Gastroesophageal reflux disease K21.9

Gastroesophageal reflux: Reflux of gastric contents into the esophagus. The cause is an insufficient sphincter closure.

Gastroesophageal reflux disease: inflammation of the esophagus caused by reflux of acidic gastric juice. The cause is acid-related erosive damage to the esophageal mucosa. It is not uncommon for multiple factors to be causative (Ates F et al. 2014).

Endoscopic negative reflux disease (NERD = non erosive reflux disease): Frequent reflux complaints without evidence of reflux esophagitis.

Endoscopic positive reflux disease = reflux esophagitis (ERD = erosive reflux disease): Reflux disease with macroscopic or histological mucosal inflammation.

Primary gastroesophageal reflux disease: insufficiency of the UES of unclear etiology (most common).

Secondary gastroesophageal reflux disease with known cause such as: abdominal obesity, in advanced pregnancy (50% of pregnant women, often in the last trimester). Condition after surgical treatment of athanasia, gastric outlet stenosis, scleroderma.

Approximately 20% of the population of Western industrialized countries is affected by gastroesophageal reflux disease. 60% of this clientele have no detectable lesions endoscopically (NERD). 40% have recognizable erosive lesions (ERD) and thus reflux esophagitis with macroscopic and/or histologic confirmation. 5% of GERD patients develop Barret's esophagus, which is considered a long-term sequela of reflux esophagitis and is an increased risk for developing adenocarcinoma of the esophagus (precancerous).

Dysfunction of the lower esophageal sphincter. Ultimately, the exact etiology is unknown. Promoting factors are impaired barrier function (physiologically, a constant pressure barrier between the esophagus and stomach (lower esophageal pressure is physiologically 10-25mm Hg higher than gastric pressure)), abnormal contraction processes in the lower esophagus, resulting in reduced cleansing function (clearance), reduced neutralization, mucosal factors (mucoresistance), gastric dysfunction, genetic factors.

Main cause: insufficiency of the UES and aggressive reflux.

Heartburn (75% of patients) and retrosternal pressure sensation (Mikami DJ et al. 2015), optional painful dysphagia (60%); air burping (60%); meteorism; flatulence; epigastric pain and burning (30%). However, reflux esophagitis may have an asymptomatic course and is discovered incidentally, e.g., during gastroscopy.

Extraesophageal manifestation of reflux disease:

Possibly stenocardial symptoms (cardiac reflex pathway).

Irritative cough (reflux bronchitis - chronic cough (D'Urzo A et al. 2002)); triggering or exacerbating bronchial asthma, triggering chronic bronchitis.

Possibly hoarseness due to laryngo-pharyngeal reflux (reflux laryngitis).

Diagnostic clarification is performed endoscopically (gastroscopy).

Long-term pH-metry: The pH value in the lower esophagus is measured over 24 hours in order to determine the acid load in these areas.

X-ray examinations of the esophagus give only a poorly informative indication of the disease. Therefore, they are not recommended.

According to the number and extent of the lesions, reflux esophagitis can be divided into different degrees of severity according to Savary and Miller or Siefert-Ottenjahn:

• Stage 0: normal mucosa
• stage I: patchy lesions (with (Ib) or without (Ia) fibrinous coating)
• Stage II: streaky lesions (IIa without fibrinous coating; IIb with fibrinous coating)
• Stage III: circular confluent lesions
• Stage IV: complications, such as Barrett's esophagus.

Other schemes for staging reflux esophagitis include the Los-Angeles classification and Armstrong's MUSE classification.

The therapy of reflux disease is based on 3 essential measures:

• general measures
• drug therapy of the symptoms
• surgical treatment of the acid reflux.

Change in eating habits: no fatty and spicy foods, no alcohol (no strong drinks) and cigarettes, no acidic drinks,

Weight reduction, no constricting clothes, no late evening meals 3 hours before going to sleep (Yang JH et al. 2014), avoidance of drugs that lower the pressure in the USE such as: anticholinergics, beta-adrenegics, calcium antagonists, nitro preparations, theophylline, peppermint.

A reflux disease can be effectively treated with medication. Proton pump inhibitors (PPI) are used. These drugs inhibit transporters in the mucous membrane of the stomach that are involved in the production of stomach acid (so-called proton pumps). By inhibiting these transporters, the amount of gastric acid produced is reduced and thus the cause of the symptoms is eliminated (omeprazole, pantoprazole, lansoprazole, esomeprazole, dexlansoprazole). Other substances should only be used for mild reflux complaints without esophagitis (e.g. H2-rezptorant gonists, antacids).

Reflux disease without esophagitis (NERD): with H2 blockers or low-dose proton pump inhibitors.

Peptic erosive reflux esophagitis (ERD): PPI for 8 weeks in 1-2 times the standard dose. In case of frequent recurrences long-term prophylaxis with PPI.

Therapy-refractory severe peptic reflux esophagitis: high-dose PPI. In young patients with large reflux volumes or large axial axial hiatus hernia, surgical intervention in case of intolerance to medical therapy (Frazzoni M et al. 2014).

Surgical procedure: A fundus cuff is wrapped around the lower esophagus. This causes an increase in pressure in the lower esophageal sphincter, which restores physiological conditions.

The reflux disease without esophagitis usually takes a benign but chronic course. Complicated reflux esophagitis has a much worse prognosis:

Complications are ulcers, peptic stenosis, tearing of the mucosa (Mallory-Weiss tear), complete rupture of the esophagus (Boerhaave syndrome); Barrett's esophagus (Rubenstein JH et al. 2014).

Barrett's esophagus: with an uncomplicated course - consistent long-term acid suppression with PPI. In case of severe dysplasia mucosectomy or local resection with small intestine interposition (op according to Merendino). In the presence of invasive adenocarcinoma an oesophageal resection is indicated.

Flax gruel:

Soak freshly ground flaxseed - 3 tablespoons / 500 ml water overnight. Boil briefly, sieve the excess water in a close-meshed kitchen sieve or cloth made of linen. Squeeze the solid through the cloth or strainer and remove from the outside with a spoon. Drink in sips.

Works even if resistant to the sometimes controversial PPI, no side effects.

It is important to have a surveillance strategy in Barrett's esophagus (Barrett's esophagus is not included in erosive reflux esophagitis because Barrett's epithelium may be present without inflammatory changes).

Physiological reflux: Occasionally occurring in healthy people (e.g. after fatty meals, after wine consumption)

1. Achem SR et al (2014) Gastroesophageal reflux disease and the elderly. Gastroenterol Clin North Am 43:147-160.
2. Ates F et al (2014) Refractory gastroesophageal reflux disease: advances and treatment. Expert Rev Gastroenterol Hepatol 8: 657-667.
3. D'Urzo A et al (2002) Chronic cough. Three most common causes. Can Fam Physician 48:1311-1316.
4. Frazzoni M et al (2014) Laparoscopic fundoplication for gastroesophageal reflux disease. World J Gastroenterol 20:14272-14279.
5. Mikami DJ et al (2015) Physiology and pathogenesis of gastroesophageal reflux disease. Surg Clin North Am 95:515-525.
6. Rubenstein JH et al (2014) Epidemiology of gastroesophageal reflux disease. Gastroenterol Clin North Am 43:1-14.
7. Yang JH et al. (2014) Recurrence of gastroesophageal reflux disease correlated with a short dinner-to-bedtime interval. J Gastroenterol Hepatol 29:730-735.