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

 

Presentation:

• 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

 

Complications:

• 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

 

Diagnosis:

• 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

 

Treatment:

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 (1^st 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

---

References:

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