Dysphagia presents with a vast array of aetiologies and is a common presenting complaint in the general practice setting.1 In addition to being a potential symptom of malignancies, dysphagia represents a common chronic disability within our ageing Australian population.2 Timely recognition and early management of dysphagia have been shown to improve patient outcomes and quality of life and to reduce hospitalisations from secondary complications.3,4
Aim
This article provides an overview of dysphagia to support general practitioners (GPs) in terms of assessment, common treatment options and the recommended management pathways.
Epidemiology
Dysphagia is a complex anatomical and/or functional disruption of the aerodigestive tract resulting in a poor swallow.5
Causes of dysphagia can be broken down into two broad categories relating to the affected anatomical location – oropharyngeal or oesophageal dysphagia – and similarly by its pathophysiology either being a motility disorder or an obstructive disorder.5 A list of differential diagnoses and their categorisations can be found in Table 1.
Dysphagia carries a significant disease burden among our communities, with notably high morbidity and mortality rates,6 although global reports vary with population-based incidences estimated to be between 2 and 20%.7,8 Australian-specific reports reflect these data, indicating that 20% of Australians aged >50 years experience dysphagia, which increases to up to 50% in those residing in long-term care facilities.6,8 Aspiration pneumonitis was the leading cause of death in people with a disability living in New South Wales residential care facilities in 2016.9 Although multifactorial, risk factors in the geriatric population include previous strokes, dementia and occasionally motor neurone disease. Dysphagia is more prevalent in women than men across all age groups.5,10
Table 1. Differential diagnoses of dysphagia |
Oropharyngeal pathology |
Oesophageal pathology |
Mechanical obstructions |
Oropharyngeal malignancy |
Squamous cell carcinoma is the most common cause of head and neck malignancy. Other cancers include lymphoma and salivary gland tumours |
Oesophageal malignancy |
Adenocarcinomas are the most common oesophageal malignancy, with dysphagia usually presenting as a sign of late-stage disease |
Pharyngitis and abscess formation |
Laryngitis, pharyngitis and tonsilitis might progress into parapharyngeal
or deep neck space infections |
Peptic/Oesophageal stricture dysfunction |
Stricture formation secondary to chronic gastric reflux is treated by endoscopic dilatations and gastric acid suppression |
Pharyngeal diverticulum |
Zenker’s diverticulum is the most common pharyngeal diverticulum due to a spasmodic upper oesophageal sphincter resulting in a high-pressure pharynx. This can often be identified in barium swallow studies in the community |
Schatzki ring |
A pathological narrowing of the distal oesophageal lumen. The pathophysiology is still unclear |
Radiation injury |
Post-radiotherapy side effects for head and neck cancer treatment include mucositis, xerostomia, fibrosis and strictures. Regular gum chewing to promote salivation, increasing daily fluid intake and using oral lubricants might help with xerostomia. Strictures can be seen on barium swallows and will require endoscopic dilatation |
Foreign body |
Patients present with hypersalivation, odynophagia and bolus regurgitation. Endoscopic treatment is only considered when medical therapies such as glucagon, benzodiazepines, calcium channel blockers and carbonated liquids have failed |
Cervical vertebral osteophytes |
Osteophytes commonly seen on barium swallows might protrude into pharyngeal mucosa creating discomfort during the transfer of a food bolus. Osteophytectomy is not routinely recommended |
|
Thyroid goitre/cancers |
Thyroid goitre results in extrinsic compression of the upper aerodigestive tract. Sonographic and CT neck and chest scans are helpful initial investigations |
Motility disorders |
Stroke |
Central disorders result in dyscoordination of pre-oral, oral and pharyngeal phases of swallowing. Reflexive swallow is delayed, bolus propulsion is blunted, and airway protection is limited |
Eosinophilic oesophagitis |
A chronic relapsing food-related inflammatory disorder results in over deposition of eosinophils and subsequent oesophageal fibrosis. Treatment involves targeted allergenic food avoidance and topical corticosteroids |
Parkinson’s disease |
Dysphagia secondary to muscular rigidity and bradykinesia increases the likelihood of silent aspiration. Swallow assessments and rehabilitation with a speech pathologist is vital in slowing the progression of dysphagia |
Achalasia |
Achalasia results from an inappropriate contraction of the lower oesophageal sphincter |
Alzheimer’s disease |
Dysphagic geriatric populations with dementia often develop malnutrition, dehydration, cachexia, social isolation and a general decline in quality of life |
Distal oesophageal spasm |
Distal oesophageal spasms result from rapid prolonged propagations of peristalsis resulting in oesophageal muscular hypertrophy over time |
Amyotrophic lateral sclerosis |
A progressive neurodegenerative disease affecting motor neurones of the central nervous system. This disease might manifest with progressive bulbar pathology. No reversible treatment options are available. Management revolves around swallow rehabilitation through a speech pathologist. These patients will require neurology and ENT input to manage sialorrhoea, reduce aspiration and improve communication |
Myasthenia gravis |
Myasthenia gravis is a rare autoimmune inflammatory myopathy induced by antibody-associated destruction of neuromuscular endplates of voluntary muscle. Although many different muscles are affected, patients might describe ‘fluctuating and fatigable swallowing’ |
Scleroderma |
Scleroderma is an autoimmune disorder that results in the recomposition of oesophageal musculature into fibrotic aperistaltic tissue |
Multiple sclerosis |
Multiple sclerosis is an autoimmune demyelination disease of the central nervous system. Dysphagia is a prevalent symptom in these patients, though there is a paucity of evidence-based management options to guide clinicians |
Autonomic neuropathy |
The most common cause of autonomic neuropathy is diabetes mellitus, which results in dysregulation of the autonomic system |
Functional dysphagia |
Functional dysphagia is a diagnosis of exclusion and refers to a psychogenic aetiology that is not explained by other causes |
|
Laryngopharyngeal reflux |
An impaired upper oesophageal sphincter results in gastric reflux irritating pharyngeal and laryngeal mucosa. Patients often complain of throat clearing |
CT, computed tomography; ENT, ear–nose–throat. |
Overview and subtypes of dysphagia
Oropharyngeal dysphagia
Oropharyngeal dysphagia relates to either a dysmotility or a mechanical obstruction at or above the level of the upper oesophageal sphincter (UES).
Several neurological conditions can result in dysmotility. Central causes include cerebrovascular accidents (CVAs) and neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease. Peripheral causes include diabetic neuropathy or myasthenia gravis.11,12 CVAs are the leading cause of oropharyngeal dysphagia, and are also associated with a higher risk of aspiration due to an uncoordinated swallow and an inability to protect the airway. As a result, up to one-third of stroke survivors will develop aspiration pneumonia in their first month of recovery.13 Dysphagia related to neurological disorders is often chronic and can result in significant disability, especially within the institutionalised geriatric population.14–16
The most common mechanical obstruction of the oropharynx includes benign or malignant lesions of the head and neck (H&N), strictures, post-radiation changes and external compressive pathologies (ie goitre, cervical osteophytes).
The most common malignancy of the oropharynx is squamous cell carcinoma (SCC), which accounts for >90% of H&N malignancies.17 These SCCs can be classified as non-human papillomavirus (HPV)-related SCCs, commonly associated with tobacco smoking and heavy alcohol use, or by HPV-associated SCC, which is steadily rising in incidence.18
Oesophageal dysphagia
Oesophageal dysphagia relates to dysmotility or a mechanical obstruction below the level of the UES. The most common mechanical obstruction is a stricture secondary to gastroesophageal reflux disease (GORD).19 Recurrent gastric acid reflux can result in oesophagitis, which can lead to benign peptic stricture development. Alternatively, GORD can also result in the dysplastic process of Barrett’s oesophagus due to chronic irritation.20 This histological change is a precursor to the development of oesophageal adenocarcinoma, which might result in progressive dysphagia, typically a sign of advanced disease.
Oesophageal motility disorders can be divided into primary oesophageal disorders or systemic diseases with a secondary effect on oesophageal motility. Achalasia is the most common motility disorder and is characterised by incomplete relaxation of the lower oesophageal sphincter, resulting in oesophageal aperistalsis.21 Less common primary motility diseases include diffuse oesophageal spasm and nutcracker oesophagus.22 The most common secondary oesophageal motility disorders are scleroderma and diabetic autonomic neuropathy, with both affecting the contractility of the oesophagus and resulting in aperistalsis.23
History-taking
A thorough history and examination is required for all patients with suspected dysphagia. Refer to Table 2 for a focused summary. For appropriate escalation and management, it is important to address two broad questions. First, whether the dysphagia involves the oropharyngeal or oesophageal region; and second, whether it is caused by a mechanical obstruction or a motility disorder.
Differentiating between locations
Oropharyngeal pathology will typically result in a delay in swallow initiation, coughing, choking or nasal regurgitation with food. Patients with oesophageal obstructions often have difficulty self-localising the level of obstruction; however, they might present with symptoms such as a catching sensation in the throat or the chest.24 Important red flag symptoms associated with malignancy include odynophagia, otalgia, neck masses, unintentional weight loss and bloody expectoration.
Differentiating between mechanisms
The primary way to differentiate between an obstructive or a dysmotility disorder is by assessing for foods that trigger dysphagia. Motility disorders affect solid and liquid foods, whereas obstructive disorders are typically initially associated with solid foods and patients might report substituting their usual diet with pureed textured food. Many of the medications found in Table 3 can lead to and contribute to dysphagia.25,26
Table 2. Key considerations for history-taking in the work-up of dysphagia |
General history considerations |
Presenting complaint
|
|
|
- Delayed swallow initiationA
- Coughing, choking or nasal regurgitationA,B
- Dysphonia,A,B otalgiaB
- XerostomiaA
- HaemoptysisB
- Exposure to HPV or high-risk sexual behavioursB
- Recent intubation
- Recurrent pneumonia
|
- Reflux or heartburnA
- Bolus regurgitationA,B
- Catching sensation in the throat or chest
- Difficulty localising the level of obstruction22
- HaematemesisB
|
- OdynophagiaB
- New neck lumps or swellingB
- Neurological deficitsA
- Food consistency: solid intolerance,A,B liquid intoleranceA
|
Constitutional symptoms |
- Unexplained weight loss (>10% over a 6-month period)B
- Generalised malaise and lethargy
- Anorexia
- Night sweatsB
|
Past medical history |
- Central neuropathies:
- Stroke or transient ischaemic attacksA
- Alzheimer’s diseaseA
- Peripheral neuropathyA
- Neurodegenerative diseasesA
- Gastroesophageal disease and peptic ulcer disease
- Diabetes mellitusA
- Thyroid disorders
- AsthmaA
|
Medications: refer to Table 3 |
Allergies |
- Drug and food hypersensitivities
|
Vaccinations |
- Up-to-date and recommended travel vaccinations
- COVID-19 vaccination status
|
Family history |
- History of head and neck cancers
- History of autoimmune disorders
|
Social |
- Smoking historyB
- Alcohol consumptionA,B
- Dietary modifications
- Assessment of activities of daily living
- Level of home assistance and food preparation independence
|
ADysmotility/physiological pathology.
BObstructive pathology.
ECOG, Eastern Cooperative Oncology Group; HPV, human papillomavirus. |
Table 3. Medication-induced dysphagia |
Category |
Mechanism |
Examples |
Sedative drugs |
- These drugs result in cognitive inhibition, resulting in oropharyngeal swallow dyscoordination
- Elderly patients are more vulnerable to its effects
|
- Benzodiazepines: lorazepam, alprazolam, diazepam
- Opiates: codeine, hydromorphone, fentanyl, oxycodone
|
Antipsychotics |
- These drugs create an antagonistic effect on central nigrostriatal dopamine D2 receptors, which suppress all phases of deglutition
|
- Clozapine, haloperidol, lithium, olanzapine, quetiapine, risperidone
|
Xerostomia-related medications |
- These medications have an inhibitory effect on the parasympathetic system, reducing salivary production, leading to xerostomia
|
- Angiotensin-converting enzyme: perindopril
- Antiemetics: metoclopramide, ondansetron, promethazine, prochlorperazine
- Decongestants: diphenhydramine, pseudoephedrine
- Selective serotonin reuptake inhibitors: citalopram, fluoxetine, venlafaxine, paroxetine, sertraline, amitriptyline
|
Anticholinergics and antimuscarinics |
- These medications have an inhibitory effect
on the parasympathetic system that can
result in the impairment of oesophageal
peristalsis. These medications can also
result in xerostomia
|
- Atropine, benztropine, hyoscine, ipratropium, oxybutynin
|
Medications that cause oesophageal mucosal injury |
- Some medications might cause caustic irritation of the oesophageal mucosa and with overexposure, might lead to stricture formation
|
- Antibiotics: clindamycin, doxycycline, erythromycin
- Bisphosphonates: alendronate, risedronate, zoledronic acid
- Non-steroidal anti-inflammatory drugs: aspirin, ibuprofen, naproxen, indomethacin
- Supplementary medications: iron-containing tablets, potassium chloride, vitamin C tablets
|
Clinical examination
The examination begins with assessing the symmetry of the face, neck and oral cavity, followed by palpation of the neck and supraclavicular region. The oral examination is performed with a tongue depressor and a light source with careful attention to the tonsils, tongue and the floor of the mouth. The clinician should also perform a cranial nerve examination and identify global or focal neurological pathologies. A focused examination can be found in Table 4.
Table 4. Key elements in the physical examination for dysphagia |
General inspection |
- Sarcopenia
- Tobacco-stained fingers or Raynaud’s phenomenon (indicating scleroderma)
- Jaundice
- Vital signs
- Surgical scars and neck masses
- Gait abnormality
- Facial tone and symmetry
- Ptyliasim/drooling/inability to tolerate secretions
- Quality of voice (eg wet, hoarse, hot potato)
|
Oral cavity |
- Assessment of trismus, dental occlusion, temporomandibular joint and trismus
- Tongue
- Deviation, fasciculations, thrush, tongue and base of tongue palpation
- Soft and hard palate, gingiva, buccal surfaces and floor
- of mouth
- Symmetry, ulcers, lesions, bleeding sites, dental hygiene
- and thrush
- Tonsils and tonsillar fossa
- Comment on size (Brodsky grading scale) and symmetry
|
Neck |
- Range of neck motion and assessment of torticollis
- Palpation of cervical and supraclavicular lymph nodes (Virchow’s node)
- Palpation of thyroid gland
|
Abdomen |
- Palpate for abdominal masses
- Gastrostomy tube
- Hepatosplenomegaly
|
Neurological examination |
- Cranial nerves
- Specifically V, VII, IX, X, XI and XII
- Unilateral or focal weakness
|
Swallow assessment |
- Water sip test and assessing for oral spillage, choking or coughing
|
Investigations and management
The history and examination can reliably identify the location and mechanism of dysphagia, which then allows for targeted investigations and the appropriate referral pathway to be actioned. When obstructive oropharyngeal dysphagia is suspected, a referral to an ear–nose–throat (ENT) specialist should be made for a nasoendoscopy and biopsies, as required. Patients suspected of oropharyngeal malignancy also benefit from computed tomographic imaging of the neck and chest to assess for primary lesions and associated lymphadenopathy. Isolated enlarged lymph nodes require an ultrasound-guided biopsy for further histological assessment.
Any patient suspected of having oesophageal dysphagia must be referred to a gastroenterologist for an upper gastrointestinal endoscopy (UGIE) to exclude an oesophageal malignancy, with biopsies taken as required.27 An UGIE will also assess for other benign obstructive pathologies.
Specialised investigation for motility disorders can be undertaken when mechanical obstructions are broadly excluded. A non-invasive study such as a barium swallow study is a helpful primary investigation that can be organised by the GP, which might demonstrate patterns of barium stasis within the oropharynx and oesophagus. Following this, more specialised testing can be considered. A speech pathologist can assist with further assessments of oropharyngeal motility disorders. They can organise specialised testing in the form of a video fluoroscope swallow study, which is a dynamic radiological assessment of swallow, assessed in a multidisciplinary fashion by both radiologists and speech pathologists.28,29 Magnetic resonance imaging of the brain can help diagnose neurological diseases that might be contributing to oropharyngeal dysfunction. Certain gastroenterologists and general surgeons might arrange manometric testing to delineate between different oesophageal motility disorders. Table 5 describes the various investigations in detail.
Table 5. Imaging and investigative modalities |
Investigation |
Indication |
Barium swallow |
- This type of imaging can inform the clinician of the level of pathology and assist in assessing for dysmotility and obstructive and diverticular pathologies
|
Modified barium swallow study/VFSS |
- This study is performed by a speech pathologist and radiologist and focuses on the swallowing of foods and fluids of varying consistencies up to the level of the upper oesophageal sphincter
|
FEES |
- A FEES is performed by a speech pathologist with a flexible nasoendoscopy to directly visualise the larynx during the swallowing of foods/fluids of various textures
|
MRI |
- An MRI assists in staging and characterising H&N lesions by providing information such as depth of invasion, associated structural invasion and lymphadenopathy
|
CT of the head, neck and chest |
- A CT scan is a useful initial imaging tool to assess for any H&N or oesophageal mass and identify any lymphadenopathy
|
Ultrasound |
- An ultrasound might assist in identifying neck lymphadenopathy and glandular pathologies and characterising thyroid masses
- A radiologist will often provide recommendations for further fine needle aspiration
|
Flexible nasoendoscopy |
- This is performed by an ENT specialist under topical local anaesthesia to assess the pharynx and larynx and to perform an in-clinic biopsy
|
Upper endoscopy |
- An upper endoscopy allows the proceduralist to perform a biopsy, dilatation of a stricture, steroid infiltration or
a foreign body retrieval
|
Manometry |
- A manometry assessment assesses the contractility
of the oesophageal sphincter
- Contraction pressures with a catheter probe can map the type and location of dysmotility
|
CT, computed tomography; ENT, ear–nose–throat; FEES, flexible endoscopic evaluation of swallow;
H&N, head and neck; MRI, magnetic resonance imaging; VFSS, video fluoroscopic swallow study. |
Community management
Most presentations of dysphagia are secondary to reflux.30 First-line treatments can be instituted with an empiric prescription of proton pump inhibitors and liquid antacids for at least eight weeks.31,32 GPs should counsel the patient on lifestyle modifications such as head elevation during sleep, avoidance of late-night meals, and avoiding exacerbating foods.33 Not only does tobacco smoking cause laryngopharyngeal irritation, it leads to many aetiologies of dysphagia and therefore cessation counselling should be provided. In patients without any red flags, a referral to a specialist should be made when the dysphagia persists.
There is a significant burden of disability related to chronic dysphagia and the associated risks of aspiration, malnutrition and dehydration. Speech pathologists can provide education on postural techniques and dynamic manoeuvres to protect the airway during ingestion, while also altering food consistencies appropriate to the degree of dysfunction.34 Oral hygiene maintenance reduces the colonisation of gastric microbes in the oropharynx and can reduce the risk of aspiration pneumonia in vulnerable patients.1,35 This can be ensured by educating patients on the importance of routine dental hygiene and review. Referral to a dietitian can help with maintaining appropriate caloric and fluid requirements, which need to be tailored around dietary restrictions. In addition to these risks, chronic dysphagia can also have significant social and psychological ramifications due to the inability to enjoy eating, as well as the lack of participation in social dining, and attention should be directed towards these emotions.2 Overall, given the holistic implications of the disability, it is important that any counselling and management also involve families and carers.36,37
In severe cases of chronic dysphagia, enteral feeding may be considered. Families should be counselled about the harms and limited benefits of long-term enteral feeding with a nasogastric or percutaneous gastrostomy tube, especially in those with advanced dementia.38
Conclusion
Dysphagia is a challenging complaint to manage. The aetiologies are broad and complex and as such, patients need a multifaceted approach. These patients would benefit from the integration of speech pathologists, dietitians and primary and tertiary care specialists. This article provides primary physicians with a guided template of pathologies and investigations that might help narrow the diagnosis.
Key points
- The prevalence of adult-onset dysphagia in Australia will continue to rise with a rapidly growing ageing population.
- Chronic dysphagia is common in the geriatric population and is a serious risk factor for the development of aspiration pneumonia.
- A thorough work-up allows the GP to delineate between oropharyngeal and oesophageal dysphagia and proceed with the relevant referral to either a gastroenterologist or an ENT specialist.
- Red flags for urgent specialist referrals include history of head and neck malignancy, history of heavy alcohol or tobacco use, new onset of persistent hoarseness, unexplained weight loss, haemoptysis and haematemesis, otalgia, unrelenting pain and obstructive dysphagia.
- Incorporating allied health professionals such as speech pathologists, dietitians, nurses and carers into dysphagia treatment is vital to setting up safe-feeding measures.