Treatment for Skin Allergy

1. Urticaria (Hives) and Angioedema

• Common triggers include foods (seafood, tree nuts, eggs), medications (penicillin, aspirin, NSAIDs, ACE inhibitors), infections, stress, insect stings, and latex.

• Second-generation, non-sedating antihistamines are the mainstay of treatment (e.g., cetirizine, loratadine, fexofenadine, bilastine). These are preferred during daytime because they do not cause sedation.
• First-generation antihistamines (e.g., diphenhydramine, hydroxyzine, chlorphenamine) are alternatives but cause sedation - useful at night for sleep disruption from itch.
• H2 blockers (famotidine, ranitidine) can be added alongside H1 antihistamines for refractory cases.

• Omalizumab (anti-IgE monoclonal antibody) is indicated when urticaria does not respond to antihistamines even at high doses.
• Immunosuppressives (cyclosporine, systemic corticosteroids short-term) may be used for severe, refractory disease.

• Epinephrine (intramuscular) is first-line if anaphylaxis is present.
• Short courses of oral or IV corticosteroids reduce late-phase reactions.

2. Allergic Contact Dermatitis

• Rosen's Emergency Medicine, p. 1792-1799

3. Atopic Dermatitis (Eczema)

• Regular moisturizer/emollient use to restore skin barrier
• Identify and avoid personal triggers (irritants, sweat, certain soaps/detergents)
• Lukewarm baths followed immediately by moisturizer

• Topical corticosteroids - the primary treatment for flares; potency chosen based on body site and age
• Topical calcineurin inhibitors (tacrolimus, pimecrolimus) - steroid-sparing alternatives, especially for face and skin folds
• Dupilumab (anti-IL-4/IL-13 biologic) - for moderate-to-severe atopic dermatitis unresponsive to topicals; highly effective
• JAK inhibitors (upadacitinib, abrocitinib) - newer oral options for moderate-to-severe disease
• Oral corticosteroids - short-term only, for severe flares
• Phototherapy (narrowband UVB) - for chronic, widespread disease

4. Allergic Rhinitis with Skin Component

5. General Principles Across All Skin Allergies

Note: This is a general overview. A dermatologist or allergist should evaluate the specific type of skin allergy for targeted patch testing, allergen identification, and personalized treatment.

Sources: Fitzpatrick's Dermatology Vol. 1-2; Goldman-Cecil Medicine; Rosen's Emergency Medicine; 2026 ARIA-EAACI guidelines.

Emergency Management of Acute Asthma - With Dosages

Step 1 - Rapid Severity Assessment

Immediate transfer to ICU if: drowsy, confused, silent chest, or cyanosis.

Step 2 - Oxygen

• Target SpO2: 93-95% in adults/adolescents; ≥94% in children 6-12 years
• Deliver via nasal cannula or face mask - titrate to target
• Use non-rebreather mask if SpO2 <90% despite low-flow O2
• Avoid high-flow uncontrolled O2 - hyperoxygenation can worsen V/Q mismatch

Step 3 - Short-Acting Beta-2 Agonists (SABA) - FIRST-LINE

GINA 2025 note: Doses of SABA for initial treatment have been clarified to avoid excessive use. For mild exacerbations, a single dose is sufficient before reassessment.

Clinical tip: pMDI + spacer is as effective as nebulizer in cooperative patients. Nebulize with oxygen in severe exacerbations.

Step 4 - Ipratropium Bromide (SAMA) - Add for Moderate-Severe

Onset: 30-120 min; duration: up to 6 hours. Do NOT use alone - it's an add-on to SABA. For hospitalized patients, no additional benefit has been shown beyond the ED phase.

Step 5 - Systemic Corticosteroids - Give Within 1 Hour

Taper: Not needed for courses <2 weeks. Tapering is only needed if the patient was already on chronic systemic steroids.

Step 6 - IV Magnesium Sulfate - For Severe/Refractory Cases

GINA 2025: Nebulized magnesium is no longer recommended. IV magnesium only. Evidence: Beneficial in adults with severe airway obstruction (FEV1 <25% predicted); reduces hospital admissions. Side effects (dose-related): Warmth/flushing, nausea, muscle weakness, loss of DTRs, hypotension, respiratory depression - monitor closely.

Step 7 - Reassess at 1 Hour

• Improving (PEF >40-60%, SpO2 recovering): Continue SABA as needed, taper frequency, continue oral steroids. Can consider discharge with plan.
• Not improving (PEF <40%, persistent hypoxia): Admit, continue intensive nebulization, consider magnesium sulfate if not already given.
• Deteriorating: Consider ICU transfer, NIV, or intubation.

Step 8 - Life-Threatening Asthma / Near-Fatal Attack

Epinephrine (Adrenaline)

• Indicated only if anaphylaxis is also present - not routine for standard asthma exacerbations
• IM: 0.3-0.5 mg (0.3-0.5 mL of 1:1000) into the mid-outer thigh
• IV epinephrine reserved for peri-arrest scenarios

Terbutaline (parenteral - if inhaled SABAs ineffective)

• Children: 0.01 mg/kg SC/IM (max 0.3 mg), repeat every 20 min x 3 doses
• Adults: 0.25 mg SC; repeat after 15-30 min (max 0.5 mg in 4 hours)

Heliox (60-80% helium / 20-40% O2)

• Consider when PEF <30% predicted, labile asthma, previous intubation, or failure of ventilation
• Reduces airway resistance and work of breathing; improves distal delivery of nebulized bronchodilators
• Delivered by non-rebreather mask or via mechanical ventilator

Non-Invasive Ventilation (NIV / BiPAP)

• Consider in severe refractory asthma in children and selected adults to avoid intubation
• Used with caution - increasing use reported in paediatric severe asthma

Intubation - Last Resort

• Indications: respiratory arrest, progressive exhaustion, altered consciousness, worsening hypercapnia/acidosis
• Use rapid sequence intubation (RSI)
• Post-intubation strategy: low RR (10-14/min), high inspiratory flow, long expiratory time (I:E 1:3 or longer) to avoid breath-stacking (auto-PEEP)
• Avoid benzodiazepines and sedatives in non-intubated patients

Ketamine

• IV dissociative anaesthetic with bronchodilator properties
• Not yet recommended as routine for non-intubated patients (insufficient evidence)
• May be considered at induction for RSI in severe asthma (dissociative anaesthetic dose: 1.5-2 mg/kg IV)

What NOT to Do

• No sedatives in non-intubated patients (respiratory depression risk)
• No nebulized magnesium (GINA 2025 no longer recommends it)
• No IV methylxanthines (theophylline/aminophylline) routinely - no added efficacy, increased adverse events
• No antibiotics unless clear objective evidence of bacterial infection
• No routine chest X-ray or blood gases unless clinical indication (suspected pneumothorax, pneumonia, monitoring ventilation)
• No LABAs alone as rescue - only in combination with ICS

Summary Algorithm

Acute Asthma → Assess Severity
        ↓
OXYGEN → target SpO2 93-95%
        ↓
SABA (salbutamol) → 4-10 puffs pMDI or 2.5 mg nebulized q20 min x 3
        ↓ (if moderate-severe)
+ IPRATROPIUM 0.5 mg nebulized x 3 doses alongside SABA
        ↓
SYSTEMIC STEROIDS within 1 hour:
   Oral prednisolone 40-50 mg (adults) / 1-2 mg/kg (children)
        ↓
Reassess at 1 hour
        ↓
If severe, not responding:
   IV MAGNESIUM SULFATE 2 g over 20 min (adults)
        ↓
Still failing:
   Parenteral beta-agonist / Heliox / NIV / Intubation (ICU)

Recent evidence (2025): Two 2025 systematic reviews (PMID 40562458 and 40562459) confirm IV magnesium sulfate reduces hospital admissions when added to standard SABA + steroids in children with acute asthma. Aminophylline provides no additional benefit in children over standard first-line treatment.

Sources: Rosen's Emergency Medicine; Goodman & Gilman's Pharmacology; GINA 2025 Summary Guide; ABEM Practice Advance 2025

Answer: B. Perioral Dermatitis ✓

Why This is the Correct Diagnosis

1. Red itchy rash around the mouth - perioral distribution of papules/pustules
2. Sparing of the vermilion border - this is the pathognomonic feature of perioral dermatitis. There is a characteristic clear zone of ~5 mm between the lip margin and the affected skin. The lip itself is always spared.

Why the Other Options are Wrong

About Perioral Dermatitis

• Who gets it: Young women aged 20-35 are the classic demographic (also occurs in children)
• Presentation: Small inflammatory papules and pustules grouped around the mouth, with variable scaling; occasionally itchy or burning
• Key triggers: Fluorinated topical corticosteroids (most common cause), fluoride-containing toothpastes, inhaled corticosteroids
• Histology: Perifollicular and perivascular lymphohistiocytic infiltrate - resembles rosacea

Treatment

1. Stop any topical/inhaled fluorinated corticosteroids (first and most important step - though expect a brief "rebound flare" initially)
2. Topical: Metronidazole, azelaic acid, adapalene, ivermectin, or pimecrolimus 1% cream
3. Oral antibiotics (for moderate-severe): Doxycycline (adults), erythromycin (children)
4. Tacrolimus 0.1% ointment - useful to bridge the rebound period after stopping steroids

Sources: Fitzpatrick's Dermatology Vol. 1-2, p. 1484; Andrews' Diseases of the Skin, p. 296

Topical Treatments for Perioral Dermatitis

Step 0 - Stop the Trigger First

Topical Antibiotics (First-Line)

Topical Anti-inflammatory / Calcineurin Inhibitors

These are especially valuable if the patient was on prolonged topical corticosteroids - they help calm the rebound flare while avoiding further steroid use.

Topical Retinoid

Topical Keratolytic / Anti-inflammatory

Topical Antiparasitic (for Demodex-associated cases)

What to AVOID Topically

• Fluorinated topical corticosteroids (betamethasone, clobetasol, triamcinolone) - they perpetuate and worsen the condition
• Even mild non-fluorinated steroids should be used with great caution if at all
• Greasy heavy moisturizers/cosmetics that may occlude pores

Practical Treatment Approach

Mild (steroid-triggered):
  Stop topical corticosteroid (gradually) 
  + Topical metronidazole 0.75% gel BD x 8 weeks
  + Pimecrolimus 1% cream to manage rebound

Mild (no steroid exposure):
  Topical metronidazole 0.75% gel OR azelaic acid 15-20% BD x 6-8 weeks

Moderate-Severe or Refractory:
  Topical agent + Oral doxycycline 100 mg daily (adults) 
                 OR Oral erythromycin (children)
  Duration: 6-8 weeks

Sources: Fitzpatrick's Dermatology, p. 1485; Andrews' Diseases of the Skin, p. 296; Dermatology 5e (Bolognese)