Esophagitis overview

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Esophagitis from other Diseases

Epidemiology and Demographics

Risk Factors

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Natural History, Complications and Prognosis

Diagnosis

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History and Symptoms

Physical Examination

Laboratory Findings

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:

Overview

Esophagitis is a general term for any inflammation, irritation, or swelling of the esophagus. The inflammation can be due to a variety of causes such as gastroesophageal reflux disease, viruses, or chemical injuries.

Historical Perspective

GERD is believed to be first described and treated by the ancient Egyptians according to the papyrus which was discovered by Edwin Smith at Thebes. The esophagus itself was named by the ancient Greeks. Friedenwald, and Feldman described the symptoms of GERD in 1925. Robbins and Jankelson used the radiological procedures to observe GERD in 1926. In 1981, Picus and Frank reported a case of a 16-year-old boy with progressive dysphagia for 1.5 years, endoscopic findings were suggestive of multiple 1-mm nodular filling defects in the esophagus in an area of stricture with dilatation above. The radiology showed a luminal narrowing, wall rigidity, and high circulating eosinophil count assumed to be a variant of eosinophilic gastroenteritis.

Classification

Esophagitis may be classified according to the Los Angeles Classification into 4 grades.

Pathophysiology

The esophagus is a part of the gastrointestinal tract which is responsible of moving the food from the mouth to the rectum. Esophagitis is defined as inflammation of mucosal layer of esophagus. Based on the etiology of inflammation esophagitis can be classified into reflux esophagitis and eosinophilic esophagitis. Any condition that lead to the reflux of the gastric acidic contents into the esophagus results in reflux esophagitis. Eosinophilic esophagitis is an immunoallergic disorder resulting from the interaction between genetics and environmental triggers such as repeated exposure to food and aeroallergens. TH2 inflammatory cell response play a major role in the production of eosinophils. Activated TH2 response leads to the recruitment and activation of eosinophils and mast cells. Characteristic gross pathology findings of esophagitis include fixed esophageal ring, white exudates, longitudinal furrows/ fibrosis, mucosal pallor, Diffuse esophageal narrowing. Characteristic microscopic findings of esophagitis include edema and basal hyperplasia (non-specific inflammatory changes), Lymphocytic infiltration (non-specific), neutrophilic infiltration, Eosinophilic infiltration, Goblet cell intestinal metaplasia or Barrett's esophagus and elongation of the papillae.

Causes

Common causes of esophagitis include gastroesophageal reflux disease, Barrett's esophagus, caustic burns, and chemical injury by either alkaline or acid solutions. Among immuncompromised patients, the most common causes of esophagitis are Candidiasis, Cytomegalovirus, and Herpes simplex virus

Differentiating Esophagitis overview from Other Diseases

Esophagitis must be differentiated from gastritis, peptic ulcer disease, gastroesophageal reflux disease, acute coronary syndrome, angina pectoris, cholecystitis, biliary colic, pulmonary embolism and esophageal perforation, rupture and tears.

Epidemiology and Demographics

In the USA and Europe, the prevalence of GERD ranges from low of 10,000 per 100,000 persons to high of 20,000 per 100,000 people. In Asia, the prevalence of GERD is 5,000 per 100,000 people. The prevalence of EoE is approximately 50-100 per 100,000 individuals worldwide. In the USA, the incidence of GERD is 5,400 per 100,000 persons. In Europe, the incidence of GERD is 840 per 100,000 persons. The incidence of EoE is approximately 10 per 100,000 individuals worldwide. The prevalence of GERD increases with age. GERD affects all age groups but it affects more the people older than 40 years. Patients of all age groups may develop EoE. Men and women are affected equally by GERD. Males are more commonly affected by EoE than females. There is no racial predilection for GERD. EoE usually affects individuals of the white race.

Risk Factors

Common risk factors in the development of esophagitis are immunosuppression, alcohol use, smoking, excessive vomiting, certain medications, and surgery or radiation to the chest.

Screening

There is insufficient evidence to recommend routine screening for Esophagitis.

Natural History, Complications, and Prognosis

If left untreated, 20% of patients with GERD may progress to develop esophageal stricture due to excessive acid in the lower esophagus. Complications of GERD include barrett's esophagus, erosive esophagitis, esophageal ulcer, and esophageal adenocarcinoma. Prognosis of GERD is good with the appropriate treatment.The natural course of primary EoE is, in patients with EoE, symptoms persist over years raising suspicion that a chronic inflammatory process is an underlying event responsible for it. The inflammatory activity is proportional to the density of the eosinophilic infiltration in the esophageal tissue. Similar to asthma, EoE has chronic persistent eosinophilic inflammation and can eventually lead to irreversible structural changes of the esophagus which is called re-modeling of the esophagus. The esophageal mucosa in patients with a longstanding EoE is characterized by a loss of elasticity. On histologic examination of the subepithelial compartments of the esophagus show an increase in the fibrous tissue. In patients with EoE, the chronic eosinophilic inflammation leads to an increased deposition of the fibrous connective tissue which in turn causes the remodeling of the esophagus hindering the esophageal transport.The complications of the EoE are as follows: Scarring of esophagus-leading to dysphagia, Esophageal stenosis, Tears or perforation during the endoscopy or retching leading to boerhaave syndrome. The long-term prognosis of the EoE is unclear but patients diagnosed with EoE have an unaffected lifespan.

Diagnosis

Diagnostic Criteria

History and Symptoms

The signs and symptoms of the esophagitis are as follows Halitosis. Chest pain, in the middle of the chest, often radiating to the back, usually associated with swallowing or soon after a meal. Dysphagia, odynophagia, food getting stuck in the throat. Hoarseness, oral ulcers, Nausea, Sore throat, Vomiting. Symptoms of underlying diseases that cause esophagitis include: Indigestion, heartburn, metallic taste, Excessive belching.

Physical Examination

The physical examination usually is not helpful in confirming the diagnosis of uncomplicated esophagitis. However, the examination may reveal other potential sources of chest or abdominal pain.

Laboratory Findings

A complete blood count (CBC) is performed in patients with neutropenia or who are immunosuppressed. A CD4 count and HIV test are performed in patients with risk factors for HIV. A collagen workup (eg, antinuclear antibody [ANA], anti-dsDNA) may be performed based on the underlying disease.

X-ray

CT

There are no CT scan findings associated with esophagitis. However, a CT scan may be helpful in the diagnosis of complications of esophagitis such as tearsperforationstrictures, etc.

MRI

There are no MRI findings associated with esophagitis. however, MRI may be helpful in the diagnosis of complications of esophagitis such as tearsperforationstrictures, etc.

Imaging Findings

Other Diagnostic Studies

There are no other diagnostic studies associated with esophagitis.

Treatment

Medical Therapy

The mainstay of therapy for reflux esophagitis is acid suppression therapy. Patients with infectious esophagitis are treated with antimicrobial therapy, whereas patients with eosinophilic esophagitis are treated with corticosteroids. Supportive therapy for esophagitis includes proton pump inhibitors, topical pain medications (gargled or swallowed), smoking and alcohol cessation, and endoscopy to remove any lodged pill fragments.

Surgery

Surgical intervention is not recommended for the management of esophagitis.

Primary prevention

There are no established measures for the primary prevention of esophagitis.

Secondary prevention

There are no established measures for the secondary prevention of esophagitis.

References


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