What is the most likely diagnosis and appropriate management for a 25‑year‑old woman presenting with painful oral ulcers and bullous eruptions on the hands and feet?

Most Likely Diagnosis: Hand, Foot, and Mouth Disease (HFMD)

The most likely diagnosis in this 25-year-old woman with oral ulcers and bullous eruptions on hands and feet is hand, foot, and mouth disease (HFMD), which should be managed with supportive care including oral corticosteroids, meticulous wound care, and pain control.

Clinical Reasoning

This presentation is classic for HFMD in an adult, which can occur after exposure to infected children. The triad of oral ulcers plus bullous lesions specifically on hands and feet is pathognomonic. While HFMD is typically considered a pediatric disease, adults can develop severe manifestations, particularly after close contact with infected children 1.

Key Diagnostic Features to Confirm:

• Recent exposure history: Contact with children (daycare, babysitting, household)
• Distribution pattern: Lesions specifically on palms/soles and oral cavity
• Timing: Acute onset (days to 1-2 weeks)
• Associated symptoms: Fever, malaise, sore throat preceding eruption

Differential Diagnoses to Exclude

Autoimmune Bullous Diseases (Less Likely)

While pemphigus vulgaris presents with oral ulcers and can have skin involvement, several features make this less likely:

• PV typically starts with oral lesions that persist for weeks to months before skin involvement 2
• Skin lesions in PV are flaccid bullae that rupture easily, not specifically localized to hands/feet
• PV affects trunk, scalp, and intertriginous areas more commonly 3
• Age 25 is younger than typical PV onset

Bullous Pemphigoid (Unlikely)

• BP typically spares mucosa or has minimal oral involvement 4
• Presents with tense bullae on trunk and limbs, not specifically hands/feet
• More common in elderly patients

Stevens-Johnson Syndrome/Erythema Multiforme (Consider if severe)

• Would expect target lesions, more extensive mucosal involvement (eyes, genitals)
• Usually medication or infection-triggered 5

Management Algorithm

Immediate Assessment (First Visit)

1. Confirm diagnosis clinically - exposure history + characteristic distribution
2. Assess severity - ability to eat/drink, pain level (VAS score), extent of lesions
3. Rule out STIs if genital involvement - HSV, syphilis testing 1

Treatment Protocol

For Moderate to Severe Cases:

• Oral prednisone: 0.5-1 mg/kg/day for 5-7 days, then taper 1
• Topical corticosteroids for oral lesions:
  • Betamethasone sodium phosphate 0.5 mg in 10 mL water as rinse-and-spit 2-4 times daily 3
  • OR clobetasol 0.05% ointment mixed in Orabase for localized lesions 3
• Pain control:
  • Topical anesthetics (lidocaine viscous) before meals
  • Barrier preparations (Gelclair) for oral comfort 3
  • Systemic analgesics as needed

For Mild Cases:

• Supportive care alone may suffice
• Topical treatments for symptom relief

Wound Care (Critical Component)

• Gentle debridement of necrotic tissue and crusts 1
• Antiseptic rinses for oral hygiene 3
• Soft paraffin or emollients for lip/skin lesions 5
• Maintain hydration and nutrition

Expected Timeline

• Resolution typically occurs over 3 weeks 1
• Oral lesions may persist longer than skin lesions

Common Pitfalls to Avoid

1. Over-investigation: Do not pursue extensive autoimmune workup (DIF, indirect IF, ELISA) if clinical picture clearly fits HFMD with appropriate exposure history
2. Under-treatment of pain: Adults experience more severe pain than children; aggressive pain management improves oral intake
3. Premature steroid discontinuation: Complete the taper to prevent rebound
4. Missing secondary infection: Monitor for bacterial superinfection of erosions

When to Reconsider Diagnosis

Refer for biopsy and autoimmune workup if:

• No improvement after 2 weeks of treatment
• Lesions persist beyond 4 weeks
• No clear exposure history
• Recurrent episodes
• Progressive worsening despite treatment
• Atypical distribution (trunk, scalp involvement)

In such cases, consider pemphigus vulgaris or bullous SLE and obtain histopathology with direct immunofluorescence 3, 6.