The substance that has been taken may often be determined by asking the person. However, if they will not, or cannot, due to an altered level of consciousness, provide this information, a search of the home or questioning of friends and family may be helpful.

Examination for toxidromes, drug testing, or laboratory test may be helpful. Other laboratory test such as glucose, urea and electrolytes, paracetamol levels and salicylate levels are typically done. Negative drug-drug interactions have sometimes been misdiagnosed as an acute drug overdose, occasionally leading to the assumption of suicide.

Definitive diagnosis relies on a blood test for alcohol, usually performed as part of a toxicology screen.

Law enforcement officers in the United States of America often use breathalyzer units and field sobriety tests as more convenient and rapid alternatives to blood tests.

There are also various models of breathalyzer units that are available for consumer use. Because these may have varying reliability and may produce different results than the tests used for law-enforcement purposes, the results from such devices should be conservatively interpreted.

Many informal intoxication tests exist, which, in general, are unreliable and not recommended as deterrents to excessive intoxication or as indicators of the safety of activities such as motor vehicle driving, heavy equipment operation, machine tool use, etc.

For determining whether someone is intoxicated by alcohol by some means other than a blood-alcohol test, it is necessary to rule out other conditions such as hypoglycemia, stroke, usage of other intoxicants, mental health issues, and so on. It is best if his/her behavior has been observed while the subject is sober to establish a baseline. Several well-known criteria can be used to establish a probable diagnosis. For a physician in the acute-treatment setting, acute alcohol intoxication can mimic other acute neurological disorders, or is frequently combined with other recreational drugs that complicate diagnosis and treatment.

As many of the clinical signs and symptoms of ethylene glycol poisoning are nonspecific and occur in many poisonings the diagnosis is often difficult. It is most reliably diagnosed by the measurement of the blood ethylene glycol concentration. Ethylene glycol in biological fluids can be determined by gas chromatography. Many hospital laboratories do not have the ability to perform this blood test and in the absence of this test the diagnosis must be made based on the clinical presentation of the patient. In this situation a helpful test to diagnose poisoning is the measurement of the osmolal gap. The patients' serum osmolality is measured by freezing point depression and then compared with the predicted osmolality based on the patients' measured sodium, glucose, blood urea nitrogen, and any ethanol that may have been ingested. The presence of a large osmolal gap supports a diagnosis of ethylene glycol poisoning. However, a normal osmolar gap does not rule out ethylene glycol exposure because of wide individual variability.

The increased osmolal gap is caused by the ethylene glycol itself. As the metabolism of ethylene glycol progresses there will be less ethylene glycol and this will decrease the blood ethylene glycol concentration and the osmolal gap making this test less useful. Additionally, the presence of other alcohols such as ethanol, isopropanol, or methanol or conditions such as alcoholic or diabetic ketoacidosis, lactic acidosis, or kidney failure may also produce an elevated osmolal gap leading to a false diagnosis.

Other laboratory abnormalities may suggest poisoning, especially the presence of a metabolic acidosis, particularly if it is characterized by a large anion gap. Large anion gap acidosis is usually present during the initial stage of poisoning. However, acidosis has a large number of differential diagnosis, including poisoning from methanol, salicylates, iron, isoniazid, paracetamol, theophylline, or from conditions such as uremia or diabetic and alcoholic ketoacidosis. The diagnosis of ethylene glycol poisoning should be considered in any patient with a severe acidosis. Urine microscopy can reveal needle or envelope-shaped calcium oxalate crystals in the urine which can suggest poisoning; although these crystals may not be present until the late stages of poisoning. Finally, many commercial radiator antifreeze products have fluorescein added to enable radiator leaks to be detected using a Wood's lamp. Following ingestion of antifreeze products containing ethylene glycol and fluorescein, a Wood's lamp may reveal fluorescence of a patient’s mouth area, clothing, vomitus, or urine which can help to diagnose poisoning.

The distribution of naloxone to injection drug users and other opioid drug users decreases the risk of death from overdose. The Centers for Disease Control and Prevention (CDC) estimates that U.S. programs for drug users and their caregivers prescribing take-home doses of naloxone and training on its utilization are estimated to have prevented 10,000 opioid overdose deaths. Healthcare institution-based naloxone prescription programs have also helped reduce rates of opioid overdose in the U.S. state of North Carolina, and have been replicated in the U.S. military. Nevertheless, scale-up of healthcare-based opioid overdose interventions is limited by providers' insufficient knowledge and negative attitudes towards prescribing take-home naloxone to prevent opioid overdose. Programs training police and fire personnel in opioid overdose response using naloxone have also shown promise in the US.

In general, the simultaneous use of multiple drugs should be carefully monitored by a qualified individual such as board certified and licensed medical doctor, either an MD or DO Close association between prescribing physicians and pharmacies, along with the computerization of prescriptions and patients' medical histories, aim to avoid the occurrence of dangerous drug interactions. Lists of contraindications for a drug are usually provided with it, either in monographs, package inserts (accompanying prescribed medications), or in warning labels (for OTC drugs). CDI/MDI might also be avoided by physicians requiring their patients to return any unused prescriptions. Patients should ask their doctors and pharmacists if there are any interactions between the drugs they are taking.

Substance intoxication is a type of substance use disorder which is potentially maladaptive and impairing, but reversible, and associated with recent use.

If the symptoms are severe, the term "substance intoxication delirium" may be used.

Generic slang terms include: getting high or being stoned or blazed (all usually in reference to cannabis), with many more specific slang terms for each particular type of intoxicant. Alcohol intoxication is even graded in intensity, from buzzed, to tipsy, all the way up to hammered, smashed, wasted, destroyed, and a number of other similar terms.

Rapid diagnosis is important to attempt to prevent further damage to the brain and further neurologic deficits. It is a diagnosis of exclusion, so a full work up for other possible etiologies (hepatic, uremic, infectious, oncologic) should be performed. Screening for heavy metals, as well as other toxins, should be done immediately as those are some of the most common causes and the patient can then remove themselves from the dangerous environment. In addition, a full examination of blood (CBC) and metabolites (CMP) should be done.

People who engage in polypharmacy and other hypochondriac behaviors are at an elevated risk of death from CDI. Elderly people are at the highest risk of CDI, because of having many age-related health problems requiring many medications combined with age-impaired judgment, leading to confusion in taking medications.

Examples (and ICD-10 code) include:

- F10.0 alcohol intoxication

- F11.0 opioid intoxication

- F12.0 cannabinoid intoxication

- F13.0 sedative and hypnotic intoxication (see benzodiazepine overdose and barbiturate overdose)

- F14.0 cocaine intoxication

- F15.0 caffeine intoxication

- F16.0 hallucinogen intoxication (See for example Lysergic acid diethylamide effects)

- F17.0 tobacco intoxication

The term contact high is sometimes used to describe intoxication without direct administration, either by second-hand smoke as with cannabis, or by placebo in the presence of others who are high.

Antifreeze products for automotive use containing propylene glycol in place of ethylene glycol are available, and are generally considered safer to use, as it possesses an unpleasant taste in contrast to the perceived "sweet" taste of toxic ethylene glycol-based coolants, and only produces lactic acid in an animal's body, as their muscles do when exercised.

When using antifreeze products containing ethylene glycol, recommended safety measures include:

- Cleaning up any spill immediately and thoroughly. Spills may be cleaned by sprinkling cat litter, sand or other absorbent material directly on the spill. Once fully absorbed, while wearing protective gloves, the material may be scooped into a plastic bag, sealed and disposed. The spill area may be scrubbed with a stiff brush and warm, soapy water. The soapy water is not recommended to be drained in a storm drain.

- Checking vehicles regularly for leaks.

- Storing antifreeze in clearly marked original sealed containers, in areas that are inaccessible to pets or small children.

- Keeping pets and small children away from the area when draining the car radiator.

- Disposing of used antifreeze only by taking to a service station.

- If antifreeze is placed in toilets, ensuring the lid is down and the door closed.

A normal liver detoxifies the blood of alcohol over a period of time that depends on the initial level and the patient's overall physical condition. An abnormal liver will take longer but still succeeds, provided the alcohol does not cause liver failure.

People having drunk heavily for several days or weeks may have withdrawal symptoms after the acute intoxication has subsided.

A person consuming a dangerous amount of alcohol persistently can develop memory blackouts and idiosyncratic intoxication or pathological drunkenness symptoms.

Long-term persistent consumption of excessive amounts of alcohol can cause liver damage and have other deleterious health effects.

In general, alcohol abusers with withdrawal symptoms, such as alcoholic hallucinosis, have a deficiency of several vitamins and minerals and their bodies could cope with the withdrawal easier by taking nutritional supplements. Alcohol abuse can create a deficiency of thiamine, magnesium, zinc, folate and phosphate as well as cause low blood sugar. However, several tested drugs have shown the disappearance of hallucinations. Neuroleptics and benzodiazepines showed normalization. Common benzodiazepines are chlordiazepoxide and lorazepam. It has been shown that management has been effective with a combination of abstinence from alcohol and the use of neuroleptics. It is also possible to treat withdrawal before major symptoms start to happen in the body. Diazepam and chlordiazepoxide have proven to be effective in treating alcohol withdrawal symptoms such as alcoholic halluciniosis. With the help of these specific medications, the process of withdrawal is easier to go through, making alcoholic hallucinosis less likely to occur.

Research is being done by organizations such as NINDS (National Institute of Neurological Disorders and Stroke) on what substances can cause encephalopathy, why they do this, and eventually how to protect, treat, and cure the brain from this condition.

The short-term effects of alcohol (also known formally as ethanol) consumption–due to drinking beer, wine, distilled spirits or other alcoholic beverages–range from a decrease in anxiety and motor skills and euphoria at lower doses to intoxication (drunkenness), stupor, unconsciousness, anterograde amnesia (memory "blackouts"), and central nervous system depression at higher doses. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream it can diffuse into nearly every cell in the body.

The concentration of alcohol in blood is measured via blood alcohol content (BAC). The amount and circumstances of consumption play a large part in determining the extent of intoxication; for example, eating a heavy meal before alcohol consumption causes alcohol to absorb more slowly. The amount of alcohol consumed largely determines the extent of hangovers, although hydration also plays a role. After excessive drinking, stupor and unconsciousness can occur. Extreme levels of consumption can lead to alcohol poisoning and death (a concentration in the blood stream of 0.40% will kill half of those affected). Alcohol may also cause death indirectly, by asphyxiation from vomit.

Alcohol can greatly exacerbate sleep problems. During abstinence, residual disruptions in sleep regularity and sleep patterns are the greatest predictors of relapse.

Alcoholic hallucinosis (or alcohol-related psychosis or alcohol-induced psychotic disorder) is a complication of alcohol withdrawal in alcoholics. Descriptions of the condition date back to at least 1907. They can occur during acute intoxication or withdrawal with the potential of having delirium tremens. Alcohol hallucinosis is a rather uncommon alcohol-induced psychotic disorder only being seen in chronic alcoholics who have many consecutive years of severe and heavy drinking during their lifetime. Alcoholic hallucinosis develops about 12 to 24 hours after the heavy drinking stops suddenly, and can last for days. It involves auditory and visual hallucinations, most commonly accusatory or threatening voices. The risk of developing alcoholic hallucinosis is increased by long-term heavy alcohol abuse and the use of other drugs.

As with all cases of hyponatremia, extreme caution must be taken to avoid the fatal consequences of rapidly correcting electrolytes (e.g. Central pontine myelinolysis, edema). Special considerations with the treatment of potomania are needed. Because this could be a chronic condition, low sodium may be normal for the patient, so an especially careful correction is warranted. It is also very important to note that due to the normal kidney function, and lack of other intrinsic or toxic cause of the electrolyte disturbance, restoration of dietary solutes will correct the electrolytes to normal serum levels. This again must be done with caution.

Medical organizations strongly discourage drinking alcohol during pregnancy. Alcohol passes easily from the mother's bloodstream through the placenta and into the bloodstream of the fetus, which interferes with brain and organ development. Alcohol can affect the fetus at any stage during pregnancy, but the level of risk depends on the amount and frequency of alcohol consumed. Regular heavy drinking and binge drinking (four or more drinks on any one occasion) pose the greatest risk for harm, but lesser amounts can cause problems as well. There is no known safe amount or safe time to drink during pregnancy.

Prenatal alcohol exposure can lead to fetal alcohol spectrum disorders (FASDs). The most severe form of FASD is fetal alcohol syndrome (FAS). Problems associated with FASD include facial anomalies, low birth weight, stunted growth, small head size, delayed or uncoordinated motor skills, hearing or vision problems, learning disabilities, behavior problems, and inappropriate social skills compared to same-age peers. Those affected are more likely to have trouble in school, legal problems, participate in high-risk behaviors, and develop substance use disorders themselves.

Due to its non-specific nature, diagnosing CSE requires a multidisciplinary "Solvent Team" typically consisting of a neurologist, occupational physician, occupational hygienist, neuropsychologist, and sometimes a psychiatrist or toxicologist. Together, the team of specialists together assesses the patient's history of exposure, symptoms, and course of symptom development relative to the amount and duration of exposure, presence of neurological signs, and any existing neuropsychological impairment.

Furthermore, CSE must be diagnosed "by exclusion". This means that all other possible causes of the patient’s symptoms must first be ruled out beforehand. Because screening and assessing for CSE is a complex and time-consuming procedure requiring several specialists of multiple fields, few cases of CSE are formally diagnosed in the medical field. This may, in part, be a reason for the syndrome’s lack of recognition. The solvents responsible for neurological effects dissipate quickly after an exposure, leaving only indirect evidence of their presence, in the form of temporary or permanent impairments.

Brain imaging techniques that have been explored in research have shown little promise as alternative methods to diagnose CSE. Neuroradiology and functional imaging have shown mild cortical atrophy, and effects in dopamine-mediated frontostriatal circuits in some cases. Examinations of regional cerebral blood flow in some imaging techniques have also shown some cerebrovascular abnormalities in patients with CSE, but the data were not different enough from healthy patients to be considered significant. The most promising brain imaging technique being studied currently is functional magnetic resonance imaging (fMRI) but as of now, no specific brain imaging techniques are available to reliably diagnose CSE.

Blackouts are commonly associated with the consumption of large amounts of alcohol; however, surveys of drinkers experiencing blackouts have indicated that they are not directly related to the amount of alcohol consumed. Respondents reported they frequently recalled having "drunk as much or more without memory loss," compared to instances of blacking out. Subsequent research has indicated that blackouts are most likely caused by a rapid increase in a person's blood-alcohol concentration. One study, in particular, resulted in subjects being stratified easily into two groups, those who consumed alcohol very quickly, and blacked out, and those who did not black out by drinking alcohol slowly, despite being extremely intoxicated by the end of the study.

In another study hospital file data showed, that of 67 participants, 39 had reported a blackout. The presence or absence of blackouts was cross-tabulated against various measures of alcohol problem severity. The presence of blackouts was associated to some degree with some indications of severity such as withdrawal and loss of control, but not with duration of problem drinking, physical complications or abnormal liver function.

The presence of blackouts was related to some measures of severity of the problem – withdrawal symptoms and loss of control. The hypotheses that blackouts either reflect a general vulnerability to the cerebral consequences of alcohol abuse or are associated with other forms of more enduring cognitive impairment did not receive any support.

In another study which looked at subjective responses to alcohol as a prime for 21st birthday alcohol consumption, subjective responses to the initial drink were viewed as a prime for more alcohol consumption during 21st birthday celebrations. Current findings show that subjective responses to alcohol have direct effects on both the final BAC achieved and on the experiences of blackouts and hangover that are not explained by level of intoxication. Where a variety of social factors, such as peer pressure and 21st birthday traditions such as 21 shots may influence the amount of alcohol people consume, their subjective experiences with alcohol have clear influences on both consumption and the physiological consequences of drinking. These physiological responses to alcohol may have a biological vulnerability that extends beyond the dose-dependent effects of alcohol.

Self reports from another study showed that 63% of patients in the study gulped their drinks rather than sipped. Five patients recollected vomiting during the drinking episode while 32 drank on an empty stomach and 41 drank more than originally planned. During the drinking episode 31% subjects described blackouts, 20% described brownouts, and 49% reported no amnesic episode.

A study published in the British Medical Journal on 10 July 2014 investigated the correlation between human variants of the ADH1B gene, which codes for the ADH1B enzyme (Alcohol dehydrogenase 1B), and cardiovascular health. The study concluded that carriers of one specific variant of this gene (A-allele of ADH1B rs1229984), which is associated with lower alcohol consumption, '...had a more favourable cardiovascular profile and a reduced risk of coronary heart disease than those without the genetic variant.' The study's authors extrapolated from this finding to suggest that '...reduction of alcohol consumption, even for light to moderate drinkers, is beneficial to health.'

This study contradicts previous findings on the causal relationship between light alcohol consumption and cardiovascular health, and has been criticized on its methodology by members of the International Scientific Forum on Alcohol Research, which stated in its analysis that '...[there are] questions about making generalized statements about the effects of alcohol on disease based on results from the analysis of a single nucleotide polymorphism of a gene.'

Moreover, the study fails to explain or discount previous findings that show a causal link between alcohol intake and cardiovascular health that can not be accounted for by genetic predisposition alone.

A drug-related blackout is a phenomenon caused by the intake of any substance or medication in which short term and long term memory creation is impaired, therefore causing a complete inability to recall the past. Blackouts are most frequently associated with GABAergic drugs. Blackouts are frequently described as having effects similar to that of anterograde amnesia, in which the subject cannot recall any events after the event that caused amnesia. Research on alcohol blackouts was begun by E. M. Jellinek in the 1940s. Using data from a survey of Alcoholics Anonymous (AA) members, he came to believe that blackouts would be a good determinant of alcoholism. However, there are conflicting views whether this is true. The negative psychological effects of an alcohol-related blackout are often worsened by those who suffer from anxiety disorders. Impairment of the liver will also allow more alcohol to reach the brain and hasten the individual's blackout.

The term "blackout" can also refer to a complete loss of consciousness, or syncope.

The normal human kidney, through suppression of anti-diuretic hormone, is normally able to excrete vast amounts of dilute urine. Thus a normal adult can drink up to 20 liters per day of water without becoming hyponatremic. However, the intake of solutes is also necessary to excrete free water. Under normal circumstances, this is clinically irrelevant. In the lack of proper solute intake, the amount of free water excretion can be severely limited. Without adequate solute intake, the normal functioning electrolyte gradient that pulls water into urine will be effectively destroyed.

Briefly, to excrete free water from urine, the urine flow (which is solute clearance + free water clearance) will equal the rate of solute excretion divided by the urine osmolality. With a diet of only solute poor beer, only about 200-300 mOSM (normal 750 mOSM to greater than 900 mOSM) of solute will be excreted per day, capping the amount of free water excretion at four liters. Any intake above 4 liters would lead to a dilution of the serum sodium concentration and thus hyponatremia.

Any vomiting or GI absorptive problems due to alcohol intoxication can also compound the effect of potomania due to additional electrolyte and acid-base disturbances.

Introduced by a working group from the World Health Organization (WHO) in 1985, WHO diagnostic criteria states that CSE can occur in three stages, organic affective syndrome (type I), mild chronic toxic encephalopathy (type II), and severe chronic toxic encephalopathy (type III). Shortly after, a workshop in Raleigh-Durham, NC (United States) released a second diagnostic criterion which recognizes four stages as symptoms only (type 1), sustained personality or mood swings (type 2A), impairment of intellectual function (type 2B), and dementia (type 3). Though not identical, the WHO and Raleigh criteria are relatively comparable. WHO type I and Raleigh types 1 and 2A are believed to encompass the same stages of CSE, and WHO type II and Raleigh type 2B both involve deficiencies in memory and attention. No other international classifications for CSE have been proposed, and neither the WHO nor Raleigh criteria have been uniformly accepted for epidemiological studies.

Treatment initially may include ketamine or midazolam and haloperidol injected into a muscle to sedate the person. Rapid cooling may be required in those with high body temperature. Other supportive measures such as intravenous fluids and sodium bicarbonate may be useful.

An alcohol enema, also known colloquially as butt-chugging, is the act of introducing alcohol into the rectum and colon via the anus. This method of alcohol consumption can be dangerous and even deadly because it leads to faster intoxication since the alcohol is absorbed directly into the bloodstream and neutralizes the body's ability to reject the toxin by vomiting.