Acute alcohol poisoning is a related medical term used to indicate a dangerously high concentration of alcohol in the blood, high enough to induce coma, respiratory depression, or even death. It is considered a medical emergency. The term is mostly used by healthcare providers. Toxicologists use the term "alcohol intoxication" to discriminate between alcohol and other toxins.

The signs and symptoms of acute alcohol poisoning include:

- severe confusion, unpredictable behavior and stupor

- sudden lapses into and out of unconsciousness or semi-consciousness (with later alcoholic amnesia)

- vomiting while unconscious or semi-conscious

- seizures

- respiratory depression (fewer than eight breaths a minute)

- pale, bluish, cold and clammy skin due to insufficient oxygen

Alcohol intoxication, also known as drunkenness among other names, is a physiological condition that may result in psychological alterations of consciousness. Drunkenness is induced by the ingestion or consumption of alcohol in a living body. Alcohol intoxication is the result of alcohol entering the bloodstream faster than it can be metabolized by the body. Metabolism results in breaking down the ethanol into non-intoxicating byproducts.

Some effects of alcohol intoxication, such as euphoria and lowered social inhibition, are central to alcohol's desirability as a beverage and its history as one of the world's most widespread recreational drugs. Despite this widespread use and alcohol's legality in most countries, many medical sources tend to describe any level of alcohol intoxication as a form of poisoning due to ethanol's damaging effects on the body in large doses. Some religions consider alcohol intoxication to be a sin.

Symptoms of alcohol intoxication include euphoria, flushed skin, and decreased social inhibition at lower doses, with larger doses producing progressively severe impairments of balance, and decision-making ability as well as nausea or vomiting from alcohol's disruptive effect on the semicircular canals of the inner ear and chemical irritation of the gastric mucosa.

Sufficiently extreme levels of blood-borne alcohol may result in coma or death.

Different concentrations of alcohol in the human body have different effects on the subject.

The following lists the common effects of alcohol on the body, depending on the blood alcohol concentration (BAC). However, tolerance varies considerably between individuals, as does individual response to a given dosage; the effects of alcohol differ widely between people. Hence, BAC percentages are just estimates used for illustrative purposes.

- Euphoria (BAC = 0.03% to 0.12%):

- Overall improvement in mood and possible euphoria

- Increased self-confidence

- Increased sociability

- Decreased anxiety

- Shortened attention span

- Flushed appearance

- Impaired judgment

- Impaired fine muscle coordination

- Lethargy (BAC = 0.09% to 0.25%)

- Sedation

- Impaired memory and comprehension

- Delayed reactions

- Ataxia; balance difficulty; unbalanced walk

- Blurred vision; other senses may be impaired

- Confusion (BAC = 0.18% to 0.30%)

- Profound confusion

- Impaired senses

- Analgesia

- Increased ataxia; impaired speech; staggering

- Dizziness often associated with nausea ("the spins")

- Vomiting (emesis)

- Stupor (BAC = 0.25% to 0.40%)

- Severe ataxia

- Lapses in and out of consciousness

- Unconsciousness

- Anterograde amnesia

- Vomiting (death may occur due to inhalation of vomit (pulmonary aspiration) while unconscious)

- Respiratory depression (potentially life-threatening)

- Decreased heart rate (usually results in coldness and/or numbness of the limbs)

- Urinary incontinence

- Coma (BAC = 0.35% to 0.80%)

- Unconsciousness (coma)

- Depressed reflexes (i.e., pupils do not respond appropriately to changes in light)

- Marked and life-threatening respiratory depression

- Markedly decreased heart rate

- Most deaths from alcohol poisoning are caused by dosage levels in this range.

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.

Dipsomania is a historical term describing a medical condition involving an uncontrollable craving for alcohol. In the 19th century, the term dipsomania was used to refer to a variety of alcohol-related problems, most of which are known today as alcoholism. Dipsomania is occasionally still used to describe a particular condition of periodic, compulsive bouts of alcohol intake. The idea of dipsomania is important for its historical role in promoting a disease theory of chronic drunkenness. The word comes from Greek "dipso" ("δίψα"= thirst) and "mania".

It is still mentioned in the WHO ICD-10 classification as an alternative description for Alcohol Dependence Syndrome, episodic use F10.26

Long-term misuse of alcohol can cause a wide range of mental health problems. Severe cognitive problems are common; approximately 10 percent of all dementia cases are related to alcohol consumption, making it the second leading cause of dementia. Excessive alcohol use causes damage to brain function, and psychological health can be increasingly affected over time. Social skills are significantly impaired in people suffering from alcoholism due to the neurotoxic effects of alcohol on the brain, especially the prefrontal cortex area of the brain. The social skills that are impaired by alcohol abuse include impairments in perceiving facial emotions, prosody perception problems and theory of mind deficits; the ability to understand humour is also impaired in alcohol abusers. Psychiatric disorders are common in alcoholics, with as many as 25 percent suffering severe psychiatric disturbances. The most prevalent psychiatric symptoms are anxiety and depression disorders. Psychiatric symptoms usually initially worsen during alcohol withdrawal, but typically improve or disappear with continued abstinence. Psychosis, confusion, and organic brain syndrome may be caused by alcohol misuse, which can lead to a misdiagnosis such as schizophrenia. Panic disorder can develop or worsen as a direct result of long-term alcohol misuse.

The co-occurrence of major depressive disorder and alcoholism is well documented. Among those with comorbid occurrences, a distinction is commonly made between depressive episodes that remit with alcohol abstinence ("substance-induced"), and depressive episodes that are primary and do not remit with abstinence ("independent" episodes). Additional use of other drugs may increase the risk of depression. Psychiatric disorders differ depending on gender. Women who have alcohol-use disorders often have a co-occurring psychiatric diagnosis such as major depression, anxiety, panic disorder, bulimia, post-traumatic stress disorder (PTSD), or borderline personality disorder. Men with alcohol-use disorders more often have a co-occurring diagnosis of narcissistic or antisocial personality disorder, bipolar disorder, schizophrenia, impulse disorders or attention deficit/hyperactivity disorder (ADHD). Women with alcoholism are more likely to experience physical or sexual assault, abuse and domestic violence than women in the general population, which can lead to higher instances of psychiatric disorders and greater dependence on alcohol.

Warning signs of alcoholism include the consumption of increasing amounts of alcohol and frequent intoxication, preoccupation with drinking to the exclusion of other activities, promises to quit drinking and failure to keep those promises, the inability to remember what was said or done while drinking (colloquially known as "blackouts"), personality changes associated with drinking, denial or the making of excuses for drinking, the refusal to admit excessive drinking, dysfunction or other problems at work or school, the loss of interest in personal appearance or hygiene, marital and economic problems, and the complaint of poor health, with loss of appetite, respiratory infections, or increased anxiety.

Symptoms can sometimes come and go with wave-like reoccurrences or fluctuations in severity of symptoms. Common symptoms include impaired cognition, irritability, depressed mood, and anxiety; all of which may reach severe levels which can lead to relapse.

The protracted withdrawal syndrome from benzodiazepines can produce symptoms identical to generalized anxiety disorder as well as panic disorder. Due to the sometimes prolonged nature and severity of benzodiazepine withdrawal, abrupt withdrawal is not advised.

Common symptoms of post-acute withdrawal syndrome are:

- Psychosocial dysfunction

- Anhedonia

- Depression

- Impaired interpersonal skills

- Obsessive-compulsive behaviour

- Feelings of guilt

- Autonomic disturbances

- Pessimistic thoughts

- Impaired concentration

- Lack of initiative

- Craving

- Inability to think clearly

- Memory problems

- Emotional overreactions or numbness

- Sleep disturbances

- Physical coordination problems

- Stress sensitivity

- Increased sensitivity to pain

- Panic disorder

- Generalized anxiety disorder

- Sleep disturbance (dreams of using, behaviors associated with the life style)

Symptoms occur intermittently, but are not always present. They are made worse by stress or other triggers and may arise at unexpected times and for no apparent reason. They may last for a short while or longer. Any of the following may trigger a temporary return or worsening of the symptoms of post-acute withdrawal syndrome:

- Stressful and/or frustrating situations

- Multitasking

- Feelings of anxiety, fearfulness or anger

- Social conflicts

- Unrealistic expectations of oneself

Post-acute-withdrawal syndrome (PAWS), or the terms post-withdrawal syndrome, protracted withdrawal syndrome, prolonged withdrawal syndromes describe a set of persistent impairments that occur after withdrawal from alcohol, opiates, benzodiazepines, antidepressants and other substances. Infants born to mothers who used substances of dependence during pregnancy may also experience a post-acute withdrawal syndrome.

While post-acute withdrawal syndrome has been reported by those in the recovery community, there have been few scientific studies supporting its existence. Because of this, the disorder is not recognized by the "Diagnostic and Statistical Manual of Mental Disorders" or major medical associations.

Drug abuse, including alcohol and prescription drugs, can induce symptomatology which resembles mental illness. This can occur both in the intoxicated state and during the withdrawal state. In some cases these substance-induced psychiatric disorders can persist long after detoxification, such as prolonged psychosis or depression after amphetamine or cocaine abuse. A protracted withdrawal syndrome can also occur with symptoms persisting for months after cessation of use. Benzodiazepines are the most notable drug for inducing prolonged withdrawal effects with symptoms sometimes persisting for years after cessation of use. Severe anxiety and depression are commonly induced by sustained alcohol abuse which in most cases abates with prolonged abstinence. Even moderate, sustained alcohol use may increase anxiety and depression levels in some individuals. In most cases these drug-induced psychiatric disorders fade away with prolonged abstinence.

Alcohol tolerance refers to the bodily responses to the functional effects of ethanol in alcoholic beverages. This includes direct tolerance, speed of recovery from insobriety and resistance to the development of alcoholism.

Acute mercury exposure has given rise to psychotic reactions such as delirium, hallucinations, and suicidal tendency. Occupational exposure has resulted in erethism, with irritability, excitability, excessive shyness, and insomnia as the principal features of a broad-ranging functional disturbance. With continuing exposure, a fine tremor develops, initially involving the hands and later spreading to the eyelids, lips, and tongue, causing violent muscular spasms in the most severe cases. The tremor is reflected in the handwriting which has a characteristic appearance. In milder cases, erethism and tremor regress slowly over a period of years following removal from exposure. Decreased nerve conduction velocity in mercury-exposed workers has been demonstrated. Long-term, low-level exposure has been found to be associated with less pronounced symptoms of erethism, characterized by fatigue, irritability, loss of memory, vivid dreams, and depression (WHO, 1976).

Effects of chronic occupational exposure to mercury, such as that commonly experienced by affected hatters, include mental confusion, emotional disturbances, and muscular weakness. Severe neurological damage and kidney damage can also occur. Neurological effects include Korsakoff's dementia and erethism (the set of neurological symptoms characteristically associated with mercury poisoning). Signs and symptoms can include red fingers, red toes, red cheeks, sweating, loss of hearing, bleeding from the ears and mouth, loss of appendages such as teeth, hair, and nails, lack of coordination, poor memory, shyness, insomnia, nervousness, tremors, and dizziness. A survey of exposed U.S. hatters revealed predominantly neurological symptomatology, including intention tremor. After chronic exposure to the mercury vapours, hatters tended to develop characteristic psychological traits, such as pathological shyness and marked irritability (box). Such manifestations among hatters prompted several popular names for erethism, including "mad hatter disease", "mad hatter syndrome", "hatter's shakes" and "Danbury shakes".

Erethism or erethism mercurialis is a neurological disorder which affects the whole central nervous system, as well as a symptom complex derived from mercury poisoning. This is also sometimes known as the mad hatter disease. Historically, this was common among old England felt-hatmakers who used mercury to stabilize the wool in a process called felting, where hair was cut from a pelt of an animal such as a rabbit. The industrial workers were exposed to the mercury vapors, giving rise to the expression “mad as a hatter.” Some believe that the character the Mad Hatter in Lewis Carroll's Alice in Wonderland is an example of someone suffering from erethism, but the origin of this account is unclear. The character was almost certainly based on Theophilus Carter, an eccentric furniture dealer who was well known to Carroll.

Mad hatter disease, or mad hatter syndrome, was an occupational disease among hatmakers, caused by chronic mercury poisoning. It affected those whose felting work involved prolonged exposure to mercury vapors. The neurotoxic effects included tremor and the pathological shyness and irritability characteristic of erethism.

Erethism is due to mercury poisoning. Mercury is an element that is found all over the earth in soil, rocks, and water. People who get erethism are usually exposed to jobs that have something to do with these elements, such as construction. People who work in factory jobs tend to have a higher chance of getting erethism. The problem with mercury is that if humans are exposed to any of the forms of mercury, depending on the amount (dose), route (ingestion, skin contact, inhalation), duration (time) of exposure, it can be toxic. Some elemental and chemical forms of mercury (vapor, methylmercury, inorganic mercury) are more toxic than other forms. The human fetus and medically compromised people (for example, patients with lung or kidney problems) are the most susceptible to the toxic effects of mercury.

It is commonly characterized through behavioral changes such as irritability, low self-confidence, depression, apathy, shyness and timidity, and in some extreme cases with prolonged exposure to mercury vapors, delirium, personality changes and memory loss occur as a result. People with erethism find it difficult to interact socially with others, with behaviors similar to that of a social phobia. Although most of the effects of erethism are neurological, some physical problems arise as well, including a decrease in physical strength, “headaches, general pain, and tremors after exposure to metallic mercury” as well as irregular heartbeat. It has been documented that “the tremor in the hands can be so severe that the victim is unable to hold a glass of water without spilling its contents.”

The primary risk factor for erethism is long-term exposure to mercury vapors and gasses at high levels. One group at risk for mercury poisoning is industrial workers and those exposed to high levels of mercury residing naturally in the environment. Erethism is not as serious an issue as it was back before acceptable working condition regulations were enforced. Preventing mercury levels from getting too high limits the amount available for inhalation.

There is a risk of mercury poisoning in the home in some cases. Exposure to mercury vapor may stem from cultural and religious reasons where mercury is sprinkled on the floor of a home or car, burned in a candle, or mixed with perfume. Due to widespread use and popular concern, the risk of toxicity from dental amalgam has been exhaustively investigated. Many studies have not revealed convincing evidence of toxicity . However, in 2015 research showed that an increased mercury release from dental amalgam restorations after exposure to electromagnetic fields is a potential hazard for hypersensitive people and pregnant women.

Alcohol tolerance is increased by regular drinking. This reduced sensitivity requires that higher quantities of alcohol be consumed in order to achieve the same effects as before tolerance was established. Alcohol tolerance may lead to (or be a sign of) alcohol dependency.

Heavy alcohol consumption over a period of years can lead to "reverse tolerance". A liver can be damaged by chronic alcohol use, leading to a buildup of fat and scar tissue. The reduced ability of such a liver to metabolize or break down alcohol means that small amounts can lead to a high blood alcohol concentration (BAC) and more rapid intoxication.

The acute porphyrias are acute intermittent porphyria (AIP), variegate porphyria (VP), aminolevulinic acid dehydratase deficiency porphyria (ALAD) and hereditary coproporphyria (HCP). These diseases primarily affect the nervous system, resulting in episodic crises known as acute attacks. The major symptom of an acute attack is abdominal pain, often accompanied by vomiting, hypertension (elevated blood pressure), and tachycardia (an abnormally rapid heart rate). The most severe episodes may involve neurological complications: typically motor neuropathy (severe dysfunction of the peripheral nerves that innervate muscle), which leads to muscle weakness and potentially to quadriplegia (paralysis of all four limbs) and central nervous system symptoms such as seizures and coma. Occasionally, there may be short-lived psychiatric symptoms such as anxiety, confusion, hallucinations, and, very rarely, overt psychosis. All these symptoms resolve once the acute attack passes. Porphyria is not a cause of chronic psychiatric illness, though an association with anxiety and depression has been suggested.

Given the many presentations and the relatively low occurrence of porphyria, patients may initially be suspected to have other, unrelated conditions. For instance, the polyneuropathy of acute porphyria may be mistaken for Guillain–Barré syndrome, and porphyria testing is commonly recommended in those situations.

Acute porphyria can be triggered by a number of drugs, most of which are believed to trigger it by interacting with enzymes in the liver which are made with heme. Such drugs include:

- Sulfonamides, including sulfadiazine, sulfasalazine and trimethoprim/sulfamethoxazole.

- Sulfonylureas like glibenclamide, gliclazide and glimepiride, although glipizide is thought to be safe.

- Barbiturates including thiopental, phenobarbital, primidone, etc.

- Systemic treatment with antifungals including fluconazole, griseofulvin, ketoconazole and voriconazole. (Topical use of these agents is thought to be safe due to minimal systemic absorption.)

- Some anesthetics like ketamine and etomidate.

- Certain antibiotics like rifapentine, rifampicin, rifabutine, isoniazid, nitrofurantoin and, possibly, metronidazole.

- Ergot derivatives including dihydroergotamine, ergometrine, ergotamine, methysergide, etc.

- Certain antiretroviral medications (e.g. indinavir, nevirapine, ritonavir, saquinavir, etc.)

- Progesterones

- Some anticonvulsants including: carbamazepine, ethosuximide, phenytoin, topiramate, valproate.

- Some painkillers like dextropropoxyphene, ketorolac, metamizole, pentazocine

- Some cancer treatments like bexarotene, busulfan, chlorambucil, estramustine, etoposide, flutamide, idarubicin, ifosfamide, irinotecan, ixabepilone, letrozole, lomustine, megestrol, mitomycin, mitoxantrone, paclitaxel, procarbazine, tamoxifen, topotecan

- Some antidepressants like imipramine, phenelzine, trazodone

- Some antipsychotics like risperidone, ziprasidone

- Some retinoids used for skin conditions like acitretin and isotretinoin

- Miscellaneous others including: cocaine, methyldopa, fenfluramine, disulfiram, orphenadrine, pentoxifylline, sodium aurothiomalate, etc.

The term was coined by the German physician C. W. Hufeland in 1819, when, in a preface to an influential book by German-Russian doctor C. von Brühl-Cramer, he translated Brühl-Cramer's term ""trunksucht"" as "dipsomania".

Due to the influence of Brühl-Cramer's pioneering work, dipsomania became popular in medical circles throughout the 19th century. Political scientist Mariana Valverde describes dipsomania as "the most medical" of the many terms used to describe habitual drunkenness in the 19th century. Along with terms such as "inebriety", the idea of dipsomania was used as part of an effort of medical professionals and reformers to change attitudes about habitual drunkenness from being a criminally punishable vice to being a medically treatable disease. As historian Roy MacLeod wrote about this dipsomania reform movement, it "illuminates certain features of the gradual transformation taking place in national attitudes towards the prevention and cure of social illnesses during the last quarter of the 19th century."

Although "dipsomania" was used in a variety of somewhat contradictory ways by different individuals, by the late 19th century the term was usually used to describe a periodic or acute condition, in contrast to chronic drunkenness. In his 1893 book "Clinical Lessons on Mental Diseases: The Mental State of Dipsomania", Magnan characterized dipsomania as a crisis lasting from one day to two weeks, and consisting of a rapid and huge ingestion of alcohol or whatever other strong, excitatory liquid was available. Magnan further described dipsomania as solitary alcohol abuse, with loss of all other interests, and these crises recurred at indeterminate intervals, separated by periods when the subject was generally sober.

Over time, the term dipsomania became less common, replaced by newer ideas and terms concerning chronic and acute drunkenness and alcoholism.

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms. Specific manifestations vary by age and by the severity of the hypoglycemia. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person do tend to be similar from episode to episode.

In the large majority of cases, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.

A rare metabolic disease of the blood-brain glucose transport system has been described in which severe neuroglycopenic effects occurred despite normal blood glucose levels. Low levels of glucose were discovered in the cerebrospinal fluid (CSF), a condition referred to as "hypoglycorrhachia" [or hypoglycorrhacia].

Hypoglycorrhachia is associated with Glucose transporter type 1 GLUT1 deficiency syndrome (GLUT1DS).

Perhaps a much more common example of the same phenomenon occurs in the people with poorly controlled type 1 diabetes who develop symptoms of hypoglycemia at levels of blood glucose which are normal for most people.

Acute uric acid nephropathy (AUAN) due to hyperuricosuria has been a dominant cause of acute kidney failure but with the advent of effective treatments for hyperuricosuria, AUAN has become a less common cause than hyperphosphatemia. Two common conditions related to excess uric acid, gout and uric acid nephrolithiasis, are not features of tumor lysis syndrome.

Tumor lysis syndrome (TLS) is a group of metabolic abnormalities that can occur as a complication during the treatment of cancer, where large amounts of tumor cells are killed off (lysed) at the same time by the treatment, releasing their contents into the bloodstream. This occurs most commonly after the treatment of lymphomas and leukemias. In oncology and hematology, this is a potentially fatal complication, and patients at increased risk for TLS should be closely monitored before, during, and after their course of chemotherapy.

Tumor lysis syndrome is characterized by high blood potassium (hyperkalemia), high blood phosphorus (hyperphosphatemia), low blood calcium (hypocalcemia), high blood uric acid (hyperuricemia), and higher than normal levels of blood urea nitrogen (BUN) and other nitrogen-containing compounds (azotemia). These changes in blood electrolytes and metabolites are a result of the release of cellular contents of dying cells into the bloodstream from breakdown of cells. In this respect, TLS is analogous to rhabdomyolysis, with comparable mechanism and blood chemistry effects but with different cause. In TLS, the breakdown occurs after cytotoxic therapy or from cancers with high cell turnover and tumor proliferation rates. The metabolic abnormalities seen in tumor lysis syndrome can ultimately result in nausea and vomiting, but more seriously acute uric acid nephropathy, acute kidney failure, seizures, cardiac arrhythmias, and death.

Clinically, patients affected with HCP present similarly to those with other acute porphyrias, such as acute intermittent porphyria (AIP) and variegate porphyria (VP). Patients with HCP and VP can present with symptoms shared between the acute and cutaneous porphyrias. This includes the acute attacks of abdominal pain, nausea, vomiting, diarrhea, tachycardia, hypertension and seizures, as well as the cutaneous findings seen in porphyria cutanea tarda (PCT), namely increased skin fragility, bullous lesions after exposure to sunlight and increased scarring.

Individuals with HCP may be asymptomatic in the absence of triggering factors. Common triggers include certain drugs, alcohol, hormonal changes, and dietary changes. Sunlight and other ultraviolet light can trigger the skin manifestations. Homozygous individuals for "CPOX" mutations can present with these findings at an earlier age than heterozygotes.

Due to its perception-altering effects, the onset of narcosis may be hard to recognize. At its most benign, narcosis results in relief of anxiety – a feeling of tranquility and mastery of the environment. These effects are essentially identical to various concentrations of nitrous oxide. They also resemble (though not as closely) the effects of alcohol or cannabis and the familiar benzodiazepine drugs such as diazepam and alprazolam. Such effects are not harmful unless they cause some immediate danger to go unrecognized and unaddressed. Once stabilized, the effects generally remain the same at a given depth, only worsening if the diver ventures deeper.

The most dangerous aspects of narcosis are the impairment of judgement, multi-tasking and coordination, and the loss of decision-making ability and focus. Other effects include vertigo and visual or auditory disturbances. The syndrome may cause exhilaration, giddiness, extreme anxiety, depression, or paranoia, depending on the individual diver and the diver's medical or personal history. When more serious, the diver may feel overconfident, disregarding normal safe diving practices. Slowed mental activity, as indicated by increased reaction time and increased errors in cognitive function, are effects which increase the risk of a diver mismanaging an incident. Narcosis reduces both the perception of cold discomfort and shivering and thereby affects the production of body heat and consequently allows a faster drop in the core temperature in cold water, with reduced awareness of the developing problem.

The relation of depth to narcosis is sometimes informally known as "Martini's law", the idea that narcosis results in the feeling of one martini for every below depth. Professional divers use such a calculation only as a rough guide to give new divers a metaphor, comparing a situation they may be more familiar with.

Reported signs and symptoms are summarized against typical depths in meters and feet of sea water in the following table, closely adapted from "Deeper into Diving" by Lippman and Mitchell:

Generally associated with exposure to beryllium levels at or above 100 μg/m, it produces severe cough, sore nose and throat, weight loss, labored breathing, anorexia, and increased fatigue.

In addition to beryllium's toxicity when inhaled, when brought into contact with skin at relatively low doses, beryllium can cause local irritation and contact dermatitis, and contact with skin that has been scraped or cut may cause rashes or ulcers. Beryllium dust or powder can irritate the eyes.

Acute hyperuricosuria is a common complication of tumor lysis syndrome. This syndrome appears not to contribute to gout and to uric acid nephrolithiasis, which is evidence that these two conditions have chronic, not acute, causes.

Chronic hyperuricosuria is associated with gout and uric acid nephrolithiasis. However, both conditions can occur in the absence of hyperuricosuria. Treatment of gout with uricosuric drugs can lead to uric acid nephrolithiasis.

Narcosis results from breathing gases under elevated pressure, and may be classified by the principal gas involved. The noble gases, except helium and probably neon, as well as nitrogen, oxygen and hydrogen cause a decrement in mental function, but their effect on psychomotor function (processes affecting the coordination of sensory or cognitive processes and motor activity) varies widely. The effects of carbon dioxide consistently result in a diminution of mental and psychomotor function. The noble gases argon, krypton, and xenon are more narcotic than nitrogen at a given pressure, and xenon has so much anesthetic activity that it is a usable anesthetic at 80% concentration and normal atmospheric pressure. Xenon has historically been too expensive to be used very much in practice, but it has been successfully used for surgical operations, and xenon anesthesia systems are still being proposed and designed.