Core EM - Emergency Medicine Podcast

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Core EM - Emergency Medicine Podcast episodes

October 26Episode 229: Iron Poisoning
Iron overdose in the ED: five stages, elemental iron math, decontamination, and deferoxamine.
Hosts:
Brian Chastain, MD
Brian Gilberti, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Iron_Poisoning.mp3
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Tags: Toxicology
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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
Iron Poisoning Stages at a Glance
Stage
Timing
What’s happening
1 · GI
30 min–6 h
Direct corrosive GI injury; abd pain, vomiting
2 · Latent
6–24 h
GI sx improve; iron redistributing into tissues
3 · Shock / acidosis
6–72 h
Profound metabolic acidosis → shock, MSOF
4 · Hepatotoxicity
12–96 h
Hepatotoxicity → fulminant liver failure
5 · GI scarring
2–8 wks
Gastric outlet obstruction, GI tract scarring
The Case
31M w/ hx depression, anxiety; found minimally responsive at home by family
EMS: HR 67, SpO2 96% on 2 L NC, BP 46/21; withdraws to pain, not opening eyes → 2 L IVF + push-dose epi en route
ED: BP ↑ to 90/61, other VS unchanged; dried vomit on lips/shirt; breathing comfortably, protecting airway
POC VBG: pH 7.24, pCO2 33, pO2 25, HCO3 14, lactate 2.5
ECG: NSR, otherwise unremarkable → get an ECG in any possible toxic ingestion
Additional 30 mL/kg bolus + norepi gtt
Family arrives → bottle of iron pills under the pt’s bed
Pathophysiology
Free iron = multisystem oxidative injury
Primary mechanism: free radical generation + lipid peroxidation → damages cellular and mitochondrial membranes throughout the body
Profound metabolic acidosis via 2 routes: uncoupled oxidative phosphorylation → anaerobic metabolism → lactate; Fe³⁺ reacts w/ water → releases 3 H⁺ → excess acid
Direct mucosal necrosis in the gut (corrosive injury)
Negative inotrope on the myocardium → hypotension, cardiogenic shock in large ingestions
Clinical Stages
Classic progression after large ingestions; stages overlap and pts can present anywhere along the timeline
Stage 1, GI (30 min–6 h): direct GI tract injury; abd pain, vomiting. Persistent vomiting = very sensitive indicator of a serious ingestion
Stage 2, latent (6–24 h): GI sx improve, but iron is redistributing into the tissues → ongoing damage
The latent-phase trap: pts look like they’re turning the corner right before they crump. Contrast: pts never symptomatic >6 h after ingestion are unlikely to develop toxicity (AAPCC 2005); GI sx that improve ≠ never symptomatic
Stage 3, shock (6–72 h): tissue iron → profound acidosis → shock, MSOF
Stage 4, hepatotoxicity (12–96 h): hepatotoxicity → fulminant liver failure
Stage 5, GI scarring (2–8 wks): gastric outlet obstruction, GI tract scarring from the initial corrosive injury
Diagnosis / Workup
Imaging
Emergent plain-film abd XR in any suspected iron ingestion → intact adult iron tabs are radiopaque
Confirms pills still in the stomach/GI tract → helps decide on WBI
Negative XR ≠ no ingestion: chewables, liquid formulations and already-dissolved tabs often don’t show up
Serum Iron
Draw 4–6 h post-ingestion for regular formulations, ~8 h for extended release
Often hard to interpret → time of ingestion and formulation frequently unknown
>500 mcg/dL → serious systemic toxicity
>1,000 mcg/dL → very significant mortality
Elemental Iron Math
Toxicity tracks the elemental iron dose, not the mass of the pill
Salt
Elemental Fe
Per 325 mg tab
Ferrous sulfate
~20%
~65 mg
Ferrous fumarate
~33%
106 mg
Ferrous gluconate
~12%
~36–38 mg
<20 mg/kg elemental Fe → usually asymptomatic
20–60 mg/kg → GI sx likely; systemic toxicity possible, esp. at the upper end
>60 mg/kg → threshold for serious toxicity, possible death
AAPCC out-of-hospital guideline: refer to an ED for ≥40 mg/kg elemental Fe (adult ferrous salt formulations) or severe/persistent sx; any self-harm ingestion → ED regardless of amount (Manoguerra 2005)
AAPCC: children’s chewable vitamins w/ iron, and unintentional carbonyl iron or polysaccharide-iron complex ingestions → home obs w/ f/u
Management
Decontamination
Activated charcoal: no role. Iron is a metal → doesn’t bind; ↑ aspiration and other complications
Whole bowel irrigation (WBI) = main decontamination strategy, esp. w/ pills on XR → flush tablets before further GI injury and systemic absorption
PEG-ELS (polyethylene glycol electrolyte solution) until rectal effluent is clear; large volume → often via NG tube
PEG-ELS rates: 1.5–2 L/h adolescents/adults (as on air); peds 500 mL/h (9 mo–6 y), 1 L/h (6–12 y) (AACT/EAPCCT 1997)
AACT/EAPCCT: consider WBI after substantial iron ingestions; contraindicated w/ bowel obstruction, perforation, ileus, hemodynamic instability or a compromised unprotected airway (Thanacoody 2015)
Gastric lavage: generally not used unless a large pill burden remains in the stomach → aspiration, direct GI injury; ED unfamiliarity ↑ complications
Get toxicology and your local poison center on the line early
Deferoxamine (DFO)
Mechanism: chelator isolated from bacteria → binds iron in the blood (ferrioxamine) → renal excretion in the urine
Indications: shock · AMS · profound metabolic acidosis · persistent GI sx (persistent vomiting) · serum iron >500 mcg/dL · predicted severe ingestion (>60 mg/kg elemental Fe) in a symptomatic pt
Reported dose >60 mg/kg in a pt w/o sx or acidosis → discuss w/ toxicology/poison center rather than chelating on pill count alone
Dosing: start 5 mg/kg/h IV → titrate to ~15 mg/kg/h. Some protocols go higher, up to ~30 mg/kg/h in the first 24 h.
Watch for hypotension: DFO can worsen existing hypotension.
FDA label: IV only for cardiovascular collapse, by slow infusion; ≤15 mg/kg/h initially; max 6 g/24 h; ARDS reported w/ excessively high IV doses; ↑ risk of Yersinia infxn.
Urine: classic “vin rosé” (red-orange) urine = ferrioxamine being excreted → helpful but not quantitative. Its absence doesn’t exclude significant toxicity or effective chelation; don’t use urine color to guide duration.
Stop when the pt is clinically well and the anion gap acidosis has resolved.
Pitfalls
Waiting for a level → a level that hasn’t peaked or looks low doesn’t exclude toxicity in a sick pt
Being reassured by GI improvement in the latent phase
Being reassured by a negative XR (chewables, liquids, dissolved tabs)
Dosing by tablet weight instead of elemental iron
Giving activated charcoal
Using urine color (or its absence) to decide when to stop DFO
Take-Home Points
Treat the patient, not the number. Shock or profound metabolic acidosis → start DFO even if the serum iron hasn’t peaked or is lower than expected; very little harm in starting it, other than hypotension
Calculate elemental iron. Formulations differ in elemental content → helps predict whether the dose is toxic
Get an X-ray. Plain film confirms tablets and guides the decision on WBI
Beware the latent phase. GI improvement ≠ toxicity over → often precedes cardiovascular collapse and shock as iron moves into the tissues
Links & References
Guidelines
Manoguerra AS, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553–570. — DOI (AAPCC)
Dart RC, et al. Expert consensus guidelines for stocking of antidotes in hospitals that provide emergency care. Ann Emerg Med. 2018;71(3):314–325.e1. — DOI
Decontamination Position Statements (AACT/EAPCCT)
Tenenbein M. Position statement: whole bowel irrigation. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35(7):753–762. — DOI
Thanacoody R, et al. Position paper update: whole bowel irrigation for gastrointestinal decontamination of overdose patients. Clin Toxicol (Phila). 2015;53(1):5–12. — DOI
Chyka PA, et al. Position paper: single-dose activated charcoal. Clin Toxicol (Phila). 2005;43(2):61–87. — DOI
Benson BE, et al. Position paper update: gastric lavage for gastrointestinal decontamination. Clin Toxicol (Phila). 2013;51(3):140–146. — DOI
Poison Center
Poison Help line (US): 1-800-222-1222
Music
Outro music: “Metalmania” Kevin MacLeod (incompetech.com). Licensed under Creative Commons: By Attribution 4.0 License

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13 min
October 19Episode 228: Tickborne Illnesses
Tickborne illnesses in the ED: attachment time, the rash, the smear, prophylaxis, & treatment.
Hosts:
Samantha Nakos, MD
Brian Gilberti, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Tickborne_Illnesses_1_.mp3
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Tags: Babesiosis, Ehrlichiosis, Infectious Diseases, Lyme Disease, Tick-Borne Illnesses
Podcast Video
Show Notes
Core EM Modular CME Course
Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. Course Highlights:
Credit: 12.5 AMA PRA Category 1 Credits™
Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.
Cost:
Free for NYU Learners
$250 for Non-NYU Learners
Click Here to Register and Begin Module 1
Lyme, Anaplasmosis, Ehrlichiosis & Babesiosis at a Glance
Lyme
Anaplasmosis
Ehrlichiosis
Babesiosis
Organism
B. burgdorferi (spirochete)
A. phagocytophilum
E. chaffeensis
B. microti (protozoan)
Vector
I. scapularis
I. scapularis
Lone star tick
I. scapularis
Attachment time
≥36–48 h
Can be <24 h
No data
Mostly >48 h
Key clue
EM rash
↓WBC, ↓plt, ↑LFTs
↓WBC, ↓plt, ↑LFTs
Hemolysis, ↓plt
Smear
—
Morulae in neutrophils
Morulae in monocytes
Intra-RBC parasites, Maltese cross
Confirm
Clinical (EM)
Smear, PCR
Smear, PCR
Smear, PCR
Treat
Doxy × 10–14 d
Doxy × 10 d
Doxy until ≥3 d afebrile
Atovaquone + azithro × 7–10 d
Background
Ixodes scapularis (deer tick) = primary US vector for Lyme, anaplasmosis, and babesiosis; I. pacificus on the West Coast. Ehrlichiosis → lone star tick (Amblyomma americanum), not the deer tick (CDC MMWR 2016)
Why attachment time matters: B. burgdorferi lives in the tick midgut → multiplies and migrates to the salivary glands only after feeding starts → built-in delay
Single infected nymph: 0 of ~90 animals infected at 24 h, ~10% by 48 h, ~70% by 72 h (Eisen 2018)
Anaplasma can transmit w/in 24 h. Babesia ≈ Lyme, not faster: earliest 36 h, mostly after 48 h. True speedster = Powassan virus (w/in 15 min). Attachment time by hx is often unreliable (IDSA Lyme 2020)
Regional variation: US Lyme = B. burgdorferi; Europe = mostly B. afzelii, B. garinii → different clinical picture. Systemic sx w/ EM more common in the US: ~65% vs ~37% in Europe (IDSA Lyme 2020)
Lyme: The Rash and the Serology
Erythema Migrans
EM in ~70–80% of infections; appears at the bite site 3–30 d post-bite (avg ~7 d) (CDC)
Usually not a bull’s-eye → most early EM is uniformly red
Expanding erythematous patch + endemic area = Lyme until proven otherwise
Serology
2-tier: EIA or IFA → IgM/IgG Western blot (or modified 2-tier: 2 EIAs, no blot)
Early localized dz → often seronegative (as few as ~20% positive w/in 1 wk of noticing EM) → EM in an endemic area = clinical dx, per IDSA (IDSA Lyme 2020)
The Other Three: Labs and the Smear
Babesiosis
Hunt for hemolytic anemia: ↓Hgb, ↑LDH, ↓haptoglobin, reticulocytosis; ↓plt and ↑LFTs common
Smear: intraerythrocytic parasites. Maltese cross (tetrad) = pathognomonic but infrequent; ring forms more common. PCR more sensitive than smear (IDSA Babesiosis 2020)
Anaplasmosis & Ehrlichiosis
Near-identical presentations. Classic triad: leukopenia, thrombocytopenia, transaminitis
Smear: morulae → Anaplasma in neutrophils, Ehrlichia in monocytes. Smear is insensitive → whole-blood PCR confirms (CDC MMWR 2016)
Management
Post-Bite Prophylaxis (Lyme)
High-risk bite only → all 3: Ixodes tick, highly endemic area, attached ≥36 h (by engorgement or hx); give w/in 72 h of removal (IDSA Lyme 2020)
Doxycycline 200 mg PO × 1 (adults); 4.4 mg/kg PO × 1, max 200 mg (kids)
Landmark RCT: 482 pts w/ I. scapularis bites → EM 0.4% doxy vs 3.2% placebo, efficacy 87% (Nadelman 2001)
Kids <8: doxy traditionally avoided (tooth staining), but a relative CI only → benefit wins. No staining seen w/ short courses; CDC/AAP: doxy = drug of choice for tickborne rickettsial dz at any age (CDC MMWR 2016)
Active Disease
Early localized Lyme: Doxycycline 100 mg PO BID × 10–14 d (CDC: shorter end preferred; IDSA: 10 d)
No 1st-gen cephalosporins (e.g., cephalexin) → ineffective vs B. burgdorferi
EM vs cellulitis unclear → cefuroxime 500 mg PO BID × 14 d covers both. If using amoxicillin-clavulanate, dose it TID (500/125 mg) to match the TID amoxicillin regimen (CDC EM Treatment)
Anaplasmosis: same doxy dose × 10 d (covers incubating Lyme). Ehrlichiosis: same dose until ≥3 d afebrile, usually 5–7 d total (CDC MMWR 2016)
Babesiosis: Atovaquone 750 mg PO BID + azithromycin 500 mg day 1, then 250 mg daily × 7–10 d (IDSA Babesiosis 2020)
Severe Babesiosis
Inpatient: Atovaquone 750 mg PO BID + azithromycin 500 mg IV daily → all-PO once sx subside, 7–10 d total. Alternative: IV clindamycin + PO quinine (CDC Babesiosis)
Consider RBC exchange transfusion for parasitemia >10% or severe hemolysis; IDSA also lists severe pulmonary, renal, or hepatic compromise (IDSA Babesiosis 2020)
Asplenia → ↑ risk of severe dz, but not itself an exchange criterion
The Case
35M, no PMH → 1 wk nausea, severe myalgias, arthralgias, HA, fatigue, fevers. Hiked upstate NY 1 wk prior; multiple tick bites to legs, none reportedly attached >24 h
VS: BP 144/76, HR 69, RR 16, T 98.7°F s/p acetaminophen, SpO2 98% RA
Exam: pruritic, painful papular rash w/ healing vesicles on bilateral wrists + anterior chest; tender bilateral axillary LAD; diffuse muscle and leg-joint tenderness
Labs: plt 87K, Hgb 12.3, transaminitis
Dx: concurrent babesiosis + poison ivy
Lessons: poison ivy = red herring while hunting for EM; antipyretic masked the fever; ↓plt in a febrile hiker → smear; reported “<24 h” attachment didn’t exclude Babesia (hx unreliable)
Pitfalls
Waiting for a bull’s-eye → most EM is uniformly red
Sending serology to rule out early EM → often neg; treat clinically
Cephalexin for “cellulitis” in tick season → misses EM
Trusting pt-reported attachment time → runs short
Fever persisting on doxy → think Babesia (coinfection is common); doxy doesn’t treat it (IDSA Lyme 2020)
Take-Home Points
Don’t wait for the bull’s-eye. Most EM is solid red. An expanding erythematous patch in an endemic area is Lyme until proven otherwise.
Watch the clock and the tick. Lyme needs ~36–48 h of attachment; Anaplasma can transmit w/in 24 h. Pts underestimate how long the tick was on.
The smear is your friend. Thrombocytopenia in a febrile hiker → manual peripheral smear for morulae or a Maltese cross.
Doxycycline is your workhorse. Covers Lyme, Anaplasma, and Ehrlichia → first-line for most tickborne febrile syndromes. Babesia needs atovaquone + azithromycin.
Links & References
Guidelines
Lantos PM, et al. Clinical practice guidelines by the Infectious Diseases Society of America (IDSA), American Academy of Neurology (AAN), and American College of Rheumatology (ACR): 2020 guidelines for the prevention, diagnosis and treatment of Lyme disease. Clin Infect Dis. 2021;72(1):e1–e48. — doi.org/10.1093/cid/ciaa1215
Krause PJ, et al. Clinical practice guidelines by the Infectious Diseases Society of America (IDSA): 2020 guideline on diagnosis and management of babesiosis. Clin Infect Dis. 2021;72(2):e49–e64. — doi.org/10.1093/cid/ciaa1216
Biggs HM, et al. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever and other spotted fever group rickettsioses, ehrlichioses, and anaplasmosis — United States. MMWR Recomm Rep. 2016;65(2):1–44. — doi.org/10.15585/mmwr.rr6502a1
Key Studies
Eisen L. Pathogen transmission in relation to duration of attachment by Ixodes scapularis ticks. Ticks Tick Borne Dis. 2018;9(3):535–542. — doi.org/10.1016/j.ttbdis.2018.01.002
Nadelman RB, et al. Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite. N Engl J Med. 2001;345(2):79–84. — doi.org/10.1056/NEJM200107123450201
CDC
CDC. Signs and symptoms of untreated Lyme disease. — cdc.gov/lyme/signs-symptoms
CDC. Clinical treatment of erythema migrans rash. — cdc.gov/lyme/hcp/clinical-care/erythema-migrans-rash
CDC. Clinical care of babesiosis. — cdc.gov/babesiosis/hcp/clinical-care

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8 min
September 24Episode 227: Diarrhea
Acute diarrhea in the ED: stool testing, treatment, and a spotlight on Cyclospora.
Hosts:
Neya Vishwanath, MD
Brian Gilberti, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Diarrhea.mp3
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Tags: Gastrointestinal, Gastrointestinal Diseases
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
Framing the Patient
Acute is <2 weeks, persistent is 2–4 weeks, chronic is >30 days. Most acute diarrhea is self-limited and needs only supportive care.
Stool cultures are positive in only 2–6% of unselected patients. Yield rises with >4 stools/day and longer duration.
The ED job is not to name the organism. It is to find volume depletion, rule out the dangerous mimic, and decide who needs testing, antibiotics, or admission.
Don’t-Miss Mimics
Diarrhea is a symptom, not a diagnosis. In anyone who looks sick, gastroenteritis is a diagnosis of exclusion.
Abdominal catastrophes: mesenteric ischemia (pain out of proportion, vascular risk factors), early appendicitis, partial obstruction with overflow stool, diverticulitis.
Systemic disease presenting through the gut: sepsis from another source, DKA, adrenal insufficiency.
Fulminant C. diff or toxic megacolon: distension, fever, tachycardia, peritonitis. The diarrhea may actually stop as the colon dilates.
GI bleeding masquerading as dark diarrhea, and in women of childbearing age, ectopic pregnancy.
History & Exam
Duration, frequency, and appearance. Watery and high-volume suggests small bowel. Small, painful, frequent stools suggest colon.
Volume status: urine output, dark concentrated urine, dry mucous membranes, orthostatic symptoms.
Exposures: recent foods, travel, sick contacts, occupation (animal or sewage contact), recent antibiotics or hospitalization.
Timing after ingestion: <6 hours suggests a preformed toxin (Staph aureus, Bacillus cereus), 8–16 hours suggests Clostridium perfringens, and >16 hours suggests viral or other bacterial causes.
High-risk hosts: pregnancy → Listeria, cirrhosis → Vibrio, hemochromatosis → Yersinia (both siderophilic).
Exam: volume status plus a real abdominal exam. A soft belly does not end the evaluation.
Who Gets Testing
Ask first whether the result will change anything. If the patient is going home on supportive care, a stool study often just generates a callback.
Test when the patient is likely to be admitted or is higher risk: febrile, hypovolemic, elderly (roughly >70), known cardiac disease, immunocompromised, IBD, or pregnant.
Bloodwork is not routine. Send a BMP and CBC for significant hypovolemia, persistent vomiting, bloody stool, or the elderly and comorbid.
Routine cultures cover Salmonella, Campylobacter, Shigella. Ask the lab specifically for Vibrio, Yersinia, Aeromonas, or Listeria.
Know your multiplex GI PCR panel. At many shops it already includes C. diff, so ordering it separately is redundant. One call to your lab settles this.
Bloody stool → send Shiga toxin. Bloody but fecal WBC negative → consider amoebiasis.
Bloody diarrhea plus anemia, thrombocytopenia, or a rising creatinine → think HUS, especially in young children.
Antibiotics or hospitalization within 3 months → C. diff moves up the differential.
Neutropenic patient on active chemotherapy → consider typhlitis (enterocolitis of the cecum).
CT only for peritoneal signs or focal tenderness. It is not part of the routine workup.
Management
Oral rehydration solution is the mainstay for anyone tolerating PO — water, salt, sugar. Preferred over sports drinks and flavored electrolyte powders, which are not ORS-formulated. A commercial ORS packet is ideal, and the home recipe works when you do not have one. One liter of water, six level teaspoons of sugar, half a teaspoon of salt.
IV fluids for severe hypovolemia, intractable vomiting, or if labs are being drawn anyway.
Most non-bloody, non-traveler’s diarrhea does not need antibiotics.
Suspected Shiga toxin E. coli: no antibiotics. Lysing the organism releases toxin and raises HUS risk.
When empiric coverage is warranted: azithromycin for severe inflammatory diarrhea, fever, dysentery risk, or fluoroquinolone resistance. Otherwise cipro or levofloxacin, and IV ceftriaxone if PO is not tolerated.
Traveler’s diarrhea: most cases are self-limited. Reserve antibiotics for moderate to severe illness, and reach for azithromycin given widespread quinolone resistance in South and Southeast Asia.
Confirmed C. diff: oral vancomycin 125 mg four times daily for 10 days, or fidaxomicin. Stop the inciting antibiotic where you can.
Loperamide: generally avoid. If diarrhea is mild and the patient is afebrile, let it run.
Bismuth subsalicylate is an option — avoid in younger patients (Reye’s syndrome) and in salicylate allergy or intolerance.
Diet: eat what is tolerated. Early refeeding is fine and BRAT is not required. Dairy can transiently make things worse. Probiotics are unlikely to change the course.
Disposition
Set expectations: we often never identify the organism, and in a stable acute patient there is no routine test and no routine cure.
Food handlers and healthcare workers may need occupational clearance before returning to work.
Return precautions: bloody stools, fever, falling urine output, or an inability to keep fluids down.
No improvement past 1–2 weeks warrants re-evaluation for parasitic or non-infectious causes, including IBD.
Cyclospora
Protozoan with no person-to-person spread — transmission is poop to produce to person. Humans are the only natural host.
Oocysts need days to weeks to sporulate, so long-shelf-life produce is the culprit: berries, basil, cilantro, and leafy greens.
Incubation is about a week. Presents as watery, explosive diarrhea, typically non-bloody and afebrile.
Untreated, it drags on for weeks and tends to relapse, often with profound fatigue, anorexia, and weight loss.
Included on many multiplex GI PCR panels. Microscopy requires a special stain or it will be missed.
Treatment is Bactrim (TMP-SMX), one DS tablet twice daily for 7–10 days, which disrupts the parasite’s folate synthesis. Azithromycin does not cover Cyclospora — this is the exception to the usual workhorse. Ciprofloxacin is the fallback for sulfa allergy, and it is less effective.
Washing produce does not kill it. Only heat does.
Take Home Points
Most acute diarrhea is self-limited. If the patient tolerates PO, is afebrile, and the course is short, supportive care and discharge is the right answer.
Before you call it gastroenteritis, make sure it is not mesenteric ischemia, DKA, or a surgical abdomen.
Bloody diarrhea with concern for Shiga toxin gets no antibiotics.
For Cyclospora, wash and cook your produce — and remember it is Bactrim, not azithro.

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15 min
August 11Episode 226: Superwarfarin Toxicity
Superwarfarin toxicity: recognition, reversal, and prolonged vitamin K therapy.
Hosts:
Mac Josh Reandelar, DO
Avir Mitra, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Superwarfarin_Toxicity.mp3
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Tags: Toxicology
Show Notes
Toxicology & Pathophysiology
Long-acting vitamin K antagonists (LA-VKAs), developed as potent rodenticides
Examples: brodifacoum, bromadiolone, difenacoum, chlorophacinone
Much more potent + far longer acting than warfarin
MOA: inhibits VKORC1 → ↓ vitamin K recycling → impaired γ-carboxylation
↓ factors II, VII, IX, X + proteins C/S
Highly lipophilic → extensive tissue/fat sequestration + slow redistribution
Effect can persist weeks-months; occasionally much longer
Not dialyzable
Exposure: large acute ingestion OR repeated low-dose exposure
Source may be unclear, concealed, or initially unknown
Presentation
Often delayed + insidious
Severe coagulopathy may precede obvious bleeding
Early: epistaxis, gingival bleeding, bruising/ecchymoses, hematuria
Classic clue: well-appearing pt + extraordinarily abnormal coagulation studies
Severe bleeding: RP hemorrhage, ICH, spinal hemorrhage, tamponade, major GI/GU bleeding
RP bleed → flank/back pain ± CVA tenderness
Labs & Diagnosis
PT/INR: profoundly elevated, sometimes beyond assay range
aPTT: may also be markedly prolonged with severe factor depletion
CBC/plts: often initially preserved unless major blood loss/other process
LFTs: often relatively normal
Profound INR + no warfarin + preserved liver function → think superwarfarin
CT based on bleeding site; CT A/P for suspected RP hemorrhage
Confirm: specialized serum/blood testing for long-acting anticoagulants, typically chromatography/mass spec
Do NOT delay resuscitation/treatment for confirmatory testing
Elevated INR: Differential
Superwarfarin exposure
Warfarin toxicity
Severe vitamin K deficiency: malnutrition, malabsorption, prolonged abx
Liver failure/cirrhosis
DIC
Acquired factor deficiency/inhibitor
Helpful discriminators
Liver dz → abnormal hepatic profile/clinical context
DIC → ↓ plts, ↓ fibrinogen, ↑ D-dimer
No warfarin + massive INR + relatively normal LFTs/plts → superwarfarin rises on the differential
ED Management
Major/Life-Threatening Bleeding
Goal: replace factors NOW + restore endogenous synthesis
4F-PCC = preferred factor replacement
Fast, predictable correction
Small volume
No thawing/type matching
FFP if PCC unavailable
Slower + large volume/TACO risk
Give IV vitamin K concurrently
PCC = immediate bridge; vitamin K = sustained factor synthesis
Recheck INR + clinical bleeding response
Repeat PCC generally not routine; reassess before redosing
No Major Bleeding, Critical INR
Vitamin K is primary therapy
High-dose PO vitamin K often preferred when clinically stable
Avoid unnecessary PCC/FFP if no major bleeding
Serial INR monitoring essential
Poison Control
Call early
Helps with:
Confirmatory testing
Vitamin K dosing
Duration of therapy
Monitoring/taper strategy
Outpatient planning
The Long Game
This is NOT standard warfarin toxicity
Vitamin K requirements may persist for months
Discharge only when bleeding controlled + clinically stable on oral regimen
Close serial INR follow-up mandatory
Slowly taper vitamin K under laboratory guidance
Stopping too early → rebound INR elevation + recurrent bleeding
Take Home Points
Massive unexplained INR + relatively normal liver function → think superwarfarin
Major bleeding → 4F-PCC + IV vitamin K
Expect prolonged vitamin K therapy + meticulous INR follow-up

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14 min
July 14Episode 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
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Group_A_Strep.mp3
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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)

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June 08Episode 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
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Nephrolithiasis.mp3
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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.

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20 min
May 15Episode 223: Thyroid Storm
Diagnosis, workup, and the four-step treatment protocol for thyroid storm.
Hosts:
Annaliese Elam, MD
Brian Gilberti, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Thyroid_Storm.mp3
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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.

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10 min
April 07Episode 222: Local Anesthetic Systemic Toxicity (LAST)
We discuss this ominous complication of providing local anesthesia.
Hosts:
Elaine Jonas, MD
Brian Gilberti, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3
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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.

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0 min
March 24Episode 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
https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3
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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.

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19 min
March 03Episode 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
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Post-ROSC_care.mp3
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).

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0 min