for the above differential including medications (NSAIDs and aspirin) and alcohol use as well as warning signs such as evidence of malignancy or upper GI bleeding
  • On labs, check for IDA that may be a sign of ulcerative lesion or gastritis
  • Consider checking for H pylori
  • Withdraw offending agents
  • Initiate a PPI

When do we use the “test and treat” strategy for H pylori infection?

  • H pylori is contracted in childhood and prevalent in 50% of the US population
  • It is asymptomatic in many, but of infected people, 1-10% will develop gastric or duodenal ulcers, 0.3-3% gastric cancer and < 0.01% MALT lymphoma
  • American College of Gastroenterology recommends testing and treating patients that are <55 and have no alarm symptoms as well as patients that have known PUD, MALT lymphoma or gastric cancers

What test do I use?

  • Biopsy and histologic examination
    • Gold standard
    • Invasive
  • Urease breath tests
    • Good for active disease and response to treatment
    • Sensitivity 95%, specificity 95%
    • Less sensitive if on PPI and antibiotics
  • Fecal antigen test
    • Sensitivity 94%, specificity 98%
    • Test of choice if on PPI
  • Serologic tests
    • No longer recommended due to their low predictive value <50%
    • Also cannot determine the effectiveness of treatment

When do patients need EGD?

  • Endoscopy is indicated for patients with alarm symptoms:
    • Weight loss, persistent N/V, odynophagia/dysphagia, GI bleeding or IDA
    • Or older patients at greater risk of malignancy, age cutoffs vary based on guidelines from 45-55 years old
    • Patients not responding to PPI, medication withdrawal or triple therapy for H pylori

What follow up is required?

  • Patients with uncomplicated duodenal ulcers with resolution of sx do not need follow up endoscopy. Patients with large duodenal ulcers should have repeat endoscopy.
  • The follow up for gastric ulcers is under wide debate and may depend on the experience of the endoscopist and the adequacy of initial biopsy.
    • Consider the following approach: Do not repeat an upper endoscopy on patients with benign-appearing gastric ulcers that have been adequately biopsied with no evidence of malignancy or dysplasia on biopsies. In patients at high-risk for malignancy, perform a follow-up endoscopy (with biopsies of the ulcer if still present) after six weeks of therapy. High-risk gastric ulcers include the following:
      • Occurrence in ethnic groups raised in endemic areas (eg, Asians, Latinos), or a family history of gastric cancer
      • The absence of recent NSAID use
      • The presence of H. pylori, particularly if associated with gastric atrophy
      • Age greater than 50 years
      • The absence of either a concomitant duodenal ulcer or a prior history of duodenal ulcer (duodenal ulcers require higher acid secretion, which is incompatible with the pangastritis typical of most gastric cancers)
      • Giant ulcers (>2 to 3 cm)
  • Non invasive confirmation of eradication is recommended in all patients by European consensus group and for the following by the American College of Gastroenterology:
    • Associated ulcer, persistent sx, MALT lymphoma, resection of early gastric cancer

Tomorrow will cover an overview of MALT lymphoma so stay tuned!

Refer to the NEJM for further reading:,

Differential Diagnosis of Dysphagia

  • Intraluminal foreign bodies (usually a cause of acute dysphagia)
  • Mucosal diseases:
    • Peptic stricture secondary to gastroesophageal reflux disease
    • Esophageal rings and webs (i.e. Plummer–Vinson syndrome)
    • Esophageal tumors
    • Chemical injury (e.g., caustic ingestion, pill esophagitis, sclerotherapy for varices)
    • Radiation injury
    • Infectious esophagitis
    • Eosinophilic esophagitis
  • Mediastinal diseases:
    • Tumors (e.g., lung cancer, lymphoma)
    • Infections (e.g., tuberculosis, histoplasmosis)
    • Cardiovascular (dilated auricula, vascular compression)
  • Diseases affecting smooth muscle and its innervation:
    • Achalasia (both idiopathic and associated with Chagas disease)
    • Scleroderma
    • Other motility disorders
    • Postsurgical (i.e., after fundoplication, antireflux devices)

Esophageal Motility Disorders

A little information on esophageal mobility disorders from an article by our own Dr. Stuart Spechler!

Classification of esophageal motility abnormalities

Inadequate LES relaxation
 Classic achalasia
 Atypical disorders of LES relaxation
Uncoordinated contraction
 Diffuse esophageal spasm
 Nutcracker esophagus
 Isolated hypertensive LES
 Ineffective esophageal motility

Continue reading Esophageal Motility Disorders