Core EM - Emergency Medicine Podcast

Podcast Video

Show Notes

Core EM Modular CME Course

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

• Credit: 12.5 AMA PRA Category 1 Credits™


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


• Cost:
  
  
  
  • Free for NYU Learners
  
  
  • $250 for Non-NYU Learners
  
  
  
  

Click Here to Register and Begin Module 1

Iron Poisoning Stages at a Glance

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

• <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

1. 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


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


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


4. 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

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

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

1. 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.


2. 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.


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


4. 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

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

1. 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.


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


3. Bloody diarrhea with concern for Shiga toxin gets no antibiotics.


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

Show Notes

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:

1. 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.


2. New infection.


3. 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

1. 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.


2. 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.


3. Treatment prevents rheumatic fever, NOT PIGN — and impetigo can cause PIGN too.


4. 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)