Excellent - I now have rich, detailed content from both Andrews', Rosen's, and Tintinalli's on all 6 dermatological emergencies. Here is the complete focused answer:
Dermatological Emergencies
From the conditions listed, the following 6 are true dermatological emergencies - they carry significant mortality if not recognized and treated immediately in the ED.
1. Meningococcemia
Causative organism: Neisseria meningitidis (gram-negative diplococcus)
Who is affected: Children <2 years (highest risk), adolescents/young adults 16-21 years; fatal in ~10% of cases
Clinical progression:
- Early: Fever, malaise, leg pain, cold hands/feet, pallor/mottling - these precede the rash
- Rash appears in ~50% as the first classic symptom - begins as nonspecific macules, rapidly evolves to petechiae (1-2 mm, discrete, non-blanching, trunk and lower body, soft palate, conjunctiva)
- Petechiae coalesce into purpura and ecchymosis
- ~10% develop Waterhouse-Friderichsen syndrome: shock + massive intracutaneous hemorrhage + adrenal failure
Workup: Blood cultures, CSF cultures, skin scraping cultures; CBC (thrombocytopenia + leukocytosis)
Treatment - do not delay:
- Ceftriaxone or cefotaxime IV (3rd-generation cephalosporin) + vancomycin
- Add dexamethasone if meningitis suspected
- Treat shock aggressively
The petechial rash directly reflects the degree of thrombocytopenia and DIC potential. Early identification is essential - progression to fulminant DIC/sepsis can occur within hours.
2. Rocky Mountain Spotted Fever (RMSF)
Causative organism: Rickettsia rickettsii - tick-borne (many patients deny tick exposure)
Geography: Despite name, most US cases are from the southeastern United States
Clinical course:
- Abrupt onset: headache, high fever, nausea/vomiting, myalgias, chills
- Disease lasts up to 3 weeks; can involve CNS, heart, lungs, kidneys, cause DIC or shock
Rash (appears day 2-6):
- Starts as blanching erythematous macules at the wrists and ankles
- Spreads centripetally up extremities to trunk and face
- Becomes petechial or hemorrhagic
- Palms and soles involvement is characteristic
Diagnosis: Clinical only in the ED - Weil-Felix reaction and immunofluorescence are not available acutely
Treatment - initiate on clinical diagnosis alone:
- Doxycycline - drug of choice; failure to treat promptly dramatically increases morbidity and mortality
- Chloramphenicol for tetracycline-allergic patients or children <9 years
- Avoid: sulfa drugs (worsen disease), penicillins, cephalosporins, aminoglycosides, erythromycin (all ineffective)
3. Necrotizing Fasciitis
Pathology: Acute necrotizing infection of the fascia, with rapid progression to gangrene
Microbiology:
- Type I (polymicrobial): Mixed aerobic/anaerobic bacteria (most common)
- Type II (monomicrobial): Group A Streptococcus or community-acquired MRSA
Progression timeline:
- Hours 0-48: Redness, pain, and edema
- By 48 hours: Central dusky-blue discoloration ± serosanguineous blisters
- Day 4-5: Purple areas become gangrenous
- Key sign: Anesthesia of the involved skin (due to nerve destruction)
Red flags (LRINEC score components): Elevated CRP, leukocytosis, low Hb, hyponatremia, elevated creatinine, hyperglycemia
Diagnosis:
- MRI is most definitive imaging (detects fascial plane involvement)
- Bedside finger test: 2-cm incision to fascia - lack of bleeding, murky "dishwater" discharge, and lack of resistance to probing finger = positive
- Soft tissue gas on plain X-ray or CT is pathognomonic when present
Treatment:
- Immediate surgical debridement - this is non-negotiable and life-saving
- Broad-spectrum IV antibiotics: vancomycin or linezolid + piperacillin-tazobactam OR carbapenem OR ceftriaxone + metronidazole
- Supportive ICU care
- Mortality ~20% even with optimal management; poor prognosis: age >50, diabetes, truncal involvement, diagnosis delayed >7 days
4. Stevens-Johnson Syndrome (SJS) / Toxic Epidermal Necrolysis (TEN)
Classification by % body surface area (BSA) epidermal detachment:
| Entity | BSA Detachment |
|---|
| SJS | <10% |
| SJS-TEN overlap | 10-30% |
| TEN | >30% |
Common causative drugs: TMP-SMX, sulfonamides, lamotrigine, carbamazepine, allopurinol (most common in Europe), nevirapine, NSAIDs, penicillins, other anticonvulsants; acetaminophen in children
Genetic risk: HLA-B*1502 (Han Chinese and other Asians) strongly associated with carbamazepine-induced SJS/TEN - HLA typing recommended before starting carbamazepine in Asian patients
Clinical presentation:
- Prodrome: Fever + influenza-like symptoms 1-3 days before skin involvement
- Skin: Deep-red/dusky macules on face and trunk, rapidly spreading over 4 days; central desquamation, bullae formation, then sloughing
- Mucosal involvement is hallmark of SJS - ≥2 surfaces: oral mucosa (hemorrhagic crust, erosions), conjunctiva (photophobia), urogenital, respiratory
- Nikolsky sign positive: lateral pressure on skin causes epidermal sliding
Complications: Ocular scarring (most common long-term sequela), cutaneous scarring, vision loss, sicca syndrome, nail/hair abnormalities
Treatment:
- Immediately stop the offending drug (single most important intervention)
- Admit to burns unit or ICU
- Supportive care: fluid/electrolyte replacement, wound care, temperature management
- Ophthalmology consult urgently (ocular involvement is the main determinant of long-term morbidity)
- Cyclosporine has emerging evidence for benefit; IVIg/TNF-alpha antagonists under investigation
- Do NOT use systemic corticosteroids (controversial; most evidence suggests harm)
SCORTEN Score - predicts mortality in TEN (scores 0-7 based on: age >40, malignancy, HR >120, initial BSA >10%, BUN >10 mmol/L, serum glucose >14 mmol/L, bicarbonate <20 mmol/L)
5. Staphylococcal Scalded Skin Syndrome (SSSS)
Causative organism: Phage group 2 exotoxin-producing Staphylococcus aureus (exfoliative toxins A and B cleave desmoglein-1)
Who is affected: Primarily children ≤6 years (neonates most vulnerable); rarely immunocompromised adults
Clinical progression:
- Erythema + crusting around the mouth (perioral)
- Erythema spreads down the body
- Bulla formation and superficial desquamation
- Mucous membranes are SPARED (key distinction from SJS/TEN)
- Clinical resolution in 3-7 days after appropriate treatment
Key distinction from TEN:
- SSSS: Cleavage is intraepidermal (superficial, at the granular layer) - caused by hematogenously spread exotoxin, mucosa spared
- TEN: Cleavage is at the dermoepidermal junction (full thickness) - caused by drug reaction, mucosa involved
Treatment:
- IV antistaphylococcal antibiotics: nafcillin, oxacillin, or vancomycin (if MRSA suspected or penicillin allergic)
- Alternatives: clarithromycin, cefuroxime
- Fluid/electrolyte support; wound care (gentle, as skin is fragile)
6. Toxic Shock Syndrome (TSS)
Causative organisms:
- Staphylococcus aureus (TSST-1 superantigen) - ~50% menstrual-associated
- Streptococcus pyogenes (streptococcal TSS - often more severe, higher mortality)
Associations: Tampon use, surgery, burns, postpartum, osteomyelitis, fasciitis, abscesses, pharyngitis
Diagnostic criteria (all 4 required):
- Temperature ≥38.9°C
- Systolic BP ≤90 mmHg
- Rash
- Involvement of ≥3 organ systems (GI, muscular, CNS, renal, hepatic, hematologic)
Rash characteristics:
- Diffuse, blanching, macular erythroderma - like a "sunburn" rash
- Accompanying non-exudative mucosal inflammation (pharyngitis with "strawberry tongue," conjunctivitis, vaginitis)
- Rash fades within 3 days
- Followed by full-thickness desquamation of palms and soles (1-2 weeks later)
Treatment:
- Aggressive IV fluid resuscitation
- Vasopressors if refractory hypotension
- Ventilatory support as needed
- Remove source of infection (remove tampon, drain abscess, debride infected wound)
- Antibiotics: anti-staphylococcal agent (nafcillin/vancomycin) + clindamycin (to suppress toxin production)
- Consider IVIG for severe streptococcal TSS
Quick Comparison: The 6 Emergencies at a Glance
| Emergency | Key Skin Finding | Mortality Risk | Immediate Action |
|---|
| Meningococcemia | Petechiae → purpura (non-blanching, trunk) | ~10% | Ceftriaxone IV stat |
| RMSF | Blanching macules → petechiae, wrists/ankles first, palms/soles | High if delayed | Doxycycline stat (clinical diagnosis) |
| Necrotizing Fasciitis | Dusky skin → gangrene, anesthesia, crepitus | ~20% | Surgical debridement + broad-spectrum ABx |
| SJS/TEN | Mucosal erosions + skin detachment, Nikolsky+ | TEN: 30-50% | Stop causative drug, burns/ICU care |
| SSSS | Superficial blistering + desquamation, mucosa spared, perioral | Low in children | IV antistaphylococcal ABx |
| TSS | Diffuse erythroderma + desquamation palms/soles | Significant | Source control + clindamycin + vancomycin |
Sources:
- Tintinalli's Emergency Medicine: A Comprehensive Study Guide, Chapter 142 (Meningococcemia)
- Rosen's Emergency Medicine: Concepts and Clinical Practice, Chapter 107 (Necrotizing Fasciitis, Meningococcal Infection, RMSF, SSSS, TSS)
- Andrews' Diseases of the Skin: Clinical Dermatology, Chapters 6 (SJS/TEN), 14 (Necrotizing Fasciitis), and the Meningococcemia section