Skin disorders in emergency room and its management Elaborate major skin Emergencies

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Major Skin Emergencies in the Emergency Room

Skin emergencies are conditions where dermatological pathology is immediately life-threatening or organ-threatening. The clinician must recognize these rapidly and act decisively - delay worsens mortality in most of them.

Overview: Classification of Skin Emergencies

CategoryConditionKey Threat
Severe drug reactionsSJS / TEN / DRESSSepsis, multi-organ failure
Necrotizing infectionsNecrotizing fasciitisSeptic death, limb loss
Septicemia with skin signsMeningococcemia / Purpura fulminansDIC, shock, death
Autoimmune blisteringPemphigus vulgaris / Bullous pemphigoidFluid/protein loss, sepsis
Anaphylaxis/urticariaAnaphylaxis with angioedemaAirway compromise
ErythrodermaExfoliative dermatitisThermoregulation failure
Staphylococcal toxinSSSS (Staphylococcal scalded skin syndrome)Sepsis, fluid loss (esp. children)

1. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)

What They Are

SJS and TEN exist on a continuum of severity - both are severe cutaneous adverse reactions (SCARs) and potentially fatal blistering drug eruptions. They are distinct from erythema multiforme (EM), which is largely HSV-associated.
  • SJS: <10% body surface area (BSA) epidermal detachment
  • SJS/TEN overlap: 10-30% BSA detachment
  • TEN (Lyell syndrome): >30% BSA detachment
Incidence: 0.4-1.2 per million person-years for TEN; 1.2-6.0 per million for SJS.

Causative Drugs

"More than 100 medications have been reported to cause SJS and TEN."
  • TMP-SMX (1-3 per 100,000)
  • Nevirapine
  • Lamotrigine (1:1,000 adults; 3:1,000 children)
  • Carbamazepine (14:100,000) - especially in HLA-B*1502-positive Asians
  • Allopurinol (most common cause in Europe currently)
  • NSAIDs, other anticonvulsants, antibiotics (sulfonamides, penicillins)
Genetic warning: HLA-B*1502 (Han Chinese, SE Asian populations) dramatically increases SJS/TEN risk with carbamazepine. HLA typing before starting carbamazepine is recommended in all Asian patients.

Clinical Presentation

  • Prodrome: fever, influenza-like symptoms 1-4 days before rash
  • Skin: deep red/dusky macules on face and trunk, spreading rapidly; "2-zone" or atypical targetoid lesions; central desquamation; bullae formation, then sloughing
  • Two or more mucosal surfaces are almost always involved in SJS: oral (hemorrhagic crusting), conjunctival, urethral, vaginal, anal
  • Symptoms: photophobia, dysphagia, dysuria, cough (tracheobronchial involvement)
  • "Pure TEN": dusky macular erythema with rapid full-thickness epidermal separation (no targetoid lesions)
SJS - severe oral mucosal erosions with hemorrhagic crusting and perioral skin lesions
Fig: Stevens-Johnson Syndrome - oral mucosa erosions. (Andrews' Diseases of the Skin)

Mortality Risk: SCORTEN

Score 1 point each for:
  • Age >40
  • Malignancy present
  • BSA involved >10%
  • Tachycardia (HR >120)
  • BUN >28 mg/dL
  • Serum bicarbonate <20 mEq/L
  • Blood glucose >14 mmol/L
SCORTENMortality
0-13.2%
212.1%
335.3%
458.3%
≥5>90%
Respiratory tract involvement (bronchial TEN + ARDS) carries ~70% mortality.

Management

  • Immediate cessation of causative drug - single most important intervention
  • ICU or burn unit admission; multidisciplinary team
  • Fluid resuscitation: approximately 2/3 of the Parkland formula (less than burn victims)
  • Nutritional support and monitoring for sepsis
  • Wound care: leave involved epidermis in place as biological dressing; nonstick dressings; silver-impregnated dressings; minimize tape-to-skin; IV lines at uninvolved sites
  • Mucosal care: nonstick dressings to separate eroded mucosal surfaces; ophthalmology consult (risk of symblepharon/blindness); gynecology and urology consults as needed; amniotic membrane application for eyes
  • Systemic immunosuppression (controversial, no consensus):
    • European practice: Cyclosporine 3-6 mg/kg/day (divided)
    • US practice: IVIG 1 g/kg/day for 4 days ± corticosteroids
    • Etanercept: shown beneficial in moderate RCT (Asia)
    • Early short-course high-dose steroids may help in some cases
Source: Andrews' Diseases of the Skin, Clinical Dermatology

2. Necrotizing Fasciitis

Definition

A rapidly progressive, life- and limb-threatening infection of the skin, subcutaneous tissue, and deep fascia characterized by widespread fascial necrosis with relative sparing of overlying skin initially.

Risk Factors

Diabetes mellitus, tobacco use, postoperative/peripartum state, IV drug use, obesity, immunosuppression.

Clinical Recognition - "Hard to Diagnose Early"

Early signs are subtle and may mimic simple cellulitis:
  • Erythema, warmth, swelling, pain "out of proportion to appearance"
  • Skin becomes brawny, violaceous, then dusky/gray
  • Late: skin necrosis, bullae, frank gangrene, crepitus (gas-forming organisms)
  • Systemic: fever, tachycardia, hypotension, altered mental status
  • Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC score): CRP, WBC, Hgb, Na, creatinine, glucose

Pathogenic Types

  • Type I (polymicrobial): streptococci, staphylococci, gram-negatives, anaerobes (most common)
  • Type II (monomicrobial): Group A Streptococcus (flesh-eating disease) or Staphylococcus aureus
  • Type III: Clostridial (gas gangrene - myonecrosis)
  • Type IV: Fungal (Candida, Mucor) - immunocompromised hosts

Management - Surgical Emergency

"Rapid surgical intervention remains the mainstay of therapy...Surgical intervention less than 24 hours following onset is associated with improved clinical outcomes." - Fitzpatrick's Dermatology
  1. Immediate surgical consult - do not delay for further imaging if clinical diagnosis is clear
  2. Radical debridement of all necrotic tissue; staged daily re-debridements until clean
  3. Wound closure: vacuum-assisted closure (VAC) devices + skin grafting after source control
  4. Amputation may be required for severe limb disease (especially in diabetics)
  5. Broad-spectrum antibiotics (IDSA 2014 guidelines): vancomycin OR linezolid OR daptomycin PLUS one of: piperacillin-tazobactam / carbapenem / ceftriaxone + metronidazole / fluoroquinolone + metronidazole - narrow based on tissue culture
  6. Fluid resuscitation + electrolyte monitoring (significant wound drainage)
  7. IVIG: limited evidence; may consider in Group A Strep NF (neutralizes exotoxins)
  8. Hyperbaric oxygen: insufficient data; ongoing research

3. Meningococcemia and Purpura Fulminans

Meningococcemia - A Classic Emergency

Caused by Neisseria meningitidis. The rash is the critical clinical clue.
Cutaneous findings (from Fitzpatrick's Dermatology, Vol. 1):
  • Initial: small, irregular petechiae with a "smudged" appearance
  • Distribution: extremities most common; also palms, soles, mucous membranes, conjunctiva
  • Petechiae in 60% of patients on presentation; higher in children 1-18 years (74%)
  • Critical sign: rapid increase in number and size of petechiae correlates with fulminant disease
Petechiae of acute meningococcemia on skin (A) and conjunctiva (B)
Fig: Petechiae of acute meningococcemia on skin and conjunctiva. (Fitzpatrick's Dermatology)

Purpura Fulminans

Occurs when meningococcemia progresses to severe DIC:
  • Retiform purpura (branching, stellate necrosis)
  • Skin necrosis extending to subcutaneous tissue, muscle, and bone
  • Low protein C levels
  • Gangrene of digits and distal extremities
Purpura fulminans from meningococcemia - retiform purpura (A) and digit gangrene (B)
Fig: Purpura fulminans - retiform purpura and digital/extremity gangrene. (Fitzpatrick's Dermatology)

Management

  1. Immediate IV benzylpenicillin (or ceftriaxone 2g IV if penicillin allergy) - do not delay for LP if patient is unstable
  2. Blood cultures before antibiotics if possible - but do not delay treatment
  3. ICU admission, sepsis resuscitation (fluids, vasopressors, oxygen)
  4. DIC management: FFP, cryoprecipitate, platelets as guided by coagulation profile
  5. Protein C concentrate may be considered in purpura fulminans
  6. Surgical care for gangrenous tissue (may require amputation)
  7. Close contacts: chemoprophylaxis (rifampicin, ciprofloxacin, or ceftriaxone)

4. DRESS Syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms)

Also known as Drug-Induced Hypersensitivity Syndrome (DiHS).

Features

  • Onset: 2-8 weeks after starting offending drug (longer latency than SJS)
  • Rash: morbilliform eruption (face, upper trunk, extremities), often with facial edema
  • Systemic involvement: fever, lymphadenopathy, hepatitis (most common), nephritis, pneumonitis, myocarditis, thyroiditis
  • Hematologic: eosinophilia (hallmark), atypical lymphocytes
  • Viral reactivation: HHV-6, EHV-7, CMV, EBV commonly reactivate and may drive severity
Common culprit drugs: allopurinol, carbamazepine, lamotrigine, phenytoin, dapsone, vancomycin, minocycline, sulfonamides

Management

  1. Stop the offending drug immediately
  2. Systemic corticosteroids: prednisone 1-2 mg/kg/day (mainstay; taper slowly over weeks to months to prevent relapse)
  3. Monitor liver function, renal function, CBC regularly
  4. Monitor for HHV-6 reactivation; antivirals (valganciclovir) if severe or HHV-6-driven
  5. Avoid re-exposure to causative drug; cross-reactivity within anticonvulsant class

5. Staphylococcal Scalded Skin Syndrome (SSSS)

Features

  • Primarily affects neonates and children <5 years (adults if immunocompromised/renal failure)
  • Caused by exfoliative toxins A and B from Staphylococcus aureus (usually phage type 71)
  • Toxins cleave desmoglein-1 in the superficial epidermis
  • Prodrome: fever, irritability, skin tenderness
  • Rash: starts perioral/periorbital, then generalized erythema, then flaccid bullae and desquamation
  • Nikolsky sign positive (lateral pressure on erythematous skin causes epidermal slipping)
  • No mucosal involvement (distinguishes from SJS/TEN - mucosae contain desmoglein-3 which is not affected by the toxin)

Management

  1. Hospitalization; neonates to NICU
  2. Anti-staphylococcal antibiotics: IV nafcillin or oxacillin; clindamycin (inhibits toxin production); vancomycin if MRSA suspected
  3. Fluid and electrolyte replacement
  4. Wound care: gentle handling; nonstick dressings; emollients
  5. Prognosis: excellent in children with treatment (mortality <5%); worse in adults (~60%)

6. Anaphylaxis with Urticaria/Angioedema

Skin Signs

  • Urticaria: pruritic, raised, evanescent wheals; can be anywhere on body
  • Angioedema: deeper, non-pitting swelling; face, lips, tongue, throat (life-threatening when laryngeal)
  • Together with systemic features (bronchospasm, hypotension, tachycardia) = anaphylaxis

Management (ABC-first approach)

  1. Epinephrine 0.3-0.5 mg IM (anterolateral thigh) - first-line, do not delay
  2. Airway: supplemental O2; early intubation or surgical airway if laryngeal edema
  3. IV fluids: 1-2 L normal saline for hypotension
  4. Antihistamines: diphenhydramine (H1) + ranitidine/famotidine (H2) - adjuncts only, NOT first-line
  5. Systemic corticosteroids: methylprednisolone IV - reduces biphasic reactions
  6. Observe for minimum 4-6 hours (24 hours if severe); prescribe epinephrine auto-injector on discharge
  7. Allergist referral for identification and avoidance of trigger

7. Erythroderma (Exfoliative Dermatitis)

Definition

Generalized redness and scaling involving >90% of body surface area.

Causes ("5 Ps + D")

  • Psoriasis (most common underlying disease)
  • Pityriasis rubra pilaris
  • Primary dermatoses (atopic dermatitis, contact dermatitis, seborrheic)
  • Drugs (sulfonamides, gold, isoniazid, captopril, many others)
  • Paraneoplastic (Sézary syndrome - cutaneous T-cell lymphoma)
  • De novo / idiopathic (in ~30%)

Systemic Complications

  • Hypothermia or hyperthermia (disrupted thermoregulation)
  • High-output cardiac failure (massive cutaneous vasodilation - up to 30% increase in skin blood flow)
  • Protein/fluid loss through skin
  • Hypoalbuminemia, edema
  • Secondary bacterial infection/sepsis
  • Renal failure

Management

  1. Hospitalize - often ICU
  2. Treat precipitating cause (stop drug, treat underlying psoriasis/dermatitis)
  3. Temperature control: warm room, blankets (patients cannot thermoregulate)
  4. Fluid and electrolyte replacement
  5. Nutritional support (high caloric needs from hypermetabolic state)
  6. Emollients and wet compresses for skin comfort
  7. Skin biopsy for diagnosis (especially to exclude Sézary syndrome)
  8. Treat secondary infections with appropriate antibiotics
  9. Disease-specific systemic therapy once diagnosis is confirmed

Quick ER Reference Summary

EmergencyKey ClueImmediate Action
SJS/TENMucosal erosions + skin sloughing after drugStop drug; burn unit; IVIG or cyclosporine
Necrotizing FasciitisPain out of proportion; skin necrosis; crepitusSurgical debridement + broad-spectrum ABx
MeningococcemiaNon-blanching petechiae/purpura + feverIV ceftriaxone STAT; ICU
Purpura FulminansRetiform purpura + DICSepsis management; FFP; protein C
DRESSMorbilliform rash + eosinophilia + organ dysfunctionStop drug; systemic steroids
SSSSChildren with skin tenderness + positive Nikolsky; no mucosal involvementIV anti-staphylococcal ABx
AnaphylaxisUrticaria + angioedema + systemic featuresIM epinephrine FIRST
Erythroderma>90% BSA erythema + scaling + systemic compromiseHospitalize; thermoregulation; treat cause

Sources consulted:

Emergency room skin disorders based on tintinalli and rosens

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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:
  1. Severe generalized drug/immune reactions (SJS, TEN, DRESS, pemphigus)
  2. Infectious emergencies with skin signs (meningococcemia, necrotizing fasciitis, cellulitis)
  3. 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
Classic target (iris) lesion of erythema multiforme
Fig: Target (iris) lesions of erythema multiforme - FIGURE 249-3 (Tintinalli's Emergency Medicine)
Management (Tintinalli TABLE 249-2):
SeverityTreatmentDisposition
EM MinorPrednisone 60-80 mg/day PO x 3-5 days; oral antihistamine; acyclovir if HSV-relatedOutpatient; 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 infectionAdmit - 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:
StepAction
Remove triggerStop all suspected causative drugs immediately
ResuscitationAirway (respiratory involvement possible), circulatory support
FluidsFluid + electrolyte management (~2/3 of burn Parkland formula)
Wound careBurow's solution compresses; nonstick dressings; leave sloughed epidermis in place as biologic dressing
InfectionAntibiotics only for confirmed infection - NOT prophylactic
Specialist careOphthalmology, gynecology, urology as indicated; dermatologist mandatory
DispositionICU 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:
SeverityTreatmentDisposition
MinorRemove trigger; symptomatic care (oral pain agents, antihistamines PRN)Outpatient; PCP/derm follow-up
MajorResuscitate; fluid/electrolytes; warm environment (thermoregulation impaired); emollients; treat infection; systemic therapy per dermatologistAdmit; 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
DRESS syndrome caused by phenytoin - diffuse erythrodermatous rash over trunk
Fig: DRESS syndrome caused by phenytoin - FIGURE 249-7 (Tintinalli's Emergency Medicine)
Management (Tintinalli):
  1. Immediate cessation of suspected culprit drug
  2. Systemic steroids in severe cases (hepatitis, pneumonitis, or extensive exfoliative dermatitis)
  3. Supportive care: antipyretics, antipruritic medications
  4. 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):
FormFeatures
BacteremiaFebrile illness ± rash; no meningeal signs
Meningococcal meningitisFever, headache, neck stiffness; rash in >50%; seizures in 20%
Meningococcal septicemiaLethargy, poor perfusion, cyanosis; hemorrhagic skin lesions in 28-77%
Fever + non-blanching rashUp to 30% - can progress to fulminant disease if untreated
Purpura fulminansRapidly 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
Meningococcemia - early petechiae evolving into purpuric lesions
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):
SituationAntibiotic
Standard proven meningococcemiaPenicillin 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-allergicChloramphenicol
  • 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):
  1. Widespread ecchymoses
  2. Hemorrhagic bullae
  3. 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:
SeverityAntibiotic
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 antibioticsFor 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):
  1. Antibiotics - Triple therapy: Penicillin or cephalosporin + aminoglycoside + clindamycin (clindamycin inhibits toxin production)
  2. Immediate surgical debridement - do not delay
  3. 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:
AgentDoseNotes
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 SCBradykinin B2 receptor antagonist; effective in HAE + ACE-I angioedema; single dose highly effective; 90% local reactions
Epinephrine0.3-0.5 mg IMFor life-threatening laryngeal/allergic angioedema
H1 antihistaminesStandard dosesAdjunct - limited benefit in bradykinin-mediated angioedema
CorticosteroidsMethylprednisolone IVAdjunct
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:
  1. Bilateral non-exudative conjunctivitis
  2. Cervical lymphadenopathy
  3. Erythema of lips and oral mucosa (strawberry tongue)
  4. Skin changes of extremities (erythema, edema, desquamation)
  5. 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

ConditionDispositionKey First Steps in ED
EM MinorOutpatientSteroids, antihistamines, acyclovir if HSV
SJS (EM Major)Admit - ICU/Burn UnitStop drug; resuscitate; fluids; ophthalmology
TENAdmit - ICU/Burn UnitStop drug; resuscitate; burn care principles
PemphigusAdmit - ICU/Burn UnitFluids; IVIG; immunosuppression
DRESSAdmitStop drug; systemic steroids if severe
Erythroderma MajorAdmitWarm environment; fluids; dermatology before steroids
MeningococcemiaAdmit - ICUCeftriaxone IV STAT; blood cultures; LP if stable
Purpura FulminansAdmit - ICUAntibiotics; FFP; vasopressors; DIC management
Necrotizing FasciitisAdmit - ORSurgical debridement + triple antibiotics
Cellulitis (severe)AdmitIV vancomycin ± beta-lactam; mark borders
Angioedema (laryngeal)Admit - ICUAirway FIRST; C1 inhibitor/icatibant; epinephrine

Sources:

Emergency room skin disorders management

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Emergency Room Skin Disorders - Management

Based on Tintinalli's Emergency Medicine & Rosen's Emergency Medicine


ED APPROACH TO SKIN DISORDERS

Tintinalli's advises a structured approach: determine whether the presentation is a dermatologic emergency first, then systematically characterize lesion morphology, distribution, mucosal involvement, and systemic features.
Key history points (Tintinalli Ch. 248):
  • Duration, rate of progression, % BSA involved
  • Medication history (especially drugs started within 2-8 weeks) - EM, SJS, TEN, DRESS are drug-induced
  • Exposures: chemicals, foods, animals, insects, plants, travel, occupational, ill contacts
  • Sexual history where relevant
  • Painful rash = red flag; rarely self-limiting
Examination principle:
"Use the burn rule of nines to estimate the degree of skin involvement in disorders with widespread distribution."
A painful rash is always a red flag. Mucosal involvement in a blistering eruption demands immediate hospitalization.

PART 1 - LIFE-THREATENING SKIN EMERGENCIES

1. Stevens-Johnson Syndrome (SJS) / Toxic Epidermal Necrolysis (TEN)

Classification:
  • SJS: <10% BSA epidermal detachment
  • SJS/TEN overlap: 10-30%
  • TEN: >30% BSA - mortality up to 90% with SCORTEN ≥5
Causative agents: TMP-SMX, carbamazepine, phenytoin, lamotrigine, allopurinol, NSAIDs, penicillins, nevirapine
ED Management (Tintinalli TABLE 249-2):
ActionDetail
Stop causative drugSingle most important step
ResuscitateAirway (bronchial involvement possible), circulatory support
Fluid management~2/3 Parkland formula (less than burns); fluid + electrolytes
Wound careBurow's solution (5% aluminum acetate) + cool compresses for blisters; nonstick dressings; leave epidermis in situ as biologic dressing
Mucosal careDiphenhydramine + viscous lidocaine rinses for oral lesions; ophthalmology for ocular involvement
AntibioticsOnly for confirmed/suspected infection - NOT prophylactic
Systemic RxMethylprednisolone 125 mg IV q6h (or equivalent); IVIG or cyclosporine per specialist
DispositionICU or burn unit; intensivist + dermatologist
SCORTEN Mortality Predictor (1 point each):
ParameterThreshold
Age>40 years
Heart rate>120 bpm
BSA involved>10%
BUN>28 mg/dL
Blood glucose>14 mmol/L
Bicarbonate<20 mEq/L
MalignancyPresent
Score 0-1 = 3.2% mortality; Score ≥5 = >90% mortality

2. Pemphigus Vulgaris

Autoimmune blistering with flaccid bullae, mucosal erosions; risk of fluid/protein loss and sepsis.
Management (Tintinalli TABLE 249-2):
  • Remove any drug trigger
  • Fluid and electrolyte resuscitation
  • Immunosuppressive therapy (prednisone + rituximab or azathioprine)
  • IVIG (immunoglobulin therapy)
  • Plasmapheresis for severe cases
  • Antibiotics only for confirmed infection
  • Admit: ICU/burn unit; intensivist + dermatologist

3. Exfoliative Dermatitis (Erythroderma)

Generalized erythema and scaling >90% BSA. Causes: psoriasis, drug reaction, atopic dermatitis, Sézary syndrome.
Management (Tintinalli TABLE 249-2):
SeverityTreatmentDisposition
MinorRemove trigger; oral analgesics and antihistamines PRNOutpatient; PCP/derm follow-up
MajorResuscitate; fluid/electrolyte replacement; warm room (thermoregulation impaired); emollients; treat secondary infectionAdmit; correct hypothermia/hypovolemia; obtain dermatology consult before systemic corticosteroids

4. DRESS Syndrome

Onset 2-8 weeks after drug initiation. Fever + rash + organ involvement (liver > kidney > hematologic).
Tintinalli key points:
  • Eosinophilia occurs in ~30% of cases
  • Rash may resemble exfoliative dermatitis OR SJS
  • Genetic predisposition is present - discuss risk with patient's family members
ED Management:
  1. Immediately stop the causative drug
  2. Systemic corticosteroids for severe cases with hepatitis, pneumonitis, or extensive dermatitis
  3. Antipyretics and antipruritic agents (supportive)
  4. Admit to hospital; monitor LFTs, renal function, CBC, eosinophil count

5. Purpura Fulminans

Tintinalli (Ch. 249):
"Purpura fulminans is a rare vascular disorder characterized by fever, shock, multiorgan failure, and the rapid development of hemorrhagic skin necrosis."
Clinical triad:
  1. Widespread ecchymoses
  2. Hemorrhagic bullae
  3. Epidermal necrosis (nose, ears, genitalia, distal extremities)
Management:
  • Treat underlying sepsis (antibiotics + vasopressors)
  • DIC management: FFP, cryoprecipitate, platelets
  • Protein C concentrate
  • ICU; surgical care for gangrenous areas

PART 2 - INFECTIOUS SKIN EMERGENCIES

6. Necrotizing Fasciitis

Tintinalli (Ch. 152):
"Hallmark of fasciitis are the presence of marked systemic toxicity and pain out of proportion to local findings."
Necrotizing fasciitis - large cutaneous bullae filled with dark purple fluid on the leg
FIGURE 152-6 (Tintinalli): Necrotizing fasciitis with hemorrhagic bullae and dusky skin necrosis
LRINEC Score - Laboratory Risk Indicator for Necrotizing Fasciitis (Tintinalli TABLE 152-6):
LabThresholdPoints
CRP>150 mg/L+4
WBC>15,000/mm³ (or >25,000)+1
Hemoglobin<13.5 g/dL (or <11)+1
Sodium<135 mmol/L+2
Creatinine>1.6 mg/dL+2
Glucose>180 mg/dL+1
Note (Tintinalli): LRINEC ≥6 has been proven to miss many cases, especially Vibrio species and neck infections. Clinical judgment remains paramount.
Imaging: CT: asymmetric fascial thickening, gas tracking along fascial planes, focal fluid collections. MRI is sensitive but not fully specific.
Management:
  1. Immediate surgical consultation - do not wait for imaging if clinical diagnosis clear
  2. IV antibiotics: triple therapy - penicillin/cephalosporin + aminoglycoside + clindamycin
  3. Surgical debridement within <24 hours - staged daily re-debridements
  4. Fluid resuscitation + electrolyte monitoring
  5. ICU admission

7. Cellulitis and Erysipelas

Tintinalli Disposition rule:
"Mark the patient's skin with an indelible marker along the perimeter of infection so healing can be determined at follow-up."
Admit if: Systemic toxicity, diabetes mellitus, alcoholism, or immunosuppression present.
Tintinalli TABLE 192-4 - Empiric Antibiotic Treatment:
SeverityIndicationTreatment
Mild - No antibioticsHealthy patient, complete abscess drainage, no systemic infectionNone required
Moderate - OralPurulent cellulitis without systemic infection; drainable abscess + mild systemic signsTMP-SMX DS 1-2 tabs PO BID × 7-10 days OR Doxycycline 100 mg PO BID × 7-10 days OR Clindamycin 300-450 mg PO QID × 7-10 days
Severe - IV (MRSA coverage)Purulent cellulitis + systemic infection/sepsis; immunocompromisedVancomycin 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 OR Clindamycin 600 mg IV q8h
Sepsis/unclear etiologyAdd broad coverage+ Piperacillin-tazobactam 4.5 g IV q6h OR Meropenem 500-1000 mg IV q8h OR Imipenem-cilastatin 500 mg IV q6h
Water exposureFresh water (Aeromonas) or salt water (Vibrio)+ Doxycycline 100 mg IV q12h + Ceftriaxone 1 g IV q24h

8. Skin Abscesses, Furuncles, and Carbuncles

(Tintinalli Ch. 152)
Management:
  • Small furuncles: warm compresses to promote drainage; reassess in 2-3 days
  • Sitz baths for buttock/perineal furuncles
  • Large furuncles, carbuncles, abscesses: incision and drainage (I&D) required
    • Simple needle aspiration inadequate for MRSA abscesses
    • Use No. 11 or 15 scalpel blade over area of greatest fluctuation
    • Use US to guide incision length and depth
    • Break up loculations with a hemostat
    • Pack the cavity with gauze; reassess at 48 hours
Incision and Drainage Technique (Tintinalli):
  1. Obtain consent; universal precautions including face shield
  2. Position for access; prep with povidone-iodine; drape
  3. Infiltrate from the side over the abscess; distend cavity with lidocaine
  4. Incise over area of greatest fluctuation
  5. Express contents; break loculations
  6. Pack with gauze wick; arrange 48-hour follow-up
Antibiotic indication after I&D: Only if moderate-severe systemic signs (see cellulitis table above)

PART 3 - VIRAL SKIN CONDITIONS IN THE ED

9. Herpes Zoster (Shingles)

(Tintinalli TABLE 250-2)
Clinical features: Vesicles and pustules on erythematous base in unilateral dermatomal distribution; associated pain, pruritus, dysesthesias. A unilateral band-like arrangement on the thorax is diagnostic.
Ramsay Hunt Syndrome: External auditory canal involvement + facial nerve paralysis + vestibulocochlear dysfunction.
ConditionDrugDoseDuration
Herpes zosterAcyclovir800 mg PO 5 times/day7 days
Herpes zosterValacyclovir1000 mg PO TID7 days
  • Initiate within first 72 hours of symptom onset for maximum benefit
  • Reduces healing time, new lesion formation, risk of postherpetic neuralgia
  • Immunocompromised patients with severe involvement: hospitalize for IV acyclovir
  • Local care: aluminum acetate compresses TID + antibiotic ointment
  • Treat pain aggressively (may be severe)

10. Herpes Simplex (HSV)

(Tintinalli TABLE 250-2)
Diagnosis: HSV type-specific NAATs are tests of choice (most sensitive/specific with active lesions). Viral culture is specific but less sensitive.
EpisodeDrugDoseDuration
Initial episodeAcyclovir400 mg PO TID or 200 mg PO 5x/day7-10 days
Initial episodeValacyclovir1000 mg PO BID7-10 days
RecurrenceAcyclovir800 mg PO TID2 days
RecurrenceValacyclovir500 mg PO BID3 days
RecurrenceFamciclovir1000 mg PO BID1 day
Suppressive therapyValacyclovir500-1000 mg PO dailyLong-term
ImmunocompromisedAcyclovirIV formulationInpatient

PART 4 - PAPULOSQUAMOUS AND COMMON ED CONDITIONS

11. Scabies

(Rosen's Ch. 84; Tintinalli TABLE 35-2)
Cause: Sarcoptes scabiei mite. Transmission: direct contact, infested linens. Features: Intense pruritus (hypersensitivity reaction); characteristic burrows; excoriations, papules, nodules on groin, genitalia, axilla, interdigital web spaces. Diagnosis: Microscopic exam of scrapings - reveals mites.
AgentDose/Application
Permethrin 5% cream (first-line)One application at bedtime, entire body from neck down; wash off in 8-12 h; repeat in 7 days
Ivermectin (oral)200 mcg/kg PO once; repeat in 7 days
Topical ivermectin 1%Alternative topical option
Key instructions (both Tintinalli and Rosen's):
  • Treat all household members and close contacts concurrently
  • Wash linens and recently worn clothes in hot water; dry on high heat

12. Contact Dermatitis and Atopic Dermatitis

(Tintinalli TABLE 250-5, TABLE 35-2)
ConditionTreatment
Poison ivy/oak (severe)Oral antihistamines + clobetasol 0.05% or fluocinonide 0.05% topical; if severe: Prednisone 0.5 mg/kg/day × 2-3 weeks
Allergic contact dermatitisIdentify + avoid allergen; mid- to high-potency topical steroids (triamcinolone 0.1%, fluocinonide 0.05%); severe cases: oral prednisone 40-60 mg PO daily tapered over 3 weeks
Atopic dermatitisHigh-potency: clobetasol 0.5%, halobetasol 0.5%; Mid-potency: triamcinolone 0.1%; Low-potency: hydrocortisone 2.5%; fexofenadine 180 mg morning + antihistamine at night
PhotosensitivityPhotoprotection; identify and avoid photosensitizer

13. Fungal Infections

(Tintinalli TABLE 250-3, TABLE 251-2, TABLE 35-2)
Tinea versicolor - hypopigmented macules with fine scale on the back
FIGURE 251-8 (Tintinalli): Tinea versicolor - hypopigmented macules with fine scale
ConditionTreatmentNotes
Tinea capitisGriseofulvin microsize 20-25 mg/kg/day PO × 8 weeks OR Terbinafine 125-250 mg/day × 6 weeksAdd ketoconazole 2% or selenium sulfide 2.5% shampoo TID × 2 weeks; treat all close contacts simultaneously
Tinea corporis/crurisClotrimazole, miconazole topical; refractory: oral fluconazole or itraconazole
Tinea barbaeGriseofulvin microsize 500 mg PO daily × 6 weeks OR Terbinafine 250 mg daily × 2-4 weeksAvoid if hepatic disease; consider baseline LFTs
Pityriasis versicolorKetoconazole 2% shampoo as body wash daily × 7 days OR Ketoconazole/miconazole cream BID × 2-4 weeksDiscoloration may persist months after successful treatment

14. Head/Scalp Conditions

(Tintinalli TABLE 250-3)
ConditionClinical FeaturesTreatment
Pediculosis capitisScalp pruritus (especially behind ears); lice + nits along hair shaftPermethrin cream / pyrethrin lotion / ivermectin lotion / malathion cream; repeat in 7-10 days; machine wash linens
Dissecting cellulitis of scalpTender suppurative nodules; sinus tracts; scarring; alopeciaOTC antibacterial wash; doxycycline or minocycline 100 mg PO BID; I&D for fluctuant nodules; referral to dermatology
Seborrheic dermatitisWhite-yellow scale on scalp, eyebrows, nasolabial folds, chestOTC antidandruff shampoo; ketoconazole 2% shampoo/cream; desonide 0.05% or hydrocortisone 2.5%

15. STI-Related Skin Conditions

(Rosen's Ch. 84)
ConditionFirst-Line TreatmentNotes
Primary/Secondary syphilisBenzathine penicillin G 2.4 million units IM single dosePenicillin allergy: doxycycline or tetracycline × 2 weeks (except pregnancy/neurosyphilis)
Genital herpes (initial)Acyclovir 400 mg PO TID × 7-10 days OR Valacyclovir 1000 mg BID × 7-10 daysExtend if not healed at 10 days
ChancroidAzithromycin 1 g PO single dose OR Ceftriaxone 250 mg IM single doseIncise and drain fluctuant buboes
Condyloma acuminata (HPV)Provider-administered: cryotherapy, TCA/BCA, surgical excision; Patient-applied: imiquimod, podofilox, sinecatechinsED may defer and refer; not a true emergency
Scabies (genital)Permethrin 5% cream; treat all contactsSee scabies section above
Molluscum contagiosumRefer for cryotherapy or curettageNot emergent

16. Urticaria and Angioedema

(Tintinalli Ch. 14)
Urticaria management:
  • Identify and remove offending agent
  • H1 antihistamines ± corticosteroids (note: adding steroids to non-sedating antihistamines alone may not reduce relapse risk)
  • H2 antihistamine (ranitidine/famotidine) in severe/chronic/unresponsive cases
  • Epinephrine 0.3-0.5 mg IM for severe or refractory cases
  • Cold compresses for symptomatic relief
Angioedema - special considerations:
  • ACE inhibitor angioedema occurs in 0.1-0.7% of ACE-I users
  • Mechanism: bradykinin/substance P mediated - does NOT respond well to antihistamines/steroids/epinephrine
  • Airway must be secured early - progression can be rapid and unpredictable
Tintinalli TABLE 14-6 - Specific Angioedema Agents:
AgentDoseIndication
C1 esterase inhibitor [human] (Berinert)20 U/kg IV (HAE); 1000 U IV (ACE-I)Hereditary angioedema (HAE) + ACE-I angioedema
C1 esterase inhibitor [recombinant] (Ruconest)50 U/kg IV (max 4200 U)HAE
Icatibant (Firazyr)30 mg SCHAE + ACE-I angioedema; bradykinin B2 receptor antagonist; ~10% need second dose

PART 5 - TOPICAL THERAPY PRINCIPLES IN THE ED

(Tintinalli Ch. 248)
General topical rule:
"If it's dry, wet it; if it's wet, dry it."
Vehicle selection:
  • Ointments (petroleum base, no preservatives): best for chronic dry conditions; winter months
  • Creams (oil + water + preservative): most versatile; suitable for any body surface; may cause drying with chronic use
  • Gels: useful for scalp, beard areas
  • Patients allergic to cream preservatives: switch to ointment formulation
Corticosteroid Cream Dosing (Tintinalli TABLE 248-10):
Body AreaSuggested PotencyAmount to Dispense
FaceLow45 g
ArmIntermediate/Low90 g
LegIntermediate/Low180 g
Hand or footIntermediate/Low45 g
ForearmIntermediate/Low45 g
Chest or backIntermediate/Low180 g
(Based on TID application × 10 days)
Non-steroidal topical agents:
  • Emollients/moisturizers: reduce dryness, skin friction, and tightness; ointments best for chronic conditions
  • Open wet dressings (tap water or saline): reduce discomfort; cleanse by painlessly loosening crusts
  • Capsaicin 0.025% TID × 4 weeks: antipruritic via substance P depletion; not for age <10 years
  • Pramoxine 1-2% or EMLA: topical anesthetics for pruritus; limited high-quality evidence

RAPID REFERENCE: Disposition by Condition

ConditionDispositionPriority
SJS/TENAdmit - ICU/Burn UnitCRITICAL
Pemphigus vulgarisAdmit - ICU/Burn UnitCRITICAL
Necrotizing fasciitisAdmit - OR urgentSURGICAL EMERGENCY
MeningococcemiaAdmit - ICUCRITICAL
Purpura fulminansAdmit - ICUCRITICAL
DRESS syndromeAdmitURGENT
Exfoliative dermatitis (major)AdmitURGENT
Cellulitis (severe/systemic signs)AdmitURGENT
Angioedema (laryngeal)Admit - ICUAIRWAY EMERGENCY
Herpes zoster (immunocompromised)Admit for IV acyclovirURGENT
Cellulitis (mild, no systemic signs)Discharge with 2-3 day follow-up + skin markingROUTINE
EM minorDischarge with PCP/derm follow-upROUTINE
Urticaria (mild/moderate)Discharge + antihistaminesROUTINE
ScabiesDischarge + permethrin + contact treatmentROUTINE
Tinea/fungalDischarge + antifungalROUTINE
Contact dermatitis (mild)Discharge + topical steroidsROUTINE

Sources:

Secondary lesions, Labs and management of skin disorders in Emergency room

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Secondary Lesions, Diagnostic Labs, and Management of Skin Disorders in the Emergency Room

Source: Tintinalli's Emergency Medicine (Ch. 246-249, 251) and Rosen's Emergency Medicine

PART 1 - SKIN LESION MORPHOLOGY

Primary vs. Secondary Lesions

Primary lesions arise directly from pathophysiological processes. Secondary lesions have had their appearance altered due to disease evolution or external factors (scratching, trauma, treatment).
"Secondary lesions...include crusts, scales, fissures, erosions, ulcerations, excoriations, atrophy, scarring, and lichenification." - Tintinalli TABLE 248-3

TINTINALLI TABLE 248-3 - Complete Lesion Morphology

PRIMARY LESIONS:
DescriptorMorphologyHeight
MaculeFlat, circumscribed discoloration ≤1 cm; color variesFlat
PatchFlat, circumscribed discoloration >1 cmFlat
PapuleSolid, elevated lesion ≤1 cmElevated
PlaqueElevated, flat-topped lesion >1 cm; may be formed by coalescence of papulesElevated
WhealTransient, edematous, variably sized papule or plaque; evanescent (urticaria)Elevated
VesicleFluid-filled blister ≤1 cm; clear or hemorrhagicElevated
BullaFluid-filled blister >1 cmElevated
PustuleVesicle filled with purulent fluidElevated
NodulePalpable solid lesion <1 cmElevated
TumorPalpable solid lesion >1 cmElevated
CystSac containing liquid or semi-solid materialElevated
AbscessTender, erythematous, fluctuant nodule filled with pusElevated
PetechiaeNonblanching purple spots <2 mmFlat
PurpuraNonblanching purple discoloration of skin (>3 mm)Flat
TelangiectasiaSmall, blanchable superficial capillariesFlat
SECONDARY LESIONS:
DescriptorMorphologyHeight
ScaleAccumulation of dead stratum corneum cells (keratin flakes)Elevated
CrustDried serum, blood, or pus overlying damaged epidermisElevated
LichenificationThickened skin with exaggerated skin markings from chronic rubbingElevated
ExcoriationLinear marks from scratching - breaks the epidermisFlat/depressed
ErosionLoss of epidermis only; moist, shallow; heals without scarringDepressed
UlcerFull-thickness epidermal or dermal tissue loss; heals with scarringDepressed
FissureLinear crack in the skin surface (heel, fingertip, anal)Flat
ScarSclerotic area of skin following tissue repairFlat or elevated
KeloidHypertrophied scar extending beyond wound marginsElevated
AtrophyThinning of epidermis or dermis; shiny, wrinkled skinDepressed
SclerosisFirm, indurated skinFlat or elevated

TINTINALLI TABLE 248-2 - Lesion Configuration Descriptors

ConfigurationMeaning
AnnularRing-like
ArcuateCurved
ConfluentBlending together
DermatomalBelt-like, unilateral, follows anatomic dermatome
DiscreteSeparate, individual lesions
Grouped / HerpetiformClustered
GuttateScattered ("drop-like")
IrisConcentric circles (target lesion)
LinearIn a line
RetiformNet-like (purpura fulminans)
SerpiginousSnake-like

TINTINALLI TABLE 248-4/5 - Differential Diagnosis by Lesion Morphology

Primary Lesion Morphology → Key Differentials:
LesionKey Diagnoses to Consider
MaculeDrug eruption, nevus, viral exanthem, secondary syphilis, meningococcemia (early), ecchymosis, vitiligo, tinea versicolor, early cellulitis
PapuleAcne, warts, molluscum contagiosum, atopic dermatitis, urticaria, folliculitis, vasculitis, psoriasis, scabies, poison ivy, erythema multiforme, varicella (early), gonococcemia
PlaqueEczema, pityriasis rosea, tinea corporis/versicolor, psoriasis, seborrheic dermatitis, urticaria, secondary syphilis, erythema multiforme
NoduleBasal cell/squamous cell/metastatic carcinoma, melanoma, erythema nodosum, furuncle, lipoma
WhealUrticaria, angioedema, insect bites, erythema multiforme
PustuleAcne, folliculitis, gonococcemia, herpes (zoster, simplex, varicella), impetigo, psoriasis, pyoderma gangrenosum
VesicleHSV, herpes zoster, varicella, impetigo, poison ivy/oak, thermal burn, friction blister, TEN, bullous pemphigoid, pemphigus vulgaris
BullaBullous impetigo, poison ivy/oak, thermal burn, TEN, bullous pemphigoid, pemphigus vulgaris
Secondary Lesion Morphology → Key Differentials:
LesionKey Diagnoses to Consider
ScalesPsoriasis, pityriasis rosea, toxic/infectious erythemas, secondary syphilis, tinea, tinea versicolor, xerosis, first-degree thermal burn
CrustsEczema, tinea, impetigo, contact dermatitis, insect bite
ErosionsCandidiasis, tinea, varicella, HSV, impetigo, pemphigus vulgaris, SJS
UlcersDiabetic/venous/arterial ulcer, syphilis (chancre), chanroid, pyoderma gangrenosum, pressure ulcer
ExcoriationsScabies, atopic dermatitis, any pruritic dermatosis
FissuresAthlete's foot, cheilitis, anal fissure, xerosis
LichenificationAtopic/contact dermatitis (chronic), lichen simplex chronicus

Distribution Pattern → Differential Diagnosis (Tintinalli TABLE 246-1)

DistributionDifferential Diagnosis
Flexor surfacesAtopic dermatitis, candidiasis, eczema, ichthyosis
Sun-exposed areas (face, upper thorax, distal extremities)Sunburn, photosensitive drug eruption, SLE, viral exanthem, porphyria
Distal extremitiesViral exanthem, atopic/contact dermatitis, eczema, Rocky Mountain spotted fever, gonococcemia
Front and back of chestPityriasis rosea, secondary syphilis, drug eruption, psoriasis, atopic/contact dermatitis
Clothing-covered areasContact dermatitis, psoriasis, folliculitis
Face + upper thorax (acneiform)Acne, drug-induced acne, irritant dermatitides

PART 2 - DIAGNOSTIC TESTS FOR SKIN DISORDERS IN THE ED

(Tintinalli Ch. 248 - Diagnostic Approach)

1. Potassium Hydroxide (KOH) Preparation

Uses: Dermatophyte infections (tinea), molluscum contagiosum, pityriasis versicolor
Specimen sources: Loose skin scales, nail parings, subungual debris, short residual hairs, small pearly globules (from molluscum body)
KOH Prep Steps (Tintinalli TABLE 248-6):
  1. Place skin scrapings on a glass slide
  2. Add a coverslip
  3. Apply KOH 10-40% solution to the edge of the coverslip - it will be drawn under by capillary action
  4. Apply heat to the underside of the slide (match or lighter) until bubbles appear under coverslip
  5. Visualize under 10× magnification; use low condenser and light settings; focus up and down rapidly
Findings:
  • True hyphae (dermatophyte infection): long, branching green rods of constant width that cross cell borders
KOH prep showing hyphae from tinea pedis - branching fungal filaments crossing epithelial cell borders
FIGURE 248-1 (Tintinalli): Hyphae in KOH scraping from tinea pedis
  • Molluscum bodies: oval discs with homogeneous cytoplasm
  • Spores in hair: small, round spores packed closely within the hair shaft (endothrix = Trichophyton; ectothrix = Microsporum)

2. Tzanck Smear

Uses: Diagnose herpetic infections - HSV-1, HSV-2, varicella-zoster virus
"The presence of the multinucleated giant cell does not distinguish between herpes simplex, herpes zoster, and varicella syndromes." - Tintinalli
Specimen: Scrape the base of a recently unroofed vesicle or pustule; remove purulent fluid from base with scalpel; place on microscope slide
Steps:
  1. Air-dry the specimen
  2. Stain with Giemsa or Wright stain
  3. View under low power - scan for epithelial cells
  4. Positive finding: multinucleated giant cells (syncytium of epidermal cells with multiple overlapping nuclei)
Limitation: Does not differentiate HSV-1, HSV-2, or VZV; NAATs (PCR) are more sensitive and specific for definitive typing

3. Wood's Lamp Examination

Mechanism: UV light source at 365 nm wavelength
Fluorescent findings (Tintinalli):
Condition / OrganismFluorescence Color
Erythrasma (Corynebacterium minutissimum)Red or pink (coral-red)
Tinea capitis (Microsporum species)Green or yellow
Tinea versicolor (Malassezia species)Green or yellow
Pseudomonas skin infectionYellow or green
Porphyria cutanea tardaUrine fluoresces orange or red
Nits (lice eggs)Fluoresce
Note: >90% of tinea capitis is due to Trichophyton species which do NOT fluoresce - Wood's lamp has limited utility for tinea capitis in most regions.
Other uses: Detect extent of melasma (darker under Wood's lamp), assess depigmentation in vitiligo

4. Scabies Preparation

Best sites for specimen: Burrows (10 mm elongated papule with vesicle/pustule) on fingers, wrists, elbows
Steps:
  1. Identify burrow - a small black dot within represents the mite
  2. Apply a single drop of mineral oil to scalpel blade (keeps scrapings adherent)
  3. Hold skin taut; scrape across the lesion with scalpel tip
  4. Place material on slide with additional mineral oil drop; add coverslip
  5. View under low power
Positive findings:
  • Mite (8-legged creature)
  • Eggs (smooth ovals)
  • Feces (clusters of red-brown pellets)
Microscopic view of scabies mite with visible eggs and feces
FIGURE 248-4 (Tintinalli): Scabies mite with eggs and feces under microscopy
Classic scabies burrow - linear, slightly raised skin lesion with arrows indicating the burrow track
FIGURE 248-3 (Tintinalli): Classic scabies burrows on skin

5. Lice Preparation

Lice are usually found on scalp, eyelashes, and pubic areas - may be visible to the naked eye. Nits (eggs) adhere to the hair shaft; confirm by microscopy.

6. Ancillary Labs for Systemic Assessment

(Tintinalli Ch. 248 - ED Diagnosis)
"Ancillary studies may also be required to assess for systemic involvement." - Tintinalli
Lab FindingWhat It Suggests
Fever + leukocytosisUnderlying infectious disorder or autoimmune reaction
Elevated transaminases (patient on anticonvulsant)DRESS syndrome - hepatic involvement
DIC (↑PT/PTT, ↓fibrinogen, ↓platelets, ↑D-dimer)Bacteremia, meningococcemia, purpura fulminans, toxic shock syndrome
ThrombocytopeniaBacteremia, sepsis, toxic shock, TTP
Acute kidney injury (↑creatinine)Meningococcemia (DIC), DRESS, TEN
Eosinophilia (>500/µL)DRESS syndrome (present in ~30%)
HyperglycemiaNecrotizing fasciitis, severe sepsis (also SCORTEN factor for TEN mortality)
Hyponatremia (<135)Necrotizing fasciitis (LRINEC score)
CRP >150 mg/LNecrotizing fasciitis (highest LRINEC weight = +4 points)
Blood culturesMeningococcemia, necrotizing fasciitis with sepsis, cellulitis with systemic signs
ASO titerGroup A streptococcal infection
Imaging:
  • CT scan: assess depth of tissue involvement; gas tracking along fascial planes in necrotizing fasciitis; detect foreign bodies
  • X-ray: subcutaneous gas in necrotizing fasciitis/gas gangrene
  • Ultrasound: differentiate abscess from cellulitis; guide I&D; assess depth of soft tissue infection; detect foreign bodies

7. Skin Biopsy (ED Context)

Indications in the ED:
  • Confirm diagnosis of TEN/SJS (frozen section if available - rapid diagnosis)
  • Rule out malignancy (referral basis)
  • Bullous disorders (pemphigus vs. pemphigoid - direct immunofluorescence needed)
  • Vasculitis confirmation
Tintinalli on SJS/TEN biopsy: Histology shows lymphocytic infiltrate at dermoepidermal junction with keratinocyte necrosis - often full-thickness; cellular necrosis out of proportion to infiltrate.

PART 3 - ED MANAGEMENT FRAMEWORK

STEP 1: Identify Emergencies First

Tintinalli trigger signs for immediate action:
SignConsider
Widespread skin sloughing / positive Nikolsky signSJS/TEN → stop drug, admit ICU/burn unit
Petechiae + fever + ill-appearingMeningococcemia → IV ceftriaxone STAT
Pain out of proportion to skin findings + systemic toxicityNecrotizing fasciitis → surgical consult STAT
Skin + eosinophilia + organ dysfunctionDRESS → stop drug, admit
>90% BSA erythema + systemic compromiseErythroderma → admit, thermoregulation
Angioedema approaching larynxSecure airway; C1 inhibitor/icatibant/epinephrine

STEP 2: Systemic Corticosteroids

(Tintinalli Ch. 248 - ED Treatment)
"Some severe widespread dermatologic syndromes, such as erythema multiforme, toxic epidermal necrolysis, and vasculitis, are best treated with systemic steroids only after consultation with a dermatologist."
Use systemic steroids without dermatology consult for:
  • Urticaria and angioedema
  • Contact/allergic dermatitis (Toxicodendron/poison ivy)
  • Other allergic reactions
Systemic steroid protocols:
ConditionRegimen
Severe contact dermatitis / poison ivyPrednisone 0.5 mg/kg/day × 2-3 weeks taper
SJS (EM major)Methylprednisolone 125 mg IV q6h (or equivalent)
DRESS (severe)Prednisone 1-2 mg/kg/day; taper slowly over weeks-months
Exfoliative dermatitisOnly after dermatology consult
Urticaria/angioedemaMethylprednisolone 125 mg IV (or equivalent oral)

STEP 3: Antihistamines - Dosing Table

(Tintinalli TABLE 248-8)
DrugAdult DosePediatric DoseClass
Diphenhydramine (Benadryl)25-50 mg PO/IV/IM QID5 mg/kg/day in 4 divided doses (max 300 mg/day)H1 (sedating)
Hydroxyzine25-100 mg PO TID-QID2 mg/kg/day PO in 4 divided dosesH1 (sedating)
Cetirizine (Zyrtec)5-10 mg PO once daily≥6 years: 5-10 mg PO once dailyH1 (non-sedating)
Fexofenadine (Allegra)60 mg PO BID≥6 years: 30 mg PO BIDH1 (non-sedating)
Loratadine (Claritin)10 mg PO once daily≥6 years: 10 mg PO once dailyH1 (non-sedating)
Famotidine (Pepcid)20 mg PO BID0.5 mg/kg/day in 2 divided doses (max 40 mg/day)H2 (adjunct in severe reactions)
Ranitidine (Zantac)150 mg PO BID5-10 mg/kg/day in 2 divided doses (max 300 mg/day)H2 (adjunct)

STEP 4: Topical Corticosteroids - Potency Classification

(Tintinalli TABLE 248-7)
US GroupPotencyRepresentative Agents
1 - SuperpotentVery PotentClobetasol (Temovate) 0.05% cream/ointment; Halobetasol 0.05%; Betamethasone (Diprolene)
2 - PotentPotentFluocinonide (Lidex) 0.05% ointment; Halcinonide 0.1% cream; Mometasone (Elocon) 0.1% ointment
3 - Upper mid-strengthBetamethasone (Diprolene) 0.05% lotion; Fluticasone (Cutivate) 0.005% ointment; Triamcinolone 0.1% ointment
4 - Mid-strengthMometasone (Elocon) 0.1% cream/lotion
5 - Lower mid-strengthModerateBetamethasone 0.1% cream; Fluocinolone (Synalar) 0.025% cream; Fluticasone (Cutivate) 0.05% cream
6 - MildAlclometasone 0.05%; Desonide (Desonate) 0.05% cream; Triamcinolone 0.025% cream
7 - Least PotentMildHydrocortisone 1% or 2.5% cream/lotion/ointment
Body area selection rule:
  • Face, intertriginous areas, children: Low potency (Group 6-7) only
  • Extremities, trunk: Intermediate (Group 3-5)
  • Thick plaques (psoriasis, palms, soles): High potency (Group 1-2)
  • Never use superpotent steroids on face, groin, or under occlusion chronically

STEP 5: Topical Antibiotics

(Tintinalli Ch. 248)
AgentUse
Mupirocin (Bactroban) 2%Impetigo - as effective as oral antibiotics for superficial skin infection
Polymyxin BWound dressing adjunct; reduce bacterial colonization
BacitracinWound dressing; prevent adherence of dressings to wounds
NeomycinCombined wound dressings (note: common sensitizer - contact allergy risk)
Silver sulfadiazineBurn wounds; do NOT apply to face (causes staining); wipe off prior application before reapplying
Oral tetracycline rinsesAphthous stomatitis
"Topical antibacterial agents are rarely useful as primary therapy for superficial bacterial infections of the skin. The exception is topical mupirocin." - Tintinalli

STEP 6: Antipruritic (Non-Steroidal) Agents

(Tintinalli Ch. 248)
AgentDoseNotes
Capsaicin 0.025% topicalApply TID × up to 4 weeksDesensitizes nerve fibers via substance P depletion; not for age <10 years
Pramoxine 1-2%Apply as directedTopical anesthetic; limited evidence
EMLA (lidocaine 2.5% + prilocaine 2.5%)Apply as directedTopical anesthetic for pruritus; evidence limited
Domeboro solution (aluminum sulfate 1:10)Soaks/compressesAstringent; relieves weeping, pruritic lesions
Oatmeal bathsAs neededSoothing antipruritic for widespread pruritus
Open wet dressings (tap water or saline)TIDCleanse crusts and exudates painlessly; reduce discomfort
Emollients/moisturizersAfter bathing while skin still moistRestore water and lipids; reduce pruritus and tightness

PART 4 - MANAGEMENT SUMMARY BY SECONDARY LESION TYPE

Secondary LesionMost Common DiagnosesED Management
ScalesPsoriasis, tinea, pityriasis rosea, drug eruptionKOH prep → antifungals or topical steroids
CrustsImpetigo, eczema, contact dermatitisMupirocin for impetigo; wet compresses to loosen crusts; topical steroids for eczema
ErosionsHSV, pemphigus, candida, impetigoTzanck smear → antivirals; antifungals; wound care
UlcersSyphilis, chanroid, diabetic/pressure ulcersSTI testing; wound care; appropriate antibiotics; vascular/wound surgery referral
FissuresTinea pedis, xerosis, anal fissureAntifungals; emollients; topical steroids; stool softeners
ExcoriationsScabies, atopic dermatitisScabies prep → permethrin; antihistamines; topical steroids
LichenificationChronic eczema, lichen simplexHigh-potency topical steroids; antihistamines for itch-scratch cycle
Crusted + weeping vesiclesHerpes zoster, impetigo, contact dermatitisTzanck; NAATs; antivirals; wet compresses; mupirocin
Purpura (non-blanching)Meningococcemia, vasculitis, ITPURGENT: blood cultures, CBC, coagulation; IV antibiotics if meningococcemia suspected
BullaeTEN, SJS, pemphigus, bullous impetigoSCORTEN; stop drug; burn/ICU care; IV antibiotics for impetigo

Sources:
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