Core EM - Emergency Medicine Podcast

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

Hosts:

Annaliese Elam, MD

Brian Gilberti, MD





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





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Tags: Critica Care, Endocrine, Thyroid Storm





Show Notes

I. Pathophysiology & Diagnosis

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

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

Clinical Presentation:

Hyperpyrexia (e.g., 104.2°F)

Tachycardia/Arrhythmias (e.g., 155 bpm)

Altered Mentation: Agitation, delirium, or psychosis; often the primary differentiator between “storm” and “compensated” hyperthyroidism

Warm, moist skin

Precipitating Events:

Infection, trauma, or surgery

Parturition

Abrupt cessation of antithyroid medications

Burch-Wartofsky Point Scale (BWPS):

≥ 45: Highly suggestive of Thyroid Storm

25–44: Suggestive of impending storm

< 25: Storm unlikely

Note: High sensitivity but low specificity; can be skewed by unrelated febrile illness.

II. Laboratory & Ancillary Findings

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

Metabolic Abnormalities:

Mild hyperglycemia (catecholamine-induced insulin inhibition)

Mild hypercalcemia

Elevated LFTs and leukocytosis

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

III. Management: The Four-Step Blocking Strategy

Step 1: Sympathetic Blockade (Beta Blockers)

Agent of Choice: Propranolol

Mechanism: Non-selective blockade; in high doses, inhibits peripheral conversion of T₄ to T₃.

Dosing:

PO: 60–80 mg every 4–6 hours

IV: 0.5–1 mg over 10 minutes

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

Step 2: Inhibition of Hormone Synthesis (Thionamides)

Agent of Choice: Propylthiouracil (PTU) preferred over Methimazole in life-threatening storm.

Mechanism: Blocks synthesis of new hormone and inhibits peripheral T₄-to-T₃ conversion (decreases T₃ by ~45% in 24 hours).

Dosing: 200–250 mg PO every 4 hours

Step 3: Inhibition of Hormone Release (Iodine)

Agents: Potassium iodide (SSKI) or Lugol’s solution

Critical Timing: Must wait at least 60 minutes AFTER thionamide administration.

Rationale: Immediate iodine administration provides substrate for new hormone synthesis (Wolff-Chaikoff effect bypass), potentially worsening thyrotoxicosis.

Step 4: Inhibition of Peripheral Conversion & Adrenal Support

Agent: Glucocorticoids (Hydrocortisone)

Mechanism: Inhibits peripheral T₄ to T₃ conversion and treats potential relative adrenal insufficiency.

Dosing: 300 mg IV loading dose, followed by 100 mg IV every 8 hours

IV. Supportive Care & Avoidance Measures

Hyperpyrexia Management:

Acetaminophen is the standard of care

Avoid Aspirin: Salicylates displace thyroid hormone from thyroid-binding globulin (TBG), increasing free T₄/T₃ levels

Volume Resuscitation:

Aggressive IV fluids; patients are often profoundly dehydrated

May require 3–5 liters of isotonic crystalloid per 24 hours

Take Home Points

I. Diagnostic Essentials

Clinical Diagnosis: Based on hyperpyrexia, cardiovascular dysfunction, and altered mentation.

Key Differentiator: Altered mentation (agitation, delirium, psychosis) is often the sole finding distinguishing “storm” from “compensated” thyrotoxicosis.

Burch-Wartofsky Point Scale (BWPS):

≥ 45: Highly suggestive of storm.

25–44: Suggests impending storm.

< 25: Storm unlikely.

Note: High sensitivity, low specificity (e.g., hyperthyroid + flu can score > 45).

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

II. The Four-Step Blocking Strategy

Beta Blockade (Propranolol):

Dose: 60–80 mg PO q4–6h or 0.5–1 mg IV over 10 min.

Action: Blocks symptoms and inhibits peripheral T4 to T3 conversion.

Caution: Avoid in acute decompensated heart failure with systolic dysfunction.

Thionamides (PTU):

Dose: 200 to 250 mg every four hours. (note: some resources suggest a loading dose beforehand)

Action: Preferred over methimazole; blocks new hormone synthesis and peripheral T4 to T3 conversion.

Iodine (SSKI/Lugol’s):

Timing: Must wait ≥ 60 minutes AFTER thionamide dose.

Action: Blocks hormone release.

Pitfall: Early iodine provides substrate for new hormone synthesis, worsening the condition.

Glucocorticoids (Hydrocortisone):

Dose: 300 mg IV load, then 100 mg IV q8h.

Action: Blocks conversion and provides adrenal support.

III. Critical Supportive Care

Hyperpyrexia: Use Acetaminophen.

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

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





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We discuss this ominous complication of providing local anesthesia.

Hosts:

Elaine Jonas, MD

Brian Gilberti, MD





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





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Tags: Critical Care, Toxicology





Show Notes

I. Pathophysiology & Mechanisms

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

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

Agent Profile: Bupivacaine (High Risk)

Highly lipophilic with high protein binding.

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

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

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

Contributing Factors:

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

Hypoxemia: Exacerbates myocardial depression and lowers seizure threshold.

II. Risk Assessment & Prevention

Patient-Specific Risk Factors

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

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

Organ Dysfunction:

Hepatic: Reduced metabolism of amide LAs.

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

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

Pregnancy: Increased sensitivity to cardiotoxicity.

Procedural Risk Factors

Vascularity of Site (Highest to Lowest Risk):

Intercostal blocks (highest absorption rate).

Caudal/Epidural.

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

Psoas compartment/Sciatic.

Brachial plexus.

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

Prevention Mandates

Weight-Based Dosing:

Lidocaine (Plain): Max 4.5 mg/kg.

Lidocaine (with Epi): Max 7 mg/kg.

Bupivacaine: Max 2.5–3 mg/kg.

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

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

III. Clinical Presentation

Neurologic Phase (Early to Late)

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

Objective: Visual disturbances, agitation, confusion, tremors.

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

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

Cardiovascular Phase

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

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

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

Contractility: Profound, refractory hypotension and cardiogenic shock.

IV. Immediate Management Algorithm

Goal: Prevent hypoxia/acidosis and sequester the toxin.

1. Initial Actions

Stop Injection: Immediately halt all LA administration.

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

Airway Management:

100% O2​.

Hyperventilate slightly if needed to counter respiratory acidosis.

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

2. Seizure Control

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

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

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

3. Lipid Emulsion Therapy 20%

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

Bolus: 1.5 mL/kg IV over 1 minute.

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

If Instability Persists:

Repeat bolus (up to 2 times).

Increase infusion to 0.5 mL/kg/min.

Upper Limit: ≈12 mL/kg total dose.

4. Modified ACLS

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

Antiarrhythmics: Amiodarone is preferred.

CONTRAINDICATED:

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

Vasopressin: Associated with poor outcomes in animal LAST models.

Calcium Channel Blockers / Beta Blockers: Exacerbate myocardial depression.

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

V. Differential Diagnosis for the Peri-Procedural Patient

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

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

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

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

VI. Post-Resuscitation & Complications

Observation:

At least 2 hours after a CNS-only event.

At least 4–6 hours after a CV event.

Lipid Complications:

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

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

Fat Embolism/Overload: Rare pulmonary complications.

VII. Clinical “Red Flags” for Toxicity

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

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

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

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





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