Episode 174: GERD in Adults

Common and atypical symptoms are presented. Pathophysiology, diagnosis, and management are discussed. H. pylori's role is discussed during this episode.

Written by Jacquelyn Garcia MS4 Ross University School of Medicine. Comments by Hector Arreaza, MD.

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Definitions:

Gastroesophageal reflux (GER): occasional backflow of stomach acid into the esophagus. It's a common physiological process that happens to many people, especially after meals. Occurs less than twice a week. Associated with mild and temporary symptoms such as heartburn or regurgitation.

Gastroesophageal reflux disease (GERD): a chronic and more severe form of GER. It occurs when acid reflux happens frequently, typically more than twice a week, and/or causes esophageal injury/complications.

-Non-erosive reflux disease (NERD)= GER without evidence of esophageal injury on endoscopy.

-Erosive reflux disease (ERD)= GER with evidence of esophageal injury on endoscopy.

AFP Journal, January 2024: “Nonerosive GERD does not increase the likelihood of esophageal cancer. However, erosive GERD is associated with a doubled, but still low, risk of developing cancer, with the likelihood increasing over time.”

Pathophysiology:

The main pathophysiology behind GERD is lower esophageal sphincter (LES) dysfunction which can occur due to the following:

-LES Pressure: The LES is a muscular ring at the junction of the esophagus and stomach. It normally maintains a high-pressure zone to prevent reflux. In GERD, the intragastric pressure is higher than the pressure created by the LES. The tone of the LES can be reduced by caffeine, nitroglycerin, and scleroderma.

-Transient LES Relaxations (TLESRs): These are normal relaxations of the LES that occur independently of swallowing. In GERD, these relaxations are more frequent or prolonged, allowing acid to reflux into the esophagus.

-Anatomic abnormalities: A hiatal hernia occurs when a portion of the stomach protrudes through the diaphragm into the chest cavity. This disrupts the normal anatomy of the gastroesophageal junction, reducing the pressure barrier and promoting reflux.

Epidemiology:

It affects 10-20% of adults in Western cultures and less than 5% in Asia. Prevalence in the US ranges from 18.1% to 27.8% with a slightly higher rate in men.

Risk factors:

-Obesity, pregnancy, scleroderma, hiatal hernia; smoking, caffeine, alcohol, stress, fatty/fried/spicy foods. Spicy foods can be a challenge in some cultures (e.g. Mexican and Indian.) Sometimes, patients may ask for “something” to stop GERD but all they may need is dietary modification.

-Medications:

-aspirin, ibuprofen, clindamycin, tetracycline, bisphosphonates (irritate the esophagus and cause heartburn pain similar to GERD)

-anticholinergics, TCA’s, CCB’s, ACEi, statins, benzodiazepines, theophylline, opioids, progesterone (increase acid reflux and worsen GERD)

Clinical features:

Typical symptoms:

-heartburn (burning retrosternal pain)

-regurgitation (acidic stomach contents)

Atypical symptoms:

-chest pain (can mimic angina pectoris, squeezing/burning substernal, radiates to back/neck/jaw/arm)

-water brash (hypersalivation)

-globus sensation (lump in throat)

-nausea

-belching

-bloating

Alarm features in GERD:

-dysphagia

-odynophagia (pain with swallowing)

-new onset of dyspepsia in ≥60yo

-weight loss

-GI bleeding

-vomiting

-anemia

Diagnosis:

-There is no gold standard test

-Patient with typical symptoms: diagnosis can be based on clinical symptoms alone

-Patient with atypical symptoms: these symptoms can be seen in GERD but are not sufficient for diagnosis of GERD in the absence of typical symptoms. Need to rule out other disorders before associating the symptoms with GERD. (ex: chest pain r/o other causes such as MI with ECG)

-Patient with alarm features: refer to GI for upper GI endoscopy.

Complications:

-Esophagitis: Erosive reflux disease (ERD) = GER with evidence of esophageal distal injury on endoscopy; in untreated GERD 30% have esophagitis.

-Iron deficiency anemia: due to mucosal ulcerations -> chronic bleeding.

-Esophageal stricture: narrowing near GE junction, solid food dysphagia.

-Barrett Esophagus: intestinal metaplasia of esophagus due to chronic GERD (stratified squamous epithelium replaced by columnar epithelium)

-Risk factors: GERD for 5-10 years, >50yo, males, obesity, Caucasian, Tobacco use, family history

-Predisposes to esophageal adenocarcinoma

Role of H. pylori.

Sometimes we tend to think that H. pylori is the cause of GERD. “H. pylori infection appears to protect the esophagus from gastroesophageal reflux disease, Barrett's esophagus, dysplasia in Barrett's esophagus, and esophageal adenocarcinoma, perhaps by causing chronic gastritis that interferes with acid production.”

It is unclear whether long-term use of PPIs heightens the risk of atrophic gastritis in patients with H. pylori. Consequently, routine screening for H. pylori infection and empiric eradication of H. pylori are NOT advised for patients with GERD. However, if H. pylori is diagnosed in the setting of GERD, eradication of H. pylori has been associated with an improvement of symptoms in patients with antral-predominant gastritis.

Treatment:

Two categories:

Mild/intermittent symptoms (<2 times per week)

“Step up approach”

1. Lifestyle modifications (weight loss, elevation of head of bed if have nighttime symptoms, diet modification/elimination of triggers) and low dose histamine 2 receptor antagonists or H2RA (famotidine, nizatidine, cimetidine) PRN for 4 weeks; antacids if symptoms <1/week

2. Symptoms persistà standard dose H2RA BID for 2 weeks

3. Symptoms persistà low dose PPI (omeprazole, pantoprazole, esomeprazole) qd for 4-8 weeks

4. Symptoms persistà standard dose PPI qd for 4-8 weeks

5. Symptoms persistà refractory GERD tx

Arreaza: What if the symptoms improve?

-Symptoms improved on PPIà taper and discontinue PPI if asymptomatic for 8 weeks (do not do if have erosive esophagitis or Barrett’s)

-Symptoms improved on H2RA à continue as PRN + lifestyle modifications

Arreaza: What if symptoms come back?

-Recurrent symptoms ≥3months of discontinuing meds: resume previous therapy for 8 weeks

-Recurrent symptoms within 3 months of discontinuing meds: upper GI endoscopy and long-term maintenance therapy

Jacquelyn:

Severe/frequent symptoms (≥2 times per week), ERD, Barrett’s esophagus

“Step down approach”

1. Lifestyle modifications AND standard dose PPI qd for 4-8 weeks.

2. Symptoms persistà refractory GERD tx

Refractory GERD tx:

1. Discuss with pt med compliance and usage

2. Symptoms persistà different PPI for 8 weeks or PPI BID for 8 weeks

3. Symptoms persistà upper GI endoscopy

Alarm features: upper GI endoscopy.

The Choosing Wisely campaign recommends that you discuss stopping PPI every year with your patient because PPIs are not free of harms.

PPI adverse effects: associated with increased risk of C. diff according to FDA safety announcement in 2012. Even without recent antibiotic use. So, patients may have to switch to another alternative due to this adverse effect of PPIs.

-others: GI upset (nausea, diarrhea, and abdominal pain), decreased iron, B12, calcium, and magnesium absorption (FDA 2010 advises possible increased risk of fractures in elderly).

PPIs were a breakthrough medication in 1989, before that time, people got surgery for gastritis, but over time PPIs became popular, but they can be a double-edged sword, it is excellent for symptom control at the expense of potential short- and long-term side effects.

-Other treatment options if there is no improvement with medical management, if a large hiatal hernia is present, or if complications occur despite medical therapy, surgical treatment is recommended.

Conclusion: GERD is very common in our clinics/hospitals. It is important to recognize classic symptoms and differentiate symptoms from mild to severe. We need to start treatment and refer to GI promptly. Primary care is in a special position in evaluating these patients so we can avoid them developing potential complications like cancer.

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References:

El-Serag HB, Sweet S, Winchester CC, Dent J. Update on the epidemiology of gastroesophageal ref...