The Possible Complications of Acid Reflux Disease
Most heartburn sufferers will develop none of these complications. These complications tend to develop in patients with severe GERD and those who have prolonged reflux esophagitis. Consult your physician if you are worried that you may have any of the problems described below.
Hemorrhage and perforation
Fortunately, the serious complications of bleeding (hemorrhage) and esophageal perforation (a hole in the gullet allowing leakage of fluid into the central chest) are rare complications of reflux esophagitis (inflammation of the esophagus or gullet) and GERD. They are usually associated with deep ulcers in the esophagus or severe spread out (diffuse) esophagitis. Clinically important hemorrhage has been reported in 7%–18% of patients with GERD in one study but this overstates the risk of bleeding for the average patient with GERD. Bleeding is a rare complication most patients with heartburn. Esophageal perforations are very rare since the advent of treatment with proton pump inhibitors (PPI's). If a perforation does occur in the esophagus, this is extremely serious as it results in infection and inflammation in the mediastinum (central chest area). This is known as mediastinitis which can be fatal if not diagnosed and treated quickly.
Peptic oesophageal strictures
Peptic strictures (narrowings) occur in around 7%–23% of patients with untreated reflux esophagitis. This is a particular problem in elderly men. Strictures of the esophagus usually develop over many years and are possibly related to the to the long-term use of nonsteroidal inflammatory drugs (NSAIDs). The way that strictures arise is complicated. They start with inflammation in the esophageal lining. This is reversible. There is edema (fluid), infiltration with inflammatory cells and vascular congestion. This the gradually progresses to the laying down (deposition) of connective tissue and collagen. The end result is fibrosis (scar tissue) and narrowing of the gullet, which is not reverersible.
The symptom of a stricture is food or liquid becoming stuck or lodged in the esophagus. People complain that foods, especially bread, get stuck after being swallowed and before the food reaches the stomach. This may or may not be painful. This symptom always needs investigation because it may be the first symptom of cancer of the esophagus. This symptom is known medically as dysphagia.
In the case of a benign peptic stricture, when dysphagia starts there is often less heartburn. This is probably because the stricture is working as a barrier to acid reflux. The dysphagia is usually restricted to solid food but it may worsen and affect the swallowing of liquids. Patients with benign strictures, unlike malignant (cancerous) strictures, have a good appetite, alter their diet maybe to a heartburn or GERD diet, and lose little or no weight.
When a barium swallow or esophagram is performed, peptic strictures show up as smooth-walled, tapered, circumferential narrowings in the lower esophagus. They are usually short being less than 1 cm long but can occasionally be as long as 8 cm. If a long stricture is found then specialists will suspect that the patient has an underlying or predisposing condition. Causes include: the Zollinger–Ellison syndrome, superimposed pill esophagitis, or prolonged nasogastric intubation. If a stricture is found in the middle to upper esophagus then doctors will be concerned that this is a sign of Barrett esophagus or cancer of the esophagus. A Schatzki ring is now thought to be the start of a peptic esophageal stricture.
In all cases, the nature of a peptic stricture needs to be investigated with an endoscopy. Samples of tissue (biopsies) from the stricture need to be taken during the endoscopy. This is because some patients will have Barrett esophagus or unsuspected cancer of the esophagus.
In some patients with gastroesophageal reflux disease, the cells lining the lower esophagus change in nature. The lower esophagus is lined with squamous epithelium. In Barret esophagus the squamous cells are replaced by specialized columnar epithelium resembling that of the intestine and containing goblet cells. This was first described by Dr. Norman Barrett. He thought that this lesion was a congenitally shortened esophagus. However studies have consistently shown that these patients have severe acid reflux (GERD) with low lower esophageal sphincter (LES) pressures, impaired esophageal motility, large hiatus hernias. They also have extensive stomach acid and bile reflux.
In addition, most patients have had long term reflux symptoms for greater than 10 years.
Studies involving animals have been carried out. When the lining mucosa, consisting of squamous cells, of the the distal (lower) esophagus is cut out and the area is exposed to acid reflux, the lining cells which regenerate are different. The new cells are called columnar cells. The columnar epithelium has grown in the area previously occupied by squamous epithelium. If reflux is prevented then the mucosal lining will regenerate with squamous epithelium.
Pluripotential stem cells which are derived from the stratified squamous epithelium are the origin of the specialized columnar epithelium.
Barrett esophagus used to be thought to be a rare condition. However it has been extensively studied and is now thought to not be that uncommon. Estimates of its frequency at autopsy vary from 1 in 57 to 1 in 105 cases. When general endoscopy surveys are carried out it Barrett esophagus was found in 1 in 100 cases. Research using endoscopic studies on patients with GERD it was found to be present in a frequency which varied from 10-15%. This shows that it is not uncommon. it is thought to affect almost 700,000 adults in the United States.
It is interesting, that when a study was carried out in Minnesota (in Olmsted County) on people who had died it was found that most cases of Barrett esophagus had not been diagnosed when these patients were alive. This raises the problem that these undiagnosed cases are not accessible for cancer surveillance programs.
Barrett esophagus most commonly affects white men. It is three times more frequent in men than in women and is rare in African American and Asian populations. It occurs mainly in middle-aged and older adults. The mean age at diagnosis is about 55 years. However it can even occur in children has been diagnosed in children over the age of 5 years. It is very rare in children.
The prevalence of Barrett esophagus increases with age and parallels that of reflux esophagitis. But the length of the affected segment which is lined with columnar cells remains remarkably stable, even when followed up over many years by endoscopy. This interesting finding suggests that Barrett esophagus appears very quickly in the vulnerable acid reflux-damaged lower esophagus and early on in the course of disease. There are cases of families where many members have Barrett esophagus, some with esophageal cancer which as been found in more than one generation.
Having Barrett esophagus does not cause symptom. But most patients will complain of heartburn and regurgitations due to the existence of GERD and acid reflux. However about a quarter of patients with Barrett esophagus found when endoscoped no esophageal symptoms.
Barrett esophagus has a typical appearnace at endoscopy and the doctor carrying out the investigation will suspect Barrett esophagus and take biopsies (tissue samples) The diagnosis is confirmed by and histological examination of the biopsies. The columnar epithelium of the stomach has a reddish pink appearance. The junction between the glossy white squamous mucosa of the esophagus and the columnar mucosa of the stomach is known as the Z-line. It is normally found at the lower end of the tubular esophagus, just above the proximal (lower) folds of a hiatal hernia, if one is present.
In Barrett esophagus, the lower (distal) esophagus is lined with columnar epithelium, which extends up for a variable distance. This is often as much as 3–10 cm, but may very rarely affect most of the esophagus. The lower margin may be horizontal or there may be present tongue-shaped, irregular, upward extensions of columnar mucosa (lining).
At endoscopy some people will have pale areas like islands of residual or regrowing squamous epithelium. Other patients will have small roundish benign ulcers in the columnar mucosa region. Esophagitis and esophageal strictures and esophagitis may be seen at the new squamo-columnar junction.
The specialist performing the endoscopy will look very carefully any for evidence of esophageal adenocarcinoma (cancer). This shows up as nodularity or masses in the lining of the esophagus.
When the esophageal tissue samples are examined with a microscope, the characteristic appearance (histological finding) in Barrett esophagus is a distinctive specialized intestinal epithelium. This is a glandular epithelium (surface lining) with mucin-type cells and the distinguishing presence of goblet cells. These are easily seen when the biopsy is stained with hematoxylin and eosin-stains and can be demonstrated more prominently in sections stained with a special stain: Alcian blue. It occupies most or all of the columnar-lined area and is the type of lining (epithelium) in which esophageal cancer develops.
There are other types of epithelia seen with Barrett esophagus. These include cardia-type and gastric fundic epithelia. However these alone do not make the diagnosis of Barrett esophagus and neither are they associated with adenocarcinoma.
The classification of Barrett esophagus is debated by gastroenterology specialists and remains controversial.
- Long-segmented or classical Barrett esophagus requires at least 3 cm of esophagus to be lined with columnar epithelium. This is the most-studied subset of Barrett esophagus. There are traditional demographic features and a definite increased risk of becoming adenocarcinoma.
- Short-segment Barrett esophagus refers to shorter lengths or tongues of columnar epithelium which are less than 3 cm, in the distal esophagus. There is intestinal metaplasia on biopsy. This type is three to five times more common than the long-segment variant. Based on anecdotal reports, the risk of cancer appears to be lower.
- The presence of intestinal metaplasia at the junction of the stomach and esophagus, refers to microscopic findings on biopsy but no visible columnar epithelium in the esophagus at endoscopy.This finding has been reported by gastroenterologists in a range of 10%–32% of biopsies from patients who were unselected. Many of these patients had no symptoms of reflux. The percentage of woman and African American people with this lesion is also higher than the percentage with either long- or short-segment Barrett esophagus. The cause of this type is controversial. Some specialists have suggested that this is the earliest form of GERD. Others think that these changes are do Helicobacter pylori infection. The risk of esophageal cancer risk is thought to be extremely low or non-existent.
Patients who have long-segment Barrett esophagus have an increaed risk of developing esophageal cancer This has been variously estimated at between 30–125 times that of the general population.
Early studies suggested that the median cancer incidence was 1 per 100 patient-years of follow-up, but subsequent studies with longer follow-up suggest a lower cancer incidence of 1 per 200–250 patient-years.
This means that the annual incidence of esophageal cancer is about 0.5%, with about 500 cases of adenocarcinoma diagnosed annually in the United States. However, since the early 1980s, the incidence of squamous cell carcinoma has stayed constant, whereas the incidence of adenocarcinoma of the esophagus and esophagogastric junction has increased by a factor of five. This growth rate exceeds that of any other type of cancer.
Adenocarcinoma accounts for more than half of all esophageal cancers in the United States. Despite their increased cancer risk, most patients with Barrett esophagus die of unrelated causes. More than 95% of patients who develop cancer present with symptoms caused by the tumor itself and are unaware of their antecedent Barrett esophagus. Research of the epidemiology of Barrett esophagus suggests that the mean length of time from the start of Barrett esophagus to the development of cancer of the esophagus is around 20–30 years.