Dysphagia is defined as difficulty in swallowing. The term odynophagia is used to indicate painful swallowing. Odynophagia is marked in ulcerative / inflammatory lesions of oral cavity and food passages.
Physiology of deglutition:
In order to better understand dysphagia physiology of deglutition should be understood. The process of swallowing is known as deglutition. The act of swallowing can be divided into three stages for easy understanding.
1. Oral stage: This is the only voluntary stage in the act of swallowing. It consists of:
Mastication of food making it into a bolus fit to be swallowed. The main muscles involved in the act of chewing are:
These muscles of mastication are supplied by the mandibular division of the trigeminal nerve.
The tongue plays a vital role in this phase and is supplied by the hypoglossal nerve.
The facial nerve also plays a vital role by supplying the Buccinator and orbicularis oris. These muscles prevent drooling of food from the mouth and keeps the contents inside the oral cavity by their contraction. In patients with facial palsy the buccinator and orbicularis oris are paralyzed causing drooling on that side of the mouth.
2. Pharyngeal stage: Is involuntary and is very complex. It passes the masticated food through the oropharynx, through the cricopharynx into the upper oesophagus. This passage is facilitated by relaxation of cricopharyngeus muscle.
During this phase the nasopharynx is shut off from the oropharynx by the contraction of muscles of soft palate and posterior pharyngeal wall, thus preventing nasal regurgitation of masticated food.
During this phase the laryngeal musculature should also constrict to prevent aspiration.
This stage relies on the coordination of many muscle groups including the muscles of the soft palate which is supplied by the 5th, 7th, 9th and 12th cranial nerves.
The pharyngeal muscles also play a vital role in propelling the food through the cricopharynx. These muscles are supplied by the 9th and 10th cranial nerves. The cricopharyngeus muscle is supplied by the 10th cranial nerve and sympathetic nerves.
Neurological disorders affecting the pharynx impair swallowing by altering motor and / or sensory functions in the oral and pharyngeal stages.
3. Oesophageal stage: This stage is again involuntary. It propels the food bolus down the oesophagus. This phase is mediated by the 10th and sympathetic nerves. This phase is dependent on the peristalsis of the oesophageal musculature. During swallowing, peristaltic waves pass down the oesophagus with waves of positive pressure reaching (50-100mmHg). When liquids and semisolids are swallowed, there is an initial negative wave caused by elevation of the larynx drawing on the cervical oesophagus. This is followed by a abrupt positive wave, which coincides with the entry of the bolus into the oesophagus. This wave is known as the primary peristaltic wave. This wave is followed by a smaller positive wave known as the stripping wave, which clears the left over food material from the oesophagus.
Secondary peristaltic waves are generated in the oesophagus in response to dilatation of oesophagus
Tertiary peristaltic waves are irregular, non propulsive contractions involving large segments of oesophagus. This occurs during emotional stress.
When fluid is swallowed, it may be projected from the pharynx to the oesophago gastric junction in about 1 second flat (when the subject is standing). This occurs well ahead of the peristaltic wave. Thus it should be borne in mind that this fact causes burns due to swallowing of corrosive fluids more at the distal end of oesophagus.
The rate of progression of peristaltic wave varies in different portions of oesophagus:
1. In the upper part of oesophagus the peristaltic wave progresses rapidly.
2. The waves are more sluggish in the lower third of oesophagus.
These differences are due to the fact that the musculature is striated in the upper portion of oesophagus and smooth at the lower 1/3 of oesophagus.
Cause of dysphagia could be preoesophageal (i.e. due to disturbance in the oral / pharyngeal phases of deglutition) or esophageal (when disturbance is in esophageal phase). This classification is rather useful as majority of preoesophageal causes can easily be excluded by physical examination. Esophageal causes ofcourse require investigation.
Preoesophageal causes of dysphagia:
Trismus, fractures of mandible, tumors of upper/ lower jaw and disorders of TM joint.
Poor salivary secretion:
This condition is seen in xerostomia following radiotherapy / Mikulicz's disease. Lack of salivary secretion causes lubrication problems making the bolus rather dry adding to swallowing difficulties.
Distrubances in tongue mobility:
Paralysis of tongue muscles, painful ulcers involving tongue, tumors of tongue, and in patients who have undergone total glossectomy swallowing is rather difficult because the propulsive action of tongue is lost.
Presence of cleft palate / oroantral fistula can interfere with oral cavity phase of swallowing.
Lesions of floor of buccal cavity:
Elevatory movement of the floor of buccal cavity plays an important role in propulsion of food bolus into the esophagus. This important movement could be hampered in the presence of stomatitis, ulcerative lesions in the floor of the mouth and Ludwig's angina.
Disturbances in pharyngeal phase of deglutition:
During the normal swallow, food bolus should enter the pharynx and then be directed towards esophageal opening. All unnecessary communications into the nasopharynx, larynx and oral cavity should be closed. Disturbances involving this phase could be due to:
Obstructive lesions of pharynx:
This include tumors of tonsil, soft palate, pharynx, tongue base, supraglottic larynx, and hypertrophic tonsils.
Inflammatory lesions of pharynx:
Inflammatory conditions like acute tonsillitis, peritonsillar abscess, retropharyngeal abscess, parapharyngeal abscess, acute epiglottis can interefere with this phase of swallowing mechanism as these conditions cause intense pain.
Conditions that cause spasm of pharyngeal musculature like tetanus and rabies can interfere with swallowing.
This includes soft palate paralysis which cause regurgitation into the nasal cavity. Paralysis of larynx can cause aspiration of food into the larynx.
Esophageal causes of dysphagia:
These include intraluminal / extraluminal lesions that cause compression of esophagus.
Intraluminal obstruction - can occur in aresia of esophagus, impacted foreign body, strictures, tumors (both benign and malignant).
Conditions involving the esophageal wall:
This could be acute / chronic esophagitis, motility disorders. Motility disorders could be hypomotility disorders and hypermotility disorders.
Hypomotility disorders include achalasia, scleroderma and amyotrophic lateral sclerosis.
Hypermotility disorders include cricopharyngeal muscle spasm, diffuse esophageal spasm.
Lesions causing extraesophageal compression can affect esophageal phase of swallowing include:
Enlarged thyroid gland
Presence of vascular rings (dysphagia lusoria)
An accurate history can invariably detect the cause for dysphagia. direct investigation combined with an accurate history increases the diagnostic yield to nearly 80%.
Long standing intermittent sensation of lump in the thorat not associated with history of weight loss in a young women always points towards the diagnosis of globus. Globus is defined as a passive symptom that usually presents itself at rest and is frequently relieved by the act of swallowing.
On the contrary dysphagia that is progressive and is associated with weight loss needs to be investigated to find out the exact cause.
The following points should be focussed during history taking:
1. Nature of dysphagia (whether it is for solids, semisolids or liquids)
2. Duration of dysphagia
3. Timing of dysphagia (whether it is continuous / intermittent)
4. Rate of progression of dysphagia (months, weeks or years)
5. Weight loss
6. Other associated symptoms like aspiration, regurgitation, coughing, choking, dysponia, dyspepsia, haemoptysis, haematemesis and referred otalgia
7. History of substance abuse (alcohol, tobacco)
A comprehensive otolaryngologic examination of oral cavity, pharynx, larynx can be performed in the outpatient department, and invariably a correct diagnosis can be arrived at. Subtle clues may present itself during examination of oral cavity and oropharynx that could point at the diagnosis. Presence of angular chelitis and a bald ironed out tongue indicates the presence of anaemia and that too in a female it could indicate the presence of post crioid web.
The three areas of the oropharynx i.e. soft palate, tonsils and tonsillar fossae should next be examined. Deep seated lesions involving posterior third of tongue are not readily visible. In co-operative patients palpation could reveal the abnormality.
Flexible esophagoscopy should be performed to definitely look out for esophageal lesions. Intraluminal lesions and narrowings caused by extraluminal lesions could be clearly made out during flexibule esophagoscopy. Biopsy of suspicious looking lesions can also be performed in the same sitting.
This is a dynamic imaging procedure that is used to characterize oropharyngeal dysphagia. Real time visualization of the integrated movements that take place during oral preparative, oral and pharyngeal stages of swallowing will help to identify structural and functional abnormalities that contribute to dysphagia. This is a multidisciplinary assessment tool that is used in conjunction with speech and language therapists and radiologists.
During this test the patient is asked to swallow food of varying volumes and viscosities during the fluroscopy and the findings are scored with the swallowing performance status scale.
This test is indicated for the evaluation of dysphagia that is not definitively diagnosed by means of endoscopy / radiology. This is considered to be the most accurate method to diagnose primary esophageal motility disorders like achalais and diffuse esophageal spasm.