Last updated date: 09-Feb-2023
Medically Reviewed By
Medically reviewed by
Dr. Lavrinenko Oleg
Originally Written in English
Gastroesophageal reflux disease (GERD)
The most frequent gastrointestinal diagnosis documented during outpatient clinic visits is gastroesophageal reflux disease. It is believed that 14 to 20% of people in the United States are afflicted, however such figures are only estimations given the disease's vague description and that such estimates are based on the prevalence of self-reported chronic heartburn.
What is GERD?
GERD is a disorder characterized by troubling symptoms and problems caused by the reflux of stomach contents into the esophagus.
The illness is now defined as "a condition that arises when the reflux of stomach contents generates bothersome symptoms (i.e., at least two bouts of heartburn per week) and/or problems." Several extraesophageal symptoms of the illness, such as laryngitis and cough, are widely known.
Based on the presence or absence of esophageal mucosal damage visible on endoscopy, GERD is categorized as non-erosive reflux disease (NERD) or erosive reflux disease (ERD).
Understanding the etiology of reflux requires a thorough understanding of the anatomy of the esophagus, stomach, and esophagogastric junction.
There are 3 parts of the esophagus: cervical, thoracic, and abdominal. The esophagus's body is composed of inner circular and outer longitudinal muscular layers. The esophagus is made up of striated muscle in the proximal third and smooth muscle in the distal two thirds. The upper esophageal sphincter (UES), which is made up of the cricopharyngeus and thyropharyngeus muscles, is located in the proximal esophagus.
The distal thoracic esophagus is placed on the midline's left side. The thoracic esophagus becomes the abdominal esophagus as it reaches the abdomen through the diaphragm's esophageal hiatus. The diaphragm's right crus forms a sling around the esophagus with the right and left pillars, causing the esophagus to narrow as the diaphragm contracts.
The exact role of the diaphragm in maintaining a sufficient length of intra-abdominal esophagus is unknown; nevertheless, careful identification and approximation of the pillars during surgical therapy is critical for preventing reflux disease recurrence.
GERD Risk factors
Older age, a high body mass index (BMI), smoking, anxiety/depression, and a lack of physical exercise at work are all risk factors for GERD. 6–8 Eating habits, such as the acidity of food, as well as the amount and timing of meals, particularly with regard to sleep, may potentially contribute to GERD. Except when conducted post-prandially, recreational physical exercise appears to be protective.
Gastroesophageal reflux is essentially a dysfunction of the lower esophageal sphincter (LES), however it can be caused by a number of causes. GERD is influenced by both physiologic and pathologic variables. Transient lower esophageal sphincter relaxations(TLESRs) are the most prevalent cause.
TLESRs are short intervals of lower esophageal sphincter tone inhibition that occur independently of swallowing. While they are physiologic in nature, there is a rise in frequency in the postprandial period, and they play a significant role in acid reflux in GERD patients. Other risk factors include low LES pressure, hiatal hernias, poor esophageal clearance, and delayed stomach emptying.
The issue of hiatal hernia must be addressed while examining the mechanics of GERD. Hiatal hernias are common in individuals with reflux illness; nevertheless, it has been well established that not all patients with hiatal hernias have symptomatic reflux.
The lower esophageal sphincter may migrate proximally towards the chest, losing its abdominal high-pressure zone (HPZ), or its length may shorten. A big hernia may enlarge the diaphragmatic hiatus, impairing the crura's capacity to serve as an external sphincter.
Finally, during LES relaxation, stomach contents may become trapped in the hernial sac and reflux proximally into the esophagus. Reducing hernias and closing the crural opening are important to restoring an appropriate intra-abdominal length of the esophagus and reconstructing the HPZ.
Heartburn is the classic and most frequent symptom of GERD. Heartburn is characterized by a burning feeling in the chest that radiates to the mouth as a result of acid reflux into the esophagus. However, only a tiny proportion of reflux episodes are symptomatic. Heartburn is frequently coupled with a sour taste in the back of the mouth, with or without refluxate regurgitation.
GERD, in particular, is a prevalent cause of non-cardiac chest discomfort. Because of the potentially catastrophic consequences of cardiac chest pain and the various diagnostic and therapeutic algorithms based on etiology, it is critical to distinguish between the underlying cause of the chest pain. In individuals with non-cardiac chest discomfort, a good clinical history may trigger GERD symptoms, pointing to GERD as a possible cause.
Although typical GERD symptoms are easily identified, extraesophageal GERD manifestations are very frequent but not often detected. Extraesophageal symptoms are more common as a result of reflux into the larynx, which causes throat clearing and hoarseness. Patients with GERD frequently complain of a sense of fullness or a lump in the back of their throat, known as globus sensation.
The origin of globus is unknown, however it is hypothesized that acid exposure of the hypopharynx causes greater tonicity of the upper esophageal sphincter (UES). Furthermore, acid reflux can cause bronchospasm, which can aggravate underlying asthma, resulting in coughing, dyspnea, and wheezing. Chronic nausea and vomiting may occur in certain GERD patients.
It is critical to evaluate patients for GERD-related warning symptoms, since they should prompt endoscopic examination. Alarm symptoms may indicate an underlying cancer. In the presence of typical GERD symptoms, an upper endoscopy is not necessary.
Endoscopy, on the other hand, is indicated in the presence of alarm symptoms and for screening of individuals at high risk for problems (i.e. Barrett's esophagus, particularly those with chronic and/or recurrent symptoms, age > 50 years, Caucasian race, and central obesity).
Dysphagia (difficulty swallowing) and odynophagia (painful swallowing) are alarm signs that may indicate the existence of problems such as strictures, ulceration, and/or cancer. Anemia, bleeding, and weight loss are just a few of the other warning signs and symptoms.
GERD symptoms should be distinguished from dyspepsia. Dyspepsia is characterized as epigastric pain that lasts more than a month and is not caused by heartburn or acid regurgitation. Bloating/epigastric fullness, belching, nausea, and vomiting are all possible symptoms. Dyspepsia is treated differently from GERD and may necessitate endoscopic examination as well as H. pylori tests.
Esophagitis occurs when excessive acid and pepsin reflux causes necrosis of the surface layers of the esophagus mucosa, resulting in erosions and ulcers. In many individuals, impaired clearance of refluxed gastric fluid from the esophagus also leads to injury.
While some gastroesophageal reflux is normal (and is related to the ability to belch), several factors, including hiatus hernia, lower esophageal sphincter hypotension, loss of esophageal peristaltic function, abdominal obesity, increased compliance of the hiatal canal, gastric hypersecretory states, delayed gastric emptying, and overeating, may predispose patients to pathologic reflux. Multiple risk factors are frequently present.
The clinical manifestations of GERD in pregnant women are comparable to those seen in the general population. The primary symptoms are heartburn and regurgitation. A comprehensive history and physical examination are part of the diagnostic evaluation.
GERD in Pregnancy
GERD symptoms are prevalent during pregnancy. However, problems such as esophageal irritation are quite rare (esophagitis). Symptoms of heartburn usually improve once the baby is born. Treatment for pregnant women with GERD is similar to treatment for other persons with GERD.
GERD is often diagnosed clinically based on the presence of characteristic symptoms and a response to acid suppression. Heartburn with or without regurgitation is usually enough to rule out GERD, especially if the symptoms worsen postprandially or when lying down.
Treatment with (H2) receptor blockers or proton pump inhibitors (PPIs) with subsequent symptom relief is deemed diagnostic. In the absence of warning characteristics or symptoms, no additional workup is necessary in individuals who respond to empiric therapy.
Reflux symptoms may remain in some individuals after therapy with high-dose PPIs. Additional testing may be required to rule out other reasons of their symptoms and to check for GERD complications. It should be noted that the intensity of reflux symptoms does not always correlate with the degree of mucosal damage.
Upper gastrointestinal endoscopy, also known as esophagogastroduodenoscopy, is the most often used diagnostic procedure for GERD and its potential consequences (EGD). Endoscopy has the major advantage of allowing direct sight of the esophagus mucosa. This aids in the identification of GERD problems such as esophagitis, strictures, and Barrett's esophagus.
Many of these options are addressed via endoscopy, with the proviso that screening for a potential cardiac etiology of the presenting symptoms should always be emphasized. In addition, the endoscopist should have a low threshold for collecting specimens from esophageal or gastric biopsy in order to detect alternative diagnoses such as eosinophilic esophagitis and Helicobacter pylori gastritis.
The barium esophagram, while useful in assessing individuals with dysphagia, is a poor screening test for GERD. When compared to endoscopy, it has a relatively low sensitivity (26%) and specificity (50%) for mild esophagitis. In symptomatic patients, barium reflux does not always correspond well with acid reflux, and it can be positive in up to 20% of instances in healthy people.
Coughing, valsalva, and rolling from supine to the right lateral position can all help to increase sensitivity. Fluoroscopic barium testing detects more severe esophagitis, peptic strictures, and hiatal hernias.
Even for this use, however, it has a very low sensitivity and specificity for detecting acid reflux when compared to ambulatory pH monitoring. As a result of its limited usefulness, it is not recommended for regular GERD diagnosis.
GERD, if left untreated, can lead to a number of severe problems, including esophagitis and Barrett's esophagus. The severity of esophagitis can vary greatly, with severe instances resulting in significant erosions, ulcerations, and constriction of the esophagus. Esophagitis can also cause bleeding in the gastrointestinal tract (GI).
Upper GI bleeding can manifest as anemia, hematemesis, coffee-ground emesis, melena, and, in severe cases, hematochezia. Chronic esophageal inflammation caused by acid exposure can result in scarring and the formation of peptic strictures, which generally present with the primary symptom of dysphagia.
Patients who have recurrent acid reflux may be at risk for Barrett's esophagus, which is described as esophageal intestinal metaplasia. As a result of acid exposure, the normal squamous cell epithelium of the esophagus is replaced by columnar epithelium containing goblet cells in Barrett's esophagus.
Barrett's esophagus changes can spread proximally from the gastroesophageal junction (GEJ) and proceed to esophageal adenocarcinoma, making early identification critical in the prevention and therapy of malignant transformation.
Patients with GERD should be evaluated for alarm signs, which should require an immediate endoscopic examination. If no warning signs are present, the first therapy of GERD should focus on lifestyle changes. It is crucial to remember, however, that the bulk of research on lifestyle and nutritional modifications in GERD have been underpowered. Nonetheless, lifestyle modifications continue to be the first-line treatment for GERD, with the primary objective being symptom reduction and quality of life enhancement.
Many lifestyle changes are suggested as treatment for gastroesophageal reflux disease. These include avoiding meals that lower lower esophageal sphincter pressure and hence predispose to reflux, minimizing exposure to acidic foods that are naturally unpleasant, and adopting habits to lessen reflux or heartburn. Although clinical studies of the clinical effectiveness of dietary or behavioral modifications are lacking,20 clinical experience shows that certain interventions may assist specific individuals.
Patients suffering from nocturnal heartburn, for example, may benefit from elevating the head of the bed, but this suggestion is generally unnecessary for a patient who does not suffer from overnight symptoms. Given the significant link between an increased BMI and the risk of symptoms, weight loss should be frequently suggested in overweight individuals.
Head of bed (HOB) elevation is the only validated lifestyle change for the treatment of GERD. In individuals with supine GERD, head of bed elevation has been found to reduce esophageal acid exposure and esophageal clearance time, resulting in a reduction in symptoms.
Furthermore, it is recommended that variables that contribute to the occurrence of TLESRs be limited or avoided. Smoking, excessive alcohol consumption, big evening meals, late-night munchies, and a high dietary fat intake are all examples.
Weight loss is strongly advised in GERD patients who are overweight, but there is little evidence of benefit in those who are normal weight. Despite the fact that obesity is a risk factor for GERD, most bariatric procedures aggravate reflux. Furthermore, because of their function in altering physiologic mucosal protection systems, all patients with GERD should avoid nonsteroidal anti-inflammatory medications (NSAIDs).
Medication therapy for GERD is aimed at reducing symptoms and limiting mucosal damage caused by acid reflux. With the exception of Zollinger-Ellison syndrome, there does not appear to be a strong link between GERD severity and high stomach acid levels, despite the fact that acid suppression is effective in the treatment of GERD.
Before seeking medical treatment, many individuals with heartburn attempt over-the-counter antacids. H2 blockers and proton pump inhibitors are the most often used acid suppression medicines. By blocking histamine activation of the parietal cell, H2 blockers reduce stomach acid production.
Proton pump inhibitors operate by reducing the quantity of acid released into the stomach lumen by parietal cells. H2 blockers have been found to provide modest clinical improvement above placebo, although PPIs are the most effective treatment in those who do not have a contraindication. Prokinetic drugs, such as metoclopramide, have no apparent role in the therapy of GERD.
The most powerful class of antacid medicines is proton pump inhibitors. They are used once or twice day and work best if taken 30 to 60 minutes before meals. Many individuals will experience a recurrence of symptoms after discontinuing PPI, necessitating lifetime treatment.
PPIs have recently been linked to the development of bone fractures, electrolyte deficits, infections (e.g., Clostridium difficile, pneumonia), and renal insufficiency. Given the theoretical risk of adverse effects from PPI medication, the lowest dose necessary for maintenance should be utilized, and weaning trials should be undertaken on a regular basis.
There is some evidence that adding a nocturnal H2 blocker to GERD patients who are resistant to twice daily PPI dosage can be helpful.
Proton-pump inhibitors' most common adverse effects include headache, diarrhea, constipation, and stomach discomfort. Long-term usage of proton-pump inhibitors may result in secondary hypergastrinemia, malabsorption, and hypochlorhydria.
Avoid or eat them in moderate amounts:
- Onion rings and French fries
- full-fat dairy items including butter, whole milk, normal cheese, and sour cream
- fatty or fried beef, pig, or lamb chops
- Lard, bacon fat, and ham fat
- Ice cream and potato chips are examples of desserts or snacks.
Surgery, most frequently Nissen fundoplication, in which the proximal stomach is wrapped around the distal esophagus to establish an antireflux barrier, is an alternate treatment option for persistent gastroesophageal reflux disease.
The use of anti-reflux surgery (fundoplication) has been a source of contention. Studies suggest that surgery has very little long-term clinical benefits over PPI treatment, with a higher incidence of dysphagia and dyspepsia.
Patients who respond well to surgery are often those who respond well to PPIs and can thus be treated medically. PPI-refractory individuals, on the other hand, are unlikely to benefit from surgery.
Approximately half of all patients who undergo surgery require surgical revision at some point. Given the near-negligible effectiveness difference between surgery and PPI, as well as the risk of surgical complications and death, surgery should be reserved for a small group of patients. Selecting the best patients for anti-reflux surgery is still a clinical concern.
Most GERD patients respond well to medicines, however relapses after discontinuing pharmacological therapy are common and suggest the need for long-term maintenance therapy.
It is critical to identify and treat the subset of individuals who are at risk of developing the most serious consequences of GERD. In these patients, surgery at an early stage is most likely indicated. Approximately 92 percent of individuals had their symptoms resolved after a laparoscopic Nissen fundoplication.
The majority of cases of gastric reflux in babies and very young children are benign and respond to nonpharmacologic therapy (developmental impairments are a significant diagnostic exception); 80 percent resolve by the age of 18 months (55 percent resolve by age 10 mo).
Some individuals require a "step-up" in acid-lowering medicines, whereas only a tiny percentage require surgery. Long-term hazards are raised because symptomatic gastroesophageal reflux after the age of 18 months is likely to be a chronic disease. Long-term antisecretory treatment is typically necessary for individuals whose gastroesophageal reflux continues throughout later childhood.
In refractory instances or when problems linked to reflux illness (e.g., stricture, aspiration, airway disease, Barrett esophagus) are detected, surgical therapy (fundoplication) is usually required. With surgery, the prognosis is deemed favorable. Patients with complicated medical conditions in addition to gastroesophageal reflux have a greater surgical morbidity and mortality.
Gastroesophageal reflux disease (GERD) is a widespread clinical condition that affects millions of individuals worldwide. Early detection of symptoms is critical for preventing GERD consequences. Behavioral adjustments and advancements in acid suppression continue to be important components of its treatment.
Clinical experience shows that dietary modifications may be useful if apparent dietary precipitants (coffee, chocolate, or fatty foods) exist, and that lifestyle changes are required to reduce obesity, smoking, or excessive alcohol consumption if they exist. However, lifestyle changes alone are unlikely to alleviate his problems.
Patients are identified by a combination of traditional and unusual symptoms. In many people with GERD, acid suppression treatment relieves symptoms and avoids problems. Diagnostic and therapeutic advances have enhanced our capacity to recognize and manage illness consequences.
GERD is generally diagnosed based on classic symptoms and an empiric trial's response to acid suppression. GERD is a major public health problem since it is linked to reduced quality of life and substantial morbidity. 4 Treatment of GERD symptoms has been linked to considerable improvements in quality of life, including less physical discomfort, more vigor, physical and social function, and emotional well-being.
While GERD medicines are not exceptionally expensive, the cost of treating GERD patients has been estimated to be two times that of comparable persons who do not have GERD. This cost disparity is most likely attributable to increased morbidity in GERD patients as well as the greater expense of addressing consequences of improperly treated GERD.
Although proton-pump inhibitors are more successful than H2-blockers in general, the latter will suffice for certain individuals, and as-needed treatment will suffice for others. Other individuals will require twice-daily proton-pump inhibitor therapy; in these situations, medicine should be taken 30 to 60 minutes before breakfast and supper.
There is no evidence that any existing medicinal or surgical therapy reduces the risk of esophageal adenocarcinoma. Patients whose heartburn has not responded satisfactorily to twice-daily proton-pump inhibitor treatment should be referred to a specialist.
If a patient's symptoms are resistant to proton-pump inhibitors (particularly those caused by regurgitation) or he or she cannot tolerate such therapy, antireflux surgery may be explored; patients should be aware that there are risks and that medication is frequently required following surgery.
Medically Reviewed By
Medically reviewed by
Dr. Lavrinenko Oleg