Makindo Medical Notes

Related Subjects: |Drug Toxicity - clinical assessment |Metabolic acidosis |Aspirin or Salicylates toxicity |Ethylene glycol toxicity |Ethanol toxicity |Methanol toxicity |Ricin toxicity |Carbon Tetrachloride Toxicity |Renal Tubular Acidosis |Lactic acidosis |Iron Toxicity |Tricyclic Antidepressant Toxicity |Opiate Toxicity |Carbon monoxide Toxicity |Benzodiazepine Toxicity |Paracetamol (Acetaminophen) toxicity |Amphetamine toxicity |Beta Blocker toxicity |Calcium channel blockers toxicity |Cannabis toxicity |Cyanide toxicity |Digoxin Toxicity |Lithium Toxicity |NSAIDS Toxicity |Ecstasy toxicity |Paraquat toxicity |Quinine toxicity |SSRI Toxicity |Theophylline Toxicity |Organophosphate (OP) Toxicity |Toxin elimination by dialysis |Drug Toxicity with Specific Antidotes

Cocaine is a commonly available drug. Inquiring about its usage is important, as patients may not readily admit to it unless directly asked.

Aetiology

• Cocaine toxicity is primarily due to central nervous system stimulation, leading to increased alertness and energy.
• Derived from the leaves of the coca plant, cocaine works by blocking the reuptake of dopamine, serotonin, and norepinephrine, which intensifies their effects in the brain.
• This blockade raises neurotransmitter levels, leading to the drug's stimulant effects, such as heightened mood and energy levels.
• Chronic usage may accelerate atherosclerosis due to prolonged vascular effects, increasing the risk of cardiovascular diseases.
• The pleasurable effects of cocaine stem from elevated dopamine levels in the mesolimbic reward centers, reinforcing the behavior of drug use.
• Cocaine may also cause neurotoxic effects, leading to changes in brain structure and function with long-term use.

Administration

• Snorting: Cocaine is absorbed via the nasal mucosa, leading to vasoconstriction and potential nasal tissue damage over time, which can result in chronic rhinitis or nasal septum perforation.
• Smoking/IV use: This method provides a rapid but shorter-lasting high, increasing the risk of addiction and overdose. Other methods include oral ingestion, rubbing on gums, and less commonly, rectal administration.
• Cocaine is also used as a local anesthetic in some ophthalmic and ENT surgeries due to its anesthetic and vasoconstrictive properties, aiding in procedures by reducing bleeding.

Effects

• Cocaine-induced chest pain often results from coronary artery spasm rather than atherosclerotic blockage, making thrombolysis generally inappropriate unless indicated otherwise.
• Chronic users may develop coexisting atherosclerotic disease, which increases susceptibility to coronary artery spasms and myocardial ischaemia.
• Effects can include anxiety, agitation, and psychotic symptoms such as paranoia and hallucinations, especially at higher doses.

Clinical Features

• Common symptoms include chest pain, neurological signs due to ischemic or hemorrhagic stroke, and aortic dissection.
• May present with hypertension, tachycardia, hyperthermia, euphoria, and psychosis, which can lead to dangerous behavioral changes.
• Physical signs may include dilated pupils, signs of myocarditis, and evidence of atherosclerosis in long-term users, such as decreased exercise tolerance.
• Withdrawal symptoms can occur with cessation after chronic use, leading to depression and increased craving for the drug.

Investigations

• Blood Tests: FBC, U&E, and Troponin at baseline and after 12 hours to assess for myocardial injury and electrolyte imbalances.
• ECG: Monitor for ischaemia, STEMI, or left ventricular hypertrophy (LVH); changes can indicate acute coronary syndrome.
• Imaging: CXR for cardiomegaly and CT head if neurological symptoms are present, as well as echocardiography to assess cardiac function.
• Urine Toxicology Screening: To confirm recent cocaine use, although it may not reflect current impairment.

Management

• Persisting ST Elevation: Proceed with Primary PCI for STEMI; timely intervention is crucial.
• Thrombolysis: Generally avoided, especially if the patient is markedly hypertensive, as it may exacerbate bleeding risk.
• Administer sublingual and then IV nitrates as a prelude to PPCI to manage chest pain and control hypertension.
• Avoid unopposed beta-blockade: This can worsen hypertension due to alpha effects; if necessary, use a beta-blocker with careful monitoring.
• Treat hyperthermia with IV fluids, active cooling methods (e.g., cooling blankets), and consider dantrolene if severe muscle rigidity is present.
• Avoid haloperidol and phenothiazines due to the risk of seizures; consider diazepam for agitation or seizures instead, carefully titrating to effect.
• Provide psychological support, as users may experience anxiety, paranoia, or hallucinations during acute intoxication.

References

• Cocaine Toxicity Management
• Clinical Features of Cocaine Intoxication