Beyond Acid Reflux: Mastering the Complex Inpatient Diagnosis and Tailored Management of Esophagitis

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.