Drugs of abuse

Introduction

Illicit use of drugs currently accounts for 1.8% of the total burden of disease and injury in Australia. In 2016, 43% of people aged over 14 years reported using illicit drugs at least once during their lifetime and 15.6% reported use within the previous 12 months, most commonly cannabis (10.4%), prescription and over-the-counter (OTC) analgesics (3.6%), cocaine (2.5%), ecstasy (2.2%) and methamphetamine (1.4%). While most users of illicit drugs are adults aged 20 to 29 years, the average age of illicit drug users is increasing, with people aged over 50 years accounting for more than 20%. Nine percent of the population report being the victim of a drug-related incident within the past year.

In Victoria, annual opioid dispensing has increased by 78% since 2006, with hospital presentations for opioid toxicity increasing by 10% per year. Deliberate self-poisoning accounts for 56% of these admissions.

Misuse of pharmaceutical agents refers to the use of pharmaceutical medications supplied OTC or on prescription, either for nonmedical purposes or in doses or frequencies greater than those prescribed, to induce or enhance the drug effect. Opioid and prescription analgesic misuse is most common (3.6%), with codeine and oxycodone accounting for the majority. Although misuse is common in young adults, users tend to be older on average (45 years) than other illicit drug users (34 years). New restrictions on OTC codeine-based products may help to reduce the misuse of these agents in the future.

In assessment and management planning, consider the primary toxic effect of the agent, complications of intoxication and complications of the administration/injection technique. Complications of poor injection technique include cellulitis, thrombophlebitis, intra-arterial injection and embolization, mycotic aneurysm, endocarditis, anaerobic infection and blood-borne virus infection. A high index of suspicion is required.

Presentation to an emergency department (ED) with acute intoxication or complications of drug use indicates ongoing hazard and provides an opportunity for intervention. Patients should be counselled regarding strategies to avoid future overdose and if willing, should be referred to rehabilitation agencies.

Amphetamines

Epidemiology

In 2016, 6.3% of Australians over 14 years reported using amphetamine derivatives in their lifetime. MDMA use was also common, with 11.2% of people over age 14 years reporting lifetime use. Amphetamine use has been declining in younger age groups since 2001.

Clinical features

Predominant symptoms are CNS excitation and peripheral sympathomimetic response. Euphoria, apprehension and agitation are common. Tachypnoea, mydriasis, tremor, diaphoresis and hyperpyrexia may also occur. Psychosis may occur with visual and tactile hallucinations, severe agitation and paranoia resembling paranoid schizophrenia. Myocardial infarction, aortic dissection, rhabdomyolysis, acidosis, acute cardiomyopathy, shock, renal failure and coagulopathy are documented. Symptoms may persist for several days. Death is secondary to hyperthermia, arrhythmia, intracerebral haemorrhage or trauma.

Hyponatraemia with cerebral oedema presenting as altered consciousness and seizures is reported following MDMA use and may be fatal. Mechanisms contributing to hyponatraemia include psychogenic polydipsia and inappropriate secretion of antidiuretic hormone.

Chronic abuse of amphetamines may be complicated by a necrotizing vasculitis which may involve multiple organ systems and lead to renal failure, myocardial ischaemia and cerebrovascular disease.

Amphetamine dependence and withdrawal is recognized. Withdrawal is characterized by neurasthenic symptoms, including somnolence and intense cravings for amphetamines. Management is supportive.

Differential diagnosis

Intoxication by an amphetamine derivative may not be discernible clinically from cocaine, except for the increased psychotic features and longer duration of action. The differential diagnosis also includes anticholinergic delirium, serotonin syndrome, alcohol and benzodiazepine withdrawal, sepsis, thyrotoxicosis and phaeochromocytoma.

Clinical investigations

Physical examination and investigations should be directed at excluding complications and alternative diagnoses. Seizures or coma should prompt investigation for complications, such as intracerebral haemorrhage or electrolyte disturbance. All patients should have a blood glucose measurement.

Treatment

Resuscitation for immediate life threats should proceed along standard lines. Care in a quiet area away from excessive stimulation may be advantageous. Patients exhibiting psychomotor acceleration or psychosis should be managed with titrated intravenous sedation.

Hyperthermia and seizures should be managed aggressively. Hyperthermia is an important contributing factor to morbidity and mortality. Core temperature should be measured in all patients and continuous monitoring is recommended if the temperature is elevated. Mild-to-moderate hyperthermia (<39°C) usually responds to benzodiazepine sedation and fluid resuscitation. If temperature continues to rise, intubation and paralysis are indicated. The use of dantrolene is not indicated.

Benzodiazepines are first-line therapy for seizures, followed by barbiturates, then general anaesthesia. Seizures in the context of acute hyponatraemia require initial rapid sodium replacement. Patients with persistent psychotic features may respond to an antipsychotic agent.

Disposition

The duration of observation in the ED and the need for admission will depend on the severity of intoxication, the influence of co-ingested drugs, comorbidities and complications. Patients with mild intoxication may be observed in the ED and discharged when vital signs and mental status have returned to normal. The long half-lives of the amphetamines may dictate inpatient care if symptoms or abnormal vital signs do not resolve within a few hours.

Cocaine

Epidemiology

The prevalence of cocaine use is increasing in Australia, with 9% of the population aged over 14 years reporting cocaine use in their lifetime in 2016.

Clinical features

The predominant symptoms are those of Central nervous system (CNS) excitation and peripheral sympathomimetic response. CNS manifestations include agitation, altered mental state, seizures, dyspnoea, transient focal neurological signs, intracranial haemorrhage and coma. Cerebral infarction, transient ischaemic attacks, subarachnoid haemorrhage, cerebral vasculitis and migraine-like headache are described. Contributing mechanisms include hypertension, vasoconstriction, vasculitis, increased coagulability, altered cerebrovascular autoregulation and embolization of particulate matter.

Cardiovascular manifestations include tachycardia, hypertension, supraventricular or ventricular tachydysrhythmias and syncope. Chest pain may be due to musculoskeletal, pulmonary or cardiovascular causes. Cocaine-induced myocardial ischaemia is multifactorial; increased myocardial oxygen demand, immediate or delayed coronary artery vasospasm, increased platelet aggregation, impaired thrombolysis and accelerated atherosclerosis all contribute. Aortic dissection associated with cocaine use is reported. A retrospective study of patients intoxicated with cocaine presenting with chest pain consistent with ischaemia found 6% suffered acute myocardial infarction.

Smoking cocaine may lead to respiratory complications including thermal airway injury, pneumothorax, pneumomediastinum, noncardiac pulmonary oedema, interstitial pneumonitis and bronchiolitis obliterans. Tachypnoea, mydriasis, tremor, diaphoresis and hyperpyrexia may also be seen. Mesenteric vasoconstriction and vasculitis may lead to bowel ischaemia and infarction. Rhabdomyolysis complicated by renal failure and hyperkalaemia is reported.

Differential diagnosis

The differential diagnosis includes intoxication with other sympathomimetic agents, hallucinogenic agents, anticholinergic delirium, serotonin syndrome, alcohol and benzodiazepine withdrawal, sepsis, thyrotoxicosis and phaeochromocytoma.