Esophagitis and Esophageal Injury

Candida, HSV, and CMV look different

Immune status narrows the pathogens, and ulcer shape separates the finalists.

Candida, the most common cause of infectious esophagitis, coats inflamed mucosa with adherent white plaques or pseudomembranes.

HSV typically creates multiple small, well-circumscribed or punched-out ulcers; diagnostic viral cytopathic change is best sampled at an ulcer edge.

CMV more often forms large linear or longitudinal distal ulcers, with diagnostic inclusions in stromal and endothelial cells from the ulcer base.

White plaques suggest Candida, punched-out ulcers suggest HSV, and long linear ulcers suggest CMV.

Five routes to esophagitis

The offending exposure or host defect usually names the inflammatory route.

Repeated gastric-content exposure injures the distal esophagus and can produce heartburn, regurgitation, dysphagia, or odynophagia.

Tetracyclines, bisphosphonates, potassium chloride, iron, and selected NSAIDs can cause pill esophagitis when swallowed with little water just before lying down.

Eosinophilic, infectious, and caustic esophagitis arise from immune inflammation, impaired host defense, and direct chemical injury, respectively, despite overlapping odynophagia.

Primary diagnostic image

Odynophagia identifies injured lining; dysphagia asks whether the lumen also narrowed or stiffened.

Depth raises urgency

Similar pain can hide very different depths of injury.

Uncomplicated esophagitis remains mainly mucosal, whereas a Mallory-Weiss tear reaches mucosa and submucosa near the gastroesophageal junction.

Boerhaave syndrome breaches the full wall, creating far greater risk of mediastinitis, sepsis, shock, and death when treatment is delayed.

Hematemesis after vomiting fits Mallory-Weiss; pain with escaped air fits Boerhaave.

The esophageal wall contains the leak until it does not

Injury depth determines whether the outcome is bleeding, stricture, or mediastinal contamination.

Mucosal inflammation may erode, bleed, ulcerate, or heal with fibrosis, yet the lumen remains contained until deeper muscular and connective-tissue layers fail.

Because most of the esophagus lacks a protective serosal coat, full-thickness perforation can rapidly soil the mediastinum and adjacent pleural spaces.

Narrowing at the upper sphincter, aortic arch or left main bronchus, and diaphragmatic hiatus helps explain pill impaction and instrumentation injury.

Vomiting injuries differ by wall depth

One bout of retching can end as a shallow bleeding split or a contaminated chest.

Forceful retching drives intragastric and intraesophageal pressure upward against a closed or poorly relaxing upper sphincter.

A Mallory-Weiss lesion is a longitudinal mucosal or submucosal laceration near the junction that usually presents with post-vomiting hematemesis.

Boerhaave syndrome is often a distal full-thickness rupture that releases air, saliva, gastric contents, and microbes into the mediastinum and pleural space.

Plummer-Vinson links iron, webs, and cancer risk

This uncommon triad links epithelial iron deficiency to a structural cause of dysphagia.

Plummer-Vinson syndrome combines iron-deficiency anemia, dysphagia, and thin proximal esophageal webs, sometimes accompanied by glossitis, angular cheilitis, fatigue, or other signs of iron deficiency.

Iron-dependent epithelial and muscular dysfunction may contribute, although the syndrome remains a clinical association without one proven pathway.

Because upper aerodigestive squamous-cell carcinoma risk is increased, persistent or recurrent symptoms merit examination rather than iron replacement alone.