Gastroesophageal Reflux Disease (GERD)/Nonerosive Reflux Disease (NERD)/Erosive Esophagitis (EE)
(Am J Gastroenterol 2005;100:190-200)
DEFINITION:
GERD: Pathologic condition of chronic symptoms or histopathologic injury via percolation of gastroduodenal contents into the esophagus
EPIDEMIOLOGY:
Symptoms: 7% daily, 14% weekly, 15-40% monthly
Note that the prevalence varies markedly from country to country due to physicians’ awareness and understanding the condition
♀ = ♂, but ♂ experience more complications: esophagitis 2:1, Barrett’s 10:1
GERD becomes more common with increasing age (incidence increases markedly after age 40)
Actual organ damage is less frequent as <50% of patients who present with reflux symptoms have esophagitis
ETIOLOGIES:
PATHOPHYSIOLOGY:
Excessive transient LES relaxations (tLES) or incompetent LES (normal pressure: 10-30 mmHg) or ↑ abdominal pressure
↑ LES pressure: cholinergic agonist, protein, gastrin, motilin, antacids, metoclopramide, domperidone
Hiatal hernia: contributes to ↓ LES tone; acts as reservoir for refluxed gastric contents; may widen diaphragmatic hiatus
Size may be the best predictor of the severity of esophagitis
Esophageal mucosal damage (esophagitis) due to prolonged contact with gastric contents: acid, pepsin and duodenal contents: bile salts
Protective: Swallowing; Reflux can trigger salivary production; Saliva has neutral pH, can clear reflux, and contains healing growth factors
Swallowing #/hr: awake/upright: 70/hr; meals 200/hr; sleep <10/hr; Reduced with sedatives/alcohol
Scleroderma/CREST and Sjogren’s syndrome have reduced amounts of saliva production
Saliva is naturally decreased at night, hence nighttime reflux has less saliva and gravity clearance = more injury
CLINICAL MANIFESTATIONS/PHYSICAL EXAM:
Heartburn, retrosternal burning discomfort and regurgitation of stomach contents; atypical “angina”; dysphagia as a complication
Waterbrash (foam at mouth as salivary glands produce up to 10 ml of saliva/min as an esophagosalivary response to acid reflux)
Extraesophageal manifestations (most patients lack classic GERD symptoms and there is no gold standard for diagnosing GERD):
Pulmonary: asthma, chronic bronchitis, aspiration pneumonitis, sleep apnea, atelectasis, interstitial pulmonary fibrosis
ENT: cough (chronic nocturnal aspiration), hoarseness (vocal cord inflammation), sore throat, posterior laryngitis, sinusitis,
Laryngealpharyngeal Reflux: hoarseness, contact ulcers/granulomas, vocal cord nodules, globus, arytenoid fixation
Other: dental erosions, globus, scleroderma/mixed connective tissue disease (MCTD)
An empiric trial of PPI bid for 3 months is preferred diagnostic and treatment approach; If symptoms persist than a pH study on therapy can prove one way or the other if acid reflux playing a role
Reflex: esophagus, bronchial tree and ENT share innervations via vagus; acid infusion of esophagus/ENT can irritate vagus
Reflux: microaspiration of acid into bronchial tree/ENT irritates the respiratory epithelium, stimulating inflammatory mediators
Clues GERD (rather than asthma): adult onset, nonallergic, poor response to asthma medications, nocturnal cough, related to meals
Clues GERD related cough: normal CXR, non smoker/exposure to irritants, no use of ACE-I, negative methacholine challengeRelated posts:
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