Ronald Estrada Seminario

Dysphagia is the sensation of hindering the passage of food from the mouth to the stomach. Patients report that food stalls, does not move, stops, or simply does not go down as it should.

Dysphagia is a common symptom, occasionally reporting associated pain (odynophagia); reason why a detailed and exact anamnesis suggests its etiology and allows to correctly define the cause in 80 to 85% of patients.

Pathophysiology and clinic

Multiple factors are involved in the pathophysiology of dysphagia, alterations occur in the various mechanisms of swallowing, peristalsis, or the function of the upper (UES) or lower esophageal sphincters (LES).

The coordinated motor pattern of the esophagus that is initiated by the act of swallowing is called primary peristalsis. A rapid and progressive pharyngeal contraction moves the bolus through the relaxed UES into the esophagus. As the LES closes, a progressive circular contraction begins in the upper esophagus and advances distally through the esophageal body to drive the bolus through the relaxed LES. Then it closes with a prolonged contraction.

Secondary peristalsis is a progressive contraction in the esophageal body, which is not induced by swallowing but by stimulation of sensory receptors in the esophageal body, bolus distension.

Tertiary peristalsis is a scanning wave in the smooth muscle segment of the esophagus that generally responds as a defensive mechanism to the presence of gastroesophageal reflux.

If these contractile movements do not develop orderly or do not progress, the food bolus accumulates and distends the lumen of the esophagus causing the dull discomfort that constitutes dysphagia.

Motor disorders at the level of the UES and cervical esophageal region are mainly due to a failure in sequential excitation through extrinsic innervation or from striated muscle disease.

Motor disorders at the level of the distal esophageal body and LES region are mainly due to two groups of abnormalities. Firstly, hypomotility that manifests with contractions of less amplitude or even absence and is frequently seen in the elderly (presbyophagus) or in scleroderma. In the LES, low pressure is observed at rest, which is manifested with gastroesophageal reflux.

Secondly, hypermobility and in this case the swallowing waves can be of great amplitude, prolonged or repetitive (esophageal spasm); spontaneous contractions are usually frequent, the intraesophageal pressure is feasible to be elevated, the LES is hypertensive, hypersensitive to excitatory stimuli with little or no relaxation during swallowing (achalasia).

This hypermobility promotes functional obstruction with chest pain and symptoms of impaired traffic.

Since these motor abnormalities sometimes do not appear with each swallow, dysphagia can present paroxysms.

Mechanical narrowing of the esophageal lumen can interrupt the orderly passage of the bolus despite adequate peristaltic contractions.

In minimally obstructive lesions, dysphagia occurs only with large, poorly chewed solid boluses of foods such as meat or dry bread; Lesions that completely obstruct the esophageal lumen are symptomatic for both solids and liquids.

Classification

Oropharyngeal dysphagia:  The most common causes are neuromuscular diseases that affect the hypopharynx and the upper part of the esophagus. The patient is unable to initiate swallowing so he repeatedly swallows to propel the bolus from the hypopharynx through the EES into the body of the esophagus. This oropharyngeal or transfer dysphagia is located specifically at the level of the cervical esophagus region and appears in the first second of swallowing.

In the case of liquids, they frequently enter the respiratory tract and manifest with a cough accompanying dysphagia; in recurrent cases it is accompanied by lung infections.

Hoarseness may appear as a reason for consultation due to dysfunction of the recurrent laryngeal nerves or in case of muscular diseases, there is dysarthria or pharyngonasal regurgitation, due to weakness of the soft palate or of the constrictor muscles of the pharynx.

Esophageal dysphagia: Motility disorders or mechanical obstructive injuries are causes of this type of dysphagia. In the analysis of the same it is important to know what type of food produces the symptom, how is its evolution over time (intermittent or progressive) and if it is accompanied by heartburn (retrosternal burning).

Dysphagia that occurs with both solids and liquids is probably due to esophageal motility disorders and in this case, patients try to alleviate the symptom with repeated swallowing, raising the arms above the head or moving the shoulders back. In spastic motility disorders, sensitivity to hot or cold liquids and chest pain predominate. In achalasia, soft regurgitation of undigested food generally accompanies dysphagia at night. In scleroderma what accompanies Reynaud's phenomenon is severe heartburn. Striated muscles are affected in myasthenia gravis, producing palpebral ptosis and may debut with dysglusia and then dysphagia. Paterson Kelly or Plummer-Vinson's disease (sideropenic dysphagia) is associated with dysglusia due to the presence of membranes located in the upper esophagus, glossitis, iron deficiency anemia, and achlorhydria. In Zenker's disease (pharyngoesophageal diverticulum), dysphagia sets in as the patient ingests food, the diverticulum fills, and compresses the esophagus causing dysphagia.

In dysphagia that appears after the intake of solids and never of liquids, generally, the cause is mechanical obstruction; in this case it is insidious, selective and progressive, first to solids (meats) then to semi-solids (porridge) and finally to liquids (water). In this case, the main differential diagnosis is peptic esophageal narrowing and carcinoma.

Study methodology

Interrogation: The physician should assess the location, form of onset, course, selectivity, and concomitant symptoms.

Radiology of the esophagus with double contrast and gastroduodenal series. Radiology will generally show the different functional and organic pathologies of the esophagus. The double-contrast esophagogram does not establish an etiological diagnosis but rather an organic lesion, in particular two very common pathologies, such as esophageal cancer and achalasia with megaesophagus, where the study must always be completed with endoscopy, biopsy and cytology. Gastroduodenal series will be performed to rule out gastric ceiling cancer spread to the lower esophagus.

Endoscopy: It allows the topographic macroscopic diagnosis of the lesion to be made, but fundamentally it facilitates biopsy and cytology, which will ultimately be the methods that will give the definitive etiological diagnosis.

Biopsy and cytology. The biopsy, in addition to the etiological diagnosis of cancer, will indicate whether it is an epidermoid carcinoma or an adenocarcinoma, and therefore will provide guidance regarding therapeutic, medical (cobalt therapy) or surgical behavior.

Other studies: The study of esophageal motility and the determination of the intraesophageal pH confirmed the diagnosis of achalasia. Esophageal motility is investigated fluoroscopically by observing the swallowing of the barium bolus. If abnormalities exist, they are confirmed by manometric records, where the pressure generated by the peristaltic wave and its ability to drive the bolus are evaluated, and also if the sphincter relaxation is complete, of adequate duration and coordinated with the peristaltic wave.