Core EM - Emergency Medicine Podcast

https://coreem.net/podcast/episode-230-dress/

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

Hosts:
Nir Lavi-Romer, MD
Brian Gilberti, MD

Download Leave a Comment Tags: Allergy + Immunology, Critical Care, Dermatology, DRESS, Rash

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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

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) — https://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) — https://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) — https://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. — https://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) — https://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) — https://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) — https://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) — https://doi.org/10.1002/cpt.1004

Calculator

• RegiSCAR Score for DRESS — MDCalc

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https://coreem.net/podcast/episode-229-iron-poisoning/

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

Hosts:
Brian Chastain, MD
Brian Gilberti, MD

Download Leave a Comment 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 (https://incompetech.com). Licensed under Creative Commons: By Attribution 4.0 License

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https://coreem.net/podcast/episode-228-tickborne-illnesses/

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

Hosts:
Samantha Nakos, MD
Brian Gilberti, MD

Download Leave a Comment 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 to transmit ≥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. — https://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. — https://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. — https://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. — https://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. — https://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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https://coreem.net/podcast/episode-227-diarrhea/

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

Hosts:
Neya Vishwanath, MD
Brian Gilberti, MD

Download Leave a Comment Tags: Gastrointestinal, Gastrointestinal Diseases

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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

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.

Read More

https://coreem.net/podcast/episode-226-superwarfarin-toxicity/

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

Hosts:
Mac Josh Reandelar, DO
Avir Mitra, MD

Download Leave a Comment 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

Read More

https://coreem.net/podcast/episode-225-group-a-strep/

Group A strep in the pediatric ED: from strep throat to invasive disease and toxic shock.

Host:
Ellen Duncan, MD, PhD
Brian Gilberti, MD

Download Leave a Comment Tags: Infectious Diseases, Pediatrics

Show Notes

Background

• Group A strep = Streptococcus pyogenes — gram-positive organism that colonizes the pharynx, but also the perianal and genital mucosa (worth remembering when the source isn’t the throat).
• Extremely common. The episode cites an estimated ~289 million cases/yr of strep pharyngitis in children 5–14 (NIH). For a U.S.-specific, verifiable anchor: the CDC estimates strep throat drives ~5.2 million outpatient visits/yr in people <65.
• No true beta-lactam resistance. GAS remains uniformly susceptible to penicillin and amoxicillin. Note this is not true for macrolides/clindamycin — roughly 1 in 3 invasive isolates are now erythromycin/clindamycin resistant.

Pathophysiology — the throughline

• Exotoxins (superantigens) tie the whole spectrum together — they drive scarlet fever, streptococcal toxic shock syndrome (STSS), and are implicated in the Kawasaki overlap discussed below.
• The organism is the same from a sore throat to a life-threat; what changes is host response and toxin burden.

Clinical Presentation

• Core findings: tonsillar inflammation/exudate, tender anterior cervical lymphadenopathy, fever.
• Classic strep tells to hunt for:

• Palatal petechiae
• Strawberry tongue
• Perioral pallor

• Scarlet fever — fine, sandpapery rash, typically starts on the trunk and spreads outward; later desquamation of the fingers and toes.
• Extrapharyngeal clues: kids commonly present with abdominal pain or headache even when the throat looks unimpressive. Low threshold to test with fever + abd pain or fever + headache.

Diagnosis / Workup

Centor / Modified (McIsaac) Score

• Centor Score (Modified/McIsaac) — MDCalc
• One point each: fever, tonsillar exudates, tender anterior cervical lymphadenopathy, absence of cough. The Modified (McIsaac) version adds age.
• Developed and validated in adults (≥16). It is not reliable in young children — don’t lean on it in peds the way you would in an adult.
• For reference, McIsaac culture-positive probabilities: ~2.5% (0 criteria), 6.5% (1), 15% (2), 32% (3), 56% (4).

Testing

• Rapid PCR — high sensitivity and specificity; increasingly the front-line test.
• Rapid antigen detection test (RADT) — highly specific but less sensitive. Per IDSA, a negative RADT in a child/adolescent should be backed up with a throat culture (culture is the more sensitive gold standard). Backup culture is not required in adults.

Who not to test

• Generally don’t test/treat children <3 — acute rheumatic fever is rare in this group.
• Exception: the symptomatic young child with a close contact recently diagnosed with strep.

Management

• First-line: amoxicillin 50 mg/kg once daily, max 1 g/dose. GAS stays beta-lactam susceptible (penicillin and amoxicillin remain treatments of choice per IDSA 2012).
• IM penicillin G / benzathine (bicillin) for kids who can’t tolerate oral meds — one shot, done.
• Return to school: after one full day of treatment (~12–24 h), provided afebrile and feeling well.
• Contact prophylaxis:

• Pharyngitis — routine prophylaxis of asymptomatic contacts is not standard; consider it for households with recurrent infection or a history of rheumatic fever.
• Invasive GAS — more aggressive. Prophylaxis is recommended for household contacts who are immunosuppressed, pregnant, post-recent-surgery, or have an open wound (CDC).

The Bounce-Back / Treatment Failure

The kid who finishes amox and is back a week later. Sort into three buckets:

• Chronic carrier — GAS carriage in children runs 2–20%. Carriers test positive but are asymptomatic, with low risk of transmission or complications. Don’t chase them.
• New infection.
• True treatment failure → ask why:

• The shield effect — the throat is co-colonized with beta-lactamase producers (Staph aureus, H. influenzae, Moraxella) that degrade amoxicillin before it can act, effectively shielding the GAS.
• This is NOT true resistance — the strep is still beta-lactam susceptible; the neighbors are the problem.
• Fix: switch to a beta-lactamase–stable agent — amoxicillin-clavulanate or a first-generation cephalosporin.

Complications

• Suppurative: peritonsillar abscess, sinusitis, meningitis, bacteremia.
• Non-suppurative:

• Acute rheumatic fever — typically 1–5 wks post-infection; Jones criteria (AHA 2015 revision · ACC summary · CDC).
• Post-infectious glomerulonephritis (PIGN) — several weeks out; hematuria / “Coca-Cola” urine. Note strep impetigo can also seed PIGN.

• The pearl: we treat strep to prevent rheumatic fever — but treatment does NOT prevent PIGN.

Invasive Group A Strep (iGAS)

Why it’s on the radar

• Rates have been climbing since 2014, and preliminary 2023 data hit a 20-year high (CDC). A CDC/ABCs analysis flagged a roughly 3-fold pediatric increase in Colorado/Minnesota in late 2022 (MMWR).
• Keep it in mind when a child isn’t following the typical strep course or just looks sicker than expected.

The spectrum

• STSS, necrotizing fasciitis, meningitis, bacteremia, peritonitis.
• Increasingly common and worth highlighting: bone and joint disease — septic arthritis, osteomyelitis — often traveling with pyomyositis.

The trap — nonspecific early presentation

• Symptoms are often nonspecific: fever, “not acting like themselves,” localized pain.
• Septic joint/osteo may show a limp or focal pain — but not always.
• When your gut fires, cast a wide net.

Workup

• Blood cultures, CBC, chemistries, CRP, ESR.
• Imaging — tailor to the suspected site:

• Suspected joint → start with X-ray + ultrasound.
• Worried about osteomyelitis or pyomyositis → MRI (the recommended modality for pyomyositis per IDSA SSTI).

Management

• Broad-spectrum: vancomycin + piperacillin-tazobactam (concordant with IDSA SSTI).
• In shock / STSS: ADD clindamycin or linezolid for toxin suppression — this is on top of vanc/zosyn, not a coverage swap. (IDSA: penicillin plus clindamycin for documented GAS necrotizing infection; consider IVIG in STSS.)

The Kawasaki overlap

• Meaningful overlap between iGAS and Kawasaki disease.
• Proposed mechanism: strep superantigens activate a shared inflammatory (T-cell) pathway that may contribute to KD; some data suggest kids with iGAS may be at higher risk of developing Kawasaki.
• Get rheumatology involved early — they’ll want those inflammatory markers and can help sort KD from mimics.

Take-Home Points

• Adult tools don’t translate to peds. Centor was built for ≥16 and is unreliable in young kids — diagnose on exam, the eponyms, and testing. Low threshold to swab the febrile kid with abdominal pain or headache.
• The bounce-back is a triage problem — carrier (2–20%) vs. new infection vs. true failure. True failure is usually the shield effect (beta-lactamase co-colonizers, not resistance) → switch to amox-clav or a first-gen cephalosporin.
• Treatment prevents rheumatic fever, NOT PIGN — and impetigo can cause PIGN too.
• iGAS is rising and hides behind nonspecific symptoms. When your gut fires, work it up broadly and escalate to MRI for osteo/pyomyositis. Treat with vanc + pip-tazo, and in shock add clindamycin/linezolid for toxin suppression. Keep Kawasaki in the differential and call rheum early.

Links & References

Calculators

• Centor Score (Modified/McIsaac) for Strep Pharyngitis — MDCalc

Guidelines

• Shulman ST, et al. Clinical Practice Guideline for the Diagnosis and Management of Group A Streptococcal Pharyngitis: 2012 Update. IDSA / Clin Infect Dis. 2012;55(10):e86–e102. — IDSA · Full text
• Stevens DL, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update. IDSA / Clin Infect Dis. 2014;59(2):e10–e52. (necrotizing infection, STSS, clindamycin adjunct, MRI for pyomyositis) — IDSA · Full text
• Gewitz MH, et al. Revision of the Jones Criteria for the Diagnosis of Acute Rheumatic Fever in the Era of Doppler Echocardiography. AHA / Circulation. 2015;131:1806–1818. — Circulation · ACC “10 Points to Remember”

CDC

• Group A Strep Disease Surveillance and Trends (invasive disease rising since 2014; 2023 20-year high)
• MMWR — Increase in Pediatric Invasive Group A Streptococcus Infections, Colorado and Minnesota, Oct–Dec 2022
• Diagnosing Acute Rheumatic Fever (clinician guidance)

Read More

https://coreem.net/podcast/episode-224-kidney-stones/

A guide to diagnosing, imaging, and managing acute renal colic and nephrolithiasis in the ED.

Hosts:
Brian Gilberti, MD
Avir Mitra, MD

Download Leave a Comment Tags: Kidney Stones, Urology

Show Notes

1. CLINICAL CORE & PHYSIOLOGIC FRAMEWORK

•

Epidemiologic Risk Profiles

• Lifetime incidence parameters hover around 1 in 11, presenting with a prominent male sex skew.
• Peak demographic manifestation concentrated within the 30–60 age band.
• High-yield temporal parameter: 50% recurrence vector within a 5-year post-initial-insult window.

•

Mineralogical Composition Vectors

• Calcium oxalate crystals represent the predominant structural matrix.
• Struvite configurations (magnesium ammonium phosphate matrix) account for 1–2% of cohorts.
• Struvite stones function explicitly as infection-driven configurations secondary to upper tract proliferation; higher distribution index noted in female cohorts.

•

Etiological & Modifiable Relational Dynamics

• Profound systemic dehydration or low baseline fluid throughput states.
• High-sodium diet structures and heavy animal-protein consumption loads.
• Positive genetic/familial history variables.
• Relative risk modulation: Each variable independently operates to expand baseline risk by a factor of 2x to 3x.

•

Pathophysiologic Symptom Complexes

• Acute, sudden-onset, maximum-intensity (10/10) unilateral flank pain.
• Classic structural radiation vector tracking downward toward the ipsilateral groin/genitourinary dermatomes.
• Distinctive behavioral marker: Renal colic pacing/writhing behavior with zero antalgic position availability.
• Concomitant autonomic triggers: Nausea and emesis manifest in 50% of acute presentations.

•

Physical Exam Discordance Metrics

• Severe subjective distress contrasted with a characteristically soft, completely non-tender abdominal palpation exam.
• CVA tenderness is completely variable and lacks reliable negative predictive value.
• Atypical Presentation Classifications
• Vague, poorly localized abdominal pain presentations occurring in up to 20% of active cases.
• Isolated lower urinary tract irritative signs including acute frequency or severe urgency.

•

Incidental & Asymptomatic Dynamics

• Silent intrarenal or ureteral stones found incidentally.
• Longitudinal tracking demonstrates up to 33.3% of initially asymptomatic cohorts convert to fully symptomatic renal colic within a multi-year tracking window.

2. EXCLUSION DIAGNOSES & CRITICAL PATHWAY RED FLAGS

• Vascular Mimics: AAA rupture/expansion. This is a mandatory exclusion pathway in elderly cohorts presenting with acute flank or back pain. Physical tracking requires active exploration for an expansile, pulsatile abdominal mass.
• Gynecologic Emergencies: Ruptured ectopic pregnancy. Demands universal screening protocols via rapid beta-hCG testing in all female patients of childbearing potential presenting with lower abdominal/pelvic localization.
• Infectious Upper Tract Decompensation: Acute uncomplicated pyelonephritis. Differentiated via persistent high spikes, high fevers, systemic shaking chills, and profound pyuria.
• Genitourinary Structural Crises: Acute testicular torsion. Mandates a thorough, explicit scrotal/testicular structural exam if the flank pain radiates into the scrotum.
• Gastrointestinal and Adnexal Torsional Confounds: Acute appendicitis variants, acute mesenteric/bowel ischemia, and ovarian torsion syndromes.

3. LABORATORY TESTING & PHYSIOLOGIC EVALUATION

•

Urinalysis Interpretation Nuances

• Microscopic or gross hematuria presents in approximately 66% to 90% of acute cases.
• Critical Pathological Caveat: Complete absence of hematuria documented in 20% to 33.3% of confirmed, acute obstructing ureteral stones.
• Diagnostic rule: A pristine urinalysis with zero red blood cells is entirely insufficient to exclude acute ureterolithiasis.

•

Urinary pH as a Composition Clue

• Consistently low urinary pH parameters (pH < 5.5) point strongly toward a uric acid crystalline composition.
• Elevated urinary pH parameters (pH > 7.5) indicate the presence of urease-producing microbial pathogens, pointing toward a struvite infection stone.

•

Infectious Screening Metrics

• Active tracking for marked pyuria, positive leukocyte esterase, and bacterial nitrites to rule out an obstructed, infected upper urinary tract system.

•

BMP

• Immediate quantification of baseline serum creatinine to establish accurate eGFR values.
• Targeting detection of post-renal AKI from bilateral obstruction, unilateral obstruction in a single functioning kidney, or severe volume depletion.

•

CBC

• Evaluation for marked leukocytosis.
• Physiologic Nuance: Mild-to-moderate white blood cell count elevations frequently represent non-specific stress demargination driven by severe pain and repetitive vomiting.
• High-grade white blood cell shifts demand immediate exclusion of systemic bacteremia or an infected, obstructed urinary system.

•

Adjunctive Lab Pathways

• Rapid qualitative urine hCG testing.
• Reflex urine culture execution whenever urinalysis metrics display significant inflammatory profiles or clinical suspicion of UTI is high.

4. IMAGING MODALITIES & ALGORITHMIC CLINICAL SELECTION

•

Non-Contrast CT Diagnostics

• Gold standard; diagnostic sensitivity and specificity parameters exceed 95% for stones >2 mm.
• Provides precise quantification of stone diameter (mm), exact localization (proximal, mid, or distal ureter), and degree of secondary hydronephrosis.
• Excellent structural visualization for detecting or ruling out alternate retroperitoneal, vascular, or intra-abdominal pathologies.

•

Contrast-Enhanced CT Protocols

• Indicated when alternative intra-abdominal surgical pathology is highly suspected over isolated renal colic.
• Retains diagnostic capability to identify urinary tract stones >3 mm even within contrast-enhanced phases.

•

NCCT Structural Architecture Limitations

• Standard stone protocol CT scans are executed in a prone position without IV contrast enhancement. It does not opacify the ureteral lumen.
• Presents a cumulative radiation exposure penalty when utilized serially across recurrent ED presentations.

•

POCUS / Radiology Ultrasound

• Direct stone visualization capabilities are modest, operating at approximately 50% to 60% sensitivity, and is highly dependent on anatomical positioning at the extreme proximal ureter or the UVJ.
• Secondary obstruction tracking: Demonstration of hydronephrosis operates at a high sensitivity of approximately 80%.

•

POCUS Clinical Utility Metrics

• Eliminates ionizing radiation exposure and allows immediate, rapid real-time execution directly at the patient’s bedside.
• Confirmation of significant hydronephrosis within a classic clinical presentation yields high post-test probability for stone presence while lowering suspicion for vascular catastrophes like a AAA.

•

KUB Radiography

• Extremely poor overall diagnostic sensitivity, hovering around 57%.
• Fails to image radiolucent configurations (pure uric acid matrices) or small stones measuring <5 mm.
• Avoided in acute ED diagnostic pathways; selectively considered as a low-radiation tracking step in pediatric cohorts or pregnant populations.

5. Ultrasonography versus Computed Tomography for Suspected Nephrolithiasis

•

Core Trial Architecture

• Large-scale multi-center randomized controlled trial assessing POCUS first vs. Radiology US first vs. NCCT first pathways in acute ED cohorts.

•

Primary Clinical Outcomes

• No statistically significant variations in missed high-risk alternative diagnoses (AAA, appendicitis, bowel ischemia, or adnexal torsion rates remained rare at ~0.4%).
• No differences noted in serious adverse event rates, subjective pain-control scores, return ED visits, or overall hospitalization frequencies.

•

Radiation Modulation Impact

• An ultrasound-first initial strategy reduced cumulative, downstream radiation exposure by approximately 50%.

•

Algorithmic Selection Guidelines

• Establishes the clinical premise that raw diagnostic sensitivity does not automatically equate to superior clinical utility or better patient outcomes.
• An ultrasound-first diagnostic pathway paired with selective escalation to NCCT is safe and indicated for recurrent, young, clinically stable cohorts.

6. IMAGING SELECTION MATRIX

•

Indications Favoring an Ultrasound-First Approach

• Age parameters <35 years to mitigate lifetime cumulative radiation risks.
• Confirmed, well-documented history of recurrent nephrolithiasis presenting with identical symptoms to prior events.
• Hemodynamic stability paired with reassuring, classic clinical tracking.

•

Indications Favoring Immediate NCCT Imaging

• Advanced age parameters.
• First-time presentation with zero history of stone disease.
• Atypical clinical presentation or diagnostic uncertainty.
• Persistent, unmitigated symptoms refractory to standard ED interventions.
• High pre-test probability of immediate surgical or urological decompression.

7. EMERGENCY PHARMACOTHERAPY & COLIC MANAGEMENT

•

First-Line Analgesic Paradigms

• NSAIDs: Specifically Ketorolac (Toradol) titrated at 15–30 mg.
• High-Yield Data Marker: Multiple trials confirm IV NSAIDs provide equivalent pain reduction scores to titrated IV opioids in acute renal colic.
• Mechanism: Targets localized ureteral smooth muscle spasms and downregulates prostaglandin-mediated hyper-filtration and local tissue inflammation.

•

NSAID Absolute/Relative Contraindications

• Significantly depressed GFR or active acute renal failure states.
• Active gastrointestinal hemorrhage risks or history of severe peptic ulcerations.
• Third-trimester pregnancy.

•

Second-Line Analgesic Titration

• Intermittent titration of IV opioids (e.g., Morphine) indicated if the NSAID maximum ceiling effect is reached or if explicit contraindications prevent NSAID administration.

•

Antiemetic Adjuvant Therapy

• Concomitant use of Ondansetron (Zofran) to manage reflex nausea and vomit-induced dehydration.

•

Fluid Resuscitation Realities

• Targeted IV fluids to correct explicit volume deficits driven by emesis or reduced oral intake.
• Physiologic Caveat: Aggressive, high-volume fluid hydration does not accelerate stone transit speed or improve the spontaneous passage rate.

8. MEDICAL EXPULSIVE THERAPY (MET) CLINICAL PARAMETERS

•

Pharmacologic Agent

• Tamsulosin (Flomax) dosed at 0.4 mg orally once daily for a maximum duration of 28 days.

•

Target Efficacy Window

• Highly specific for distal ureteral stones measuring between 5 mm and 10 mm.
• Yields modest improvements in spontaneous clearance rates within this specific size band.

•

Literature Controversies

• A 2015 Lancet randomized controlled trial demonstrated neutral primary endpoints.
• Subsequent large-scale meta-analyses and network meta-analyses identify a significant signal for benefit, particularly for combinations.

•

Stones Measuring <5 mm

• MET is generally not indicated or cost-effective.
• Spontaneous passage rates are high, making the side effect profile of alpha-blockade unjustifiable.

•

Side Effect Profile

• Orthostatic hypotension, transient dizziness, and retrograde ejaculation.

9. SPONTANEOUS PASSAGE PROBABILITIES

•

Size-Dependent Passage Vectors

•

• Stones <5 mm: 70% to 90% spontaneous passage rate. Managed conservatively.
• Stones 5–10 mm: 50% to 60% spontaneous passage rate. Candidates for MET.
• Stones >10 mm: <10% spontaneous passage rate. Spontaneous transit is rare; requires urologic intervention.

•

Anatomical Location Passage Vectors

•

• Distal Ureter (UVJ area): ~75% spontaneous passage likelihood.
• Mid-Ureter (Crossing point of iliac vessels): ~60% spontaneous passage likelihood.
• Proximal Ureter (UPJ to upper third): ~48% spontaneous passage likelihood.

•

Transit Timeline Dynamics

•

• Mean passage window spans 2 to 4 weeks for complete structural clearance.
• Temporal Risk Threshold: Unremitting ureteral obstruction lasting >4 weeks carries an elevated risk of irreversible renal parenchymal injury, persistent AKI, and permanent loss of nephron function.

10. ADMISSION ARCHITECTURE & UROLOGIC CONSULTATION CRITERIA

Mandatory Surgical Emergency Decompression Criteria

Obstructed Urinary Tract + Concomitant Infection: Co-existence of an obstructing stone and upper tract infection (fever, systemic chills, pyuria, nitrites, leukocytosis) is a urologic emergency. It carries a high risk for rapid progression to pyonephrosis, perinephric abscess, overwhelming urosepsis, and cardiovascular collapse. Requires emergent urologic consultation for surgical retrograde stent placement or percutaneous nephrostomy tube insertion.

Refractory Symptom Complexes

•

•

• Intractable pain scores or persistent emesis failing aggressive ED parenteral therapies.

High-Risk Patient Anatomy / Physiology

•

•

• Solitary functioning kidney or renal transplant anatomy presenting with acute obstruction (high risk for sudden anuric renal failure).
• Complete clinical anuria.
• High-grade, progressive acute kidney injury (AKI) that fails to stabilize following targeted volume resuscitation.
• Acute obstructing ureterolithiasis manifesting within a pregnant patient.

High Structural Stone Burden

•

•

• Stone diameter >10 mm. Spontaneous resolution is unlikely; needs shockwave lithotripsy, ureteroscopy, or specialized stenting.

Prolonged Structural Symptoms

•

•

• Documented stone impaction or symptom tracking extending past a 4-week timeline without clear passage.

11. OUTPATIENT DISCHARGE MATRICES & SAFETY NETTING

•

Discharge Criteria Checklists

• Pain score controlled with oral medications; tolerating adequate PO oral fluids; stable renal function panel; zero systemic or local signs of infection.
• Outpatient Prescribing Packets

• Scheduled or high-dose PRN oral NSAIDs plus short-course rescue oral opioids for breakthrough colic episodes.
• Tamsulosin 0.4 mg once daily if stone localization is distal and diameter measures 5–10 mm.
• Oral anti-emetics for home management.

•

Discharge Guidance and Counseling

• Vigorous oral hydration to maintain constant, high volumetric urine throughput.
• Provide a urine strainer to capture the stone matrix for metabolic and chemical composition testing.

•

Explicit Return Precautions

• Instruct the patient to return to the ED for temperature spikes, shaking chills, or unmanageable pain spikes.
• Instruct the patient to return for relentless vomiting preventing fluid retention.

•

Clinical Follow-up Tracking

• Ensure structured outpatient urology follow-up within a 1- to 2-week window.

12. CLINICAL PEARLS & QUICK-REFERENCE SUMMARY NOTES

• The Hematuria Diagnostic Confound: Up to 33% of patients with a confirmed obstructing stone will exhibit a completely normal urinalysis with zero RBCs. Never drop nephrolithiasis from the differential based on a negative dipstick.
• Leukocytosis Interpretation: Severe colic and violent vomiting induce physiological demargination. Treat the overall clinical presentation and temperature curve; do not over-interpret an isolated WBC.
• Hydrative Fluid Mechanics: Fluids address dehydration from emesis. Over-hydrating a patient in acute colic does not push the stone out faster and may worsen pain by increasing renal capsular hydrostatic pressure.
• The 4-Week Functional Boundary: Ureteral obstruction lasting longer than 4 weeks requires specialized intervention to prevent permanent nephron damage.
• Size and Anatomy Rules: A 3 mm stone at the UVJ passes spontaneously in ~90% of cases. An 11 mm stone in the proximal ureter has a <10% clearance rate and requires early urologic involvement.

Read More

https://coreem.net/podcast/episode-223-thyroid-storm/

Diagnosis, workup, and the four-step treatment protocol for thyroid storm.

Hosts:
Annaliese Elam, MD
Brian Gilberti, MD

Download Leave a Comment Tags: Critica Care, Endocrine, Thyroid Storm

Show Notes

I. Pathophysiology & Diagnosis

Definition: Life-threatening hypermetabolic state resulting from decompensated thyrotoxicosis.

Hormonal Profile: Absolute levels of total T₄/T₃ often mirror uncomplicated thyrotoxicosis; storm is driven by rapid rate of rise, increased catecholamine sensitivity, or increased free T₄/T₃ concentrations.

Clinical Presentation:

• Hyperpyrexia (e.g., 104.2°F)
• Tachycardia/Arrhythmias (e.g., 155 bpm)
• Altered Mentation: Agitation, delirium, or psychosis; often the primary differentiator between “storm” and “compensated” hyperthyroidism
• Warm, moist skin

Precipitating Events:

• Infection, trauma, or surgery
• Parturition
• Abrupt cessation of antithyroid medications

Burch-Wartofsky Point Scale (BWPS):

• ≥ 45: Highly suggestive of Thyroid Storm
• 25–44: Suggestive of impending storm
• < 25: Storm unlikely
• Note: High sensitivity but low specificity; can be skewed by unrelated febrile illness.

II. Laboratory & Ancillary Findings

Thyroid Panel: Characteristically low TSH with elevated free T₄ and T₃.

Metabolic Abnormalities:

• Mild hyperglycemia (catecholamine-induced insulin inhibition)
• Mild hypercalcemia
• Elevated LFTs and leukocytosis

Cardiovascular: EKG may show sinus tachycardia or atrial fibrillation with rapid ventricular response.

III. Management: The Four-Step Blocking Strategy

• Step 1: Sympathetic Blockade (Beta Blockers)

• Agent of Choice: Propranolol
• Mechanism: Non-selective blockade; in high doses, inhibits peripheral conversion of T₄ to T₃.
• Dosing:

• PO: 60–80 mg every 4–6 hours
• IV: 0.5–1 mg over 10 minutes

• Critical Pitfall: Avoid in patients with acute decompensated heart failure with systolic dysfunction; risk of cardiovascular collapse.

• Step 2: Inhibition of Hormone Synthesis (Thionamides)

• Agent of Choice: Propylthiouracil (PTU) preferred over Methimazole in life-threatening storm.
• Mechanism: Blocks synthesis of new hormone and inhibits peripheral T₄-to-T₃ conversion (decreases T₃ by ~45% in 24 hours).
• Dosing: 200–250 mg PO every 4 hours

• Step 3: Inhibition of Hormone Release (Iodine)

• Agents: Potassium iodide (SSKI) or Lugol’s solution
• Critical Timing: Must wait at least 60 minutes AFTER thionamide administration.
• Rationale: Immediate iodine administration provides substrate for new hormone synthesis (Wolff-Chaikoff effect bypass), potentially worsening thyrotoxicosis.

• Step 4: Inhibition of Peripheral Conversion & Adrenal Support

• Agent: Glucocorticoids (Hydrocortisone)
• Mechanism: Inhibits peripheral T₄ to T₃ conversion and treats potential relative adrenal insufficiency.
• Dosing: 300 mg IV loading dose, followed by 100 mg IV every 8 hours

IV. Supportive Care & Avoidance Measures

Hyperpyrexia Management:

• Acetaminophen is the standard of care
• Avoid Aspirin: Salicylates displace thyroid hormone from thyroid-binding globulin (TBG), increasing free T₄/T₃ levels

Volume Resuscitation:

• Aggressive IV fluids; patients are often profoundly dehydrated
• May require 3–5 liters of isotonic crystalloid per 24 hours

Take Home Points

I. Diagnostic Essentials

• Clinical Diagnosis: Based on hyperpyrexia, cardiovascular dysfunction, and altered mentation.
• Key Differentiator: Altered mentation (agitation, delirium, psychosis) is often the sole finding distinguishing “storm” from “compensated” thyrotoxicosis.
• Burch-Wartofsky Point Scale (BWPS):

• ≥ 45: Highly suggestive of storm.
• 25–44: Suggests impending storm.
• < 25: Storm unlikely.
• Note: High sensitivity, low specificity (e.g., hyperthyroid + flu can score > 45).

• Triggers: Infection, trauma, parturition, or abrupt cessation of antithyroid drugs.

II. The Four-Step Blocking Strategy

• Beta Blockade (Propranolol):

• Dose: 60–80 mg PO q4–6h or 0.5–1 mg IV over 10 min.
• Action: Blocks symptoms and inhibits peripheral T4 to T3 conversion.
• Caution: Avoid in acute decompensated heart failure with systolic dysfunction.

• Thionamides (PTU):

• Dose: 200 to 250 mg every four hours. (note: some resources suggest a loading dose beforehand)
• Action: Preferred over methimazole; blocks new hormone synthesis and peripheral T4 to T3 conversion.

• Iodine (SSKI/Lugol’s):

• Timing: Must wait ≥ 60 minutes AFTER thionamide dose.
• Action: Blocks hormone release.
• Pitfall: Early iodine provides substrate for new hormone synthesis, worsening the condition.

• Glucocorticoids (Hydrocortisone):

• Dose: 300 mg IV load, then 100 mg IV q8h.
• Action: Blocks conversion and provides adrenal support.

III. Critical Supportive Care

• Hyperpyrexia: Use Acetaminophen.

• NEVER Use Aspirin: Displaces thyroid hormone from binding proteins, acutely increasing free T4/T3 levels.

• Volume: Aggressive fluid resuscitation; patients may require 3–5 L/day due to profound dehydration.

Read More

https://coreem.net/podcast/episode-222-local-anesthetic-systemic-toxicity-last/

We discuss this ominous complication of providing local anesthesia.

Hosts:
Elaine Jonas, MD
Brian Gilberti, MD

Download Leave a Comment Tags: Critical Care, Toxicology

Show Notes

I. Pathophysiology & Mechanisms

•

Definition: Systemic toxicity secondary to local anesthetic (LA) via accidental intravascular injection or excessive systemic absorption.

•

Threshold: Occurs when plasma concentration exceeds the safety threshold for cardiac and neural tissue.

•

Agent Profile: Bupivacaine (High Risk)

•

Highly lipophilic with high protein binding.

•

“Fast-on, Slow-off” Kinetics: Strong Na+ channel binding with extremely slow dissociation during diastole.

•

Myocardial Depression: Direct inhibition of Ca2+ release from the sarcoplasmic reticulum, impairing contractility.

•

Low CC:CNS Ratio: The dose required for cardiac collapse is very close to the dose that triggers seizures (narrow safety margin).

•

Contributing Factors:

•

Acidosis/Hypercapnia: Increases the fraction of free drug and promotes ion trapping in the brain/heart; shifts the LA-binding curve toward higher toxicity.

•

Hypoxemia: Exacerbates myocardial depression and lowers seizure threshold.

II. Risk Assessment & Prevention

Patient-Specific Risk Factors

•

Extremes of Age: Neonates (low α-1-acid glycoprotein) and elderly (reduced clearance).

•

Body Composition: Low muscle mass/frailty (decreased volume of distribution).

•

Organ Dysfunction:

•

Hepatic: Reduced metabolism of amide LAs.

•

Renal: Accumulation of metabolites; risk of metabolic acidosis lowering seizure threshold.

•

Cardiac: Reduced cardiac output slows hepatic delivery/clearance; heart failure patients are more sensitive to Na+ channel blockade.

•

Pregnancy: Increased sensitivity to cardiotoxicity.

Procedural Risk Factors

•

Vascularity of Site (Highest to Lowest Risk):

•

Intercostal blocks (highest absorption rate).

•

Caudal/Epidural.

•

Interfascial plane blocks (e.g., TAP block).

•

Psoas compartment/Sciatic.

•

Brachial plexus.

•

Technique: Large volume infiltration, lack of ultrasound, lack of incremental injection.

Prevention Mandates

•

Weight-Based Dosing:

•

Lidocaine (Plain): Max 4.5 mg/kg.

•

Lidocaine (with Epi): Max 7 mg/kg.

•

Bupivacaine: Max 2.5–3 mg/kg.

•

Incremental Injection: 3–5 mL aliquots with frequent aspiration.

•

Intravascular Marker: Use Epinephrine (1:200,000) to detect accidental IV placement (HR increase >10 bpmor SBP increase >15 mmHg).

III. Clinical Presentation

Neurologic Phase (Early to Late)

•

Subjective: Metallic taste, tinnitus, circumoral numbness/tingling.

•

Objective: Visual disturbances, agitation, confusion, tremors.

•

Critical: Generalized tonic-clonic seizures, rapid progression to CNS depression, coma, and apnea.

•

Note: Early phases are often masked in patients receiving midazolam or propofol.

Cardiovascular Phase

•

Initial: Hypertension and tachycardia (if epi used) or transient stimulatory phase.

•

Conduction Defects: PR prolongation, QRS widening (classic sign), bundle branch blocks.

•

Dysrhythmias: Bradycardia (most common), VT/VF, PEA, asystole.

•

Contractility: Profound, refractory hypotension and cardiogenic shock.

IV. Immediate Management Algorithm

Goal: Prevent hypoxia/acidosis and sequester the toxin.

1. Initial Actions

•

Stop Injection: Immediately halt all LA administration.

•

Call for Help: Specify “LAST Protocol” and “Intralipid Kit.”

•

Airway Management:

•

100% O2​.

•

Hyperventilate slightly if needed to counter respiratory acidosis.

•

Low threshold for intubation (hypoxia/acidosis rapidly worsen LAST).

2. Seizure Control

•

First-line: Benzodiazepines (e.g., Midazolam).

•

Avoid: Propofol if hemodynamically unstable (exacerbates cardiac depression).

•

Neuromuscular Blockers: May be needed for ventilation, but remember they do not stop CNS seizure activity.

3. Lipid Emulsion Therapy 20%

•

Indications: Start at first sign of serious toxicity (airway compromise, seizures, or CV instability).

•

Bolus: 1.5 mL/kg IV over 1 minute.

•

Infusion: 0.25 mL/kg/min immediately following bolus.

•

If Instability Persists:

•

Repeat bolus (up to 2 times).

•

Increase infusion to 0.5 mL/kg/min.

•

Upper Limit: ≈12 mL/kg total dose.

4. Modified ACLS

•

Epinephrine: Use low doses (<1 mcg/kg) to avoid worsening arrhythmias and interfering with lipid rescue.

•

Antiarrhythmics: Amiodarone is preferred.

•

CONTRAINDICATED:

•

Lidocaine: (Class Ib antiarrhythmic—will worsen toxicity).

•

Vasopressin: Associated with poor outcomes in animal LAST models.

•

Calcium Channel Blockers / Beta Blockers: Exacerbate myocardial depression.

•

Refractory Arrest: Early consultation for ECMO or Cardiopulmonary Bypass (CPB).

V. Differential Diagnosis for the Peri-Procedural Patient

•

High Spinal: Ascending sensory/motor block, profound sympathectomy (hypotension/bradycardia).

•

Anaphylaxis: Urticaria, wheezing (rare with amides, more common with esters).

•

Air/Gas Embolism: Sudden dyspnea, “mill-wheel” murmur, acute right heart strain.

•

Vasovagal Syncope: Bradycardia/hypotension, usually lacks the QRS widening or seizure activity.

VI. Post-Resuscitation & Complications

•

Observation:

•

At least 2 hours after a CNS-only event.

•

At least 4–6 hours after a CV event.

•

Lipid Complications:

•

Lab Interference: Lipemia interferes with hemoglobin, creatinine, and electrolyte measurements (draw labs before ILE if possible).

•

Pancreatitis: Rare, delayed complication of high-dose ILE.

•

Fat Embolism/Overload: Rare pulmonary complications.

VII. Clinical “Red Flags” for Toxicity

•

Unexpected Agitation: In a patient who just received a block, don’t assume “anxiety.”

•

Wide QRS: Any widening of the QRS complex post-injection is LAST until proven otherwise.

•

Refractory Arrest: Standard ACLS failing in a patient who received LA. Lipid must be given.

Critical Note: LAST is a clinical diagnosis. Do not wait for serum lidocaine levels or laboratory confirmation to initiate Lipid Emulsion Therapy. Immediate correction of pH and PaCO2​ is as vital as the lipid itself.

Read More

https://coreem.net/podcast/episode-221-high-output-heart-failure/

We discuss the diagnosis and treatment of one of EM's paradoxes: High-Output Heart Failure.

Hosts:
Nicolas Gonzalez, MD
Brian Gilberti, MD

Download Leave a Comment Tags: Cardiology

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

1. Core Definition & Hemodynamic Profile

•

Clinical Paradox: Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function.

•

Hemodynamic Criteria:

•

Cardiac Index (CI): >4.0 L/min/m2.

•

Cardiac Output (CO): >8 L/min.

•

Systemic Vascular Resistance (SVR): Pathologically low (vasodilated or shunted state).

•

The “Warm” Phenotype: Unlike standard HFrEF/HFpEF (often “Cold and Wet”), HOHF presents as “Warm and Wet” due to low SVR and bounding pulses.

2. Pathophysiology: The Hemodynamic Paradox

•

Primary Insult: Decreased SVR (either via peripheral vasodilation or arteriovenous shunting).

•

Effective Arterial Blood Volume: Paradoxically low despite high total CO.

•

Neurohormonal Cascade:

•

Activation of Renin-Angiotensin-Aldosterone System (RAAS).

•

Increased Sympathetic Nervous System tone.

•

Increased Antidiuretic Hormone (ADH) secretion.

•

Resultant State: Avid renal salt and water retention leading to massive plasma volume expansion.

•

Cardiac Response: Chronic volume overload → eccentric remodeling → chamber dilation → eventual secondary myocardial failure/dilated cardiomyopathy.

3. Differential Diagnosis: Etiological “Buckets”

Category A: Increased Metabolic Demand (Systemic)

•

Hyperthyroidism/Thyrotoxicosis:

•

Direct T3 effects: increased chronotropy/inotropy.

•

Indirect effects: metabolic byproduct accumulation causing peripheral vasodilation.

•

Myeloproliferative Disorders:

•

High cell turnover and increased oxygen consumption drive compensatory CO increase.

•

Sepsis (Hyperdynamic Phase):

•

Cytokine-mediated global vasodilation.

•

Note: Often transient; may transition to sepsis-induced myocardial depression.

Category B: Peripheral Vascular Effects (Shunting/Vasodilation)

•

Arteriovenous Fistulas (AVF) / Malformations (AVM):

•

Most Common Cause: Iatrogenic AVF for Hemodialysis (ESRD population).

•

Bypasses high-resistance capillary beds, dumping arterial blood directly into venous circulation.

•

Chronic Liver Disease (Cirrhosis):

•

Formation of “spider angiomata” and internal AV shunts.

•

Impaired clearance of endogenous vasodilators (e.g., Nitric Oxide).

•

Thiamine Deficiency (Wet Beriberi):

•

Accumulation of pyruvate/lactate → systemic vasodilation.

•

Histopathology: Vacuolation, myofiber hypertrophy, and interstitial edema.

•

Chronic Lung Disease:

•

Hypoxia/Hypercapnia-driven systemic vasodilation.

•

Concomitant pulmonary HTN (RV remodeling) but preserved/high LV output.

•

Others: Paget’s disease of bone (extensive micro-shunting), Carcinoid syndrome, Mitochondrial diseases, Acromegaly, Erythroderma.

4. Special Focus: Hemodialysis Access-Induced HOHF

Physiologic Phases of AVF Creation:

•

Acute Phase:

•

Immediate ↓ SVR.

•

↑ Stroke volume and Heart Rate (SNS-mediated).

•

Endothelial shear stress → Nitric Oxide release → further arterial dilation.

•

Subacute Phase (Days to 2 Weeks):

•

RAAS-driven volume expansion.

•

↑ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP).

•

Natriuretic peptide surge (BNP/ANP) peaks around Day 10.

•

Chronic Phase (Weeks to Months):

•

Adaptive hypertrophy.

•

Decompensation occurs when dilation exceeds contractility limits.

5. Point-of-Care Physical Exam & Maneuvers

•

Nicoladoni-Branham Sign (Pathognomonic for Shunt-driven HOHF):

•

Maneuver: Manually compress the AVF (or inflate cuff to >50 mmHg above SBP) for 30 seconds.

•

Positive Result: Reflexive bradycardia or a transient rise in systemic BP.

•

Significance: Confirms the shunt is a major contributor to the cardiac workload.

•

Peripheral Pulse Assessment:

•

Water Hammer Pulses: Rapid upstroke and collapse.

•

Quincke’s Pulse: Visible capillary pulsations in the nail beds.

•

Traube’s Sign: “Pistol-shot” sounds auscultated over the femoral arteries.

•

Volume Status: Rales, S3 gallop, peripheral edema (standard HF signs).

6. Diagnostic Workup (Technical Targets)

POCUS / Echocardiography:

•

Left Ventricle: Hyperdynamic function; EF typically >60%.

•

Left Atrium: Significant dilation (Left Atrial Volume Index >34 mL/m2; Case study noted 72 mL/m2).

•

IVC: Plethoric with minimal respiratory variation.

•

Doppler: High flow velocities across the AV access if applicable.

Laboratory Evaluation:

•

BNP/NT-proBNP: Often markedly elevated (e.g., >70,000 in severe cases), though mean values in literature hover around 700–800 pg/mL.

•

Hematology: CBC to evaluate for severe anemia (trigger for HOHF if Hgb<7–8 g/dL) or myeloproliferative markers.

•

Endocrine/Metabolic: TSH (Thyrotoxicosis), Serum Thiamine (Beriberi), LFTs (Cirrhosis).

7. Management Strategy: A Stepwise Approach

Phase 1: Immediate Stabilization (Volume Offloading)

•

Diuresis: Aggressive IV loop diuretics (Bumetanide/Furosemide).

•

Ultrafiltration: Preferred in ESRD patients failing to respond to dialysis or with refractory congestion.

•

Vasodilator Caution: Avoid aggressive Nitroglycerin or ACE-inhibitors initially.

•

Rationale: Baseline SVR is already pathologically low; further reduction may precipitate profound hypotension/circulatory collapse.

Phase 2: Targeted Therapy (Etiology Specific)

•

Anemia: Transfuse to goal Hgb>7–8 g/dL to reduce demand.

•

Beriberi: High-dose IV Thiamine (100–500 mg).

•

Thyrotoxicosis: Beta-blockers (Propranolol) + Antithyroid meds (PTU/Methimazole).

Phase 3: Surgical/Interventional Salvage (Refractory AVF Cases)

•

Closure of Accessory Sites: If multiple fistulas exist, close the non-dominant/unused sites.

•

Flow Reduction (Banding): Surgical narrowing of the fistula to target flow <600 mL/min.

•

RUDI Procedure: Revision Using Distal Inflow (moving inflow to a smaller, more distal artery).

•

Ligation: Complete closure of the AVF.

•

Note: Requires bridge to Tunneled Dialysis Catheter or AV graft (higher resistance than fistulas).

8. Key Clinical Takeaways

•

The “Normal EF” Trap: Do not be reassured by an EF of 55–65%; in the context of pulmonary edema and high CO, this is potentially HOHF.

•

Pulse Pressure: Look for a wide pulse pressure (e.g., 180/60) as a marker of low SVR.

•

ESRD Logic: If an ESRD patient is “wet” immediately after HD, the problem is likely flow (AVF), not just fluid.

Read More

https://coreem.net/podcast/episode-220-post-rosc-care/

We explore how to refine and optimize care in the vital minutes following ROSC.

Hosts:
Jonathan Elmer, MD, MS
Brian Gilberti, MD

Download Leave a Comment

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

I. Phase 1: Stabilization (Minutes 0–10)

The “Rearrest” Window & Pathophysiology

• High-Risk Period: Rearrest rates reach 30% within the first minutes post-ROSC.

• Shock Incidence: Two-thirds of patients develop profound hypotension/shock as initial resuscitative efforts subside.

• Catecholamine Washout: Super-physiologic “code-dose” epinephrine (1mg IV) typically wears off within ~3 minutes post-ROSC, leading to predictable hemodynamic collapse.

• Secondary Injuries: Evaluate for “CPR-induced trauma” (blunt thoracic trauma, rib fractures, pneumothorax, liver/splenic lacerations).

Immediate Resuscitative Actions

• Vascular Access:

• Transition rapidly from IO to reliable IV access within 1–2 minutes.

• Prioritize Intraosseous (IO) placement within 5 minutes if IV attempts fail; intra-arrest data suggests no significant difference in early outcomes.

• Vasoactive “Bridge”:

• Maintain a “bolus-dose” pressor at the bedside for immediate push-dose titration.

• Options: Phenylephrine, dilute Epinephrine, or dilute Norepinephrine (titrated to effect rather than rigid dosing).

• Physician-Specific Task: Arterial Line:

• Goal: Placement within 5 minutes of ROSC.

• Preferred Site: Femoral (by landmarks/blind if necessary) for speed; should be a <2-minute procedure.

• Utility: Immediate detection of rearrest and beat-to-beat titration of vasopressors.

II. Phase 2: Diagnostic Workup (Minutes 10–40)

Etiology Epidemiology

• ACS Shift: Acute Coronary Syndrome (ACS) is the cause in only 6–10% of resuscitated survivors (lower than historical estimates).

• Common Etiologies:
• Respiratory: COPD, pneumonia, mucus plugging.

• Cardiac: Arrhythmia (cardiomyopathy/scar), RV failure (PE), or LV failure.

• Neurological: Intracranial hemorrhage (SAH/ICH), status epilepticus (4–5%).

• Metabolic: Dialysis-related disarray/hyperkalemia.

• Toxicology: Overdose accounts for ~10% of cases in urban centers.

The “Broad Net” Strategy

• “Rainbow Labs”: Comprehensive panel including toxicology and serial biomarkers.

• Pan-Scan Protocol:

• Components: CT/CTA Head/Neck, Contrast CT Chest/Abdomen/Pelvis.

• Diagnostic Yield: 50% for clinically significant findings (causes or consequences of arrest).

• Contrast Risk: Negligible (1–2% increase in AKI risk) compared to the high diagnostic utility.

• Avoid Anchoring: Do not assume ischemic EKG changes are the cause; they are frequently a consequence of the global arrest-induced ischemia.

III. Hemodynamic & Respiratory Targets

Mean Arterial Pressure (MAP)

• Autoregulation Shift: In acute brain injury/post-arrest, the lower limit of cerebral autoregulation shifts right, often requiring MAPs of 110–120 mmHg for adequate perfusion.
• Clinical Target: Aim for MAP >80 mmHg.

• The BOX Trial Nuance: While the BOX trial showed no difference between MAP 63 vs. 77, its cohort (Denmark) had exceptionally high survival rates (70% back to work) and short response times, which may not generalize to North American populations with lower shockable rhythm incidence.

• Permissive Hypertension: If the patient is “self-driving” to higher pressures, do not aggressively lower them, as this may be a physiologic demand for cerebral blood flow.

Ventilation and Oxygenation

• PaCO2 Management:

• Target: High-normal to slightly hypercarbic (45–55 mmHg).

• Rationale: Avoid accidental hyperventilation (PaCO2 <30), which can cut cerebral blood flow by 50%.

• PaO2 Management: Maintain normoxia; avoid extreme hyperoxia, though trial data (BOX trial) suggests small variances (70 vs 90 mmHg) are likely neutral.

IV. Neurological Prognostication & Communication

The “Stunned” Brain

• Anoxic Depolarization: Occurs within ~2 minutes of pulselessness as ATP-dependent ion pumps fail.

• Clinical Pitfall: Early neurological exams (absent pupils, no motor response) are unreliable in the first hours as they reflect global neuronal “stunning” rather than definitive permanent injury.

• Time Horizon: Meaningful recovery is measured in days/weeks, not minutes/hours.

Family Engagement

• Presence: Bring family to the bedside immediately, including during procedures or continued resuscitation.

• Psychological Impact: Significantly reduces PTSD, anxiety, and depression in survivors’ families.

• Prognostic Honesty: Explicitly state “I don’t know” regarding etiology and outcome.

• Framing: Define “No News” as the best possible early outcome (preventing rearrest and stabilization).

Read More

https://coreem.net/podcast/episode-219-meningitis-2-0/

We review diagnosing and managing bacterial meningitis in the ED.

Hosts:
Sarah Fetterolf, MD
Avir Mitra, MD

Download Leave a Comment Tags: CNS Infections, Infectious Diseases, Neurology

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

Patient Presentation & Workup

• Patient: 36-year-old male, currently shelter-domiciled, presenting with 3 weeks of generalized weakness, fevers, weight loss, and headaches.
• Vitals (Initial): BP 147/98, HR 150s, Temp 100.2°F, RR 18, O2 99% RA.
• Clinical Evolution: Initial assessment noted cachexia and a large ventral hernia. Following initial workup, the patient became acutely altered (A&O x0) and febrile to 102.9°F.
• Physical Exam Findings:

• Brudzinski Sign: Positive (knees flexed upward upon passive neck flexion).
• Kernig Sign: Discussed as highly specific (resistance/pain during knee extension with hip flexed at 90°).
• Meningeal Triad: Fever, nuchal rigidity, and AMS (present in 40% of cases; 95% of patients have at least two of the four cardinal symptoms including headache).

• Imaging:

• Chest X-ray: Scattered opacities (pneumonia) and a small pneumothorax.
• CT Abdomen/Pelvis: Confirmed asplenia (secondary to 2011 GSW/exploratory laparotomy).
• Head CT: Ventricle enlargement concerning for obstructive hydrocephalus and diffuse sulcal effacement.

CSF Analysis & Microbiology

• Bacterial Meningitis

• Opening Pressure: Elevated (Normal is <170 mm H2​O).
• Color: Cloudy or turbid.
• Gram Stain: Positive in 60%–80% of cases before antibiotics; drops to 7%–41% after antibiotics.
• Cell Count: Very high (>1000–2000/mm3 WBC); dominated by neutrophils (>80% PMN).
• Glucose: Low (<40 mg/dL); CSF/blood glucose ratio is <0.3–0.4.
• Protein: High (>200 mg/dL).
• Cytology: Negative.

• Viral Meningitis

• Opening Pressure: Normal.
• Color: Clear or bloody.
• Gram Stain: Negative.
• Cell Count: Slightly elevated (<300/mm3 WBC); dominated by lymphocytes (<20% PMN).
• Glucose: Normal.
• Protein: Moderately elevated (<200 mg/dL).
• Cytology: Negative.

• Fungal Meningitis

• Opening Pressure: Normal to elevated.
• Color: Clear or cloudy.
• Gram Stain: Negative.
• Cell Count: Elevated (<500/mm3 WBC).
• Glucose: Normal to slightly low.
• Protein: High (>200 mg/dL).
• Cytology: Negative.

• Neoplastic (Cancer-related) Meningitis

• Opening Pressure: Normal.
• Color: Clear or cloudy.
• Gram Stain: Negative.
• Cell Count: Elevated (<300/mm3 WBC).
• Glucose: Normal to slightly low.
• Protein: High (>200 mg/dL).
• Cytology: Positive (this is the key differentiator).

Management Protocol

• Immediate Treatment: Early administration of antibiotics/antivirals is critical to reduce mortality.

• Antibiotics: Ceftriaxone 2g IV q12h + Vancomycin (or Rifampin in cephalosporin-resistant areas).
• Listeria Coverage: Add Ampicillin for patients > 50 years old.
• Antivirals: Acyclovir 10 mg/kg q8h.
• Steroids: Dexamethasone 10 mg IV q6h for 4 days (proven to reduce mortality and improve outcomes).

• Surgical Intervention: Neurosurgery performed an emergent EVD in the ED to relieve pressure from obstructive hydrocephalus.
• Post-Exposure Prophylaxis: Indicated only for N. meningitidis (not S. pneumoniae) for contacts < 24 hours from diagnosis.

• Regimens: Rifampin for 2 days, single-dose Ciprofloxacin, or IM Ceftriaxone (if pregnant).

Stats & Clinical Pearls: Austrian Syndrome

• The Triad: Concurrent pneumonia, endocarditis, and meningitis caused by Streptococcus pneumoniae.
• Risk Factors: Asplenia (due to the spleen’s role in filtering encapsulated bacteria), alcohol use disorder, and immunosuppression.
• Mortality Rate: Extremely high at 28%; mortality is highest when there is CNS involvement.
• Incidence: Worldwide, S. pneumoniae is the leading cause of bacterial meningitis, accounting for 3,000–6,000 cases annually.

Read More

https://coreem.net/podcast/episode-218-sympathetic-crashing-acute-pulmonary-edema-scape/

We discuss the diagnosis and management of SCAPE in the ED.

Hosts:
Naz Sarpoulaki, MD, MPH
Brian Gilberti, MD

Download Leave a Comment Tags: Acute Pulmonary Edema, Critical Care

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

The Clinical Case

• Presentation: 60-year-old male with a history of HTN and asthma.
• EMS Findings: Severe respiratory distress, SpO₂ in the 60s on NRB, HR 120, BP 230/180.
• Exam: Diaphoretic, diffuse crackles, warm extremities, pitting edema, and significant fatigue/work of breathing.
• Pre-hospital meds: NRB, Duonebs, Dexamethasone, and IM Epinephrine (under the assumption of severe asthma/anaphylaxis).

Differential Diagnosis for the Hypoxic/Tachypneic Patient

• Pulmonary: Asthma/COPD, Pneumonia, ARDS, PE, Pneumothorax, Pulmonary Edema, ILD, Anaphylaxis.
• Cardiac: CHF, ACS, Tamponade.
• Systemic: Anemia, Acidosis.
• Neuro: Neuromuscular weakness.

What is SCAPE?

Sympathetic Crashing Acute Pulmonary Edema (SCAPE) is characterized by a sudden, massive sympathetic surge leading to intense vasoconstriction and a precipitous rise in afterload.

• Pathophysiology: Unlike HFrEF, these patients are often euvolemic or even hypovolemic. The primary issue is fluid maldistribution (fluid shifting from the vasculature into the lungs) due to extreme afterload.

Bedside Diagnosis: POCUS vs. CXR

POCUS is the gold standard for rapid bedside diagnosis.

• Lung Ultrasound: Look for diffuse B-lines (≥3 in ≥2 bilateral zones).
• Cardiac: Assess LV function and check for pericardial effusion.
• Why not CXR? A meta-analysis shows LUS has a sensitivity of ~88% and specificity of ~90%, whereas CXR sensitivity is only ~73%. Importantly, up to 20% of patients with decompensated HF will have a normal CXR.

Management Strategy

1. NIPPV (CPAP or BiPAP)

Start NIPPV immediately to reduce preload/afterload and recruit alveoli.

• Settings: CPAP 5–8 cm H₂O or BiPAP 10/5 cm H₂O. Escalate EPAP quickly but keep pressures to avoid gastric insufflation.
• Evidence: NIPPV reduces mortality (NNT 17) and intubation rates (NNT 13).

2. High-Dose Nitroglycerin

The goal is to drop SBP to < 140–160 mmHg within minutes.

• No IV Access: 3–5 SL tabs (0.4 mg each) simultaneously.
• IV Bolus: 500–1000 mcg over 2 minutes.
• IV Infusion: Start at 100–200 mcg/min; titrate up rapidly (doses > 800 mcg/min may be required).
• Safety: ACEP policy supports high-dose NTG as both safe and effective for hypertensive HF. Use a dedicated line/short tubing to prevent adsorption issues.

3. Refractory Hypertension

If SBP remains > 160 mmHg despite NIPPV and aggressive NTG, add a second vasodilator:

• Clevidipine: Ultra-short-acting calcium channel blocker (titratable and rapid).
• Nicardipine: Effective alternative for rapid BP control.
• Enalaprilat: Consider if the above are unavailable.

Troubleshooting & Pitfalls

The “Mask Intolerant” Patient

Hypoxia is the primary driver of agitation. NIPPV is the best sedative. * Pharmacology: If needed, use small doses of benzodiazepines (Midazolam 0.5–1 mg IV).

• AVOID Morphine: Data suggests higher rates of adverse events, invasive ventilation, and mortality. A 2022 RCT was halted early due to harm in the morphine arm (43% adverse events vs. 18% with midazolam).

The Role of Diuretics

In SCAPE, diuretics are not first-line.

• The problem is redistribution, not volume excess. Diuretics will not help in the first 15–30 minutes and may worsen kidney function in a (relatively) hypovolemic patient.
• Delay Diuretics until the patient is stabilized and clear systemic volume overload (edema, weight gain) is confirmed.

Disposition

• Admission: Typically requires CCU/ICU for ongoing NIPPV and titration of vasoactive infusions.
• Weaning: As BP normalizes and work of breathing improves, infusions and NIPPV can be gradually tapered.

Take-Home Points

• Recognize SCAPE: Hyperacute dyspnea + severe HTN. Trust your POCUS (B-lines) over a “clear” CXR.
• NIPPV Immediately: Don’t wait. It saves lives and prevents tubes.
• High-Dose NTG: Use boluses to “catch up” to the sympathetic surge. Don’t fear the dose.
• Avoid Morphine: Use small doses of benzos if the patient is struggling with the mask.
• Lasix Later: Prioritize afterload reduction over diuresis in the hyperacute phase.

Read More

https://coreem.net/podcast/episode-217-prehospital-blood-transfusion/

We discuss the shift to prehospital blood to treat shock sooner.

Hosts:
Nichole Bosson, MD, MPH, FACEP
Avir Mitra, MD

Download Leave a Comment Tags: EMS, Prehospital Care, Trauma

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

What is prehospital blood transfusion

•

Administration of blood products in the field prior to hospital arrival

•

Aimed at patients in hemorrhagic shock

Why this matters

•

Traditional US prehospital resuscitation relied on crystalloid

•

ED and trauma care now prioritize early blood

•

Hemorrhage occurs before hospital arrival

•

Delays to definitive hemorrhage control are common

•

Earlier blood may improve survival

Supporting rationale

•

ATLS and trauma paradigms emphasize blood over fluid

•

National organizations support prehospital blood when feasible

•

EMS already manages high risk, time sensitive interventions

Evidence overview

•

Data are mixed and evolving

•

COMBAT: no benefit

•

PAMPer: mortality benefit

•

RePHILL: no clear benefit

•

Signal toward benefit when transport time exceeds ~20 minutes

•

Urban systems still experience long delays due to traffic and geography

•

LA County median time to in hospital transfusion ~35 minutes

LA County program

•

~2 years of planning before launch

•

Pilot began April 1

•

Partnerships:

•

LA County Fire

•

Compton Fire

•

Local trauma centers

•

San Diego Blood Bank

•

14 units of blood circulating in the field

•

Blood rotated back 14 days before expiration

•

Ultimately used at Harbor UCLA

•

Continuous temperature and safety monitoring

Indications used in LA County

•

Focused rollout

•

Trauma related hemorrhagic shock

•

Postpartum hemorrhage

Physiologic criteria:

•

SBP < 70

•

Or HR > 110 with SBP < 90

•

Shock index ≥ 1.2

•

Witnessed traumatic cardiac arrest

Products:

•

One unit whole blood preferred

•

Two units PRBCs if whole blood unavailable

Early experience

•

~28 patients transfused at time of discussion

•

Evaluating:

•

Indications

•

Protocol adherence

•

Time to transfusion

•

Early outcomes

•

Too early for outcome conclusions

California collaboration

•

Multiple active programs:

•

Riverside (Corona Fire)

•

LA County

•

Ventura County

•

Additional programs planned:

•

Sacramento

•

San Bernardino

•

Programs meet monthly as CalDROP

•

Focus on shared learning and operational optimization

Barriers and concerns

•

Trauma surgeon concerns about blood supply

•

Need for system wide buy in

•

Community engagement

•

Patients who may decline transfusion

•

Women of childbearing age and alloimmunization risk

•

Risk of HDFN is extremely low

•

Clear communication with receiving hospitals is essential

Future direction

•

Rapid national expansion expected

•

Greatest benefit likely where transport delays exist

•

Prehospital Blood Transfusion Coalition active nationally

•

Major unresolved issue: reimbursement

•

Currently funded largely by fire departments

•

Sustainability depends on policy and payment reform

Take-Home Points

•

Hemorrhagic shock is best treated with blood, not crystalloid

•

Prehospital transfusion may benefit patients with prolonged transport times

•

Implementation requires strong partnerships with blood banks and trauma centers

•

Early data are promising, but patient selection remains critical

•

National collaboration is key to sustainability and future growth

Read More

https://coreem.net/podcast/episode-216-brue-brief-resolved-unexplained-event/

We review BRUEs (Brief Resolved Unexplained Events).

Hosts:
Ellen Duncan, MD, PhD
Noumi Chowdhury, MD

Download Leave a Comment Tags: Pediatrics

Show Notes

What is a BRUE?

• BRUE stands for Brief Resolved Unexplained Event.
• It typically affects infants <1 year of age and is characterized by a sudden, brief, and now resolved episode of one or more of the following:

•

Cyanosis or pallor

•

Irregular, absent, or decreased breathing

•

Marked change in tone (hypertonia or hypotonia)

• Altered level of responsiveness

Crucial Caveat: BRUE is a diagnosis of exclusion. If the history and physical exam reveal a specific cause (e.g., reflux, seizure, infection), it is not a BRUE.

Risk Stratification: Low Risk vs. High Risk

Risk stratification is the most important step in management. While only 6-15% of cases meet strict “Low Risk” criteria, identifying these patients allows us to avoid unnecessary invasive testing.

Low Risk Criteria

To be considered Low Risk, the infant must meet ALL of the following:

•

Age: > 60 days old

•

Gestational Age: GA > 32 weeks (and Post-Conceptional Age > 45 weeks)

•

Frequency: This is the first episode

•

Duration: Lasted < 1 minute

•

Intervention: No CPR performed by a trained professional

•

Clinical Picture: Reassuring history and physical exam

Management for Low Risk:

•

Generally do not require extensive testing or admission.

•

Prioritize safety education/anticipatory guidance.

•

Ensure strict return precautions and close outpatient follow-up (within 24 hours).

High Risk Criteria

Any infant not meeting the low-risk criteria is automatically High Risk.

Additional red flags include:

•

Suspicion of child abuse

•

History of toxin exposure

•

Family history of sudden cardiac death

•

Abnormal physical exam findings (trauma, neuro deficits)

Management for High Risk:

•

Requires a more thorough evaluation.

•

Often requires hospital admission.

• Note: Serious underlying conditions are identified in approx. 4% of high-risk infants.

Differential Diagnosis: “THE MISFITS” Mnemonic

•

T – Trauma (Accidental or Non-accidental/Abuse)

•

H – Heart (Congenital heart disease, dysrhythmias)

•

E – Endocrine

•

M – Metabolic (Inborn errors of metabolism)

•

I – Infection (Sepsis, meningitis, pertussis, RSV)

•

S – Seizures

•

F – Formula (Reflux, allergy, aspiration)

•

I – Intestinal Catastrophes (Volvulus, intussusception)

•

T – Toxins (Medications, home exposures)

•

S – Sepsis (Systemic infection)

Workup & Diagnostics

Step 1: Stabilization

•

ABCs (Airway, Breathing, Circulation)

•

Point-of-care Glucose

•

Cardiorespiratory monitoring

Step 2: Diagnostic Testing (For High Risk/Symptomatic Patients)

•

Labs: VBG, CBC, Electrolytes.

•

Imaging:

•

CXR: Evaluate for infection and cardiothymic silhouette.

•

EKG: Evaluate for QT prolongation or dysrhythmias.

• Neuro: Consider Head CT/MRI and EEG if there are concerns for trauma or seizures.

Clinical Pearl: Only ~6% of diagnostic tests contribute meaningfully to the diagnosis. Be judicious—avoid “shotgunning” tests in low-risk patients.

Prognosis & Outcomes

•

Recurrence: Approximately 10% (lower than historical ALTE rates of 10-25%).

•

Mortality: < 1%. Nearly always linked to an identifiable cause (abuse, metabolic disorder, severe infection).

•

BRUE vs. SIDS: These are not the same.

•

BRUE: Peaks < 2 months; occurs mostly during the day.

•

SIDS: Peaks 2–4 months; occurs mostly midnight to 6:00 AM.

Take-Home Points

•

Diagnosis of Exclusion: You cannot call it a BRUE until you have ruled out obvious causes via history and physical.

•

Strict Criteria: Stick strictly to the Low Risk criteria guidelines. If they miss even one (e.g., age < 60 days), they are High Risk.

•

Education: For low-risk families, the most valuable intervention is reassurance, education, and arranging close follow-up.

•

Systematic Approach: For high-risk infants, use a structured approach (like THE MISFITS) to ensure you don’t miss rare but reversible causes.

Read More

https://coreem.net/podcast/episode-215-marburg-virus-and-global-em/

Lessons from Rwanda’s Marburg Virus Outbreak and Building Resilient Systems in Global EM.

Hosts:
Tsion Firew, MD
Brian Gilberti, MD

Download Leave a Comment Tags: Global Health, Infectious Diseases

Show Notes

Context and the Rwanda Marburg Experience

•

The Threat: Marburg Virus Disease is from the same family as Ebola and has historically had a reported fatality rate as high as 90%.

•

The Outbreak (Sept. 2024): Rwanda declared an MVD outbreak. The initial cases involved a miner, his pregnant wife (who fell ill and died after having a baby), and the baby (who also died).

•

Healthcare Worker Impact: The wife was treated at an epicenter hospital. Eight HCWs were exposed to a nurse who was coding in the ICU; all eight developed symptoms, tested positive within a week, and four of them died.

•

The Turning Point: The outbreak happened in city referral hospitals where advanced medical interventions (dialysis, mechanical ventilation) were available.

•

Rapid Therapeutics Access: Within 10 days of identifying Marburg, novel therapies (experimental drugs and monoclonal antibodies) and an experimental vaccine were made available through diplomacy with the US government/CDC and agencies like WHO, Africa CDC, CEPI and more.

•

The Outcome: This coordinated effort—combining therapeutics, widespread testing, and years of investment in a resilient healthcare system—helped curb the fatality rate down to 23%.

Barriers and Enablers in Outbreak Preparedness

•

Fragmented Systems: Emergency and surveillance functions often operate in silos, leading to delayed or missed outbreak identification (e.g., inconsistent travel screening at JFK during early COVID-19 vs. African countries).

•

Solution: Empowering Emergency Departments and the community as the sentinel site can bridge this gap.

•

Limited Frontline Capacity and Protection: Clinicians are often undertrained and underprotected and are frequently not part of the decision-making for surveillance.

•

Weak Governance and Accountability: Unclear command structures and lack of feedback discourage early reporting.

•

Enabler: Strong governance and accountability in Rwanda helped contain the virus.

•

Dependence on External Programs: Many low-income countries rely on outside sources for vaccines and therapeutics, slowing response.

•

Solution: Invest in local production (e.g., Rwanda’s pre-outbreak investment in developing its own mRNA vaccines).

•

Lack of Resource-Smart Innovation: Gaps exist in things like integrating digital triage tools and surveillance systems.

Four Pillars of a Responsive and Equitable Emergency System

•

Workforce: Invest in pre-service and in-service training, mentorship, and fair compensation to ensure a skilled, protected, and motivated team.

•

Integration into the Health System: Emergency care (including pre-hospital services) must not operate in silos; it needs to be embedded in national health strategies and linked to surveillance, referral, and financing systems.

•

Equity in Design and Policy: The system must address the needs and protection of vulnerable groups and work closely with policymakers.

•

Data: Utilize real-time data and dashboards to provide a feedback loop between clinicians and policymakers, enabling tailored and innovative interventions.

Advice for Clinicians in Global Health Work

•

Start Small and Build Trust: Meaningful work requires humility and relationship over scale or visibility. Focus on local priorities and sustainable change through long-term partnership, not just presence. Avoid the “savior mindset”.

•

Be T-Shaped: Be deep in one specialty (e.g., EM) but fluent across other critical areas like policy, finance, and data, as these drive decision-making.

•

Focus on Knowledge Transfer: True impact means making yourself less essential over time. Prioritize mentorship, co-creation, and sharing leadership opportunities.

Looking Ahead: Global Threats Shaping the Next Decade

The future of EM will be shaped by the convergence of several complex challenges:

•

Climate and Environmental Crisis: Extreme heat, floods, and vector-borne illnesses will strain emergency systems.

•

Preparation: Invest in climate-resilient infrastructure for both EDs and the community.

•

Outbreaks and Biosecurity: Future outbreaks will emerge faster than current systems can handle, coupled with challenges from anti-microbial resistance.

•

Conflict, Displacement, and Urbanization: Mass migration and overcrowded cities will require new models of emergency care that are mobile, scalable, and inclusive.

•

Preparation: Building resilient healthcare systems ready for crisis mental health and cross-border coordination.

•

Digital Tools and AI: These can augment solutions, but investment is needed in data governance and ethical AI that preserves local control and adapts to local capacity.

Read More

https://coreem.net/podcast/episode-214-acute-pulmonary-embolism/

We review the diagnosis, risk stratification, & management of acute pulmonary embolism in the ED.

Hosts:
Vivian Chiu, MD
Brian Gilberti, MD

Download One Comment Tags: Pulmonary

Show Notes

Core Concepts and Initial Approach

• Definition: Obstruction of pulmonary arteries, usually from a DVT in the proximal lower extremity veins (iliac/femoral), but may be tumor, air, or fat emboli.
• Incidence & Mortality: 300,000–370,000 cases/year in the USA, with 60,000–100,000 deaths annually.
• Mantra: “Don’t anchor on the obvious. Always risk stratify and resuscitate with precision.”
• Risk Factors: Broad, including older age, inherited thrombophilias, malignancy, recent surgery/trauma, travel, smoking, hormonal use, and pregnancy.

Clinical Presentation and Risk Stratification

• Presentation: Highly variable, showing up as anything from subtle shortness of breath to collapse.
• Acute/Subacute: Dyspnea (most common), pleuritic chest pain, cough, hemoptysis, and syncope. Patients are likely tachycardic, tachypneic, hypoxemic on room air, and may have a low-grade fever.
• Chronic: Can mimic acute symptoms or be totally asymptomatic.
• Pulmonary Infarction Signs: Pleuritic pain, hemoptysis, and an effusion.
• High-Risk Red Flags: Signs of hypotension (systolic blood pressure < 90 mmHg for over 15 minutes), requirement of vasopressors, or signs of shock → activate PERT team immediately.
• Crucial Mimics: Think broadly; consider pneumonia, ACS, pneumothorax, heart failure exacerbation, and aortic dissection.

Workup & Diagnostics

• History/Scoring: Ask about prior clots, recent surgeries, hospitalizations, travel. Use Wells/PERC criteria to assess pretest probability.
• Labs:

• D-dimer: A good test to rule out PE in a patient with low probability. If suspicion is high, proceed directly to imaging.
• Troponin/BNP: Act as RV stress gauges. Elevated levels are associated with increased risk of a complicated clinical course (25-40%).
• Lactate: Helpful in identifying patients in possible cardiogenic shock.
• EKG: Most common finding is sinus tachycardia. Classic RV strain patterns (S1Q3T3, T-wave changes/inversions) are nonspecific.

• Imaging:

• CXR: Usually normal, but quick and essential to rule out other causes.
• CTPA: The usual standard and gold standard for stable patients. High sensitivity (> 95%) and can detect RV enlargement/strain.
• V/Q Scan: Option for patients with contraindications to contrast (e.g., severe contrast allergies).
• POCUS (Point-of-Care Ultrasound): Useful adjunct for unstable patients.

• Bedside Echo: Can show signs of RV strain (enlarged RV, McConnell sign).
• Lower Extremity Ultrasound: Can identify a DVT in proximal leg veins.

Treatment & Management

• Resuscitation (Reviving the RV):

• Oxygenation: Give supplementally as needed (nasal cannula, non-rebreather, high flow).
• Intubation: Avoid if possible; positive pressure ventilation can worsen RV dysfunction.
• Fluids: Be judicious; even the smallest amount can worsen RV overload.
• Vasopressors: Norepinephrine is preferred as first-line for hypotension/shock.

• Anticoagulation (Start Immediately):

• Initial choice is UFH or LMWH (Lovenox).
• Lovenox is preferred for quicker time to therapeutic range, but is contraindicated in renal dysfunction, older age, or need for emergent procedures.
• DOACs can be considered for stable, low-risk patients as an outpatient.

Escalation for High-Risk PE

• Systemic Thrombolytics: Consider for very sick patients with shock/cardiac arrest (e.g., Alteplase 100 mg over two hours or a bolus in cardiac arrest). High risk of intracranial hemorrhage; weigh risks versus benefits.
• PERT Activation: Engage multidisciplinary teams (usually including ICU, CT surgery, and interventional radiology).
• Interventions: Consult specialists for catheter-directed thrombolysis or suction embolectomy. Surgical embolectomy can also be considered.
• Bridge to Care: Activate the ECMO team early for unstable patients to buy valuable time.

Prognosis & Disposition

• Mortality: Low risk < 1%; intermediate 3-15%; high risk 25-65%.
• Complications: 3-4% of patients develop Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Others may have long-term RV dysfunction and chronic shortness of breath.
• Recurrence: ∼ 30% chance in the next few weeks to months, if not treated correctly.
• Disposition:

• ICU: All high-risk and some intermediate-high risk patients.
• Regular Floor: Intermediate-low risk patients.
• Outpatient Discharge: Low-risk patients can be sent home on anticoagulation. Use PSI or HESTIA scores to risk stratify suitability, typically starting a DOAC.

• Shared Decision-Making: Critical to ensure care is safe and consistent with the patient’s wishes.

Read More

https://coreem.net/podcast/episode-213-pneumothorax/

We break down pneumothorax: risks, diagnosis, and management pearls.

Hosts:
Christopher Pham, MD
Brian Gilberti, MD

Download Leave a Comment Tags: Chest Trauma, Pulmonary, Trauma

Show Notes

Risk Factors for Pneumothorax

• Secondary pneumothorax

• Trauma: rib fractures, blunt chest trauma (as in the case).
• Iatrogenic: central line placement, thoracentesis, pleural procedures.

• Primary spontaneous pneumothorax

• Young, tall, thin males (10–30 years).
• Connective tissue disorders: Marfan, Ehlers-Danlos.
• Underlying lung disease: COPD with bullae, interstitial lung disease, CF, TB, malignancy.

• Technically, anyone is at risk.

Symptoms & Differential Diagnosis

• Typical PTX presentation: Dyspnea, chest pain, pleuritic discomfort.
• Exam clues: unilateral decreased breath sounds, focal tenderness/crepitus.
• Red flags (suggest tension PTX):

• JVD
• Tracheal deviation
• Hypotension, shock physiology
• Severe tachycardia, hypoxia

• Differential diagnoses:

• Pulmonary: asthma, COPD, pneumonia, pulmonary edema (SCAPE), ILD, infections.
• Cardiac: ACS, CHF, pericarditis.
• PE and other acute causes of dyspnea.

Diagnostics

• Bloodwork: limited role, except type & screen if intervention likely.
• EKG: reasonable given chest pain/shortness of breath.
• Imaging:

• POCUS (bedside ultrasound)

• High sensitivity (86–96%) & specificity (97–100%).
• Signs:

• Seashore sign: normal lung sliding.
• Barcode sign: absent lung sliding.
• Lung point: most specific for PTX.

• CXR

• Sensitivity ~70–90% for small PTX.
• May show pleural line, hyperlucency.

• CT chest (gold standard)

• Defines size/severity.
• Rules out mimics (bullae, pleural effusion, hemothorax).
• Guides intervention choice.

Management

• First step for all: Oxygen supplementation (non-rebreather if possible).

• Accelerates resorption of pleural air.

• Stable vs. unstable decision point:

• Unstable/tension PTX

• Immediate needle thoracostomy (14-g angiocath, 2nd ICS midclavicular).
• Temporizing until chest tube/pigtail placed.

• Stable, small PTX (<2 cm on O₂)

• Observation, supplemental O₂, conservative management.

• Stable, larger PTX or symptomatic

• Chest tube or pigtail catheter insertion.
• Pigtail catheters: less invasive, more comfortable, similar efficacy for simple PTX.
• Large bore tubes: indicated if associated with blood, pus, large collections.

Disposition

• Admit all patients with chest tubes; cannot be discharged with tube in place.
• Service responsible varies by hospital: trauma, CT surgery, MICU, etc.
• Level of care (ICU vs. floor) depends on stability:

• ICU if unstable course, intubated, shock physiology.
• Stepdown/floor if stable and straightforward.

Take Home Points

• Always broaden differential in dyspnea/chest pain → don’t anchor on asthma/COPD.
• Exam findings + history (trauma, risk factors) crucial to raising suspicion.
• Ultrasound is more sensitive than CXR and highly specific when lung point found.
• Oxygen is first-line; intervention determined by size + stability.
• Pigtail catheters increasingly favored for simple, stable PTX.
• All patients with intervention require admission; service varies by institution.

Read More

https://coreem.net/podcast/episode-212-angioedema/

Angioedema – Recognition and Management in the ED

Hosts:
Maria Mulligan-Buckmiller, MD
Brian Gilberti, MD

Download Leave a Comment Tags: Airway

Show Notes

Definition & Pathophysiology

Angioedema = localized swelling of mucous membranes and subcutaneous tissues due to increased vascular permeability.

Triggers increased vascular permeability → fluid shifts into tissues.

Etiologies

• Histamine-mediated (anaphylaxis)

• Associated with urticaria/hives, pruritus, and redness.
• Triggered by allergens (foods, insect stings, medications).
• Rapid onset (minutes to hours).

• Bradykinin-mediated

• Hereditary angioedema (HAE): C1 esterase inhibitor deficiency (autosomal dominant).
• Acquired angioedema: Associated with B-cell lymphoma, autoimmune disease, MGUS.
• Medication-induced: Most commonly ACE inhibitors; rarely ARBs.
• Typically lacks urticaria and itching.
• Gradual onset, can last days if untreated.

• Idiopathic angioedema

• Unknown cause; diagnosis of exclusion.

Clinical Presentations

• Swelling

• Asymmetric, non-pitting, usually non-painful.
• May involve lips, tongue, face, extremities, GI tract.

• Respiratory compromise

• Upper airway swelling → stridor, dyspnea, sensation of throat closure.
• Airway obstruction is the most feared complication.

• Abdominal manifestations

• Bowel wall angioedema can mimic acute abdomen:

• Nausea, vomiting, diarrhea, severe pain, increased intra-abdominal pressure, possible ischemia.

Key Differentiating Features

• Histamine-mediated: rapid onset, hives/itching, resolves quickly with epinephrine, antihistamines, and steroids.
• Bradykinin-mediated: slower onset, lacks urticaria, prolonged duration, less responsive to standard anaphylaxis medications.

Diagnostic Approach in the ED

• Focus on airway (ABCs) and clinical assessment.
• Labs (e.g., C4 level) useful for downstream diagnosis (esp. HAE) but not for acute management.
• Imaging: only if symptoms suggest abdominal involvement or to rule out other causes.

Treatment Strategies

• Airway protection is always priority:

• Early consideration of intubation if worsening obstruction or inability to manage secretions.

• Histamine-mediated (anaphylaxis):

• Epinephrine (IM), antihistamines, corticosteroids.

• Bradykinin-mediated:

• Epinephrine may be tried if unclear etiology (no significant harm, lifesaving if histamine-mediated).
• Targeted therapies:

• Icatibant: bradykinin receptor antagonist.
• Ecallantide: kallikrein inhibitor (less available).
• C1 esterase inhibitor concentrate: replenishes deficient protein.
• Fresh frozen plasma (FFP): contains C1 esterase inhibitor.
• Tranexamic acid (TXA): off-label, less evidence, considered if no other options.

Complications to Watch For

• Airway compromise: rapid deterioration possible.
• Abdominal compartment syndrome from bowel edema (rare, surgical emergency).

Take-Home Points

• Secure the airway if in doubt.
• Differentiate histamine-mediated vs bradykinin-mediated by presence/absence of hives/itching and speed of onset.
• Use epinephrine promptly if suspecting histamine-mediated angioedema or if uncertain.
• Consider bradykinin-targeted therapies for confirmed hereditary, acquired, or ACE-inhibitor–related angioedema.
• Recognize ACE inhibitors as the most frequent medication trigger; ARBs rarely cause it.
• Labs and imaging generally don’t change initial ED management but aid diagnosis for follow-up care.

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https://coreem.net/podcast/episode-211-granulomatosis-with-polyangiitis/

Granulomatosis with Polyangiitis (GPA) – Recognition and Management in the ED

Hosts:
Phoebe Draper, MD
Brian Gilberti, MD

Download One Comment Tags: Rheumatology

Show Notes

Background

• A vasculitis affecting small blood vessels causing inflammation and necrosis
• Affects upper respiratory tract (sinusitis, otitis media, saddle nose deformity), lungs (nodules, alveolar hemorrhage), and kidneys (rapidly progressive glomerulonephritis)
• Can lead to multi-organ failure, pulmonary hemorrhage, renal failure

Red Flag Symptoms:

• Chronic sinus symptoms
• Hemoptysis (especially bright red blood)
• New pulmonary complaints
• Renal dysfunction
• Constitutional symptoms (fatigue, weight loss, fever)

Workup in the ED:

• CBC, CMP for anemia and AKI
• Urinalysis with microscopy (hematuria, RBC casts)
• Chest imaging (CXR or CT for nodules, cavitary lesions)
• ANCA testing (not immediately available but important diagnostically)

Management:

• Stable patients: Outpatient workup, urgent rheumatology consult, prednisone 1 mg/kg/day
• Unstable patients: High-dose IV steroids (methylprednisolone 1 g daily x3 days), consider plasma exchange, cyclophosphamide or rituximab initiation, ICU admission

Conditions that Mimic GPA:

• Goodpasture syndrome (anti-GBM antibodies)
• TB, fungal infections
• Lung malignancy
• Other vasculitides (EGPA, MPA, lupus)

ANCA Testing Utility:

• C-ANCA/PR3-ANCA positive in 80-90% of GPA cases
• P-ANCA/MPO-ANCA more common in MPA
• Don’t delay treatment while awaiting results if suspicion is high

Outcomes:

• Without treatment: Fatal within a year (renal failure, respiratory complications)
• With treatment: 5-year survival ~75-90%, but ~50% relapse rate
• Long-term rheumatology follow-up is essential

Take-Home Points:

• Always include vasculitis in the differential for unexplained respiratory, renal, or systemic symptoms.
• Recognize pulmonary-renal syndromes early.
• Initiate high-dose steroids immediately for unstable patients without waiting for ANCA results.
• GPA is rare but life-threatening – early recognition saves lives.

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