Overview of Dysphagia

Original Editor - Ewa Jaraczewska based on the course by Srishti Banerjee

Top Contributors - Ewa Jaraczewska  

Introduction

Swallowing (deglutition) impairment effects individual's safety and efficacy during drinking or eating. 1 of 6 adults report difficulty swallowing, but only half of them discuss their symptoms with a clinician. The consequence of deglutition difficulties are malnutrition, dehydration, and increase the risk of aspiration pneumonia. Additionally, dysphagia has a significant impact on social and psychological well-being because eating and drinking are important social and pleasurable activities. Understanding dysphagia helps with its early detection and management and lead to reduction in patient's hospital stay, improvement in rehabilitation outcomes, and decreasing morbidity and mortality.This course discusses dysphagia as a dysfunction of one or more parts of the swallowing apparatus.

Definition

Dysphagia is defined as the difficulty or impossibility to swallow liquids, food or medication and can occur during the oropharyngeal or the oesophageal phase of swallowing.

Dysphagia can lead to severe complications: (1) aspiration pneumonia, (2) dehydration, (3)malnutrition, and (4) death because of choking. According to Wilkinson et al.,initial assessment should base on patients' symptoms, "rather than their perceived location."

Oropharyngeal Dysphagia

"Oropharyngeal dysphagia is characterised by inability to initiate the swallow process."

"Oropharyngeal dysphagia is a clinical symptom, defined by the difficulty to move the alimentary bolus from the mouth to the oesophagus."

Oropharyngeal dysphagia may lead to two types of clinically relevant complications:

1. Malnutrition and/or dehydration when there is a presence of a decrease in deglutition efficacy

2. Pneumonia with an associated mortality caused by a decrease in deglutition safety and development of airway obstruction with chocking.

Oropharyngeal dysphagia is associated with abnormalities in the structures (structural alterations) in the oral cavity and the pharynx , or it may result from functional disorder of deglutition.

Structural alterations effects bolus progression. The following abnormalities can lead to oropharyngeal dysphagia:

• oesophageal and ENT tumors
• neck osteophytes
• post surgical oesophageal stenosis
• as a complication following head & neck cancer

The normal swallow response in healthy humans ranges form 0.6–1 s. Functional disorder of deglutition affects oropharyngeal swallow response. It can be caused by:

• ageing
• stroke
• systemic or neurological diseases

Prevalence of Oropharyngeal Dysphagia

The prevalence of oropharyngeal dysphasia varies as it depends on the screening method and the type of population tested. Symptoms may be often neglected by a patient or a caregiver and not reported to the physician.Percentage of patients with oropharyngeal dysphasia is high and include:

• over 30% of patients with a cerebrovascular accident
• 52%–82% of patients with Parkinson’s disease
• 84% of patients with Alzheimer’s disease
• up to 40% adults aged 65 years and older
• an increasing trend by increasing the age
• more than 60% of elderly institutionalised patients
• in the systematic review study of Takizawa et al. the prevalence of oropharyngeal dysphasia was as follow:
  • between 8.1 and 80% in stroke patients
  • between 11–81% in the Parkinson’s disease
  • between 27–30% in the traumatic brain injury patients
  • 91.7% in the community-acquired pneumonia

Countries and populations vary in the prevalence of the oropharyngeal dysphasia, with the highest percentage on the African continent ( 64.2% ) and the lowest in Australia ( 7.3%).

According to Rajati et al.the prevalence of oropharyngeal dysphasia in the pediatric population is high and may be due to the following:

• abnormalities or dental problems
• large tongue and tonsils
• craniofacial abnormalities as a result of problems with prenatal development of cranial bones and structures of the mouth and throat
• esophageal obstruction related to prenatal abnormalities of the gastrointestinal tract,
• tracheovasophageal fistula after prolonged exposure to a ventilator (which may occur in premature infants or very sick children)
• vocal cord paralysis
• tracheostomy surgery
• oesophageal stimulation or ulceration due to gastric acid in gastroesophageal reflux disease

Mechanisms of Oropharyngeal Dysphagia

1. Velopharyngeal incompetence occurs when " velum and lateral and posterior pharyngeal walls fail to separate the oral cavity from the nasal cavity during speech and deglutination." It can be caused by:
   • vagus nerve and pharyngeal plexus impairment due to neurological and neurosurgical conditions
   • brainstem stroke
   • decompression of the foramen magnum
   • head and neck cancer treatment due to intentional or inadvertent damage of the nerve supply to the palatal muscles
   • tumours of the oropharynx
   • radiotherapy to the nasopharynx
2. Absent, inefficient, or infrequent laryngeal elevation takes place when the thyrohyoid and suprahyoid muscles fail to assist with anterior and superior movement of the hyolaryngeal complex. As a result, the cricopharynx does not relax. This pathology arises with the following neurological and neurosurgical conditions:
   • posterior circulatory stroke
   • cerebellopontine angle surgery
   • high level spinal injuries or tumours
   • head and neck cancer surgery with removal of suprahyoid musculature and its nerve supply
   • floor of mouth resection
   • radiotherapy
3. Inappropriate laryngeal closure results in suboptimal diversion of the food bolus. It can be caused by:
   • partial or complete epiglottic resection
   • a high vagal injury with involvement of superior laryngeal nerves
   • brainstem lesions
   • brainstem surgery
4. Weakness or paralysis of the thyropharyngeal contraction leads to the stasis of the food bolus in the pyriform fossa on the affected side and can be caused by:
   • neurosurgery involving cranial nerves IX, X, and XI
   • stroke
5. Cricopharyngeal dysmotility as a primary or secondary cause affecting the proper functioning of the cricopharyngeus:
   • Primary due to problems in its neurological control
   • Secondary due to lack of elevation of the larynx
6. Idiopathic spasm of the cricopharyngeal which is characterised by simultaneous contraction of both thyropharyngeus and cricopharyngeus leading to development of a condition known as Zenker’s diverticulum.

Clinical Presentation of Oropharyngeal Dysphagia

Clinical presentation can often provide helpful information for diagnosis of oropharyngeal dysphasia:

• Nasal regurgitation is often associated with velopharyngeal incompetence, and occasionally with cricopharyngeal dysfunction.
• Multiple attempts to swallow are consistent with laryngeal elevation or cricopharyngeal dysmotility.
• Coughing immediately after the swallowing may indicate unilateral or bilateral laryngeal incompetence.
• A delayed cough implies a hypopharyngeal dysfunction
• Additional symptoms include hoarseness and breathing difficulty.

Oesophageal Dysphagia

"Oesophageal dysphagia is characterised by difficulty in transporting the food down the oesophagus."

Oesophageal dysphagia is associated with mechanical (structural ) problems, or motor disorders.

Mechanical (structural) disorders include a barrier that is obstructing the flow and can be suspected when an individual is experiencing difficulties with swallowing solids.Mechanical disorder can be intrinsic or extrinsic and can include:

Intrinsic:

• Carcinoma
• Benign tumours
• Diverticulum (small pouch inside the oesophagus)
• Eosinophilic oesophagitis (inflammation of the oesophagus)
• Peptic stricture (narrowing or tightening of the oesophagus)
• Oesophageal rings and webs
• Schatzski ring ( narrowing of the lower oesophagus)
• Foreign body
• Pill-induced stricture, for example alendronate, potassium chloride tablets
• Strictures related to tracheoesophageal fistula or its treatment

Extrinsic:

• Mediastinal mass
• Vascular compression
• Spinal osteophyte

Motility (motor) disorders result in peristaltic failure. These disorders can lead to problems with both solid and liquid boluses, however difficulties swallowing solids occur more frequently. Motility disorders can be further divided into primary or secondary. The following are examples of the primary and secondary motility disorder leading to oesophageal dysphagia:

Primary:

• Achalasia (failure of relaxation of the lower esophageal sphincter)
• Distal oesophageal spasm
• Hypercontractile (jackhammer) oesophagus
• Hypertensive lower oesophageal sphincter/gastroesophageal junction outflow obstruction
• Other peristaltic abnormalities

Secondary

• Chagas disease (disease caused by the protozoan parasite Trypanosoma cruzi )
• Reflux-related dysmotility
• Systemic sclerosis and other rheumatologic disorders
• Medications: anticholinergics, antiepileptics, benzodiazepines, calcium channel blockers, nitrates, phosphodiesterase inhibitors, opioids, tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors

Prevalance of Oesophageal Dysphagia

The prevalence of oesophageal dysphagia increases with age and comorbidities.

• individuals with gastroesophageal reflux disease experience an increase by 30%, patients with eosinophilic oesophagitis (EOE) by 8%, and those with oesophageal stricture by 4.5%
• Australia and Argentina report prevalence rates of 16% and 13% respectively
• China reports low prevalence rate of 1.7%

Clinical Presentation of Oesophageal Dysphagia

Oesopharyngeal dysphagia may have different clinical features depending on the cause of dysphagia.

Primary motility disorders:

• dysphagia to liquids as the predominant symptom may indicate neuromuscular motility disorders
• significant, progressive dysphagia for both liquids and solids, which can be relieved with repeated swallows, Valsalva maneuvers, or positional changes is associated with achalasia. Additional symptoms include regurgitation of undigested food, particularly at night, coughing, heartburn, weight loss, and aspiration
• intermittent, non-progressive dysphagia without weight loss in addition to patient's reporting globus sensation, regurgitation, and heartburn is consistent with a diffuse oesophageal spasm

Secondary motility disorders:

• regurgitation and heartburn effect 60% of patients with scleroderma

Obstructive intrinsic structural lesions:

• intermittent non-progressive dysphagia for only solid food indicates an obstructive lesion, like oesophageal ring or web
• “steakhouse syndrome” is a term used for symptoms in Schatzki connective tissue B ring. Dysphagia occurs after eating bread and meat, especially when the meal is consumed quickly. It is consistent with meat or food impaction with prolonged inability to pass an ingested bolus

Extrinsic diseases:

• progressive dysphagia, heartburn, odynophagia (pain when swallowing), food impaction, weight loss, and chest pain imply narrowing of the oesophageal lumen through inflammation, neoplasm, or fibrosis
• oropharyngeal ulcerations, oedema, and erythema with coughing, crying, vomiting, drooling, and varying degrees of respiratory distress and stridor characterise thermal or chemical burns to the oesophagus
• progressive dysphagia for solids and later liquids within weeks to months is common in oesophageal carcinoma

Resources

• Dysphagia - Pathophysiology of Swallowing Dysfunction, Symptoms, Diagnosis and Treatment
• Dziewas R, Allescher HD, Aroyo I, Bartolome G, Beilenhoff U, Bohlender J, Breitbach-Snowdon H, Fheodoroff K, Glahn J, Heppner HJ, Hörmann K, Ledl C, Lücking C, Pokieser P, Schefold JC, Schröter-Morasch H, Schweikert K, Sparing R, Trapl-Grundschober M, Wallesch C, Warnecke T, Werner CJ, Weßling J, Wirth R, Pflug C. Diagnosis and treatment of neurogenic dysphagia - S1 guideline of the German Society of Neurology. Neurol Res Pract. 2021 May 4;3(1):23.
• Dysphagia (difficulty swallowing)