ICU Toxicology: Lethal poisonings and ODs – How to best manage them

Today we have Dr. Fermin F. Barrueto, Clinical Associate Professor of EM here at U-Maryland and all-around tox guru, to share his wisdom on the topic of critical care toxicology. Over the last 10 years Dr. Barrueto has seen nearly every type of poisoning as head of our medical toxicology consult service. Over the next hour he will give you tips and tricks on what to look for to make the diagnosis easy and allow you to avoid costly errors of management. He even introduces the newest antidote on the block: lipid emulsion therapy. I implore you to watch this lecture more than once, because it’s not a matter of IF you will see these toxidromes, but WHEN!

Anticholinergic Toxidrome:
“Blind as a bat, mad as a hatter, red as a beet, hot as Hades, dry as a bone, the bowel and bladder lose their tone, and the heart runs alone.” (Mydriasis, hallucinations, flushed, hyperthermia, dry skin, ileus, urinary retention and tachycardia.)

Treatment: Physostigmine 0.5-2mg slow IV over 2-5 min (0.02mg/kg IV)

Cholinergic Toxidrome: 

DUMBBELLS – Diarrhea, Urination, Miosis, Bradycardia, Bronchorrhea/Bronchospasm, Emesis, Lacrimation, Lethargy and Salivation and seizures

Treatment: Antimuscarinics (Atropine)

ICU Hyperthermia

1) Serotonin Syndrome

  • Hunter Criteria: 

Dunkley EJ et al. QJM. 2003;96(9):639.

  • Treatment: #1 Supportive care, #2 Benzos, Cyproheptadine (antihistamine, anticholinergic, serotonin blocking)

2) Malignant Hyperthermia

  • Usually due to inhalational anesthetics (immediate in OR)
  • Hypercatabolic syndrome due to MASSIVE calcium influx from sarcoplasmic reticulum (SR)
  • Treatment: Dantrolene (allows calcium reuptake to SR!)

3) Neuroleptic Malignant Syndrome

  • Antipsychotics (usually older, ex: Haldol) due to an antidopaminergic effect
  • Lead pipe rigidity is distinguishing
  • #1: Benzos, #2 Dantrolene (but not proven), then Dopaminergics: Bromocriptine or Amantadine

Acetaminophen Toxicity

www.pediatricsconsultant360.com

  • Treatment: N-acetylcysteine: 100% effective in 1st 8-10hrs
  • ↓ Phosphate implies survival

Lipid Emulsion Therapy

  • Anecdotal evidence in CCB and local anesthetic overdoses
  • Additionally: augments hemodynamic stability (↑BP, positive ionotropy, and rhythm improvement)
  • Dose: 1.5ml/kg of 20% lipid emulsion, repeated in 15 mins and then start a 0.25ml/kg/min gtt

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Comments

  1. Alex Kobzik

    Great talk. I’d like to add something that one of my attendings/toxicologists discussed with me recently. Bromocriptine for NMS carries a risk or serotonergic activation, particularly in the (albeit rarer) instances of NMS causes by atypical antipsychotics. This may induce or worsen a concomitant serotonin syndrome. If the offending agent is unknown, would avoid bromocriptine as part of the arsenal, even as 3rd line.

  2. mjanderson972

    I can’t say I have seen 20% or 50-60% of patients with a QTc > 500 or even > 600 msec without severe hypoK and hypoMg that have progressed to TdPs. Moreover, the patient’s I have seen were not even on medications prior to hospitalization that prolong the QTc. I’m wondering where Dr Barrueto gets this data? Anecdotally, I can’t say I have seen any patient on multiple QT prolonging medications with a QTc > 500-600 that have progressed to TdPs even after I’ve given them a QT prolonging medication.

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