This page compiles our content related to substance use disorders and overdose. For further information on diagnosis and treatment, follow the links below to our full BMJ Best Practice topics on the relevant conditions and symptoms.
Introduction
Relevant conditions
Opioid use disorder | go to our full topic on Opioid use disorder An opioid is a synthetic or natural agent that stimulates opioid receptors and produces opium-like effects. Opiates are a type of opioid that are naturally derived from the opium poppy (e.g., codeine, morphine, opium). They are used to treat pain but may also be misused because of their euphoric effects. Initiation of opioid use disorder is related to familial and environmental influences such as peer pressure, disrupted family dynamics, and history of availability of opioids in the family.[5][6] The diagnosis of opioid use disorder is clinical, and therefore a thorough history and psychiatric and medical exam, along with appropriate laboratory tests, are essential for making a diagnosis. Patients with opioid use disorder may present with chronic constipation, weight loss, or symptoms of either tolerance or withdrawal. |
|---|---|
Opioid overdose | go to our full topic on Opioid overdose Overdose occurs when larger quantities than physically tolerated are taken, resulting in central nervous system (CNS) and respiratory depression, miosis, and apnea. Can be fatal if not treated rapidly. Over 80% of deaths associated with opioid overdose in North America involve fentanyl, a synthetic opioid with a very high potency.[7] The diagnosis of opioid overdose is primarily based on history and physical exam. History of opioid use or misuse is a key factor. Other risk factors include recent abstinence from opioid use in chronic users and a history of chronic pain.[8] |
Cocaine use disorder | go to our full topic on Cocaine use disorder Cocaine is a controlled illicit, highly addictive stimulant drug that is usually either insufflated (snorted), injected, or smoked in its freebase form (crack). Cocaine use is normally occasional, with the majority of users not meeting the criteria for cocaine use disorder. In 2022, approximately 23 million people had used cocaine globally.[1] Genomic studies and twin and family cohort studies suggest that there are genes with allelic variants that do predispose to stimulant dependence.[9][10] Diagnosis of cocaine use disorder is based on clinical assessment via a combination of patient interview, collateral history, and review of available medical records. Chronic use can lead to scarring of heart tissue and myocardial hypertrophy and other changes collectively known as myocardial remodeling. These changes constitute the substrate for the occurrence of lethal arrhythmias. Cocaine use causes a hyperadrenergic state associated with abnormal mentation. The symptoms of any hyperadrenergic state include nausea, jitteriness, trouble concentrating, anxiety, paranoia, and euphoria. |
Cocaine toxicity | go to our full topic on Cocaine toxicity Cocaine toxicity usually occurs in the setting of recreational misuse. Refers to adverse events that occur within minutes or hours of excessive cocaine use. More rarely, unintentional toxicity occurs in individuals carrying drugs in body cavities for the purpose of smuggling (body packing) or avoiding legal punishment (body stuffing). These events, which can occur in combination or isolation, include hyperthermia, rhabdomyolysis, dysrhythmia, ischemia, intracranial hemorrhage, agitation, psychosis, and seizures. Some patients may die suddenly before treatment can be given. |
Amphetamine and methamphetamine use disorder | go to our full topic on Amphetamine and methamphetamine use disorder Amphetamine and methamphetamine are noncatecholamine sympathomimetic amines that may be taken by various routes including inhalation, intravenous, intramuscular, or transmucosal (oral/nasal). In 2022, approximately 30 million people had used amphetamine-type stimulants globally.[1] The etiology is unclear, although a number of predisposing factors exist, including comorbid psychiatric disorders and adverse childhood events. Psychiatric comorbidity is complex, given the overlap in symptoms (e.g., psychosis and depression) and presence of shared risk factors.[11][12] Diagnosis is based on clinical assessment via a combination of patient interview, collateral history, and review of available medical records. Early warning features suggestive of a need for close monitoring due to potential impending risk to life include: dyspnea, angina, palpitations, cough, and hemoptysis.[13] |
Amphetamine overdose | go to our full topic on Amphetamine overdose Amphetamine overdose represents a large burden of dependency and toxicity worldwide, stemming from both legitimate and recreational ingestion of amphetamine and its derivatives. The diagnosis of amphetamine toxicity is primarily clinical. Patients usually present with sympathetic nervous system hyperactivity and a history of legitimate (licit) or illicit drug use in the immediate past. Patients with amphetamine toxicity will often present with agitated, irrational, restless, and aggressive behavior, and may show signs of hypervigilance, paranoia, and psychosis.[14] Overdose and toxicity strike inconsistently among new, occasional, chronic, and binge users. Intentional overdose is also encountered. |
Cannabis use disorder | Cannabis is the most commonly used drug worldwide, with an estimated 228 million users in 2022.[1] Acute health effects include impaired cognitive and psychomotor performance. Chronic health effects may include sustained cognitive impairment (and impaired cognitive development in children and adolescents), dependence, increased risk of schizophrenia and social anxiety, exacerbation of bipolar disorders, worsened respiratory symptoms, and increased frequency of chronic bronchitis associated with smoking cannabis.[15] |
Inhalant use disorder | The deliberate inhalation of a volatile substance to achieve an altered mental state.[16] Inhalants used include volatile solvents from household and industrial products; aerosol propellants; gases from household, industrial, and medical products; and nitrites and nitrous oxide. Hypoxia and heart failure can occur within minutes. Longer-term adverse effects include hearing loss, peripheral neuropathies, and liver and kidney damage. |
Hallucinogen use disorder | The DSM-5-TR divides problematic hallucinogen use into two categories: phencyclidine use disorder and other hallucinogen use disorder. Phencyclidine use disorder includes pharmacologically similar substances such as ketamine, cyclohexamine, and dizocilpine. Other hallucinogen use disorder covers a diverse group of substances including phenylalkylamines (e.g., mescaline, MDMA), indoleamines (e.g., psilocybin, dimethyltryptamine [DMT]), ergolines (e.g., LSD), and hallucinogenic plants (e.g., Salvia divinorum, jimsonweed). Psychological effects can be unpredictable. Long-term adverse effects of hallucinogens are rare, but may include persistent psychosis or hallucinogen persisting perception disorder.[17] |
Benzodiazepine overdose | go to our full topic on Benzodiazepine overdose Occurs when excessive amounts of benzodiazepine drugs are taken. Commonly known as minor tranquilizers or sleeping pills, benzodiazepines are prescribed for sedative, anxiolytic, hypnotic, and anticonvulsant purposes. Overdose can be intentional (e.g., as an act of self-harm), as part of recreational misuse, or accidental (e.g., medication error). The key feature of overdose is excessive sedation. Larger doses can cause coma, respiratory depression, and, without appropriate treatment, even death, particularly in the context of mixed ingestion with other CNS depressants, such as alcohol and opioids. Benzodiazepine overdose is usually determined by the patient's history, either from his or her own report, or by circumstantial evidence, such as benzodiazepine prescriptions or a history of psychiatric illness or previous overdose. Key risk factors include depression, history of illicit drug or alcohol use, history of benzodiazepine use, drug administration error, comorbidity, suicidal ideation or behavior, and history of polydrug or unknown substance ingestion. |
Tricyclic antidepressant overdose | go to our full topic on Tricyclic antidepressant overdose An antidepressant overdose occurs when a person ingests an amount of drug that is more than a reasonable and normal dose.[18] Tricyclic antidepressants have a narrow therapeutic index and therefore become potent cardiovascular and CNS toxins in moderate doses. One UK cohort study found that tricyclic and tetracyclic antidepressants (ICD-10 code T43.0) were the tenth most common poisoning substance, accounting for 624 (2.7%) of all common poisoning events between 1998 and 2014 (n=23,326).[19] Best markers for suspected overdose are a history of depression, suicidality, and overdose, with a sudden deterioration in mental status and vital signs. At 1 to 2 hours after ingestion, there is a rapid decline in mental and cardiovascular status. Diagnosis is established on clinical grounds and classic ECG changes (sinus tachycardia progressing to wide complex tachycardia and ventricular arrhythmias with increasing severity of intoxication). |
Anabolic steroid use disorder | go to our full topic on Anabolic steroid use disorder The use of testosterone derivatives (or other drugs that increase endogenous testosterone production) to improve athletic performance or to increase lean body mass and muscle size. The global lifetime prevalence rate of anabolic-androgenic steroid use is 3.3%.[20] Misuse differs from that of other drugs, such as heroin or cocaine, as the desire to use them does not generally come from effects of the drug, but rather from wanting to change appearance or improve athletic performance. They are used at doses 10 to 100 times higher than those required to treat medical conditions. Diagnosis requires a high index of suspicion and observing various signs and symptoms in addition to laboratory tests. |
Acetaminophen overdose | go to our full topic on Acetaminophen overdose Overdose may occur after excessive ingestion of acetaminophen or acetaminophen-containing medication as an acute or staggered overdose, or therapeutic excess. In 2023, 5053 deaths related to drug poisoning were registered in England and Wales; 259 of these were related to acetaminophen poisoning.[21][22] Patients are often asymptomatic or have only mild gastrointestinal symptoms at initial presentation. Acetaminophen overdose usually occurs as a self-harm attempt or a therapeutic error. Untreated acetaminophen poisoning may cause varying degrees of liver injury over the 2 to 4 days following ingestion, including fulminant hepatic failure. Patients are often asymptomatic or have only mild gastrointestinal symptoms at initial presentation. Rarely, massive overdose may initially present with coma and severe metabolic acidosis. |
Overview of chronic alcohol use | go to our full topic on Overview of chronic alcohol use Alcohol-use disorder, particularly when chronic and severe, can be associated with a variety of medical and psychiatric sequelae. In 2019, harmful alcohol use resulted in an estimated 2.6 million deaths globally.[23] Young people are disproportionately affected by alcohol consumption - people ages 20-39 years made up 13% of alcohol-attributable deaths in 2019.[23] Unintentional injuries, digestive diseases, disabilities, and alcohol use disorders are the leading contributors to the alcohol-related burden of disease.[23] |
Smoking cessation | go to our full topic on Smoking cessation Cigarette smoking is the most common cause of preventable death and disease.[24] The goal of smoking cessation is to assist the person in changing their behavior to help them achieve abstinence from smoking or other tobacco use. Physicians and other healthcare professionals should play a central role in motivating and assisting patients who smoke to stop.[25] Globally, the prevalence of current use of smoking tobacco among individuals ages 15 years and older is 32.7% among males and 6.6% among females.[26] Tobacco smoking usually begins in adolescence or early adulthood (typically before the age of 24 years).[27] Smoking behavior is influenced by biologic, genetic, behavioral, social, and environmental factors. |
Toxic ingestions in children | go to our full topic on Toxic ingestions in children Children may ingest a toxic substance accidentally while exploring their environment, or deliberately in response to stress or underlying mental problems, or in an attempt to get "high." Agents consumed may be pharmaceutical substances; drugs of abuse (including alcohol); toxic plants, berries, or mushrooms; or chemicals. In a study of fatal poisonings in Australia between 2003 and 2013, acute poisoning death was most common in children ages 0-4 years (26.7%) and 13-16 years (58.9%); 61.1% of cases were unintentional and 17.8% were intentional self-harm.[28] Pediatric patients who have ingested poisons or drugs in toxic amounts may have any number of symptoms or signs. These include, but are not limited to, seizures, cardiac dysrhythmias, autonomic instability, hypoglycemia, movement disorders due to rigidity or ataxia, hepatic failure, lethargy, agitation, acute kidney injury, breathlessness, rashes, changes in mental status, visual disturbances, and hypotonia/weakness. Diagnosis is based on a combination of thorough clinical evaluation and comprehensive laboratory investigation to identify all ingested substances. |
Contributors
Authors
Editorial Team
BMJ Publishing Group
Disclosures
This overview has been compiled using the information in existing sub-topics.
References
Key articles
United Nations Office on Drugs and Crime. World drug report 2024. Jun 2024 [internet publication].Full text
Reference articles
A full list of sources referenced in this topic is available to users with access to all of BMJ Best Practice.
Patient information
Quitting smoking
More Patient information
Log in or subscribe to access all of BMJ Best Practice
Use of this content is subject to our disclaimer