GI - Dysphagia, GERD, Esophageal Cancer Flashcards
Define Dysphagia, Oropharyngeal dysphagia and Esophageal dysphagia
Dysphagia: difficulty in swallowing, Failure to clear good and drink through upper digestive tract into stomach at appropriate rate
Oropharyngeal dysphagia
- Difficulty with initial phases of swallowing, from mouth to esophagus
- Usually functional (i.e. due to neuromuscular diseases)
Esophageal dysphagia
- failure of peristaltic delivery of food through oesophagus
- Can be functional or mechanical
- Sensation of food or liquid obstructed in passage from mouth to stomach
Define 3 physiological phases of swallowing
Oral phase
Oropharyngeal phase
Esophageal phase
Describe oral phase of swallowing
Oral phase: voluntary, striated muscles
→ Mastication of solid to form food bolus
→ Tongue movement to achieve glossopalatal seal → push food bolus or fluid against hard palate
Describe oropharyngeal phase of swallowing
Oropharyngeal phase: involuntary
→ Activation of mechanoreceptors of pharynx → initiation of swallowing reflex
→ Soft palate elevates (levator veli palatini) → nasal cavity closed off
→ Larynx elevates (suprahyoid muscles) → larynx closed off (by epiglottis)
→ Pharyngeal muscles contract → food bolus delivered from pharynx into oesophagus
Describe esophageal phase of swallowing
Oesophageal phase: involuntary
→ Peristaltic movement of muscularis propria
→ food bolus delivered into stomach
Neurological control of swallowing
3 key questions for suspected dysphagia
- Is it real dysphagia? Globus hystericus or Odynophagia?
- Oropharyngeal or Esophageal dysphagia?
- Mechanical/ anatomical or Functional motility problem?
Causes of oropharyngeal dysphagia
- Functional?
- Mechanical?
- Iatrogenic?
Functional:
- Diseases of CNS:
Bulbar palsy, pseudobulbar palsy, Parkinson’s disease
- Diseases of motor neurones:
Motor neuron disease, peripheral neuropathy, poliomyelitis, syphilis
- Diseases of NMJ/muscles:
Myasthenia gravis, myopathies (muscular dystrophy, polymyositis, dermatomyositis)
Mechanical:
- Mural causes:
Pharyngeal pouch, oropharyngeal tumours, strictures
- Extramural causes:
Goitre, lymphadenopathy, cervical osteophytes, retropharyngeal abscess
Iatrogenic:
- Radiotherapy causing salivary gland atrophy
Causes of esophageal dysphagia
Primary motility disorders:
Achalasia, diffuse oesophageal spasm, nutcracker oesophagus, hypertensive LES
Secondary motility disorders:
Diabetic neuropathy, scleroderma, Sjogren’s syndrome, multiple sclerosis
Intraluminal causes: Foreign bodies (fishbone commonest), lower oesophageal rings, oesophageal webs
Mural causes:
Oesophageal/cardia tumours, oesophagitis, strictures
Extramural causes:
Anterior mediastinal masses, CA lung, TB, cardiovascula
Esophagitis:
Causes
Peptic: acid reflux
Post-radiation
Chemical
Infectious:
Healthy: Candida albicans, HSV
HIV: fungal, viral (esp CMV), mycobacteria, protozoan, ulcers
Drugs:
tetracyclines, NSAIDs, KCl, alendronate
Extramural causes of esophageal dysphagia
Anterior mediastinal masses (thyroid, thymus, teratoma, terrible lymphoma)
CA lung
TB
S/S of oropharyngeal dysphagia
- Difficulty in initiating swallowing
- Nasal regurgitation, choking and weak cough
- Halitosis
- Recurrent aspiration pneumonia
- A/w other neurological signs:
Nasal speech (soft palate paralysis)
Drooling of saliva, dysarthria
Dysphonia
S/S esophageal dysphagia
C/O food getting stuck in throat or chest
Region localized is poorly correlated with exact site of abnormality
Retrosternal: usually corresponds to site
Suprasternal: commonly referred from below
Differentiate mechanical vs functional cause of dysphagia
- Onset
- Progression
- Solid and fluid swallowing
- Variation with temp.
- Intermittent causes
- Progressive causes
Explain why pharyngeal pouch can cause halitosis
Zenker diverticulum/ Pharyngeal pouch
Outpouching arise from the Kilian Dehiscence between thyro- and cricopharyngeus
Cricopharyngeal (CP) muscle fails to relax during swallowing + Incoordination of swallowing within pharynx → herniation through cricopharyngeus muscle
→ formation of a pouch
> > Easy to lodge food there and causing dysphagia and foul smell
Ddx intermittent mechanical dysphagia
Webs and rings
- hiatus hernia (97%) and eosinophilic oesophagitis
- Plummer-Vinson syndrome, Zenker’s diverticulum, bullous dermatological disease and GVHD
Esophagitis
CVS causes (rare)
- Dysphagia lusoria due to aberrant right subclavian artery
- Dysphagia aortica due to thoracic aorta aneurysm
- Dysphagia megalatriensis due to LA dilatation
Ddx progressive mechanical dysphagia
Benign strictures
- Reflux: acid regurgitation, heartburn
- Post-RT strictures
- Previous oesophagitis
CA oesophagus, cardia of stomach
- RFs of CA oesophagus, eg. chronic GERD, smoking, FHx
Ddx Functional esophageal dysphagia
Achalasia
- progressive dysphagia
- regurgitation of undigested food/saliva
- Must exclude pseudoachalasia due to carcinoma infiltrating myenteric plexus
Other motility disorder:
- intermittent, non-progressive dysphagia
- Hypertensive disorders, eg. diffuse oesophageal spasm, nutcracker oesophagus
Scleroderma/ Systemic sclerosis
- a/w heartburn (GERD symptom) and progressive dysphagia
- Look for systemic features: Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasia
Ddx Odynophagia and dysphagia
□ Oesophagitis: drug-induced, radiation, infectious, reflux
□ Caustic ingestion
□ Late CA oesophagus
Specific investigations for dysphagia
Video fluoroscopy swallowing study (VFSS)
Barium swallow
Upper Endoscopy
Fiberoptic endoscopic evaluation of swallowing (FEES)
High resolution manometry (HRM)
Endoluminal Functional Lumen Imaging Probe (EndoFLIP)
Outline different types of Primary esophageal motility disorders
Achalasia
- Hypertensive LES + hypoperistalsis
Hypercontracting oesophagus
- Hypertensive LES
- Nutcracker/jackhammer oesophagus
- Hypertensive peristalsis
Hypocontracting oesophagus
- Hypotensive LES
- Ineffective oesophageal motility (IEM)
Dyscoordinated motility
- Diffuse oesophageal spasm
Outline different types of secondary esophageal motility disorders
Systemic sclerosis
- Hypotensive LES + distal hypoperistalsis + normal proximal oesophagus and UES
Chagas’ disease
- Hypertensive LES + hypoperistalsis (= idiopathic achalasia)
DM neuropathy
Sjogren’s syndrome
Management options for esophageal motility disorders
□ Antispasmodics: CCB, nitrates, anticholinergics
□ Surgical options:
→ Endoscopic pneumatic dilatation
→ Surgical or minimally invasive myotomy
→ Intrasphincteric injection of botox
□ Psychological Mx:
→ Benzodiazepines, anxiolytics, antidepressants
→ Psychological and behavioural therapies
→ Reassurance
Achalasia
- Characteristic features
- Demographics
characterized by
□ Hypertonic LES
□ Failure of LES to relax in swallowing
□ Hypoperistalsis: failure of propagation of oesophageal contraction → progressive dilatation of oesophagus
Demographics: M:F ≈ 1:1, age infancy to 9th decade (but majority 20-40y)
Causes of Achalasia
□ Primary (idiopathic): HLA-DQw1 and HSV-1 infection
□ Secondary: Chagas’ disease, infiltrative (amyloidosis, sarcoidosis), paraneoplastic (CA lung, cholangiocarcinoma)
□ (Pseudoachalasia): OGJ cancer → mechanical obstruction + infiltration of nerve plexus
Pathophysiology of idiopathic achalasia
Normal innervation by
→ Excitatory (cholinergic) motor neurones
→ Inhibitory (nitric oxide) motor neurones
Early: loss of inhibitory neurones → ↑basal LES pressure + failure of LES relaxation during swallowing
Later: loss of excitatory neurones → oesophageal hypo/aperistalsis
Clinical features of Achalasia
Complications of achalasia
□ Progressive dysphagia:
→ Initially intermittent, gradually worsens
→ Worse for solids, eased by drinking liquids, by standing and moving around after eating
□ Regurgitation: immediately after meals
□ Cough: esp when recumbent
□ chest pain due to oesophageal spasms (may not resolve even after treatment)
□ Recurrent aspiration pneumonia/bronchitis in late stages
Complications:
□ SCC of oesophagus (28× risk)
□ Food stasis may result in erosions or candida oesophagitis
Manometric subtypes of achalasia
Function of sub-typing
therapeutic and prognostic significance
□ Type I (classic): impaired LES relaxation + no oesophageal body pressurization
□ Type II (compressive): impaired LES relaxation + oesophageal compression
□ Type III (spastic): impaired LES relaxation + spastic oesophageal contractions
Investigations and typical findings for achalasia
OGD + Biopsy: mainly to r/o pseudoachalasia
→ Dilated oesophagus with stasis of food and secretions (frothy)
→ LES appears tight
CXR:
→ Widened mediastinum with air-fluid level
→ Absence of gastric air bubble
Barium swallow: bird’s beak / rat’s tail appearance
→ Tapered narrowing of lower oesophagus
→ Dilated proximal oesophagus + air-fluid level in late stage
→ Obstruction often relieved by drinking more fluid
High-resolution manometry: for definitive diagnosis
→ Aperistalsis with low-amplitude simultaneous oesophageal body contraction
→ Hypertensive LES (>45mmHg) + pressurized oeso body
→ Failure of LES relaxation (>8mmHg) with swallowing
List treatment options for different manometry subtypes of achalasia
Pneumatic dilatation / surgery for type I/II
POEM for type III
Options:
- Endoscopic pneumatic dilatation: Dilatation of LES using endoscopically placed balloon
- Surgical myotomy (Heller’s operation) + partial fundoplication: Laparoscopic or open cutting of LES fibers + reduce GERD symptoms
- Peroral endoscopic myotomy (POEM): endoscopic diathermy of LES muscles
- Endoscopic botox injection, Nitrates / CCB if failed botox
- Oesophagectomy in end-stage
Diffuse esophageal spasm
- Clinical presentation
- Investigations and typical findings
- Management
Clinical presentation:
□ Late middle age
□ Episodic chest pain (may mimic angina)
□ Sometimes a/w transient dysphagia or occur in response to gastroesophageal reflux
Ix:
Manometry:
→ Simultaneous contraction of oesophageal body
→ Intact LES relaxation**
Barium swallow: cockscrew appearance**
→ Due to simultaneous contractions of circular muscle of oesophageal body
Mx:
□ PPI when gastroesophageal reflux is present
□ Oral/sublingual nitrates or nifedipine to relieve attacks of pain
Zenker’s diverticulum
- Pathogenesis
- S/S
- Ix
- Tx
Pathology:
□ Cricopharyngeus and thyropharyngeus do not overlap → physiological weak spot
□ Incoordination of swallowing within pharynx → herniation through cricopharyngeus muscle → formation of a pouch
S/S:
□ asymptomatic
□ long Hx of halitosis and recurrent sore throats
□ Regurgitation: food without acid/bitter taste
□ Dysphagia if pressing on oesophagus
□ ± neck swelling
Ix:
□ Barium swallow: visualizes pouch, incoordination of swallowing ± pulmonary aspiration
□ C/I endoscopy: risk of perforation!!
Mx:
□ Surgical myotomy ± resection of pouchq
Medications that cause esophageal ulceration?
Pills that lodge in esophageal wall can cause erosions:
NSAIDs
Tetracyclines
Potassium chloride
Alendronate
GERD
- Pathophysiology
- Complications
Reflux: reflux of gastric content into lower oesophagus due to
→ Incompetent LES (hiatus hernia or dietary factors)
→ Increased intra-abdominal pressure due to obesity, tight garments, large meal, pregnancy
→ Gastric dysmotility: gastric emptying often delayed
Acid damage: mucosal inflammation due to exposure to acidic gastric content
→ Gastric content: acid, pepsin, bile
→ Ineffective oesophageal clearance
Chronic inflammation causes complications → Oesophagitis → Strictures → Barrett’s oesophagus → Adenocarcinoma
Risk factors of GERD
Low LES tone:
→ Genetic determinants
→ Hiatus hernia
→ Diet/environment: alcohol, caffeine, smoking
→ Drugs (that cause sm relaxation), eg. NSAIDs, CCB, BB, nitrates, α-blocker, theophylline, anticholinergic
High intra-abdominal pressure: pregnancy, chronic cough, obesity, constipation
Clinical presentation of GERD
Heartburn and regurgitation
- characteristically posturally aggravated
Water brash: reflex salivary gland stimulation as acid enters throat
Odynophagia due to oesophagitis and ulcers
Dysphagia due to strictures
Extra-oesophageal symptoms
- Laryngo-pharyngeal reflux (LPR)
- Asthma
- Recurrent chest infections
- Dental erosions
- Sleep disturbances
(large overlap between GERD, NCCP and dyspepsia)
Classification of GERD
Montreal classification
□ Non-erosive reflux disease (NERD) (60-80%):
→ Typical GERD symptoms but normal oesophageal mucosa with OGD
□ GERD with erosive oesophagitis (20-35%)
□ GERD with Barrett’s oesophagitis (1-5%)
Diagnosis of GERD
Non-invasive tests for clinical diagnosis
→ Clinical symptomatology ± diagnostic questionnaire
→ Proton pump inhibitor test (PPI test)
OGD
24h oesophageal impedance pH testing: GERD symptoms refractory to treatment
Manometry
Management of GERD
- Lifestyle modification
□Stop smoking and drinking
□ Reduce weight
□ Elevate head of bed + avoid tight clothing
□ Diet changes: Eat small meals, avoid late meals, Avoid reflux-promoting agents, eg. alcohol, coffee, chocolate etc (not evidence-based) - Medication:
→ Acid-reducing agents: antacids, H2RA, PPI
→ Prokinetics: metoclopramide, cisapride - Surgery, eg. Nissen fundoplication
Esophageal cancer
- 2 main histological subtypes
- Prevalence and demographics
Gender: M (9.9/100k) >F (2.3/100k)
Asian population, SCC > adenocarcinoma
Western population, adenocarcinoma > SCC
Incidence of SCC decreasing: less smoking
Incidence of Adenocarcinoma increasing: due to ↑obesity, ↑GERD
Risk factors for SCC esophagus
Age >60y, male gender, FHx
Genetics: Peutz-Jegher syndrome, PTEN
Race: African, Asians
Smoking + alcohol**
Diet: ↓fresh vegetables/fruit ↑hot soup, beverages ↑pickles, salted fish (nitrosamines) ↓micronutrients, eg. β-carotene, folate, vitamin C/E, selenium
Oesophageal diseases
Achalasia
Caustic injuries/strictures
Others, eg. Plummer-Vinson syndrome, diverticula, webs
H&N cancers: field cancerization by similar RFs
HPV infection
Risk factors for esophageal adenocarcinoma
Age >60y, male gender, FHx
Race: Caucasians
Smoking (NOT alcohol)
Obesity and metabolic syndrome
Oesophageal diseases
- Chronic GERD
- Barrett’s oesophagus (40×)
Compare SCC and adenocarcinoma of esophagus
- Site
- Pathogenesis
- Metastasis propensities
- Malignant behavior
SCC:
- Middle 1/3 esophagus
- Carcinoma-in-situ»_space; invasive SC
- Early invasion of submucosal wall, intrathoracic LN, trachea and aorta
- Early metastasis (30% at presentation): liver, bone, lung
Adenocarcinoma:
- Distal 1/3 esophagus, near EGJ
- Chronic GERD»_space; Barrett’s esophagus»_space; dysplastic changes»_space; invasive adenocarcinoma
- Early LN invasion (lower abdominal LN)
- Late metastasis to intra-abdominal organs
Why does esophageal cancer carry poor prognosis?
□ Late presentation with early spread of disease
□ Anatomically deep-seated with important surrounding structures
□ Typically occur in elderly population with comorbid diseases
Clinical presentation of esophageal cancer
Asymptomatic/non-specific for early stage disease
Progressive painless dysphagia, especially solids
Odynophagia: late extra-oesophageal involvement
Regurgitation
Systemic S/S:
- Weight loss
- Anaemia
Local invasion:
- Profuse UGIB from vascular invasion
- Recurrent pneumonia/ intractable cough from tracheobronchial fistula
- Hoarseness from RLN invasion
Systemic metastatic S/S
- Bone, Liver, Lungs, Brain, LN …etc
First-line investigations, staging Ix and expected findings for esophageal cancer
OGD + biopsy:
- Appearance: large mucosal mass pathognomonic
Barium swallow: irregular stricture with shouldering
Staging Ix:
- Endoscopic ultrasound (EUS) for T/N (locoregional) staging
- PET-CT for M (systemic) ± T/N staging
- Bronchoscopy for airway involvement
- Laryngoscopy
Management of esophageal cancers:
- Early cancer
- Superficial cancers
- Resectable local cancers
- Unresectable cancer
Early: Endoscopic Tx
- Endoscopic mucosal resection (EMR)
- Endoscopic submucosal dissection (ESD)
- ± adjuvant: photodynamic therapy (PDT), RFA
Superficial: Esophagectomy only
Resectable/ locally advanced: Resection + neoadjuvant chemo/RT + adjuvant chemo/RT (if adenocarcinoma)
Unresectable: Palliative chemo/RT
chemo/RT:
→ Cisplatin + 5-FU + RT for SCC
→ Carboplatin + paclitaxel + RT for adenocarcinoma
Esophagectomy
Phases/ number of areas operated on
Fields of LN dissection
Phase, i.e. number of areas operated on
- I: oesophagogastrectomy, transhiatal
- II: Lewis-Tanner operation (most common)
- III: McKeown operation
Field of LN dissection:
- II: thorax + abdomen
- III: thorax + abdomen + neck**
Esophagectomy
- Choices of conduits
- Route of anastomosis
- Approaches
→ Conduit: stomach, colon, jejunum
→ Route of anastomosis: orthotopic, retrosternal, subcutaneous (rare)
→ Approach: open, VATs, totally minimally invasive, robotic
Complications of esophagectomy
CVS: post-oesophagectomy AF, acute MI, VTE
Pulmonary: atelectasis, pneumonia, ARDS, sputum retention
Surrounding structure injury:
- RLN injury → hoarseness
- Tracheo-bronchial injury → can lead to fistula formation
Anastomotic complications:
- Anastomotic leak leading to mediastinitis
- Anastomotic strictures due to healed anastomotic leaks
- Conduit ischaemia
Chylothorax due to thoracic duct damage
Hiatal herniation of bowel
Post-esophageal GERD
