Friday, July 12, 2013

Toxidromes

Morning report on Wednesday July 10 was a case of toxic ingestion.

In the approach to toxidromes, there are some guiding principles.

1.) Is this an emergency?
2.) What did they take (think of co-ingestions), how did they take it, when did they take it
3.) Treatment consists in general of: Antidote if avaialble, decrease absorption, increase elimination, treat complications.

History is often difficult in these cases as the patient may be alone, and may have an altered mental status. Collateral, family, friends is key.

The physical exam is so important and often you will see tables breaking down toxidromes and the patterns on physical.

Key parameters are:
Mental status
Temperature
BP
HR
RR
Pupils
axilla

Major toxidromes are sympathomimetic, anticholinergic, cholingergic, opioid, and what I think of as others including serotonin syndrome, NMS.

Some (usually) defining features:

Anticholinergic: DRY as a chip!

Cholinergic: opposite, everything is leaking

Opioid: pinpoint pupils

Serotonin syndrome: hyperreflexia, clonus. Often is a faster onset than NMS.

This was a young female who had ingested 45 tablets of "222" which consists of codeine, caffeine, and ASA.

This case brought up the concern of both the codeine and the ASA.

She had no evidence of opioid overdose. As a side note, codeine as we know is metabolized by CYP2D6 to morphine. ~5-7% of Caucasians are deficient in CYP2D6, ~1% Asians. Some populations over express CYP2D6 and may run into problems of toxicity, or may require smaller doses. 

ASA toxicity can be difficult to manage as there is no specific antidote. Treatment principles include:

1. Monitoring of levels to ensure decreasing. Beware that ongoing absorption may occur.

2. Acid-base and electrolytes

Classically salicylate toxicity causes an anion gap metabolic acidosis and a respiratory alkalosis. 

Remember that HS ↔ H+  + S-  It is the neutral HS that can enter the CSF and tissues.

Thus treatment aims at alkanilizing the urine to keep in the anion form and prevent entry into tissue.

These patients can become neuroglycopenic so pay close attention to glucose.

3. GI decontamination

If appropriate and no contraindications activated charcoal or even whole bowel irrigation can be considered. Particularly in early cases.

4. Airway

Remember that the respiratory alkalosis is also helping maintaining alkalemia. Intubating a patient may worsen toxicity if hyperventilation is not maintained as the pH may drop and further push towards the neutral HS that can enter tissues. This is tricky as these patients may very well require intubation especially as their mental status deteriorates. Monitor the pH, minute ventilation, and pCO2

5. Enhancing elimination

As mention urine alkalnilization is part of this.

Dialysis ultimately is an effective means to eliminate.

This information and further detail can be found using the link below to the ACMT recently published recommended treatment guidelines/considerations for Salicylate Toxicity.

Also, always remember to call poison control, they can help tremendously!

http://www.acmt.net/_Library/Position_Drafts/Management_Priorities_in_Salicylate_Toxicity_APPROVED_03_13_13.pdf

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