Gastroesophageal Reflux Disease

Normal Anatomy and Physiology:


Physiologic reflux:

  • LES remains actively closed -> opens by relaxation once pharyngeal swallow is initiated
  • unguarded moments” where some of the gastric juices reflux up the esophagus, due to open LES and pressure gradient (higher abdominal pressure than intrathoracic)
  • But w\ effective peristalsis, once the bolus moves downwards, the esophagus should be cleared from the gastric juices

Anti-reflux mechanism:

  • Efficient esophageal clearance
  • Adequately functioning gastric revoir
  • Mechanically effective LES
Neural Hormonal Drugs Foods
Increase LES tone Alpha stimulation Gastrin, motilin Antacids, cholinergics, domperidone, metoclopramide __
Decrease LES tone Beta stimulation Cholecystokinin, estrogen\progesterone, glucagon, somatostatin, secretin Anticholinergics, barbiturates, CCB, diazepam, meperidine, theophylline Peppermint, chocolate, caffeine, ethanol, smoking, fatty meals

Characteristics of LES which maintain its tone:

  • Its resting pressure
  • Its overall length
    • Imagine the stomach as a balloon and the LES as the neck of the balloon
    • The more you inflate the balloon (stomach), the shorter the neck (LES) becomes -> higher pressure is required to close it -> which decreases the resting pressure
    • Gastric distension can be from over-eating\eating large meals, fatty meals (delay gastric emptying)
    • Once the pt feels heartburn -> swallow more, why? Saliva is alkaline (high PH) -> neutralizes the gastric juices -> temporarily relieve the heartburn. But increased\repetitive swallowing of “air” -> bloating, belching, and gastric distention -> further LES dysfunction. VICIOUS CYCLE!
  • Its intra-abdominal length that is exposed to the positive pressure (most common defect)
    • Why is it important? Periods of increased abdominal pressure (e.g. obesity), the pressure applied to the stomach needs to be the same to a portion of LES to prevent reflux
    • Pts w\ hiatal hernia (where the LES is completely intra thoracic) are more liable for reflux

Permanently defective sphincter is defined as:

  1. Mean resting pressure < 6 mmHg
  2. Overall length < 2 cm
  3. Intra-abdominal length < 1 cm



  • Typical sx: heartburn, regurgitation, dysphagia
  • Atypical sx: cough, wheezing, hoarseness, post-prandial fullness, vomiting, chest pain, asthma, aspiration

1» Heartburn:

  • Substernal discomfort, burning in character
  • Begins in epigastrium, radiating upwards
  • Aggravated by meals, spicy\fatty foods, chocolate, coffee
  • Worse in supine position
  • Relieved by antacids

2» Regurgitation:

  • Effortless return of acid\bitter gastric contests into the chest, pharynx, mouth
  • Particularly severe at night when supine, or when bending over
  • May result in associated pulmonary sx: cough, hoarseness, asthma, recurrent pneumonia (due to bronchospasm)

3» Dysphagia:

  • Sensation of difficulty of food passage from the mouth to stomach
  • Can be divided into oropharyngeal and esophageal etiologies
  • Can be a sign of underlying malignancy -> investigate thoroughly
  • May be accompanied by pain (odynophagia), relieved by passage of bolus

4» Chest pain:

  • Exertional chest pain similar to angina
  • Difficult\impossible to distinguish between them on clinical grounds only
  • Some characteristics which suggest esophageal origin:
    • Precipitated by meals
    • Occurs at night while supine
    • Non-radiating
    • Responsive to antacids
    • Accompanied by other sx: dysphagia or regurgitation



  • Combination of refluxed gastric juices and duodenal juice (contains bile and pancreatic secretions) is more noxious than gastric juices alone

1) Esophagitis:

2) Ulcerations, hemorrhage, dysmotility

3) Strictures:

  • Luminal stricture develops from submucosal and eventually intramural fibrosis
  • Occurs at the site of maximal inflammatory injury (i.e. the columnar-squamous epithelial interface)
  • Resistant to dilation
  • Incidence has lessened since the introduction of PPI

4) Schatzki’s ring:

  • Constrictive band at the squamo-columnar junction
  • Composed of fibrotic mucosa and submucosa (not esophageal muscle)
  • May result in dysphagia

5) Barret’s esophagus:

  • Traditionally, it used to be defined by the presence of columnar mucosa, extending at least 3 cm into the esophagus
  • Presently, dx is made given any length of endoscopically identifiable columnar mucosa + on biopsy, proving the presence of intestinal mucosa
  • Hallmark of IM? Presence of intestinal goblet cells
  • It can lead to ulceration (similar to peptic ulceration, having the same propensity to bleed, penetrate, or perforate)
  • Ulcerations and stricture in BE have become less common w\ PPI, unlike the incidence of adenocarcinoma
  • Adenocarcinoma:
    • 10% of GERD pts develop BE
    • Pts of BE, have a lifetime risk of 7% of developing adenocarcinoma


6) Respiratory complications:

  • Repetitive aspirations -> recurrent\aspiration pneumonia, asthma, lung abscess, bronchiectasis pulmonary fibrosis



  • Upper GI series; barium study:

    • Look for anatomical cause for reflux (hiatal hernia)
    • Check for pathology resulting from long-standing reflux (ulcer or stricture)
    • 40% of pts w\ classical GERD sx -> show spontaneous reflux
    • Signs of reflux:
      • Abnormal motility -> weakened primary peristalsis
      • Mucosal nodularity: in early ds -> due to edema and inflammation
      • Thickened folds
      • Ulcerations and erosions
  • 24-hr ambulatory PH monitoring:

    • A probe w\ pH electrodes -> inserted into the pt’s esophagus for 24 hrs
    • Gold standard for GERD dx (sensitivity and specificity of 96%)
    • Determines the severity of reflux by DeMeester’s parameters



  • Esophageal manometry:

    • Evaluates competence of LES
  • Endoscopy (EGD):

    • Evaluates mucosa to rule out BE
    • Used to biopsy
    • Indications:
      • Extremes of ages
      • Malignancy
      • Bleeding
      • Chronicity (>5 yrs)
      • Failure of medical therapy
      • Extra GI sx



1. Non-pharmacological; life-style modification:

  • Elevations of the head-end of bed
  • Avoid alcohol, coffee, chocolate, peppermint, nicotine
  • Eat small, frequent meals
  • Avoid tight clothing
  • Avoid eating 2-4 hrs before sleep

2. Medical:

  • Antacids -> symptomatic relief
  • H2 antagonists (ranitidine)
  • PPI (omeprazole)
  • Pt should undergo a trial of medical therapy for 6-12 wks before further investigation
  • Metoclopramide -> promotes gastric emptying, beneficial early in the ds
  • Drugs that increase LES pressure: Metoclopramide and bethanechol

3. Surgery:

  • Indications:
    • If medical management fails
    • If pt develops esophageal complications: chronic esophagitis, strictures, ulcers ± BE
    • Respiratory complication
  • Types of procedures:
  • Nissen procedure: the procedure of choice
    • 360° fundoplication -> wrapping the fundus of the stomach around the distal portion of the esophagus to create a sphincter (1st line is laparoscopic)
    • Works in 85% of pts
    • Goals:
      1. Increase LES tone
      2. Elongate LES ≈ 3 cm
      3. Return LES into abdominal cavity
    • Post op complications:
      1. Immediate: pneumothorax, bleeding (short gastric arteries or spleen itself), perforation
      2. Early (2-4 wks): wound infection, obstructive Sx, cont. reflux, hernia
      3. Late: gas bloat syndrome (no burping\vomiting), Wt loss, recurrence
  • Partial fundoplication:
    • 270° fundoplication
    • Indicated if poor motility
    • e.g.: Belsy (transthoracic) or Toupet (laparoscopic)



Download the PDF version: here


  • Dr Albargawi’s clinical notes
  • Schwartz’s principles of surgery
  • First aid for the surgical clerkship
  • Monte Reid
  • Surgical recall

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