Updated: Jan 31, 2022
  • Author: Nam-Jong Paik, MD, PhD; Chief Editor: Elizabeth A Moberg-Wolff, MD  more...
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Practice Essentials

As typically defined, dysphagia is a condition in which disruption of the swallowing process interferes with a patient’s ability to eat. It can result in aspiration pneumonia, malnutrition, dehydration, weight loss, and airway obstruction. The goals of dysphagia treatment are to maintain adequate nutritional intake for the patient and to maximize airway protection.

Chest radiography is a simple assessment for pneumonia. The image below shows aspiration of liquid barium into the distal bronchus.

Delayed posteroanterior chest image shows aspirati Delayed posteroanterior chest image shows aspiration of liquid barium into the distal bronchus.

Signs and symptoms of dysphagia

Signs and symptoms of oral or pharyngeal dysphagia include the following:

  • Coughing or choking with swallowing

  • Difficulty initiating swallowing

  • Food sticking in the throat

  • Sialorrhea

  • Unexplained weight loss

  • Change in dietary habits

  • Recurrent pneumonia

  • Change in voice or speech (wet voice)

  • Nasal regurgitation

Signs and symptoms of esophageal dysphagia include the following:

  • Sensation of food sticking in the chest or throat

  • Change in dietary habits

  • Recurrent pneumonia [1]

  • Symptoms of gastroesophageal reflux disease (GERD), including heartburn, belching, sour regurgitation, and water brash

Other associated factors/symptoms of dysphagia include the following:

  • General weakness

  • Mental status changes

See Clinical Presentation for more detail.


Since history and physical examination alone may not be adequate to make a diagnosis in cases of silent aspiration, additional diagnostic tests, such as the following, may be needed:

  • Transnasal esophagoscopy

  • Cervical auscultation

  • Blood tests: Including thyroid-stimulating hormone, vitamin B-12, and creatine kinase; may be useful, especially in neurogenic dysphagia

  • Imaging studies: May include videofluoroscopy, computed tomography (CT) scanning, magnetic resonance imaging (MRI), and chest radiography

  • Endoscopic examination

  • Esophageal pH monitoring: The criterion standard for diagnosing reflux disease

  • Pulmonary function tests

See Workup for more detail.


Pharmacologic treatment

Medications used in the treatment of dysphagia include the following:

  • Botulinum toxin type A (BoNT-A)

  • Diltiazem

  • Cystine-depleting therapy with cysteamine

  • Nitrates

Dietary treatment

Dietary modification is the key component in the general treatment program of dysphagia. Diets for patients with dysphagia include the following:

  • Dysphagia diet 1: Thin liquids (eg, fruit juice, coffee, tea)

  • Dysphagia diet 2: Nectar-thick liquids (eg, cream soup, tomato juice)

  • Dysphagia diet 3: Honey-thick liquids (ie, liquids that are thickened to a honey consistency)

  • Dysphagia diet 4: Pudding-thick liquids/foods (eg, mashed bananas, cooked cereals, purees)

  • Dysphagia diet 5: Mechanical soft foods (eg, meat loaf, baked beans, casseroles)

  • Dysphagia diet 6: Chewy foods (eg, pizza, cheese, bagels)

  • Dysphagia diet 7: Foods that fall apart (eg, bread, rice, muffins)

  • Dysphagia diet 8: Mixed textures

Because fluid intake is restricted in most patients with dysphagia, these individuals are at risk of dehydration. Therefore, the patient's hydration status must be closely monitored.

Exercise and facilitation techniques

The following types of exercise can be recommended to patients with dysphagia:

  • Indirect (eg, exercises to strengthen swallowing muscles)

  • Direct (eg, exercises to be performed while swallowing)

Facilitation techniques used in the treatment of dysphagia include the following:

  • Somatosensory stimulation: In the form of an electrical current applied to the pharynx

  • Deep pharyngeal neuromuscular stimulation (DPNS)

  • Tactile-thermal stimulation (TTS)

Compensatory techniques

Maintaining oral feeding often requires compensatory techniques to reduce aspiration or improve pharyngeal clearance. These include the following:

  • Use of the chin-tuck position

  • Rotation of the head to the affected side

  • Tilting of the head to the strong side

  • Lying on one's side or back during swallowing

  • Supraglottic swallow

  • Bolus-clearing maneuvers

Enteral feeding

  • Nasogastric tube (NGT) feeing

  • Oroesophageal tube feeding

  • Percutaneous endoscopic gastrostomy (PEG)

Surgery for chronic aspiration

  • Medialization: This helps to restore glottic closure and subglottic pressure during the swallow

  • Laryngeal suspension: The larynx is in a relatively protected position under the tongue base

  • Laryngeal closure: This may be performed to close the glottis off, in this way protecting the airway at the expense of phonation

  • Laryngotracheal separation-diversion: This procedure may be done to separate the airway from the alimentary tract

See Treatment for more detail.



The term dysphagia, a Greek word that means disordered eating, typically refers to difficulty in eating as a result of disruption in the swallowing process. Dysphagia can be a serious health threat because of the risk of aspiration pneumonia, malnutrition, dehydration, weight loss, and airway obstruction, and it exerts a large influence on the outcome of rehabilitation (eg, length of hospital stay, mortality/morbidity). [2] (See Prognosis and Treatment.)

Dysphagia can be secondary to defects in any of the 3 phases of swallowing, which are as follows [3] :

  • Oral phase: Which involves the oral preparatory phase and the oral transit phase

  • Pharyngeal phase

  • Esophageal phase

A number of etiologies have been attributed to dysphagia in populations with neurologic and nonneurologic conditions. (See Pathophysiology and Etiology.)

Dysphagia should be differentiated from disorders that prevent transfer of food to the mouth or beyond the stomach but that are not characterized by difficulty swallowing. For example, feeding disorder, which is the inability to get food to the mouth, and gastric outlet obstruction, which is the inability of food to pass from the stomach into the small intestine, are not types of dysphagia. On average, 10 million Americans are evaluated for swallowing disorders annually. (See Epidemiology and DDx.)

Advances have been made in the treatment of swallowing disorders, especially with regard to dysphagia-related malnutrition, and with the available tests and management options for swallowing disorders, the prognosis for patients with dysphagia has improved. (See Prognosis, Clinical Presentation, Workup, and Treatment.)

An understanding of the anatomy and physiology of the areas of the body affected by dysphagia is of paramount importance in the diagnosis and management of swallowing disorders (see the image below). Early involvement of specialists such as nutritionists, gastroenterologists, general surgeons, speech-language therapists, and ear, nose, and throat (ENT) surgeons offers a good prognosis for the management of swallowing disorders. (See Treatment.)

Lateral projection of the videoprint of a videogra Lateral projection of the videoprint of a videographic swallowing study shows the epiglottis (E), pyriform sinuses (P), tongue (Tg), trachea (Tr), and vallecula (V).

Pediatric patients

Certain factors make dysphagia in children unique. Successful oral feeding and growth in infants and children depend not only on functional deglutition but also on a broad range of neurodevelopmental skills involving sensory systems, cognition, communication, and gross and fine motor behaviors. [4, 5]

Prematurity by itself and neurologic impairment (eg, cerebral palsy) are common causes of dysphagia in young patients. Children with cerebral palsy typically manage solid boluses more easily than they do liquid boluses and manage small liquid boluses more easily than large liquid boluses.

Congenital structural lesions (eg, choanal atresia, cleft lip and palate, craniofacial syndromes) can interfere with normal anatomic transport of a bolus. [6] Prosthetic devices or adaptive feeding equipment may be necessary.

Gastroesophageal reflux disease (GERD) is a common problem in children. Choking, food refusal, and food "getting stuck" are nonspecific symptoms that may arise because of reflux and esophagitis.

Childhood achalasia appears to be more common in boys than in girls. Regurgitation of food and dysphagia are the most common symptoms. In about 18% of patients, symptoms begin during infancy.

Management of pediatric dysphagia requires a special approach. Cognitive, developmental, and behavioral issues can affect the treatment options. Treatment does not necessarily imply feeding therapy. Tone abnormalities, postural control, adverse behavior, and primitive reflexes should be managed. Hypoxemia can occur while a child with dysphagia eats, so pulse oximetry during mealtime can be useful. [7]

Geriatric patients

The prevalence of dysphagia increases with age, making dysphagia is a major health-care problem in elderly patients. Normal aging alters some aspects of the swallowing function; problems include increased oral and pharyngeal transit times, poor bolus control and coordination, increased magnitude and duration of pharyngeal pressures, and increased incidence of pharyngeal residue after swallowing. [8]

Other factors, such as the following, can cause a predisposition to dysphagia or can aggravate the condition:

  • Poor dentition

  • Atrophy of the tongue and alveolar ridge

  • Diminished taste and smell sensitivity

  • Decreased muscle tone

  • Increased ligamentous laxity

  • Limited laryngeal elevation



Deglutition is the act of swallowing, which allows a food or liquid bolus to be transported from the mouth to the pharynx and esophagus, through which it enters the stomach. Normal deglutition is a smooth, coordinated process that involves a complex series of voluntary and involuntary neuromuscular contractions and typically is divided into distinct phases: oral, pharyngeal, and esophageal. Each stage facilitates a specific function; if the stages are impaired by a pathologic condition, specific symptoms may result.

The process of swallowing is organized with sensory input from receptors in the base of the tongue, as well as in the soft palate, faucial arches, tonsils, and posterior pharyngeal wall; this input is transmitted to the swallowing center, located within the pontine reticular system, through the facial (VII), glossopharyngeal (IX), and vagus (X) cranial nerves.

Information from the swallowing center then is conveyed back to the muscles that help in swallowing through trigeminal (V), facial (VII), glossopharyngeal (IX), vagus (X), and hypoglossal (XII) cranial nerves, with the trigeminal, hypoglossal, and nucleus ambiguus constituting the efferent levels.

The act of swallowing usually interrupts the expiratory phase of ventilation, while the completion of expiration occurs when swallowing ends. In situations in which the swallowing is initiated during the inspiratory phase of ventilation, a brief expiration ensues after the completion of swallowing.

Oral phase

The oral phase of swallowing is divided into the following 2 parts:

  • Oral preparatory phase: The processing of the bolus to render it swallowable

  • Oral propulsive (or transit) phase: The propelling of food from the oral cavity into the oropharynx

With single swallows of liquid, the entire sequence lasts about 1 second. For swallows of solid foods, a delay of 5-10 seconds may elapse while the bolus accumulates in the oropharynx.

Oral preparatory phase

The process begins with contractions of the tongue and striated muscles of mastication. The muscles work in a coordinated fashion to mix the food bolus with saliva, with the taste, temperature, touch, and proprioception senses required to form a bolus of the right size and consistency. (See image below.)

Oral preparatory phase of normal swallowing. Oral preparatory phase of normal swallowing.

Oral propulsive phase

This segment of the swallowing process involves manipulation of the bolus formed in the preparatory stage in the central portion of the tongue. The bolus is then pushed toward the pharynx posteriorly with a sequential anterior-to-posterior tongue elevation in order to trigger the swallowing reflex as the bolus enters the pharyngeal phase.

This process requires that a labial seal be maintained to prevent food from leaking from the mouth and that there be buccal musculature tension to prevent food from getting into the recess between the mandible and cheek. (See the image below.)

Oral propulsive phase of normal swallowing. Oral propulsive phase of normal swallowing.

Pharyngeal phase

The pharyngeal phase is of particular importance, because without intact laryngeal protective mechanisms, aspiration (the passage of food or liquid through the vocal folds) is most likely to occur during this phase. This phase involves a rapid sequence of overlapping events. The soft palate rises, the hyoid bone and larynx move upward and forward, the vocal folds move to the midline, the epiglottis folds backward to protect the airway, and the tongue pushes backward and downward into the pharynx to propel the bolus downward. [9] The tongue is assisted by the pharyngeal walls, which move inward with a progressive wave of contraction from top to bottom.

The upper esophageal sphincter relaxes during the pharyngeal phase of swallowing and is pulled open by the forward movement of the hyoid bone and larynx. This sphincter closes after passage of the food, and the pharyngeal structures then return to the reference position. (See the image below.)

Pharyngeal phase of normal swallowing. Pharyngeal phase of normal swallowing.

The pharyngeal phase of swallowing is involuntary and totally reflexive, so no pharyngeal activity occurs until the swallowing reflex is triggered. This swallowing reflex lasts approximately 1 second and involves the motor and sensory tracts from cranial nerves IX (glossopharyngeal) and X (vagus).

Esophageal phase

In the esophageal phase, the bolus is propelled downward by a peristaltic movement. The lower esophageal sphincter relaxes at initiation of the swallow, and this relaxation persists until the food bolus has been propelled into the stomach. Unlike the upper esophageal sphincter, the lower sphincter is not pulled open by extrinsic musculature. Rather, it closes after the bolus enters the stomach, thereby preventing gastroesophageal reflux. (See the image below.)

Esophageal phase of normal swallowing. Esophageal phase of normal swallowing.

The medulla controls this involuntary swallowing reflex, although voluntary swallowing may be initiated by the cerebral cortex.

An interval of 8-20 seconds may be required for contractions to drive the bolus into the stomach.

Patient education

For patient education information, see the Cancer Center, as well as Cancer of the Mouth and Throat.



Aspiration is a term referring to the passive entry of any food item into the trachea (eg, during inhalation), although the word often is used to denote any entry of a bolus into the trachea in any manner

Penetration refers to the active entry of any food item into the trachea (eg, during swallowing), although the term often is used to denote the entry of any bolus into the laryngeal vestibule

A lesion in the cerebral cortex or the brainstem can cause swallowing disorders as a result of the following:

  • Decrease in range of motion (ROM) of muscles of mastication and bolus propulsion, especially those responsible for buccal, labial, and lingual strength and the cricopharyngeus

  • Decreased sensation

  • Delayed or absent pharyngeal swallowing and reductions in pharyngeal peristalsis [10]

  • Delayed or absent laryngeal adduction and elevation

The locations of specific lesions, however, do not show correlation with findings on computed tomography (CT) or magnetic resonance imaging (MRI) scans.

Disorders of swallowing may be categorized according to the swallowing phase affected. A number of dysphagic problems can be identified during each phase of deglutition.

Oral-phase disorders

Pocketing of food in the mouth, circumoral leakage, and early pharyngeal spill can occur with weakness and poor coordination of the lips, cheeks, and tongue. Weak posterior tongue can lead to abnormal tongue thrusting.

Aspiration of food or drink, especially during inhalation, can occur before pharyngeal swallowing due to premature pharyngeal spillage.

Changes in mental status with cognitive deficits also may affect the initiation of swallowing, increasing the tendency to pocket food in the lateral sulci and leading to possible aspiration.

Logemann's Manual for the Videofluorographic Study of Swallowing cites the following oral-phase swallowing symptoms and disorders [11] :

  • Inability to hold food in the mouth anteriorly due to reduced lip closure

  • Inability to form a bolus or residue on the floor of the mouth due to reduced range of tongue motion or coordination

  • Inability to hold a bolus due to reduced tongue shaping and coordination

  • Inability to align teeth due to reduced mandibular movement

  • Entry of food material into the anterior sulcus or the presence of residue in the anterior sulcus due to reduced labial tension or tone

  • Entry of food material into the lateral sulcus or the presence of residue in the lateral sulcus due to reduced buccal tension or tone

  • Abnormal hold position or dropping of material to the floor of the mouth due to tongue thrust or reduced tongue control

  • Delayed oral onset of swallow due to apraxia of swallow or reduced oral sensation

  • Searching motion or inability to organize tongue movements due to apraxia of swallow

  • Forward tongue movement to start the swallow due to tongue thrust

  • Residue of food on the tongue due to reduced tongue range of movement or strength

  • Disturbed lingual contraction (peristalsis) due to lingual discoordination

  • Incomplete tongue-to-palate contact due to reduced tongue elevation

  • Inability to mash material due to reduced tongue elevation

  • Adherence of food to hard palate due to reduced tongue elevation or reduced lingual strength

  • Reduced anterior-posterior lingual action due to reduced lingual coordination

  • Repetitive lingual rolling in Parkinson disease [12]

  • Uncontrolled bolus or premature loss of liquid or pudding consistency into the pharynx due to reduced tongue control or linguavelar seal

  • Piecemeal deglutition

  • Delayed oral transit time

Pharyngeal-phase disorders

If pharyngeal clearance is severely impaired, a patient may be unable to ingest sufficient amounts of food and drink to sustain life. In people without dysphagia, small amounts of food commonly are retained in the valleculae or pyriform sinus after swallowing. If there is weakness in or a lack of coordination of the pharyngeal muscles or if there is a poor opening of the upper esophageal sphincter, patients may retain excessive amounts of food in the pharynx and experience overflow aspiration after swallowing.

Dysfunction or abnormalities of the soft palate and superior pharynx (eg, cleft palate) can lead to nasopharyngeal reflux following uvulectomy.

Logemann's Manual for the Videofluorographic Study of Swallowing cites the following pharyngeal-phase swallowing symptoms and disorders [11] :

  • Delayed pharyngeal swallow

  • Nasal penetration during swallow due to reduced velopharyngeal closure

  • Pseudoepiglottis (after total laryngectomy): Fold of mucosa at the base of the tongue

  • Cervical osteophytes

  • Coating of pharyngeal walls after the swallow due to bilateral reduction of pharyngeal contraction

  • Vallecular residue due to reduced posterior movement of the tongue base

  • Coating in a depression on the pharyngeal wall due to scar tissue or pharyngeal pouch

  • Residue at top of airway due to reduced laryngeal elevation

  • Laryngeal penetration and aspiration due to reduced closure of the airway entrance (arytenoid to base of epiglottis)

  • Aspiration during swallow due to reduced laryngeal closure

  • Stasis of residue in pyriform sinuses due to reduced anterior laryngeal pressure

  • Delayed pharyngeal transit time

Esophageal-phase disorders

Impaired esophageal function can result in retention of food and liquid in the esophagus after swallowing. This retention may result from a mechanical obstruction, a motility disorder, or an impairment of the opening of the lower esophageal sphincter.

Achalasia can lead to reduced gastroesophageal junction relaxation or absent esophageal peristalsis.

Logemann's Manual for the Videofluorographic Study of Swallowing cites the following swallowing symptoms and disorders of the esophageal phase [11] :

  • Esophageal-to-pharyngeal backflow due to esophageal abnormality

  • Tracheoesophageal fistula

  • Zenker diverticulum

  • Reflux

Zenker diverticulum can lead to swallowing difficulty, with possible nocturnal aspiration of residue in the diverticulum.

Other defects in the wall of the esophagus or in the external structures (eg, in the hilar lymph nodes) can lead to dysfunction in the propulsion of the bolus from the esophagus to the stomach (eg, esophageal webs, rings, strictures; intraluminal obstruction from solids) and result in weak esophagopharyngeal peristalsis due to scleroderma or other conditions.

A study by Kawaguchi et al determined that primary esophageal motility disorder was present in 58 out of 100 study patients with dysphagia, indicating that it has a not uncommon association with swallowing difficulties. [13]


As previously mentioned, aspiration is the passage of food or liquid through the vocal folds. People without swallowing abnormalities routinely aspirate microscopic amounts of food and liquid. Gross aspiration, however, is abnormal and may lead to respiratory complications, including pneumonia. (See the images below.) [14]

Lateral projection of the videoprint of a videogra Lateral projection of the videoprint of a videographic swallowing study shows residues on the vallecula (Vr) and pyriform sinuses (Pr) and a small amount of aspirated liquid barium in the trachea (As).
Lateral projection of the videoprint of a videogra Lateral projection of the videoprint of a videographic swallowing study shows subglottic aspiration.
Delayed posteroanterior chest image shows aspirati Delayed posteroanterior chest image shows aspiration of liquid barium into the distal bronchus.

Several factors influence the effects of aspiration: quantity, depth, physical properties of the aspirate, and pulmonary clearance mechanisms.

Aspirating material into the distal airways is more dangerous than aspiration into the vocal folds. Solid food may cause fatal airway obstruction, and acidic material is dangerous because the lungs are highly sensitive to the caustic effects of acid. Aspirating material laden with infectious organisms or even normal mouth flora can cause bacterial pneumonitis.

Pulmonary clearance mechanisms include ciliary action and coughing, with aspiration normally provoking a strong reflex cough. If sensation is impaired, silent aspiration may occur.

The severity of aspiration can be described by estimating the percentage of the total bolus aspirated or by estimating the depth of bolus invasion into the airway. The Eight-Point Penetration-Aspiration Scale is an example of an estimation tool. [15]



Central nervous system disorders

Central nervous system (CNS) pathologies that can produce dysphagia include the following:

  • Alzheimer disease

  • Brain tumors

  • Guillain-Barré syndrome

  • Huntington disease

  • CNS infections

  • Stroke

  • Traumatic brain injury (TBI) [16]

  • Parkinson disease [12, 17]

  • Poliomyelitis

  • Cerebral palsy

  • Multiple sclerosis

  • Amyotrophic lateral sclerosis (ALS) [18]

Research by Suntrup-Krueger et al indicated that the location of brain lesions in stroke affects the specific elements of swallowing dysfunction. The investigators found an association between cough reflex disturbance and lesions on the limbic structures of the right hemisphere and sensory regions of the left hemisphere, while oropharyngeal residue and impaired swallow response were found in association with lesions of the parietal-temporal regions of the right hemisphere. [19, 20]

Muscular disorders

Muscular disorders that can cause dysphagia include the following:

  • Muscular dystrophies

  • Spinal muscular atrophy

  • Polymyositis

  • Dermatomyositis

Neuropathic disorders

Dysphagia can result from sensory neuropathies affecting the laryngeal nerves. [21, 22]

Endocrine disorders

Dysphagia can result from the following:

  • Secondary myopathies in Cushing syndrome, hyperthyroidism, and hypothyroidism

  • Vitamin B-12 deficiency: Leading to pseudobulbar palsy secondary to corticobulbar tract dysfunction

Pharmacologic causes

Various medications, including the following, can produce dysphagia by causing a decrease in cognition or giving rise to drug-induced myopathies:

  • CNS depressants

  • Antipsychotics

  • Corticosteroids

  • Lipid-lowering agents

  • Colchicine

  • Aminoglycosides

  • Anticholinergic drugs

Mucosal injury may be caused by the following drugs:

  • Potassium chloride tablets

  • Nonsteroidal anti-inflammatory drugs (NSAIDs)

  • Antibiotics (eg, doxycycline, tetracycline, clindamycin, trimethoprim-sulfamethoxazole)

Xerostomia may be caused by the following agents:

  • Anticholinergics

  • Alpha-adrenergic blockers

  • Angiotensin-converting enzyme (ACE) inhibitors

  • Antihistamines

Surgical causes

Surgeries that can lead to dysphagia include the following:

  • Laryngectomy

  • Pharyngectomy, esophagectomy reconstructed by gastric pull-up

  • Head and neck surgery (oral cavity cancer) [23]

  • Surgery involving the pharyngeal plexus during cervical fusion or carotid endarterectomy


The frequency of aspiration in patients with a tracheostomy is 50-83%. The tracheostomy tube affects airway protection and swallowing in many ways. It impairs the glottic closure reflex, reduces subglottic pressure and laryngeal elevation, impairs hypopharyngeal and laryngeal sensation, and leads to disuse muscle atrophy.

Tracheostomy alters the essence of normal respiratory flow by diverting air through the neck instead of the pharynx, especially when an inflated tracheostomy tube cuff is present. The previous belief that an inflated tracheostomy tube cuff prevents aspiration of food has been refuted. An inflated cuff causes secretions to stagnate and collect above it, and these secretions can trickle down past the cuff and potentially lead to infection. Increasing the pressure of the cuff may lead to malacia, stenosis, fistula of the tracheal wall, or dragging of the cuff on the larynx as the larynx elevates during a swallow (laryngeal excursion).

Subglottic airway pressure is disrupted in patients with open tracheostomy tubes. The expiratory phase is shortened because the function of the normal vocal folds to maintain lung volumes throughout the physiologic prolongation of the expiratory phase is impaired. Furthermore, reduced subglottic pressure precludes effective coughing.

Superior and anterior laryngeal excursion during swallowing facilitates vertical closure of the laryngeal vestibule, assisting in airway protection and opening of the upper esophageal sphincter. The tracheostomy tube may attach the larynx to the surrounding neck tissue, anchoring it in position and reducing laryngeal elevation.

The tracheostomy desensitizes laryngeal and hypopharyngeal receptors, delaying onset of the laryngeal adductor reflex response and leading to aspiration. The sensory response, and hence the organization of the swallowing mechanism, can be improved by restoring the transglottic airflow by downsizing the tracheostomy tube, placing a fenestrated tube, or occluding the tracheostomy tube with a cap or with a 1-way speaking valve.

Endotracheal intubation

Endotracheal intubation also affects swallowing function, directly and indirectly. The direct effect of the endotracheal tube on laryngeal structures is caused by laryngeal trauma, which manifests as vocal-fold and supraglottic edema, granulation tissue in the posterior larynx, subluxation of one or both arytenoid cartilages, and permanent or temporary palsy of the recurrent laryngeal nerve. Supraglottic and glottic edema reduces the patient's ability to sense the presence of secretions in the larynx or hypopharynx, which in turn can inhibit the timely triggering of the pharyngeal swallow response, causing aspiration.

Indirect effects on swallowing caused by endotracheal intubation relate to the coordination required between respiration and the swallowing function. An increased respiratory rate in patients with suboptimal oxygenation can disrupt the regular swallowing and respiration pattern and predispose the patient to aspiration of saliva and secretions.

For example, continuous, positive airway pressure delays the latency of the swallow response and reduces the number of swallows, because it alters the peripheral sensory receptors that assist with the triggering of a pharyngeal swallow.

Additional iatrogenic causes of dysphagia

These include the following:

  • Use of a cervical brace

  • Ventilator dependency

Psychogenic dysphagia

This diagnosis is one of exclusion. The condition is characterized by oral apraxia with intact speech and pharyngoesophageal and neurologic function.

Associated psychiatric conditions include anxiety, depression, somatoform disorders, hypochondriasis, conversion disorders, and eating disorders. Psychiatric evaluation and treatment often are needed.

Instances of swallowed foreign bodies do occur (bezoars), especially in patients with developmental disabilities, and this possibility also should be considered.

Motility disorders

Motility disorders that can produce dysphagia include the following:

  • Diffuse esophageal spasms (DES)

  • Achalasia (megaesophagus)

  • Scleroderma

  • Presbyesophagus

  • Cricopharyngeal dysfunction


The following may also result in dysphagia [24] :

  • Gastroesophageal reflux disease (GERD)

  • Infectious esophagitis (eg, as in human immunodeficiency virus [HIV], herpes, candidiasis)

  • Radiation esophagitis: Especially after radiation treatments of 4500 to 6000 rad over 6-8 weeks

  • Medication-induced esophagitis: May develop from enteric-coated nonsteroidal anti-inflammatory drugs (NSAIDs); substances such as quinidine, potassium, vitamins, and FeSO4 also may produce esophageal injury

Structural disorders

These include the following:

  • Zenker diverticulum at the upper esophagus or epiphrenic diverticula at the midesophagus or distal esophagus

  • Esophageal strictures, webs, or rings

  • Tracheoesophageal fistula

  • Schatzki rings

  • Plummer-Vinson or Paterson-Kelly syndromes and hypopharyngeal webs with iron deficiency anemia

  • Cervical spondylosis



Occurrence in the United States

Neurologic swallowing disorders are encountered more frequently in rehabilitation medicine than in most other medical specialties. Stroke is the leading cause of neurologic dysphagia, with the condition occurring in approximately 51-73% of patients with stroke. Dysphagia can delay functional recovery in patients with stroke and is also the most significant risk factor for the development of pneumonia in this population.

Race- and age-related demographics

According to the US National Medicare database, the incidence of poststroke dysphagia is higher in Asians and other minority groups than in whites, suggesting racial disparities in the development of dysphagia after stroke. [25, 26]

As previously mentioned, the prevalence of dysphagia increases with age, and dysphagia is a major health-care problem in elderly patients.

A study by Kooi-van Es et al found that of 295 children with neuromuscular disease, dysphagia and dysarthria had a pooled overall prevalence of 47.2% and 31.5%, respectively. The investigators reported that 90.0% of children with dysphagia had chewing problems, while 43.0% had swallowing problems, and 33.3% demonstrated difficulties with both chewing and swallowing. [27]



Stroke patients recover swallowing function gradually, and therapeutic interventions for dysphagia generally are successful. In a prospective investigation of 128 patients admitted because of acute stroke, a swallowing abnormality was detected in 51% on clinical examination and in 64% on videofluoroscopy at initial presentation. [28] At 6 months after stroke, 87% of patients had returned to their prestroke diet.

In conditions in which recovery is possible (eg, TBI, stroke), the normalization of swallowing may take from 3 weeks to approximately 6 months or longer. [29, 1] Many patients tolerate normal oral caloric intake 9 months after a stroke, while some may require partial or nonoral caloric supplementation. In patients who have sustained a stroke, continued swallowing dysfunction after 6 months is associated with increased morbidity and mortality.

In static or progressive conditions (eg, neuromuscular disorders, postpolio syndrome), periodic evaluation of swallowing disorders is mandatory, especially with the onset of new symptoms, and the appropriate strategies (the use of nonoral feeding techniques or new compensatory mechanisms) should be considered.

Aspiration pneumonia

Pneumonia accounts for about 34% of all stroke-related deaths and represents the third highest cause of death during the first month after a stroke. Although not all of these cases of pneumonia are attributable to the aspiration of food, the early detection and treatment of dysphagia in patients who have sustained a stroke is nonetheless very critical. [30]

In a study of 124 patients with acute stroke, 39% of them had failing results on initial swallow screening. [31] However, because of early management (eg, altered dietary texture) of their dysphagia, no patients developed aspiration pneumonia. Early swallow screening and dysphagia management in patients with acute stroke reduces their risk of aspiration pneumonia, is cost effective, and helps to ensure good-quality care with optimal outcomes.


Patients who have had a stroke are likely to decrease their dietary intake, which increases their risk of malnutrition or exacerbates existing malnourishment. [32] In an investigation of the nutritional status of patients with stroke who were admitted to a rehabilitation service, 49% had malnutrition, and 65% of those with dysphagia were malnourished. [33]

In another study, no differences were found in the nutritional parameters of patients admitted for stroke with or without dysphagia on admission. However, after 1 week, 48.3% of the patients with dysphagia were malnourished, compared with only 13.6% of those without dysphagia.

Malnutrition is a risk factor for pneumonia because it renders the person susceptible to altered colonization in the oropharynx and reduced resistance to infection by depressing the immune system. Malnutrition may also lead to lethargy, weakness, and reduced alertness, all of which may increase the probability of aspiration. In addition, malnutrition may reduce the strength of cough and mechanical clearance in the lungs.

A study by Gourin et al indicated that dysphagia-associated malnutrition is a significant risk factor for health outcomes in patients with head and neck cancer. In a study of 93,663 patients treated with ablative therapy for malignant neoplasms of the oral cavity, larynx, hypopharynx, or oropharynx, the investigators found that dysphagia was the most significant of several factors related to weight loss in these patients. The study also indicated that an association exists between weight loss and increases in medical and surgical complications, as well as in length of hospital stay and hospital-related costs, in patients who undergo head and neck cancer surgery. [34]


Dysphagia can potentially lead to dehydration, while dehydration may itself be a risk factor for pneumonia for several reasons. First, it decreases salivary flow, which promotes altered colonization of the oropharynx; second, it may lead to lethargy, mental confusion, and increased aspiration; and third, it makes the person susceptible to infection by depressing the immune system.