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Gastroesophageal reflux disease, Etiopathogenesis, Symptoms, Diagnosis

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Definition of Gastroesophageal reflux disease
Gastroesophageal reflux disease (GERD) includes all the symptoms that result from ferux of gastric content into the  esophagus.
Gastroesophageal reflux (GERD) represents the physiologic phenomenon of gastric content passage into the esophagus, which becomes pathological when the antireflux mechanisms are surpassed.
Reflux esophagitis (RE) consists of esophageal lesions induced by GER, occurring only in certain cases of pathological GER.

Etiopathogenesis (causes)
A. Physiologic causes:
  • Decreasing of the lower esophageal sphincter (LES) pressure. Normally the LES pressure is 20-25 mmHg and it only disappears during swallowing. GER occurs either when LES transiently relaxes because of swallowing, or when the LES basal pressure decreases less than 6 mmHg, thus allowing the castric content to pass into the esophagus. LESpressure can be reduced by drugs (anticholinergic, aminophylline, nitrates, benzodiazepines, calcium channel blockers), food (chocolate, fatty foods, onion, citric, tomato juice mint), coffee, smoking, alcohol.
  • Decreasing of gastric motility with delayed gastric emptying.
  • Disorder of esophageal clearance by refluxed acid gastric content.

B. Mechanical causes:
  • Hiatal hernia – produces a decrease in LES tonus, which allows the reflux.
  • Increasing of intraabdominal pressure: pregnant women, obese, patients with giant abdominal tumors or ascites.
  • The widening of his angle. This angle between the esophagus and stomach is usually very sharp, having the role of a valve at the stomach entrance. In the obese, it enlarges.
  • The relaxation of diaphragmatic crura, the muscular channel through which the esophagus passes from thorax into the abdomen. The relaxation cavity volume increases (emphysema).
  • Sclerodermia. The motor disorders of the esophagus are the result of fibrosis and atrophy of the smooth muscle, the so-called “glass-esophagus”.

The development and severity of reflux esophagitis depend on 3 conditions:
  • the increasing of reflux frequency
  • the increasing of reflux duration
  • the action of aggressive gastric content of the esophageal mucosa

Clinical features (symptoms)

  • Pyrosis is characterized by burning retrosternal discomfort, climbing up the throat. It is aggravated by maneuvers that increase intraabominal pressure (bending forward, load straining, lying recumbent immediately after eating) accompanied sometimes by acid regurgitations as well. If the LES incompetence is severe, solid food can also be regurgitated.
  • Retrosternal pain is often a problem of differential diagnosis with the cardiac pathology. It may appear isolated, without pyrosis, mainly when ingesting irritating food. Odynophagia (painful swallowing) appears during spastic contractions of LES. Dyspagia – difficult swallowing.
  • Respiratory symptoms (stifling, nocturnal dyspneea, asthma crises) or ENT (laryngitis, pharyngeal paralysis, dysphonia) are due to the regurgitation of refluxed acid gastric content and its aspiration.
Paraclinical findings (investigations)
  • Superior digestive andoscopy (esogastrocopy). When confronting with annoying, persistent esophageal symptoms (mainly pain or dysphagia), an esogastroscopy will be done. It will reveal or exclude the possible esophageal lesions (esopagitis, stenosis)., gastroduodenal lesion. Also by means of endoscopy, a discovered lesion may be diopsied.
  • Barium examination it may show the esophageal motor disorders (achalasia, esophageal diffuse spasm), a possible esophageal stenosis, a hiatal hernia.
  • Esophageal pH – metry is very useful to discover the reflux duration.
  • Esophageal manometry allows the subtle discovering of esophageal motor disorders and their possible linking to the clinical symptoms.
Other tests, more rarely used are esophageal scintigraphy or the Berstein test.
Diagnosis of Gastroesophageal reflux disease
Positive diagnosis – is mainly clinical, but most be paraclinical confirmed.

Differential diagnosis
A. With digestive diseases:
  • gastroduodenal ulcer having as typical symptom the epigastric pain;
  • the differenciation between the acid reflux and the alkaline one (mostly after colecistectomy), when the patient complains of bitter taste in the morning.
  • the esophageal diverticula’s, achalasia, esophageal ulcer or cancer.

B. With nondigestive digeases:
  • retrosternal or thoracic pain must be differentiated from a cardiac pain (ECG or the effort test is necessary; in doubtful cases, coronarography is useful)
  • the bronchic asthma crisis may be sometimes induced by the acid reflux, therefore, correlating the crises with pH – metry may be useful for the therapy.
Evolution, complications
The evolution is prolonged with good periods alternating with less good ones, generally because of food intake and life style.

The complications of reflux disease are:
  • reflux esophagitis, of different degrees, resulting in esophageal peptic ulcer and esophageal stenosis.
  • The Barrett epithelium (endobranchiesophagus) is a columnar epithelial metaplasia of normal squamous mucosa, because of reflux disease healing, after acid exposure, and it represents a premalignant condition to the esophageal cancer.
  • Superior digestive hemorrhage (hematemesis and/or melena) is a rare complication. It generally appears as melena, because the hemorrhages are mild, produced by ulcer or severe esophagitis.
Treatment of Gastroesophageal reflux disease
A. Diet
  • dietary restrictions: avoiding bulky meals, avoiding food that decreases LES pressure:coffee, chocolate, carbonated drinks, mint products, fatty foods, alcohol or foods that increase the acid secretion: orange juice, carbonated drinks, white vine, and acid food);
  • avoiding smoking. It is said that smoking increases the acid secretion and lowers the LES pressure;
  • avoiding lying recumbent immediately after eating;
  • weight loss in the obese patients (reducing the abdominal pressure);
  • avoiding medications that decrease the LES pressure: nifedipin (calcium channel blockers), nitrates, aminophylline, caffeine and anticholinergics. These are also studies suggesting that NSAIDS and aspirin are associated with esophageal lesions, being able to induce esophagitis and even esophageal strictures.
B. Medication – involves 2 types of drugs:

1. Antisecretory drugs. This treatment decreases the acid secretion:
Proton pump blockers are the most potent antisecretory drugs:
  • Esomeprazole (Nexium) 40 mg/day.
  • Omeprazole (Losec, Ultop, Antra) 20 mg bid;
  • Pantoprazole (Controloc) 40 mg/day;
  • Lanzoprazole (Lanzap) 30 mg/day;
  • Rabeprazole 20 mg/day;
The duration of treatment is 4-8 weeks, or a few months in resistant cases.
H2 blocking agents:
  • Ranitidine 150 mg bid;
  • Famotidine 40 mg/day;
  • Nizatidine (Axid) 150 mg bid.
  • H2 blocking agents; they may be used 2-6 weeks or even more in resistant cases.

2. Prokinetic
  • Metoclopramide, 10 mg tid, 30 bid minutes before meals. Its effect  is the increasing of LES tone; it also increases the esophageal clearance and hastens the gastric emptying.
  • Domperidone (Motilium) is effective on the LES and gastrokietic; the effect on the reflux is lower than that of Metoclopramide.
3. Antiacids - medication with direct neutralizing effect: Maalox, Novalox, Rennie, Dicarbocalm, containing magnesium and aluminium salts; the patients se them when the symptoms appear, with a spectacular disappearance of symptoms. They effect is only symptomatic, the esophagitis lesions persisting. An interesting drug of this group is the sodium alginate (Gaviscon, Nicon), which forms a protective layer over the esogastric mucosa.
4. Mucosal protectives. Sucralfate is an aluminium polisulfatate sucrose, which links the billiary acids and pepsin and stimulates the gastric secretion of prostaglandins and epidermic growth factor, thus favoring the epithelium healing. It is sometimes indicated in esophagitis.
The strategy of treatment is to begin, generally, in case of acid reflux, with PPI, in case of failure, a prokinetic is added. If the patients complain of billiary reflux, the therapy will be prokinetic.
C. Endoscopic
  • Esophageal structures. The most preffered treatment in peptic strictures is done endoscopically, by Savary probe dilators or pressure balloons.
  • Superior digestive hemorrhage. The severe cases require endoscopic hemostasis by Adrenaline injections, Argon Beamer photocoagulation or hemoclips application.
  • Barrett’s esophagus. The columnar epithelium patches with different degrees of dysplasia may be destroyed by Argon plasma photocoagulation.
  • Endoscopic fondoplicature – represents a new noninvasive method, in which the gastric fundus is wrapped around the esophagus thus creating a very sharp His angle.
D. Surgical
In rare cases with severe esophagitis without response to drug therapy, surgery may be needed.                                       

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