『Episode 226: Superwarfarin Toxicity』のカバーアート

Episode 226: Superwarfarin Toxicity

Episode 226: Superwarfarin Toxicity

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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 Download Leave a Comment Tags: Toxicology Show Notes Toxicology & Pathophysiology Long-acting vitamin K antagonists (LA-VKAs), developed as potent rodenticidesExamples: brodifacoum, bromadiolone, difenacoum, chlorophacinoneMuch more potent + far longer acting than warfarinMOA: inhibits VKORC1 → ↓ vitamin K recycling → impaired γ-carboxylation↓ factors II, VII, IX, X + proteins C/SHighly lipophilic → extensive tissue/fat sequestration + slow redistributionEffect can persist weeks-months; occasionally much longerNot dialyzableExposure: large acute ingestion OR repeated low-dose exposureSource may be unclear, concealed, or initially unknown Presentation Often delayed + insidiousSevere coagulopathy may precede obvious bleedingEarly: epistaxis, gingival bleeding, bruising/ecchymoses, hematuriaClassic clue: well-appearing pt + extraordinarily abnormal coagulation studiesSevere bleeding: RP hemorrhage, ICH, spinal hemorrhage, tamponade, major GI/GU bleedingRP bleed → flank/back pain ± CVA tenderness Labs & Diagnosis PT/INR: profoundly elevated, sometimes beyond assay rangeaPTT: may also be markedly prolonged with severe factor depletionCBC/plts: often initially preserved unless major blood loss/other processLFTs: often relatively normalProfound INR + no warfarin + preserved liver function → think superwarfarinCT based on bleeding site; CT A/P for suspected RP hemorrhageConfirm: specialized serum/blood testing for long-acting anticoagulants, typically chromatography/mass specDo NOT delay resuscitation/treatment for confirmatory testing Elevated INR: Differential Superwarfarin exposureWarfarin toxicitySevere vitamin K deficiency: malnutrition, malabsorption, prolonged abxLiver failure/cirrhosisDICAcquired factor deficiency/inhibitor Helpful discriminators Liver dz → abnormal hepatic profile/clinical contextDIC → ↓ plts, ↓ fibrinogen, ↑ D-dimerNo warfarin + massive INR + relatively normal LFTs/plts → superwarfarin rises on the differential ED Management Major/Life-Threatening Bleeding Goal: replace factors NOW + restore endogenous synthesis4F-PCC = preferred factor replacement Fast, predictable correctionSmall volumeNo thawing/type matching FFP if PCC unavailable Slower + large volume/TACO risk Give IV vitamin K concurrentlyPCC = immediate bridge; vitamin K = sustained factor synthesisRecheck INR + clinical bleeding responseRepeat PCC generally not routine; reassess before redosing No Major Bleeding, Critical INR Vitamin K is primary therapyHigh-dose PO vitamin K often preferred when clinically stableAvoid unnecessary PCC/FFP if no major bleedingSerial INR monitoring essential Poison Control Call earlyHelps with: Confirmatory testingVitamin K dosingDuration of therapyMonitoring/taper strategyOutpatient planning The Long Game This is NOT standard warfarin toxicityVitamin K requirements may persist for monthsDischarge only when bleeding controlled + clinically stable on oral regimenClose serial INR follow-up mandatorySlowly taper vitamin K under laboratory guidanceStopping too early → rebound INR elevation + recurrent bleeding Take Home Points Massive unexplained INR + relatively normal liver function → think superwarfarinMajor bleeding → 4F-PCC + IV vitamin KExpect prolonged vitamin K therapy + meticulous INR follow-up Read More
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