Esophagitis

Article Author:
Catiele Antunes
Article Editor:
George Mathew
Updated:
11/18/2018 7:54:09 PM
PubMed Link:
Esophagitis

Introduction

Esophagitis refers to inflammation or injury to the esophageal mucosa. There are many causes of esophagitis and essentially the presentation is similar.[1][2]

Etiology

Professionals have identified several etiologies. Reflux or erosive esophagitis that occurs as a consequence of reflux of gastric contents into the stomach leading to mucosal injury is one of the most common causes of esophagitis. Radiation, infections, local injury caused by medications (pill esophagitis), and eosinophilic esophagitis (EoE) are also other possible etiologies.[3]

Epidemiology

Epidemiology varies depending on the subset to which one refers.[4][5][6]

  • Professionals estimate that 1% of the population suffers from erosive esophagitis.
  • Medication-induced esophagitis has an estimated incidence of 3.9 per 100,000 population per year with a mean age at diagnosis of 41.5 years.
  • Many studies have tried to identify the most accurate incidence and prevalence of eosinophilic esophagitis. The estimated incidence is 0.35 per 100,000 population with a prevalence of 55 per 100,000 population.
  • Radiation esophagitis is a relatively frequent complication of radiation therapy. Acute injury invariably occurs at doses of 6000 cGy given in fractions of 1000 cGy per week. Lower doses or longer schedules are associated with lower rates of radiation esophagitis.  
  • For infectious esophagitis, the numbers are not very easy to define. One thing that is certain is that is way more prevalent is patients who are immunocompromised such as HIV-infected patients and patients with hematological malignancies.

Pathophysiology

The pathophysiology also depends in large part on the subset of esophagitis to which one refers.[7][8][9]

  • Reflux esophagitis: This is the pathophysiology involved in reflux of gastric content into the esophagus leading to mucosal injury. Several mechanisms take place in the pathophysiology of reflux. See more information in the Gastroesophageal Reflux Disease (GERD) chapter. Briefly, the lower esophageal sphincter (LES) seems to have decreased tone and increased transient relaxations. These factors facilitate the anterograde flow of acid. Also, patients with large hiatal hernias seem to have a higher incidence of reflux for since they contribute to a decreased tone in the LES. In contrast, any conditions that decrease esophageal peristalsis or affects saliva content can affect the protective mechanisms in place to prevent esophageal injury, contributing to the development of reflux esophagitis.
  • Medication-induced esophagitis: The pathogenesis of medication-induced esophagitis involves a direct irritant effect and disruption of cytoprotective barriers. Researchers hypothesize that prolonged contact of irritants with the esophageal mucosa can lead to damage. Medications like doxycycline, tetracyclines, and ferrous sulfate can cause local caustic injury as they have a pH of less than three once dissolved in water or saliva. Other medications such as potassium chloride can cause tissue destruction and vascular injury due to its hyperosmolar nature.
  • Eosinophilic esophagitis: The pathogenesis of EoE is incompletely defined. Considerable evidence suggests that eosinophilic esophagitis is an allergic disorder induced by antigen sensitization either through foods and/or aeroallergens. Eotaxin, interleukin 5 (IL-5) and STAT6 may play important roles. Some patients have at least partially improved symptoms with acid suppression therapy suggesting that acid reflux may be a contributor.
  • Radiation esophagitis: The pathophysiology involves DNA damage and cell death from high-energy electrons leading to the formation of volatile oxygen free radicals. The radiation injury can be acute or chronic. In the acute phase, radiation destroys epithelial cells and interferes with proliferation. Small doses can lead to villous blunting and minor alterations in mucosal formation, but larger doses can denude extensive regions of the mucosa. The chronic injury seems to involve small vessel ischemic injury. Endothelial inflammation coupled with smooth muscle and fibroblast proliferation compromise blood flow into the small vessels. Excessive fibrosis and the presence of atypical fibroblasts characterizes the chronic radiation injury. Progressive injury can lead to stricturing, ulceration, fistulization and even perforation.
  • Infectious esophagitis: Candida albicans infection is the most common cause of infectious esophagitis. The first step in the pathophysiology involves colonization with mucosal adherence and proliferation. The second step involves impairing the host defense mechanisms. C. albicans is a normal component of oral flora, but it can become a problem if their number increases (e.g., with the use of antibiotics) or if the patient is immunosuppressed (e.g., by therapy with corticosteroids). Herpes simplex virus (HSV) is the most common cause of viral esophagitis. It infects the squamous epithelium leading to vesicles and then ulcerations. Cytomegalovirus (CMV), Epstein-Barr (EBV) and varicella-zoster (VZV) are other viral causes of viral esophagitis.

History and Physical

The most common symptoms are chest pain, odynophagia, and dysphagia. Patients with EoE can present with food impaction. If the esophagitis is severe and leads to strictures, fistulization, and perforation, patients can present with symptoms related to those.

Evaluation

Diagnosis is usually achieved with endoscopy and biopsies. If the history is very suggestive of medication-induced (pill) esophagitis, endoscopy may not be initially required. Patients with eosinophilic esophagitis will have a characteristic eosinophilic infiltration (> 15 eosinophils per high-power field). Histology can also be helpful in diagnosis infectious etiologies. Multinucleated giant cells with ballooning and degeneration of squamous cells are diagnostic of HSV esophagitis with Cowdry type A inclusions being pathognomonic. Large cells with both intracytoplasmatic inclusions and amphophilic intranuclear inclusions are suggestive of CMV esophagitis.[10][4]

Patients with eosinophilic esophagitis will have a characteristic eosinophilic infiltration (> 15 eosinophils per high-power field). Histology can also be helpful in diagnosis infectious etiologies. Multinucleated giant cells with ballooning and degeneration of squamous cells are diagnostic of HSV esophagitis with Cowdry type A inclusions being pathognomonic. Large cells with both intracytoplasmatic inclusions and amphophilic intranuclear inclusions are suggestive of CMV esophagitis.

Furthermore, the appearance of the mucosal lesions on endoscopy can help with diagnosis. In patients with suspected eosinophilic esophagitis, endoscopy may reveal white exudates or papules, red furrows, corrugated concentric rings, and strictures; but endoscopy may be normal in up to 10% of patients. Endoscopic signs of candidiasis are diffuse, linear, yellow-white plaques adherent to the mucosa. CMV esophagitis is characterized by several large, shallow, superficial ulcerations. HSV esophagitis results in multiple small, deep ulcerations.

Treatment / Management

Treatment depends on the etiology. If the etiology is acid reflux, use of H2 blockers or proton-pump inhibitors is indicated, along with lifestyle modifications. If the etiology is medication-induced esophagitis, the medication should be stopped if possible or otherwise; the patient should be instructed to take pills with 4 oz of water and remain upright for 30 min after taking the pills. If EoE is the etiology, the treatment will include acid suppression, topical or systemic steroids, dietary modification and endoscopic therapies such as dilations is strictures are present. If etiology is infectious, target therapy is indicated. For C.  albicans, esophagitis treatment is with Nystatin or Fluconazole. For HSV esophagitis, treatment is oral or intravenous acyclovir and Foscarnet for those who are non-responders. For CMV esophagitis, treatment is with Gancyclovir intravenously.[11][12][13]

Surgical Oncology

  • Pericarditis
  • Esophageal stricture
  • Coronary artery disease
  • Pneumonia
  • Peptic ulcer disease
  • Pulmonary embolism

Complications

  • Bleeding
  • Stricture
  • Barrett esophagus
  • Perforation
  • Laryngitis
  • Aspiration pneumonitis

Enhancing Healthcare Team Outcomes

There are many causes of esophagitis and healthcare workers in many disciplines will encounter these patients. To avoid delay in diagnosis, a multidisciplinary approach is necessary. The prognosis for most patients is good with prompt treatment, but ultimately the outcomes depend on the underlying cause. When esophagitis is recurrent, it can lead to anxiety and absenteeism from work because of the need to rule out other more serious causes of chest pain. Untreated esophagitis can lead to stricture formation and malnutrition. Both bleeding and perforation are also relatively common complications. Some patients may aspirate and develop pneumonitis or worsening of asthma. In most patients who do not change their lifestyle, recurrences are common, and thus life long therapy is required. In immunocompromised patients, both candida and herpes can lead to severe pain, dysphagia, and weight loss. Patient education is key when a diagnosis of esophagitis is made. The patient should be told to sleep with the head of bed elevated, avoid lying supine after a meal and lose weight. The patient should also avoid caffeinated beverages, alcohol and discontinue smoking. Finally, the patient should be told to avoid NSAIDS.[14][15]