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Esophageal Achalasia

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Esophageal achalasia is a motor disorder in which the lower esophageal sphincter, or LES, fails to relax, and peristalsis in the distal esophagus may be abnormal or absent.

This functional obstruction impairs food from entering the stomach, leading to progressive dysphagia, regurgitation, and chest discomfort.

The cause is often indeterminate, possibly triggered by infections such as herpes simplex virus type 1 or human papillomavirus, and may involve immune-mediated inflammation.

This inflammation is hypothesized to cause degeneration of inhibitory neurons in the myenteric plexus, reducing the nitric oxide and vasoactive intestinal peptide required for LES relaxation.

Persistent LES contraction and absent peristalsis cause food retention above the sphincter, leading to esophageal dilation and increased pressure.

Chronic stasis promotes mucosal inflammation and bacterial overgrowth and increases the risk of esophageal cancer.

Clinically, patients experience significant weight loss, aspiration, recurrent pneumonia, and, in severe cases, esophageal rupture.

Overview

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Esophageal achalasia is a chronic neurogenic disorder characterized by impaired relaxation of the lower esophageal sphincter (LES) and absent or ineffective peristalsis in the distal esophagus. This leads to a functional obstruction without a physical blockage, despite significant disruption of esophageal motility.

Etiology

Achalasia is caused by degeneration of the myenteric (Auerbach's) plexus, specifically the loss of inhibitory ganglion cells that produce vasoactive intestinal peptide (VIP) and nitric oxide, which are crucial for relaxation of the lower esophageal sphincter (LES). The trigger for this degeneration remains unclear, but an immune-mediated mechanism involving cell and antibody responses to a possible viral antigen has been suggested. Chagas disease, caused by Trypanosoma cruzi, has a similar pathogenesis, causing damage to esophageal neural plexuses and mimicking idiopathic achalasia.

Pathophysiology

Normal esophageal motility is governed by coordinated neural inputs that regulate both tonic contraction and phasic relaxation of the LES. In achalasia, this coordination is lost due to the selective depletion of inhibitory neurons. The LES remains hypertonic and fails to relax during swallowing, leading to stasis of ingested food. Concurrently, the absence of peristalsis in the esophageal body exacerbates this stasis. Over time, this functional obstruction causes progressive dilation of the esophagus, sometimes transforming it into a capacious reservoir for retained food and secretions, potentially holding up to one liter. This retention can promote microbial colonization and lead to chronic inflammation. As a result, the risk of esophageal carcinoma also increases.

Clinical Manifestations

Patients with achalasia typically experience a gradual onset of dysphagia, regurgitation, chest discomfort, and significant weight loss in advanced stages. The dilated esophagus can lead to regurgitation and aspiration, increasing the risk of respiratory infections and aspiration pneumonia. Chronic irritation may cause ulceration, and disease progression can lead to serious complications like esophageal rupture.

Transcript

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Esophageal Achalasia

Lower Esophageal Sphincter

Myenteric Plexus

Inhibitory Neurons

Esophageal Motility

Dysphagia Regurgitation

Esophageal Dilation

Neurogenic Disorder

Functional Obstruction