Abstract

Achalasia cardia is the best characterised oesophageal motility disorder. It is characterised by progressive ganglion cell degeneration in the oesophageal myenteric plexus, which results in impaired lower oesophageal sphincter (LES) relaxation upon swallowing and aperistalsis in the distal smooth muscle segment of the oesophagus. The usual presenting features are dysphagia to both liquids and solids from onset, regurgitation of undigested food, retrosternal pain, heartburn, and weight loss. Initial investigations include upper gastrointestinal (GI) endoscopy and timed barium oesophagogram, whereas high resolution manometry is diagnostic. Therapy in achalasia cardia is directed towards biochemical or mechanical reduction in LES pressures. If candidates are fit for surgery, pneumatic dilatation, peroral endoscopic myotomy, and laparoscopic Heller’s myotomy are the mainstays of therapy that act by mechanical disruption of LES. On the other hand, botulinum toxin and pharmacotherapy (nitrates and calcium channel blockers) act by biochemical reduction of LES and are reserved for surgically unfit patients with limited life expectancy because of their short-lived efficacy. Oesophagectomy is reserved for treating refractory longstanding cases, who have previously failed multiple therapies.

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