An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
PURPURIC RASHES
Purpura may be benign vascular leakage—or the visible surface of meningococcemia, DIC, TTP, or catastrophic thrombocytopenia. The fatal error is waiting for a complete laboratory explanation while an immediately treatable syndrome progresses.
A 27-year-old woman arrives with purple pinpoints scattered across her legs and fresh bruises blooming along her forearms. She says her gums bled while brushing her teeth this morning, and her partner noticed she was “not quite herself” during the drive in. In the triage chair, she develops a sudden, severe headache and asks the nurse what the spots mean. The CBC and smear are still pending.
— What’s your move? Read on.
Before you read
What single bedside distinction separates platelet failure from coagulation-factor failure?
When should empiric treatment begin before confirmatory testing?
When to Think of It
Enter purpura into the differential with nonblanching petechiae, palpable purpura, ecchymoses, mucosal bleeding, or rapidly progressive skin discoloration. Fever, hypotension, altered mental status, severe headache, renal injury, neurologic findings, pregnancy/postpartum state, new medications, or hemolysis should raise the urgency.
Sick or Not Sick
The key call is stable isolated skin findings versus systemic illness with possible infection, DIC, TTP, or profound thrombocytopenia. Shock, rapidly spreading purpura, fever, encephalopathy, focal neurologic findings, renal failure, or active bleeding means resuscitation and specialty consultation now—not outpatient dermatology.
The First Fifteen Minutes
Place on monitor; obtain two IVs, bedside glucose, CBC with smear, PT/INR, aPTT, fibrinogen, CMP, lactate, type and screen, urinalysis, pregnancy test, and blood cultures if febrile.
If septic appearance, fever, or rapidly progressive purpura suggests meningococcemia: ceftriaxone 2 g IV now, because rapid bactericidal therapy reduces invasive meningococcal mortality. Add vancomycin 15–20 mg/kg IV when resistant pneumococcus or an undifferentiated bacterial meningitis syndrome remains plausible; check institutional dosing/renal-adjustment guidance.
If TTP is strongly suspected—thrombocytopenia plus microangiopathic hemolytic anemia, neurologic findings, renal injury, or fever—send ADAMTS13 before therapy if it will not delay treatment and call hematology for plasma exchange. Give methylprednisolone 1 g IV daily when hematology agrees, because immune suppression reduces ongoing autoantibody-mediated ADAMTS13 inhibition; regimen varies by protocol.
If life-threatening bleeding with severe thrombocytopenia: platelet transfusion is generally one adult apheresis unit IV, because it temporarily raises the platelet mass; avoid routine platelet transfusion in suspected TTP unless hemorrhage is immediately life-threatening or directed by hematology.
If major hemorrhage or DIC with low fibrinogen: activate a massive-transfusion protocol as indicated; cryoprecipitate dosing varies by laboratory and product, commonly 10 units IV, because it restores fibrinogen. Use the institutional transfusion protocol.
If hypotension: crystalloid 500–1,000 mL IV bolus, reassessing perfusion; if shock persists, norepinephrine 0.05–0.1 mcg/kg/min IV infusion, titrated to a MAP around 65 mm Hg, because vasoconstriction restores perfusion pressure.
Definitive Care & Disposition
Treat the cause: plasma exchange urgently for suspected TTP; antibiotics and source control for sepsis; stop offending medications; manage DIC with treatment of the underlying process and targeted blood products. Admit patients with systemic symptoms, severe thrombocytopenia, active bleeding, hemolysis, coagulopathy, renal injury, or diagnostic uncertainty. ICU care is appropriate for shock, neurologic deterioration, respiratory compromise, rapidly progressive purpura, or need for plasma exchange or massive transfusion. Stable, isolated, mild purpura with reassuring testing may receive expedited hematology or dermatology follow-up.
How This One Kills
The dangerous miss is labeling purpura “ITP” without reviewing the smear and hemolysis markers, allowing TTP to progress to irreversible neurologic injury, renal failure, or death while awaiting ADAMTS13.
The Differential — What Else Looks Like This
Petechiae from isolated thrombocytopenia — normal coagulation studies and no hemolysis; confusing it with TTP delays plasma exchange.
DIC — prolonged PT/aPTT, elevated D-dimer, and low fibrinogen; confusing it with TTP leads to the wrong blood-product and source-control strategy.
Meningococcemia — fever, toxicity, rapidly spreading purpura, shock; confusing it with a noninfectious rash delays antibiotics.
Small-vessel vasculitis — palpable, often dependent purpura with renal or joint involvement; confusing it with sepsis may delay biopsy and immunologic evaluation.
The Second-Day Story
Older adults may present with weakness, confusion, or anemia rather than obvious bleeding; patients with dark skin may have purpura that is easier to feel than see; and partially treated sepsis may lack fever. Do not let a modest-appearing rash reassure you: palpate for nonblanching lesions, inspect mucosa, trend mental status and urine output, and use the smear, platelet count, hemolysis profile, and coagulation studies to identify systemic disease.
Back to Our Patient
Back to our 27-year-old woman: her petechiae, mucosal bleeding, headache, and confusion make this a sick purpuric presentation, not an outpatient rash. The CBC shows severe thrombocytopenia, hemoglobin is low, creatinine is elevated, smear shows schistocytes, and coagulation studies are near normal—recognition of suspected TTP. After blood is sent for ADAMTS13 without delaying treatment, hematology is called, methylprednisolone 1 g IV is given, and she is transferred emergently for plasma exchange and ICU monitoring.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 27-year-old woman with acute petechiae, mucosal bleeding, headache, and new confusion. Symptoms began today without trauma, and she has no fever, diarrhea, pregnancy, or known liver disease. She is tachycardic but maintaining pressure, with diffuse nonblanching petechiae and scattered ecchymoses, without meningismus or focal infection. Her CBC shows severe thrombocytopenia and anemia, the smear has schistocytes, creatinine is elevated, and PT and aPTT are near normal. I’m concerned for TTP rather than isolated thrombocytopenia or DIC, so I’ve sent ADAMTS13, called hematology, started empiric steroid therapy, and am arranging emergent plasma exchange and ICU admission.”
Study Directive
Draw a bedside algorithm separating platelet disorders, coagulation disorders, vasculitis, and sepsis.
Memorize the TTP pattern: thrombocytopenia + MAHA + neurologic/renal features + usually normal coagulation studies.
Review one peripheral smear and identify schistocytes, spherocytes, blasts, and giant platelets.
Practice stating the empiric management of suspected TTP in one sentence without waiting for ADAMTS13.
SJS/TEN is a rapidly progressive mucocutaneous emergency with epidermal loss, ocular injury, airway risk, infection, and multiorgan failure. Mortality rises...
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The Case
A 38-year-old man sits forward, lips cracked and stuck together with dried blood. His eyes are red and painfully light-sensitive, and dusky patches have spread from his chest across his back since yesterday. He started a new prescription two weeks ago and now says swallowing feels like “glass.” The skin is beginning to lift with gentle pressure, but the extent of injury has not yet been mapped.
Before You Read
Which findings distinguish SJS/TEN from a routine morbilliform drug eruption?
What must happen before any disease-specific debate?
How should burn-unit transfer and fluid needs be determined?
Why It Matters
SJS/TEN is a rapidly progressive mucocutaneous emergency with epidermal loss, ocular injury, airway risk, infection, and multiorgan failure. Mortality rises when the culprit drug is continued or when the patient is managed as a simple dermatologic admission.
When to Think of It
Think SJS/TEN with fever or malaise followed by skin pain, dusky atypical targets, blistering, epidermal detachment, and involvement of at least two mucosal surfaces—oral, ocular, genital, or respiratory. Common triggers include sulfonamides, anticonvulsants, allopurinol, oxicam NSAIDs, nevirapine, and other medications, often within 1–8 weeks of initiation.
Sick or Not Sick
The critical call is epidermal detachment with mucosal/systemic involvement versus an uncomplicated drug eruption. Assess airway, hemodynamics, urine output, temperature, ocular function, pain, and percent body surface area detached or detachable. Calculate SCORTEN after initial stabilization; involve dermatology, burn surgery, ophthalmology, and critical care early.
The First Fifteen Minutes
Stop every nonessential medication, especially the suspected culprit, and document the exposure; removing the antigen is the most important disease-modifying action.
Assess airway early. If airway edema or progressive respiratory compromise: intubate with a cuffed endotracheal tube using a difficult-airway plan; SJS/TEN mucosal edema can rapidly make later intubation hazardous.
If hypovolemia or hypotension: give balanced crystalloid 500–1,000 mL IV bolus, then reassess urine output and perfusion; fluid loss resembles a burn but usually requires less than classic burn formulas. If shock persists, norepinephrine 0.05–0.1 mcg/kg/min IV infusion, titrated to MAP, restores vascular tone.
For severe pain: fentanyl 25–50 mcg IV, repeated every 5 minutes to effect with respiratory monitoring, because denuded skin can cause profound pain; use lower doses in frail or hypoventilating patients.
For fever or mild pain when enteral intake is possible: acetaminophen 650–1,000 mg PO, keeping the total at or below 4 g/day in healthy adults and lower with liver disease or heavy alcohol use.
For ocular irritation while awaiting ophthalmology: preservative-free artificial tears, commonly 1–2 drops in each affected eye every 1–2 hours, protect the cornea; avoid topical anesthetic for ongoing use.
Do not routinely give prophylactic antibiotics or empiric systemic steroids in the first minutes; antibiotics are triggered by documented or strongly suspected infection, and immunomodulatory regimens require dermatology/burn expertise.
Definitive Care & Disposition
Transfer SJS/TEN to a burn center or ICU-capable dermatology service. Provide temperature-controlled, nonadherent wound care, careful fluid/electrolyte replacement, nutrition, VTE prophylaxis when safe, and frequent renal, pulmonary, and infectious monitoring. Urgent ophthalmology evaluation is required; genital and urinary involvement may require urology. Diagnosis is supported by skin biopsy. Cyclosporine, etanercept, IVIG, or systemic corticosteroids may be considered early by specialists, but comparative evidence and dosing vary; verify Lexicomp, UpToDate, or institutional protocol.
How This One Kills
The classic fatal failure is continuing the culprit medication—or discharging the patient with “allergic rash”—while epidermal detachment expands and ocular, airway, and fluid-loss complications become irreversible.
The Atypical Presentation
Older adults, immunocompromised patients, and partially treated patients may have little fever despite extensive epidermal loss. Darker skin can make dusky erythema harder to recognize, while mucosal disease may precede visible skin findings by a day or more. Skin pain, ocular photophobia, oral erosions, genital dysuria, and a recent high-risk medication should trigger a full skin-and-mucosa examination even when the rash looks nonspecific.
Back to Our Patient
Back to our 38-year-old man: painful dusky lesions, epidermal sloughing, cracked lips, photophobia, and odynophagia after a recent medication identify SJS/TEN, and his mucosal and skin findings make him sick even before hypotension develops. The suspected drug is stopped immediately, airway and ocular assessments begin, IV access and monitoring are established, and analgesia and carefully titrated crystalloid are provided. Dermatology, burn surgery, ophthalmology, and critical care accept him for ICU/burn-center transfer, where biopsy, wound care, nutrition, and complication surveillance continue.
Patient Presentation to Attending
“This is a 38-year-old man with two days of feverish malaise followed by painful dusky skin lesions, oral erosions, photophobia, and dysphagia after starting a new medication two weeks ago. He has no prior similar eruption and no sick contacts. Exam shows tender atypical targets with early epidermal detachment, hemorrhagic crusting of the lips, conjunctival injection, and genital mucosal erosions, without focal pneumonia or shock currently. I’m concerned for SJS/TEN rather than erythema multiforme or DRESS. I’ve stopped the suspected medication, assessed his airway and fluid status, started monitored analgesia, obtained labs and skin-biopsy consultation, and am arranging urgent burn-center, dermatology, and ophthalmology admission.”
Study Directive
Memorize the high-risk medication classes and typical latency windows.
Practice estimating detached/detachable body surface area using the patient’s palm as approximately 1%.
Review SCORTEN variables and calculate it for three practice cases.
Build a first-hour checklist covering culprit-drug withdrawal, airway, eyes, fluids, analgesia, biopsy, consultation, and disposition.
Key Medications
Fentanyl 25–50 mcg IV, titrated every 5 minutes with monitoring.
Acetaminophen 650–1,000 mg PO/IV every 6 hours as needed, maximum 4 g/day in healthy adults; use a lower maximum with hepatic disease or alcohol use.
Norepinephrine 0.05–0.1 mcg/kg/min IV infusion, titrated to perfusion.
Preservative-free artificial tears 1–2 drops every 1–2 hours while awake.
Specialist-directed cyclosporine is often 3–5 mg/kg/day PO or IV divided doses, but dosing, renal contraindications, and monitoring vary—check Lexicomp, UpToDate, or local protocol.
IVIG regimens vary substantially, commonly total 2 g/kg divided over 2–5 days; verify specialist and institutional guidance.
Pediatric patients require burn-center consultation and weight-based analgesic/fluid planning; do not extrapolate adult medication limits.
High-Yield Pearls
Skin pain and mucosal erosions are more discriminating than the visual appearance of the rash.
Ocular involvement is an emergency even when total skin detachment is limited; early ophthalmology can prevent corneal scarring and blindness.
SJS/TEN fluid needs are burn-like but not automatically the full Parkland formula; titrate to perfusion, urine output, and ongoing losses.
The Mimics
Staphylococcal scalded-skin syndrome — superficial split with positive Nikolsky but usually spares mucosa and occurs mainly in children; confusing it with SJS/TEN changes antibiotic and infection-control priorities.
DRESS — facial edema, eosinophilia, organ injury, and usually less epidermal detachment; confusing it with TEN may underrecognize delayed hepatitis or nephritis.
Erythema multiforme — fixed classic targets, often acral and HSV-associated, with limited detachment; confusing it with SJS/TEN underestimates the need for ICU-level care.
Generalized bullous fixed drug eruption — sharply demarcated recurrent lesions at prior sites; confusing it with TEN may lead to unnecessary extensive burn management, though severe cases can overlap.
Board Question
A patient has 25% epidermal detachment, severe oral and ocular erosions, and skin pain after starting lamotrigine. Which intervention has the highest immediate priority?
AContinue lamotrigine and start antihistamines
BStop lamotrigine and transfer to a specialized burn/ICU service
CApply topical corticosteroid and discharge
DStart prophylactic broad-spectrum antibiotics in the absence of infection
Reveal answer
Correct: B
Stop lamotrigine and transfer to a specialized burn/ICU service. Immediate withdrawal of the culprit drug and supportive critical care are foundational. Routine prophylactic antibiotics are not recommended without evidence of infection.
Use this guideline to standardize immediate supportive care, including prompt culprit-drug withdrawal, severity assessment, wound and mucosal care, fluid management, temperature control, analgesia, nutrition, and early multidisciplinary ref
3 of 4
DERMATOLOGIC MANIFESTATIONS OF VZV
VZV can cause localized dermatomal disease, blindness, encephalitis, pneumonitis, and disseminated infection. Early antiviral therapy is time-sensitive,...
A 61-year-old woman presses a cool washcloth against the left side of her face. Clusters of clear blisters run from her ear toward her scalp, and she says the pain began before the rash, like an electric wire under the skin. Her left eye feels gritty, and her smile appears slightly uneven in the room’s reflection. She has not yet had her vision or hearing formally tested.
Before You Read
Which VZV skin distribution turns a rash into an ophthalmic emergency?
When is oral therapy inadequate?
What findings require airborne isolation and evaluation for dissemination?
Why It Matters
VZV can cause localized dermatomal disease, blindness, encephalitis, pneumonitis, and disseminated infection. Early antiviral therapy is time-sensitive, especially with facial, ocular, neurologic, or immunocompromised presentations.
When to Think of It
Look for grouped vesicles on an erythematous base in a unilateral dermatome, usually with neuropathic pain. Varicella produces successive crops of pruritic lesions in different stages, beginning on the trunk and face. Red flags include V1 involvement, Hutchinson sign, immunocompromise, pregnancy, neonatal exposure, diffuse lesions, respiratory symptoms, severe headache, altered mental status, or cranial neuropathies.
Sick or Not Sick
The key call is localized, uncomplicated zoster versus ocular, neurologic, visceral, or disseminated VZV. Any V1 rash, eye pain, photophobia, vision change, immunocompromise, diffuse eruption, pneumonia, or encephalopathy requires same-day specialty evaluation and often admission or IV therapy.
The First Fifteen Minutes
Place suspected varicella or disseminated zoster on airborne and contact precautions; localized zoster in an immunocompetent patient can be covered and managed with standard precautions.
If uncomplicated localized zoster in an immunocompetent adult within 72 hours of rash onset: valacyclovir 1 g PO three times daily for 7 days, because it suppresses viral replication and reduces lesion duration and acute pain; adjust for renal function.
If disseminated disease, visceral involvement, severe immunocompromise, or inability to take oral medication: acyclovir 10 mg/kg IV every 8 hours, because IV exposure is reliable in high-risk disease; adjust for renal function and hydrate to reduce nephrotoxicity.
For pain: acetaminophen 650–1,000 mg PO every 6 hours as needed, maximum 4 g/day in healthy adults; use a lower maximum with liver disease. Severe pain may require fentanyl 25–50 mcg IV, titrated with monitoring.
If bacterial superinfection is clinically apparent: obtain cultures and treat with an antibiotic selected for the site and severity; do not give antibiotics solely because vesicles are present.
Obtain fluorescein examination and urgent ophthalmology consultation for eye pain, photophobia, vision change, conjunctival injection, or V1 involvement; avoid topical ocular steroids unless directed by ophthalmology.
Definitive Care & Disposition
Ophthalmic zoster requires urgent ophthalmology, slit-lamp evaluation, and systemic antiviral therapy. Admit immunocompromised patients with extensive disease, disseminated lesions, pneumonia, hepatitis, encephalitis, severe pain, or inability to maintain hydration. Suspected VZV encephalitis requires CSF evaluation when safe and IV acyclovir. Provide wound care, analgesia, and counseling about avoiding contact with pregnant, immunocompromised, and unvaccinated individuals until lesions crust. Consider postherpetic neuralgia prevention and vaccination counseling after recovery.
How This One Kills
The dangerous miss is treating a V1 eruption as routine shingles and failing to examine the cornea; keratitis, uveitis, and retinal disease can progress while external skin lesions appear limited.
The Atypical Presentation
In older adults, pain may precede the eruption by several days, and lesions may be sparse or absent in zoster sine herpete. Immunocompromised patients may have hemorrhagic, necrotic, diffuse, or minimally vesicular lesions. When the distribution is unclear, test vesicle fluid with PCR and let the host status, pain pattern, cranial-nerve findings, and systemic symptoms determine urgency.
Back to Our Patient
Back to our 61-year-old woman: the unilateral vesicles and neuropathic pain suggest zoster, but V1/facial involvement, gritty eye symptoms, and facial asymmetry make this a high-risk presentation. She is placed in appropriate precautions, receives valacyclovir 1 g PO three times daily while renal function is checked, and undergoes urgent fluorescein and ophthalmologic assessment; if ocular or neurologic disease is confirmed, therapy escalates to IV acyclovir. She is admitted or placed in closely coordinated specialty follow-up depending on corneal, neurologic, and social findings—not discharged as uncomplicated shingles before the eye is evaluated.
Patient Presentation to Attending
“This is a 61-year-old woman with two days of left facial pain followed by grouped vesicles across the left forehead, scalp, and ear. She reports gritty eye discomfort but no vision loss, fever, dyspnea, or confusion; her smile is mildly asymmetric. Exam shows a unilateral V1-predominant vesicular eruption with possible external-ear involvement, and I have not yet excluded corneal disease. I’m concerned for ophthalmic zoster with possible cranial neuropathy rather than HSV or dermatitis. I’ve initiated precautions, started renal-adjusted systemic antiviral therapy, arranged fluorescein examination and urgent ophthalmology, and will admit if ocular, neurologic, or disseminated involvement is found.”
Study Directive
Sketch the trigeminal dermatomes and mark the ocular-risk territory.
Practice distinguishing localized zoster, disseminated zoster, and primary varicella from photographs or cases.
Memorize oral valacyclovir and IV acyclovir adult dosing, including the need for renal adjustment.
Write a one-minute ocular zoster plan including isolation, fluorescein, ophthalmology, antivirals, and disposition.
Key Medications
Valacyclovir 1 g PO three times daily for 7 days for typical adult herpes zoster; renal adjustment is required.
Acyclovir 10 mg/kg IV every 8 hours for severe/disseminated disease or significant immunocompromise; use ideal/adjusted weight and renal-adjusted institutional guidance when appropriate.
Acetaminophen 650–1,000 mg PO/IV every 6 hours as needed, maximum 4 g/day in healthy adults.
Fentanyl 25–50 mcg IV, titrated with cardiorespiratory monitoring for severe pain.
Pediatric varicella/zoster dosing is weight-based and age-dependent; consult a pediatric infectious disease or dosing reference.
Antiviral dosing varies with renal function, pregnancy, and immunocompromise; check Lexicomp, UpToDate, or institutional protocol if uncertain.
High-Yield Pearls
Pain before rash is common in zoster; absence of visible vesicles does not exclude VZV.
Disseminated zoster is defined clinically by widespread lesions outside the primary or adjacent dermatomes, especially in an immunocompromised host.
Ear vesicles plus facial weakness suggest Ramsay Hunt syndrome and require attention to hearing, vestibular symptoms, and corneal protection.
The Mimics
HSV — recurrent vesicles often localized to the same site and may cross dermatomes; confusing it with VZV can miss disseminated zoster risk and appropriate isolation.
Contact dermatitis — pruritic and patterned rather than neuropathic and dermatomal; confusing it with zoster delays antivirals.
Impetigo — honey-colored crust rather than grouped vesicles; confusing it with VZV may miss bacterial infection.
Disseminated HSV — widespread vesicles with severe systemic disease, especially in immunocompromised patients; confusing it with localized zoster underestimates visceral risk.
Board Question
An immunocompetent 68-year-old man presents with vesicles on the tip of his nose and right forehead, with eye pain and photophobia. What is the best next step?
AReassurance and topical antibiotic ointment
BUrgent ophthalmologic evaluation and systemic antiviral therapy
CIncision and drainage of the vesicles
DOral prednisone alone
Reveal answer
Correct: B
Urgent ophthalmologic evaluation and systemic antiviral therapy. Nasal-tip involvement, or Hutchinson sign, suggests nasociliary V1 involvement and increased ocular risk. Eye examination should not be delayed while waiting for progression.
A practical reference for recognizing the cutaneous patterns of primary varicella and herpes zoster, including atypical presentations that may alter isolation, testing, and antiviral decisions in the ED.
HSV may be a localized nuisance, but eczema herpeticum, disseminated HSV, neonatal exposure, and HSV keratitis can threaten vision, organs, and life. The...
A 24-year-old man arrives with a painful cluster of tiny blisters at the corner of his mouth and several new lesions on his forearm. He has eczema, and the forearm lesions are tender rather than itchy; he reports fever and chills since last night. His right eye is beginning to burn, though he denies vision loss. The rash is expanding while the question of how far the infection has traveled remains unanswered.
Before You Read
Which HSV skin patterns require systemic rather than topical management?
How do you recognize eczema herpeticum before it becomes disseminated?
What eye findings prohibit empiric steroid treatment?
Why It Matters
HSV may be a localized nuisance, but eczema herpeticum, disseminated HSV, neonatal exposure, and HSV keratitis can threaten vision, organs, and life. The combination of painful monomorphic vesicles, systemic illness, and impaired skin barrier should accelerate treatment.
When to Think of It
Typical manifestations include grouped painful vesicles or erosions on the lips, face, genitals, buttocks, fingers, or mucosa. Eczema herpeticum presents with abrupt, painful, monomorphic “punched-out” vesicles or erosions over eczematous skin, often with fever and toxicity. Consider disseminated disease with widespread lesions, hepatitis, pneumonitis, encephalitis, immunocompromise, or ocular involvement.
Sick or Not Sick
The decisive call is localized mucocutaneous HSV versus eczema herpeticum, ocular disease, neonatal disease, or dissemination. Eye pain, photophobia, visual change, lesions near the eye, systemic toxicity, extensive disease, pregnancy, immunocompromise, or inability to take oral medication requires urgent consultation and usually systemic therapy.
The First Fifteen Minutes
Inspect the eyes, oral cavity, genitals, and entire skin surface; obtain HSV PCR from a fresh vesicle or ulcer when the diagnosis is uncertain or disease is severe.
If eczema herpeticum, disseminated disease, encephalitis, severe immunocompromise, or inability to tolerate oral medication: acyclovir 10 mg/kg IV every 8 hours, because reliable systemic levels suppress potentially invasive viral replication; adjust for renal function.
If localized mucocutaneous HSV in an immunocompetent adult: acyclovir 400 mg PO five times daily for 7–10 days, or valacyclovir 1 g PO twice daily for 7–10 days, because oral nucleoside analog therapy shortens active viral replication; exact duration depends on site and recurrence.
For painful lesions: acetaminophen 650–1,000 mg PO every 6 hours as needed, maximum 4 g/day in healthy adults; reduce the maximum with liver disease. Severe pain may be treated with fentanyl 25–50 mcg IV, titrated with monitoring.
If bacterial superinfection is suspected: obtain a culture and start site-appropriate antibiotics; crusting alone is not proof of bacterial infection.
If eye pain, photophobia, foreign-body sensation, or visual change is present: urgent ophthalmology evaluation and fluorescein/slit-lamp examination; do not apply topical ocular corticosteroids unless ophthalmology directs them, because they can worsen active epithelial HSV keratitis.
Definitive Care & Disposition
Admit patients with eczema herpeticum who are toxic, extensive, immunocompromised, unable to hydrate, or failing oral treatment; evaluate for bacterial superinfection and systemic involvement. HSV encephalitis requires IV acyclovir and neurologic/CSF evaluation. Suspected keratitis requires same-day ophthalmology. Provide contact precautions for draining lesions, wound care, hydration, pain control, and counseling about sexual and skin-to-skin transmission. Neonates, pregnant patients near delivery, and severely immunocompromised patients require specialist-directed management.
How This One Kills
The catastrophic error is treating eczema herpeticum as an eczema flare with topical steroids alone, allowing rapid viral dissemination, bacterial superinfection, ocular injury, or encephalitis.
The Atypical Presentation
In immunocompromised patients, lesions may be necrotic, verrucous, or minimally vesicular, and fever may be absent. In darker skin, erythema is less obvious, so the key clues are pain, monomorphic punched-out erosions, rapid spread, and systemic symptoms. A negative swab from a crusted or late lesion does not reliably exclude HSV; sample the base of a fresh lesion and use PCR when stakes are high.
Back to Our Patient
Back to our 24-year-old man: painful monomorphic lesions spreading over eczematous skin, fever, and new eye burning identify eczema herpeticum with possible ocular involvement, not a routine eczema flare. He is assessed as sick because of rapid spread, systemic symptoms, and an eye complaint; fresh lesions are swabbed for PCR, ophthalmology is contacted, and IV acyclovir 10 mg/kg every 8 hours is started while renal function is assessed. He is admitted for antiviral therapy, ocular surveillance, hydration, and monitoring for dissemination or bacterial superinfection.
Patient Presentation to Attending
“This is a 24-year-old man with eczema who developed painful grouped vesicles at the mouth yesterday and rapidly spreading monomorphic punched-out erosions on the forearm, accompanied by fever and new right-eye burning. He has no confusion, dyspnea, or visual loss, but the lesions are tender rather than pruritic and are expanding. Exam shows vesicles and punched-out erosions over eczematous skin, without hypotension or focal neurologic deficit. I’m concerned for eczema herpeticum with possible ocular HSV rather than an eczema flare or impetigo. I’ve obtained a fresh-lesion PCR, started IV acyclovir, avoided ocular steroids, called ophthalmology, and recommend admission for treatment and monitoring.”
Study Directive
Compare HSV, VZV, impetigo, and eczema herpeticum using distribution, pain, lesion morphology, and host factors.
Memorize oral versus IV acyclovir/valacyclovir indications and doses.
Practice a complete eye screen for facial HSV: pain, photophobia, vision, fluorescein, and urgent ophthalmology.
Review the indications for admission in eczema herpeticum and write them from memory.
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Mechanism Pearl of the Day: The skin is both a diagnostic map and a barrier: dermatomal nerve distribution points to VZV, recurrent mucocutaneous sites point toward HSV, epidermal detachment signals immune-mediated barrier failure in SJS/TEN, and nonblanching purpura signals blood or vessel-wall pathology. When the barrier fails—or when the host is immunocompromised—the same visible rash can conceal rapidly invasive disease.
Key Medications
Acyclovir 400 mg PO five times daily for 7–10 days for localized adult mucocutaneous HSV.
Valacyclovir 1 g PO twice daily for 7–10 days as an alternative for initial or significant mucocutaneous disease; renal adjustment required.
Acyclovir 10 mg/kg IV every 8 hours for eczema herpeticum with systemic illness, disseminated disease, CNS disease, or severe immunocompromise; verify renal-adjusted dosing.
Acetaminophen 650–1,000 mg PO/IV every 6 hours as needed, maximum 4 g/day in healthy adults.
Fentanyl 25–50 mcg IV, titrated with monitoring for severe pain.
Pediatric and neonatal acyclovir dosing is weight- and age-dependent and must be checked in a pediatric reference or institutional protocol.
Acyclovir/valacyclovir dosing varies with renal function and indication; check Lexicomp, UpToDate, or institutional guidance if uncertain.
High-Yield Pearls
“Painful and monomorphic” is the eczema-herpeticum clue; ordinary eczema is usually pruritic and polymorphic.
Never use topical ocular steroids for suspected epithelial HSV keratitis without ophthalmology direction.
Sampling the base of a fresh vesicle is more useful than swabbing a dry crust.
The Mimics
Eczema flare or impetiginized eczema — usually pruritic and polymorphic rather than painful, monomorphic punched-out erosions; confusing it with eczema herpeticum delays IV antiviral therapy.
Varicella-zoster virus — typically dermatomal in zoster, whereas HSV often recurs at the same mucocutaneous site; confusing disseminated VZV and HSV can impair isolation and antiviral selection.
Hand-foot-and-mouth disease — oral and acral lesions with a characteristic distribution, generally in children; confusing it with HSV may lead to unnecessary invasive evaluation.
Bacterial cellulitis — diffuse warmth and tenderness without grouped vesicles; confusing it with HSV delays antibiotics and source assessment.
Board Question
A patient with severe atopic dermatitis develops fever and numerous monomorphic punched-out erosions over the face and trunk. Which treatment is most appropriate?
AHigh-potency topical corticosteroid alone
BOral antihistamine alone
CSystemic acyclovir
DIncision and drainage of each lesion
Reveal answer
Correct: C
Systemic acyclovir. Painful monomorphic punched-out erosions with fever over eczematous skin are characteristic of eczema herpeticum. Systemic antiviral therapy is required, with IV therapy for toxic, extensive, immunocompromised, or otherwise high-risk patients.
Reviews cutaneous HSV disease and emerging topical immune-directed therapies, offering context for persistent or recurrent lesions that respond poorly to standard antiviral treatment.
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
A 24-year-old man is brought in with palpitations, chest tightness, and lightheadedness that began abruptly an hour ago. He is anxious, diaphoretic, and pale, with a blood pressure of 96/58. What’s the diagnosis, and the first move?
Check your answer
Atrial Fibrillation in Pre-excitation (WPW). If the patient is unstable, go straight to urgent synchronized DC cardioversion. If stable, avoid every AV nodal blocking drug and treat with procainamide; refer for accessory pathway ablation as the definitive long-term therapy.
From the July 10 edition
Today, three days ago: Calcium Gluconate. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
Hyperkalemia: 1–3 g IV of 10% calcium gluconate over 5–10 min; repeat if ECG changes persist. Magnesium toxicity: calcium gluconate 1 g IV. Digoxin toxicity is a historical caution; life-threatening hyperkalemia still usually warrants calcium with expert awareness.
From the July 3 edition
A 45-year-old man presents with periorbital edema, frothy urine, albumin 1.8 g/dL, and 4+ protein on urinalysis. Which complication is he at greatest risk for?
ABrain abscess
BRenal cell carcinoma
CVenous thromboembolism
DUremic pericarditis
Reveal answer
Correct · C
Venous thromboembolism. Nephrotic syndrome causes urinary loss of anticoagulant proteins and a hypercoagulable state, increasing risk of DVT and PE. The ED should look for thrombotic complications and not be reassured by preserved creatinine alone.
Journal Watch
From the FOAMed wire
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
In adults with sickle cell disease hospitalized for acute chest syndrome (ACS) without pulmonary artery macrothrombosis, does therapeutic-dose anticoagulation with tinzaparin shorten ACS duration compared with prophylactic-dose anticoagulation? The post The TASC Trial:...
Podcast Picks
Two for the shift
Critical Care Perspectives in Emergency Medicine2026-05-23
Acute hypoxemic respiratory failure is a leading cause of ICU admission worldwide. Oxygen is first-line therapy for patients with acute hypoxemic respiratory failure and can be given via nasal cannula (NC), non-rebreather mask (NRB), high-flow nasal cannula (HFNC), or noninvasive ventilation (NIV). At present, the literature is inconsistent on which mode...
Source
Critical Care Perspectives in Emergency Medicine
Published
2026-05-23
Host
Critical Care Perspectives in Emergency Medicine, Critical Care Perspectives in Emergency Medicine
This week Ilene, Al, and Jeff talk pediatric stridor, Miz and Mel talk measles, and Cardy brings us a case of a bruise in an odd spot. Megan and Mel also continue working through June EMA papers. 1. Introduction 2....
Critical Care Corner
Matched to today’s topics
A critical-care reference from LITFL’s Critical Care Compendium, tied to today’s differential.
SJS/TEN turns a dermatologic eruption into critical illness through extensive epidermal loss, with burn-style priorities: airway surveillance, fluid and electrolyte management, temperature control, analgesia, and infection prevention.
= immune complex mediated hypersensitivity -> severe erythema multiforme. Separation of the epidermis from the dermis; most authors believe toxic epidermal necrolysis (TEN) and SJS are different ends of the same spectrum of disease
Pharmacology Corner
Two drugs for the shift
One antimicrobial and one other ED workhorse — selected daily, with sources and last-reviewed dates so every dose is cross-checkable.
Antimicrobial of the Day
Piperacillin-Tazobactam
Beta-lactam / beta-lactamase inhibitor
Indication
Broad-spectrum coverage for nosocomial pneumonia, intra-abdominal infection, complicated UTI, neutropenic fever, and undifferentiated sepsis with Pseudomonas risk.
What’s your dose? — reveal dosing & cautions
ED Dose
3.375 g IV q6h (extended infusion 4 h preferred for serious infection); 4.5 g IV q6h for severe pseudomonal infection or critical illness.
Renal Adjustment
CrCl 20–40: 3.375 g q8h. CrCl < 20: 2.25 g q8h. Hemodialysis: 2.25 g q8h plus 0.75 g after each session.
Contraindications
Penicillin or beta-lactam anaphylaxis history.
Interactions
Vancomycin (increased AKI risk per recent observational data); methotrexate (decreased clearance); probenecid (prolongs half-life).
Monitoring
Renal function, electrolytes (sodium load), platelets with prolonged courses.
ED Pearl
Order the loading dose immediately on sepsis recognition — every hour of antibiotic delay in septic shock raises mortality. Use extended-infusion protocols if your pharmacy supports them.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Rhythm
Normal Sinus Rhythm
The default rhythm: a regular narrow-complex rhythm at 60-100 bpm with a normal P wave before every QRS and a constant PR.
The Tracing
A healthy 18-year-old man presents for a pre-participation sports evaluation with no complaints. Vitals are normal. His 12-lead shows a regular rhythm at 84 bpm. Each QRS is narrow, under 100 ms, and is preceded by a P wave that is upright in leads I and II and inverted in aVR. The PR interval is constant from beat to beat, and every P wave is followed by a QRS. The complexes are of normal amplitude with no ST or T wave abnormality. Nothing on the tracing departs from what you would expect in a well young adult.
Regular rhythm at a rate of 60-100 bpm (or age-appropriate rate in children)
Each QRS complex preceded by a normal P wave
Normal P wave axis: upright in leads I and II, inverted in aVR
Constant PR interval
QRS complexes <100 ms wide (unless a co-existent interventricular conduction delay is present)
Pearls
The P wave axis is the quiet workhorse: upright in I and II and inverted in aVR confirms the impulse is coming from the sino-atrial node, not an ectopic or junctional focus.
Rate alone doesn't unseat sinus rhythm — sinus tachycardia (>100) and sinus bradycardia (<60) are still sinus, defined by the same normal P wave and constant PR.
Beat-to-beat variation in the P-P interval with otherwise normal sinus P waves is sinus arrhythmia, a normal variant, not a pathologic irregularity.
Pitfalls
Assuming any narrow, regular, appropriately-rated rhythm is sinus without confirming a normal P wave precedes each QRS — junctional and ectopic atrial rhythms can masquerade.
Using child rates against adult thresholds — normal newborn rates run 110-150 bpm, so 'tachycardia' must be judged against the age-appropriate range.
Forgetting that a QRS can exceed 100 ms and still sit on sinus rhythm when there is a co-existent interventricular conduction delay.
At the Bedside
Confirming normal sinus rhythm establishes the baseline against which every abnormality is judged — it reassures you the conduction pathway from SA node through AV node and His-Purkinje is intact and directs attention to the clinical question rather than the rhythm.
For educational use only. Verify ECG interpretation against the LITFL entry and your institution’s practice before clinical decision-making.
Case of the Day
From the lead · PURPURIC RASHES
Self-Examination
Test Your Understanding
A 42-year-old woman has petechiae, confusion, fever, thrombocytopenia, anemia, elevated LDH, low haptoglobin, and schistocytes. PT and aPTT are normal. ADAMTS13 testing will not return for several days. What is the best next step?
APlatelet transfusion and outpatient hematology follow-up
BImmediate plasma exchange
CVitamin K and fresh frozen plasma
DSkin biopsy before treatment
Reveal answer
Correct answer · B
Immediate plasma exchange. The combination of thrombocytopenia and microangiopathic hemolytic anemia with neurologic symptoms and relatively preserved coagulation studies is highly concerning for TTP. Treatment should not await ADAMTS13 results.
Study Pace4 topics today; 4 remaining; Day 42 of 43Deadline · June 1, 2026