GERD- gastro-oesophagial reflux disease

Pathophysiology

Reflux of gastric acid and pepsin into the oesophagus
Necrosis of the oesophageal mucosa causing erosions and ulcers.
Impaired clearance of the refluxed gastric juice.
GE junction incompetence-
- Three mechanisms-
  - transient LES relaxations (vasovagal reflex in which LES relaxation is elicited by gastric distension)
  - LES hypotension
  - Anatomic distortion of the esophagogastric junction.
Reduced salivary function-
- Normally after acid reflux peristalsis return the refluxed fluid back to stomach.
- And also titrated with bicarbonate in swallowed saliva.
Bile reflux can also cause esophagitis and play role in barrettes esophagitis.

Symptoms

Risk factors–

Obesity.
Hiatus hernia.
Pregnancy.
Exogenous oestrogens.
Foods- high fat, chocolate, peppermint, caffeine, alcohol, smoking.
Drugs- anticholinergic, antidepressants, opioids, theophylline, diazepam, barbiturates.
Helicobacter pylori infestation.

Diagnostic tests

Clinical history- heartburn and/or regurgitation.
Upper G.I endoscopy- routine endoscopy not required in typical symptoms of GERD.
- To evaluate for dysphagia or look for oesophageal mucosa (erosions/ metaplasia, dysplasia or mass lesions)
- Grading of esophagitis:
  - Grade A – One or more mucosal breaks each ≤5 mm in length.
  - Grade B – At least one mucosal break >5 mm long, but not continuous between the tops of adjacent mucosal folds.
  - Grade C – At least one mucosal break that is continuous between the tops of adjacent mucosal folds, but which is not circumferential.
  - Grade D – Mucosal break that involves at least three-fourths of the luminal circumference.
Oesophageal manometry  manometry cannot diagnose GERD, but can be performed to exclude oesophageal motility disorders.
Ambulatory oesophageal pH monitoring  to confirm the diagnosis of GERD in those with persistent symptoms when twice daily trial of PPI has failed.
- Can be performed with either a trans nasally placed catheter or a wireless, capsule shaped device that is affixed to the distal oesophageal mucosa.

Management

Life-style and dietary modification-
- Weight loss
- Elevation of head of the bed.
- Elimination of dietary triggers  coffee, chocolate, spicy foods, food with high fat content, carbonated beverages and peppermint.
- Avoid tight fitting garments.
- Promotion of salivation through oral lozenges/ chewing gum to neutralize refluxed acid.
- Avoidance of tobacco and alcohol.
Antacids:
- Magnesium trisilicate
- Aluminium hydroxide or calcium carbonate.
Surface agents:
- sucralfate (aluminium sucrose sulphate)- adheres to the mucosal surface, promotes healing and protects from peptic injury by mechanisms that are incompletely understood.
- Sodium alginate
Histamine 2 receptor antagonist:
- Decreases secretion of acid by inhibiting Histamine 2 receptor on gastric parietal cell.
- Develop tachyphylaxis within 2 weeks of use- hence limited use.
Proton pump inhibitors:
- Potent inhitors of gastric acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump.
- Standard doses for eight weeks relieve symptoms of GERD and heal esophagitis in upto 86% of patients.

Surgical management:

Failed medical management.
Intolerance of medical therapy
Complication of GERD (peptic stricture, severe esophagitis, barrettes oesophagus, carcinoma, dysplasia)
Procedures:
- Radiofrequency treatment – endoscopic
- Transoral incisionless fundoplication- endoscopic
- Surgical- laparoscopic hill gastropexy
- Laparoscopic partial fundoplication
- Laparoscopic Nissen fundoplication (complete)

Complications of GERD:

Everything Gastro