- Dysphagia – difficulty swallowing. Clinically, this includes the inability to initiate swallowing and / or the sensation that swallowed solids or liquids adhere to the esophagus.
- Odinophagy refers to pain with swallowing. In some disorders, dysphagia may be accompanied by odnophagia.
- Globus hystericus describes the sensation of a “lump in the throat,” which is momentarily relieved by swallowing.
Preesophageal or orophysophageal dysphagia
Patients with this disorder have problems with the initial stages of swallowing. They may have difficulty delivering food to the larynx. If the food passes normally to the larynxopharynx, the presence of pain, intra- or extraluminal mass lesion, or neuromuscular disorder may interfere with the ordered sequence of pharyngeal contraction, closure of the epiglottis, relaxation of the upper esophageal sphincter and the occurrence of peristalsis, contraction of the striated muscle of the upper esophagus.
Signs and symptoms. These patients usually cough and expel swallowed food through their mouth and nose, or inhale when trying to swallow. Their symptoms are worse with liquids than with solids. They may have “wet” voice quality, reduced cough, congestion in the upper respiratory tract and aspiration pneumonitis.
- The state of the central nervous system. Cerebral vascular incidents (bulbar or pseudobulbar palsy), multiple sclerosis, amyotrophic lateral sclerosis, Wilson’s disease, Parkinson’s disease, Friedreich’s ataxia, back shifts, brain stem tumors, paraneoplastic disorders, reaction to drugs or toxins, nervous disorders of the central nervous system and other congenital malformations of the system.
- The condition of the peripheral nervous system. Poliomyelitis (bulbar), diphtheria, rabies, botulism, diabetes mellitus, demyelinating diseases, Guillain-Barr syndrome.
- Disorders of the mioneural transition. Myasthenia gravis, Eaton-Lambert syndrome.
- Muscle disorders. Dermatomyositis, muscular dystrophies, myotonic disorders, congenital myopathies, metabolic myopathies (thyrotoxicosis, myodema, steroid myopathy), collagen vascular diseases, amyloidosis.
- Toxins Tetanus, botulism, teak paralysis, arsenic, lead, mercury poisoning.
- Local structural lesions. Diseases of the mouth, pharynx and larynx.
- Infection or inflammation. abscess; tuberculosis; syphilis; viral, bacterial and fungal infections; Lyme disease diphtheria; rabies.
- Cosmic defeat. Neoplasms, congenital tissues, Plummer-Winson syndrome.
- External compression. Cervical spine, lymphadenopathy, thyromegaly, Zenker diverticulum.
- Injury. Surgical recovery, ingestion of a foreign body, caustic injury.
Violations of the motility of the upper esophageal sphincter. Hypertensive upper esophageal sphincter, hypotensive upper esophageal sphincter with esophageal-pharyngeal regurgitation, abnormal relaxation of the upper esophageal sphincter (incomplete relaxation: achalasia of the cricopharyngeal, premature closure, delayed relaxation).
Esophageal dysphagia describes difficulties in transporting food through the esophagus after the bolus has been successfully transferred to the proximal lumen of the esophagus. Any disorder, structural or neuromuscular, affecting the body of the esophagus, lower esophageal sphincter or gastroesophageal junction, can lead to dysphagia or a feeling of “jamming” of food behind the sternum. If the patient can localize the symptom at some point along the sternum, a good correlation with the anatomical site is possible. However, if symptoms are felt at the sternum level, the anatomical site of the lesion cannot be predicted.
Structural abnormalities are usually caused by discrete damage, such as a neoplasm, stricture, or external compression, which interferes with the transport of an ingested bolus. Initially, dysphagia occurs with solid foods. However, since the lumen narrows with an increase in lesions, the passage of fluids also worsens.
Squamous cell carcinoma accounts for approximately one third of all cases of esophageal cancer. Excessive alcohol consumption and cigarette smoking seem to increase the risk. Other predisposing factors include head and neck cancer, Plummer-Winson syndrome (anemia and esophageal network), tylosis, achalasia and alkali stricture.
Esophageal adenocarcinoma accounts for about two thirds of esophageal cancer. It is believed that it arises as a result of the expansion of carcinoma of the stomach, esophagus or, more often, columnar metaplasia of the esophagus (Barrett’s epithelium).
Kaposi’s sarcoma, lymphoma, melanoma and metastatic tumors of the lungs, pancreas, breast and other structures can also affect the esophagus.
Benign esophageal tumors are rare and make up less than 10% of esophageal tumors. These tumors most often arise from neuro-mesenchymal elements. Leiomyomas arising from the smooth muscles of the esophagus are the most common. These intramural lesions are covered with normal squamous epithelium of the esophagus. They protrude into the lumen, which ultimately causes a narrowing of the passage. Other lesions, such as fibroadenomas, although rare, can become very long and large and can cause obstruction.
- Peptic strictures. Most esophageal strictures are found in the distal or middle esophagus and are the result of chronic inflammation caused by gastroesophageal reflux. Peptic strictures are usually benign, but those associated with Barrett’s epithelium can be malignant.
- Burns caused by ingestion of caustic substances (e.g. strong alkalis and acids) can lead to esophageal stricture in one or more places in the esophagus.
- Some pill-shaped medications can settle in the esophagus and cause local inflammation, ulceration, and stricture.
- Foreign bodies (such as coins or button batteries) can be swallowed and cause obstruction or damage to the esophagus.
Rings and tissues are usually thin peripheral mucous shelves that protrude into the lumen of the esophagus and cause intermittent dysphagia, especially in the solid. Spider webs are found in the upper esophagus and may be associated with iron deficiency anemia (Plummer-Winson syndrome).
Rings (Schatzki) are most commonly found in the gastroesophageal junction. Shatsky’s rings seem to be associated with chronic gastroesophageal reflux. Most of them contain only elements of the mucous membrane; however, thicker ones may also contain a thickened muscle layer.
External compression. The lumen of the esophagus can be narrowed by compression by external damage. These lesions include the following: mediastinal tumors, primary or metastatic.
Vascular lesions, such as an aberrant right subclavian artery (dysphagia lusoria), an enlarged aneurysmal aorta, or an enlarged heart chamber.
Cervical osteoarthritis and bone spurs.
Esophageal diverticula can cause dysphagia when they become large and stretch with food and secretions. They tend to occur in three main parts of the esophagus: just above the upper esophageal sphincter (Zenker), in the middle (extension) and near the diaphragm (epiphrenic). It is believed that the diverticulums of Zenker and epiphrenics are the result of motor disorders of the esophagus. Despite the fact that diverticula of the middle esophagus are associated with stretching on the walls of the esophagus by external inflammatory and fibrotic processes (for example, tuberculosis or sarcoidosis), they can also be the result of abnormal motility of the esophagus.
Gastroesophageal reflux. Reflux of gastroduodenal contents into the esophagus can cause dysphagia in some patients, especially if severe inflammation, ulceration, or stricture develops. With the resolution of inflammation and edema, dysphagia can decrease. In some patients, gastroesophageal reflux can lead to impaired esophageal motility, which can lead to dysphagia and chest pain.
Neuromuscular or motor disorders lead to dysphagia of both fluids and solids due to aberrant peristalsis. These disorders are present in approximately half of patients with dysphagia without obvious structural abnormalities. With these disorders, peristalsis is either absent, or weak, or too strong and stable, or not coordinated. The function of the lower esophageal sphincter may also be abnormal. The pressure of the lower esophageal sphincter may be too high or low, and the sphincter may not completely relax when swallowed.
Primary motor disorders
Achalasia is a violation of the smooth muscle function of the esophagus with three diagnostic prerequisites. Firstly, there is a complete absence of primary and secondary peristalsis in the smooth muscles of the esophagus. Skeletal muscle function is generally normal. Secondly, the lower esophageal sphincter does not completely relax when swallowed. Thirdly, the pressure in the lower esophageal sphincter is usually high. The absence of peristalsis and a stable zone of high pressure in the gastroesophageal connection leads to a delay in swallowed material and secretions in the oral cavity in the esophagus with a gradual loss of tone and progressive dilatation of the esophagus body.
Cause. Achalasia, most likely, is the result of neuronal disorders, and not primary myopathy. Lesions were found in the dorsal part of the vagus nerve in the brainstem, in the vagus trunks and in the myenteric ganglia of the esophagus. Secondary achalasia may resemble primary achalasia. This may be the result of invasion of the tumor into the lower esophageal sphincter, narrowing of malignant nodes or paraneoplastic syndromes.
Signs and symptoms. Patients with achalasia constantly suffer from dysphagia of both solids and liquids. Sometimes in the early stages of the disease and in patients with severe achalasia, chest pain may occur. Regurgitation of the contents of the esophagus, often with aspiration of the trachea, is a common complication of the disease.
Achalasia treatment is intended to reduce pressure in the lower esophageal sphincter. This allows the aperistric esophagus to empty upright. Myotomy of the lower esophageal sphincter can be performed surgically (open or laparoscope) or by forced dilation using an inflatable pneumatic oral balloon dilator or by intramuscular injection of botulinum toxin endoscopically. Medical management of achalasia is usually unsuccessful. In some patients, calcium channel blockers can reduce pressure in the lower esophageal sphincter and lead to temporary symptomatic improvements.
Diffuse spasm of the esophagus. This subject makes up about 10-15% of patients with impaired esophageal motility. Patients with this disorder have simultaneous high amplitude contractions in the smooth muscle of the esophagus. Skeletal muscle function is normal. “Spastic” waves are usually initiated by swallows, but can occur randomly, interspersed with normal peristalsis. The lower esophageal sphincter may have normal or high pressure and may not completely relax when swallowed.
Signs and symptoms. In these patients, dysphagia is intermittent. This happens with both liquids and solids. This is sometimes exacerbated by hot or cold food and can cause chest pain. In fact, chest pain with diffuse spasm of the esophagus is often confused with angina pectoris. Therefore, it is important for these patients to rule out possible heart disease.
Treatment of diffuse esophageal spasm is usually aimed at reducing the frequency and intensity of simultaneous contractions. Smooth muscle relaxants, including nitrates (for example, nitroglycerin, 0.4 mg sublingually variable and pr); isosorbide dinitrate, 30 mg per os (po) 30 minutes of alternating current; hydralazine 25 to 50 mg orally three times a day; calcium channel blockers (e.g., nifedipine, 10-20 mg, four times a day); psychotropic drugs (for example, diazepam 1-5 mg orally four times a day; trazodone 50-100 mg orally twice a day; doxepin 50 mg orally, hour); and anticholinergics (eg, dicyclomine 10–20 mg orally four times a day) were tested with variable result.
Since in patients with dysphagia secondary to dysmobility, abnormal motility is not always documented, attempts can be made to provoke symptoms and obtain gauge data using drugs. Edrofonium is the most tolerated and most effective drug available today.
Bougienage and pneumatic dilatation sometimes provide temporary relief of symptoms. In difficult cases, surgical myotomy can be tried. The result is often varied, and successful relief of symptoms is rare.
“Energetic achalasia.” Some patients have a partial match between diffuse spasm of the esophagus and achalasia called achalasia. In this state, in addition to simultaneous high-amplitude contractions in the distal esophagus, as with diffuse spasm of the esophagus, the function of the lower esophageal sphincter is similar to that of achalasia. Symptoms are usually chest pain and dysphagia. Such a coincidence, as well as the transition from diffuse spasm of the esophagus to achalasia in some patients, suggests that these two disorders can be different manifestations of the spectrum of esophageal dysfunction in smooth muscles.
The esophagus nutcracker or “super compressor” is a motor disorder that occurs in about half of patients with esophageal chest pain and in one tenth of patients with dysphagia. These patients have normal lower esophageal sphincter function and peristalsis; however, the contraction amplitude is usually two to three times higher than the normal value. Most of these patients also have an abnormal lengthening of the peristaltic wave. A subgroup of patients with waves of normal amplitude reduction, but of long duration, was also described.
Symptoms of patients with an esophageal nutcracker are similar to those associated with diffuse spasm of the esophagus. Patients may have prolonged chest pain, which may be nocturnal, and intermittent dysphagia. The esophagus The nutcracker can develop into a diffuse spasm of the esophagus, suggesting that these disorders are related. Treating an esophageal nutcracker is similar to treating a diffuse esophageal spasm.
Nonspecific disorders of the motility of the esophagus. Most patients with symptoms of esophageal motility impairment cannot be clearly divided into specific groups. The frequency of these disorders of the peristaltic wave or function of the lower esophageal sphincter is at least five times higher than with achalasia and diffuse esophageal spasm combined. Patients may have an isolated anomaly of the lower esophageal sphincter (high blood pressure, incomplete relaxation, hypertonic lower esophageal sphincter) with abnormal contractions of the esophagus or without them (increased amplitude or duration, simultaneous contractions, involuntary waves).
Treatment. There is no reliable therapy for patients with non-specific esophageal disorders. As with diffuse esophageal spasm, smooth muscle relaxants with variable results were tried. Probing can provide temporary relief in some patients.
Patients with diabetes mellitus may have abnormal motility of the esophagus, such as poor peristaltic wave propagation and diffuse spasm, most likely due to visceral neuropathy.
Secondary motor disorders. Esophageal smooth muscle dysfunction may be associated with a number of systemic disorders.
In approximately 80% of patients with scleroderma, especially those with the Raynaud phenomenon, the peristalsis amplitude is reduced in the smooth muscle of the esophagus with reduced pressure in the lower esophageal sphincter. Initially, the disorder seems nervous; however, as disease progresses, collagen deposition and smooth muscle fibrosis are observed. These patients cause severe reflux esophagitis, which is often complicated by the formation of Barrett’s stricture and esophagus.
Other diseases Disorders of esophageal motility associated with scleroderma have been reported in some patients with other diseases of the collagen vessels and Raynaud’s phenomenon. Patients with polymyositis and lupus may also have esophageal dysfunction in smooth muscles.
An achalosing disease is considered a secondary disease with Chagas disease (Trypanosoma cruzi infection).
Tumors of the mediastinum, lower esophagus, gastroesophageal junction and gastric cardia, as well as lymphoma, pancreatic cancer and bronchogenic cancer, can also manifest as achalasia. Tumors can invade the micellar plexus or cause obstruction in the gastroesophageal junction; thus, the aperistal may be secondary to neural invasion or a reaction to obstruction of the lower esophageal sphincter.
Chronic idiopathic intestinal pseudo-obstruction usually affects the esophagus, as well as all other parts of the gastrointestinal tract. The esophageal abnormality includes aperistalsis and incomplete relaxation of the lower esophageal sphincter, causing functional obstruction. Patients with this disease usually have either congenital or acquired neuromuscular degeneration of the entire intestine, affecting the plexuses and mental ganglia.
Reflux esophagitis and impaired esophageal motility. It has been shown that in patients with gastroesophageal reflux and reflux esophagitis there are a number of disorders of smooth muscle function. These include low pressure in the lower esophageal sphincter; abnormal, long periods of relaxation of the lower esophageal sphincter; and reduced esophagus clearance due to disturbance of the primary and secondary peristaltic waves. It is difficult to determine whether these defects are the main cause of reflux or the result of associated esophagitis.