Esophageal ulcer induced by GERD and certain drugs presents both esophageal and gastric symptoms. The intermittent reflux of gastric contents produces discomfort in swallowing resulting in dysphagia, odynophagia and ultimately weight loss . The reflux of acid is characterized by pain behind the sternum and heartburn . A common clinical feature of esophageal ulcer caused by esophageal tuberculosis is hematemesis which produces lesions in the esophagus.
Diagnosis is based on evaluation of signs and symptoms, physical assessment and an X-ray imaging to obtain an esophagram. Barium swallow is typically used to identify anatomic abnormalities of the esophagus . Esophagogastroduodenoscopy (EGD) is used to perform endoscopic evaluation of the esophagus and identify the cause of an esophageal ulcer. Suspected cases of infectious esophagitis are confirmed by histopathological study following tissue biopsy and blood cultures. In the presence of psychiatric illnesses associated with severe depression, psychiatric evaluation is needed .
Identification of the definite cause of esophageal ulcer is of utmost importance as management is based on treating the cause. Severe cases of esophageal injury are managed by intubation with nasogastric tube, administration of intravenous fluids, chemoprophylaxis with antibiotics, pain relief with analgesics and treating the ulcer with H2 receptor anatagonists and PPIs.
Treatment of esophageal ulcer caused by GERD is aimed at symptomatic management, promoting persitalsis and controlling acid secretion. Temporary relief from symptoms is achieved by the use of H2 receptor antagonists. The commonly used H2 receptor blockers are cimetidine, ranidtidine, famotidine and nizatidine. However, long-term resolution is achieved by the use of PPIs which directly inhibit acid secretion from gastric parietal cells by blocking proton pumps. Available PPIs used to treat GERD include omeprazole, esomeprazole, lasoprazole, pantoprazole and rabeprazole. Additionally, esophageal clearance can be promoted by prokinetics that increase motility of the gastrointestinal tract. Cisapride and metoclopramide are the commonly employed prokinetics to promote esophageal peristalsis.
If GERD occurs secondary to Helicobacter pylori infection, the standard treatment is followed which is based on triple therapy with a PPI and two antibiotics. The standard treatment regimens available for eradication of Helicobacter pylori include administration of ompeprazole, amoxicillin and clarithromycin (OAC) for 10 days, bismuth subsaclicylate, metronidazole and tetracyline (BMT) for 14 days and lansoprazole, amoxicillin and clarithromycin (LAC) for 10-14 days .
Treatment of drug-induced esophageal ulcer includes discontinuation of the drug causing mucosal damage and administration of PPIs and gastroprotective agents . Esophageal ulcer occurring as a result of esophageal tuberculosis requires standard antitubercular treatment based on IREP therapy (Isoniazid, rifampicin, ethambutol and pyrazindamide). The duration of treatment varies from 6-9 months, depending on patient's condition.
Antimicrobial agents are used to treat mucosal damage caused by infectious esophagitis. Infection caused by cytomegalovirus is treated with ganciclovir whereas fluconazole is the preferred choice in treatment of esophageal candidiasis. HIV infected patients with esophageal ulcer have been found to respond well to antiretroviral therapy. Idiopathic esophageal ulcers are treated with corticosteriods although the risk of developing opportunistic infections is increased due to immunosuppressive effects of steroids.
Prognosis is good in patients strictly following treatment regimen and maintaining appropriate diet. Disease recurrence after treatment with proton pump inhibitors is common and such patients require maintenance therapy to avoid relapse . A serious complication of GERD with poor prognosis is the development of esophageal adenocarcinoma. However, the risk for developing adenocarcinoma is extremely rare occurring in about 0.1% patients .
Typical etiologic factors that cause esophageal ulcers comprise preexisting esophageal disorders such as GERD and achalasia, infectious esophagitis and use of certain drugs. Damage to the esophageal mucosa due to any cause can lead to esophageal ulcer formation. The most common cause of mucosal damage is acid reflux that occurs in GERD. The lower esophageal sphincter (LES) which is responsible for preventing the back flow of acid becomes weak in GERD due to which it fails to hinder the acid reflux and consequently exposure of esophageal mucosa to gastric acid causes ulceration. Moreover, forced vomiting that ensues repeated expulsion of gastric contents in patients with bulimia nervosa periodically exposes the esophageal mucosa to gastric acid causing open sores.
Another common cause is inflammation of the esophagus that occurs from infection. The infections can be viral, bacterial, fungal or parasitic in origin and often emerge in immunocompromised individuals, such as those suffering from acquired immunodeficiency syndrome (AIDS) and diabetes mellitus  . Commonly involved causative agents in infectious esophagitis are herpes simplex virus (HSV), human immunodeficiency virus (HIV), candida albicans, cytomegalovirus (CMV) and mycobacterium tuberbulosis. The risk of developing opportunistic infection in the form oroesophageal candidiasis is increased by prolonged and recurrent use of antibiotics and chemotherapeutic agents as their use inhibits the normal protective flora of the esophagus making it prone to be infected by opportunistic pathogens.
Some drugs adversely affect the esophagus on prolonged contact with the esophageal mucosa or through side effects following systemic absorption. Use of drugs that may weaken LES or alter its tonicity can also cause acid reflux. Drugs that may cause esophageal ulcer include tetracyclines, NSAIDs , bisphosphonates, potassium chloride and iron compounds. Chronic consumption of acid rich foods, caffeinated drinks, alcohol and cigarette smoking  worsens the condition by destroying the esophageal lining and delaying regeneration of healthy esophageal mucous membrane.
The reported prevalence rate of esophageal ulcers emerging from GERD has been found to lie between 2%-7%  .
In case of esophageal ulcer induced by GERD, the period of exposure to gastric acid and bile salts largely determines the extent of mucosal erosion. Ulceration is directly related to the number of times gastric contents flow back into the esophagus as the more the episodes of esophageal reflux, more will be the mucosal damage . Apart from this, weakened contractions of the LES causes hindrance in clearing gastric acid from the esophagus which further aggravates the condition. Furthermore, persistent acid reflux coupled with lowered resting tone of upper esophageal sphincter (UES) precipitates laryngopharyngeal symptoms causing cough, sore throat and throat clearing . The natural resistance of mucosal epithelium against gastric contents also indicates the severity of damage. Inability of the damaged mucosa to undergo regeneration and healing further worsens the ulceration.
One complication that follows GERD due to prolonged aspiration of gastric reflux contents is reflux-induced asthma and is characterized by vasovagal bronchoconstriction. A usual finding in chronic asthmatic patients is asymptomatic gastroesophageal reflux .
Since GERD is the leading cause of esophageal ulcer, controlling acid reflux and gastric hyperacidity helps in preventing the disease. Dietary modification aimed at reducing intake of spicy, acid rich foods and caffeinated beverages and incorporating alkaline foods controls acidity and prevents heart burn. Cigarette smoking, carbonated drinks and alcohol should be avoided in all cases. Regular intake of milk keeps from developing acidity as it a natural antacid.
Esophageal ulcer is the erosion of esophageal mucosa that causes the formation of an open sore. Gastroesophageal reflux disease (GERD) is the most common cause of esophageal ulcer. GERD is the flow of acid rich gastric contents back into the esophagus. Since the esophageal mucosa lacks a protective lining against gastric contents, the acid reflux damages the esophageal mucous membrane causing an esophageal ulcer. Other causes of esophageal ulcer are esophagitis and use of certain anti-inflammatory medications.
Prolonged and recurrent ulceration due to GERD can result in metaplastic change in the mucosal lining of the esophagus, a condition referred to as Barrett esophagus. Barrett esophagus is presented with symptoms similar to those of GERD such as heart burn, retrosternal pain, hematemesis and dysphagia  .
An esophageal ulcer possesses a high risk of recurrence after treatment. In such cases, aggressive treatment is required following standard regimen of proton pump inhibitors (PPI). Diagnosis is established on evaluation of patient's history, assessment of symptoms, physical examination and certain tests. Usually, barium swallow and upper GI endoscopy are utilized to identify the ulcer. Other tests include tissue biopsy and blood culture.
Treatment is aimed at resolution of the underlying cause and control of symptoms to relief discomfort. PPIs are the standard agents used to treat GERD while infectious esophagitis may require intervention with antimicrobial agents.
As the name indicates, esophageal ulcer is the formation of an ulcer or open sore inside esophagus. The esophagus is a long hollow tube that provides passage of food from the throat to the stomach. Several causes of esophageal ulcer have been identified. The most common cause is gastroesophageal reflux disease (GERD). The disease is characterized by reverse flow of stomach contents into the esophagus. The continuous exposure of acid in stomach contents with the inner lining of esophagus damages it, causing esophageal ulcer. Infection caused by bacteria, virus, fungus or parasite can also provoke esophageal ulcer. Common disease causing organisms that have been identified are herpes simplex virus (HSV), cytomegalovirus (CMV) and candida albicans. Esophageal ulcer can also result from side effects of certain medications. In some cases, excessive cigarette smoking, intake of alcohol, colas and spicy food can also damage the esophagus and cause ulcers.
Diagnosis is based on disease history, evaluation of signs and symptoms, physical examination, X-rays, endoscopy and blood tests. X-ray of the esophagus is obtained by barium swallow method. In this procedure, the patient is instructed to drink a solution of barium after which X-ray is obtained to show a clear image. Another test used to establish accurate diagnosis is endoscopy of the upper digestive tract. An endoscope is inserted in the patient's mouth through which internal structures of esophagus are visualized to see the presence of ulceration on the inner lining. In some cases, tissue biopsy is performed along with blood tests to identify any suspected case of infection.
Treatment depends on the cause of ulceration and disease severeness. Medications used to reduce production of stomach acid and antibiotics to treat infectious cause are used. The standard medications used in GERD are proton pump inhibitors (PPIs). Patients are advised to avoid spicy and acid rich foods and intake of medications that may cause acidity. Medicines that must be avoided include aspirin, ibuprofen, naproxen, diclofenace sodium, iron and potassium.