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Figure 17.2 Barium swallow in a patient with achalasia, demonstrating a dilated oesophagus with tapering at the distal end.

Pneumatic dilatation and surgical myotomy (now usually performed laparoscopically) represent the most efficacious treatments for achalasia, and each has a very high rate of treatment success in type 1 and 2 achalasia. Each is associated with a 1% perforation rate even in experienced hands; and while pneumatic dilatation is associated with less morbidity and cost, it may need to be repeated.³⁴ In recent years, the technique of peroral endoscopic myotomy (POEM) has emerged and may allow close calibration of myotomy to the manometric findings – a useful asset in the treatment of type 3 achalasia, which should otherwise be managed laparoscopically.³³ In general, either pneumatic dilatation or laparoscopic myotomy is well tolerated in the elderly; in a consecutive series of 51 patients age ≥65 undergoing the latter procedure, there were no deaths, few complications, and a median hospital stay of 3 days.³⁵ Both pneumatic dilatation and POEM can induce reflux symptoms in a minority; this can be pre‐empted with laparoscopic myotomy by performing an anti‐reflux procedure concurrently.

      For the frail elderly patient with achalasia, endoscopic injection of botulinum toxin into the LOS represents an alternative and safe therapy. Two‐thirds report improvement in dysphagia after this procedure, although the majority relapse within one year, and repeat treatments become progressively less effective.³³ Pharmacological therapy to reduce LOS pressure (nitrates, calcium channel antagonists, or phosphodiesterase type 5 inhibitors) is of limited efficacy (possibly even less in the elderly than the young), requires frequent dosing, and is associated with frequent adverse effects, so it cannot be recommended.

      Patients with achalasia have an increased risk (estimated as 16‐fold) of squamous cell carcinoma of the oesophagus, but as the absolute risk is small, the cost‐benefit ratio of surveillance endoscopy appears unlikely to be favourable.³⁶ Occasionally, patients with achalasia have persistent dysphagia despite therapy, together with a tortuous, dilated oesophagus that empties poorly; in these circumstances, esophagectomy may be required.

      Distal oesophageal spasm and ‘jackhammer’ oesophagus

These disorders are diagnosed in a minority of patients with dysphagia or chest pain, and in many cases, the relationship between symptoms and motor abnormalities is unclear. Distal oesophageal spasm (formerly termed diffuse) is characterised by the presence of simultaneous or premature pressure waves in the distal oesophagus¹⁸ (Figure 17.4). A barium swallow may show segmentation of contrast by contractions (a corkscrew appearance) in a minority of patients (Figure 17.5) but lacks sensitivity or specificity for diagnosing the disorder. Similar manometric abnormalities may occur in GORD and in association with diabetes mellitus, alcohol abuse, amyloidosis, and progressive systemic sclerosis. Hypercontractile, or ‘jackhammer’ oesophagus, is defined by high‐amplitude oesophageal pressure waves, but peristalsis is maintained and appears normal on the barium swallow. The management of both distal spasm and jackhammer oesophagus is discussed below in relation to non‐cardiac chest pain.

      Minor disorders of peristalsis

Many patients referred for investigation of symptoms such as dysphagia or chest pain have abnormal manometric features that do not meet the criteria for achalasia, distal oesophageal spasm, or hypercontractile oesophagus. Cases where peristaltic waves are of abnormally low amplitude in the distal oesophagus are categorized as ineffective oesophageal motility, while patients who exhibit large breaks in the peristaltic sequence are diagnosed with fragmented peristalsis.³⁷ These ‘minor disorders’ of oesophageal motor function are evident in more than one‐third of presentations with dysphagia in patients over age 65, in contrast to the young, where a specific diagnosis can usually be made. It is important to recognise that a causal association cannot be assumed since the presence of radiographic or manometric abnormalities of oesophageal function correlates poorly with symptoms. Moreover, no specific therapy is available. Symptomatic management includes acid suppression when GORD is a feature and optimising nutrition.

      ‘Pill esophagitis’

An important cause of dysphagia or odynophagia in older individuals is mucosal injury caused by impaction of medications in the oesophagus, the incidence of which is likely to increase as the number of medications prescribed in this group escalates. Risk factors that are more prevalent in the elderly include less saliva, delayed oesophageal transit, and immobility (particularly recumbent position). Capsules – especially if gelatin‐coated – may present a greater risk than tablets due to slower oesophageal transit, and extended‐ or sustained‐release formulations are often implicated. The most frequent sites of hold‐up are the upper and mid‐oesophagus, corresponding to extrinsic compression from the left main bronchus, aortic arch, or enlarged left atrium, and also to a zone of low‐amplitude pressure waves between the proximal and distal oesophagus. Numerous medications are associated with oesophageal injury, including potassium chloride, tetracyclines, aspirin, non‐steroidal drugs, quinidine, theophylline, ferrous sulfate, and alendronate.³⁸ Dabigatran has also recently been associated with extensive sloughing of the oesophageal mucosa.³⁹

Figure 17.3 Oesophageal manometry in achalasia (type 2), displayed as a pressure topography plot. Note the simultaneous low‐amplitude pressure waves in the oesophageal body, i.e. pan‐oesophageal pressurization, and failure of LOS relaxation on swallowing.

Figure 17.4 Manometry recording in distal oesophageal spasm, displayed as a pressure topography plot. Note the excessively rapid propagation of contractions along the oesophagus (premature contractions) as well as a hypercontractile response in the distal oesophagus.

      Symptoms usually resolve when the offending drug is withdrawn but may be persistent and related to stricture formation. Perforation and bleeding are other associated complications, particularly with potassium chloride, quinidine, and non‐steroidal drugs. The typical endoscopic or barium swallow appearance in pill esophagitis is of small superficial ulcers. There is anecdotal evidence that sucralfate is beneficial in severe or persistent disease. As a preventive measure, patients should be advised to take oral medications in the upright position, followed immediately by a full glass of water.

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