IV Fluids: not too much; max 2L.
Atropine / Pacing: can try, but generally won’t affect BP that much. Use atropine before intubation.
Calcium: has isotropy effect; consider getting calcium to 2x the normal range for these patients.
Glucagon: helpful, but old data was from studies that had insulin in the actual glucagon formulas.
Pressers: need central access anyway, Levophed. Consider bicarbonate drip if there is a wide-complex rhythm since some of the CCB/B-blockers have Na-channel affects as well (like TCA).
High Dose Insulin: With CCB toxicity, patient’s are insulin resistant so these high doses of insulin are not going to affect patient’s potential hypoglycemia as much as say a DKA patient would. Given 1 unit/kg bolus, then 0.5units/kg/hr drip.
Intralipid Therapy: lipid sink that will try and take the drug off the binding sites. Intralipid definitely used in analgesia (lidocaine) toxicity with cardiac arrest.
Extracorporeal Measures: IABP, ECMO, MARS
TOX – Calcium Channel Blockers and More, Curtis Snook, Managing Medical Emergencies 2015, EMedHome
Tylenol/APAP/Panadol/Anacin: Regular dosage: 650-1000mg; 10mg/kg in children q4-6hrs. Max dose 4g, 75mg/kg in children. Peak serum levels in 30-120min.
Overdose: glucuronidation and sulfation are saturated, APAP metabolized to NAPQI which eventually binds to hepatic cells causing necrosis. Early signs of toxicity occur within 12 hours though clinically become apparent much later.
Stage 1: First 24 hrs. Mild symptoms of N/V, malaise. Hypokalemia.
Stage 2: Day 2-3. Vomiting improves, though RUQ occurs, elevated LFTs.
Stage 3: Day 3-4. If severe enough, will progress to full liver failure. Acidosis, coagulopathy, renal failure, recurrent GI symptoms.
Stage 4: Next 2 weeks. Recovery. Complete recovery in 1-3 months if patient survives.
Consider overdose when >10g or 200mg/kg over single dose or over 24 hrs, or >6g or 150mg/kg over 2 days.
Rumack-Matthew nomogram used for terminating toxicity at 4-24hr window. Looks for possible toxicity if APAP level >150mcg/mL. Only pertinent with single ingestion and within the 20 hr window. Safety below the nomogram line corresponds to a 4hr post-ingestion of 150mcg/mL – incidence of hepatotoxicity was 1% and all patients recovered.
Consider activated charcoal in early ingestion.
Acetylcysteine: theory of why it works: acts as NAPQI binder or a sulfate substitute. Also with toxicity > 24 hrs, acts an antioxidant to lessen amount of damage. If given within 8 hours of ingestion, 100% effective at preventing hepatoxicity (LFTs >1000). Does bind to activated charcoal.
Oral: Loading dose 140mg/kg, then maintenance 70mg/kg every 4 hours for 17 doses. If able to give oral dose, dilute with chilled beverage or fruit juice. has rotten egg smell. IV dose can cause anaphylactoid reactions within 2 hours of administration. Risk is 4-17%. Asthmatics have greatest risk.
IV: Loading dose 150mg/kg over 15-60min, then 50mg/kg over 4 hours, then 100mg/kg over 16 hrs. Check LFTs and APAP levels after tx completed and continue until APAP level is not detectable or LFTs have rapidly decreased.
For patients presenting within 4 hours of ingestion, treatment begins with GI decontamination and awaiting 4hr post-ingestion level. If you can wait within the 8 hour window, then wait to treat.
Multiple ingestions: plot on the nomogram as the farthest back the patient started taking the ingestion (so the threshold for treating is a lower level.
Tintinalli, Seventh Edition, Chapter 184: Acetaminophen