Gerd

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Gastroesophageal reflux disease (GERD) PROF /GOUDA ELLABBAN MD SURGERY

Transcript of Gerd

Gastroesophageal reflux disease (GERD)

PROF /GOUDA ELLABBANMD SURGERY

Gastroesophageal reflux disease (GERD)

GERD: Any symptomatic condition or histopathologic alteration resulting from episodes of gastroesophageal reflux.

Reflux esophagitis: endoscopy

GERD Symptoms in the absence of

esophagitis-> 24-hour esophageal pH monitor

Acid sensitive esophagus No gold standard for the recognition or

exclusion of GERD. Heartburn is an indicator of GERD.

GERD in the 1970s found that 7% of individuals

experienced heartburn daily, 14% weekly, and 15% monthly.

55% to 81% no esophagitis. an autopsy study: < 1/6 patients with

Barrett's metaplasia was recognized clinically prior to death.

Risk factors of GERD

Male preponderance of esophagitis (2 :1 to 3 :1) and of Barrett's metaplasia (10 :1).

Pregnancy: 48~79% heartburn. Whites Geographic variation: very low rates in Africa

and Asia and high rates in North America and Europe.

Agents decrease LES pressure NSAIDs: peptic strictures

Erosive esophagitis

Complications: peptic stricture, pseudodiverticula, Barrett's metaplasia, inflammatory polyps, and reactive changes that can mimic dysplasia.

Perforation and fistulization: rare.

Pathogenesis Exposure of gastric secretions Functional integrity of the esophagogastric

junction: intrinsic LES pressure, extrinsic compression of the LES by the crural diaphragm, the intra-abdominal location of the LES, integrity of the phrenoesophageal ligament, and maintenance of the acute angle of His between the distal esophagus and proximal stomach with its flap valve function

Mechanisms of Reflux

1. Transient LES relaxation: mild

2. Hypotensive LES

3. Diaphragmatic sphincter, hiatal hernia, and other anatomic variables

Acid reflux during smoking

Delayed Gastric Emptying

May exacerbate GERD

A potential cofactor exacerbating GERD rather than a cause of GERD.

Esophageal Acid Clearance

Titration by swallowed saliva. Increase salivation: oral lozenges,

chewing gum, or bethanechol chloride. Salivation ceases during sleep

Esophageal Acid Clearance

Hiatal hernia: the most prolonged supine acid clearance

Correlates with both the severity of esophagitis and the presence of Barrett's metaplasia

Impairments of Esophageal Emptying

Ineffective esophageal motility: ≥ 30% hypotensive (<30 mm Hg) or failed contractions

Reflux of fluid from the hernia sac during swallowing: complete emptying with only 1/3 of test swallows

Tissue Injury

Hydrogen ion gastroesophageal refluxate is a

heterogeneous mixture: pepsin, bile acids, trypsin,lysolecithin & food hyperosmolarity

Clinical Presentation & Natural History – Typical Symptoms

The most common symptoms: heartburn, acid regurgitation, and dysphagia

Heartburn (pyrosis): Some patients with severe esophagitis or Barrett's metaplasia do not report having any heartburn.

Typical Symptoms

Regurgitation Dysphagia: > 30%; caused by peptic

stricture, a Schatzki ring (B ring), peristaltic dysfunction, or simple mucosal inflammation. Abnormal sensitivity to bolus movement during peristalsis.

Typical Symptoms -- Less common

Water brash: excessive salivation resulting from a vagal reflex triggered by esophageal acidification.

Globus sensation: perception of a lump or fullness in the throat that is felt irrespective of swallowing.

Odynophagia: likely related to an esophageal ulcer or deep erosion

Atypical Symptoms

Posterior Laryngitis: 4% to 10% evaluated by otolaryngologists; chronic hoarseness, posterior laryngeal erythema and edema, contact ulceration of the vocal folds, and vocal fold granulomata.

Asthma: effect of esophageal acid perfusion on pulmonary function is minimal on researches, but clinical data suggest that treatment of GERD in asthma patients usually improves respiratory symptoms.

Atypical Symptoms

Cough: postnasal drip, asthma, and GERD (10% to 40%) constitute an estimated 80% to 90% of cases in chronic cough. acid stimulation of nerve endings in the esophagus-> activate the cough center; besides, actived vagally mediated esophagotracheobronchial reflex

Noncardiac Chest Pain About 30% of patients have normal CAG. Once cardiac ischemia is ruled out,

esophagus is often implicated. Episodes of chest pain were often

associated with reflux The mechanism is unclear: maybe

esophageal afferent nerves discriminate poorly.

Natural History

1 to 3 years prior to seeking medical attention Esophagitis: recurrence in approximately 80%,

most within 3 months of discontinuation of therapy

Mortality (other than adenocarcinoma) is minimal: 0.1 per 100,000.

Peptic stricture: 8% to 20% Ulceration: 5%-> decreasing due to PPI. Bleeding <2%

Differential Diagnosis

Infectious esophagitis, pill esophagitis, peptic ulcer disease, dyspepsia, biliary colic, CAD, and esophageal motor disorders.

CAD must be given early consideration because of its potentially lethal implications

Associated condition Pregnancy: 50% to 80% Scleroderma: 90% with esophageal

function impairment (diminished peristaltic amplitude in the smooth muscle segment of the esophagus and diminished or absent LES pressure). MCTD can occur also.

Associated condition

Sjögren's syndrome: disrupts normal salivary secretion and interferes with esophageal acid clearance

Diabetic gastroparesis, intestinal pseudo-obstruction, and collagen vascular disorders: Changes in gastric emptying

Zollinger-Ellison syndrome

Management The primary goal: symptom relief. Diagnostic evaluation: in selected GERD

patients to confirm the diagnosis, direct therapy, or identify complications.

Severe or atypical symptoms: intensive medical therapy is appropriate as the initial treatment plan and may in fact help establish the diagnosis of GERD.

Diagnostic Evaluation Indication: extremely chronic heartburn

(possibility of Barrett's metaplasia?), refractory to treatment, or warning signs of dysphagia, odynophagia, gastrointestinal bleeding, or weight loss.

Endoscopy: the first diagnostic test; specificity of 90% to 95% in erosive esophagitis, but sensitivity is poor (only 30~40% of patients with GERD have esophagitis indicated by endoscopy). Grading: the Los Angeles system A-D.

Further tests

(1) Atypical symptoms (2) identifying why GERD therapy has failed.

Bernstein test: reproduce symptoms by perfusing the esophagus with 0.1 N HCl. Typical symptoms: sensitivity 42%~100%, and specificity 50%~100%. Atypical symptoms: sensitivity 7%~27%; high specificity is maintained.

Further test -- Ambulatory 24-hour pH monitor

The most widely used test probe 5 cm above LES Abnormal: time of pH <4; value >3.5%. Lack of high sensitivity (25~30%) The principal indication: patients without

endoscopic esophagitis or evaluating the efficacy of medical or surgical treatment

Further test Empirical trial of potent antisecretory

therapy: PPI for 1- to 2-week; including no reflux in 24 hr pH monitor

False-positive : peptic ulcer disease or malignancy ?

Esophageal manometry: minimal use except detecting major motor disorders or evaluating peristaltic function prior to antireflux surgery.

Nonprescription Therapy

>36% of the U.S. population suffers from heartburn at least once a month (Am J Dig Dis

21:953, 1976), but few seek medical care. 27% of adult Americans take antacids more than twice a month.

life-style modifications over-the-counter histamine-2 (H2)

receptor antagonists

Life-style modifications Head of the bed elevation, avoidance of

tight fitting garments, weight loss, dietary modification, restriction of alcohol use and elimination of smoking.

Avoid a supine position after meals and should not eat within 3 hours of bedtime

Chewing gum for mild GERD.

Acid Suppressive Medications The most common and effective

treatment H2RA: Tachyphylaxis & inability to

suppress meal related acid secretion effectively. (therapeutic gain 10~24%)

PPI: only act on membrane bound activated H+, K+-ATPase-> 30 minutes before meals.

Prokinetic Drugs Metoclopramide: antidopaminergic agent, also

acts as a 5-HT3 antagonist, a 5-HT4 agonist, and a cholinomimetic. Minimal effect but 25% P’ts have CNS side effects.

Cisapride: 5-HT3 antagonist and 5-HT4 agonist activity, release of acetylcholine from postganglionic nerve endings of the myenteric plexus. As efficacious as standard H2RA therapy in controlling symptoms and healing grade 1 to 2 esophagitis. Cardiotoxic effects especially in combination with agents that are metabolized by the cytochrome P-450 system.

Maintenance Therapy A study: Omeprazole significantly more

effective than either ranitidine or cisapride alone, and the combination of omeprazole and cisapride was the most effective.

The median dose to maintain remission: at or near the dose required for healing esophagitis.

Nonerosive GERD

Elimination of heartburn: a more difficult therapeutic end point than esophagitis healing

Data do not support “ nonerosive GERD is more responsive to therapy than erosive esophagitis, and easily treated with less potent antisecretory therapy”.

Intermittent or on-demand therapy may be adequate for symptom control in endoscopy-negative GERD.

Antireflux Surgery

Laparoscopic Nissen (360°) fundoplication and the Toupet (270°) fundoplication

Repair hiatal hernia and increase resting LES pressure; decrease frequency and/or effectiveness of tLESR.

Mortality rate of 0.2% Dysphagia, gas bloating, and flatulence: some

(4/57 in a study) need reoperation.

Antireflux Surgery Indication: (1) failed medical therapy (2)

medical success in a young healthy patient unwilling to take or intolerant of long-term PPI therapy (3) persistent symptoms due to regurgitation (laryngitis, asthma, bronchiectasis).

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