GASTRO-ESOFAGIAN REFLUX

Gastro-oesophageal reflux disease (GERD) comprises all the symptoms produced by the
reflux of gastric contents in the esophagus.
Gastroesophageal reflux (GGE) is the passage of gastric contents in the
esophagus, a physiological phenomenon that becomes pathological (ER) when antireflux mechanisms are
overcome.
In esophageal reflux (ER), oesophageal lesions induced by the RGE are not found in
all cases. BRGE is a relatively common clinical entity in clinical practice and has a
symptomatic, often polymorphic picture .
The prevalence of
ER is ~ 4% in the general population, increasing with age. The current trend is to
increase it.
etiopathogeny
There are two major causes that determine the ineffectiveness of the antireflux mechanism:
A. Physiological causes
1. Lower esophageal sphincter (SEI) pressure. Under normal conditions,
SEI pressure is 20-25 mmHg and does not disappear until swallowing.
RGE occurs either when SEI is transiently relaxed outside of swallowing or when
baseline SEI falls below 6 mmHg, allowing the gastric contents to pass
through the esophagus. SEI pressure can be reduced by medication factors (anticholinergics,
aminophylline, nitrites, benzodiazepines, calcium channel blockers), food
(chocolate, fat, onion, citrus, tomato juice
, , alcohol (also increases gastric acid secretion).
2. Decreased gastric motility with delayed gastric emptying.
3. Impairment of esophageal clearance of reflex gastric acid content. This
clearance together with swallowed saliva is to buffer the reflex acid.
B. Mechanical Causes
1. Hiatal hernia produces a decrease in SEI tone that favors reflux.
2. Increasing intra-abdominal pressure leads to widening diaphragmatic hiatus,
explaining the occurrence of RGE in pregnant, obese patients with giant abdominal tumors
or ascites.
3. Widening the angle of His. This angle between the esophagus and the stomach is usually very
sharp, having the role of a valve at the entrance of the stomach. In the obese he widen and
lose his physiological role.
4. Relaxation of the diaphragmatic forearm. This brush is formed by the diaphragm,
the muscular canal through which the esophagus passes from the chest to the abdomen. Relaxation
occurs when intra-abdominal pressure or chest cavity
(emphysema) increases.
5. Scleroderma. Oesophageal motor disorders are caused by the processes of
fibrosis and smooth muscle atrophy, the so-called „glass esophagus”.

The development and severity of reflux esophagitis are conditioned by the presence of three conditions:
– increased frequency of reflux;
– increasing the duration of reflux;
– the aggressive effect of gastric contents on the esophagus mucosa.
Clinical picture
It is relatively typical, translating through acidic or heartburn with a continuous or
discontinuous character . Symptoms can only be occasional, but sometimes quasi-permanent.
Retrospective pain or dysphagia are quite rare. The presence of these two last symptoms
must make us think of a more severe pathology. More rarely, in atypical forms,
symptoms may mimic a cardiac pathology with angina-like pain or the onset of
asthma attacks .
Heartburn is the retrosternal burning sensation that climbs to the throat. It is accentuated by maneuvers
that increase intraabdominal pressure (bending forward, lifting weights, sleeping immediately
after a meal), sometimes accompanied by acid regurgitation. If SEI incompetence is
major, food may be regurgitated.
Retrosternal pain often causes differential diagnosis problems with
cardiac pathology . It may appear isolated, not accompanied by heartburn.
Odinophagia (painful swallowing) occurs in case of spastic contraction of SEI.
Dysphagia is defined as difficult swallowing.
Respiratory symptoms (suffocation, nocturnal dyspnea, asthma attacks) or ENT (laryngitis,
pharyngitis, dysphonia) are due to regurgitation of reflex acid and
aspiration.
Paraclinical
investigations Investigations needed to evaluate gastroesophageal reflux will include:
esogastroscopy, ph-metria and esophageal manometry. Which of these tests do we do and
when? In an attempt not to be too invasive, but wishing not to get rid of serious injuries, it is quite
difficult to decide the means of diagnosis.
Superior digestive endoscopy
In the presence of persistent, troublesome esophageal symptoms (but especially when we have
pain or dysphagia), eso-gastroscopy will be performed.
It will reveal possible esophageal lesions (esophagitis, stenosis) or exclude them. It will
also reveal a gastro-duodenal lesion associated or even causing symptoms.
The presence of a hiatal hernia can be highlighted. Also through endoscopy an uncovered lesion
can be biopsy (emphasizing a Barrett epithelium).
The most typical consequence of gastroesophageal reflux is reflux oesophagitis, which is
an oesophageal mucosal lesion (denudation) under the effect of acidic or alkaline reflux.
The severity of endoscopic lesions is appreciated by the Los Angeles classification.
According to this classification, esophagitis may have several degrees (AD):
A) One or more loss areas of less than 5 mm.
B) At least one substance loss greater than 5 mm but non-confluent.
C) At least one extended substance loss between 3 or 4
mucous, but non-circumferential folds .
D) Loss of circumferential substance.
The 24-hour esophageal Ph-metria (usually ambulatory) is very useful
to discover the duration of reflux, the time spent by the lower esophagus at a pH below 4
(acid). It also uses the correlation between clinical symptoms and acidic pH, or
correlates with atypical symptoms (temporary pain, asthma attacks) with reflux.
The impediments are related to the price of the device and its affordability rather low.

Esophageal manometry usually coupled with esophageal pH, allows for the detection
of oesophageal motor disorders and eventually coupling with clinical symptoms. It’s an
older method.
The passage of barium (with a questionable utility in this condition) can highlight
esophageal motor disorders (acalasia, esophageal diffuse spasm), eventual oesophageal stenosis, a
hiatal hernia (in the Trendelenburg position). Evidence of oesophageal lesions is not
possible, so examination has a very limited value.
Diagnosis
Positive
Diagnosis The diagnosis of the disease is clinical, but must be confirmed paraclinically. We have two
special situations : differentiation between gastroesophageal reflux as a discomfort generator and
reflux esophagitis as a consequence of reflux. In most patients who have
occasional oesophageal reflux , explorations will not show lesions. In case of persistent (permanent) reflux,
esophageal morphologic lesions will exist.
Differential diagnosis
A. With digestive diseases:
– Gastroduodenal ulcer has a typical symptom of epigastric pain; the presence of pyrosis
indicates the concomitance of an acid reflux.
– Differentiation between acidic and alkaline reflux (especially postcolecistectomy), when
mature or quasi-permanent bitter taste occurs.
– Esophageal diarrhea, achalasia, esophageal ulcer, esophageal cancer.
In the face of any dysphagia, especially in the elderly (but not necessarily), or of a
distress (intense pain during swallowing), we must think of a possible
esophageal neoplasm and perform a mandatory diagnostic endoscopy (attention:
barium passage can lead to diagnostic errors).
B. With non-digestive diseases:
– Retrosternal or thoracic pain will be distinguished from cardiac pain (EKG
or effort test is needed, in case of doubt the coronarography is useful).
– The bronchial asthma crisis can sometimes be triggered by acid reflux, so
correlation of pH-metric seizures can be useful for therapy; the problem is often
important in the child.
Evolution, complications
Evolution is long-lasting with good and less good periods, generally related to
diet, lifestyle.
Complications that occur in reflux disease are:
– reflux oesophagitis, varying degrees, going to esophageal ulcer and
oesophageal stenosis (exceptional situations rare in us, where A
and B esophagitis prevails in the Los Angeles classification).
– The Barrett epithelium (endo-brachis-esophagus) is a cylindrical epithelial metaplasia of
normal malpig mucosa as a consequence of healing reflux disease after
exposure to acid and is a premalignant condition for esophageal cancer.
Endoscopically, the metaplastic Barrett mucosa appears red, unlike the
pink esophageal mucosa . Topographic, can be circular, in the form of languages ​​or islands.
Two forms of Barrett esophagus are described:
· long – is present more than 3 cm above the esophagus junction;
· Short – is located in the first 2-3 cm above the esophagus junction.
Diagnosis of certainty is histopathological – intestinal metaplasia.

Since 2004 there has been a new classification of the Barrett epithelium – the Prague classification.
In this classification there are two parameters: the circumferential Barrett and the
maximum Barrett (c and m, both in centimeters).
The essential issue of Barrett’s esophagus is its increased malignancy risk,
30-125 times higher than in the rest of the population; on average,
one of 125 subjects with Barrett’s esophagus is cancer yearly .
Therapeutic guidance for the early detection of
Barrett’s esophagus malignancy is based on the histological appearance:
– intestinal metaplasia without dysplasia – medical treatment with
endoscopic surveillance and biopsy at 2 years;
– low grade dysplasia – medical treatment and annual
biopsy surveillance ;
– high grade dysplasia – surgical or endoscopic treatment (
endoscopic mucosectomy or radioablation destruction).
If not, then medical treatment, with biopsies serialized at 3-6 months.
– upper digestive haemorrhage (haematemesis and / or melena) is a rare complication.
It usually appears as melen, because bleeding is mild or moderate,
caused by severe ulcer or esophagitis.
Treatment
A. Igieno-dietetic
Most cases are resolved by sustained dietary measures. These measures would be:
– Dietary Rrestrics: avoiding bulky meals, avoiding foods that lower
SEI pressure: coffee, chocolate, carbonated drinks, mints, fat,
alcohol or foods that increase acid secretion: orange juice,
carbonated drinks , wine white, acidic foods.
– Avoiding smoking: smoking is believed to increase acid secretion and lower SEI pressure.
– Avoiding full stomach licking or bent positions immediately after the meal.
– Obese people will be advised to lose weight (abdominal press).
– Avoiding medications that lower SEI pressure: nifedipine, nitrates, euphiline or
caffeine.
B. Medicaments There
are two types of medication:
1. Antisecretor
This treatment decreases acid secretion.
Proton pump blockers (proton pump inhibitors (PPIs))
are the most potent antisecretory agents. Several proton pump blockers are known today
: omeprazole (Losec, Omeran, Ultop, Antra, Omez) 2 × 20 mg / day, pantoprazole
(Controloc) 40 mg / day, lanzoprazole (Lanzop, Lanzap) rabeprazole 20 mg / day.
Esomeprazole (Nexium, Emanera) 40 mg / day is the second-generation IPP.
In case of reflux oesophagitis, the duration of treatment is 4-8 weeks (after the
severity of esophagitis). Antisecretory therapy can be used if needed (in
case of intermittent acid reflux).
2. Prokinetic
– Classic Metoclopramide, given 3x1tb (10 mg) 30 minutes before a
meal. The effect is to increase SEI tone; also increases
esophageal clearance and gastric emptying rate.
– Domperidone (Motilium) has SEI effect and gastric kinetics.
It does not give extrapyramidal phenomena. This prokinetic is preferred to Metoclopramide,
with reduced side effects.

3. Antacids
Medication with direct neutralizing effect: Maalox, Novalox, Rennie, Dicarbocalm,
containing magnesium and aluminum salts; the patients consume them in case of symptoms, which
make them disappear immediately. They have only a symptomatic effect, for the moment, not knowing the
lesions of esophagitis.
The treatment strategy is generally in the case of acid reflux with an
antisecretory medication , preferably with IPP. In case of failure, a prokinetic
(Domperidon) is added . If patients complain of biliary reflux, therapy will be prokinetic.
C. Endoscopic
– Esophageal Stenosis The
treatment of peptic stenosis is endoscopic by dilatation with
Savary probes or pressure balloons.
– Higher digestive haemorrhage
Severe forms benefit from endoscopic hemostasis by adrenaline injection,
Argon Beamer photocoagulation or hemobiography.
– Barrett
Esophagus Cylindrical epithelial beaches with varying degrees of dysplasia can be destroyed
by radiofrequency (RFA) ablation , dynamic phototherapy or endoscopic mucosctomy.
– Endoscopic Bonepulsion
It is a new, non-invasive method, which consists in creating a sharp His angle, through the
endoscopic embossing of the gastric face of SEI. Several types
of endoscopic endoscopic devices are currently available for endoscopic fundoplication.
D. Surgery
Rare cases that have a severe and unresponsive oesophagitis may have
operative indication (exceptionally rare in us). This consists of the Nissen follicularization
(making a gastric sleeve around the distal esophagus), which is currently
laparoscopic.

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