Esophagitis: Infectious, Pill-Induced & Caustic Injury
Read the ulcer, respect the pill, and never make a caustic patient vomit
Infectious esophagitis
Odynophagia. Painful swallowing signals mucosal inflammation or ulceration rather than obstruction. In a patient with HIV and a low CD4 count, a transplant, chemotherapy, or steroid therapy, think Candida, HSV, or CMV; in a healthy patient who just swallowed a pill with little water, think pill esophagitis.
| Feature | Candida | HSV | CMV |
|---|---|---|---|
| Host | HIV (AIDS-defining), diabetes, steroids, antibiotics | Immunocompromised, also healthy hosts | HIV with CD4 <50, transplant |
| Endoscopy | Adherent white-yellow plaques | Multiple small punched-out "volcano" ulcers with raised edges | Few large, shallow, longitudinal ulcers |
| Histology | Yeast and pseudohyphae | Ulcer edge: multinucleated giant cells, ground-glass nuclei, Cowdry A inclusions | Ulcer base: enlarged cells with owl's-eye intranuclear and cytoplasmic inclusions |
| Treatment | Oral fluconazole 14–21 days | Acyclovir (IV if unable to swallow) | IV ganciclovir, then valganciclovir; foscarnet if resistant |
Candida. The most common infectious esophagitis. Odynophagia plus oral thrush in a patient with HIV justifies empiric systemic fluconazole without endoscopy; if symptoms do not improve within 3–5 days, perform EGD with biopsy to look for a viral cause or resistant yeast. Topical nystatin or clotrimazole can treat thrush but not esophageal disease, and fluconazole-refractory infection is treated with an echinocandin or another azole.
HSV. Usually HSV-1, with abrupt severe odynophagia, often fever, and sometimes herpes labialis. It occurs in immunocompetent hosts as well.
CMV. Pain tends to be more gradual. Because CMV infects endothelial and stromal cells, the diagnostic cells lie in the ulcer base, whereas HSV infects squamous epithelium and is found at the ulcer edge. Both viruses need tissue (histology, immunostains, PCR), whereas Candida is usually recognized by its plaques.
Pill-induced esophagitis
Mechanism. A tablet that lodges in the esophagus releases concentrated drug against the mucosa, producing a discrete ulcer with normal surrounding mucosa, usually at a point of narrowing such as the level of the aortic arch. Risk rises when pills are taken with little water or right before lying down.
- Doxycycline and other tetracyclines (the classic acne or travel-medicine scenario)
- Bisphosphonates such as alendronate
- Potassium chloride tablets, NSAIDs, ferrous sulfate, quinidine
Presentation and care. Sudden retrosternal pain and odynophagia, sometimes hours after a bedtime dose. Stop the drug or switch to a liquid formulation where possible and give supportive acid suppression, sucralfate, and analgesia; most ulcers heal within days to weeks.
Prevention: take high-risk pills with a full glass of water (about 240 mL) and stay upright for at least 30 minutes. Bisphosphonates are taken on waking with plain water, fasting and upright for 30 minutes (60 minutes for ibandronate).
Caustic ingestion
Alkali versus acid. Alkalis (lye, drain and oven cleaners) are often odorless and swallowed in larger volumes; they cause liquefactive necrosis that penetrates deeply, so the esophagus bears the brunt and perforation is a real risk. Acids (toilet bowl and pool cleaners, battery acid) cause coagulative necrosis, and the resulting eschar limits depth; the stomach, especially the antrum and pylorus, is injured more.
Never induce emesis (re-exposes the esophagus), attempt neutralization (heat-generating reaction), give activated charcoal (does not bind caustics and obscures endoscopy), or pass a blind nasogastric tube (can perforate burned tissue).
- AirwayStridor, hoarseness, or drooling signal airway injury; intubate early, preferably fiberoptically.
- SupportNPO, IV fluids, analgesia.
- Exclude perforationChest, back, or abdominal pain, peritonitis, or subcutaneous air: upright films and CT; perforation requires surgery.
- EGD within 24 hoursGrades the burn (Zargar scale) and guides feeding and disposition; avoid scoping roughly 5–15 days after ingestion, when the healing wall is weakest.
Late complications. Deep circumferential or necrotic burns (grade 2b–3) scar into strictures over weeks to months and are treated with serial dilation; corticosteroids do not prevent them. Acid injury can cause gastric outlet obstruction. Lye injury raises the risk of esophageal squamous cell carcinoma (not adenocarcinoma, which arises from Barrett esophagus) decades later, so long-term endoscopic surveillance is advised.
Food bolus and foreign-body impaction
Timing. Perform EGD within 24 hours for a food bolus or foreign body in the esophagus. Go emergently for complete obstruction (drooling, inability to handle secretions), a button battery, or a sharp object in the esophagus. A button battery shows a double-ring (halo) sign on x-ray and starts damaging tissue within about 2 hours, risking fistula into the aorta or trachea.
Pitfalls. Barium swallow risks aspiration and coats the mucosa before endoscopy. Glucagon is sometimes tried but should not delay endoscopy, and papain (meat tenderizer) is contraindicated because it can digest the esophageal wall.
Find the cause. After clearing the impaction, biopsy for eosinophilic esophagitis (a young atopic man with recurrent food impaction is the classic patient) and look for a Schatzki ring or peptic stricture.