I now have comprehensive content from both Tintinalli's and Rosen's. Let me compile the full response.
Emergency Room Skin Disorders
Based on Tintinalli's Emergency Medicine & Rosen's Emergency Medicine
Approach to the Dermatologic Patient in the ED
Both Tintinalli and Rosen emphasize a structured approach: identify whether the presentation is life-threatening first, then characterize the morphology, distribution, and associated systemic findings. The most dangerous skin disorders in the ED fall into three groups:
- Severe generalized drug/immune reactions (SJS, TEN, DRESS, pemphigus)
- Infectious emergencies with skin signs (meningococcemia, necrotizing fasciitis, cellulitis)
- Vascular/purpuric disorders (purpura fulminans)
PART 1 - SEVERE GENERALIZED SKIN DISORDERS
(Tintinalli Chapter 249; Rosen's Chapter 118/23)
1. Erythema Multiforme (EM)
Tintinalli's perspective:
"Until the early 1990s, erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis were classified as a continuum of a spectrum of disease; it is now appreciated that erythema multiforme is distinct from the more serious or even life-threatening Stevens-Johnson syndrome and toxic epidermal necrolysis."
Causes:
- Adults: drugs (barbiturates, penicillins, sulfonamides, NSAIDs, phenothiazines)
- Children: predominantly infections - HSV-1/HSV-2 account for 70-90% of all EM cases; Mycoplasma pneumoniae also common
Clinical Features:
- Abrupt onset rash, sometimes preceded by burning; pruritus usually absent
- Classic "target" (iris) lesion: 2-3 zones - dark center, lighter surrounding zone, red outer ring
- Symmetric distribution on hands, feet, extensor surfaces
- EM minor: limited distribution
- EM major: oral mucosal involvement; ophthalmologic lesions in ~70% of cases
Fig: Target (iris) lesions of erythema multiforme - FIGURE 249-3 (Tintinalli's Emergency Medicine)
Management (Tintinalli TABLE 249-2):
| Severity | Treatment | Disposition |
|---|
| EM Minor | Prednisone 60-80 mg/day PO x 3-5 days; oral antihistamine; acyclovir if HSV-related | Outpatient; PCP/derm follow-up |
| EM Major (SJS) | Remove trigger; resuscitate; fluid/electrolytes; methylprednisolone 125 mg IV q6h or equivalent; diphenhydramine + viscous lidocaine rinses for oral lesions; Burow's solution (5% aluminum acetate) with cool compresses for blisters; ophthalmology consult; antibiotics only if established infection | Admit - acute care/burn unit; intensivist + dermatologist consults |
2. Stevens-Johnson Syndrome (SJS) / Toxic Epidermal Necrolysis (TEN)
Classification (Tintinalli):
"Some authorities include Stevens-Johnson syndrome as a severe form of erythema multiforme major, whereas others consider it a less severe form of toxic epidermal necrolysis. Perhaps the most appropriate classification approach for the emergency physician is to recognize that the severity and extent of epidermal detachment reflects the spectrum of disease."
- SJS: <10% BSA epidermal detachment
- SJS/TEN overlap: 10-30% BSA
- TEN: >30% BSA detachment
Precipitating drugs: Sulfonamides (TMP-SMX most common), anticonvulsants (phenytoin, carbamazepine, lamotrigine), allopurinol, antibiotics, NSAIDs, nevirapine.
ED Clinical Presentation:
- Flu-like prodrome (fever, malaise, myalgias) 1-4 days before skin lesions
- Maculopapular rash progressing rapidly to confluent erythema, bullae, and skin sloughing
- Mucous membranes: painful erosions of oral, ocular, urogenital mucosae in virtually all SJS cases
- Positive Nikolsky sign (lateral pressure causes epidermal separation)
- May have ARDS, hepatitis, renal failure
Tintinalli TABLE 249-2 - Management of TEN:
| Step | Action |
|---|
| Remove trigger | Stop all suspected causative drugs immediately |
| Resuscitation | Airway (respiratory involvement possible), circulatory support |
| Fluids | Fluid + electrolyte management (~2/3 of burn Parkland formula) |
| Wound care | Burow's solution compresses; nonstick dressings; leave sloughed epidermis in place as biologic dressing |
| Infection | Antibiotics only for confirmed infection - NOT prophylactic |
| Specialist care | Ophthalmology, gynecology, urology as indicated; dermatologist mandatory |
| Disposition | ICU or burn unit; intensivist + dermatologist consults |
Prognostic score - SCORTEN (1 point each for: age >40, HR >120, BSA involved >10%, BUN >28 mg/dL, serum glucose >14 mmol/L, bicarbonate <20 mEq/L, malignancy): mortality 3.2% at 0-1 points, >90% at ≥5 points.
3. Pemphigus Vulgaris
Autoimmune blistering disorder producing flaccid bullae that rupture easily, causing extensive skin and mucosal erosions. Risk of superinfection and sepsis.
Tintinalli TABLE 249-2 - Management:
| Action |
|---|
| Remove any drug trigger |
| Resuscitate (respiratory +/- circulatory) |
| Fluid and electrolyte management |
| Antibiotics only for confirmed infection (not prophylactic) |
| Immunosuppressive therapy |
| Plasmapheresis |
| Immunoglobulin therapy (IVIG) |
| Disposition: Admit - acute care/burn unit; intensivist + dermatologist |
4. Exfoliative Dermatitis (Erythroderma)
Generalized erythema and scaling covering >90% BSA. Causes: psoriasis, atopic dermatitis, drug reaction, Sézary syndrome (T-cell lymphoma), idiopathic.
Tintinalli TABLE 249-2:
| Severity | Treatment | Disposition |
|---|
| Minor | Remove trigger; symptomatic care (oral pain agents, antihistamines PRN) | Outpatient; PCP/derm follow-up |
| Major | Resuscitate; fluid/electrolytes; warm environment (thermoregulation impaired); emollients; treat infection; systemic therapy per dermatologist | Admit; correct hypothermia/hypovolemia; dermatology consult before systemic corticosteroids |
5. DRESS Syndrome (Drug Rash with Eosinophilia and Systemic Symptoms)
(Tintinalli Chapter 249)
"DRESS syndrome is a severe adverse drug reaction that usually develops within 8 weeks of initiation of drug therapy. Aromatic anticonvulsants (such as phenytoin and phenobarbital), allopurinol, and sulfa medications are the most common culprits."
Clinical features:
- Onset 2-8 weeks after drug initiation
- Fever + rash + internal organ involvement (liver, kidneys, hematologic most common)
- Rash polymorphic: can mimic exfoliative dermatitis or SJS
- Eosinophilia in ~30%; hepatic and renal dysfunction
- Genetic predisposition present; must warn family members
Fig: DRESS syndrome caused by phenytoin - FIGURE 249-7 (Tintinalli's Emergency Medicine)
Management (Tintinalli):
- Immediate cessation of suspected culprit drug
- Systemic steroids in severe cases (hepatitis, pneumonitis, or extensive exfoliative dermatitis)
- Supportive care: antipyretics, antipruritic medications
- Hospital admission; monitor LFTs, renal function, CBC
PART 2 - PURPURIC / VASCULAR EMERGENCIES
(Tintinalli Chapter 249; Rosen's Chapter 118)
6. Meningococcemia
(Rosen's: Chapter 118 - "Bacterial Meningitis and Meningococcemia")
(Tintinalli: Chapter 249 - "Purpuric Disorders")
"A rash is frequently noted on presentation and is an invaluable clue to the correct diagnosis early in the disease course." - Tintinalli
Pathogen: Neisseria meningitidis (gram-negative diplococcus)
Population: <20 years; highest risk in children/infants <5 years; military recruits, college dorms
Clinical spectrum (Rosen's):
| Form | Features |
|---|
| Bacteremia | Febrile illness ± rash; no meningeal signs |
| Meningococcal meningitis | Fever, headache, neck stiffness; rash in >50%; seizures in 20% |
| Meningococcal septicemia | Lethargy, poor perfusion, cyanosis; hemorrhagic skin lesions in 28-77% |
| Fever + non-blanching rash | Up to 30% - can progress to fulminant disease if untreated |
| Purpura fulminans | Rapidly spreading ecchymoses + gangrene; most advanced form |
Skin findings (Tintinalli):
- Petechiae, urticaria, hemorrhagic vesicles, macules, maculopapules
- Classic: petechiae on extremities and trunk, palms, soles, head, mucous membranes
- Petechiae evolve into palpable purpura with gray necrotic centers - pathognomonic
- Mechanism: organism invades and destroys endothelium causing infectious vasculitis
Fig: Early meningococcemia with petechiae evolving into purpuric lesions - FIGURE 249-8 (Tintinalli's)
Investigations (Rosen's):
- Blood cultures (positive in 50-80%); obtain before antibiotics if no delay
- Lumbar puncture in stable patients without DIC
- Gram stain of petechial scrapings: gram-negative diplococci in up to 2/3 of cases
- PCR of buffy coat/CSF - most sensitive and specific; unaffected by prior antibiotics
- CBC (bandemia typical), coagulation profile, metabolic panel, CXR, lactate, echo if myocarditis suspected
Treatment (Rosen's):
| Situation | Antibiotic |
|---|
| Standard proven meningococcemia | Penicillin G 4 million units IV q4h (adults); 250,000-300,000 units/kg/day IV q4h (children) |
| First-line empirical (ID uncertain) | Ceftriaxone or cefotaxime IV |
| Penicillin-allergic | Chloramphenicol |
- Dexamethasone 0.4-0.6 mg/kg/day q6h x 4 days for bacterial meningitis - give before first antibiotic dose if possible
- Corticosteroids in meningococcemia without meningitis: controversial; consider only if persistent shock despite fluids + vasopressors (possible adrenal insufficiency)
- Fulminant meningococcemia: airway management + IV fluid resuscitation + vasopressors; FFP for DIC bleeding; hemodialysis if anuric; correct electrolyte/acid-base abnormalities
- Plasmapheresis, blood exchange, ECMO: described but limited data
Chemoprophylaxis for close contacts (Rosen's):
- Rifampin 10 mg/kg (max 600 mg) PO q12h x 4 doses (neonates: 5 mg/kg; warn about urine/secretion discoloration)
- Alternative: Ceftriaxone IM 125 mg (children <15 years) or 250 mg (>12 years) - preferred in pregnancy
- Alternative: Ciprofloxacin 500 mg PO single dose (adults)
7. Purpura Fulminans
(Tintinalli Chapter 249)
"Purpura fulminans is a rare vascular disorder characterized by fever, shock, multiorgan failure, and the rapid development of hemorrhagic skin necrosis."
Causes: Hereditary or acquired Protein C/S deficiency; activated protein C resistance; any cause of DIC (including meningococcemia)
Dermatologic triad (Tintinalli):
- Widespread ecchymoses
- Hemorrhagic bullae
- Epidermal necrosis
Also: cyanosis with necrosis of nose, ears, genitalia; distal extremity gangrene
Management:
- Treat underlying sepsis aggressively
- DIC management: FFP, cryoprecipitate, platelets
- Protein C concentrate where available
- ICU; surgical care for gangrenous tissue
PART 3 - INFECTIOUS SKIN EMERGENCIES
(Tintinalli Chapters 192-194)
8. Cellulitis and Erysipelas
Tintinalli Disposition and Follow-up:
- Admit if: systemic toxicity, diabetes mellitus, alcoholism, immunosuppression
- Discharge if: healthy, no systemic toxicity - outpatient with 2-3 day follow-up; mark the perimeter of infection with indelible marker to monitor progression
Tintinalli TABLE 192-4 - Empiric Antibiotic Treatment:
| Severity | Antibiotic |
|---|
| Mild (no systemic infection, drainable abscess, immunocompetent) | No antibiotics required after complete drainage |
| Moderate (purulent cellulitis, no systemic infection) | TMP-SMX DS 1-2 tabs PO BID x 7-10 days OR Doxycycline 100 mg PO BID x 7-10 days OR Clindamycin 300-450 mg PO QID x 7-10 days |
| Severe (systemic infection/sepsis, immunocompromised) - IV antibiotics | For MRSA: Vancomycin 15 mg/kg IV q12h OR Linezolid 600 mg IV q12h OR Daptomycin 4 mg/kg IV q24h OR Telavancin 10 mg/kg IV q24h |
For non-purulent cellulitis and erysipelas (primarily streptococcal): beta-lactams are appropriate (cefazolin IV, or oral cephalexin/dicloxacillin for mild-moderate).
9. Necrotizing Fasciitis
(Tintinalli Chapter 149 / Chapter 7 in postoperative complications section)
"Hallmark of fasciitis are the presence of marked systemic toxicity and pain out of proportion to local findings." - Tintinalli
Risk factors: Diabetes mellitus, hypertension, obesity, alcoholism, immunosuppression, peripheral vascular disease - but also occurs in young, healthy individuals.
Early differentiation from cellulitis is difficult - Tintinalli notes CT findings that help:
- Asymmetric fascial thickening
- Gas tracking along fascial planes (pathognomonic)
- Focal fluid collections
- MRI: sensitive but not entirely specific
Late signs: Deep pain with surface hypesthesia; crepitation; bullae; rapidly progressing skin necrosis
Management (Tintinalli):
- Antibiotics - Triple therapy: Penicillin or cephalosporin + aminoglycoside + clindamycin (clindamycin inhibits toxin production)
- Immediate surgical debridement - do not delay
- ICU admission; fluid resuscitation; monitor electrolytes
PART 4 - URTICARIA, ANGIOEDEMA, AND ANAPHYLAXIS
(Tintinalli Chapter 14)
10. Urticaria
"Urticaria, or hives, is a cutaneous reaction marked by acute onset of pruritic, erythematic wheals of varying size that generally are described as 'fleeting.'" - Tintinalli
ED Management (Tintinalli):
- Identify and remove offending agent
- H1 antihistamines ± corticosteroids (note: adding corticosteroids to non-sedating antihistamines may not improve relapse or itch reduction)
- Epinephrine for severe or refractory cases
- H2 antihistamine (ranitidine/famotidine) in severe/chronic/unresponsive cases
- Cold compresses for symptomatic relief
- Refer to allergist for severe, recurrent, or refractory cases
11. Angioedema
(Tintinalli Chapter 14 - TABLE 14-6)
"Angioedema of the tongue, lips, and face has the potential for airway obstruction." - Tintinalli
ACE inhibitor-induced angioedema occurs in 0.1-0.7% of patients on ACE inhibitors. Mechanism involves bradykinin and substance P - does NOT respond well to antihistamines/steroids/epinephrine.
Tintinalli TABLE 14-6 - Pharmacologic Treatment of Angioedema:
| Agent | Dose | Notes |
|---|
| C1 esterase inhibitor [human] (Berinert) | 20 U/kg IV (HAE); 1000 U IV (ACE-inhibitor angioedema) | Effective in HAE and ACE-I angioedema; adverse: headache, GI symptoms |
| C1 esterase inhibitor [recombinant] (Ruconest) | 50 U/kg IV (max 4200 U) | Effective in HAE; no data for ACE-I angioedema |
| Icatibant (Firazyr) | 30 mg SC | Bradykinin B2 receptor antagonist; effective in HAE + ACE-I angioedema; single dose highly effective; 90% local reactions |
| Epinephrine | 0.3-0.5 mg IM | For life-threatening laryngeal/allergic angioedema |
| H1 antihistamines | Standard doses | Adjunct - limited benefit in bradykinin-mediated angioedema |
| Corticosteroids | Methylprednisolone IV | Adjunct |
Priority: Secure the airway early. Angioedema can progress rapidly and unpredictably.
PART 5 - PEDIATRIC INFECTIOUS SKIN EMERGENCIES
12. Kawasaki Disease
(Tintinalli Chapter 142 - Rashes in Infants and Children)
"Kawasaki's disease is the leading cause of acquired heart disease in children."
Diagnostic criteria (Classic disease): Fever ≥5 days PLUS 4 of:
- Bilateral non-exudative conjunctivitis
- Cervical lymphadenopathy
- Erythema of lips and oral mucosa (strawberry tongue)
- Skin changes of extremities (erythema, edema, desquamation)
- Rash (variable morphology; vesicles not described; perineal predilection)
- Peak age: 18-24 months; <6 months or >9 years have poorer outcomes
- Mortality <0.5% - mainly from coronary artery aneurysm rupture
- Most devastating complication: sudden cardiac death from coronary aneurysms
Quick Reference: Disposition Summary
| Condition | Disposition | Key First Steps in ED |
|---|
| EM Minor | Outpatient | Steroids, antihistamines, acyclovir if HSV |
| SJS (EM Major) | Admit - ICU/Burn Unit | Stop drug; resuscitate; fluids; ophthalmology |
| TEN | Admit - ICU/Burn Unit | Stop drug; resuscitate; burn care principles |
| Pemphigus | Admit - ICU/Burn Unit | Fluids; IVIG; immunosuppression |
| DRESS | Admit | Stop drug; systemic steroids if severe |
| Erythroderma Major | Admit | Warm environment; fluids; dermatology before steroids |
| Meningococcemia | Admit - ICU | Ceftriaxone IV STAT; blood cultures; LP if stable |
| Purpura Fulminans | Admit - ICU | Antibiotics; FFP; vasopressors; DIC management |
| Necrotizing Fasciitis | Admit - OR | Surgical debridement + triple antibiotics |
| Cellulitis (severe) | Admit | IV vancomycin ± beta-lactam; mark borders |
| Angioedema (laryngeal) | Admit - ICU | Airway FIRST; C1 inhibitor/icatibant; epinephrine |
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