Heartburn

Overview

Heartburn, also known as pyrosis, cardialgia, or acid indigestion, is a burning feeling in the upper central chest or belly. Heartburn is often caused by the regurgitation of stomach acid into the esophagus (gastric reflux). It is the most classic symptom of gastroesophageal reflux disease (GERD).

Gastroesophageal reflux disease (GERD) is a highly prevalent digestive condition that affects 18.1–27.8 % of people in North America. Approximately half of all individuals will experience reflux symptoms at some point in their lives. GERD is a disorder characterized by troubling symptoms and consequences caused by the reflux of stomach contents into the esophagus.

Belching, nausea, squeezing, stabbing, or a feeling of pressure on the chest are all typical characteristics for heartburn, in addition to burning. The discomfort frequently begins in the chest (just beneath the breastbone) and may extend to the neck, throat, or arm angle. Because the chest contains other vital organs than the esophagus (such as the heart and lungs), it is crucial to note that not all heartburn symptoms are esophageal in nature.

GERD is often 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 poor quality of life and considerable morbidity.

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 drugs 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 difference is most likely attributable to increased morbidity in GERD patients as well as the greater expense of addressing consequences of improperly treated GERD.

 

Incidence and prevalence of GERD-associated heartburn

GERD is one of the most prevalent gastrointestinal disorders, affecting around 20% of individuals in Western culture. According to a comprehensive study, the prevalence of GERD in the United States ranges from 18.1 % to 27.8 %.

However, because more people have access to over-the-counter acid-reducing drugs, the real prevalence of this condition may be greater. Men have a somewhat greater prevalence of GERD than women.

Women with GERD symptoms are more likely to develop non-erosive oesophageal reflux disease (NERD) than males with erosive esophagitis. Men with long-standing GERD symptoms, on the other hand, had a greater incidence of Barrett's esophagus (23%) than women (14%).

 

How & why GERD- associated heartburn developed?

The pathophysiology of GERD is complicated and best described by the multiple processes involved, which include the effect of lower esophageal sphincter tone, the existence of a hiatal hernia, esophageal mucosal protection against refluxate, and esophageal motility.

 

Impaired Lower Esophageal Sphincter (LES) Function and Transient Lower Esophageal Sphincter Relaxations:

The LES is a 3-4 cm tonically contracted smooth muscle segment found at the esophagogastric junction that, along with the crural diaphragm, forms the physiological esophagogastric junction barrier, preventing acidic gastric contents from migrating retrograde into the esophagus. 

In generally healthy individuals, the LES maintains a high-pressure zone above intragastric pressures, with temporary relaxation of the LES occurring physiologically in reaction to a meal, allowing food to enter into the stomach.

Patients with GERD symptoms may experience frequent transient LES relaxations that are not initiated by swallowing, resulting in intragastric pressures surpassing LES pressures and allowing reflux of gastric contents into the esophagus. Alcohol, smoking, caffeine, pregnancy, and some drugs like as nitrates and calcium channel blockers all have an effect on LES tone.


Hiatal hernia:

Hiatal hernia is usually associated with GERD; however, it can also persist without generating symptoms. Nonetheless, the existence of a hiatal hernia is important in the etiology of GERD because it impairs LES function. Patients with GERD, whether they had a minor hiatal hernia or not, displayed identical LES function problems and acid clearance.

Patients with extensive hiatal hernias, on the other hand, had shorter and weaker LES, leading in more reflux episodes. It was also mentioned that patients with significant hiatal hernias had more esophagitis. A research that looked at the association between hiatal hernia and reflux esophagitis found hiatal hernia in 94 percent of individuals with reflux esophagitis.


Impaired esophageal mucosal defense against the gastric refluxate:

The esophageal mucosa is made up of a variety of structural and functional features that act as a protective defensive barrier against the luminal chemicals encountered in GERD. Prolonged exposure to the refluxate, which contains both acidic gastric contents (hydrochloric acid and pepsin) and alkaline duodenal contents (bile salts and pancreatic enzymes), can penetrate this protective barrier, causing mucosal injury.


Defective esophageal peristalsis:

Acidic stomach contents that enter the esophagus are normally removed by regular esophageal peristalsis and neutralized by salivary bicarbonate. In a prospective research, 21% of GERD patients were shown to have reduced esophageal peristalsis, resulting in poor clearance of gastric reflux, severe reflux symptoms, and mucosal injury.

 

Histopathologic features of affected esophageal mucosa

The esophagus squamous epithelium acts as a preventive defensive barrier against refluxate retrograde migration. This epithelial defense is frequently disrupted in GERD and NERD. 

Because of the minimum biopsy criteria for diagnosis and varied sensitivity and specificity in the diagnosis, the histopathological characteristics of GERD are not exclusive to this condition. In fact, the histopathologic diagnosis of GERD is based on a variety of microscopic characteristics, including inflammation, basal cell hyperplasia, papilla elongation, and intercellular gap dilatation.

 

Signs and symptoms of GERD

Heartburn is the classic and most prevalent 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 linked 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 significant 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 explanation.

Although traditional GERD symptoms are easily identified, extraesophageal GERD manifestations are very frequent but not usually detected. Extraesophageal symptoms are more prevalent 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 etiology of globus is unknown, however it is assumed 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 assess patients for GERD-related warning symptoms, since they should prompt endoscopic investigation. Alarm symptoms may indicate an underlying cancer. In the presence of typical GERD symptoms, an upper endoscopy is not indicated. 

Endoscopy, on the other hand, is advised in the presence of alarm symptoms and for screening of individuals at high risk for problems (i.e. Barrett's esophagus, especially 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 assessment as well as H. pylori tests.

 

How to diagnose GERD?

Because there is no gold standard test for GERD, diagnosis is ambiguous. GERD is diagnosed purely on the basis of presenting symptoms or in conjunction with other variables such as response to antisecretory medication, esophagogastroduodenoscopy, and ambulatory reflux monitoring.


PPI (proton pump inhibitor) trial:

Most individuals with typical symptoms of heartburn and regurgitation can be presumptively diagnosed as GERD. Unless there are no concomitant warning symptoms such as dysphagia, odynophagia, anemia, weight loss, and hematemesis, most individuals can be started on empiric pharmacological therapy with proton pump inhibitors (PPIs) with a response to treatment confirming the diagnosis of GERD. 


Esophagogastroduodenoscopy (EGD):

Patients who present with normal GERD symptoms together with any of the warning signs should be assessed with an EGD to rule out GERD complications. These include erosive esophagitis, Barrett's esophagus, esophageal stricture, and esophageal cancer, as well as the exclusion of peptic ulcer disease.

According to current American College of Gastroenterology (ACG) guidelines, distal esophageal biopsies are not regularly advised for the diagnosis of GERD.

Patients with GERD symptoms who have a high index of suspicion for coronary artery disease should be evaluated for underlying cardiovascular disease.

Patients presenting with noncardiac chest discomfort suspected of being caused by GERD, on the other hand, should undergo a diagnostic evaluation, including an EGD and pH monitoring, before starting PPIs. In individuals with GERD symptoms, current ACG guidelines advise against screening for Helicobacter pylori infection.


Radiographic studies:

Barium radiography, for example, can reveal moderate to severe esophagitis, esophageal strictures, hiatal hernia, and malignancies. Their usefulness in the assessment of GERD, however, is restricted, and they should not be used to diagnose GERD.


Ambulatory esophageal reflux monitoring:

Medically refractory GERD is becoming more widespread, and patients frequently have standard endoscopic assessment since PPIs are quite effective in healing esophagitis caused by reflux. Ambulatory esophageal reflux monitoring can determine the relationship between symptoms and inappropriate acid exposure.

It is suggested in individuals with medically resistant GERD and extraesophageal symptoms suggestive of GERD. Ambulatory reflux (pH or impedance in combination) monitoring makes use of a telemetry pH capsule or a transnasal catheter.

It is the only test on the market that identifies pathological acid exposure, the frequency of reflux episodes, and the connection of symptoms with reflux episodes. In patients without erosive esophagitis, current practice recommendations require obligatory preoperative ambulatory pH monitoring.

 

Treatment of GERD associated heartburn

GERD therapies may include dietary modifications, lifestyle changes, medications, and, in some cases, surgery. A proton-pump inhibitor, such as omeprazole, is commonly used as the first line of therapy. A person with GERD symptoms may be able to manage them in certain situations by taking over-the-counter medications. This is frequently safer and less expensive than using prescription medications. Because of cost and safety concerns, some guidelines advocate trying to address symptoms with an H2 antagonist before employing a proton-pump inhibitor.

1. Lifestyle changes:

Certain foods may contribute to GERD, although most dietary therapies are ineffective. Some data shows that eating less sugar and eating more fiber can help. Those suffering from GERD should avoid certain meals and avoid eating before lying down. Coffee, alcohol, chocolate, fatty meals, acidic foods, and spicy foods are all known GERD triggers.

Weight loss may help reduce the intensity and frequency of symptoms. When lying down, elevating the head of the entire bed with blocks or using a wedge cushion that lifts the individual's shoulders and head may reduce GERD. Although moderate activity might help with GERD symptoms, intense exercise can make them worse. Breathing exercises may help to alleviate GERD symptoms.


2. Medications:

Proton-pump inhibitors, H2 receptor blockers, and antacids with or without alginic acid are the most often used drugs for GERD. Acid suppression therapy is a standard treatment for GERD symptoms, and many patients receive more of it than their condition warrants. The misuse of acid suppression is an issue due to the negative side effects and high expenses.

  • Proton-pump inhibitors:

The most effective are proton-pump inhibitors (PPIs) such as omeprazole, followed by H2 receptor blockers such as ranitidine. If a once-day PPI is only partially successful, it can be taken twice daily. They should be taken half an hour to an hour before a meal. There is no discernible difference in PPIs. When using these drugs on a long-term basis, the lowest effective dose should be utilized. They can also be used solely when symptoms arise in persons who have regular issues. H2 receptor blockers result in a 40 percent improvement.

  • Antacids:

Antacids provide a marginal effect of around 10%, but a combination of an antacid and alginic acid (such as Gaviscon) may relieve symptoms by 60%. Metoclopramide (a prokinetic) is not indicated alone or in conjunction with other medications due to safety concerns. The prokinetic mosapride has a little advantage.

  • Other agents:

Sucralfate works similarly to H2 receptor blockers; however, sucralfate must be taken numerous times each day, restricting its usage. While effective, baclofen, has the same difficulties of needing frequent doses as well as more bad effects when compared to other drugs.


3. Surgery

The Nissen fundoplication is the primary surgical therapy for severe GERD. The top section of the stomach is wrapped around the lower esophageal sphincter in this surgery to strengthen the sphincter, reduce acid reflux, and repair a hiatal hernia. It is only advised for people who do not improve with PPIs. 

Quality of life is better in the short term as compared to medical therapy, but the advantages of surgery against long-term medical care with proton pump inhibitors remain unknown. When comparing different fundoplication procedures, partial posterior fundoplication surgery outperforms partial anterior fundoplication surgery, and partial fundoplication outperforms whole fundoplication.

 

Consequences associated with untreated GERD

Erosive Esophagitis:

Erosive Esophagitis is distinguished by esophageal mucosal erosions or ulcers. Patients may be asymptomatic or have increasing GERD symptoms. Endoscopically, the degree of esophagitis is assessed using the Los Angeles esophagitis classification system, which applies the A, B, C, D grading system based on criteria such as the length, position, and circumferential severity of esophageal mucosal breaks.


Esophageal Strictures:

Chronic acid irritation of the distal esophagus can cause scarring, which can lead to the establishment of a peptic stricture. Patients may present with esophageal dysphagia or food impaction symptoms. To avoid the need for recurrent dilations, ACG recommendations urge esophageal dilation and the continuation of PPI medication.


Barrett's Esophagus:

Chronic abnormal acid exposure to the distal esophageal mucosa causes this problem. The distal esophageal mucosa, which is ordinarily bordered by stratified squamous epithelium, undergoes a histological transition to metaplastic columnar epithelium. Barrett's esophagus is more frequent in Caucasian males over the age of 50, is associated with obesity, and has a history of smoking, and it predisposes to the development of esophageal adenocarcinoma.

 

Conclusion

Heartburn is a burning sensation in the chest produced by stomach acid ascending to the esophagus (acid reflux). If this occurs repeatedly, it is referred to be gastro-oesophageal reflux disease (GERD).

Gastroesophageal reflux disease (GERD) is a chronic condition in which stomach contents leak into the esophagus, producing mucosal irritation. The primary cause of reflux is an abnormal, temporary relaxation of the lower esophageal sphincter (LES).

Obesity, stress, specific eating habits (e.g., large meals or lying down soon after eating), and changes in the architecture of the esophagogastric junction are also risk factors (e.g., hiatal hernia). Typical symptoms include retrosternal burning sensation (heartburn) and regurgitation, however the presentation can vary and may include symptoms such as chest discomfort and dysphagia.

The majority of individuals with suspected GERD should be treated empirically with proton pump inhibitors (PPIs). Diagnostic investigations, such as esophagogastroduodenoscopy (EGD) and/or a 24-hour pH test, may be recommended to confirm the diagnosis or rule out other possible causes of symptoms.

Management entails dietary changes, medication, and, in certain circumstances, surgery. Esophagitis treatment is critical because prolonged mucosal damage can lead to Barrett esophagus, a premalignant disease that can proceed to adenocarcinoma.