Cocaine usage has historical dual effects spanning thousands of years.
Cocaine is a strong stimulant from coca plant leaves. High potential for abuse and addiction affects the central nervous system.
Cocaine toxicity leads to serious physiological and psychological effects. Cocaine increases sympathetic activity to block neurotransmitter reuptake in synapses.
Euphoria and energy increase but with significant risks. Cocaine toxicity stimulates cardiovascular, CNS, and thermoregulatory systems.
In 2018, U.S. cocaine-related deaths reached 14,666 for the third consecutive year.
ED patients with cocaine toxicity frequently use other drugs, which may significantly contribute to drug-related fatalities.
Cocaine has influenced societies for millennia as this noted for its dual effects since at least 2000 BC.
Crack is sold as rocks, but also in larger slabs resembling sticks of chewing gum, often scored for easier breaking into smaller pieces.
Crack cocaine is smokable and stable to pyrolysis unlike cocaine. Cocaine crack users are young adults aged 18-30 from low socioeconomic backgrounds in central cities.
Epidemiology
The 2019 CDC report highlighted drug-related risks and outcomes findings from 2018. In 2018, approximately 977,000 individuals reported a cocaine-related substance use disorder.
In 2020, the UNODC estimated 21.5 million cocaine users globally in the past year.
A “pocket shot” involves injecting the internal jugular vein by directing the needle into the neck above the clavicle.
Women using intranasal cocaine have lower plasma levels than men. Men experience cocaine effects quicker and report more euphoria and dysphoria.
Anatomy
Pathophysiology
Cocaine blocks norepinephrine reuptake and causes significant norepinephrine release.
Synergistic effects boost norepinephrine at nerve terminal. Cocaine affects serotonin and dopamine levels moderately.
Sodium channel blockade produces local anesthetic effects to inhibit nerve impulse conduction and reducing potential.
Cocaine arrives in the U.S. as hydrochloride salt, refined from the original coca leaf. Crack smokers aggressively inhale from a pipe then exhale or blow the drug to others.
Etiology
The causes of cocaine toxicity are:
Route and Dose of Cocaine Use
Drug Purity and Adulterants
Individual Susceptibility
Chronic Use and Sensitization
Dose-Dependent Toxicity
Genetics
Prognostic Factors
Cocaine significantly impacts mortality through homicide, suicide, and accidents.
Cocaine-related deaths stem from direct effects and traumatic injuries.
Alcohol and illicit drugs elevate suicide risk 16-fold significantly higher than each substance individually.
Half of Hispanic male suicides test positive for cocaine. Cocaine users resort to violence and firearms.
Cocaine use increases risk of HIV and sexually transmitted infections.
Clinical History
Collect details including the presenting complaints, substance Use history, and medical history to understand clinical history of patients.
Physical Examination
Neurological Examination
Cardiovascular Examination
Respiratory Examination
Gastrointestinal Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Acute symptoms are:
Agitation, paranoia, violent behavior, Seizures or status epilepticus
Chronic symptoms are:
Paranoia, psychosis, severe insomnia, fatigue, depression, chronic hypertension, cardiomyopathy
Differential Diagnoses
Acute Hypoglycemia
Delirium Tremens
Pneumothorax
Hallucinogen Toxicity
Pneumothorax
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Patients with cocaine toxicity require evaluation, stabilization, ABCs attention, oxygen, IV access, and monitoring.
Hyperthermic patients may experience rising temperature from agitation or restraints.
Routine pregnancy testing essential due to increased cocaine toxicity risks.
Medications for cocaine’s pathophysiologic effects may exacerbate adverse effects, hence raises concerns about epinephrine, lidocaine, and beta-blockers in acute toxicity.
American Heart Association (AHA) guidelines state no evidence supports cocaine-specific interventions for cardiac arrest from overdose.
Ventricular ectopy is transiently managed through observation and benzodiazepines to reduce cocaine-related CNS stimulation.
Positive-pressure ventilation or intubation effectively treats resistant hypoxemia with positive end-expiratory pressure.
Patients should be moved into a quiet/dim room to minimize loud noises and sudden interactions.
Avoid excessive cooling to prevent shivering and heat production.
Aggressive BP reduction is essential to prevent stroke from hypertension.
Provide structured withdrawal care in a safe environment and monitor for cocaine crash symptoms.
Proper awareness about cocaine toxicity should be provided and its related causes with management strategies.
use-of-benzodiazepines
Diazepam:
It depresses all levels of CNS to increase GABA activity.
Midazolam:
It increases neuronal membrane permeability with chloride ions.
Use of Cardiovascular agents
Lidocaine:
It increases electrical stimulation threshold of ventricle that slows conduction velocity.
Phentolamine:
It blocks circulating epinephrine and norepinephrine action to reduce hypertension.
Norepinephrine:
It stimulates alpha and beta1-adrenergic receptors which increases cardiac muscle contractility.
Use of GI agents
Polyethylene glycol:
It is laxative with strong electrolyte effect indicated for treating cocaine ingestion in body-packers.
Use of Nutrients
Thiamine:
It forms thiamine pyrophosphate when combines with ATP.
Dextrose:
It absorbed from intestine and used by tissues. While direct oral absorption increases blood glucose concentrations.
Procedural interventions in cocaine toxicity should be initiated based on clinical severity including airway protection, cooling, and cardiac interventions.
use-of-phases-in-managing-cocaine-toxicity
In the initial stabilization phase, the goal is to stabilize the patient, prevent complications, and ensure long-term recovery.
Pharmacologic therapy is effective in the treatment phase as it includes the use of benzodiazepines, cardiovascular agents, GI agents, and nutrients.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
Cocaine usage has historical dual effects spanning thousands of years.
Cocaine is a strong stimulant from coca plant leaves. High potential for abuse and addiction affects the central nervous system.
Cocaine toxicity leads to serious physiological and psychological effects. Cocaine increases sympathetic activity to block neurotransmitter reuptake in synapses.
Euphoria and energy increase but with significant risks. Cocaine toxicity stimulates cardiovascular, CNS, and thermoregulatory systems.
In 2018, U.S. cocaine-related deaths reached 14,666 for the third consecutive year.
ED patients with cocaine toxicity frequently use other drugs, which may significantly contribute to drug-related fatalities.
Cocaine has influenced societies for millennia as this noted for its dual effects since at least 2000 BC.
Crack is sold as rocks, but also in larger slabs resembling sticks of chewing gum, often scored for easier breaking into smaller pieces.
Crack cocaine is smokable and stable to pyrolysis unlike cocaine. Cocaine crack users are young adults aged 18-30 from low socioeconomic backgrounds in central cities.
The 2019 CDC report highlighted drug-related risks and outcomes findings from 2018. In 2018, approximately 977,000 individuals reported a cocaine-related substance use disorder.
In 2020, the UNODC estimated 21.5 million cocaine users globally in the past year.
A “pocket shot” involves injecting the internal jugular vein by directing the needle into the neck above the clavicle.
Women using intranasal cocaine have lower plasma levels than men. Men experience cocaine effects quicker and report more euphoria and dysphoria.
Cocaine blocks norepinephrine reuptake and causes significant norepinephrine release.
Synergistic effects boost norepinephrine at nerve terminal. Cocaine affects serotonin and dopamine levels moderately.
Sodium channel blockade produces local anesthetic effects to inhibit nerve impulse conduction and reducing potential.
Cocaine arrives in the U.S. as hydrochloride salt, refined from the original coca leaf. Crack smokers aggressively inhale from a pipe then exhale or blow the drug to others.
The causes of cocaine toxicity are:
Route and Dose of Cocaine Use
Drug Purity and Adulterants
Individual Susceptibility
Chronic Use and Sensitization
Dose-Dependent Toxicity
Cocaine significantly impacts mortality through homicide, suicide, and accidents.
Cocaine-related deaths stem from direct effects and traumatic injuries.
Alcohol and illicit drugs elevate suicide risk 16-fold significantly higher than each substance individually.
Half of Hispanic male suicides test positive for cocaine. Cocaine users resort to violence and firearms.
Cocaine use increases risk of HIV and sexually transmitted infections.
Collect details including the presenting complaints, substance Use history, and medical history to understand clinical history of patients.
Neurological Examination
Cardiovascular Examination
Respiratory Examination
Gastrointestinal Examination
Acute symptoms are:
Agitation, paranoia, violent behavior, Seizures or status epilepticus
Chronic symptoms are:
Paranoia, psychosis, severe insomnia, fatigue, depression, chronic hypertension, cardiomyopathy
Acute Hypoglycemia
Delirium Tremens
Pneumothorax
Hallucinogen Toxicity
Pneumothorax
Patients with cocaine toxicity require evaluation, stabilization, ABCs attention, oxygen, IV access, and monitoring.
Hyperthermic patients may experience rising temperature from agitation or restraints.
Routine pregnancy testing essential due to increased cocaine toxicity risks.
Medications for cocaine’s pathophysiologic effects may exacerbate adverse effects, hence raises concerns about epinephrine, lidocaine, and beta-blockers in acute toxicity.
American Heart Association (AHA) guidelines state no evidence supports cocaine-specific interventions for cardiac arrest from overdose.
Ventricular ectopy is transiently managed through observation and benzodiazepines to reduce cocaine-related CNS stimulation.
Positive-pressure ventilation or intubation effectively treats resistant hypoxemia with positive end-expiratory pressure.
Acidosis negatively impacts heart contractility and enhances catecholamine effects.
Patients with rhabdomyolysis may need 20 L of fluid in the first 24 hours, with monitoring of cardiac status required.
Cocaine ingestion in stable patients can be treated with activated charcoal administration.
Carriers purge their GI tract with laxatives and consume clear liquids until delivering drug packages.
Emergency Medicine
Patients should be moved into a quiet/dim room to minimize loud noises and sudden interactions.
Avoid excessive cooling to prevent shivering and heat production.
Aggressive BP reduction is essential to prevent stroke from hypertension.
Provide structured withdrawal care in a safe environment and monitor for cocaine crash symptoms.
Proper awareness about cocaine toxicity should be provided and its related causes with management strategies.
Emergency Medicine
Diazepam:
It depresses all levels of CNS to increase GABA activity.
Midazolam:
It increases neuronal membrane permeability with chloride ions.
Emergency Medicine
Lidocaine:
It increases electrical stimulation threshold of ventricle that slows conduction velocity.
Phentolamine:
It blocks circulating epinephrine and norepinephrine action to reduce hypertension.
Norepinephrine:
It stimulates alpha and beta1-adrenergic receptors which increases cardiac muscle contractility.
Emergency Medicine
Polyethylene glycol:
It is laxative with strong electrolyte effect indicated for treating cocaine ingestion in body-packers.
Emergency Medicine
Thiamine:
It forms thiamine pyrophosphate when combines with ATP.
Dextrose:
It absorbed from intestine and used by tissues. While direct oral absorption increases blood glucose concentrations.
Emergency Medicine
Procedural interventions in cocaine toxicity should be initiated based on clinical severity including airway protection, cooling, and cardiac interventions.
Emergency Medicine
In the initial stabilization phase, the goal is to stabilize the patient, prevent complications, and ensure long-term recovery.
Pharmacologic therapy is effective in the treatment phase as it includes the use of benzodiazepines, cardiovascular agents, GI agents, and nutrients.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
Cocaine usage has historical dual effects spanning thousands of years.
Cocaine is a strong stimulant from coca plant leaves. High potential for abuse and addiction affects the central nervous system.
Cocaine toxicity leads to serious physiological and psychological effects. Cocaine increases sympathetic activity to block neurotransmitter reuptake in synapses.
Euphoria and energy increase but with significant risks. Cocaine toxicity stimulates cardiovascular, CNS, and thermoregulatory systems.
In 2018, U.S. cocaine-related deaths reached 14,666 for the third consecutive year.
ED patients with cocaine toxicity frequently use other drugs, which may significantly contribute to drug-related fatalities.
Cocaine has influenced societies for millennia as this noted for its dual effects since at least 2000 BC.
Crack is sold as rocks, but also in larger slabs resembling sticks of chewing gum, often scored for easier breaking into smaller pieces.
Crack cocaine is smokable and stable to pyrolysis unlike cocaine. Cocaine crack users are young adults aged 18-30 from low socioeconomic backgrounds in central cities.
The 2019 CDC report highlighted drug-related risks and outcomes findings from 2018. In 2018, approximately 977,000 individuals reported a cocaine-related substance use disorder.
In 2020, the UNODC estimated 21.5 million cocaine users globally in the past year.
A “pocket shot” involves injecting the internal jugular vein by directing the needle into the neck above the clavicle.
Women using intranasal cocaine have lower plasma levels than men. Men experience cocaine effects quicker and report more euphoria and dysphoria.
Cocaine blocks norepinephrine reuptake and causes significant norepinephrine release.
Synergistic effects boost norepinephrine at nerve terminal. Cocaine affects serotonin and dopamine levels moderately.
Sodium channel blockade produces local anesthetic effects to inhibit nerve impulse conduction and reducing potential.
Cocaine arrives in the U.S. as hydrochloride salt, refined from the original coca leaf. Crack smokers aggressively inhale from a pipe then exhale or blow the drug to others.
The causes of cocaine toxicity are:
Route and Dose of Cocaine Use
Drug Purity and Adulterants
Individual Susceptibility
Chronic Use and Sensitization
Dose-Dependent Toxicity
Cocaine significantly impacts mortality through homicide, suicide, and accidents.
Cocaine-related deaths stem from direct effects and traumatic injuries.
Alcohol and illicit drugs elevate suicide risk 16-fold significantly higher than each substance individually.
Half of Hispanic male suicides test positive for cocaine. Cocaine users resort to violence and firearms.
Cocaine use increases risk of HIV and sexually transmitted infections.
Collect details including the presenting complaints, substance Use history, and medical history to understand clinical history of patients.
Neurological Examination
Cardiovascular Examination
Respiratory Examination
Gastrointestinal Examination
Acute symptoms are:
Agitation, paranoia, violent behavior, Seizures or status epilepticus
Chronic symptoms are:
Paranoia, psychosis, severe insomnia, fatigue, depression, chronic hypertension, cardiomyopathy
Acute Hypoglycemia
Delirium Tremens
Pneumothorax
Hallucinogen Toxicity
Pneumothorax
Patients with cocaine toxicity require evaluation, stabilization, ABCs attention, oxygen, IV access, and monitoring.
Hyperthermic patients may experience rising temperature from agitation or restraints.
Routine pregnancy testing essential due to increased cocaine toxicity risks.
Medications for cocaine’s pathophysiologic effects may exacerbate adverse effects, hence raises concerns about epinephrine, lidocaine, and beta-blockers in acute toxicity.
American Heart Association (AHA) guidelines state no evidence supports cocaine-specific interventions for cardiac arrest from overdose.
Ventricular ectopy is transiently managed through observation and benzodiazepines to reduce cocaine-related CNS stimulation.
Positive-pressure ventilation or intubation effectively treats resistant hypoxemia with positive end-expiratory pressure.
Acidosis negatively impacts heart contractility and enhances catecholamine effects.
Patients with rhabdomyolysis may need 20 L of fluid in the first 24 hours, with monitoring of cardiac status required.
Cocaine ingestion in stable patients can be treated with activated charcoal administration.
Carriers purge their GI tract with laxatives and consume clear liquids until delivering drug packages.
Emergency Medicine
Patients should be moved into a quiet/dim room to minimize loud noises and sudden interactions.
Avoid excessive cooling to prevent shivering and heat production.
Aggressive BP reduction is essential to prevent stroke from hypertension.
Provide structured withdrawal care in a safe environment and monitor for cocaine crash symptoms.
Proper awareness about cocaine toxicity should be provided and its related causes with management strategies.
Emergency Medicine
Diazepam:
It depresses all levels of CNS to increase GABA activity.
Midazolam:
It increases neuronal membrane permeability with chloride ions.
Emergency Medicine
Lidocaine:
It increases electrical stimulation threshold of ventricle that slows conduction velocity.
Phentolamine:
It blocks circulating epinephrine and norepinephrine action to reduce hypertension.
Norepinephrine:
It stimulates alpha and beta1-adrenergic receptors which increases cardiac muscle contractility.
Emergency Medicine
Polyethylene glycol:
It is laxative with strong electrolyte effect indicated for treating cocaine ingestion in body-packers.
Emergency Medicine
Thiamine:
It forms thiamine pyrophosphate when combines with ATP.
Dextrose:
It absorbed from intestine and used by tissues. While direct oral absorption increases blood glucose concentrations.
Emergency Medicine
Procedural interventions in cocaine toxicity should be initiated based on clinical severity including airway protection, cooling, and cardiac interventions.
Emergency Medicine
In the initial stabilization phase, the goal is to stabilize the patient, prevent complications, and ensure long-term recovery.
Pharmacologic therapy is effective in the treatment phase as it includes the use of benzodiazepines, cardiovascular agents, GI agents, and nutrients.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
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