In this episode of Hospital Medicine Unplugged, we sprint through esophagitis—spot it fast, pin the cause, heal the mucosa, prevent complications.

We open with the do-firsts: identify alarm features (dysphagia, weight loss, GI bleed, IDA), review meds (bisphosphonates, NSAIDs, tetracyclines), immune status, tube size/position, and supine time. Frame the epidemiology for inpatients: ~1/3 of scoped inpatients have esophagitis, morbidity is meaningful, and higher short-term mortality usually mirrors comorbidity—not the mucositis itself. Prefer fine-bore NG tubes when you must feed.

Call the diagnosis: symptoms alone are messy. Endoscopy for alarms or refractory symptoms—grade erosions, biopsy to confirm EoE, rule out Candida/HSV/CMV, pill injury, Barrett’s, strictures, or malignancy. Add pH monitoring/manometry only when the picture stays hazy or before surgery.

Etiology plays (treat what you find):
• Reflux (GERD)—most common inpatient cause.
• EoE—eosinophilic infiltration; dysphagia/food impaction.
• Pill injury—temporal to culprit med, worse if taken without water/lying down.
• Infectious—Candida/HSV/CMV in the immunocompromised.
• Don’t forget motility disorders and functional overlap.

Treatment—build the anti-acid backbone for reflux esophagitis:
• PPIs first-line for symptoms + mucosal healing; H2RAs for mild or if PPIs can’t be used. Use the lowest effective dose long term; reassess need to avoid PPI baggage (infections, micronutrients).
• Refractory? BID PPI, switch agents, add H2RA at night, alginates, or baclofen (careful selection).
• Surgery (fundoplication) only for documented pathologic reflux with persistent symptoms on optimal therapy; endoscopic options are investigational.

Eosinophilic esophagitis (EoE) moves:
• Start with PPI therapy (anti-inflammatory effects beyond acid).
• Add topical steroids (swallowed fluticasone or viscous budesonide) for histologic remission.
• Dietary elimination works but watch feasibility.
• Endoscopic dilation for fixed rings/strictures or severe dysphagia.

Infectious & pill-induced:
• Candida → systemic azoles; HSV/CMV → antivirals guided by histology/NAAT.
• Stop/substitute offending pills; insist on water + remaining upright ≥30 min.

ICU & hospital specifics:
• Stress ulcer prophylaxis only for true indications (coagulopathy, prolonged ventilation). IV acid suppression (PPI or H2RA) acceptable—no clear winner for prophylaxis.
• For acute upper GI bleeding, IV PPI post-hemostasis to reduce rebleed.
• Minimize supine time, elevate HOB, and choose fine-bore tubes to reduce mechanical injury/bile reflux.

Prevention & follow-up:
• Lifestyle nudges: HOB elevation, no late meals, weight loss when relevant, trim trigger foods and tobacco.
• Reassess need for chronic PPI; step-down/stop when safe (no erosive disease/Barrett’s).
• Arrange follow-up for healing, stricture detection, and Barrett’s surveillance when indicated.

Complications—don’t miss them: UGIB, strictures, Barrett’s, rare perforation/fistula with aspiration risk—act early (endoscopic therapy, CT + surgical consult for suspected perforation).

System moves that stick: (1) triage by alarm features; EGD + biopsy when indicated; (2) default PPI-first for erosive disease with dosing/meal-timing education; (3) EoE pathway (PPI → topical steroid → diet ± dilation); (4) targeted infectious therapy after sampling; (5) medication stewardship to avoid pill injury; (6) ICU prophylaxis by criteria only; (7) tube care protocol favoring fine-bore and HOB elevation; (8) deprescribing and surveillance plan at discharge.

Fast, endoscopy-led, and cause-targeted—treat reflux with PPIs, tailor therapy to EoE/infectious/pill injury, protect the mucosa, and engineer the inpatient environment to prevent harm.