Core EM - Emergency Medicine Podcast

DRESS in the ED: Diagnosing this delayed drug reaction behind rash and shock & how to manage.

Hosts:

Nir Lavi-Romer, MD

Brian Gilberti, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/DRESS.mp3





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Tags: Allergy + Immunology, Critical Care, Dermatology, DRESS, Rash





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Core EM Modular CME Course

Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.  Course Highlights:

Credit: 12.5 AMA PRA Category 1 Credits™

Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics.

Cost:

Free for NYU Learners

$250 for Non-NYU Learners

Click Here to Register and Begin Module 1

DRESS vs SJS/TEN vs Anaphylaxis at a Glance

DRESS
SJS/TEN
Anaphylaxis

Onset after drug
~2–8 wks; hrs–days on re-exposure
~1–3 wks
Min–hrs

Skin
Diffuse, infiltrated erythema; blisters rare
Dusky lesions → blisters, sloughing
Urticaria, flushing

Nikolsky
Neg
Pos
Neg

Mucosa
Mild, if any
Severe, hemorrhagic
Angioedema

Big clues
Facial edema, lymphadenopathy, eos, organ injury
Epidermal detachment
Wheeze, ↓BP, GI sx

Response to epi
None
None
Expected

Background

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS): drug exposure → rash + systemic involvement (liver, kidneys, lungs, heart, pancreas)

Systemic dz is what makes pts critically ill → think ICU. Mortality up to ~10% in retrospective series; 1.7% in a prospective multinational registry (SEAIC 2020)

Eosinophilia not universal → also called drug-induced hypersensitivity syndrome (DIHS)

Rare, but can’t-miss

Pathophysiology

Type IV, T-cell–mediated delayed hypersensitivity; Th2 cytokines (IL-5) recruit eosinophils (SEAIC 2020)

Not IgE-mediated → don’t expect an anaphylaxis-style response to epi

Exact cause unclear. Two leading contributors:

Genetics: HLA polymorphisms, e.g., HLA-A*31:01 w/ carbamazepine DRESS (CPIC 2018)

Herpesvirus reactivation (HHV-6, HHV-7, EBV, CMV) in up to ~75%; cause vs consequence still unsettled

The Culprit Drugs

200+ drugs implicated; a short list does most of the damage:

Allopurinol, vancomycin, TMP-SMX & other sulfas

Aromatic antiepileptic drugs (AEDs): phenytoin, phenobarbital, carbamazepine, lamotrigine

Less common: NSAIDs, antiretrovirals, ACEi, CCBs, atypical antipsychotics

Latency: classically 2–8 wks after starting the drug; re-exposure → hrs to days (SEAIC 2020)

Med rec has to look back: SEAIC treats any drug started <6 mo & stopped <14 d before onset as a compatible suspect

Clinical Presentation

Rash: itchy morbilliform eruption → diffuse, confluent, infiltrated erythema, often >50% BSA; can be tender. Blisters & sloughing rare

Facial edema: classic

Lymphadenopathy (LAD), fever

Mucosa: mild, ~half of pts, usually 1 site (mouth/pharynx)

Organs: liver most common (~75%) & the leading cause of death; kidney (esp. allopurinol), lungs, heart (myocarditis), pancreas (SEAIC 2020)

Sick end of the spectrum: shock, hypoxemia, AMS, multi-organ failure

Diagnosis

Clinical Dx

Built on hx (new drug, wks back) + exam. Labs & biopsy support it; neither should hold up tx

Sorting the Dangerous Rashes

Anaphylaxis: min–hrs after exposure; urticaria, angioedema. No response to epi → reconsider

Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN): blisters, sloughing, severe hemorrhagic mucosal dz, Nikolsky pos

Pemphigus vulgaris: flaccid bullae; Nikolsky & Asboe-Hansen pos

Necrotizing soft tissue infection: pain out of proportion, crepitus

Nikolsky: pressure on skin → epidermis shears/sloughs

Asboe-Hansen: pressure on a bulla → fluid spreads laterally past its border

Points to DRESS: delayed onset after a new drug, facial edema, LAD, no blistering/sloughing, mild mucosal dz

Labs

Gauge severity/end-organ damage, not the dx. Can be normal early → don’t use to exclude

SEAIC admission panel: CBC w/ diff (eos, atypical lymphs), LFTs/INR, Cr + UA, lipase, CK, troponin (SEAIC 2020)

Delphi: ECG for all; troponin/BNP only if cardiac involvement suspected (Delphi consensus 2024). Crashing pt → send the full panel up front

Delphi grades severity on liver, kidney & blood derangement; any other organ involved = severe (Delphi consensus 2024)

RegiSCAR Score

Quantifies suspicion (MDCalc): <2 excluded, 2–3 possible, 4–5 probable, >5 definite (SEAIC 2020)

Early on, eos may not have appeared & a course ≥15 d can’t be confirmed (scores −1) → a low ED score doesn’t exclude

Management

Stop the Drug, Hold New Ones

Stop every possible culprit

Careful adding drugs to a sick pt; SEAIC specifically avoids empiric abx (esp. amoxicillin) & NSAIDs acutely (SEAIC 2020)

Aromatic AED cross-reactivity 40–80% → avoid phenytoin, phenobarbital, lamotrigine, oxcarbazepine; benzos considered safe

Resuscitate

ABCs first, like any crashing pt

Epi for any concern of anaphylaxis: unlikely to hurt, may help

IVF titrated to dynamic measures & UOP; pressors for refractory shock

Large BSA → burn-like insensible losses; extensive erythroderma/exfoliation may need a burn center (SEAIC 2020)

Anticipate RRT, intubation, central & arterial lines

Steroids

Prednisone equivalent 0.5–1 mg/kg/day; start early

Prolonged taper (wks–mos) to prevent relapse (~10–15%); Delphi: 6 wk–3 mo for mild/moderate, 3–6 mo for severe (Delphi consensus 2024)

Delphi: steroids for all confirmed DRESS; very high-potency topicals for mild, topicals or systemic for moderate, systemic for severe

Don’t wait for consultants or biopsy if suspicion is high & pt unstable

Refractory Disease

Usually ICU-initiated: cyclosporine, anti–IL-5 antibodies, IVIG, JAK inhibitors; antivirals w/ viral reactivation

Delphi backs cyclosporine, anti–IL-5/IL-5R & IVIG for steroid-refractory dz; ganciclovir/valganciclovir for high CMV load (Delphi consensus 2024)

Disposition

ICU; burn center if extensive skin involvement

All hands early: derm, nephro, ID (viral reactivation), ophtho (ocular involvement), critical care

The Case

61M w/ hx of seizures, started carbamazepine 6 wks ago

Itchy rash on arms ~2 wks ago → trunk, face, oral mucosa; worsening. Family calls 911 for AMS

EMS: hypotensive, diffuse red rash → EpiPen, no improvement

ED: hypotensive, tachycardic, tachypneic, hypoxemic on RA. Diffuse tender, blanching erythema; no blisters, sloughing, vesicles, bullae, or petechiae; Nikolsky & Asboe-Hansen neg; facial edema; cervical LAD

Why DRESS: aromatic AED, ~4-wk latency, facial edema, LAD, no epidermal detachment, no response to epi

Pitfalls

Anchoring on anaphylaxis when epi isn’t working

Missing the culprit because it started wks before the rash

Using normal early labs to exclude DRESS

Holding steroids for consultants or biopsy in an unstable pt

Reflexive new drugs: empiric abx, NSAIDs, another aromatic AED

Calling consultants late

Take-Home Points

DRESS is systemic. Diffuse rash + hypotension + liver or kidney injury → keep DRESS high on the ddx.

Look back weeks to months. Allopurinol, sulfa drugs & anticonvulsants are the classic offenders.

Let the exam sort the rash. Sloughing skin and severe hemorrhagic mucosal dz point to SJS/TEN.

Steroids early. High suspicion + unstable pt → start them; don’t wait on consultants or a biopsy.

Trust your resuscitation skills. Supportive EM/ICU care carries these pts.

Links & References

DRESS Guidelines & Consensus

Brüggen MC, et al. Management of Adult Patients With Drug Reaction With Eosinophilia and Systemic Symptoms: A Delphi-Based International Consensus. JAMA Dermatol. 2024;160(1):37–44. (54-expert international panel: severity grading, steroid taper, refractory tx) — doi.org/10.1001/jamadermatol.2023.4450

Cabañas R, et al. Spanish Guidelines for Diagnosis, Management, Treatment, and Prevention of DRESS Syndrome. J Investig Allergol Clin Immunol. 2020;30(4):229–253. (SEAIC: organ-specific steroid dosing, AED cross-reactivity, RegiSCAR) — doi.org/10.18176/jiaci.0480

Mizukawa Y, et al. Guidelines for the management of drug-induced hypersensitivity syndrome 2023. J Dermatol. 2025;52(3):e189–e209. (Japanese MHLW study group; DIHS & HHV-6) — doi.org/10.1111/1346-8138.17609

Ingen-Housz-Oro S, et al. French national protocol for diagnosis and management of drug reaction with eosinophilia and systemic symptoms (DRESS) in adults and children. Ann Dermatol Venereol. 2025;152(3):103381. — doi.org/10.1016/j.annder.2025.103381

Related Society Guidelines

Creamer D, et al. U.K. guidelines for the management of Stevens-Johnson syndrome/toxic epidermal necrolysis in adults 2016. Br J Dermatol. 2016;174(6):1194–1227. (British Association of Dermatologists) — doi.org/10.1111/bjd.14530

Golden DBK, et al. Anaphylaxis: A 2023 practice parameter update. Ann Allergy Asthma Immunol. 2024;132(2):124–176. (AAAAI/ACAAI Joint Task Force) — doi.org/10.1016/j.anai.2023.09.015

Khan DA, et al. Drug allergy: A 2022 practice parameter update. J Allergy Clin Immunol. 2022;150(6):1333–1393. (AAAAI/ACAAI Joint Task Force) — doi.org/10.1016/j.jaci.2022.08.028

Phillips EJ, et al. Clinical Pharmacogenetics Implementation Consortium Guideline for HLA Genotype and Use of Carbamazepine and Oxcarbazepine: 2017 Update. Clin Pharmacol Ther. 2018;103(4):574–581. (CPIC) — doi.org/10.1002/cpt.1004

Calculator

RegiSCAR Score for DRESS — MDCalc





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Iron overdose in the ED: five stages, elemental iron math, decontamination, and deferoxamine.

Hosts:

Brian Chastain, MD

Brian Gilberti, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/Iron_Poisoning.mp3





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Tags: Toxicology





Podcast Video



Show Notes

Core EM Modular CME Course

Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.  Course Highlights:

Credit: 12.5 AMA PRA Category 1 Credits™

Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics.

Cost:

Free for NYU Learners

$250 for Non-NYU Learners

Click Here to Register and Begin Module 1

Iron Poisoning Stages at a Glance

Stage
Timing
What’s happening

1 · GI
30 min–6 h
Direct corrosive GI injury; abd pain, vomiting

2 · Latent
6–24 h
GI sx improve; iron redistributing into tissues

3 · Shock / acidosis
6–72 h
Profound metabolic acidosis → shock, MSOF

4 · Hepatotoxicity
12–96 h
Hepatotoxicity → fulminant liver failure

5 · GI scarring
2–8 wks
Gastric outlet obstruction, GI tract scarring

The Case

31M w/ hx depression, anxiety; found minimally responsive at home by family

EMS: HR 67, SpO2 96% on 2 L NC, BP 46/21; withdraws to pain, not opening eyes → 2 L IVF + push-dose epi en route

ED: BP ↑ to 90/61, other VS unchanged; dried vomit on lips/shirt; breathing comfortably, protecting airway

POC VBG: pH 7.24, pCO2 33, pO2 25, HCO3 14, lactate 2.5

ECG: NSR, otherwise unremarkable → get an ECG in any possible toxic ingestion

Additional 30 mL/kg bolus + norepi gtt

Family arrives → bottle of iron pills under the pt’s bed

Pathophysiology

Free iron = multisystem oxidative injury

Primary mechanism: free radical generation + lipid peroxidation → damages cellular and mitochondrial membranes throughout the body

Profound metabolic acidosis via 2 routes: uncoupled oxidative phosphorylation → anaerobic metabolism → lactate; Fe³⁺ reacts w/ water → releases 3 H⁺ → excess acid

Direct mucosal necrosis in the gut (corrosive injury)

Negative inotrope on the myocardium → hypotension, cardiogenic shock in large ingestions

Clinical Stages

Classic progression after large ingestions; stages overlap and pts can present anywhere along the timeline

Stage 1, GI (30 min–6 h): direct GI tract injury; abd pain, vomiting. Persistent vomiting = very sensitive indicator of a serious ingestion

Stage 2, latent (6–24 h): GI sx improve, but iron is redistributing into the tissues → ongoing damage

The latent-phase trap: pts look like they’re turning the corner right before they crump. Contrast: pts never symptomatic >6 h after ingestion are unlikely to develop toxicity (AAPCC 2005); GI sx that improve ≠ never symptomatic

Stage 3, shock (6–72 h): tissue iron → profound acidosis → shock, MSOF

Stage 4, hepatotoxicity (12–96 h): hepatotoxicity → fulminant liver failure

Stage 5, GI scarring (2–8 wks): gastric outlet obstruction, GI tract scarring from the initial corrosive injury

Diagnosis / Workup

Imaging

Emergent plain-film abd XR in any suspected iron ingestion → intact adult iron tabs are radiopaque

Confirms pills still in the stomach/GI tract → helps decide on WBI

Negative XR ≠ no ingestion: chewables, liquid formulations and already-dissolved tabs often don’t show up

Serum Iron

Draw 4–6 h post-ingestion for regular formulations, ~8 h for extended release

Often hard to interpret → time of ingestion and formulation frequently unknown

>500 mcg/dL → serious systemic toxicity

>1,000 mcg/dL → very significant mortality

Elemental Iron Math

Toxicity tracks the elemental iron dose, not the mass of the pill

Salt
Elemental Fe
Per 325 mg tab

Ferrous sulfate
~20%
~65 mg

Ferrous fumarate
~33%
106 mg

Ferrous gluconate
~12%
~36–38 mg

<20 mg/kg elemental Fe → usually asymptomatic

20–60 mg/kg → GI sx likely; systemic toxicity possible, esp. at the upper end

>60 mg/kg → threshold for serious toxicity, possible death

AAPCC out-of-hospital guideline: refer to an ED for ≥40 mg/kg elemental Fe (adult ferrous salt formulations) or severe/persistent sx; any self-harm ingestion → ED regardless of amount (Manoguerra 2005)

AAPCC: children’s chewable vitamins w/ iron, and unintentional carbonyl iron or polysaccharide-iron complex ingestions → home obs w/ f/u

Management

Decontamination

Activated charcoal: no role. Iron is a metal → doesn’t bind; ↑ aspiration and other complications

Whole bowel irrigation (WBI) = main decontamination strategy, esp. w/ pills on XR → flush tablets before further GI injury and systemic absorption

PEG-ELS (polyethylene glycol electrolyte solution) until rectal effluent is clear; large volume → often via NG tube

PEG-ELS rates: 1.5–2 L/h adolescents/adults (as on air); peds 500 mL/h (9 mo–6 y), 1 L/h (6–12 y) (AACT/EAPCCT 1997)

AACT/EAPCCT: consider WBI after substantial iron ingestions; contraindicated w/ bowel obstruction, perforation, ileus, hemodynamic instability or a compromised unprotected airway (Thanacoody 2015)

Gastric lavage: generally not used unless a large pill burden remains in the stomach → aspiration, direct GI injury; ED unfamiliarity ↑ complications

Get toxicology and your local poison center on the line early

Deferoxamine (DFO)

Mechanism: chelator isolated from bacteria → binds iron in the blood (ferrioxamine) → renal excretion in the urine

Indications: shock · AMS · profound metabolic acidosis · persistent GI sx (persistent vomiting) · serum iron >500 mcg/dL · predicted severe ingestion (>60 mg/kg elemental Fe) in a symptomatic pt

Reported dose >60 mg/kg in a pt w/o sx or acidosis → discuss w/ toxicology/poison center rather than chelating on pill count alone

Dosing: start 5 mg/kg/h IV → titrate to ~15 mg/kg/h. Some protocols go higher, up to ~30 mg/kg/h in the first 24 h.

Watch for hypotension: DFO can worsen existing hypotension.

FDA label: IV only for cardiovascular collapse, by slow infusion; ≤15 mg/kg/h initially; max 6 g/24 h; ARDS reported w/ excessively high IV doses; ↑ risk of Yersinia infxn.

Urine: classic “vin rosé” (red-orange) urine = ferrioxamine being excreted → helpful but not quantitative. Its absence doesn’t exclude significant toxicity or effective chelation; don’t use urine color to guide duration.

Stop when the pt is clinically well and the anion gap acidosis has resolved.

Pitfalls

Waiting for a level → a level that hasn’t peaked or looks low doesn’t exclude toxicity in a sick pt

Being reassured by GI improvement in the latent phase

Being reassured by a negative XR (chewables, liquids, dissolved tabs)

Dosing by tablet weight instead of elemental iron

Giving activated charcoal

Using urine color (or its absence) to decide when to stop DFO

Take-Home Points

Treat the patient, not the number. Shock or profound metabolic acidosis → start DFO even if the serum iron hasn’t peaked or is lower than expected; very little harm in starting it, other than hypotension

Calculate elemental iron. Formulations differ in elemental content → helps predict whether the dose is toxic

Get an X-ray. Plain film confirms tablets and guides the decision on WBI

Beware the latent phase. GI improvement ≠ toxicity over → often precedes cardiovascular collapse and shock as iron moves into the tissues

Links & References

Guidelines

Manoguerra AS, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553–570. — DOI (AAPCC)

Dart RC, et al. Expert consensus guidelines for stocking of antidotes in hospitals that provide emergency care. Ann Emerg Med. 2018;71(3):314–325.e1. — DOI

Decontamination Position Statements (AACT/EAPCCT)

Tenenbein M. Position statement: whole bowel irrigation. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35(7):753–762. — DOI

Thanacoody R, et al. Position paper update: whole bowel irrigation for gastrointestinal decontamination of overdose patients. Clin Toxicol (Phila). 2015;53(1):5–12. — DOI

Chyka PA, et al. Position paper: single-dose activated charcoal. Clin Toxicol (Phila). 2005;43(2):61–87. — DOI

Benson BE, et al. Position paper update: gastric lavage for gastrointestinal decontamination. Clin Toxicol (Phila). 2013;51(3):140–146. — DOI

Poison Center

Poison Help line (US): 1-800-222-1222

Music

Outro music: “Metalmania” Kevin MacLeod (incompetech.com). Licensed under Creative Commons: By Attribution 4.0 License





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Tickborne illnesses in the ED: attachment time, the rash, the smear, prophylaxis, & treatment.

Hosts:

Samantha Nakos, MD

Brian Gilberti, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/Tickborne_Illnesses_1_.mp3





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Tags: Babesiosis, Ehrlichiosis, Infectious Diseases, Lyme Disease, Tick-Borne Illnesses





Podcast Video



Show Notes

Core EM Modular CME Course

Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.  Course Highlights:

Credit: 12.5 AMA PRA Category 1 Credits™

Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics.

Cost:

Free for NYU Learners

$250 for Non-NYU Learners

Click Here to Register and Begin Module 1

Lyme, Anaplasmosis, Ehrlichiosis & Babesiosis at a Glance

Lyme
Anaplasmosis
Ehrlichiosis
Babesiosis

Organism
B. burgdorferi (spirochete)
A. phagocytophilum
E. chaffeensis
B. microti (protozoan)

Vector
I. scapularis
I. scapularis
Lone star tick
I. scapularis

Attachment time
≥36–48 h
Can be <24 h
No data
Mostly >48 h

Key clue
EM rash
↓WBC, ↓plt, ↑LFTs
↓WBC, ↓plt, ↑LFTs
Hemolysis, ↓plt

Smear
—
Morulae in neutrophils
Morulae in monocytes
Intra-RBC parasites, Maltese cross

Confirm
Clinical (EM)
Smear, PCR
Smear, PCR
Smear, PCR

Treat
Doxy × 10–14 d
Doxy × 10 d
Doxy until ≥3 d afebrile
Atovaquone + azithro × 7–10 d

Background

Ixodes scapularis (deer tick) = primary US vector for Lyme, anaplasmosis, and babesiosis; I. pacificus on the West Coast. Ehrlichiosis → lone star tick (Amblyomma americanum), not the deer tick (CDC MMWR 2016)

Why attachment time matters: B. burgdorferi lives in the tick midgut → multiplies and migrates to the salivary glands only after feeding starts → built-in delay

Single infected nymph: 0 of ~90 animals infected at 24 h, ~10% by 48 h, ~70% by 72 h (Eisen 2018)

Anaplasma can transmit w/in 24 h. Babesia ≈ Lyme, not faster: earliest 36 h, mostly after 48 h. True speedster = Powassan virus (w/in 15 min). Attachment time by hx is often unreliable (IDSA Lyme 2020)

Regional variation: US Lyme = B. burgdorferi; Europe = mostly B. afzelii, B. garinii → different clinical picture. Systemic sx w/ EM more common in the US: ~65% vs ~37% in Europe (IDSA Lyme 2020)

Lyme: The Rash and the Serology

Erythema Migrans

EM in ~70–80% of infections; appears at the bite site 3–30 d post-bite (avg ~7 d) (CDC)

Usually not a bull’s-eye → most early EM is uniformly red

Expanding erythematous patch + endemic area = Lyme until proven otherwise

Serology

2-tier: EIA or IFA → IgM/IgG Western blot (or modified 2-tier: 2 EIAs, no blot)

Early localized dz → often seronegative (as few as ~20% positive w/in 1 wk of noticing EM) → EM in an endemic area = clinical dx, per IDSA (IDSA Lyme 2020)

The Other Three: Labs and the Smear

Babesiosis

Hunt for hemolytic anemia: ↓Hgb, ↑LDH, ↓haptoglobin, reticulocytosis; ↓plt and ↑LFTs common

Smear: intraerythrocytic parasites. Maltese cross (tetrad) = pathognomonic but infrequent; ring forms more common. PCR more sensitive than smear (IDSA Babesiosis 2020)

Anaplasmosis & Ehrlichiosis

Near-identical presentations. Classic triad: leukopenia, thrombocytopenia, transaminitis

Smear: morulae → Anaplasma in neutrophils, Ehrlichia in monocytes. Smear is insensitive → whole-blood PCR confirms (CDC MMWR 2016)

Management

Post-Bite Prophylaxis (Lyme)

High-risk bite only → all 3: Ixodes tick, highly endemic area, attached ≥36 h (by engorgement or hx); give w/in 72 h of removal (IDSA Lyme 2020)

Doxycycline 200 mg PO × 1 (adults); 4.4 mg/kg PO × 1, max 200 mg (kids)

Landmark RCT: 482 pts w/ I. scapularis bites → EM 0.4% doxy vs 3.2% placebo, efficacy 87% (Nadelman 2001)

Kids <8: doxy traditionally avoided (tooth staining), but a relative CI only → benefit wins. No staining seen w/ short courses; CDC/AAP: doxy = drug of choice for tickborne rickettsial dz at any age (CDC MMWR 2016)

Active Disease

Early localized Lyme: Doxycycline 100 mg PO BID × 10–14 d (CDC: shorter end preferred; IDSA: 10 d)

No 1st-gen cephalosporins (e.g., cephalexin) → ineffective vs B. burgdorferi

EM vs cellulitis unclear → cefuroxime 500 mg PO BID × 14 d covers both. If using amoxicillin-clavulanate, dose it TID (500/125 mg) to match the TID amoxicillin regimen (CDC EM Treatment)

Anaplasmosis: same doxy dose × 10 d (covers incubating Lyme). Ehrlichiosis: same dose until ≥3 d afebrile, usually 5–7 d total (CDC MMWR 2016)

Babesiosis: Atovaquone 750 mg PO BID + azithromycin 500 mg day 1, then 250 mg daily × 7–10 d (IDSA Babesiosis 2020)

Severe Babesiosis

Inpatient: Atovaquone 750 mg PO BID + azithromycin 500 mg IV daily → all-PO once sx subside, 7–10 d total. Alternative: IV clindamycin + PO quinine (CDC Babesiosis)

Consider RBC exchange transfusion for parasitemia >10% or severe hemolysis; IDSA also lists severe pulmonary, renal, or hepatic compromise (IDSA Babesiosis 2020)

Asplenia → ↑ risk of severe dz, but not itself an exchange criterion

The Case

35M, no PMH → 1 wk nausea, severe myalgias, arthralgias, HA, fatigue, fevers. Hiked upstate NY 1 wk prior; multiple tick bites to legs, none reportedly attached >24 h

VS: BP 144/76, HR 69, RR 16, T 98.7°F s/p acetaminophen, SpO2 98% RA

Exam: pruritic, painful papular rash w/ healing vesicles on bilateral wrists + anterior chest; tender bilateral axillary LAD; diffuse muscle and leg-joint tenderness

Labs: plt 87K, Hgb 12.3, transaminitis

Dx: concurrent babesiosis + poison ivy

Lessons: poison ivy = red herring while hunting for EM; antipyretic masked the fever; ↓plt in a febrile hiker → smear; reported “<24 h” attachment didn’t exclude Babesia (hx unreliable)

Pitfalls

Waiting for a bull’s-eye → most EM is uniformly red

Sending serology to rule out early EM → often neg; treat clinically

Cephalexin for “cellulitis” in tick season → misses EM

Trusting pt-reported attachment time → runs short

Fever persisting on doxy → think Babesia (coinfection is common); doxy doesn’t treat it (IDSA Lyme 2020)

Take-Home Points

Don’t wait for the bull’s-eye. Most EM is solid red. An expanding erythematous patch in an endemic area is Lyme until proven otherwise.

Watch the clock and the tick. Lyme needs ~36–48 h of attachment; Anaplasma can transmit w/in 24 h. Pts underestimate how long the tick was on.

The smear is your friend. Thrombocytopenia in a febrile hiker → manual peripheral smear for morulae or a Maltese cross.

Doxycycline is your workhorse. Covers Lyme, Anaplasma, and Ehrlichia → first-line for most tickborne febrile syndromes. Babesia needs atovaquone + azithromycin.

Links & References

Guidelines

Lantos PM, et al. Clinical practice guidelines by the Infectious Diseases Society of America (IDSA), American Academy of Neurology (AAN), and American College of Rheumatology (ACR): 2020 guidelines for the prevention, diagnosis and treatment of Lyme disease. Clin Infect Dis. 2021;72(1):e1–e48. — doi.org/10.1093/cid/ciaa1215

Krause PJ, et al. Clinical practice guidelines by the Infectious Diseases Society of America (IDSA): 2020 guideline on diagnosis and management of babesiosis. Clin Infect Dis. 2021;72(2):e49–e64. — doi.org/10.1093/cid/ciaa1216

Biggs HM, et al. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever and other spotted fever group rickettsioses, ehrlichioses, and anaplasmosis — United States. MMWR Recomm Rep. 2016;65(2):1–44. — doi.org/10.15585/mmwr.rr6502a1

Key Studies

Eisen L. Pathogen transmission in relation to duration of attachment by Ixodes scapularis ticks. Ticks Tick Borne Dis. 2018;9(3):535–542. — doi.org/10.1016/j.ttbdis.2018.01.002

Nadelman RB, et al. Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite. N Engl J Med. 2001;345(2):79–84. — doi.org/10.1056/NEJM200107123450201

CDC

CDC. Signs and symptoms of untreated Lyme disease. — cdc.gov/lyme/signs-symptoms

CDC. Clinical treatment of erythema migrans rash. — cdc.gov/lyme/hcp/clinical-care/erythema-migrans-rash

CDC. Clinical care of babesiosis. — cdc.gov/babesiosis/hcp/clinical-care





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Acute diarrhea in the ED: stool testing, treatment, and a spotlight on Cyclospora.

Hosts:

Neya Vishwanath, MD

Brian Gilberti, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/Diarrhea.mp3





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Tags: Gastrointestinal, Gastrointestinal Diseases





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Core EM Modular CME Course

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Framing the Patient

Acute is <2 weeks, persistent is 2–4 weeks, chronic is >30 days. Most acute diarrhea is self-limited and needs only supportive care.

Stool cultures are positive in only 2–6% of unselected patients. Yield rises with >4 stools/day and longer duration.

The ED job is not to name the organism. It is to find volume depletion, rule out the dangerous mimic, and decide who needs testing, antibiotics, or admission.

Don’t-Miss Mimics

Diarrhea is a symptom, not a diagnosis. In anyone who looks sick, gastroenteritis is a diagnosis of exclusion.

Abdominal catastrophes: mesenteric ischemia (pain out of proportion, vascular risk factors), early appendicitis, partial obstruction with overflow stool, diverticulitis.

Systemic disease presenting through the gut: sepsis from another source, DKA, adrenal insufficiency.

Fulminant C. diff or toxic megacolon: distension, fever, tachycardia, peritonitis. The diarrhea may actually stop as the colon dilates.

GI bleeding masquerading as dark diarrhea, and in women of childbearing age, ectopic pregnancy.

History & Exam

Duration, frequency, and appearance. Watery and high-volume suggests small bowel. Small, painful, frequent stools suggest colon.

Volume status: urine output, dark concentrated urine, dry mucous membranes, orthostatic symptoms.

Exposures: recent foods, travel, sick contacts, occupation (animal or sewage contact), recent antibiotics or hospitalization.

Timing after ingestion: <6 hours suggests a preformed toxin (Staph aureus, Bacillus cereus), 8–16 hours suggests Clostridium perfringens, and >16 hours suggests viral or other bacterial causes.

High-risk hosts: pregnancy → Listeria, cirrhosis → Vibrio, hemochromatosis → Yersinia (both siderophilic).

Exam: volume status plus a real abdominal exam. A soft belly does not end the evaluation.

Who Gets Testing

Ask first whether the result will change anything. If the patient is going home on supportive care, a stool study often just generates a callback.

Test when the patient is likely to be admitted or is higher risk: febrile, hypovolemic, elderly (roughly >70), known cardiac disease, immunocompromised, IBD, or pregnant.

Bloodwork is not routine. Send a BMP and CBC for significant hypovolemia, persistent vomiting, bloody stool, or the elderly and comorbid.

Routine cultures cover Salmonella, Campylobacter, Shigella. Ask the lab specifically for Vibrio, Yersinia, Aeromonas, or Listeria.

Know your multiplex GI PCR panel. At many shops it already includes C. diff, so ordering it separately is redundant. One call to your lab settles this.

Bloody stool → send Shiga toxin. Bloody but fecal WBC negative → consider amoebiasis.

Bloody diarrhea plus anemia, thrombocytopenia, or a rising creatinine → think HUS, especially in young children.

Antibiotics or hospitalization within 3 months → C. diff moves up the differential.

Neutropenic patient on active chemotherapy → consider typhlitis (enterocolitis of the cecum).

CT only for peritoneal signs or focal tenderness. It is not part of the routine workup.

Management

Oral rehydration solution is the mainstay for anyone tolerating PO — water, salt, sugar. Preferred over sports drinks and flavored electrolyte powders, which are not ORS-formulated. A commercial ORS packet is ideal, and the home recipe works when you do not have one. One liter of water, six level teaspoons of sugar, half a teaspoon of salt.

IV fluids for severe hypovolemia, intractable vomiting, or if labs are being drawn anyway.

Most non-bloody, non-traveler’s diarrhea does not need antibiotics.

Suspected Shiga toxin E. coli: no antibiotics. Lysing the organism releases toxin and raises HUS risk.

When empiric coverage is warranted: azithromycin for severe inflammatory diarrhea, fever, dysentery risk, or fluoroquinolone resistance. Otherwise cipro or levofloxacin, and IV ceftriaxone if PO is not tolerated.

Traveler’s diarrhea: most cases are self-limited. Reserve antibiotics for moderate to severe illness, and reach for azithromycin given widespread quinolone resistance in South and Southeast Asia.

Confirmed C. diff: oral vancomycin 125 mg four times daily for 10 days, or fidaxomicin. Stop the inciting antibiotic where you can.

Loperamide: generally avoid. If diarrhea is mild and the patient is afebrile, let it run.

Bismuth subsalicylate is an option — avoid in younger patients (Reye’s syndrome) and in salicylate allergy or intolerance.

Diet: eat what is tolerated. Early refeeding is fine and BRAT is not required. Dairy can transiently make things worse. Probiotics are unlikely to change the course.

Disposition

Set expectations: we often never identify the organism, and in a stable acute patient there is no routine test and no routine cure.

Food handlers and healthcare workers may need occupational clearance before returning to work.

Return precautions: bloody stools, fever, falling urine output, or an inability to keep fluids down.

No improvement past 1–2 weeks warrants re-evaluation for parasitic or non-infectious causes, including IBD.

Cyclospora

Protozoan with no person-to-person spread — transmission is poop to produce to person. Humans are the only natural host.

Oocysts need days to weeks to sporulate, so long-shelf-life produce is the culprit: berries, basil, cilantro, and leafy greens.

Incubation is about a week. Presents as watery, explosive diarrhea, typically non-bloody and afebrile.

Untreated, it drags on for weeks and tends to relapse, often with profound fatigue, anorexia, and weight loss.

Included on many multiplex GI PCR panels. Microscopy requires a special stain or it will be missed.

Treatment is Bactrim (TMP-SMX), one DS tablet twice daily for 7–10 days, which disrupts the parasite’s folate synthesis. Azithromycin does not cover Cyclospora — this is the exception to the usual workhorse. Ciprofloxacin is the fallback for sulfa allergy, and it is less effective.

Washing produce does not kill it. Only heat does.

Take Home Points

Most acute diarrhea is self-limited. If the patient tolerates PO, is afebrile, and the course is short, supportive care and discharge is the right answer.

Before you call it gastroenteritis, make sure it is not mesenteric ischemia, DKA, or a surgical abdomen.

Bloody diarrhea with concern for Shiga toxin gets no antibiotics.

For Cyclospora, wash and cook your produce — and remember it is Bactrim, not azithro.





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Superwarfarin toxicity: recognition, reversal, and prolonged vitamin K therapy.

Hosts:

Mac Josh Reandelar, DO

Avir Mitra, MD





https://media.blubrry.com/coreem/content.blubrry.com/coreem/Superwarfarin_Toxicity.mp3





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Tags: Toxicology





Show Notes


Toxicology & Pathophysiology

Long-acting vitamin K antagonists (LA-VKAs), developed as potent rodenticides

Examples: brodifacoum, bromadiolone, difenacoum, chlorophacinone

Much more potent + far longer acting than warfarin

MOA: inhibits VKORC1 → ↓ vitamin K recycling → impaired γ-carboxylation

↓ factors II, VII, IX, X + proteins C/S

Highly lipophilic → extensive tissue/fat sequestration + slow redistribution

Effect can persist weeks-months; occasionally much longer

Not dialyzable

Exposure: large acute ingestion OR repeated low-dose exposure

Source may be unclear, concealed, or initially unknown

Presentation

Often delayed + insidious

Severe coagulopathy may precede obvious bleeding

Early: epistaxis, gingival bleeding, bruising/ecchymoses, hematuria

Classic clue: well-appearing pt + extraordinarily abnormal coagulation studies

Severe bleeding: RP hemorrhage, ICH, spinal hemorrhage, tamponade, major GI/GU bleeding

RP bleed → flank/back pain ± CVA tenderness

Labs & Diagnosis

PT/INR: profoundly elevated, sometimes beyond assay range

aPTT: may also be markedly prolonged with severe factor depletion

CBC/plts: often initially preserved unless major blood loss/other process

LFTs: often relatively normal

Profound INR + no warfarin + preserved liver function → think superwarfarin

CT based on bleeding site; CT A/P for suspected RP hemorrhage

Confirm: specialized serum/blood testing for long-acting anticoagulants, typically chromatography/mass spec

Do NOT delay resuscitation/treatment for confirmatory testing

Elevated INR: Differential

Superwarfarin exposure

Warfarin toxicity

Severe vitamin K deficiency: malnutrition, malabsorption, prolonged abx

Liver failure/cirrhosis

DIC

Acquired factor deficiency/inhibitor

Helpful discriminators

Liver dz → abnormal hepatic profile/clinical context

DIC → ↓ plts, ↓ fibrinogen, ↑ D-dimer

No warfarin + massive INR + relatively normal LFTs/plts → superwarfarin rises on the differential

ED Management

Major/Life-Threatening Bleeding

Goal: replace factors NOW + restore endogenous synthesis

4F-PCC = preferred factor replacement

Fast, predictable correction

Small volume

No thawing/type matching

FFP if PCC unavailable

Slower + large volume/TACO risk

Give IV vitamin K concurrently

PCC = immediate bridge; vitamin K = sustained factor synthesis

Recheck INR + clinical bleeding response

Repeat PCC generally not routine; reassess before redosing

No Major Bleeding, Critical INR

Vitamin K is primary therapy

High-dose PO vitamin K often preferred when clinically stable

Avoid unnecessary PCC/FFP if no major bleeding

Serial INR monitoring essential

Poison Control

Call early

Helps with:

Confirmatory testing

Vitamin K dosing

Duration of therapy

Monitoring/taper strategy

Outpatient planning

The Long Game

This is NOT standard warfarin toxicity

Vitamin K requirements may persist for months

Discharge only when bleeding controlled + clinically stable on oral regimen

Close serial INR follow-up mandatory

Slowly taper vitamin K under laboratory guidance

Stopping too early → rebound INR elevation + recurrent bleeding

Take Home Points

Massive unexplained INR + relatively normal liver function → think superwarfarin

Major bleeding → 4F-PCC + IV vitamin K

Expect prolonged vitamin K therapy + meticulous INR follow-up





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