One-liner#

GERD management centers on lifestyle modifications plus PPI therapy (omeprazole 20mg daily for 4-8 weeks), with step-down to lowest effective dose once controlled, EGD for alarm features or refractory symptoms, and indefinite PPI therapy for Barrett’s esophagus.

Quick nav#

Definition and epidemiology#

Diagnostic criteria#

GERD is a clinical diagnosis based on:

  • Typical symptoms: heartburn and/or regurgitation occurring ≥2 times per week
  • Response to empiric PPI trial supports diagnosis
  • EGD not required for diagnosis in typical presentations without alarm features

Montreal Definition: GERD is a condition that develops when reflux of stomach contents causes troublesome symptoms and/or complications.

Phenotypes:

CategoryFindingsClinical Significance
Non-erosive reflux disease (NERD)Normal EGD; symptoms presentMost common (~70%); responds to PPI but may need ongoing therapy
Erosive esophagitis (ERD)Mucosal breaks on EGD (LA grades A-D)Higher grades need longer PPI course; higher recurrence risk
Barrett’s esophagusIntestinal metaplasia on biopsyPremalignant; requires surveillance; indefinite PPI
Reflux hypersensitivityNormal acid exposure; symptoms correlate with reflux eventsFunctional component; may need neuromodulators
Functional heartburnNormal acid exposure; no symptom-reflux correlationNot true GERD; treat as functional disorder

Epidemiology#

Prevalence is 18-28% in North America and Europe; 10-20% globally. Weekly symptoms affect ~20% of US adults. Risk factors include obesity (OR 1.5-2.0 for each 5-unit BMI increase), hiatal hernia, pregnancy, smoking, family history, and connective tissue disorders. Complications include erosive esophagitis (30-40% of GERD patients), stricture (1-5%), Barrett’s esophagus (5-15% of chronic GERD), and esophageal adenocarcinoma (0.5% annual risk in Barrett’s without dysplasia).

Pathophysiology#

Mechanism (clinical understanding)#

GERD results from excessive esophageal acid exposure due to failure of the anti-reflux barrier and/or impaired esophageal clearance.

Lower esophageal sphincter (LES) dysfunction:

  • Transient LES relaxations (TLESRs): most common mechanism; inappropriate relaxations unrelated to swallowing allow reflux
  • Hypotensive LES: baseline pressure <10 mmHg allows free reflux, especially when supine or with increased intra-abdominal pressure
  • Anatomic disruption: hiatal hernia separates the LES from the crural diaphragm, eliminating the “double sphincter” effect

Hiatal hernia contribution:

  • Present in 50-90% of patients with erosive esophagitis
  • Creates an “acid pocket” above the diaphragm that refluxes easily
  • Impairs LES function and esophageal clearance
  • Larger hernias (>3 cm) correlate with more severe disease

Acid pocket phenomenon:

  • After meals, a pocket of unbuffered acid forms at the gastroesophageal junction
  • This acid pocket is the source of postprandial reflux
  • Explains why symptoms worsen after eating and when lying down

Impaired esophageal clearance:

  • Gravity and peristalsis normally clear refluxed acid
  • Impaired motility (scleroderma, diabetes) prolongs acid contact time
  • Supine position eliminates gravity assistance

Mucosal defense failure:

  • Esophageal epithelium lacks the protective mucus layer of gastric mucosa
  • Repeated acid exposure causes inflammation, erosion, and metaplasia
  • Chronic inflammation leads to Barrett’s esophagus in susceptible individuals

Why this matters for treatment:

  • PPIs reduce acid production but don’t fix the mechanical defect
  • Lifestyle modifications (weight loss, head elevation, avoiding late meals) address the mechanical component
  • Surgery (fundoplication) restores the anti-reflux barrier for patients who fail medical therapy

How to explain to patients#

Your stomach makes acid to digest food. Normally, a valve at the bottom of your food pipe (esophagus) keeps that acid in your stomach where it belongs. In GERD, this valve doesn’t work properly—it relaxes when it shouldn’t, or it’s too weak to stay closed.

When acid splashes up into your food pipe, it causes that burning feeling you know as heartburn. Your food pipe isn’t designed to handle acid like your stomach is, so the acid irritates and inflames the lining.

Think of it like a door that doesn’t close all the way. The acid can leak through, especially after meals when your stomach is full, or when you lie down and gravity can’t help keep things in place. That’s why eating late at night and lying down right after eating makes symptoms worse.

The medicines we use reduce how much acid your stomach makes. Less acid means less burning when reflux happens. But the medicines don’t fix the valve—that’s why lifestyle changes like losing weight, raising the head of your bed, and not eating before bedtime are just as important as the pills.

Clinical presentation#

Characteristic symptoms#

Typical symptoms (high specificity for GERD):

  • Heartburn: retrosternal burning, rising from epigastrium toward throat; worse postprandially, when supine, or bending over; relieved by antacids
  • Regurgitation: effortless return of gastric contents to mouth or hypopharynx; sour or bitter taste; may occur with bending or lying down

Atypical/extraesophageal symptoms (lower specificity):

  • Chronic cough: especially nocturnal or postprandial; GERD is one of the “big 3” causes of chronic cough (with asthma and upper airway cough syndrome)
  • Hoarseness/dysphonia: laryngeal irritation from reflux; worse in morning
  • Throat clearing, globus sensation: feeling of lump in throat
  • Dental erosions: enamel loss on lingual surfaces of teeth
  • Asthma exacerbation: reflux can trigger bronchospasm; consider in poorly controlled asthma
  • Chest pain: can mimic angina; must rule out cardiac causes first

Symptom patterns:

  • Postprandial: symptoms within 1-3 hours of eating, especially large or fatty meals
  • Nocturnal: symptoms when supine; may wake patient from sleep
  • Positional: worse bending over, straining, or lying flat
  • Dietary triggers: fatty foods, chocolate, caffeine, alcohol, citrus, tomatoes, mint

Physical exam findings#

Usually normal in uncomplicated GERD. Physical exam is primarily to identify complications or alternative diagnoses.

Findings that may be present:

  • Epigastric tenderness (nonspecific)
  • Dental erosions (chronic severe reflux)
  • Hoarse voice (laryngeal involvement)
  • Wheezing (if asthma component)
  • Obesity (major risk factor)

Findings suggesting complications or alternative diagnoses:

  • Weight loss, cachexia (malignancy)
  • Lymphadenopathy, especially supraclavicular (malignancy)
  • Abdominal mass (malignancy)
  • Pallor (anemia from bleeding)
  • Dysphagia with odynophagia (stricture, esophagitis, malignancy)

Red flags#

Alarm features requiring EGD (do not treat empirically):

  • Dysphagia (difficulty swallowing solids or liquids)
  • Odynophagia (painful swallowing)
  • Unintentional weight loss (>5% in 6 months)
  • GI bleeding: hematemesis, melena, iron deficiency anemia
  • Persistent vomiting
  • Palpable abdominal mass or lymphadenopathy
  • Family history of upper GI malignancy
  • Age >60 with new-onset symptoms (lower threshold for EGD)

Symptoms requiring urgent evaluation:

  • Severe chest pain (rule out cardiac causes first)
  • Complete dysphagia (unable to swallow saliva)—ED evaluation
  • Signs of GI bleeding with hemodynamic instability—ED evaluation

Diagnostic workup#

Initial evaluation#

GERD is primarily a clinical diagnosis. In patients with typical symptoms (heartburn, regurgitation) without alarm features, empiric PPI trial is both diagnostic and therapeutic.

Empiric PPI trial:

  • Omeprazole 20mg (or equivalent) once daily for 4-8 weeks
  • Take 30-60 minutes before breakfast for optimal efficacy
  • Symptom response supports GERD diagnosis
  • Sensitivity ~80% for GERD; specificity ~50-60% (functional disorders may also respond)

When to order labs:

  • CBC: if anemia suspected (chronic blood loss)
  • Iron studies: if anemia present
  • H. pylori testing: if dyspepsia component or prior to long-term PPI (test-and-treat)

H. pylori testing before long-term PPI:

  • Controversial; some guidelines recommend testing before chronic PPI therapy
  • Rationale: PPI + H. pylori may accelerate progression to atrophic gastritis
  • Practical approach: test if dyspepsia symptoms or planning >1 year PPI therapy
  • Use urea breath test or stool antigen (NOT serology)
  • Stop PPI 2 weeks before testing (false negatives)

Confirmatory testing#

EGD (esophagogastroduodenoscopy):

IndicationRationale
Alarm features presentRule out malignancy, stricture
Age >60 with new-onset symptomsHigher malignancy risk
Refractory to 8 weeks of PPIEvaluate for complications, alternative diagnoses
Recurrent symptoms after stopping PPIAssess for erosive disease, Barrett’s
Pre-surgical evaluationConfirm diagnosis, assess anatomy
Barrett’s surveillancePer surveillance protocol

EGD findings and implications:

FindingLA GradeManagement Implication
Normal mucosaN/ANERD; PPI trial appropriate; consider pH testing if refractory
Mucosal erythema onlyN/ANonspecific; treat as NERD
Mucosal breaks <5mm, ≤1 foldAMild erosive; 4-8 week PPI; high healing rate
Mucosal breaks >5mm, ≤1 foldBModerate erosive; 8 week PPI; consider maintenance
Mucosal breaks continuous between foldsCSevere erosive; 8 week PPI; likely needs maintenance
Mucosal breaks >75% circumferenceDSevere erosive; 8 week PPI; high recurrence; maintenance therapy
Barrett’s esophagusN/AIndefinite PPI; surveillance per protocol
StrictureN/ADilation; PPI; evaluate for malignancy

Ambulatory pH monitoring:

  • Gold standard for quantifying acid exposure
  • Indications: refractory symptoms despite PPI, atypical symptoms, pre-surgical evaluation, diagnostic uncertainty
  • Types: catheter-based (24-48 hours) or wireless capsule (96 hours)
  • Perform OFF PPI (7 days) to diagnose GERD; ON PPI to assess treatment adequacy
  • Metrics: DeMeester score, % time pH <4, symptom correlation (SI, SAP)

Esophageal manometry:

  • Not for GERD diagnosis
  • Indicated pre-operatively to rule out achalasia or severe dysmotility
  • Identifies patients who may not tolerate fundoplication

When to refer for specialist workup#

GI referral indications:

  • Alarm features requiring EGD
  • Refractory symptoms despite 8 weeks of optimized PPI therapy
  • Recurrent symptoms requiring continuous PPI therapy
  • Suspected Barrett’s esophagus
  • Consideration for anti-reflux surgery
  • Atypical symptoms not responding to PPI trial
  • Need for pH monitoring or manometry

Surgical referral (after GI evaluation):

  • Confirmed GERD with good PPI response but preference to avoid long-term medication
  • Refractory symptoms despite optimized medical therapy (with objective evidence of reflux)
  • Large hiatal hernia with symptoms
  • Medication intolerance or non-adherence
  • Volume regurgitation not controlled by PPI

What NOT to order#

Avoid these tests in routine GERD:

  • EGD for typical symptoms without alarm features in patients <60 (low yield; treat empirically)
  • Barium swallow for GERD diagnosis (poor sensitivity; does not change management)
  • CT scan for GERD (not indicated; does not visualize mucosal disease)
  • Serology for H. pylori (cannot confirm eradication; use breath test or stool antigen)
  • Gastrin level (only if Zollinger-Ellison suspected—refractory ulcers, diarrhea, MEN1)
  • Repeat EGD for healed erosive esophagitis (unless Barrett’s or other indication)

Cost considerations:

  • EGD: $1,000-3,000; reserve for appropriate indications
  • pH monitoring: $500-1,500; specialist test for refractory cases
  • Empiric PPI trial is cost-effective first-line approach

Treatment#

Goals of therapy#

Symptom control:

  • Complete resolution of heartburn and regurgitation
  • Improvement in quality of life and sleep
  • Ability to eat without symptoms

Mucosal healing (if erosive disease):

  • Healing of esophageal erosions on repeat EGD (if performed)
  • LA grade A/B: >90% healing at 8 weeks with PPI
  • LA grade C/D: 80-90% healing at 8 weeks; may need longer course

Complication prevention:

  • Prevent stricture formation
  • Prevent Barrett’s progression (in those with Barrett’s)
  • Minimize long-term PPI exposure when possible

Long-term strategy:

  • Step-down to lowest effective dose after initial control
  • On-demand therapy for mild intermittent symptoms
  • Maintenance therapy for erosive disease, Barrett’s, or frequent recurrence

Non-pharmacologic management#

Lifestyle modifications are as important as medication. These address the mechanical component of GERD that PPIs cannot fix.

Weight loss (most effective intervention):

  • Even modest weight loss (5-10%) improves symptoms
  • Each 5-unit increase in BMI increases GERD risk 1.5-2x
  • Counsel: “Losing weight is the single most effective thing you can do for your reflux”

Dietary modifications:

  • Avoid eating 2-3 hours before bedtime (allows gastric emptying before supine)
  • Smaller, more frequent meals (reduces gastric distension)
  • Avoid trigger foods: fatty foods, chocolate, caffeine, alcohol, mint, citrus, tomatoes, spicy foods
  • Identify personal triggers (not all patients react to all foods)

Head of bed elevation:

  • Elevate head of bed 6-8 inches using blocks under bedposts or a wedge pillow
  • Extra pillows alone are NOT effective (bends at waist, increases intra-abdominal pressure)
  • Particularly important for nocturnal symptoms
  • Counsel: “Gravity helps keep acid in your stomach—sleeping on an incline makes a real difference”

Positional changes:

  • Avoid lying down within 2-3 hours of eating
  • Left lateral decubitus position may reduce reflux (gastric anatomy)
  • Avoid bending over after meals

Other modifications:

  • Smoking cessation (smoking decreases LES pressure)
  • Avoid tight-fitting clothing (increases intra-abdominal pressure)
  • Limit alcohol (decreases LES pressure, increases acid secretion)

Pharmacologic management#

Proton pump inhibitors (PPIs) - First-line therapy:

DrugDoseContraindicationsMonitoringCostNotes
Omeprazole (Prilosec)20mg daily; 40mg for severe/erosive; max 40mg BIDNone absoluteMg if >1 year; B12 if years of use$ (generic, OTC)First-line; take 30-60 min before breakfast
Pantoprazole (Protonix)40mg daily; max 40mg BIDNone absoluteSame$ (generic)Fewer CYP2C19 interactions; preferred if on clopidogrel
Esomeprazole (Nexium)20-40mg daily; max 40mg BIDNone absoluteSame$ (generic)S-isomer of omeprazole; marginally faster onset
Lansoprazole (Prevacid)15-30mg daily; max 30mg BIDNone absoluteSame$ (generic)Available as orally disintegrating tablet
Rabeprazole (Aciphex)20mg daily; max 20mg BIDNone absoluteSame$$Less affected by CYP2C19 polymorphisms
Dexlansoprazole (Dexilant)30-60mg dailyNone absoluteSame$$$ (brand)Dual delayed-release; can take without regard to meals

PPI prescribing pearls:

  • Take 30-60 minutes before first meal (maximizes efficacy by blocking actively secreting proton pumps)
  • Once-daily dosing sufficient for most patients
  • BID dosing for severe erosive disease, nocturnal symptoms, or partial response to once-daily
  • All PPIs similarly effective at equivalent doses; choose based on cost and interactions
  • If one PPI fails, can try another (some patients respond differently due to CYP2C19 polymorphisms)
  • Generic omeprazole or pantoprazole is appropriate first-line for most patients

Drug interactions:

  • Omeprazole/esomeprazole: may reduce clopidogrel efficacy (CYP2C19 inhibition)—use pantoprazole if on clopidogrel
  • All PPIs: may reduce absorption of drugs requiring acid (ketoconazole, itraconazole, iron, B12)
  • All PPIs: may increase methotrexate levels (reduce renal clearance)

H2 receptor antagonists (H2RAs) - Second-line or adjunct:

DrugDoseContraindicationsMonitoringCostNotes
Famotidine (Pepcid)20mg BID or 40mg QHSCKD: reduce dose if eGFR <50None$ (generic, OTC)Less potent than PPI; good for step-down, breakthrough, or nocturnal symptoms
Nizatidine150mg BID or 300mg QHSCKD: reduce doseNone$Alternative H2RA

H2RA role:

  • Step-down from PPI for mild symptoms
  • Add-on for nocturnal breakthrough (H2RA at bedtime + PPI in morning)
  • Patients who cannot tolerate PPIs
  • On-demand use for intermittent symptoms
  • Note: tachyphylaxis develops with continuous use (less effective over time)

Antacids and alginates:

DrugDoseContraindicationsMonitoringCostNotes
Calcium carbonate (Tums)500-1000mg PRNHypercalcite; CKD (calcium load)None$ (OTC)Immediate relief; not for maintenance
Gaviscon (alginate)10-20mL after meals and QHSNone significantNone$ (OTC)Forms raft on gastric contents; may help postprandial symptoms

Prokinetics (limited role):

  • Metoclopramide: limited efficacy for GERD; significant side effects (tardive dyskinesia); avoid
  • Not recommended as routine GERD therapy

Patient counseling points#

For PPI initiation:

  • “Take this pill 30-60 minutes before breakfast on an empty stomach. This timing is important—the medicine works best when your stomach is about to make acid for your first meal.”
  • “It may take a few days to a week to feel the full effect. Don’t expect instant relief like an antacid.”
  • “This is not a cure—it reduces acid production but doesn’t fix the underlying valve problem. That’s why lifestyle changes matter too.”

For lifestyle modifications:

  • “Losing even 10 pounds can make a noticeable difference in your symptoms.”
  • “Don’t eat within 2-3 hours of bedtime. Your stomach needs time to empty before you lie down.”
  • “Raise the head of your bed 6-8 inches with blocks or a wedge. Extra pillows don’t work—they just bend you at the waist.”
  • “Pay attention to what triggers your symptoms. Common culprits are fatty foods, chocolate, coffee, alcohol, and citrus.”

For step-down therapy:

  • “Now that your symptoms are controlled, let’s try reducing your dose. Many people can manage with a lower dose or take the medicine only when needed.”
  • “If symptoms come back, go back to the dose that worked. We can always adjust.”

For long-term PPI use:

  • “You’ve heard about risks of long-term PPI use. The risks are real but small. For most people with ongoing reflux, the benefits outweigh the risks.”
  • “We’ll monitor your magnesium and B12 levels periodically.”
  • “Let’s make sure you still need this medication—we should try to use the lowest dose that controls your symptoms.”

For refractory symptoms:

  • “If the medicine isn’t working well, we should look further. Sometimes what seems like reflux is actually something else.”
  • “An endoscopy can help us see what’s happening and make sure we’re treating the right problem.”

Monitoring and follow-up#

Initial treatment phase:

  • Follow-up at 4-8 weeks to assess response
  • If symptoms resolved: attempt step-down (see below)
  • If symptoms persist: optimize PPI (timing, dose, adherence) before escalating

Step-down strategy (after 4-8 weeks of symptom control):

  1. Reduce PPI to lowest effective dose (e.g., omeprazole 20mg → 10mg, or daily → every other day)
  2. If stable, try switching to H2RA (famotidine 20mg BID)
  3. If stable, try on-demand therapy (PPI or H2RA PRN for symptoms)
  4. If symptoms recur at any step, return to previous effective regimen

Maintenance therapy indications (continuous PPI):

  • Erosive esophagitis LA grade C or D (high recurrence without maintenance)
  • Barrett’s esophagus (indefinite PPI regardless of symptoms)
  • Stricture history
  • Frequent symptom recurrence when attempting step-down
  • Severe symptoms significantly impacting quality of life

Long-term PPI monitoring:

  • Magnesium: check annually if on PPI >1 year (hypomagnesemia risk)
  • B12: consider checking every 2-3 years if on PPI >3 years (especially elderly)
  • Bone density: no routine screening for PPI use alone; follow standard osteoporosis guidelines
  • No routine monitoring of kidney function, C. diff, or pneumonia (be aware of risks but no specific monitoring)

Long-term PPI risks (counsel patients, but benefits usually outweigh risks):

RiskMagnitudeClinical Significance
C. difficile infectionOR 1.5-2.0Clinically relevant; counsel on symptoms
Community-acquired pneumoniaOR 1.3-1.5Small absolute risk increase
Hip fractureOR 1.2-1.4Modest risk; ensure adequate calcium/vitamin D
Hypomagnesemia~1% with long-term useMonitor annually; can cause arrhythmia, seizures
B12 deficiencyOR 1.6-2.0Check periodically in long-term users
CKD progressionControversial; OR ~1.2Observational data only; causation unclear
DementiaNo proven associationEarly studies not confirmed; likely confounding
Gastric cancerNo proven associationConfounded by indication (GERD itself is risk factor)

Patient education#

What is this condition?#

GERD stands for gastroesophageal reflux disease. It happens when acid from your stomach flows back up into your food pipe (esophagus). This causes the burning feeling in your chest called heartburn.

Your stomach makes acid to help digest food. Normally, a ring of muscle at the bottom of your food pipe acts like a one-way valve—it lets food go down but keeps acid from coming back up. In GERD, this valve does not work properly. Acid leaks up into your food pipe, which is not built to handle acid like your stomach is.

GERD is very common. About 1 in 5 adults has symptoms at least once a week. It is not dangerous for most people, but if left untreated for many years, it can cause changes to the lining of your food pipe.

What you can do#

Lose weight if you are overweight. This is the most effective thing you can do. Even losing 10 pounds can help.

Do not eat within 2-3 hours of bedtime. Your stomach needs time to empty before you lie down.

Raise the head of your bed 6-8 inches. Put blocks under the bedposts at the head of your bed, or use a wedge pillow. Extra pillows alone do not work well.

Avoid foods that trigger your symptoms. Common triggers include fatty or fried foods, chocolate, coffee, alcohol, mint, citrus fruits, and tomatoes. Everyone is different—pay attention to what bothers you.

Take your medicine correctly. If you take a PPI (like omeprazole), take it 30-60 minutes before your first meal of the day on an empty stomach.

Do not smoke. Smoking makes reflux worse.

Wear loose-fitting clothes. Tight belts and waistbands put pressure on your stomach.

When to seek care#

Call your doctor if:

  • Your symptoms do not improve after 4-8 weeks of treatment
  • You need to take medicine every day for more than a few months
  • Your symptoms come back as soon as you stop medicine
  • You have new symptoms like trouble swallowing or food getting stuck

See a doctor right away if you have:

  • Trouble swallowing or pain when swallowing
  • Unintended weight loss
  • Vomiting blood or material that looks like coffee grounds
  • Black, tarry stools
  • Severe chest pain (go to the emergency room to rule out heart problems)

Questions to ask your doctor#

  • Do I need any tests, or can we try medicine first?
  • How long should I take this medicine?
  • Can I try a lower dose or stop the medicine once I feel better?
  • Are there risks to taking this medicine long-term?
  • Should I see a specialist?
  • Could my symptoms be caused by something other than reflux?
  • What lifestyle changes will help the most?

Prognosis and monitoring#

Expected course#

With treatment:

  • 80-90% of patients achieve symptom control with PPI therapy
  • Erosive esophagitis heals in >90% (LA grade A/B) to 80-90% (LA grade C/D) at 8 weeks
  • Many patients can step down to lower doses or on-demand therapy
  • Some patients require long-term maintenance therapy

Without treatment:

  • Symptoms typically persist or worsen
  • Erosive esophagitis may progress to stricture (1-5%)
  • Barrett’s esophagus develops in 5-15% of chronic GERD
  • Quality of life significantly impacted

Natural history:

  • GERD is typically a chronic, relapsing condition
  • Symptoms may wax and wane with weight changes, diet, stress
  • Spontaneous resolution is uncommon in established disease
  • Progression to Barrett’s or adenocarcinoma is uncommon but possible

Monitoring parameters#

ParameterFrequencyTarget/Action
Symptom assessmentEach visitComplete symptom control; quality of life
PPI dose optimization4-8 weeks after initiationStep-down to lowest effective dose
Magnesium levelAnnually if on PPI >1 year>1.8 mg/dL; supplement if low
B12 levelEvery 2-3 years if on PPI >3 years>300 pg/mL; supplement if low
EGD (if Barrett’s)Per surveillance protocolDysplasia assessment
WeightEach visitEncourage weight loss if overweight

Complications to watch for#

Erosive esophagitis:

  • Mucosal damage from chronic acid exposure
  • Symptoms: worsening heartburn, odynophagia
  • Management: longer PPI course (8 weeks); maintenance therapy for severe grades

Esophageal stricture:

  • Scarring from chronic inflammation; causes dysphagia
  • Symptoms: progressive difficulty swallowing solids, then liquids
  • Management: EGD with dilation; long-term PPI; may need repeat dilations

Barrett’s esophagus:

  • Intestinal metaplasia of esophageal epithelium; premalignant
  • Risk: 0.5% annual progression to adenocarcinoma (without dysplasia)
  • Management: indefinite PPI; surveillance EGD (see below)
  • Dysplasia: low-grade (EGD every 6-12 months or ablation); high-grade (ablation or resection)

Esophageal adenocarcinoma:

  • Rare but serious; arises from Barrett’s esophagus
  • Risk factors: long-standing GERD, Barrett’s, obesity, male sex, smoking
  • Symptoms: progressive dysphagia, weight loss, anemia
  • Management: oncology referral; staging; surgery/chemo/radiation per stage

Barrett’s esophagus surveillance (GI manages; PCP awareness):

Dysplasia StatusSurveillance IntervalNotes
No dysplasiaEGD every 3-5 yearsIndefinite PPI; lifestyle modifications
Low-grade dysplasiaEGD every 6-12 months OR ablationDiscuss ablation vs surveillance with GI
High-grade dysplasiaAblation or endoscopic resectionRefer to specialized center

PCP role in Barrett’s:

  • Continue indefinite PPI therapy (regardless of symptoms)
  • Ensure patient follows up with GI for surveillance
  • Reinforce lifestyle modifications (weight loss especially)
  • Monitor for alarm symptoms (dysphagia, weight loss)

Special populations#

Elderly/geriatric#

Presentation differences:

  • May have less typical symptoms (less heartburn, more regurgitation, dysphagia)
  • Higher prevalence of complications (erosive disease, Barrett’s, stricture)
  • More likely to have hiatal hernia
  • Atypical symptoms (cough, hoarseness) may be more prominent

Treatment considerations:

  • PPIs are generally safe in elderly; no specific dose adjustment needed
  • Be aware of drug interactions (polypharmacy common)
  • Hypomagnesemia risk may be higher; monitor annually
  • B12 deficiency risk higher; check periodically
  • Hip fracture risk: ensure adequate calcium and vitamin D; fall prevention

Beers criteria considerations:

  • PPIs are NOT on Beers list as drugs to avoid
  • However, Beers recommends avoiding PPI use >8 weeks without clear indication
  • For elderly with documented GERD, erosive disease, or Barrett’s: long-term PPI is appropriate
  • Attempt step-down when possible; avoid indefinite PPI without reassessment

Polypharmacy:

  • Review for drugs that worsen GERD: calcium channel blockers, nitrates, anticholinergics, bisphosphonates, NSAIDs
  • Check for interactions: clopidogrel (use pantoprazole), methotrexate, ketoconazole

Chronic kidney disease#

Dosing:

  • PPIs: no dose adjustment required; not renally cleared
  • H2RAs: reduce dose if eGFR <50 (famotidine 20mg daily instead of BID)

Monitoring:

  • Standard PPI monitoring applies
  • Be aware of observational data suggesting PPI-CKD association (causation unclear)
  • Hypomagnesemia may be more common in CKD; monitor

Drug interactions:

  • Phosphate binders may reduce PPI absorption; separate by 2 hours
  • Avoid magnesium-containing antacids in advanced CKD

Special considerations:

  • CKD patients often on multiple medications that worsen GERD (calcium, iron, phosphate binders)
  • Optimize timing to minimize interactions
  • H. pylori testing and treatment same as general population

Other populations#

Pregnancy:

  • GERD very common in pregnancy (30-80%); due to progesterone effect on LES and increased intra-abdominal pressure
  • First-line: lifestyle modifications, antacids, sucralfate
  • H2RAs (famotidine): considered safe; category B
  • PPIs: generally considered safe; omeprazole and pantoprazole most data; use if H2RA inadequate
  • Avoid: sodium bicarbonate (sodium load), magnesium trisilicate (fetal toxicity)
  • Symptoms typically resolve postpartum

Obesity:

  • Major risk factor for GERD; weight loss is most effective intervention
  • Higher rates of erosive disease, Barrett’s, and adenocarcinoma
  • May need higher PPI doses
  • Bariatric surgery (especially gastric bypass) can improve or cure GERD
  • Sleeve gastrectomy may worsen GERD in some patients

Scleroderma/connective tissue disease:

  • Severe GERD due to esophageal dysmotility and LES dysfunction
  • Often requires high-dose PPI (BID dosing)
  • Higher complication rates
  • GI co-management recommended

Asthma:

  • GERD can trigger or worsen asthma
  • Consider GERD in poorly controlled asthma, especially with nocturnal symptoms
  • PPI trial reasonable if GERD symptoms present
  • Empiric PPI for asthma without GERD symptoms: not recommended (trials show no benefit)

Drug-induced GERD:

  • Medications that worsen GERD: NSAIDs, bisphosphonates, calcium channel blockers, nitrates, anticholinergics, potassium supplements, iron, tetracyclines
  • Review medication list; modify if possible
  • Bisphosphonates: take correctly (upright 30 min, full glass of water); consider IV if intolerant

When to refer#

Specialist referral criteria#

GI referral:

  • Alarm features (dysphagia, weight loss, GI bleeding, anemia, vomiting)
  • Age >60 with new-onset symptoms
  • Refractory symptoms despite 8 weeks of optimized PPI (correct timing, adherence, dose)
  • Recurrent symptoms requiring continuous PPI (to assess for Barrett’s, erosive disease)
  • Atypical symptoms (chronic cough, hoarseness) not responding to PPI trial
  • Known Barrett’s esophagus (for surveillance)
  • Consideration for anti-reflux surgery
  • Need for pH monitoring or manometry

Surgical referral (after GI evaluation):

  • Confirmed GERD with objective evidence (EGD or pH study) who prefer surgery over long-term medication
  • Refractory symptoms despite optimized medical therapy with objective reflux evidence
  • Large symptomatic hiatal hernia
  • Volume regurgitation not controlled by PPI
  • Medication intolerance

ENT referral:

  • Laryngeal symptoms (hoarseness, globus) not responding to PPI trial
  • Suspected laryngopharyngeal reflux (LPR) for laryngoscopy

Urgency levels#

ScenarioUrgencyAction
Typical GERD, no alarm featuresRoutineEmpiric PPI trial; f/u 4-8 weeks
Alarm features presentUrgent (1-2 weeks)GI referral for EGD
Refractory to 8 weeks PPIRoutine (2-4 weeks)GI referral for EGD
Known Barrett’s, due for surveillanceRoutineEnsure GI follow-up scheduled
Complete dysphagia (can’t swallow saliva)EmergentED evaluation
GI bleeding with hemodynamic instabilityEmergentED evaluation
Severe chest painEmergentED to rule out cardiac cause first

Smartphrase snippets#

GERD, stable on PPI: GERD on omeprazole [X] mg daily with good symptom control, no alarm features. Continue current regimen; will attempt step-down at next visit. F/u 6-12 months.

GERD, attempting step-down: GERD previously controlled on PPI, attempting step-down to [lower dose/H2RA/PRN]. If symptoms recur, return to previous effective dose. F/u 4-8 weeks.

GERD, refractory to PPI: GERD with persistent symptoms despite omeprazole [X] mg daily x [X] weeks with proper timing and adherence. GI referral for EGD to evaluate for erosive disease or Barrett’s. Continue PPI pending evaluation.

GERD with Barrett’s esophagus: Barrett’s esophagus (no dysplasia per last EGD [date]) on indefinite omeprazole [X] mg daily. No alarm features. Continue surveillance per GI (EGD every 3-5 years); next due [date].