Sympathomimetic Toxicity

Introduction

Sympathomimetics act to activate the sympathetic nervous system through adrenergic stimulation. Cocaine, amphetamines and their derivatives, ephedrine, pseudoephedrine, theophylline and caffeine all act as sympathomimetics. The vast majority of the agents in this class are taken recreationally.

Risk Assessment

Clinical features:

  • Mild – euphoria, increased alertness, bruxism, tachycardia, hypertension, mydriasis, tremor
  • Moderate – agitation, paranoia, hallucinations, diaphoresis, vomiting abdominal pain, chest pain, dysrhythmia
  • Severe – hyperthermia, metabolic acidosis, rhabdomyolysis, acute renal failure, vascular accident, seizures, coma

Baseline bloods including renal function and CK should be performed in all patients presenting with features of moderate or severe toxicity.

A CT head should be considered in patients presenting with headache given the association with intracranial haemorrhage.

An ECG should be performed on all patients.

Management

Resuscitation

Acute behavioural disturbance should be managed as outlined in the module Approach to the behaviourally disturbed patient. Droperidol is first line for acute behavioural disturbance. Titrated intravenous benzodiazepines are indicated for all other sympathomimetic related emergencies.

Further specific therapy includes;

Hyperthermic crisis

  •  Active cooling measures

 Hypertensive crisis

  •   GTN or SNIP infusion
  •   Hydralazine
  •   Beta blockersSee additional information

 Ventricular arrhythmia

  •   Bicarbonate 1mmol/kg bolus
  •   Defibrillation
  •   Lignocaine 1.5mg/kg bolus

Supportive Measures

Titrated benzodiazepines and good supportive care are paramount until the toxidrome subsides.

Disposition

The majority of patients will be suitable for transfer to SSU under the toxicology team for observation and supportive care. For those with more serious sympathomimetic related complications intensive care input may be necessary.

Additional Information

  • Traditional teaching suggests beta blockers are theoretically contra-indicated in sympathomimetic toxicity because of the potential for unopposed alpha adrenergic stimulation leading to profound vasoconstriction and hypertension. However, a recent literature review suggests otherwise,2 concluding that, based on the available evidence, beta blockers are recommended in the armament of treatment of hyperadrenergic states.
  • Cocaine in particular is associated with coronary vasospasm and myocardial infarction, however vasospasm, dissection and vessel rupture can occur in all sympathomimetic toxicity and needs to be considered in a patient presenting with concerning symptoms.

References

  1. Wikitox 2.1.11.4.8 Sympathomimetic teaching resources http://curriculum.toxicology.wikispaces.net/2.1.11.4.8+Sympathomimetics+teaching+resources
  2. Richards, J.R., et al., Treatment of toxicity from amphetamines, related derivatives, and analogues: A systematic clinical review. Drug Alcohol Depend. (2015), http://dx.doi.org/10.1016/j.drugalcdep.2015.01.040