Multiple guidelines recommend that delirium should be diagnosed when it presents to healthcare services. Much evidence suggest, however, that delirium is greatly underdiagnosed. Higher rates of detection of delirium in general settings (for the ICU see below) can be assisted by the use of validated delirium screening tools. Many such tools have been published. They differ in duration, complexity, need for training, and so on. Examples of tools in use in clinical practice are: Delirium Observation Screening Scale, the Nursing Delirium Screening Scale (Nu-DESC), the Confusion Assessment Method, the Recognizing Acute Delirium As part of your Routine (RADAR) tool and the 4 "A"s Test or 4AT.

In the ICU, international guidelines recommend that every patient gets checked for delirium every day (usually twice or more a day) using a validated clinical tool. The two most widely used are the Confusion Assessment Method for the ICU (CAM-ICU) and the Intensive Care Delirium Screening Checklist (ICDSC). There are translations of these tools in over 20 languages and they are used globally in many thousands of ICUs, and instructional videos and myriad implementation tips are available. It is not as important which tool is used as that the patient gets monitored. Without using one of these tools, 75% of ICU delirium is missed by the practicing team, which leaves the patient without any likely active interventions to help reduce the duration of his/her delirium.

The most salient component of the definition of delirium that nurses and other healthcare professionals use at the bedside is whether or not the patient can pay attention and follow simple commands (see videos and literature). The advent of daily monitoring for delirium, made easy by the CAM-ICU and other assessment tools, as well as proper documentation, had led to important changes in the culture of ICUs and rounds in that the entire team can now discuss the brain and how it is doing in terms of being “on” (not delirious) or “off” (delirious) and then focus on the several most likely causes of delirium in any specific patient. Thus, it is not the monitoring itself that changes the patient’s clinical course, but rather it is this combination of monitoring and then relaying the information on rounds in the ICU that makes such a huge difference in awareness of this form of organ dysfunction and then enables a difference to be made in clinical outcomes.

Diagnosis is mainly based on symptoms. In a person with delirium tremens it is important to rule out other associated problems such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.

Other medical conditions that can resemble excited delirium are panic attack, hyperthermia, diabetes, head injury, delirium tremens, and hyperthyroidism.

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.

Delirium tremens due to alcohol withdrawal can be treated with benzodiazepines. High doses may be necessary to prevent death. Amounts given are based on the symptoms. Typically the person is kept sedated with benzodiazepines, such as diazepam, lorazepam, chlordiazepoxide, or oxazepam.

In some cases antipsychotics, such as haloperidol may also be used. Older drugs such as paraldehyde and clomethiazole were formerly the traditional treatment but have now largely been superseded by the benzodiazepines.

Acamprosate is occasionally used in addition to other treatments, and is then carried on into long term use to reduce the risk of relapse. If status epilepticus occurs it is treated in the usual way. It can also be helpful to control environmental stimuli, by providing a well-lit but relaxing environment for minimizing distress and visual hallucinations.

Alcoholic beverages can also be prescribed as a treatment for delirium tremens, but this practice is not universally supported.

High doses of thiamine often by the intravenous route is also recommended.

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.

There is limited evidence that caffeine, in high doses or when chronically abused, may induce psychosis in normal individuals and worsen pre-existing psychosis in those diagnosed with schizophrenia.

According to the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th Edition), Cotard delusion falls under the category of somatic delusions, those that involve bodily functions or sensations. (Citation needed. DSM-5 does not specifically reference Cotard syndrome.)

There are no further diagnostic criteria for Cotard syndrome within the DSM-5, and identification of the syndrome relies heavily on clinical interpretation.

Cotard delusion should not be confused with Delusional Disorders as defined by the DSM-5, which involve a different spectrum of symptoms that are less severe and have lesser detrimental effect on functioning.

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.

Definitions vary, but currently it is defined as one continuous, unremitting seizure lasting longer than five minutes, or recurrent seizures without regaining consciousness between seizures for greater than five minutes. Previous definitions used a 30-minute time limit.

NCSE is believed to be under-diagnosed.

Treatment consists of supportive care during the acute intoxication phase: maintaining hydration, body temperature, blood pressure, and heart rate at acceptable levels until the drug is sufficiently metabolized to allow vital signs to return to baseline. Typical and atypical antipsychotics have been shown to be helpful in the early stages of treatment. This is followed by abstinence from psychostimulants supported with counseling or medication designed to assist the individual preventing a relapse and the resumption of a psychotic state.

The article "Cotard's syndrome: A Review" (2010) reports successful pharmacological treatments (mono-therapeutic and multi-therapeutic) using antidepressant, antipsychotic, and mood stabilizing drugs; likewise, with the depressed patient, electroconvulsive therapy (ECT) is more effective than pharmacotherapy. Cotard syndrome resulting from an adverse drug reaction to valacyclovir is attributed to elevated serum concentration of one of valacyclovir's metabolites, 9-carboxymethoxymethylguanine (CMMG). Successful treatment warrants cessation of the drug, valacyclovir. Hemodialysis was associated with timely clearance of CMMG and resolution of symptoms.

Many hospitals use the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol in order to assess the level of withdrawal present and therefore the amount of medication needed. When overuse of alcohol is suspected but drinking history is unclear, testing for elevated values of carbohydrate-deficient transferrin or gammaglutamyl transferase can help make the diagnosis of alcohol overuse and dependence more clear. The CIWA has also been shortened (now called the CIWA-Ar), while retaining its validity and reliability, to help assess patients more efficiently due to the life-threatening nature of alcohol withdrawal.

Other conditions that may present similarly include benzodiazepine withdrawal syndrome (a condition also mainly caused by GABA receptor adaptation).

Benzodiazepines are the preferred initial treatment after which typically phenytoin is given. First aid guidelines for seizures state that, as a rule, an ambulance should be called for seizures lasting longer than five minutes (or sooner if this is the person's first seizure episode and no precipitating factors are known, or if SE happens to a person with epilepsy whose seizures were previously absent or well controlled for a considerable time period).

Benzodiazepines are effective for the management of symptoms as well as the prevention of seizures. Certain vitamins are also an important part of the management of alcohol withdrawal syndrome. In those with severe symptoms inpatient care is often required. In those with lesser symptoms treatment at home may be possible with daily visits with a health care provider.

The symptoms of an anticholinergic toxidrome include blurred vision, coma, decreased bowel sounds, delirium, dry skin, fever, flushing, hallucinations, ileus, memory loss, mydriasis (dilated pupils), myoclonus, psychosis, seizures, and urinary retention. Complications include hypertension, hyperthermia, and tachycardia. Substances that may cause this toxidrome include the four "anti"s of antihistamines, antipsychotics, antidepressants, and antiparkinsonian drugs as well as atropine, benztropine, datura, and scopolamine.

Due to the characteristic appearance and behavior of patients with this toxidrome, they are colloquially described as "Blind as a bat, mad as a hatter, red as a beet, hot as Hades (or hot as a hare), dry as a bone, the bowel and bladder lose their tone, and the heart runs alone."

The symptoms of an opiate toxidrome include the classic triad of coma, pinpoint pupils, and respiratory depression as well as altered mental states, shock, pulmonary edema and unresponsiveness. Complications include bradycardia, hypotension, and hypothermia. Substances that may cause this toxidrome are opioids.

Psychomotor agitation is a set of signs and symptoms that stem from mental tension and anxiety. The signs are unintentional and purposeless motions; the symptoms are emotional distress and restlessness. Typical manifestations include pacing around a room, wringing the hands, uncontrolled tongue movement, pulling off clothing and putting it back on, and other similar actions. In more severe cases, the motions may become harmful to the individual, such as ripping, tearing, or chewing at the skin around one's fingernails, lips, or other body parts to the point of bleeding. Psychomotor agitation is typically found in major depressive disorder or obsessive-compulsive disorder, and sometimes the manic phase in bipolar disorder, though it can also be a result of an excess intake of stimulants. It can also be caused by severe hyponatremia. The middle-aged and the elderly are more at risk to express it.

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.

The condition is rare, with only 80 established cases reported in medical literature and incomplete evidence of a further 200.

If the symptoms of alcohol dementia are caught early enough, the effects may be reversed. The person must stop drinking and start on a healthy diet, replacing the lost vitamins, including, but not limited to, thiamine. Recovery is more easily achievable for women than men, but in all cases it is necessary that they have the support of family and friends and abstain from alcohol.

The existence of alcohol-related dementia is widely acknowledged but not often used as a diagnosis, due to a lack of widely accepted, non-subjective diagnostic criteria; more research is needed. Criteria for alcohol-induced persistent dementia in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) include the following:

There are problems with DSM diagnostic criteria, however. Firstly, they are vague and subjective. Furthermore, the criteria for diagnosis of dementia were inspired by the clinical presentation of Alzheimer's disease and are poorly adapted to the diagnosis of other dementias. This has led to efforts to develop better diagnostic models.

Oslin (Int J Geriatr Psychiatry 1998) proposed alternative clinical diagnostic criteria which were validated. The criteria include a clinical diagnosis of dementia at least 60 days after last exposure to alcohol, significant alcohol use (i.e. minimum 35 standard drinks/week for males and 28 for women) for more than 5 years, and significant alcohol use occurring within 3 years of the initial onset of cognitive deficits. Oslin proposed the new and refined diagnostic criteria for Alcohol Related Dementia because he hoped that the redefined classification system would bring more awareness and clarity to the relationship between alcohol use and dementia.

Oslin's proposed classification of ARD:

- "Definite" Alcohol Related Dementia

At the current time there are no acceptable criteria to definitively define Alcohol Related Dementia.

- "Probable" Alcohol Related Dementia

Intramuscular midazolam, lorazepam, or another benzodiazepine can be used to both sedate agitated patients, and control semi-involuntary muscle movements in cases of suspected akathisia.

Droperidol, haloperidol, or other typical antipsychotics can decrease the duration of agitation caused by acute psychosis, but should be avoided if the agitation is suspected to be akathisia, which can be potentially worsened. Also using promethazine may be useful.

In those with psychosis causing agitation there is a lack of support for the use of benzodiazepines, although they can prevent side effects associated with dopamine antagonists.

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.