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Ecmo in Acute Poisoning

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Ecmo in Acute Poisoning ECMO Conference 5/17/2019 OBJECTIVES • Indications for ECMO in acute poisoning • 3 representative cases ECMO IN ACUTE POISONING • Essential treatments • Special considerations when using ECMO in acute poisoning Clara Zamorano, MD • Conclusions Intensivist Abbott Northwestern Hospital May 17, 2019 Indications for ECMO in Acute Poisoning Cardiogenic shock in toxicology VV-ECMO VA-ECMO • Calcium channel blocker or beta-blocker • • ARDS: • Ingestions that cause Sodium channel blocker: TCAs, buproprion, SNRIs, anti- • Inhalant exposure causing lung injury cardiovascular collapse due to: epileptics (carbamazepine, lacosamide, lamotrigine, • Aspiration of toxic agents • Dysrrhythmias phenytoin), amiodarone, lidocaine and bupivicaine (LAST) • Drug side effect • Acute cardiomyopathy • Not shown to be beneficial in • Heavy metals: cobalt vasodilatory shock • Imidazolines (clonidine) • Ketamine (ACS) • Many more Patient 1: Massive Calcium Channel Overdose • 41 y/o F h/o depression found • Hypotensive, pressors titrated to Drug and confused at home with several 15mcg/kg/min dopamine, empty pill bottles 12mcg/min epinephrine, 12 Patient • Amlodipine – at least 90 tabs 5 mg mcg/min norepi, 100 mgc/min Factors in • Losartan – unknown amount phenylephrine, vasopressin 0.04 • BP on arrival of EMS 70/32 units ECMO • ED 60/p • TTE: LVEF 35% • Intubated and sent to ANW • Develops multi-organ failure • Epi, dopamine, norepi; remains in • Taken for VA ECMO cannulation refractory shock Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy, Volume: 37, Issue: 2, Pages: 221-235, First published: 08 December 2016, DOI: (10.1002/phar.1882) ©AllinaHealthSystems 1 ECMO Conference 5/17/2019 Patient 1 CCB / ßBlocker Overdose Presentation • Given trial bolus of intralipids • Hemodynamics improved by CCBs BetaBlockers • Unable to check labs until circuit HD 2-3, EF normal on TTE changed • Dihydropyridines- Relax vascular • Decrease myocardial contractility • HD #3: Converted to VV ECMO smooth muscle • Thrombocytopenia and high due to ARDS • Hypotension • Bradycardia and hypotension post-oxygenator pressures • HD#7: decannulated • Tachycardia • HYPOglycemia • Non-dihydropyridines-decrease • Develops progressive hypoxic • HD# 9: extubated. myocardial contractility • Altered mental status respiratory failure • HD#10: transferred to floor • Hypotension • Seizures • Bradycardia • Started on high dose insulin • QTc prolongation • HD #12: transferred to infusion • HYPERglycemic psychiatry unit. • Awake • Given methylene blue • Discharged home after 17 days • Difference in effect between 2 classes converges as dose increases CCB / ßBlocker OD Treatment IV Lipid Emulsion • Used as a lipid sink for lipid soluble drugs with higher LogP CCB ßB • In ECMO: • Cracking of stopcocks • Atropine 0.5-1mg q3-5 minutes up to • Clogging and malfunction of membrane oxygenator 4 mg • Increased clot formation in circuit • Calcium chloride 1g IVP, consider • ARDS/non-cardiogenic pulmonary edema (side effect even without use of ECMO) infusion • Lab interference for many hours • Dextrose for hypoglycemia • • Glucagon 5-10 mg IV, then 2-10 mg/h Could give/use prior to cannulation and plan to change circuit after 6-12 hours • Pressors (Epi/NE) if possible • High dose insulin protocol • If considering use for sequestration of lipophilic drug, ECMO circuit may be as • Intralipid effective in sequestration • 1-1.5ml/kg bolus + 0.25-0.5ml/kg/min infusion. May repeat bolus High Dose Insulin Patient 2: Sodium Channel Blocker Overdose • Increases uptake of • Degraded an eliminated by liver • 17y/o F found unresponsive ~5pm • 11AM: refractory seizures carbohydrates by myocardium and kidney • empty pill bottles holding up to 150 • HypotensionPEA arrest, pills of 150 mg Wellbutrin SR cardiogenic shock with EF 10% • Glucose preferred fuel substrate • No data regarding insulin during stress adsorption by circuit, however • EMS called to roadside, • Given intralipid and IV lidocaine to continued to seize and vomit no avail • Strong inotropic effect in patients on ECMO, relative • Accelerates oxidation of insulin resistance is common • Intubated and brought to ED at • Cannulated and initiated on VA Mercy Hospital ECMO with Impella, sent to ANW myocardial lactate • Some centers prime circuit with • EKG • Arterial vasodilation in insulin • Wide QRS and long QTc microcirculation • ANW does not do this currently • Started on sodium bicarb infusion • Propofol ©AllinaHealthSystems 2 ECMO Conference 5/17/2019 Patient 2 Sodium Channel Blockers Presentation Treatment • Harlequin syndrome noted due • HD#4:Transitioned to VV • TCAs, SSRIs, SNRIs, MAOIs • Treat seizures to severe pulmonary edema/ ECMO • Block sodium channels in • Benzos / barbiturates concomitant hypoxic respiratory • HD#6: Decannulated and myocardium conduction and • Propofol if EF and BP tolerate failure contractility derangement • Sodium bicarbonate infusion extubated • Profound CM, tachycardia, HTN • Bolus 1-3 amps • Reconfigured to VAV ECMO • HD#7: Transferred to floor • Obtundation • Infusion with pH goal >7.55 • N/V • 3% saline • Completed therapeutic • Clonus/hyperreflexia, seizures • Rehabbed and was followed by • Consider lidocaine (avoid in LAST) • QTc prolongation and widening of QRS hypothermia protocol psych while awaiting psych bed • Replace magnesium and potassium • TTE HD#3 with EF 60-65% • Discharged to psych on HD#14 • Local anesthetics • Intralipids • Anti-epileptics • GI symptoms, hyponatremia, tremor, drowsiness Bicarb Infusion Patient 3: Cobalt Poisoning • Potential benefits: • 64 F h/o CAD, mild ischemic CM, • Now with progressive AKI, • High sodium load cardiogenic shock, elevated LFTs, • Metabolic alkalosis with decreased tissue penetration and enhanced excretion in urine DJD hip s/p L hip arthroplasty encephalopathy, elevated lactate • Ionize the drug into inactive form (‘09),hypothyroidism, obesity, • Side effects: admitted to hospital following total • Transferred to ICU on HD #3: • Electrolyte abnormalities- hypo calcemia and kalemia • EF 20%, PAWP 45mmHg • Volume overload hip revision. • Creatinine 3.14 with bicarb 15 • Respiratory failure • Worsening of CHF for 2 years, also • LFT: ALT 716/AST1293 • Usually target pH 7.5 -7.55 with paresthesias, hypothyroidism, • Sodium loading and pH increase drive therapeutic effects to varying degrees • HD#4: ALT 700/AST 3511 depending on specific overdose drug previous pericardial effusions • Lactate: 9.9 • Animal and lab models • Patient had metal on metal hip • Cobalt level found to be 222.8ng/mL • ECMO circuit highly efficient for blowing of CO2 explanted on HD#1 prior to surgery (normal <1ng/mL) • Can adjust sweep to keep pH slightly alkalotic • CRRT started HD#4 • Watch for evolution of pulmonary edema/signs of volume overload Patient 3 Cobalt Toxicity • Started on dobutamine, nitrates. • After initial improvement, • Started on N-acetylcysteine, developed refractory cardiogenic • Metal on metal prosthetic joints • Interferes with calcium’s shock thiamine 500 mg TID • Insidious onset of multi-organ inotropic effects • Intubated due to progressive • EDTA obtained, started on HD#4, failure including dilated • Interrupts aerobic cellular encephalopathy HD#10 completed 5 day course cardiomyopathy, pericardial respiration • LFTs rapidly normalized • Started on VA ECMO HD#12 effusion, renal failure, liver • Citric acid cycle • Acidosis improved • Extubated HD#20 disease • CRRT initiated for renal failure • HeartMate 3 with central RVAD • Treatment: • • Gradually able to wean off Often co-exists with • Removal of exposure as able inotropes, RVAD hypothyroidism or thiamine • Chelation • Discharged to home HD #49 deficiency ©AllinaHealthSystems 3 ECMO Conference 5/17/2019 Chelating Agents Summary • Little to no published data on real • Examples: • ECMO is useful in refractory cardiogenic shock due to acute overdose of patients • EDTA-ethylenediaminetetraacetic acid many drugs • Most highly protein-bound (calciumdisodium) • DMSA-Meso-2,3-dimercaptosuccinic Acid • ECMO circuit and drug interactions impact therapy in important ways • Bind cationic metals and enhance • DMPS-sodium 2,3 Dimercaptopropane-I- • If proceeding toward ECMO in the acutely poisoned patient, consider: renal excretion sulphonate • Side effects: • Calcium trisodium • Avoiding intralipids • Renal failure diethylenetriaminepentaacetate • Titrating Sweep Flow to pH >7.4 if overdose requiring bicarb drip • CaNa DTPA • Hypocalcemia 3 • That insulin infusion may require higher than published rates of infusion • Hypotension • Deferrioxamine • Chelator use in setting of renal failure will likely require renal replacement therapy and that • Coagulopathy • N-acetylcysteine dose used may need to be higher • Zinc depletion • Chemistry suggests could be highly • Bone marrow suppression sequestered by circuit • Always involve Poison Center in overdose cases • If renal failure dialyze patient as • 1-800-222-1222 many are dialyzable Special Thanks TO CONTACT ME •Matt Lillyblad • Email: • [email protected] •Kate Katzung • [email protected] • Mail: Clara Zamorano, ANW Intensivists 800 W 28th St, Minneapolis, MN 55407 REFERENCES • Bibro C, Lasich C, et al. Critically ill patients with H1N1 influenza A undergoing extracorporeal membrane oxygenation. Crit Care Nurse Oct 2011;31(5): e8-e24 • Bou-Abboud E, Nattel S. Relative role of alkalosis and sodium ions in reversal of class I antiarrhythmic drug-induced sodium channel blockade by sodium bicarbonate. Circulation. 1996 Oct; 94(8): 1954-1961 • Ciapetti M,
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