Dysphagia and odynophagia

• Dysphagia is difficulty moving a bolus from the mouth to the stomach; odynophagia is pain on swallowing. They often occur together and have different causes.
• The first and most useful distinction is between oropharyngeal (transfer) dysphagia, where the problem is getting the bolus out of the mouth and through the pharynx, and oesophageal dysphagia, where the bolus sticks after it has been swallowed.
• Oropharyngeal dysphagia is commonly neurological: stroke, Parkinson disease, myasthenia gravis, motor neurone disease, and also follows prolonged intubation, Zenker diverticulum and head and neck cancer. It carries a real risk of aspiration.
• Oesophageal dysphagia is either mechanical (peptic stricture, Schatzki ring, eosinophilic oesophagitis, cancer, extrinsic compression) or a motility disorder (achalasia, oesophageal spasm, scleroderma), with or without an associated web or iron deficiency.
• Red flags are progressive dysphagia (solids first, then liquids), weight loss, anaemia or bleeding. These should prompt urgent upper endoscopy with biopsies.
• Oropharyngeal problems are assessed best with a videofluoroscopic swallow study (VFSS), often alongside fibreoptic endoscopic evaluation of swallowing (FEES); oesophageal problems are assessed first with upper endoscopy, with barium studies and high-resolution manometry in selected cases.

By the end of this page you should be able to:

1. Define dysphagia and odynophagia, and explain why they are not the same thing.
2. Distinguish oropharyngeal from oesophageal dysphagia using the history alone, including timing, liquids versus solids, nasal regurgitation, coughing and aspiration.
3. List the important causes of each type, grouped as neurological, mechanical and motility.
4. Recognise the alarm features that make urgent endoscopy necessary.
5. Choose the first investigation for a patient with each type of dysphagia and explain why.
6. Plan initial management, including aspiration precautions, nutrition and speech and language therapy, and match treatment to cause.
7. Adapt the approach in a low-resource setting.

The two words are often used as if they were the same, but they are not. A patient can have painless dysphagia (for example a peptic stricture or achalasia), painful swallowing with no difficulty (for example Candida oesophagitis or a pill ulcer), or both (for example eosinophilic oesophagitis during a flare). Keeping the distinction clear is the first step in making the correct diagnosis. Dysphagia localises to where the swallow fails, while odynophagia points to inflammation, ulceration or spasm of the mucosal lining.

Dysphagia is a presentation rather than a diagnosis. The swallowing pathway has two functional parts, and a problem at either part produces a different story. The oropharyngeal part prepares and propels the bolus: the tongue gathers it, the soft palate rises, the pharynx contracts and the upper oesophageal sphincter opens. The oesophageal part transports it: peristalsis and gravity move the bolus through the oesophagus and relaxation of the lower oesophageal sphincter lets it into the stomach. Understanding which part is failing tells you which tests to order and which treatments to choose.

Impairment anywhere along this chain can also cause odynophagia when the mucosa is inflamed, eroded or ulcerated. Causes of pain on swallowing are therefore better thought of as causes of oesophagitis, pill injury, infection, or severe reflux, together with muscular spasm, rather than a separate list. The sections below deal with each level in turn.

These are problems of neuromuscular control and of passage through the pharynx and upper oesophageal sphincter. They are commoner in older patients, in neurological disease, and after head and neck treatment.

• Stroke (including brainstem stroke) is the single commonest cause. Dysphagia is present in a large proportion of patients after stroke and is the reason bedside swallow screening is routine.
• Parkinson disease produces a slow, rigid tongue, reduced pharyngeal contraction and impaired airway protection. Drooling, micrographia and a shuffling gait are clues.
• Myasthenia gravis causes fatiguable weakness of the bulbar muscles, so swallowing deteriorates as a meal goes on, with nasal speech and diplopia.
• Motor neurone disease (amyotrophic lateral sclerosis) causes progressive bulbar weakness with dysarthria, tongue wasting and fasciculations. It overlaps with progressive muscular atrophy and primary lateral sclerosis.
• Prolonged intubation or tracheostomy can injure the larynx and cricopharyngeus muscle and leave a post-extubation dysphagia that improves over days to weeks.
• Zenker diverticulum is a pulsion diverticulum above the cricopharyngeus. Old food regurgitates, causing halitosis, gurgling and aspiration, often worse when lying flat.
• Head and neck cancer and its treatment (surgery, radiotherapy) can distort anatomy, narrow the pharynx, and paralyse a cranial nerve. New one-sided throat symptoms, voice change or a neck lump are alarm features.
• Other less common causes include myopathies, myositis (including inclusion body myositis), polymyositis, multiple sclerosis, Guillain-Barre syndrome, and post-polio bulbar weakness.

Mechanical causes all behave the same way at first: a solid bolus of food sticks. Liquids pass freely until the lumen is very narrow.

• Peptic stricture from long-standing gastro-oesophageal reflux: a smooth, tapered narrowing in the distal oesophagus, often in someone with years of heartburn.
• Schatzki ring: a thin mucosal ring at the gastro-oesophageal junction, often with a hiatus hernia. It causes intermittent dysphagia for solids, typically bread or meat, with impaction episodes.
• Oesophageal web with iron deficiency and glossitis, as in Plummer-Vinson syndrome (Paterson-Brown Kelly syndrome): a thin web in the proximal oesophagus, iron deficiency anaemia and smooth tongue with koilonychia and angular stomatitis. It is uncommon and is more often seen where iron deficiency is late or untreated.^[2]
• Eosinophilic oesophagitis: an immune-mediated disease of the oesophagus, increasingly diagnosed in young men and in children. Food impaction, intermittent solid-food dysphagia, atopy and ringed oesophagus on endoscopy are clues.
• Cancer of the oesophagus (squamous cell or adenocarcinoma) or cancer at the gastro-oesophageal junction. This is the diagnosis to exclude in any new progressive dysphagia in a middle-aged or older adult.
• Extrinsic compression: an enlarged thyroid or mediastinal mass, bulky lymphadenopathy, a vascular anomaly such as an aberrant right subclavian artery (arteria lusoria), an aortic aneurysm, or achalasia-like narrowing from a mediastinal tumour. Dysphagia accompanied by a neck mass, hoarseness or stridor points this way.
• Post-radiation and post-surgical strictures after treatment for head and neck or chest disease.

Motility disorders tend to affect both solids and liquids from the start, because the problem is propulsion rather than a fixed narrow point.

• Achalasia: failure of the lower oesophageal sphincter to relax on swallowing, with loss of peristalsis and progressive dilation of the oesophagus. The classic picture is progressive dysphagia for both solids and liquids, regurgitation of undigested food, chest pain, and weight loss.
• Oesophageal spasm and hypercontractile (jackhammer) oesophagus: intermittent, high-amplitude simultaneous contractions causing colicky chest pain and intermittent dysphagia.
• Scleroderma (systemic sclerosis): smooth muscle atrophy gives a weak, hypotensive lower oesophageal sphincter and ineffective peristalsis, leading to severe reflux and dysphagia for solids in someone with Raynaud phenomenon and skin thickening.
• Other causes include Chagas disease, pseudoachalasia from a tumour, and medication-induced oesophageal dysfunction.

A patient with any of the following needs urgent, specialist-level assessment, and in most health systems an urgent upper endoscopy.

• Progressive dysphagia, especially solids first and then liquids (mechanical or malignant cause until proven otherwise).
• Weight loss that is unintended, even if modest.
• Anaemia, particularly iron deficiency anaemia without another explanation.
• Bleeding from the upper gut: haematemesis, melaena, or occult blood.
• Food bolus impaction, repeated episodes.
• Onset of dysphagia in an older adult with no previous history of reflux.
• Associated neck mass, hoarse voice, stridor, or referred ear pain.
• Regurgitation of undigested food, nocturnal cough or aspiration pneumonia.
• Dysphagia after caustic ingestion or a pill known to injure the oesophagus.

A correct medical history is the single most important step, because it tells you which investigations are worth doing first and which are not.^[1] Ask the patient to describe the very first swallow that went wrong, and then ask what happens on a normal day. The most useful questions are:

• Where does it stick? Oropharyngeal dysphagia usually produces a sensation at the throat or behind the sternum within one second of swallowing, with coughing or choking. Oesophageal dysphagia is felt lower, a few seconds after the bolus has been swallowed.
• Solids, liquids, or both from the beginning? Mechanical obstruction: solids only at first, progressing from bread and meat to all solids and then liquids as the lumen narrows. Motility disease: solids and liquids difficulty from the outset. Oropharyngeal dysphagia: both solids and liquids, often worse with thin liquids, because the transfer mechanism and not the food is the problem.
• Nasal regurgitation? Food or liquid coming back through the nose points to impaired palatal elevation or upper oesophageal sphincter coordination and therefore to oropharyngeal disease. It is characteristic of stroke, neuromuscular disease and myasthenia gravis.
• Coughing, choking, or a wet voice during or just after swallowing? These point to laryngeal penetration or aspiration and therefore to oropharyngeal disease. A weak cough, a quiet wet voice, or recurrent chest infections are serious signs even when the patient does not report cough.
• Heartburn and regurgitation? Long-standing reflux suggests a peptic stricture.
• Food impaction? Episodic impaction of meat or bread suggests a Schatzki ring or eosinophilic oesophagitis.
• Weight loss, fever, and systemic features? These point to cancer, an inflammatory disease, or infection.
• Neurological symptoms? Tremor, slowness and gait change (Parkinson); fatigable weakness and diplopia (myasthenia); progressive weakness with speech change (motor neurone disease); previous stroke; medications that reduce saliva.
• Medication history. Bisphosphonates, doxycycline, iron, potassium chloride and non-steroidal anti-inflammatory drugs taken dry and at night can cause pill oesophagitis with odynophagia.
• Dentition, saliva, and oral health. Poor chewing and dry mouth (anticholinergic drugs, Sjogren syndrome, radiotherapy) produce a swallow problem that mimics higher-level disease.

The examination tailors to what the history suggests. Every patient needs a general and nutritional assessment plus a targeted test of the swallow itself.

• General and nutritional: weight, body mass index, signs of dehydration or malnutrition (temporal wasting, oedema), and a survey for iron deficiency (pallor, glossitis, angular stomatitis, koilonychia). In oropharyngeal dysphagia, patients may look well between swallows, so you have to watch them eat and drink.
• Mouth and throat: dentition, oral ulcers, candidiasis, tonsillar symmetry, palatal elevation when saying "ah", gag reflex, tongue strength and wasting, voice quality.
• Neurological: cranial nerves (especially V, VII, IX, X, XII), facial masking and rigidity, limb bradykinesia and tremor, limb weakness and hyperreflexia, eye movements, and a bedside check of speech and language.
• Neck and chest: goitre, lymphadenopathy, scars of previous surgery or radiotherapy, signs of chest infection.
• Bedside swallow screen: a recognised protocol, such as giving successive small volumes of water and watching for coughing, choking, a wet voice, or breathlessness. A failed screen means "nil by mouth" until properly assessed and is not a diagnosis.

Examination signs of aspiration are often absent, so a normal bedside test does not rule out aspiration. Any suspicion in an at-risk patient (stroke, frailty, bulbar signs) should lead to an instrumental assessment rather than reassurance.^[1]

The goal is to see the swallow happen, to check whether material is entering the airway, and to choose safe textures and manoeuvres. Clinical bedside scales are screening tools; they cannot confirm aspiration.^[1]

• Videofluoroscopic swallow study (VFSS, also called a modified barium swallow) is the method of choice, alongside fibreoptic endoscopic evaluation of swallowing (FEES), for instrumental assessment of oropharyngeal dysfunction.^[1] It visualises the oral, pharyngeal and upper oesophageal phases, identifies penetration and aspiration (including silent aspiration), shows residue, and lets the examiner test compensatory manoeuvres and different consistencies in real time.
• FEES involves passing a flexible nasal endoscope to watch the pharynx and larynx before and after the swallow. It is safe, needs no radiation, can be done at the bedside, in an intensive care unit or on mechanical ventilation, and is excellent for handling of secretions, residue and diet prescription.
• Speech and language therapy assessment determines which textures are safe, which postures or manoeuvres protect the airway, and whether the patient needs a modified diet or non-oral feeding.
• Nasogastric tube or, in selected cases, percutaneous endoscopic gastrostomy can protect nutrition while the swallow is rehabilitating or where recovery is not expected.
• Other tests: chest radiograph if aspiration pneumonia is suspected, and screening for the underlying neurological disease where the cause is not already known.

Where instrumental assessment is not available, especially in rural, remote or resource-poor settings, clinicians must rely on careful bedside swallowing evaluation and patient-reported or questionnaire-based tools, with the lowest safe texture and close observation.^[1]

Upper endoscopy comes first. It is the test that excludes the conditions that matter most to treat: cancer, a stricture, severe inflammation, eosinophilic oesophagitis, Candida oesophagitis, achalasia on endoscopic view, and an impacted bolus.

• Upper endoscopy (oesophagogastroduodenoscopy) should be performed in anyone with oesophageal dysphagia. It rules out mechanical obstruction and inflammation and, in endoscopy-negative disease, motor disorders are still suspected.^[1] In a patient with suspected eosinophilic oesophagitis, endoscopic biopsy should be taken even if the mucosa looks normal, because appearances can be subtle and histology is the arbiter.
• Barium oesophagram (barium swallow) is a useful complement. It is suggested as a complementary investigation to improve diagnosis of structural and functional oesophageal disease when endoscopy and high-resolution manometry have not fully explained symptoms, and it may be the most informative first investigation if a proximal stricture, a diverticulum (including Zenker), a very tight stricture or high perforation risk is suspected. It delineates rings, strictures, diverticula, achalasia (bird's beak, delayed emptying) and extrinsic compression better than endoscopy in some cases.^[1]
• High-resolution manometry (HRM) is the most important technology for assessing oesophageal motor function when endoscopy is negative. It is the test of choice for achalasia, spasm and other motility disorders, using a standardised classification such as the Chicago Classification v4.0.^[1]
• Endoscopic functional lumen imaging probe (EndoFLIP) is an adjunctive test for patients with dysphagia and inconclusive results after endoscopy and high-resolution manometry.^[1]
• CT (or MRI) of neck and chest and endoscopic ultrasound are used when pseudoachalasia or extrinsic compression is suspected (for example impalpable thyroid goitre, mediastinal mass, vascular compression), and for staging when cancer is found.^[1]
• Nutritional assessment: weight, caloric intake, albumin/prealbumin where available, and iron studies if a web is suspected. In older patients and in neurological disease, nutritional compromise is common and often precedes presentation.

Oropharyngeal dysphagia is associated with serious nutritional and respiratory complications, including malnutrition, dehydration and respiratory infections such as aspiration pneumonia, which in turn are linked to hospital readmission and increased morbidity and mortality.^[1] The priority at first contact is therefore to protect the airway and maintain hydration and nutrition.

• Put the patient nil by mouth if a bedside swallow screen has failed or if aspiration is strongly suspected, until further assessment.
• Position upright for all oral intake, allow plenty of time, and supervise meals if unsafe to eat alone.
• Use texture-modified food and thickened fluids as recommended by a speech and language therapist; these reduce aspiration in at-risk patients, although evidence that any one technique improves long-term outcome is limited.
• Keep the mouth clean (oral hygiene reduces the bacterial load that drives aspiration pneumonia).
• Consider a nasogastric tube early if oral intake is unsafe but the problem is expected to improve (for example after stroke in the first weeks), and percutaneous endoscopic gastrostomy when dysphagia is profound and protracted or recovery is not expected.
• Reassess the swallow regularly; a texture that was unsafe can become safe as function recovers, and unnecessary restriction causes weight loss and misery.
• Nutritional targets should be individualised; energy and protein requirements increase during rehabilitation and during radiotherapy for head and neck cancer.

Speech and language therapists are the specialists for the oropharyngeal phase. They assess, prescribe a texture and strategy, and deliver rehabilitation. Useful interventions include:

• Exercises for tongue strength, lip seal and pharyngeal contraction (effortful swallow, Mendelsohn manoeuvre, Shaker exercise).
• Postural changes (chin tuck, head turn) and swallow manoeuvres to protect the airway during the swallow.
• Diet texture modification and advice on food and fluid consistencies.
• Education for patients, carers and ward staff on cueing, pacing, and avoiding distractions at meals.
• Advice on safe medication administration (crushed tablets, liquid formulations, water swallowing).

UEG/ESNM suggest that swallow therapy may improve swallowing mechanics, reduce symptoms and enhance quality of life, and that it is more effective when using validated assessment tools, consistent treatment parameters, and long-term follow-up.^[1] The evidence base is modest and largely derived from stroke and head and neck cancer trials, so treatment should be delivered by a trained therapist and reassessed rather than prescribed as a standard package.

Refer promptly, and to the appropriate service, for:

• Any red flag (suspected cancer, progressive dysphagia, weight loss, iron deficiency anaemia, bleeding).
• Stroke, Parkinson disease, myasthenia gravis or motor neurone disease: to neurology and to a stroke or neuromuscular multidisciplinary team.
• Suspected eosinophilic oesophagitis, achalasia, significant motility disorder: to gastroenterology.
• Food impaction or foreign body: emergency endoscopy.
• Severe, progressive or intractable dysphagia with failure to maintain weight: to gastroenterology, surgery, or a feeding team.
• Head and neck cancer symptoms: to a head and neck oncology unit under a two-week pathway where that exists.
• Low-resource settings: to whatever specialist centre is reachable, even if the journey is long; delay in cancer and achalasia costs lives.

• Children: oropharyngeal dysphagia in an infant is often congenital (neurological, craniofacial, cleft palate) or acquired neonatal (prematurity, cardiorespiratory disease). Assessment and treatment need a paediatric speech and language therapist and feeding team. FEES and modified barium swallow are used with paediatric-specific protocols. Do not transfer adult thresholds and strategies unchanged.
• Older adults: presbyphagia (age-related change in swallowing) lowers reserve and turns minor illness into aspiration pneumonia. Medication review is often the most useful single intervention.
• Pregnancy: dysphagia commoner from reflux and nausea; a progressive solid-then-liquid pattern or a neck mass still needs endoscopy, which is safe in pregnancy at any gestation when indicated.
• Immunocompromised patients: odynophagia is usually infectious (Candida, herpes simplex or cytomegalovirus oesophagitis) until shown otherwise. A trial of systemic antifungal therapy, with reassessment after a few days, is reasonable when the picture is classic; endoscopy with targeted biopsies if not. See the topic on infectious oesophagitis.

• Aspiration pneumonia and lung abscess.
• Malnutrition, dehydration and weight loss.
• Recurrent food bolus impaction with risk of perforation.
• Stricture, Barrett oesophagus and, rarely, malignancy in long-standing Plummer-Vinson syndrome.^[2]
• Psychosocial: fear of eating, social isolation and reduced quality of life; dysphagia is a leading cause of choking death in frail elderly patients.

Where specialist services, endoscopy or VFSS are unavailable, the principles below keep patients safer without pretending the standard tests have been done.

• Recognise oropharyngeal dysphagia from the bedside: bedside swallow screen with water, observation of a meal, strength of cough, ability to clear secretions, and whether the patient can manage saliva.
• Keep the patient upright, use the cheapest safe texture (usually well-cooked and mashed, thickened with a household flour or commercial thickener if available), and supervise meals.
• Treat infection (aspiration pneumonia) promptly and aggressively; it is the complication that kills.
• Correct iron deficiency when Plummer-Vinson features are present; this alone may resolve dysphagia.^[2]
• Arrange referral for any red flag; even a long journey is justified if cancer or achalasia is suspected. Keep a list of the nearest centres that can do endoscopy and dilation.
• Where endoscopy is available but VFSS is not, a careful bedside assessment by a trained therapist (or a nurse with basic training) is far better than no assessment; ask available speech and language therapists in the region for a short training session.
• Nutritional support can be as simple as high-protein local foods, fortified porridges and small frequent meals; a nasogastric tube is inexpensive and safe while feeding is established.

• Dysphagia is difficulty swallowing; odynophagia is pain on swallowing. They overlap in some diseases and should be recorded separately.
• The first and most important distinction is oropharyngeal (transfer) versus oesophageal dysphagia, made mainly from a careful history.
• Oropharyngeal dysphagia gives trouble at the throat within one second of swallowing, affects liquids and solids together, and produces coughing, choking or nasal regurgitation with risk of aspiration. Stroke, Parkinson disease, myasthenia gravis, motor neurone disease, prolonged intubation, Zenker diverticulum and head and neck cancer are the main causes.
• Oesophageal dysphagia gives a food-sticking sensation lower down. Mechanical obstruction begins with solids and progresses to liquids. Motility disorders affect solids and liquids from the start.
• Alarm features are progressive dysphagia (solids then liquids), unintended weight loss, anaemia and bleeding. These require urgent endoscopy.
• VFSS (with FEES) is the method of choice for instrumental assessment of oropharyngeal dysphagia. Upper endoscopy with biopsies comes first for oesophageal dysphagia; barium oesophagram complements it; high-resolution manometry is used when endoscopy is normal.
• Treat the cause: iron repletion plus dilation for Plummer-Vinson, PPI plus dilation for peptic stricture and ring, steroids/diet/PPI for eosinophilic oesophagitis, pneumatic dilation or POEM/surgery for achalasia, oncology care for cancer, rehabilitation for neurological disease.
• Protect the airway and nutrition first, and get speech and language therapy involved early.
• In low-resource settings, bedside assessment, safe textures, correction of iron deficiency and timely referral for red flags are the priorities.