Core EM - Emergency Medicine Podcast

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





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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

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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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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