Esophagitis is inflammation of the esophageal mucosa developing from various etiologies: gastroesophageal reflux (most common), infectious (Candida, HSV, CMV — in immunosuppressed patients), eosinophilic (allergic), caustic (corrosive substance ingestion), pill (medication-induced), and radiation esophagitis. The primary CT finding is mucosal thickening and target sign — inner enhancing mucosa, middle hypodense submucosal edema line, and outer enhancing serosa. Wall thickening is usually concentric and smooth. Ulcerations, strictures, and mucosal irregularity may be seen on barium studies. Radiological findings of esophagitis may mimic esophageal carcinoma; clinical context and endoscopy provide differentiation.
Age Range
20-80
Peak Age
50
Gender
Equal
Prevalence
Common
Esophagitis pathophysiology varies by etiology. In reflux esophagitis, lower esophageal sphincter (LES) dysfunction or hiatal hernia causes gastric acid reflux into the esophagus — acid pH <4 leads to protein denaturation in epithelial cells, disruption of intercellular junctions, and mucosal erosion. In infectious esophagitis, pathogenic agents (Candida albicans, Herpes simplex, Cytomegalovirus) directly invade mucosal epithelium; Candida forms superficial plaques while HSV and CMV create deeper ulcerations. In eosinophilic esophagitis, excessive Th2 immune response to food antigens → eosinophil infiltration (≥15/HPF) → mucosal inflammation and fibrosis → concentric stricture develops. The target sign on CT reflects different degrees of inflammation in wall layers: mucosa hyperemic (increased enhancement), submucosa edematous (fluid accumulation → low density), serosa mildly inflammatory (increased enhancement). This layered pattern is the pathognomonic imaging finding of inflammatory wall changes.
Three-layered wall structure on CT in inflammatory esophagitis: inner enhancing hyperemic mucosa, middle hypodense submucosal edema line, and outer enhancing serosa. This pattern is pathognomonic for inflammatory wall changes and distinguishes from asymmetric, layer-destructive thickening of malignant infiltration.
Target sign in the esophageal wall on portal venous phase: inner layer of enhancing hyperemic mucosa, middle layer of hypodense submucosal edema, and outer layer of enhancing serosa/muscularis. Wall thickness is usually 5-15 mm (normal <3 mm). Target sign is concentric and circumferential with symmetric wall thickening. Segmental involvement (reflux: distal 1/3; radiation: radiotherapy field) or diffuse involvement (infectious) may be seen.
Report Sentence
Concentric wall thickening with target sign (enhancing mucosa, hypodense submucosal edema, enhancing outer wall) in the esophagus is observed, consistent with inflammatory esophagitis.
Increased density in periesophageal fat tissue (dirty fat) in transmural inflammation. While normal mediastinal fat density is between -80 and -120 HU, these values increase to between -20 and -60 HU with inflammatory infiltration. Periesophageal fat infiltration suggests severe esophagitis — perforation or transmural necrosis risk should be evaluated.
Report Sentence
Increased density in periesophageal fat tissue (dirty fat) is observed, suggesting transmural inflammation.
Increased mucosal enhancement (mucosal hyperemia) in the esophagus in arterial phase. While normal esophageal mucosa shows minimal enhancement in arterial phase, inflammatory mucosa demonstrates prominent enhancement. Localized in distal esophagus suggests reflux, diffuse suggests infectious etiology. Mucosal enhancement intensity may correlate with inflammation severity.
Report Sentence
Increased mucosal enhancement (mucosal hyperemia) in the esophagus in arterial phase is observed, consistent with active mucosal inflammation.
Submucosal edema on T2-weighted images — seen as a hyperintense submucosal line in the esophageal wall. While mucosa and muscularis show lower signal on T2, edematous submucosa appears markedly hyperintense. This finding is the MRI equivalent of the target sign on CT. Acute inflammation may show diffusion restriction on diffusion-weighted imaging.
Report Sentence
A hyperintense line consistent with submucosal edema in the esophageal wall on T2-weighted images is observed.
Concentric, symmetric thickening of the esophageal wall on non-contrast CT (>3 mm, usually 5-15 mm). Wall density is at soft tissue density (30-50 HU). Intraluminal air or fluid creates contrast with the thickened wall. Thickening usually continues along a long segment. Hiatal hernia and dilated esophagus support reflux esophagitis.
Report Sentence
Concentric symmetric wall thickening of the esophagus on non-contrast CT is observed, consistent with inflammatory esophagitis.
On EUS evaluation of esophageal wall layers: thickened mucosa (hyperechoic, 1st and 3rd layers), expanded submucosa (hypoechoic, 2nd layer — due to edema), preserved muscularis propria (hypoechoic, 4th layer). Preservation of layer structure supports inflammatory etiology — layer disruption is seen in carcinoma. EUS assists endoscopy in evaluating superficial ulcerations and plaques (Candida).
Report Sentence
Preserved esophageal wall layers with expanded submucosa due to edema on EUS is observed; this finding is consistent with inflammatory esophagitis.
Criteria
Most common esophagitis type. Localized to distal 1/3 of esophagus. Hiatal hernia frequently accompanies. Risk of Barrett esophagus and stricture in chronic disease.
Distinct Features
Wall thickening in distal esophagus, hiatal hernia, dilated esophagus on CT. Erosions, ulcers, peptic stricture on barium. Risk of Barrett metaplasia (adenocarcinoma precursor) in longstanding cases.
Criteria
In immunosuppressed patients (HIV, transplant, chemotherapy). Candida: diffuse, superficial plaques ('shaggy esophagus'). HSV: small discrete ulcers (volcano-like). CMV: large deep ulcers.
Distinct Features
Diffuse wall thickening, multiple ulcerations on CT. Candida: 'shaggy' mucosa on barium. HSV: discrete volcano-like ulcers with surrounding normal mucosa. CMV: single or few deep ulcers, linear or oval, usually mid-distal esophagus. Endoscopic biopsy is diagnostic.
Criteria
Atopic background, food allergy, common in young males. Dysphagia (especially with solid foods) is main symptom. ≥15 eosinophils/HPF on endoscopy is diagnostic.
Distinct Features
Long-segment concentric stricture on CT/barium ('small-caliber esophagus'), trachealization (ring-like mucosal rings — 'feline esophagus'). Longitudinal fissures on barium. Severe stricture and food impaction in advanced cases. Lack of response to PPI distinguishes from reflux esophagitis.
Criteria
After thoracic radiotherapy (especially lung, esophageal, breast cancer treatment). Risk increases with radiation dose >30 Gy. Acute (during or immediately after treatment) or chronic (months-years later).
Distinct Features
Wall thickening confined to the radiotherapy field — sharp border reflects edge of radiation field. Edema and mucosal hyperemia in acute phase. Fibrotic stricture and mucosal atrophy in chronic phase. Accompanying radiation pneumonitis or pericarditis supports diagnosis.
Distinguishing Feature
Carcinoma shows asymmetric, irregular wall thickening with layer disruption; esophagitis shows concentric symmetric thickening with target sign. Lymphadenopathy is common in carcinoma; rare in esophagitis. Endoscopic biopsy is definitive.
Distinguishing Feature
Lymphoma may have more prominent wall thickening (>2 cm) with LAP and splenomegaly; esophagitis shows thinner thickening (<1.5 cm) with target sign. Lymphoma shows very low ADC on DWI.
Distinguishing Feature
Benign stricture may be the end stage of chronic esophagitis — fibrotic thickening, smooth margin, concentric narrowing. Absence of active inflammation findings (no target sign, no mucosal hyperemia) distinguishes stricture from active esophagitis.
Distinguishing Feature
Barrett esophagus is a complication of chronic reflux esophagitis — mucosal thickening in distal esophagus on CT may be similar but mucosal irregularity and nodularity are more prominent in Barrett's. Diagnosis is made by endoscopic biopsy. Barrett is an adenocarcinoma precursor requiring surveillance.
Urgency
routineManagement
medicalBiopsy
Not NeededFollow-up
3-monthEsophagitis treatment is etiology-based: PPI + lifestyle modification for reflux esophagitis; antifungal (Candida), antiviral (HSV/CMV) for infectious esophagitis; topical steroid + elimination diet for eosinophilic esophagitis; discontinuation of responsible medication for pill esophagitis; symptomatic treatment for radiation esophagitis. Excluding carcinoma on imaging is critical — endoscopic biopsy is needed for asymmetric thickening, LAP, or layer disruption. Complications: stricture (chronic), perforation (severe acute), Barrett metaplasia (chronic reflux), tracheoesophageal fistula (rare).
Reflux esophagitis is controlled with PPI therapy. Infectious esophagitis requires antifungal/antiviral treatment. Chronic reflux carries risk of progression to Barrett esophagus and subsequently adenocarcinoma. Complications include ulcer, stricture, perforation.