Core EM - Emergency Medicine Podcast

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

Hosts:

Samantha Nakos, MD

Brian Gilberti, MD





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





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





Podcast Video



Show Notes

Core EM Modular CME Course

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

Credit: 12.5 AMA PRA Category 1 Credits™

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

Cost:

Free for NYU Learners

$250 for Non-NYU Learners

Click Here to Register and Begin Module 1

Lyme, Anaplasmosis, Ehrlichiosis & Babesiosis at a Glance

Lyme
Anaplasmosis
Ehrlichiosis
Babesiosis

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

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

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

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

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

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

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

Background

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

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

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

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

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

Lyme: The Rash and the Serology

Erythema Migrans

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

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

Expanding erythematous patch + endemic area = Lyme until proven otherwise

Serology

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

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

The Other Three: Labs and the Smear

Babesiosis

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

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

Anaplasmosis & Ehrlichiosis

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

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

Management

Post-Bite Prophylaxis (Lyme)

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

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

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

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

Active Disease

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

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

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

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

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

Severe Babesiosis

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

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

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

The Case

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

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

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

Labs: plt 87K, Hgb 12.3, transaminitis

Dx: concurrent babesiosis + poison ivy

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

Pitfalls

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

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

Cephalexin for “cellulitis” in tick season → misses EM

Trusting pt-reported attachment time → runs short

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

Take-Home Points

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

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

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

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

Links & References

Guidelines

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

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

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

Key Studies

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

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

CDC

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

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

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





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

Hosts:

Neya Vishwanath, MD

Brian Gilberti, MD





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





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Tags: Gastrointestinal, Gastrointestinal Diseases





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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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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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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