Core EM - Emergency Medicine Podcast

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Core EM Emergency Medicine Podcast

  1. 3d ago

    Iron Poisoning

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

    Iron Poisoning

  2. Oct 19

    Tickborne Illnesses

    Tickborne illnesses in the ED: attachment time, the rash, the smear, prophylaxis, & treatment. Hosts: Samantha Nakos, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Tickborne_Illnesses_1_.mp3 Download Leave a Comment Tags: Babesiosis, Ehrlichiosis, Infectious Diseases, Lyme Disease, Tick-Borne Illnesses Podcast Video Show Notes Core EM Modular CME Course Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.  Course Highlights: Credit: 12.5 AMA PRA Category 1 Credits™ Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics. Cost: Free for NYU Learners $250 for Non-NYU Learners Click Here to Register and Begin Module 1 Lyme, Anaplasmosis, Ehrlichiosis & Babesiosis at a Glance Lyme Anaplasmosis Ehrlichiosis Babesiosis Organism B. burgdorferi (spirochete) A. phagocytophilum E. chaffeensis B. microti (protozoan) Vector I. scapularis I. scapularis Lone star tick I. scapularis Attachment time ≥36–48 h Can be 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 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 Read More

  3. Sep 24

    Diarrhea

    Acute diarrhea in the ED: stool testing, treatment, and a spotlight on Cyclospora. Hosts: Neya Vishwanath, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Diarrhea.mp3 Download Leave a Comment 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 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: 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. Read More

  4. Aug 11

    Superwarfarin Toxicity

    Superwarfarin toxicity: recognition, reversal, and prolonged vitamin K therapy. Hosts: Mac Josh Reandelar, DO Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Superwarfarin_Toxicity.mp3 Download Leave a Comment 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 Read More

  5. Jul 14

    Group A Strep

    Group A strep in the pediatric ED: from strep throat to invasive disease and toxic shock. Host: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Group_A_Strep.mp3 Download Leave a Comment 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) Read More

  6. Jun 8

    Kidney Stones

    A guide to diagnosing, imaging, and managing acute renal colic and nephrolithiasis in the ED. Hosts: Brian Gilberti, MD Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Nephrolithiasis.mp3 Download Leave a Comment 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 s*****m. 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 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 10 mm: 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 nor

  7. May 15

    Thyroid Storm

    Diagnosis, workup, and the four-step treatment protocol for thyroid storm. Hosts: Annaliese Elam, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Thyroid_Storm.mp3 Download Leave a Comment 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 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. Read More

  8. Apr 7

    Local Anesthetic Systemic Toxicity (LAST)

    We discuss this ominous complication of providing local anesthesia. Hosts: Elaine Jonas, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3 Download Leave a Comment 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. Read More

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