Sympathomimetic Toxicity

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Sympathomimetic Toxicity


Symoathomimetic toxicity is commonly seen following recreation drug use, but may also result from excessive use or overdose of a number of pharmaceuticals.

It presents largely as one of afrenergic excess, with the CNS and CVS most notably effected. Treatment is largely supportive along with the provision of adequate sedation.


Sympathomimetic Agents

Agents causing sympathomimetix toxicity include:

Illicit substances:

  • Amfetamines and their derivatives e.g. metafetamine, MDMA
  • Cocaine
  • Beta-adrenergic receptor agonists e.g. clenbuterol
  • Novel psychoactives - including novel stimulants, novel hallucinogenic agents, and synthetic cannabinoid-receptor agnoists

Pharmaceuticals

  • Beta-adrenergic receptor agnoists e.g. salbutamol
  • Catecholamines e.g. adrenaline, noradrenaline, dopamine
  • Psychostimulants e.g. modafinil
  • Indirect sympathomimetics e.g. dexamfetamine, methylphenidate
  • Monoamine inhibitors e.g. phenelzine
  • Serotonin and Noradrenaline reuptake inhibitors (SNRIs) e.g. venlafaine, atomoxetine
  • Xanthines e.g. caffeine, thophylline

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Mechanism of toxic effects

There is some variability depending on the causative agent but in genreal toxicity stems from the inhibition of monoamine reuptake transporters at the preganglionic synapse. They can also act to displace monoamines from presynaptic vesicles. The result is an increase in neurotransmitter presense in the synapse.

The increase in noradrenaline mostly leads to the cardiovascular signs, dopamine to the behavioural and psychotic symptoms and serotnin for the mood and some autonomic effects, although there is crossover of effects.


Clinical Presentation

The sympathomimetic toxidrome can vary both in severity and the range of symptoms experiences based on whether the inciting agent has predominantly adrenertgic, serotonergic or dopaminergic effects. Whilst several body symptoms are usually affected, the most notable signs are normally seen in the CNS and CVS.

  • Central Nervous system
    • Excitation - agitation, anxiety, delirium
    • Acute behavioural disturabance - aggression, psychotic phenomena (commonly seen with metafetamine use)
    • Haemorrhagic or thrombotic storkes
  • Cardiovascular effects
    • Tachycardia, arrhythmias
    • Hypertension
    • Acute coronary syndrome
    • Hypotension (with severe toxicity)
  • Autonomic effects
    • Hyperthermia
    • Diaphoresis
    • Mydriasis
  • Neuromuscular effects
    • Excitation - tremor, hyper-reflexia
  • Metabolic effects
    • Hypokalaemia
    • Lactic acidosis
    • Rhabdomyolysis

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Management

The main goal of treatment is to control agitation and aggression and identify and treat any life threats including hypertheria, acute coronary/cerebrovascular syndromes and severe electrolyte derangements.

In most cases the paramount and often only treatment reuired is sedation, this is especially true of illicit recreational stimulant ingestion, which is the most common cause of sympathomimetic toxicity presenting to hospital.

wikitox/sympathomimetic_toxicity.1721790354.txt.gz · Last modified: 2024/07/23 23:05