Where does the food stick?

Retrosternal hold-up suggests that the disorder lies within the oesophagus. If the site of hold-up is in the neck, the pathology can lie either in the oesophagus or in the pharynx (Figure 2.1). Due to referred sensation, the site of perceived hold-up is above the suprasternal notch in 30% of cases where the actual hold-up is within the oesophageal body. Therefore, the next batch of questions aims to distinguish pharyngeal from oesophageal dysfunction.

FIGURE 2.1 Differentiating oesophageal disorders.

Is one or more of the four cardinal symptoms of pharyngeal dysfunction present?

The four cardinal symptoms of pharyngeal dysfunction are:

Supportive but less specific symptoms of oropharyngeal dysphagia include: bolus hold-up in the neck, piecemeal swallows, oral spill or drooling, dysphonia, throat clearing, garbled voice and weight loss.

If one or more of these symptoms is/are present the dysphagia is probably oropharyngeal, either structural or neuromyogenic, and further history and investigation should proceed accordingly (see below).

If oesophageal dysphagia is suspected, the next step is to establish whether it is a structural or motor disorder (Tables 2.1 and 2.2).

TABLE 2.1 Structural oesophageal disorders causing dysphagia

TABLE 2.2 Aetiology of pharyngeal dysphagia^*

* Common causes. List not intended to be comprehensive.

Is the dysphagia for solids or liquids?

Typically the patient with a motor disorder (e.g. achalasia, diffuse spasm) will describe dysphagia for liquid and solids while structural disorders will cause dysphagia for solids only. As the calibre of the oesophagus narrows, the size of the bolus required to cause obstruction becomes progressively smaller.

If the problem is likely to be a structural oesophageal disorder, the following enquiry will define the likely cause.

How long has dysphagia been present; is it intermittent, is it progressive?

Longstanding dysphagia is compatible with a benign condition. Slowly progressive, longstanding dysphagia, particularly if reflux is or has been experienced, is highly suggestive of a peptic stricture. A short history of dysphagia particularly with rapid progression (weeks or months) and associated weight loss is highly suggestive of oesophageal cancer. Longstanding, intermittent, non-progressive dysphagia purely for solids is indicative of a fixed structural lesion such as a distal oesophageal ring or proximal oesophageal mucosal web.

What does the patient do when the bolus sticks?

Sipping water will frequently relieve obstruction due to a structural lesion causing solid bolus dysphagia. However, if the patient sips water in the context of a solid bolus impaction, this will result in immediate regurgitation of the water indicative of complete bolus obstruction. If the bolus is catching very high (e.g. at the cricopharyngeus) patients learn very quickly not to sip water as it results in immediate coughing and spluttering due to laryngeal penetration.

Does the patient regurgitate?

While regurgitation can be associated with solid bolus hold-up during a meal, spontaneous regurgitation between meals (generally fluid and ‘frothy’ saliva) is highly suggestive of dysmotility (see below).

If the problem is likely to be an oesophageal motility disorder, the following enquiry will define the likely cause.

The three cardinal features of oesophageal dysmotility are dysphagia (for solids and liquids), chest pain and regurgitation.

Regurgitation during the meal as well as spontaneous regurgitation between meals or at night (generally fluid and saliva) is highly suggestive of dysmotility. The regurgitated fluid/food is generally not noxious to taste (unlike reflux-related regurgitation).

Does the patient experience chest pain or discomfort?

Oesophageal spasm and achalasia typically cause chest pain. While frequently described as heavy or crushing, it can be indistinguishable from the typical ‘heartburn’ of reflux. The pain frequently occurs during the meal but can be quite unpredictable and sporadic or nocturnal. Sipping antacids or even water can relieve the related dysmotility, thus further confusing distinction from reflux pain.

If oesophageal dysmotility is strongly suspected, distinction between achalasia and oesophageal spasm can be difficult at times. Achalasia is very much more common than spasm. In achalasia, chest pain is more prominent early in the disease, but over the years tends to diminish and may disappear as dysphagia and regurgitation worsen. In contrast, the chest pain of spasm is the predominant symptom and can be quite severe. Due to poor oesophageal clearance, regurgitation is frequently more impressive in achalasia than it is in the case of spasm. The oesophagus generally dilates over time in the context of achalasia, but this is less prevalent with spasm. Finally, there can be significant overlap between the two syndromes and spasm can evolve into more typical achalasia over time as they both share a similar underlying inhibitory neuropathic process. Oesophageal motility disorders can be classified as either primary (e.g. achalasia or diffuse oesophageal spasm) or secondary (e.g. scleroderma) (Table 2.3).

TABLE 2.3 Classification of oesophageal motility disorders

Primary

Secondary

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