Amphetamine:

Kinetics: Most amphetamines are quickly absorbed into the blood stream, and clinical signs can occur very quickly after ingestion .

Amphetamines are lipophilic and cross the blood – brain barrier to enter the central nervous system.

They are metabolized in the liver and both parent compound and its metabolites are excreted in the urine.

Elimination by the urine is enhanced in acidic urine.

Mechanism of Action :

Amphetamines produce their stimulatory activity through several neurotransmitters, including norepinephrine, dopamine, and serotonin in the central nervous system and through direct stimulation of α – and β – adrenergic receptors in the peripheral nervous system .

 Amphetamines also inhibit monoamine oxidase and inhibit neuronal reuptake of catecholamines, both of which can result in accumulation of excess neurotransmitters such as serotonin and norepinephrine at the postsynaptic neuron.

Clinical Signs:

Signs associated with amphetamine intoxication include agitation, restlessness, hyperactivity, aggression, vocalization, hyperthermia, tachycardia, tachypnea, ataxia, tremors, and seizures.

Treatment:

The goals of managing amphetamine exposures are to stabilize the patient, manage clinical signs, decontaminate (if feasible), and provide supportive care.

 Agitation, hyperactivity, and other stimulatory signs tend to respond well to phenothiazine tranquilizers such as acepromazine or chlorpromazine.

 Benzodiazepines should be avoided, because paradoxical worsening of the neurologic effects has been reported.

 Seizures are best controlled with injectable anesthetics (pentobarbital or propofol).

Hyperthermia should be managed by external cooling measures (ice packs, fans, etc.).

For tachycardia that persists after sedation, a beta blocker such as propranolol should be used.

Intravenous fluid therapy will aid in stabilizing the cardiovascular system as well as enhancing elimination of amphetamine via the urine.