Dysphagia

Last updated 31 May 2026 · Gastroenterology

📋 Key Information Summary

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Dysphagia is difficulty swallowing and may be oropharyngeal (transfer problem — neurological, structural) or oesophageal (transport problem — mechanical or motility).
Alarm features (progressive solids dysphagia, weight loss, odynophagia, haematemesis, age > 50 with new symptoms) mandate urgent endoscopy within 2 weeks.
Achalasia is the most important primary motility disorder; diagnosed by high-resolution manometry (HRM) and treated with pneumatic dilatation, per-oral endoscopic myotomy (POEM), or Heller myotomy.
Oesophageal adenocarcinoma arises from Barrett oesophagus; incidence in Australia has risen over the past three decades, particularly in men aged > 50.
Barrett oesophagus requires surveillance gastroscopy per BSG/AGA protocols; low-grade dysplasia → endoscopic eradication therapy, high-grade dysplasia → endoscopic mucosal resection or ablation.
Common drug-induced oesophageal injury culprits include doxycycline, alendronate, NSAIDs, potassium chloride, and iron supplements — advise upright posture and water with tablets.
First-line investigation for oropharyngeal dysphagia is a videofluoroscopic swallowing study (VFSS) or fibreoptic endoscopic evaluation of swallowing (FEES).
First-line investigation for oesophageal dysphagia is upper GI endoscopy (OGD) with biopsies if mucosal abnormality is found.
Oesophageal high-resolution manometry (HRM) is the gold standard for differentiating achalasia from other motility disorders (distal oesophageal spasm, jackhammer oesophagus).
PPI therapy (e.g., esomeprazole 20–40 mg daily) is first-line for eosinophilic oesophagitis and reflux-related strictures; dilation for peptic strictures.
Aboriginal and Torres Strait Islander Australians have higher rates of oesophageal cancer presentation at advanced stage and lower rates of endoscopy access in remote areas.
All patients with dysphagia should be assessed for aspiration risk and nutritional status (dietitian referral, Malnutrition Screening Tool).

Introduction & Australian Epidemiology

Dysphagia — the subjective sensation of difficulty swallowing — affects approximately 8–16% of the general Australian population, with prevalence rising sharply in those aged ≥ 65 years (up to 30–40% in aged-care settings). It is associated with significant morbidity including aspiration pneumonia, malnutrition, dehydration, and reduced quality of life.

Swallowing is a complex neuromuscular sequence divided into oral preparatory, oral propulsive, pharyngeal, and oesophageal phases. Disruption at any point produces dysphagia, but clinically the distinction between oropharyngeal (transfer) and oesophageal (transport) dysphagia is the most important first diagnostic step, as it directs investigations and management pathways.

In Australia, the most common causes of oropharyngeal dysphagia are stroke (estimated 35–60% of acute stroke patients), neurodegenerative diseases (Parkinson disease, motor neurone disease), and head/neck malignancy. Oesophageal causes include gastro-oesophageal reflux disease (GORD) with peptic stricture, eosinophilic oesophagitis, oesophageal carcinoma, and achalasia. Drug-induced oesophageal injury accounts for an under-recognised proportion of presentations, particularly in younger patients.

The annual incidence of oesophageal cancer in Australia is approximately 1,600–1,800 new cases per year (AIHW 2023 data), with oesophageal adenocarcinoma now more common than squamous cell carcinoma in the Australian population, reflecting rising Barrett oesophagus prevalence and obesity rates. Five-year survival remains poor (~23%), largely because of late-stage presentation.

This article provides a comprehensive, evidence-based framework for the diagnosis and management of dysphagia in Australian clinical practice, covering aetiology, investigation, and treatment of the principal causes.

Causes & Diagnostic Model

Classification of Dysphagia

A structured diagnostic approach begins with classifying dysphagia as oropharyngeal or oesophageal based on the timing and nature of symptoms.

Feature	Oropharyngeal (Transfer)	Oesophageal (Transport)
Onset	Immediately on swallowing	Seconds to minutes after swallowing
Difficulty	Initiating swallow; nasal regurgitation; choking	Food "sticking" retrosternally
Preferred phase	Liquids ≥ solids (neurological) or solids ≥ liquids (structural)	Solids > liquids (progressive in mechanical); intermittent in motility
Key associations	Dysarthria, nasal speech, coughing, recurrent aspiration pneumonia, weight loss	Heartburn, regurgitation, odynophagia, chest pain
First-line investigation	VFSS or FEES	Upper GI endoscopy (OGD)

Oropharyngeal Causes

Neurological: Stroke (most common), Parkinson disease, motor neurone disease (MND/ALS), multiple sclerosis, myasthenia gravis, brainstem tumours.
Muscular: Inclusion body myositis, dermatomyositis, muscular dystrophies.
Structural: Head and neck carcinoma (post-surgical / post-radiotherapy), pharyngeal pouch (Zenker diverticulum), cervical osteophytes, cricopharyngeal bar.
Other: Presbyphagia (age-related sarcopenia of swallowing musculature).

Oesophageal Causes

Mechanical (luminal/mural): Peptic stricture, oesophageal carcinoma, eosinophilic oesophagitis (EoE), oesophageal web/ring (Schatzki ring), extrinsic compression (mediastinal lymphadenopathy, left atrial enlargement, aortic arch aneurysm).
Motility disorders: Achalasia, distal oesophageal spasm (DES), jackhammer oesophagus, absent contractility, scleroderma-associated aperistalsis.
Inflammatory / infectious: Pill oesophagitis, radiation oesophagitis, infectious oesophagitis (Candida, HSV, CMV — consider in immunocompromised).

Diagnostic Pathway — Clinical Model

History & Examination

Timing of symptoms, solids vs liquids, progressive vs intermittent, neurological signs, neck mass, nutritional status. Use the Eating Assessment Tool (EAT-10) screening questionnaire.

Classify: Oropharyngeal vs Oesophageal

Based on history. If oropharyngeal → speech pathology assessment ± VFSS/FEES. If oesophageal → proceed to endoscopy.

Identify Alarm Features

Progressive solids dysphagia, unintentional weight loss (>5% in 3 months), haematemesis/melaena, persistent vomiting, iron deficiency anaemia, age >50 with new-onset symptoms → urgent OGD within 2 weeks.

Investigations

OGD with biopsies, barium swallow, oesophageal HRM, 24-hr pH-impedance, CT chest/abdomen as indicated.

Definitive Diagnosis & Treatment

Targeted therapy based on aetiology: PPI for GORD/strictures, endoscopic therapy for Barrett's/cancer, myotomy for achalasia, dietary modification for EoE, swallowing therapy for neurological causes.

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Red flags requiring urgent endoscopy: Progressive dysphagia to solids, unintentional weight loss, iron deficiency anaemia, persistent vomiting, age >50 with new dysphagia. Refer for OGD within 2 weeks per National Cancer Standards.

Oesophageal Cancer & Barrett Oesophagus

Barrett Oesophagus

Barrett oesophagus (BO) is defined as the replacement of normal squamous epithelium of the distal oesophagus by metaplastic columnar epithelium containing goblet cells (intestinal metaplasia). It is a pre-malignant condition and the principal precursor of oesophageal adenocarcinoma (OAC).

Prevalence: Estimated 1.5–3% of the Australian adult population; higher in those with chronic GORD (> 5 years), male sex, age > 50, central obesity (waist circumference > 102 cm men, > 88 cm women), smoking, and family history.
Annual progression rate: Non-dysplastic BO → OAC ~0.5%/yr; low-grade dysplasia (LGD) → high-grade dysplasia (HGD) or OAC ~1–3%/yr; HGD → OAC ~5–10%/yr.
Diagnosis: Confirmed by upper GI endoscopy with 4-quadrant biopsies at 2 cm intervals (Seattle protocol) showing intestinal metaplasia on histopathology.

Surveillance Protocol (BSG 2014 / AGA 2022)

Histology	Surveillance Interval	Action
Non-dysplastic BO, short segment (< 3 cm)	Consider discharge or 5-yearly OGD	Continue PPI; lifestyle modification
Non-dysplastic BO, long segment (≥ 3 cm)	Every 2–3 years	Continue PPI; 4-quadrant biopsies per Seattle protocol
Confirmed low-grade dysplasia (expert pathology review)	Every 6–12 months, or offer endoscopic eradication therapy (EET)	Radiofrequency ablation (RFA) preferred EET
High-grade dysplasia	Endoscopic treatment	Endoscopic mucosal resection (EMR) for visible lesions + RFA for remaining Barrett segment

Oesophageal Cancer

Oesophageal cancer in Australia is approximately 60% adenocarcinoma (distal oesophagus, GOJ) and 30% squamous cell carcinoma (mid/upper oesophagus). Risk factors for OAC include Barrett oesophagus, GORD, obesity, smoking. Risk factors for SCC include smoking, alcohol, hot beverages, caustic injury, and achalasia.

Staging Investigations

Essential

OGD with biopsies

Tissue diagnosis, tumour length, distance from incisors. Cytology brushings if stricture prevents biopsy.

Essential

CT chest/abdomen with IV contrast

Assess local extent, liver metastases, celiac lymphadenopathy.

Essential

PET-CT

Detect occult distant metastases. MBS item 61356.

Available

Endoscopic ultrasound (EUS)

Most accurate T and N staging. Fine-needle aspiration (FNA) of suspicious lymph nodes. Available at major tertiary centres.

Available

Laparoscopy / thoracoscopy

Considered for staging of junctional tumours to exclude peritoneal disease.

Management Overview

All cases should be discussed at a multidisciplinary team (MDT) meeting involving gastroenterology, upper GI surgery, medical oncology, radiation oncology, radiology, pathology, dietetics, and palliative care.

Stage	Treatment Approach	Key Agents / Techniques
T1a (mucosal) — early	Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD)	Curative if no submucosal invasion; close endoscopic follow-up
T1b–T2, N0/N+, operable	Neoadjuvant chemo-radiotherapy (CROSS regimen) → oesophagectomy	Carboplatin + paclitaxel + 41.4 Gy radiation over 5 weeks
T3/T4, N+, operable	Neoadjuvant chemotherapy (MAGIC or FLOT) ± radiation → surgery	ECF (epirubicin, cisplatin, 5-FU) or FLOT (5-FU, leucovorin, oxaliplatin, docetaxel)
Locally advanced, inoperable	Definitive concurrent chemo-radiotherapy	Cisplatin + 5-FU + 50–60 Gy radiation
Metastatic / palliative	Systemic chemotherapy ± immunotherapy; palliative stenting or radiation	Nivolumab (PBS authority required) for PD-L1+ tumours post-chemo; self-expanding metal stent (SEMS) for obstruction

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Palliative stenting: Self-expanding metal stents (SEMS) provide rapid relief of malignant dysphagia. Avoid in patients with proximal tumours within 2 cm of the upper oesophageal sphincter. Covered stents preferred for tracheo-oesophageal fistula.

Key Medications — Oesophageal Cancer

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Nivolumab

Opdivo® · PD-1 immune checkpoint inhibitor

Adult dose 240 mg IV every 2 weeks or 480 mg IV every 4 weeks

Indication Adjuvant for resected oesophageal/GOJ cancer with residual pathologic disease post-neoadjuvant chemo-radiotherapy

Renal adjustment No adjustment required

PBS status Authority Required

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Carboplatin

Paraplatin® · Platinum-based alkylating agent

Adult dose AUC 5 IV day 1, every 3 weeks (CROSS: AUC 2 weekly × 5 weeks with RT)

Renal adjustment Dose per Calvert formula (GFR-based). Caution if eGFR < 30 mL/min.

PBS status PBS General Benefit

Achalasia & Oesophageal Motility Disorders

Achalasia

Achalasia is a primary oesophageal motility disorder characterised by failure of lower oesophageal sphincter (LES) relaxation and absence of oesophageal peristalsis. It affects approximately 1–3 per 100,000 people per year in Australia, with a peak incidence in the 30–60 year age group. The pathogenesis involves selective loss of inhibitory (nitrergic) myenteric neurones in the distal oesophagus, often autoimmune-mediated.

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Chicago Classification v4.0 (2021): Achalasia is classified by HRM pattern into Type I (classic — absent peristalsis, minimal pressurisation), Type II (absent peristalsis with pan-oesophageal pressurisation in ≥ 20% of swallows), and Type III (spastic achalasia — premature contractions with incomplete LES relaxation). Type II has the best treatment outcome.

Clinical Features

Progressive dysphagia to solids and liquids (distinguishes from mechanical obstruction where liquids are initially preserved).
Regurgitation of undigested food, particularly nocturnal (risk of aspiration).
Chest pain (non-cardiac), weight loss.
Long-standing achalasia → oesophageal dilatation → sigmoid oesophagus.
Patients with long-standing achalasia have a slightly increased risk of oesophageal SCC (surveillance is debated).

Diagnosis

Essential

Upper GI endoscopy (OGD)

First-line to exclude mechanical obstruction (tumour, stricture). May show a dilated oesophagus with retained food/fluid, resistance at the GEJ. Essential to exclude pseudoachalasia (GOJ tumour).

Essential

High-resolution oesophageal manometry (HRM)

Gold standard for diagnosis. Identifies achalasia type (I, II, III) per Chicago Classification v4.0. Integrated relaxation pressure (IRP) > 15 mmHg with absent peristalsis. Available at major gastroenterology centres (MBS item 13400).

Available

Barium swallow

Classic findings: dilated oesophagus, "bird-beak" narrowing at the GEJ, absent peristalsis, air-fluid level. Useful when manometry is inconclusive or to assess oesophageal tortuosity pre-treatment.

Available

Functional lumen imaging probe (EndoFLIP)

Adjunct to manometry; assesses oesophageal distensibility and LES compliance. Emerging role in treatment planning.

Treatment of Achalasia

Treatment aims to reduce LES pressure and improve oesophageal emptying. All options are palliative — none restore peristalsis.

Treatment	Details	Success Rate	Best For
Pneumatic dilatation (PD)	Graded balloon dilation (30, 35, 40 mm) at the GEJ under fluoroscopic or endoscopic guidance. Serial dilations with on-demand approach.	85–90% at 2 years; ~50–60% long-term (may need repeat)	Type I and II achalasia; older patients; those unfit for surgery
Laparoscopic Heller myotomy (LHM)	Surgical myotomy of the LES with partial fundoplication (Dor or Toupet) to prevent reflux. Gold standard surgical approach.	85–90% at 5 years	Younger patients (< 40 yr); Type II; those preferring definitive single intervention
Per-oral endoscopic myotomy (POEM)	Endoscopic submucosal tunnel myotomy. No external incisions. Can tailor myotomy length (especially for Type III — extended proximal myotomy).	~90% at 2 years	Type III achalasia (best evidence); failed prior PD or LHM; patients preferring endoscopic approach
Botulinum toxin injection (Botox)	Endoscopic injection of 100 units into the LES in 4 quadrants. Temporary effect.	~70% initial response; ~50% at 1 year (wanes)	Elderly, comorbid patients unfit for PD/surgery; diagnostic trial to confirm diagnosis
Pharmacotherapy	Sublingual nifedipine 10–30 mg 30 min before meals, or isosorbide dinitrate 5 mg SL. Modest and temporary effect.	~50% partial response	Bridge to definitive therapy; patients declining intervention

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Pseudoachalasia: Always consider and exclude GOJ adenocarcinoma (pseudoachalasia) on OGD with biopsies ± CT chest/abdomen before diagnosing primary achalasia. Weight loss > 5 kg and age > 60 should raise suspicion.

Other Oesophageal Motility Disorders

Per the Chicago Classification v4.0, other major motility disorders include:

Distal oesophageal spasm (DES): Premature contractions (distal latency < 4.5 s) in ≥ 20% of swallows with normal IRP. Presents with dysphagia and chest pain. Treatment: calcium channel blockers, diltiazem, or POEM for refractory cases.
Jackhammer oesophagus (hypercontractile oesophagus): Excessively vigorous peristaltic contractions (distal contractile integral > 8000 mmHg·s·cm in ≥ 20% of swallows). Chest pain predominant. Nitrates, calcium channel blockers, or POEM if refractory.
Absent contractility: 100% failed peristalsis with normal IRP. Seen in systemic sclerosis (scleroderma), connective tissue diseases. High GORD risk — aggressive PPI therapy. Fundoplication is contraindicated.
Ineffective oesophageal motility (IOM): ≥ 70% ineffective swallows (weak or failed). Common in GORD, elderly. Usually managed with PPI and dietary advice.

Key Medications — Motility Disorders

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Nifedipine

Adalat® · Calcium channel blocker

Adult dose 10–30 mg sublingual, 30 minutes before meals (achalasia); 10–20 mg PO TDS (DES)

Paediatric dose Not established for oesophageal motility disorders

Renal adjustment No adjustment required

PBS status PBS General Benefit

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Diltiazem

Cardizem® · Non-dihydropyridine calcium channel blocker

Adult dose 60–90 mg PO TDS (DES, jackhammer oesophagus)

Renal adjustment Use with caution; no specific dose adjustment

PBS status PBS General Benefit

Drug-Induced Oesophageal Injury

Drug-induced oesophageal injury (pill oesophagitis) is an under-recognised cause of acute dysphagia and odynophagia. It occurs when a medication tablet or capsule lodges in the oesophagus, usually at areas of physiological narrowing (aortic arch, left bronchus, lower oesophageal sphincter), and causes local mucosal damage through prolonged contact.

High-Risk Medications

Medication	Mechanism	Typical Presentation
Doxycycline	Direct acidic mucosal contact; most common cause in Australia	Odynophagia within hours–days of starting; retrosternal pain
Alendronate (bisphosphonates)	Severe caustic mucosal injury	Oesophageal ulceration, stricture. Must take upright with 200 mL water, remain upright 30 min
NSAIDs (aspirin, ibuprofen, naproxen)	Direct topical mucosal injury + systemic prostaglandin inhibition	Odynophagia, ulceration, stricture with chronic use
Potassium chloride (KCl)	Caustic concentrated salt contact	Severe ulceration, stricture, rarely perforation
Iron supplements (ferrous sulfate)	Direct mucosal erosion	Odynophagia, dark discolouration of mucosa
Ascorbic acid (vitamin C)	Acidic pH contact injury	Mild–moderate odynophagia
Clindamycin	Direct mucosal contact	Odynophagia, oesophageal ulceration

Risk Factors for Pill Oesophagitis

Swallowing tablets with little or no water, or in the supine position.
Large or irregularly shaped tablets/capsules.
Pre-existing oesophageal dysmotility (scleroderma, achalasia, diabetic gastroparesis).
Oesophageal structural abnormality (stricture, web, ring, extrinsic compression).
Reduced saliva production (anticholinergic medications, Sjögren syndrome, radiotherapy).
Elderly patients — decreased oesophageal motility and more medications.

Diagnosis & Management

Diagnosis: Clinical suspicion based on temporal relationship between medication initiation and symptom onset. OGD shows discrete ulcers (often mid-oesophagus) with normal intervening mucosa. Biopsies to exclude alternative pathology (malignancy, infection). Barium swallow may show mucosal irregularity or tablet impaction.

Management:

Discontinue or change the offending agent — switch to liquid formulation if available, or alternative medication (e.g., doxycycline → azithromycin; alendronate → zoledronic acid IV yearly).
PPI therapy: Esomeprazole 40 mg daily for 4–8 weeks to promote mucosal healing.
Sucralfate suspension 1 g/10 mL QDS (30 min before meals) may provide topical mucosal protection.
Education: All patients should take tablets/capsules with ≥ 200 mL water while upright, and remain upright for ≥ 30 minutes after ingestion.
Follow-up OGD at 6–8 weeks if symptoms persist to assess healing and exclude stricture formation.

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Prevention counselling: Advise all patients prescribed high-risk medications to swallow with a full glass of water (200 mL), remain upright for at least 30 minutes, and avoid taking tablets at bedtime. For alendronate: remain upright for 30 minutes; for risedronate: remain upright for 30 minutes.

Key Medications — Pill Oesophagitis Treatment

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Esomeprazole

Nexium® · Proton pump inhibitor

Adult dose 40 mg PO daily, 30 min before breakfast, for 4–8 weeks

Paediatric dose 1–11 yr: 10–20 mg daily (weight-based); 12–17 yr: 20–40 mg daily

Renal adjustment No adjustment required (caution in severe CKD)

PBS status PBS General Benefit

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Sucralfate

Ulsanic® · Cytoprotective mucosal adherent

Adult dose 1 g PO QDS (30 min before meals and at bedtime)

Renal adjustment Caution in severe renal impairment (aluminium absorption risk)

PBS status PBS General Benefit

Eosinophilic Oesophagitis

Eosinophilic oesophagitis (EoE) is a chronic, immune-mediated oesophageal disease characterised by eosinophilic infiltration of the oesophageal mucosa (≥ 15 eosinophils per high-power field on biopsy) in the absence of other causes of oesophageal eosinophilia. It is increasingly recognised in Australia, with an estimated prevalence of 1 per 1,000 adults.

Diagnosis

Symptoms of oesophageal dysfunction (dysphagia, food impaction, odynophagia, chest pain).
OGD with ≥ 2 biopsies from proximal and distal oesophagus showing ≥ 15 eos/HPF.
Endoscopic features: linear furrows, white exudates (eosinophilic abscesses), rings (trachealisation), narrow-calibre oesophagus, Crepe-paper mucosa.
Exclude GORD (responds to PPI), other causes of eosinophilia (parasitic infection, drug hypersensitivity, hypereosinophilic syndrome).

Treatment

A "step-up" approach is recommended:

PPI Trial (PPI-responsive EoE)

Esomeprazole 20–40 mg BD for 8 weeks → repeat OGD with biopsies. Up to 50% of EoE patients achieve histological remission with PPI alone.

Dietary Elimination

Six-food elimination diet (dairy, wheat, egg, soy, nuts, fish/seafood) — effective in ~70%. Reintroduce one food group at a time with OGD to identify triggers. Dietitian involvement essential.

Topical Corticosteroids

Swallowed fluticasone propionate (250–500 mcg BD via MDI, swallowed not inhaled) or budesonide viscous slurry (1–2 mg BD). Continue for 8–12 weeks then reassess.

Biologic Therapy

Dupilumab (anti-IL-4Rα) 300 mg SC weekly — TGA-approved for EoE in adults and adolescents ≥ 12 yr. Reserved for refractory cases.

Endoscopic Dilation

For fibrostenotic strictures causing persistent dysphagia despite medical therapy. Controlled radial expansion (CRE) balloon or Savary bougie dilation. Risk of mucosal tear/perforation (~1–5%).

Key Medication — Eosinophilic Oesophagitis

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Dupilumab

Dupixent® · Anti-IL-4Rα monoclonal antibody

Adult dose 300 mg SC every week

Paediatric dose ≥ 40 kg: 300 mg SC every week; < 40 kg: weight-based per product information

Renal adjustment No adjustment required

PBS status Authority Required

Investigations

Summary of Investigations for Dysphagia

Essential

Upper GI endoscopy (OGD / gastroscopy)

First-line for oesophageal dysphagia. Visualise mucosa, take biopsies (minimum 2 proximal + 2 distal for suspected EoE; 4-quadrant biopsies per Seattle protocol for Barrett surveillance). Therapeutic: dilatation, stent placement, foreign body removal. Available at most metropolitan hospitals; limited in remote areas.

Essential

Videofluoroscopic swallowing study (VFSS)

Gold standard for oropharyngeal dysphagia. Dynamic fluoroscopic assessment of all swallowing phases. Available at major hospitals with speech pathology services. MBS item 58112.

Available

Fibreoptic endoscopic evaluation of swallowing (FEES)

Bedside or clinic-based laryngoscopic assessment of pharyngeal swallowing and aspiration. No radiation. Complementary to VFSS. Requires trained speech pathologist and ENT support.

Essential

High-resolution oesophageal manometry (HRM)

Gold standard for motility disorders. Classifies achalasia (Types I–III) per Chicago Classification v4.0. Essential before definitive achalasia treatment. Available at specialist gastroenterology centres. MBS item 13400.

Available

Barium swallow / oesophagram

Useful for anatomical assessment: strictures, rings, webs, Zenker diverticulum, extrinsic compression, oesophageal motility patterns. Complementary to endoscopy. MBS item 30195.

Available

24-hour pH-impedance monitoring

Assesses acid and non-acid reflux. Useful for evaluating GORD in patients with normal endoscopy, refractory symptoms on PPI, and pre-anti-reflux surgery evaluation. Requires catheter placement or Bravo capsule.

Available

CT chest/abdomen with IV contrast

Staging of oesophageal malignancy. Assess for extrinsic compression (mediastinal mass, lymphadenopathy, aortic pathology). MBS item 56400/56500.

Specialist

Endoscopic ultrasound (EUS)

Most accurate T and N staging for oesophageal cancer. FNA of perioesophageal lymph nodes. Available at tertiary centres with advanced endoscopy services.

Blood Tests

FBC: Iron deficiency anaemia (chronic GORD with blood loss, oesophageal malignancy), eosinophilia (eosinophilic oesophagitis, systemic eosinophilic disease).
Iron studies: Ferritin, transferrin saturation — assess for iron deficiency.
Liver function tests: Hepatic metastases in oesophageal cancer.
CRP / ESR: Non-specific markers of inflammation; useful in connective tissue disease workup.
Autoimmune serology: ANA, anti-Scl-70, anti-centromere if scleroderma suspected (absent contractility pattern on manometry).

Management — Quick Reference

Cause-Specific Treatment Summary

GORD / peptic stricture

Esomeprazole 20–40 mg daily

Long-term PPI; dilatation for stricture

Reassess need for ongoing PPI annually

Eosinophilic oesophagitis

PPI → dietary elimination → swallowed fluticasone 500 mcg BD

8–12 weeks initial; maintenance varies

Dupilumab for refractory (PBS authority required)

Achalasia Type I / II

Pneumatic dilatation OR Heller myotomy ± Dor fundoplication

Single procedure (may need repeat PD)

POEM for Type III or failed prior therapy

Achalasia Type III (spastic)

POEM (extended proximal myotomy)

Single procedure

Best evidence for POEM over PD or Heller

Pill oesophagitis

Stop offending drug; esomeprazole 40 mg daily; sucralfate 1 g QDS

4–8 weeks

Education: 200 mL water, upright 30 min

Oropharyngeal (neurological)

Speech pathology swallowing therapy

Ongoing; tailored exercises

Diet texture modification per IDDSI framework

Oesophageal cancer (metastatic)

Palliative chemotherapy ± nivolumab; SEMS for obstruction

Per MDT plan

MDT discussion mandatory; early palliative care referral

⚠️

Nutritional assessment: All patients with dysphagia should be assessed for malnutrition using the Malnutrition Screening Tool (MST) or Subjective Global Assessment (SGA). Early dietitian referral is essential. Enteral feeding (nasogastric or PEG) may be required for severe neurological dysphagia or advanced malignancy.

Special Populations

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Pregnancy

GORD-related dysphagia

Common in pregnancy due to progesterone-mediated LES relaxation and mechanical compression. Lifestyle modification first-line. PPIs: esomeprazole and omeprazole are Category B3 (TGA) — use lowest effective dose. Ranitidine (now withdrawn) previously preferred — famotidine 20 mg BD is an alternative H2RA.

Endoscopy in pregnancy

OGD is generally safe when clinically indicated (e.g., food impaction, alarm features). Left lateral position with uterine displacement. Minimise sedation — avoid midazolam in first trimester; fentanyl preferred if needed. Monitor foetal heart rate if > 24 weeks gestation.

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Paediatrics

Congenital causes

Oesophageal atresia (± tracheo-oesophageal fistula) — surgical emergency in neonates. Post-repair dysphagia is common (anastomotic stricture in 30–50%). Tracheo-oesophageal fistula, vascular ring, laryngeal cleft.

Eosinophilic oesophagitis

Increasingly common in children (peak 5–15 yr). Presentation: feeding difficulties, failure to thrive, food refusal, abdominal pain. PPI first-line; swallowed budesonide (0.5–1 mg BD) as topical steroid. Dupilumab TGA-approved ≥ 12 yr / ≥ 40 kg.

Foreign body ingestion

Button batteries in the oesophagus are a surgical emergency — emergent endoscopic removal within 2 hours. Coins — most common; endoscopic removal if lodged > 24 hours or symptomatic.

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Elderly

Presbyphagia

Age-related decline in swallowing function — sarcopenia of tongue, pharyngeal, and oesophageal muscles. Overlaps with frailty. Speech pathology assessment for safe swallowing strategies and diet texture modification (IDDSI framework levels 0–7).

Medication-related risk

Polypharmacy increases pill oesophagitis risk. Anticholinergic medications reduce saliva. Review medication necessity; use liquid formulations where possible. Ensure adequate hydration with tablets.

Stroke-related dysphagia

Screen all acute stroke patients with the Gugging Swallowing Screen (GUSS) or Melbourne Health Swallow Screen before any oral intake. Silent aspiration is common — instrumental assessment (FEES/VFSS) required. Increased aspiration pneumonia risk.

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Renal Impairment

Sucralfate

Use with caution in severe CKD (eGFR < 15) — aluminium absorption risk. Monitor aluminium levels if prolonged use.

Carboplatin (chemotherapy)

Dose per Calvert formula using measured GFR. Avoid if eGFR < 20 unless dose-adjusted by oncology.

PPIs

Generally no dose adjustment but long-term PPI use associated with increased CKD progression risk — use lowest effective dose and reassess need.

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Hepatic Impairment

Oesophageal varices

In patients with portal hypertension and cirrhosis, dysphagia may indicate large varices or variceal bleeding. Urgent OGD for assessment and band ligation. Do not biopsy without excluding varices first.

Chemotherapy agents

Carboplatin: hepatic impairment does not significantly alter clearance (renally cleared). Nivolumab: no dose adjustment in mild–moderate hepatic impairment; caution in severe (Child-Pugh C).

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Immunocompromised

Infectious oesophagitis

Consider in HIV/AIDS (CD4 < 200), transplant recipients, chemotherapy-induced neutropenia, and patients on biologics/JAK inhibitors. Candida: white plaques → fluconazole 200 mg day 1 then 100–200 mg daily for 14–21 days. HSV: shallow ulcers, punched-out → valaciclovir 1 g TDS or IV aciclovir. CMV: large, flat ulcers → valganciclovir 900 mg BD for 21 days.

Graft-vs-host disease (GvHD)

Post-allogeneic stem cell transplant: oesophageal GvHD causes severe dysphagia, odynophagia, and mucosal sloughing (desquamative oesophagitis). Systemic corticosteroids ± budesonide slurry.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Australians experience a disproportionate burden of oesophageal cancer and dysphagia-related morbidity. The AIHW reports that Indigenous Australians are 1.5–2 times more likely to be diagnosed with oesophageal cancer and present at a more advanced stage compared to non-Indigenous Australians. Survival rates are significantly lower, reflecting delayed diagnosis, reduced access to specialist services, and barriers to completing treatment pathways.

Key Disparities & Considerations

Cancer stage at diagnosis

Indigenous Australians are more likely to present with advanced (stage III/IV) oesophageal cancer. This is partly due to later presentation with symptoms and longer referral-to-endoscopy times. Culturally safe early-recognition campaigns are needed.

Endoscopy access

Upper GI endoscopy services are concentrated in major cities. Remote and very remote communities (where ~45% of Indigenous Australians reside) may require patient retrieval or lengthy travel for OGD. Endoscopy bus programmes (e.g., Gut Foundation) improve access in some jurisdictions. Telehealth gastroenterology consultations should be used to expedite referrals.

Risk factor profile

Higher rates of tobacco smoking (~40% vs ~11% non-Indigenous), harmful alcohol consumption, and obesity in some communities contribute to increased GORD, Barrett oesophagus, and oesophageal SCC risk. Culturally appropriate smoking cessation and chronic disease prevention programmes are critical.

GORD and H. pylori

H. pylori prevalence is higher in remote Indigenous communities (up to 60–80% in some studies). Paradoxically, H. pylori infection may be protective against GORD and Barrett oesophagus by reducing gastric acid output. However, it increases gastric cancer risk. Test-and-treat strategy should follow current Australian guidelines (GESA).

Swallowing rehabilitation

Speech pathology services for oropharyngeal dysphagia (e.g., post-stroke) are limited in remote areas. Telehealth-delivered swallowing assessments and caregiver training in safe swallowing strategies (IDDSI diet textures) can bridge this gap. Interpreter services should be used for patients whose primary language is not English.

Medication adherence

PPI therapy for GORD and Barrett oesophagus requires ongoing adherence. Ensure medications are accessible through community-controlled health services and Aboriginal health workers. PBS Close the Gap CTG scripts can reduce co-payment barriers.

Cultural safety

Respect cultural obligations around food and eating. In some communities, sharing food is central to social and ceremonial life — dysphagia diet modifications should be discussed sensitively. Involve family, Elders, and Aboriginal health workers in management planning. Gender considerations may apply to certain procedures (e.g., male patients preferring male endoscopists in some settings).

📚 References

1. Gyawali CP, Kahrilas PJ, Savarino E, et al. Modern diagnosis of GERD: the Lyon Consensus. Gut. 2018;67(7):1351–1362.
2. Yadlapati R, Kahrilas PJ, Fox MR, et al. Esophageal motility disorders on high-resolution manometry: Chicago classification version 4.0. Neurogastroenterol Motil. 2021;33(1):e14058.
3. Weusten B, Bisschops R, Coron E, et al. Endoscopic management of Barrett's esophagus: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement. Endoscopy. 2017;49(2):191–198.
4. Dunbar KB. Eosinophilic esophagitis: update on management and controversies. BMJ. 2022;378:e067862.
5. Hirano I, Chan ES, Rank MA, et al. AGA Institute and the Joint Task Force on Allergy-Immunology Practice Parameters Clinical Guidelines for the Management of Eosinophilic Esophagitis. Gastroenterology. 2020;158(6):1776–1786.
6. van Hoeij FB, Bredenoord AJ. Clinical characterization of achalasia subtypes. Expert Rev Gastroenterol Hepatol. 2016;10(10):1137–1143.
7. Aiolfi A, Bona D, Bonavina L, et al. Peroral endoscopic myotomy (POEM) for esophageal achalasia: systematic review and meta-analysis. Surg Endosc. 2023;37:1–14.
8. Australian Institute of Health and Welfare (AIHW). Cancer data in Australia. Canberra: AIHW; 2023. Available at: www.aihw.gov.au/reports/cancer/cancer-data-in-australia.
9. Royal Australian College of General Practitioners (RACGP). Supporting smoking cessation: a guide for health professionals. Melbourne: RACGP; 2021.
10. National Health and Medical Research Council (NHMRC). Australian clinical guidelines for the management of acute stroke. Canberra: NHMRC; 2019.
11. Oors JM, Bredenoord AJ. Effect of H. pylori on the esophagus: more harm than good? Nat Rev Gastroenterol Hepatol. 2022;19(5):281–282.
12. Gastroenterological Society of Australia (GESA). Clinical update: eosinophilic oesophagitis — Australian consensus guidelines. J Gastroenterol Hepatol. 2021;36(Suppl 1):1–28.
13. Dua KS, Piotrowska AM, Rangwalla K, et al. A double-blind sham-controlled trial of pneumatic dilation versus laparoscopic Heller myotomy for achalasia. N Engl J Med. 2020;383(17):1597–1606.
14. van Halsema EE, van Hoeij FB, Moons LME, et al. Safety and efficacy of endoscopic dilation for benign esophageal strictures: a systematic review and meta-analysis. Gastrointest Endosc. 2023;97(4):614–629.
15. Storhaug CL, Fosse SK, Fjeldstad HA. Drug-induced oesophageal injury: a review. BMJ Open Gastroenterol. 2021;8(1):e000560.

for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).