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Achalasia is a motility disorder caused by neural dysfunction which may involve both the myenteric plexus of the oesophagus, the vagal nerves, and the dorsal motor nucleus.1,2 The aetiology of the disorder is still obscure, viral infection and autoimmunity having been suggested. Recently, Park and Vaezi1 proposed that different environmental factors in patients with genetic predisposition could lead to the same clinical picture and manometric findings.
As part of an ongoing prospective study in patients with achalasia,3 we have investigated if chest trauma could be involved in the development of achalasia. Twenty consecutive achalasia patients (eight men), aged 18–79 years (median age 53) at the time of diagnosis, and 20 consecutive patients matched for sex and age (eight men; 17–83 years (median 49)), evaluated at our outpatient clinic, were included. Control patients presented with symptoms other than dysphagia and, at the end of evaluations, diagnosis of irritable bowel syndrome (n = 8), gastro-oesophageal reflux disease (n = 6), peptic ulcer disease (n = 4), chronic constipation (n = 1), and anal incontinence (n = 1) were made. Achalasia patients underwent clinical evaluation, upper endoscopy, x ray barium study, and oesophageal manometry to confirm diagnosis. All patients included in the study underwent a standard questionnaire regarding occurrence of chest trauma. Arbitrarily, only traumas serious enough to require hospitalisation or to determine loss of work of ⩾ 7 days were considered. Type of trauma and type of accident causing trauma were also recorded. Traumas were divided according to their occurrence before or after the onset of dysphagia.
Chest trauma was reported by 5/20 (25%) achalasia patients and no control patients (p<0.05 by Fisher’s exact test). All traumas occurred before the onset of dysphagia (median 2 years (range 1–13) before), being caused by a road accident in three patients and work accident in two. All traumas were non-penetrating. Hospitalisation was required in three patients. Achalasia patients with and without chest trauma had a similar age at onset of dysphagia (mean 45 (SEM 9) and 43 (5) years, respectively), clinical score (8.8 (0.5) and 7.6 (0.5)) according to Eckardt and colleagues,4 oesophageal diameter at x ray barium swallow (4.9 (0.3) and 4.4 (0.5) cm), amplitude of oesophageal pressure waves (41 (18) and 31 (7) mm Hg), and lower oesophageal sphincter pressure (26 (5) and 27 (4) mm Hg) at diagnosis. Independently of previous occurrence of chest trauma, all patients achieved stable clinical remission (that is, clinical score of ⩽3 for ⩾1 year after dilatation)3 and a low lower oesophageal sphincter pressure (<10 mm Hg)4 after one (n = 11) or two (n = 9) pneumatic dilatations. Recent retrospective data support our findings5: a history of operative or non-operative chest trauma prior to the development of dysphagia was present in 16/64 (25%) achalasia patients compared with 7/73 (9.5%; p<0.05) control patients presenting with dysphagia and normal oesophageal manometry.
In conclusion, chest trauma may be one of the aetiological factors of achalasia. This could occur through ischaemia or compression of neural structures leading to their irreversible damage in susceptible individuals.
Conflict of interest: None declared.
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