Gastro-oesophageal reflux

Section: UGI Sub-section: Gastric and Oesophagus Curriculum: Curriculum, page 94

Definition

• (Montreal Definition): Condition which develops when reflux of gastric contents into the oesophagus causes troublesome symptoms or complications
• Manifested by symptoms or endoscopic / histologic / 24h-pH studies
• Can be reliably diagnosed if pt has either of:
  • Typical Hx + ≥ 1 piece of objective evidence of reflux
    • Regurigation
    • Heartburn
  • Atypical Hx + ≥ 2 objective evidence
    • Reflux cough
    • Poor dentition
    • Sinusitis
    • Recurrent aspiriations
• Usually associated with a hiatal hernia
• Reflux oesophagitis:
  • Ulceration of distal oesophagus due to reflux

Reflux is Clinical diagnosis

• Typical syx
• Atypical syx and other diagnosis excluded

Incidence

• 10-20% of adults in Western countries have weekly sx
• 35% of population have “heartburn” >1/month
• Only ¼ pts with symptoms consult their doctor
• Only 60% with symptoms will have abnormal endoscopy
• 20% of patients with oesophagitis have no symptoms

Classification Systems

• Three types of GORD
  • Symptomatic but endoscopic negative
    • Probably due to oesophageal hypersensitivity to acid/non-acid reflux
  • Oesophagitis and erosive reflux
    • Typical sx – good response to acid suppression
  • Barrett’s Oesophagus
    • Minimal sx due to insensate nature of columnar epithelium to acid
• Grading systems for severity of oesophagitis on OGD
  • Los Angeles Classification
  • Savary-Miller Classification

Los Angeles Classification

• Grades oesophagitis severity by extent of mucosal abnormality, with complications recorded separately
• LA A
  • One or more mucosal breaks, each <5mm in length
• LA B
  • One or more mucosal breaks > 5mm long, not continuous between tops of adjacent mucosal folds
• LA C
  • One or more mucosal breaks that are continuous between the tops of adjacent folds, but < 75% circumference
• LA D
  • One or more mucosal breaks that involve at least > 75% circumference

Aetiology

• Failure of the natural anti-reflux mechanisms
• Risk factors:
  • Inherited
  • Family hx
  • Demographic
  • Age > 50
  • M>F
  • Pregnancy
• Lifestyle
  • Smoking (reduced LOS pressure)
  • Obesity
  • EtOH
• Medical
  • IBS, Gastric dysfunction, Zollinger-Ellison Syndrome
• Structural
  • Hiatus Hernia (2/3 pts with hernia have GORD)
  • Oesophageal dysmotility
• Refluxogenic stimuli:
  • Large / fatty / spicy meals, chocolate, onions, peppermint, garlic, nicotine, carbonated drinks, EtOH, caffeine, theophylline, Ca channel blockers, anticholinergics
• NB: Inverse relationship with H pylori infection
  • Protective to have H pylori as causes atrophic gastritis and reduced acid production

Clinical Presentation

NB: Development of stricture may actually improve reflux symptoms by creating barrier

Typical Symptoms

• Heartburn, non-cardiac retrosternal chest pain
  • Unable to bend over without symptoms
• Volume reflux
  • Regurgitation, acid brash (acid regurgitation) especially when bending forward, belching
• Obstruction or dysmotility
  • Forceful regurgitation
• Oesophageal diverticulum or achalasia
  • Undigested food regurgitation
  • Waterbrash - acid reflux + salivary hyper-production
• Odynophagia (pain on swallowing) > Oesophagitis
• Dysphagia for solids – in advanced GORD
  • Oedema, oesophagitis, stricture, dysmotility, large H/H (liquids – neuromuscular)

Atypical Symptoms

• Epigastric pain
• Bloating
• Extra-oesophageal
  • Pulmonary Sx (less likely to respond to therapy):
    • Cough, asthma, pneumonia
    • Respiratory Sx my occur via 2 mechanisms:
      • Direct micro-aspiration into tracheobronchial tree
      • Vagal reflex → Bronchoconstriction
  • Sx of vocal cord irritation:
    • Hoarseness (Cherry-Donner syndrome), cough
    • Cough Sx can be related to GORD if post laryngitis is seen
    • If operated on → 64% satisfaction rate / Sx improved ≥ 50% at 1yr
      • (cf 90% satisfaction post-surgery for reflux Sx)
  • Dental damage

Alarm Symptoms

• All warrant endoscopy
  • Bleeding
  • Weight loss
  • Dysphagia
  • Respiratory symptoms
  • Chest pain
  • Anaemia
  • Failure to respond to PPI over 6/52

Pathophysiology

Physiology of Normal Swallow

• On swallowing, UOS and LOS relax, and food bolus propelled distally by peristalsis to the stomach
  • Peristalsis = Sequential contraction of oesophageal body
    • Greatest pressure at midpoint of contracted segment
    • Usually few cm behind the food bolus
• Primary Peristalsis
  • Instigated centrally in the swallowing centre by swallowing
    • Vagal efferents
      • Nucleus Ambiguus initiates skeletal muscle contraction
      • Dorsal Motor Nucleus initiates smooth muscle contraction
    • Modified peripherally by local myogenic and neurohormonal elements
  • Results in synchronised contraction arising in the pharynx and extending down to GOJ
    • Both circular and longitudinal muscle involved
• Secondary Contractions
  • Triggered by any residual bolus distending the oesophagus
  • Sends a second peristaltic wave mediated by local neural mechanisms
• Tertiary Contractions
  • Aberrant synchronous contraction of oesophageal segments that plays no role in peristalsis

Anti-Reflux Mechanisms

1. The intrinsic LES sphincter (smooth muscle).
2. The crural diaphragm as an extrinsic sphincter - the left and right pillar of the right crus sling around the oesophagus.
3. The gastro-intestinal flap valve, whereby the distal esophageal sphincter enters the stomach at an oblique angle (angle of His)
4. The distal oesophagus is intra-abdominal.

Dysfunction of the anti-reflux barrier.

• The two biggest causes are advancing age, and obesity - both of which are associated with a hiatus hernia.
• A hiatus hernia causes the LES to migrate caudally and the reflux barrier to become defective.
• This causes all 3 of the anti-reflux barrier mechanisms to be compromised
• The crural diaphragms ability to act as a sphincter is reduced.
• The flap valve mechanism is disabled.
• The internal sphincter becomes stretched during pressure changes leading to further dysfunction.

Other factors which contribute to the GORD symptoms.

• Characteristics of the refluxate - pH < 2 and high bile acid content cause more severe mucosal injury.
• Impaired oesophageal acid clearance and emptying.
• Diminished salivary function - saliva is an alkali (smokers hypo salivate)
• Oesophageal sensitivity and hypersensitivity.

More Detail

• Intrinsic oesophageal mechanisms:
  • Lower Oesophageal Sphincter
  • Mucosal Defence Mechanism
  • Basal tone
  • Adaptive pressure changes
• Extrinsic mechanisms (disturbed with hiatus hernia):
  • Diaphragmatic sphincter (Pinch-cock)
  • Distal oesophageal compression intra-abdominally
  • Angle of His
    • Maintained by tonic contraction of the oblique fibres of the cardia
  • Mucosal Rosette
  • Phreno-oesophageal Ligament

Lower Oesophageal Sphincter

• Primary anti-reflux mechanism
• Not a distinct anatomic structure
  • But is composed of 4 x anatomic structures
• Resting high-pressure zone in distal oesophagus
  • Relaxes appropriately to allow swallowing/vomiting etc
• Specialised smooth muscle arranged in slings or clasps running in distal 1-4cm
  • Intrinsic tone (inherent to muscle properties)
  • Extrinsic tone (excitatory cholinergic vagal input)
• Transient LOS relaxation (TLOSR)
  • Appropriately short (< 10s) 6-8 x per hour
  • Occur after peristalsis, gastric distension and with belching/vomiting
  • Nitric Oxide is primary inhibitory neurotransmitter
  • Get small amount of physiologic reflux with this

Composition of Lower Oesophageal Sphincter

• Made up of 4 anatomic structures
  • Intrinsic musculature of the distal oesophagus
    • In a state of tonic contraction
    • Relax to allow passage of liquid or food into the stomach
    • Return to a state of tonic contraction
  • Sling fibres of the gastric Cardia
    • Oriented diagonally from the cardia-fundus junction to the lesser curve of the stomach.
    • Same depth as the circular muscle fibers of the oesophagus
    • Contribute significantly to the high-pressure zone of the LES
  • Crura of the diaphragm
    • Surround the oesophagus as it passes through the oesophageal hiatus
    • During inspiration, intrathoracic pressure decreases relative to intra-abdominal pressure, the anteroposterior diameter of the crural opening is decreased, compressing the oesophagus and increasing the measured pressure at the LES.
  • Increased intra-abdominal pressure is transmitted to the GOJ
    • When the gastro-oesophageal junction (GOJ) is firmly anchored in the abdominal cavity
    • Increases pressure on the distal oesophagus and prevents spontaneous reflux of gastric contents

Oesophageal Mucosal Defence Mechanism

• Oesophagus is not damaged by hydrochloric acid/pepsin for up to 1hr of exposure

Two main mechanisms:

• Oesophageal Clearance
  • Reflex peristalsis induced by oesophageal acid receptors
    • Abnormal motility exacerbates GORD
    • Unsure if cause or consequence present in over 50% of pts with oesophagitis
  • Aided by gravity
    • NB: Impaired during sleep!
• Tissue Resistance
  • Pre-epithelial
    • Oesophageal buffer + Saliva – to raise pH above 3 to prevent pepsin induced damage
  • Epithelial
    • Transmural electrochemical gradient, tight-cell junctions, and pH dependent cation channels
  • Post-epithelial
    • Epithelial repair

Hiatus hernia

• Often associated with GORD because abnormal anatomy compromises efficacy of LOS
• Type 1 (sliding) hernias present when GOJ migrates cephalad into posterior mediastinum
  • Occurs due to laxity of phreno-oesophageal ligament
• Small sliding hernia doesn’t necessarily mean incompetent LOS
  • But larger the size, greater the risk of GORD
  • Many small type 1 hernias don’t have symptoms and don’t require treatment
• Type 2-4 hernias often associated with obstructive symptoms

Pathology of GORD

• GORD results from a defect in one or more of the normal mechanisms protecting the oesophagus from excess exposure to gastric contents
• 65% Due to prolonged or abnormal Transient LOS relaxation (TLOSR)
• 20% Low resting LOS pressure (Sphincter failure)
• 15% Due to increased intraabdominal pressure
  • ± May be failure of ‘exit valve’ (pylorus)
  • (i.e. delayed gastric emptying or duodenogastric reflux)

Mucosal Effects of GORD

• Refluxate = Acid + Pepsin/Bile
  • Pepsin does the damage
  • Acid causes the symptoms
• Would need a sustained pH of 2 for acid alone to cause significant damage
• Reflux of bile may also contribute to development of Barrett’s
• Indicated by bilirubin measurements in the oesophagus

Histology

• Neutrophils
• Lymphocytes
• Intraepithelial Eosinophils
• Thickening of Basal Cell layer
• Elongation of LP papillae

Differential Diagnosis

• Other causes of oesophagitis:
  • Chemical induced
  • Pill induced
  • Infective oesophagitis
    • Especially candida
  • Scleroderma

Investigations

• Can try initial symptomatic response to PPI
  • 70% specific, 80% sensitive for GORD
• Aim of Investigations
  • Identify patients with complications or motility disorders
• Endoscopy – 1st Line

Gastroscopy if no improvement in 6 weeks with PPI or patient at high risk of Barretts

Endoscopy

• Prevalence of oesophagitis on OGD in patients with reflux symptoms varies (38-75%)
• Recommended for pts with dyspepsia and:
  • Chronic GI bleeding or IDA
  • Weight loss
  • Progressive dysphagia
  • Persistent vomiting
  • Epigastric mass
  • Age > 55 yrs with persistent dyspepsia
• Patients with oesophagitis/Barrett’s will have reflux but subset with reflux will have no endoscopic findings
• No OGD for reflux age < 45 with typical symptoms
• ≥ 15% of pts with symptomatic GORD show no evidence of oesophagitis on endoscopy and have normal pH studies

Contrast Swallow

• Limited role in GORD
• More to rule out other conditions you may be expecting or functional/structural disorders that may be correctable
• Double contrast oesophagram - barium/gastrograffin swallow
  • Highly effective at dx complications of GORD
  • Strictures/malignancy
• Highlights Hiatus Hernia and diverticula
• Assists in diagnosis of motility disorders

24hr Ambulatory pH Study

• Gold Standard for diagnosis of GORD
  • Sensitivity and specificity 92%
• Indications:
  • Refractory oesophagitis after PPI tx
  • Atypical presentations
  • Pre-requisite before reflux surgery
• Method
  • Catheter is placed 5cm above the manometrically-determined LES
  • Patient records events & position at time – correlate sx to reflux events
  • Begins ‘reflux episode’ when pH drops below 4, records until above 5

Normal Values

• < 5% of the time there is acid (pH < 4) in oesophagus
• No. of reflux episodes > 5mins: < 3.5
• No. of reflux episodes pH < 4: 50
• May get false –ves
  • Need to stop PPIs 2/52 before the study
• Generates a DeMeester score
  • Based on SD from the mean of reflux times, length & no of episodes
• Correlation with symptoms important for diagnosis
• NB: Normal 24 hour study but significant symptoms = Likely poor outcome from intervention
• Can add
  • Multichannel intraluminal impedance pH monitoring
  • Bilitec probe (detects bilirubin/bile reflux)

DeMeester Score

• Composite score of acid exposure during a 24hr ambulatory pH study
• Based on six variables
  • Percentage of total time pH < 4
  • Percentage of upright time pH < 4
  • Percentage of supine time pH < 4
  • Number of reflux episodes
  • Number of prolonged reflux episodes >5mins
  • Longest reflux episode
• Normal is < 14.72

Symptom Correlation

• Correlation with symptoms is important for diagnosis
• Multiple calculations to determine symptom to reflux episode association and establish response to PPI.
  • Symptom Index
  • Symptoms severity Index
  • Symptoms Association Probability

Multichannel Intraluminal Impedance pH Monitoring

• Detects changes in impedance
  • Conduction of current across oesophageal wall
  • Will be stable between reflux/swallow
    • Liquids improve conduction and impedance falls
    • Gases reduce conduction and impedance increases
• Most sensitive Ix for GORD
  • Useful for patients with symptoms despite acid suppression
  • More sensitive than pH studies alone
    • High sensitivity – can detect:
      • Swallow or reflux
      • Velocity of transit
      • How long it takes swallow/reflux to be cleared
      • Liquid or gas reflux
      • How proximal reflux extends
      • Degree of pH changes with reflux
• May identify patients who would benefit from fundoplication
  • Despite -ve pH study

Manometry

• Important to differentiate reason for reflux
  • Impaired clearance (motility disorder) vs impaired anti-reflux mechanisms
  • Require very different management
• Required for proper placement of pH probe for pH monitoring
  • 5cm above LES
• Usually done as stationary (supine) study
  • May also be done as 24hr ambulatory study
  • Resting pressure between 12 to 30mmHg
  • Long length pressure zone is protective against GORD
  • Can have 4 channels and assess peristaltic wave to fluid, should generate pressure wave around 30mmHg
• Abnormal in 20-30% of GORD pts
  • Doesn’t significantly change plan for surgery in most cases

Other Investigations

• CT scan
  • Assess large hiatus hernia only
• Bernstein test:
  • Acid is infused into mid-oesophagus to determine symptom correlation
  • Rarely used, except in cases of atypical chest pain investigation
• Radionuclide gastric emptying study
  • Reflects Vagus nerve function

Management

• Use stepwise approach
  • Life-style changes
  • Medications
  • Endoscopic therapy – poor outcomes and not recommended
  • Surgery

Lifestyle Changes

• Stop smoking
• Restriction of refluxogenic intake
  • EtOH, caffeine, chocolate, carbonated beverages relax LOS
  • Fatty foods reduce gastric emptying
  • Large meals induce transient LOS relaxation
• Small frequent meals instead
• Weight loss
  • Changes pressure gradient between thorax and abdomen
• Elevation of head of bed by 4-6 inches

Medical Management

Proton Pump Inhibitors

• Inhibit H+/K+ ATPase on luminal surface of Parietal Cells
  • 20mg OD ↓ Gastric acid production 90%
  • 40mg OD ↓acid 95%
    • Changes gastric pH from ≤ 2 to ≥3
  • Get 75% healing of oesophagitis
• Predicts outcome of surgery?
• If mild disease & respond → Can discontinue after 8-week course
  • Patients may develop recurrent symptoms once stopped
• If patients have severe disease / ulcers
  • Treat with high dose → If healing achieved → Long-term standard dose therapy
• Volume reflux & aspiration can still occur, due to incompetent LOS
  • Will not affect biliary/volume reflux

Side Effects of PPIs:

• Headache, Abdominal pain, Diarrhoea
  • Develop Fundic Gland Gastric polyps – Not pre-malignant
• Long term PPI consequences:
  • Atrophic Gastritis and metaplasia with concurrent H pylori
  • Parietal Cell Hyperplasia ~ may account for rapid recurrence of symptoms if stop PPI

Other medical therapies

H2 Receptor Blocker (Famotidine)

• Indication
  • GORD
• Dose
  • Same as Omezol
• MOA
  • H2 receptor competitive antagonist (histamine) on parietal cells
  • Reduces acid release
• Side Effects
  • Constipation or diarrhoea
  • Headaches

Prokinetics - Domperidone/Metaclopramide

• Indication
  • Volume or bile reflux
• Dose
  • 10mg PO TDS
• MOA
  • Dopamine receptor antagonist
• Side Effects
  • Dry mouth
  • Diarrhoea
  • QT prolongation](← H2-receptor antagonists
• Prokinetics (e.g. Cisapride – but NB: cardiac dysrhythmia)
• Only prokinetic shown to be better than placebo. Accelerates gastric emptying>)

Surgical Management

• Principles of Surgery
  • To create mechanical anti-reflux barrier between oesophagus and stomach
    • Only treatment that addresses the underlying cause
  • Restore normal pressure at LOS
  • Correct hiatus hernia
  • With a normal angle of His
    • ≥ 1.5cm of abdominal LOS length
  • Avoid too tight a wrap
    • “Gas-bloat” can be the most significant side effect

Indications for Surgery

• Persistent symptoms on maximal treatment
• Persistent volume reflux (regurgitation)
• Respiratory complications
  • NB: If failure to respond to PPI, warn that surgery may also not relieve symptoms
• Inability to tolerate long-term medication (includes non-compliance & cost)
• Age < 50
• Controversial:
  • Throat complications of reflux oesophagitis
  • Barrett’s – some evidence to show it improves dysplasia and may reduce length of Barrett’s
    • Poor quality evidence
    • No evidence to show surgery reduces dysplasia or progression to Ca
    • Also risk of reduced visualization of GOJ after surgery

Contraindications

• Elderly with concomitant disease
• Poor peristalsis or oesophageal dysmotility
  • Not always contraindication to surgery and may improve after anti-reflux surgery
• Highly functional symptoms

Fundoplication

• Principles of operation:
  • Mobilize lower oesophagus
  • Wrap fundus of the stomach
  • Stabilize new anatomy
• Mechanism of effect
  • Create floppy valve by opposing oesophagus to gastric fundus
  • Exaggeration of angle of His
  • Normalises basal pressure of LOS
  • Reduction in TLOSR
  • Increased gastric emptying

Nissen Fundoplication

• Gives best outcome but more gas bloat & dysphagia
  • For the exam you are only going to operate on those really suffering
  • Benign disease so err on side of caution before operating
• Success rate 90% (good/excellent long-term outcomes)
• Predictors of a good outcome from surgery
  • Objective pre-op evidence of reflux (? or very typical Sx)
  • Normal pre-op pH study is a predictor of poor outcome
  • Complete / partial response to PPIs
  • Good compliance with anti-reflux meds
• Basic elements of the operation
  • Exposure of the oesophageal hiatus
  • Reduction of Hiatus hernia
  • Completely mobilize GOJ
  • Exposure of 3-4cm of oesophagus without tension below the diaphragm
  • Crural closure (cruroplasty) – important to prevent hiatus hernia
  • Fundus mobilization
    • ± Division of short gastrics (→ ↑ fundal length available for fundoplication) but ? not needed
  • Creation of a short (< 2cm), loose wrap over a 56-60 F bougie
  • Preservation of Vagi (preserves gastric emptying)
    • No benefit; “wind related” Sx ↑ed because nerves damaged

Op Viva

• Ports = Left rectus optical entry
  • Left flank working port
  • Right subcostal MCL
  • Left subcostal MCL
  • Natheson retractor in epigastrium
• Steps
  • Expose oesophagus and mobilisation
    • Preserving accessory Left Hepatic artery (Pars flaccida)
  • Delineate Crura – Identify left crus from the right by lifting oesophagus
    • Preserve epimysium covering muscle
  • Sling the oesophagus and ensure enough abdominal length (4cm) – preserve posterior vagal nerve
  • Mobilise short gastrics (not mandatory) – 2 layers and Posterior Gastric Artery
  • Crural repair – tension free (ethibond figure 8)
    • May require biosynthetic mesh if large
  • Fundoplication – short floppy wrap, anchor top to crura, Bougie 52 F

Toupet Fundoplication

• Partial 270-degree posterior wrap
• May be good option when oesophageal motility poor

Dor Fundoplication

• Left anterolateral partial 180-degree wrap
• Often added to Heller’s myotomy for achalasia to prevent post-op reflux

Nissen Vs Partial Wrap

• Nissen
  • 10-year symptom free good, best for long term reflux control
  • ~ 25% pts will require medication again in long term
  • No reduction in rates of oesophageal adenocarcinoma cf anti-acid medication
• Partial fundoplication
  • Decreased side effects (e.g. dysphagia, gas bloat)
  • Increased recurrence
• Some new studies claim little difference in recurrence or dysphagia
  • Nissen vs. 180 ant partial after 10-yrs f/up
    • Partial posterior has reduced gas bloat/bloating/flatulence
• Anterior partial fundoplication:
  • Improved dysphagia, less bloating and preservation of belching
  • However Nissen’s had better control of reflux and decreased incidence of re-operation for reflux
• Take home points
  • After either operation 80-90% pts are satisfied with outcome
  • Nissen’s has better control of reflux but higher dysphagia, gas related sx
  • Partial has less dysphagia/gas related sx but increased chance of re-operation for reflux
  • Dividing short gastric does NOT improve reflux symptoms
    • Associated with increased symptoms of gas bloat/flatulence and disruption of fundoplication
    • Also associated with increased risk of sliding hiatus hernia

Laparoscopic Vs Open

• Benefits of laparoscopic anti-reflux surgery
  • Early benefits:
    • Less complications (respiratory/ileus)
    • Earlier mobilization/discharge
    • Earlier return to work
  • Late benefits:
    • Reduced incisional hernias
  • Cons of laparoscopic surgery
    • Longer operative time (but early DC offsets the cost)
    • Increased technical skills required
    • Slightly higher re-op rate in initial 3/12
      • but equalised at 1 year
• No overall difference in control of reflux or dysphagia/gas symptoms
• Success for both ≈ 91% at 1yr

Complications of Fundoplication (3-10%)

Operative Complications of Fundoplication

• Convert to open
• Pneumothorax 2%
  • Injury to left pleural membrane
  • CO2 – watch & wait, pneumomediastinum
• Perforation of Oesophagus / Stomach < 1%
• Bleeding
  • Injury to major vessels, liver, short gastrics
  • Liver/spleen injury
    • Spleen 2.3%

Post-operative Complications of Fundoplication

• Gas bloat 30%
  • Most settles with time
  • Due to gastric inertia – vagal injury
  • May need pyloric dilation
    • If improves symptoms, definitive treatment is Gastric antrectomy and Roux-en-Y
• Dysphagia < 30% early, 5% late
  • Higher initially due to oedema
  • Use graduated diet over 4-6 weeks; clear fluids after 6 hours, sloppy diet at 24 hours usually okay
  • Often tight hiatal repair
    • Requires release of sutures
  • Late dysphagia usually due to excessive scaring at hiatal repair
    • Managed by balloon dilation or repeat op and widening hiatus
• Slipped Wrap
• Acute recurrence
  • Crural repair failure
• Paraoesophageal hernia (5-7%)
  • Increased in laparoscopic repair
  • Exacerbated by:
    • Higher thoracic dissection
    • Breach of left pleural membrane
    • Less post op pain, means pts cough > Increased risk of stomach protruding into left hemithorax
    • Routine hiatal repair reduces risk by 80%
    • Avoid lifting/straining for 1 month
• PE
  • Increased risk with prolonged ops, steep head up, legs in stirrups
  • Minimized by mechanical and chemical VTE prophylaxis.
• Bilobed stomach - body rather than fundus used for wrap

Delayed Complications of Fundoplication

• Wrap Failure 5%
  • But 62% will stay on anti-reflux medication
• Inability to vomit
• Mortality rate 0.1%

Other Surgery

• RYGB may be more appropriate for very obese
• Consider PTFE mesh patch for very large hiatus hernia
  • Less recurrence than suture alone
• Endoscopic Options:
  • All poor outcomes and not recommended
  • Rx for mild-mod reflux (exclude > 2cm H/H) – currently not recommended
  • Stretta:
    • Burns introduced into oesophagus → Denervates mucosa → Poor outcomes
  • Endosinch
    • Mucosal suturing device → effect limited as sutures disappear
    • ≈ 50% at 3mths, ≈ 90% disappeared at 1yr
  • Full thickness Plicator
    • ? more potential: ≈ 70% of patient off PPIs at 1yr
  • Enteryx
    • Bioenert polymer injected into LES
    • Complications potentially serious if injections end up outside the wall
    • Causes adhesions around oesophagus, making subsequent surgery more difficult

PPI vs Surgery

• ? Medical therapy not as effective as surgery
  • Some RCTs say that both are equally effective
  • ? Up to 80% of pts will have recurrence of Sx if PPI discontinued
• RCT: PPIs vs. fundoplication
  • After 7 yrs:
    • Surgery more effective than PPIs (67% vs. 47% success)
  • But at the expense of post-fundoplication symptoms
    • (e.g. dysphagia, inability to belch/vomit, rectal flatulence)
  • Cost-benefit analyses
    • Surgery becomes less expensive than PPI therapy after ≈ 5yrs
  • ? Detrimental effects of long-term PPI use
    • Atrophic gastritis
    • Hypergastrinaemia
      • → Concerns re trophic stimulatory effect on the stomach

Prognosis

• Potential Complications of GORD (Natural History)
  • Oesophagitis
  • Bleeding
    • Rare to cause significant bleeding however oesophageal ulcer can erode into blood vessel and cause sig bleed
    • Most should be controlled endoscopically
  • Oesophageal strictures
    • Schatzki rings
      • Seen in 2-10% of GORD pts (Mx = Rx of GORD +/- dilatation)
    • Peptic Strictures
      • Pathognomonic for long-standing GORD, develop due to chronic inflammation
• Barrett’s Oesophagus and Oesophageal cancer
• Short oesophagus
  • From chronic inflammation and fibrosis
  • May need a Collis gastroplasty
    • Higher chance of failure of surgical intervention
    • Risk of acid producing tube above fundoplication.

Respiratory complications

• Aspiration pneumonia, Bronchiectasis
• Firm indication for surgery if pt well enough
• Halitosis, Enamel damage, Pharyngitis/laryngitis

Post Surgical Prognosis

• Symptomatic (typical Sx) improvement in 85-90%
  • Less for atypical Sx
• Reflux control achieved in 80-90% at 5-10yrs
  • Proportion of patients freed from anti-acid meds ranges 25-50% in studies
• ≈ 5% experience side-effects
  • Recurrence after surgery
    • Asymptomatic hiatus hernia recurrence up to 25%
    • Failure defined as
      • Presence of mod/sever heartburn
      • Regurgitation
      • Presence of ≥ grade 2 oesophagitis on endoscopy
      • Mod/severe dysphagia/odynophagia
      • Need for PPIs post-surgery to control sx
      • Need for reoperation
      • Need for surgery despite long-term PPI Rx
  • ¾ pts who get recurrent reflux:
    • Not as bad as pre-surgical & can be controlled with meds
  • ¼ pts with recurrence will have bad reflux
    • Re-do surgery is considered in this group
• Male pts: better outcome (heartburn & satisfaction) @ 5 yrs

Follow-up

• If severe oesophagitis:
  • Consider repeat scope after Rx trial, to check for healing
• After fundoplication:
  • 6/52 puree diet
  • Review at 3/12 post surgery, then prn