Gastro-Oesophageal Reflux


Montreal consensus: "GORD is a condition that develops when the reflux of stomach contents causes troublesome symptoms and / or complications".

GORD & Oesophagitis.
- see below for oesophagitis grading
See also related hiatal hernia.


Commonest disorder of upper GI tract.

20% people suffer episodes.
- most are over 40
- it is rare in children.




Factors contributing to the physiological LOS:
- intrinsic musculature of distal oesophagus being tonically contracted
- sling fibres of the cardia (run diagonally across LOS, raising pressure above stomach pressure).
- diaphragm: crura surround oesophagus, shutting it (hence measure manometry at mid or end-expiration for accuracy)
- intra-abdominal pressure being higher than thoracic, keeping LOS pressure high (lost in hiatal herniation).


Normally the gastro-oesophageal junction does not allowed retrograde passage of gastric contents.
- either i) the LOS pressure is low, or ii) spontaneously relaxes out of coordination with peristalsis.
Any refluxate is normally cleared by gravity and saliva and bicarbonate in the oesophagus.
Pts with symptomatic GORD usually (70%) have mechanical LOS defects (Shackelford)
- some have overly frequent sphincter relaxation
- in a few inefficient clearance from oesophagus contributes.
See also hiatal hernia

Aetiology / Predispositions
Crus / LOS malformation, pyloric stenosis.
ZE syndrome (gastrinoma).
Anything causing pyloric obstruction.
Scleroderma-like disease.
Smoking, alcohol predispose.
Smooth muscle relaxants - beta adrenergics, aminophylline, anticholinergics, Ca channel blockers, nitrates.
Surgical destruction.
Post-prandial transient LOS relaxation allow gas escape, takes refluxate with it.
- most commonly
Anything causing raised intra-abdominal pressure.
- eg pregnancy, tumours.




Often associated with hiatus hernia.
- see card for relationship.
The refluxate enters the oesophagus.
May go as far as the mouth, or be partly aspirated.

Mechanically defective LES
Relatively small subset of GORD patients = LES is ineffective.
- Manometry: pressure <6mm Hg; length <2 cm, abdo length <1 cm.
--> 75% chance of reflux if 2/3 of these, 90% if 3/3.x

Natural History of Oesophagitis
Oesophagitis is a pathological entity, and should only be used in such terms.
- correlation with GORD symptoms is often poor.
Development of oesophagitis depends on:
- duration
- frequency
- volume
- virulence of reflux
- efficiency of clearing by peristalsis (acid time in contact)
- resilience of affected cells
Ulcerative oesophagitis follows when reflux overcomes ability of mucosal cells to regenerate.
- stricture can follow concentric oesophagitis.
- scarring and muscular shortening can mean reduction of a hiatal hernia impossible without lengthening procedure.

Note on Barrett's Ulcer
Sharply circumscribed defect in the columnar epithelium, resembling a gastric ulcer.
- usually posterior & longitudinal.
- painful swallowing rather than reflux may dominate.
- may perforate.
- may haemorrhage (cf oesophagitis ulcers, which tend to just weep).
Usually do not respond to medical Rx --> resection preferred

- early symptoms are often mild and missed.
Barrett's oesophagus.


From coughing / hoarseness to recurrent severe pulmonary infections.
- chronic lung conditions eg abscess, bronchiectasis may develop.
Not prevented by PPIs, and antireflux surgery can be very beneficial.
--> VOLUME REFLUX = suggest surgery


Heartburn, regurgitation, salty salivary hyper-secretion and dysphagia

Most pathognomonic

Post-prandial posturally-aggravated substernal burning pain.
Regurgitation (54%)
- (or 'effortless vomiting')
- often occurs on bending or stooping or lying at night.
- particularly after a large meal.
- acid taste in the mouth.
- if food = volume regurgitation.
- note if food is digested or undigested
--> if latter, think pouch or achalasia etc.
Heartburn = very reliable symptom (80%)
- confined to epigastric / retrosternal areas; see below most common patterns shaded by patients (Shackelford)
- usually caustic, burning or stinging.
- not pressure and does not radiate to back.

Dysphagia for solids (23%-50%)
- pain with stuck feeling at distal sternum, relieved as bolus passes.
- may indicate peptic stricture, may just indicate inflammation.
- tumour, diverticulae should be considered.
Abdo pain (29%)
Belching (15%)
Bloating (15%)
Globus (4%)

Aspiration (14%)
- may occur in absence of GI symptoms
- wheezing (7%), cough (27%)
Recurrent pneumonia
Hoarseness (21%).
Dental erosion
Sinus irritation (runny nose, headache).

As above

Eroded dentition
Chronic sinusitis
If severe disease, this is interesting:
- patients may sit forward with lungs inflated to near vital capacity
- this flattens the LOS, keeping reflux minimized.
?Supraclavicular lymph nodes
- progression to cancer.


Identifies peptic esophageal injury.
Dx supported by oesophagitis on biopsy

(Skinner & Beasley)

I = erythema / oedema
II = superficial ulceration / fibrin overlying
Sorry! Picture not possible for you.
III = deeper ulceration, submucosal fibrosis, shortening of oesophagus.
IV = stenosis, full-thickness fibrosis & mediastinal lymphadenopathy.

The minimal lesion considered reliable for diagnosis reflux oesophagitis is a mucosal break
- an area of slough / erythema with a sharp line of demarcation from adjacent mucosa.
- (Recent Los Angeles classification system)


Extreme end of oesophageal injury, with metapastic transformation
- intestinal metaplasia arising in an endoscopically-visible columnar-line oesophagus.
- see notes.
Is objective evidence for GORD.

'Flap-valve grading'
With endoscope retroflexed, the GOJ has been graded
- grade IV being patulous opening with oesophagus in full view from stomach.

Flexible tube with pressure-sensing devices, e.g. at 5cm intervals.
Best for defining propulsion disorders:
- e.g. scleroderma, achalasia, diffuse spasm.
- resting LOS pressure (normally 12-30mmHg).
- relaxation (should relax to gastric baseline for a few seconds after swallowing initiated.
- peristalsis of oesophageal body (percentage of initiated swallows transmitted to each of four channels at 3, 8, 13, 18cm above LOS; normal being 80%).
--> also get amplitude of the wave.
--> "Ineffective esophageal motility" = <60% peristalsis or distal oesophageal amplitudes <30mmHg, often associated with significant GORD.
Degree of weakness may help decide how much of a barrier can be constructed by the anti-reflux surgeon.
New devices combine pH and impedance measurements.

24 hr pH monitoring.
Gold standard for diagnosing & quantifying acid reflux.
Can't always get it though, due to access, but helpful if you can.
Thin catheter with solid-state electrodes down oesophagus
- placed 5cm above the LES.
- spaced 5-10cm apart, sense fluctuations in pH between 2-7.
- pt records reflux in a diary, noting the time on the recorder.
- returns total number of episodes, longest episode, number lasting longer than 5 minutes, extent of reflux when upright vs supine.
--> overall score that indicates likelihood of oesophageal injury (DeMeester Score).
Another method is counting % of time pH is below 4 vs time of study.
- should be <1% in proximal 15cm, <4% in distal oesophagus.
May underestimate reflux, as patient will be less active and eat less with a catheter down their gullet.
Symptom correlation with low pH measurements is confirmatory.
Bravo capsule is a wireless system clipped 5cm above LES, pH transmitted to receiver on the belt.

Oesophagogram (Ba contrast study)

Useful. Determines anatomy of the oesophagus and distal stomach, and degree of hiatal herniation.
- may demonstrate reflux not showing with an empty stomach study.
- helps plan an operation: if the GOJ does not reduce during the study, predicts a more difficult operation.
- shows anatomical problems e.g. strictures, pouches, tumours.


Scintigraphic studies used if pt cannot tolerate naso-esophageal intubation.
Therapeutic trial (see below)
Acid perfusion test:
- 0.1 Normal HCl is infused into lower gullet via a catheter
- ?reproduction of symptoms (test with placebo to be sure).
Lignocaine test:
- pt with undifferentiated substernal pain swallows 15ml of 0.5% viscous xylocaine.
- +ve pt needs a scope.
Acid reflux test:
- 200 ml of 0.1 N HCl in stomach; measure oesophageal pH
- most sensitive, but lacks specificity.



Avoid aggravating factors.
Diet change (low fat, soluble carbohydrates).
Can try avoiding coffee, tea, alcohol, cola, citrus, tomatoes or chocolate.
- the latter impairs LOS function
Stop smoking, reduce weight, exercise, elevate head of bead.
"Chocolate, alcohol and tobacco are notorious stokers of the reflux furnace" (Shackelford).
Small frequent meals, eat slowly, chew food well.
Avoid large meals before lying down.

Aims of medical therapy
1. Decrease gastric pH
2. Promote downward traffic
3. Boost mucosal resistance

By far the most effective medical therapy.
All pts should undergo a trial of PPIs as first line therapy.
Many internists use trial of PPIs as means of confirming GORD
- heal 90% of oesophagitis, vs 30-50% pts unrelieved on H2-receptor antagonists.
- decrease acid secretion; irreversible blockers, take 4 days before full effect, persist for 4-5 days after therapy ceases.
- stabilize pt on a double dose for 6 weeks, then reduce as necessary.
- long term therapy safe, though linked to hyperplastic gastric polyp formation (benign).
- however expensive and if long-term user, may be cheaper to have an operation.
- & do not prevent aspiration of gastric contents.
- beware lack of response and investigate them carefully.

If experience prolonged symptoms despite PPIs
Or complications are suggested
--> investigate carefully.

H1 receptor agonists = not as good.
 - symptom control and mucosal healing not well correlated.
- may be useful in difficult pts in combo with PPIs.

Prokinetics, e.g. cisapride = controversial.

Few patients need fundoplication, total or partial.
Unlike medical therapy which is started on subjective evidence, surgical therapy requires objective evidence

Absolute indications for oesophageal surgery
- perforation (Barrett ulcer, PUD in intrathoracic stomach, iatrogenic)
- uncontrolled bleeding (Barrett ulcer, PUD in intrathoracic stomach)
- obstruction (extreme stenosis, hernial)
- gastric necrosis (hernial strangulation)
- malignancy proven or suspected

Indications for fundoplication
Paraoesophageal hernia (incarceration, symptomatic, intermittent obstruction, recurrent aspiration, chronic ulceration, Fe deficiency)
Reflux complications; relapse, chronicity (ulcerative oesophagitis, peptic stricture, chronic Barret ulcer)
- including extra-oesophageal complications.
Prominent regurgitation component.
Disabling symptoms; inadequate PPI control
- symptoms persisting at a young age (takes 10 years for cost-benefit analysis of surgery to outweigh PPIs).
- most common indication is persistent symptoms despite maximal medical therapy and reluctance to take medicines for life.
Patient wishes for symptom control without medication.

Do not simply assume pts with no response to PPIs need surgery; they are highly effective and the diagnosis should be scrutinized.
*Barrett's alone is not an indication for surgery*
- while it might be true, there is no proof that surgery decreases chance of high-grade dysplasia or cancer developing.
- surveillance would still be recommended, and Barrett's rarely regresses completely.
- better genetic subgroup analysis may define a group that benefit from surgery more carefully.

Obesity (weight loss measures instead)
Barret mucosa with HGD or adenoCa
Comorbidities conveying high risk
Portal hypertension

How to Select Patients?
Pts wanting to stop meds, recurrent symptoms, severe regurge, complications of reflux, and significant hernia.
Note, if anti-reflux meds are ineffective, then operation unlikely to help.

What about young patients?
Better to wait on med Rx for a while.
Although surgery is effective, it does not last forever, and repeat procedures are difficult.

Preoperative evaluation
1. Confirm presence of reflux
--> endoscopy, contrast study, and pH study
2. Define oesophagogastric anatomy
- presence / absence of hernia, type of hernia, length of oesophagus
- mucosal pathology
--> endoscopy, contrast study; CT if complex hernia
3. Rule out motility disorders of esophagus and stomach
- would be disastrous to do a fundo here; worse dysmotility, symptoms, gas bloat in gastroparesis
--> manometry if any suspicion, video contrast swallowing study; GET scintigraphy test if concern for gastroparesis.

Success depends on understanding the pathophysiology of GORD, pt selection, meticulous technique and attentive post-op care.

Continue surveillance for Barrett's?
Yes. Regression of Barrett's occurs only in less than quarter to a half of patients.
- need to continue surveillance of metaplasia after operative intervention.

What is the role of endoscopic therapies?
Attempts to augment the LOS have been tried: suturing / plication, invaginating devices (stomach into oesophagus), radiofrequency, bulking injections (now abandoned)
- suturing has shown early promise, longer-term f/up required.
- radiofrequency has shown modest benefits, this and others are undergoing clinical trials and follow-up studies so watch this space.
Bottom line: no procedure to date has effectiveness of surgery, and no RCTs comparing them to surgery
Also carry risk, eg perforation.

top D I A B M I M home

Sabistons 17th.
Shackelford's 5th.
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