Most drowning is preventable. It has been estimated that more than 85% of drownings could have been prevented by supervision, training in water skills, technology, regulation and public education.

Many pools and designated bathing areas either have lifeguards, a pool safety camera system for local or remote monitoring, or computer-aided drowning detection. However, bystanders play an important role in drowning detection and either intervention or the notification of authorities by phone or alarm.

The acronym "RID" was originated by Frank Pia to summarize important reasons why lifeguards may be unaware of a drowning. The term stands for "failure to recognize the struggle, the intrusion of non-lifeguard duties upon lifeguards' primary task-preventive lifeguarding, and the distraction from surveillance duties". In his paper on the RID factors, Pia makes a number of observations on the role, and the required behavior and training of lifeguards, as well as the importance of administrators directing lifeguards to this role and avoiding double tasking them (due to the very brief time of 20 – 60 seconds required for drowning to occur). He ended by summarizing the role of lifeguards as guardians of life, and that they should be directed exclusively to this duty and none other, while on surveillance, due to the high value placed on human life.

Accurate determination of core temperature often requires a special low temperature thermometer, as most clinical thermometers do not measure accurately below . A low temperature thermometer can be placed in the rectum, esophagus or bladder. Esophageal measurements are the most accurate and are recommended once a person is intubated. Other methods of measurement such as in the mouth, under the arm, or using an infrared ear thermometer are often not accurate.

As a hypothermic person's heart rate may be very slow, prolonged feeling for a pulse could be required before detecting. In 2005, the American Heart Association recommended at least 30–45 seconds to verify the absence of a pulse before initiating CPR. Others recommend a 60-second check.

The classical ECG finding of hypothermia is the Osborn J wave. Also, ventricular fibrillation frequently occurs below and asystole below . The Osborn J may look very similar to those of an acute ST elevation myocardial infarction. Thrombolysis as a reaction to the presence of Osborn J waves is not indicated, as it would only worsen the underlying coagulopathy caused by hypothermia.

It is usually recommended not to declare a person dead until their body is warmed to a near normal body temperature of greater than , since extreme hypothermia can suppress heart and brain function. Exceptions include if there is an obvious fatal injuries or the chest is frozen so that it cannot be compressed. If a person was buried in an avalanche for more than 35 minutes and is found with a mouth packed full of snow without a pulse, stopping early may also be reasonable. This is also the case if a person's blood potassium is greater than 12 mmol/l.

Those who are stiff with pupils that do not move may survive if treated aggressively. Survival with good function also occasionally occurs even after the need for hours of CPR. Children who have near-drowning accidents in water near can occasionally be revived, even over an hour after losing consciousness. The cold water lowers the metabolism, allowing the brain to withstand a much longer period of hypoxia. While survival is possible, mortality from severe or profound hypothermia remains high despite optimal treatment. Studies estimate mortality at between 38% and 75%.

In those who have hypothermia due to another underlying health problem, when death occurs it is frequently from that underlying health problem.

When an unconscious patient enters a hospital, the hospital utilizes a series of diagnostic steps to identify the cause of unconsciousness. According to Young, the following steps should be taken when dealing with a patient possibly in a coma:

1. Perform a general examination and medical history check

2. Make sure the patient is in an actual comatose state and or is not in locked-in state (patient is either able to voluntarily move their eyes or blink) or psychogenic unresponsiveness (caloric stimulation of the vestibular apparatus results in slow deviation of eyes towards the stimulation followed by rapid correction to mid-line. This response cannot be voluntarily suppressed, so if the patient does not have this response, psychogenic coma can be ruled out.)

3. Find the site of the brain that may be causing coma (i.e., brain stem, back of brain…) and assess the severity of the coma with the Glasgow coma scale

4. Take blood work to see if drugs were involved or if it was a result of hypoventilation/hyperventilation

5. Check for levels of “serum glucose, calcium, sodium, potassium, magnesium, phosphate, urea, and creatinine”

6. Perform brain scans to observe any abnormal brain functioning using either CT or MRI scans

7. Continue to monitor brain waves and identify seizures of patient using EEGs

Perinatal asphyxia is the medical condition resulting from deprivation of oxygen (hypoxia) to a newborn infant long enough to cause apparent harm. It results most commonly from a drop in maternal blood pressure or interference during delivery with blood flow to the infant's brain. This can occur as a result of inadequate circulation or perfusion, impaired respiratory effort, or inadequate ventilation. There has long been a scientific debate over whether newborn infants with asphyxia should be resuscitated with 100% oxygen or normal air. It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.

Diagnosis of coma is simple, but diagnosing the cause of the underlying disease process is often challenging. The first priority in treatment of a comatose patient is stabilization following the basic ABCs (standing for airway, breathing, and circulation). Once a person in a coma is stable, investigations are performed to assess the underlying cause. Investigative methods are divided into physical examination findings and imaging (such as CAT scan, MRI, etc.) and special studies (EEG, etc.)

Asphyxia or asphyxiation is a condition of severely deficient supply of oxygen to the body that arises from abnormal breathing. An example of asphyxia is choking. Asphyxia causes generalized hypoxia, which affects primarily the tissues and organs. There are many circumstances that can induce asphyxia, all of which are characterized by an inability of an individual to acquire sufficient oxygen through breathing for an extended period of time. Asphyxia can cause coma or death.

In 2015 about 9.8 million cases of unintentional suffocation occurred which resulted in 35,600 deaths. The word asphyxia is from Ancient Greek "without" and , "squeeze" (throb of heart).

Exsanguination is the process of blood loss, to a degree sufficient to cause death. One does not have to lose all of one's blood to cause death. Depending upon the age, health, and fitness level of the individual, people can die from losing half to two-thirds of their blood; a loss of roughly one-third of the blood volume is considered very serious. Even a single deep cut can warrant suturing and hospitalization, especially if trauma, a vein or artery, or another comorbidity is involved. It is most commonly known as "bleeding to death" or colloquially as "bleeding out". The word itself originated from Latin: "ex" ("out of") and "sanguis" ("blood").

Mild and moderate cerebral hypoxia generally has no impact beyond the episode of hypoxia; on the other hand, the outcome of severe cerebral hypoxia will depend on the success of damage control, amount of brain tissue deprived of oxygen, and the speed with which oxygen was restored.

If cerebral hypoxia was localized to a specific part of the brain, brain damage will be localized to that region. A general consequence may be epilepsy. The long-term effects will depend on the purpose of that portion of the brain. Damage to the Broca's area and the Wernicke's area of the brain (left side) typically causes problems with speech and language. Damage to the right side of the brain may interfere with the ability to express emotions or interpret what one sees. Damage on either side can cause paralysis of the opposite side of the body.

The effects of certain kinds of severe generalized hypoxias may take time to develop. For example, the long-term effects of serious carbon monoxide poisoning usually may take several weeks to appear. Recent research suggests this may be due to an autoimmune response caused by carbon monoxide-induced changes in the myelin sheath surrounding neurons.

If hypoxia results in coma, the length of unconsciousness is often indicative of long-term damage. In some cases coma can give the brain an opportunity to heal and regenerate, but, in general, the longer a coma, the greater the likelihood that the person will remain in a vegetative state until death. Even if the patient wakes up, brain damage is likely to be significant enough to prevent a return to normal functioning.

Long-term comas can have a significant impact on a patient's families. Families of coma victims often have idealized images of the outcome based on Hollywood movie depictions of coma. Adjusting to the realities of ventilators, feeding tubes, bedsores, and muscle wasting may be difficult. Treatment decision often involve complex ethical choices and can strain family dynamics.

Exsanguination is a relatively uncommon cause of death in human beings. Traumatic injury can cause exsanguination if bleeding is not promptly controlled, and is the most common cause of death in military combat. Non-combat causes can include gunshot or stab wounds; motor vehicle crash injuries; suicide by severing arteries, typically those in the wrists; and partial or total limb amputation, such as via accidental contact with a circular or chain saw, or becoming entangled in operating machinery.

Patients can also develop catastrophic internal hemorrhages, such as from a bleeding peptic ulcer, postpartum bleeding or splenic hemorrhage, which can cause exsanguination without any external signs of distress. Another cause of exsanguination in the medical field is that of aneurysms. If a dissecting aortic aneurysm ruptures through the adventitia, massive hemorrhage and exsanguination can result in a matter of minutes.

Blunt force trauma to the liver, kidneys, and spleen can cause severe internal bleeding as well, though the abdominal cavity usually becomes visibly darkened as if bruised. Similarly, trauma to the lungs can cause bleeding out, though without medical attention, blood can fill the lungs causing the effect of drowning, or in the pleura causing suffocation, well before exsanguination would occur. In addition, serious trauma can cause tearing of major blood vessels without external trauma indicative of the damage.

Alcoholics and others with liver disease can also suffer from exsanguination. Thin-walled, normally low pressure dilated veins just below the lower esophageal mucosa called esophageal varices can become enlarged in conditions with portal hypertension. These may begin to bleed, which with the high pressure in the portal system can be fatal. The often causative impaired liver function also reduces the availability of clotting factors (many of which are made in the liver), making any rupture in vessels more likely to cause a fatal loss of blood.

For newborn infants starved of oxygen during birth there is now evidence that hypothermia therapy for neonatal encephalopathy applied within 6 hours of cerebral hypoxia effectively improves survival and neurological outcome. In adults, however, the evidence is less convincing and the first goal of treatment is to restore oxygen to the brain. The method of restoration depends on the cause of the hypoxia. For mild-to-moderate cases of hypoxia, removal of the cause of hypoxia may be sufficient. Inhaled oxygen may also be provided. In severe cases treatment may also involve life support and damage control measures.

A deep coma will interfere with body's breathing reflexes even after the initial cause of hypoxia has been dealt with; mechanical ventilation may be required. Additionally, severe cerebral hypoxia causes an elevated heart rate, and in extreme cases the heart may tire and stop pumping. CPR, defibrilation, epinephrine, and atropine may all be tried in an effort to get the heart to resume pumping. Severe cerebral hypoxia can also cause seizures, which put the patient at risk of self-injury, and various anti-convulsant drugs may need to be administered before treatment.

There has long been a debate over whether newborn infants with cerebral hypoxia should be resuscitated with 100% oxygen or normal air. It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.

Brain damage can occur both during and after oxygen deprivation. During oxygen deprivation, cells die due to an increasing acidity in the brain tissue (acidosis). Additionally, during the period of oxygen deprivation, materials that can easily create free radicals build up. When oxygen enters the tissue these materials interact with oxygen to create high levels of oxidants. Oxidants interfere with the normal brain chemistry and cause further damage (this is known as "reperfusion injury").

Techniques for preventing damage to brain cells are an area of ongoing research. Hypothermia therapy for neonatal encephalopathy is the only evidence-supported therapy, but antioxidant drugs, control of blood glucose levels, and hemodilution (thinning of the blood) coupled with drug-induced hypertension are some treatment techniques currently under investigation. Hyperbaric oxygen therapy is being evaluated with the reduction in total and myocardial creatine phosphokinase levels showing a possible reduction in the overall systemic inflammatory process.

In severe cases it is extremely important to act quickly. Brain cells are very sensitive to reduced oxygen levels. Once deprived of oxygen they will begin to die off within five minutes.

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.

There is ongoing research on the treatment of ARDS by interferon (IFN) beta-1a to aid in preventing leakage of vascular beds. Traumakine (FP-1201-lyo), is a recombinant human IFN beta-1a drug developed by Faron pharmaceuticals, is undergoing international phase-III clinical trials after an open-label, early-phase trial showed a 81% reduction-in-odds of 28-day mortality in ICU patients with ARDS. The drug is known to function by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine, such that vascular leaking and escalation of inflammation are reduced.

Despite converging agreement about the definition of persistent vegetative state, recent reports have raised concerns about the accuracy of diagnosis in some patients, and the extent to which, in a selection of cases, residual cognitive functions may remain undetected and patients are diagnosed as being in a persistent vegetative state. Objective assessment of residual cognitive function can be extremely difficult as motor responses may be minimal, inconsistent, and difficult to document in many patients, or may be undetectable in others because no cognitive output is possible (Owen et al., 2002). In recent years, a number of studies have demonstrated an important role for functional neuroimaging in the identification of residual cognitive function in persistent vegetative state; this technology is providing new insights into cerebral activity in patients with severe brain damage. Such studies, when successful, may be particularly useful where there is concern about the accuracy of the diagnosis and the possibility that residual cognitive function has remained undetected.

The position of lung infiltrates in acute respiratory distress syndrome is non-uniform. Repositioning into the prone position (face down) might improve oxygenation by relieving atelectasis and improving perfusion. If this is done early in the treatment of severe ARDS, it confers a mortality benefit of 26% compared to supine ventilation.

Cardiac arrest is synonymous with clinical death.

A cardiac arrest is usually diagnosed clinically by the absence of a pulse. In many cases lack of carotid pulse is the gold standard for diagnosing cardiac arrest, as lack of a pulse (particularly in the peripheral pulses) may result from other conditions (e.g. shock), or simply an error on the part of the rescuer. Nonetheless, studies have shown that rescuers often make a mistake when checking the carotid pulse in an emergency, whether they are healthcare professionals or lay persons.

Owing to the inaccuracy in this method of diagnosis, some bodies such as the European Resuscitation Council (ERC) have de-emphasised its importance. The Resuscitation Council (UK), in line with the ERC's recommendations and those of the American Heart Association,

have suggested that the technique should be used only by healthcare professionals with specific training and expertise, and even then that it should be viewed in conjunction with other indicators such as agonal respiration.

Various other methods for detecting circulation have been proposed. Guidelines following the 2000 International Liaison Committee on Resuscitation (ILCOR) recommendations were for rescuers to look for "signs of circulation", but not specifically the pulse. These signs included coughing, gasping, colour, twitching and movement. However, in face of evidence that these guidelines were ineffective, the current recommendation of ILCOR is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally. Another method is to use molecular autopsy or postmortem molecular testing which uses a set of molecular techniques to find the ion channels that are cardiac defective.

Acute alcohol poisoning is a medical emergency due to the risk of death from respiratory depression and/or inhalation of vomit if emesis occurs while the patient is unconscious and unresponsive. Emergency treatment for acute alcohol poisoning strives to stabilize the patient and maintain a patent airway and respiration, while waiting for the alcohol to metabolize. This can be done by removal of any vomitus or, if patient is unconscious or has impaired gag reflex, intubation of the trachea using an endotracheal tube to maintain adequate airway:

Also:

- Treat hypoglycaemia (low blood sugar) with 50 ml of 50% dextrose solution and saline flush, as ethanol induced hypoglycaemia is unresponsive to glucagon.

- Administer the vitamin thiamine to prevent Wernicke-Korsakoff syndrome, which can cause a seizure (more usually a treatment for chronic alcoholism, but in the acute context usually co-administered to ensure maximal benefit).

- Apply hemodialysis if the blood concentration is dangerously high (>400 mg/dL), and especially if there is metabolic acidosis.

- Provide oxygen therapy as needed via nasal cannula or non-rebreather mask.

- Provide parenteral Metadoxine.

Additional medication may be indicated for treatment of nausea, tremor, and anxiety.

Hypoxic hypoxia is a result of insufficient oxygen available to the lungs. A blocked airway, a drowning or a reduction in partial pressure (high altitude above 10,000 feet) are examples of how lungs can be deprived of oxygen. Some medical examples are abnormal pulmonary function or respiratory obstruction. Hypoxic hypoxia is seen in patients suffering from chronic obstructive pulmonary diseases (COPD), neuromuscular diseases or interstitial lung disease.

There is little data on the effects of screening the general population on the ultimate rate of suicide. Screening those who come to the emergency departments with injuries from self harm have been shown to help identify suicide ideation and suicide intention. Psychometric tests such as the Beck Depression Inventory or the Geriatric Depression Scale for older people are being used. As there is a high rate of people who test positive via these tools that are not at risk of suicide, there are concerns that screening may significantly increase mental health care resource utilization. Assessing those at high risk however is recommended. Asking about suicidality does not appear to increase the risk.

Persistent vegetative state is the standard usage (except in the UK) for a medical diagnosis, made after numerous neurological and other tests, that due to extensive and irreversible brain damage a patient is "highly unlikely" ever to achieve higher functions above a vegetative state. This diagnosis does not mean that a doctor has diagnosed improvement as impossible, but does open the possibility, in the US, for a judicial request to end life support. Informal guidelines hold that this diagnosis can be made after four weeks in a vegetative state. US caselaw has shown that successful petitions for termination have been made after a diagnosis of a persistent vegetative state, although in some cases, such as that of Terri Schiavo, such rulings have generated widespread controversy.

In the UK, the term 'persistent vegetative state' is discouraged in favor of two more precisely defined terms that have been strongly recommended by the Royal College of Physicians (RCP). These guidelines recommend using a continuous vegetative state for patients in a vegetative state for more than four weeks. A medical definition of a permanent vegetative state can be made if, after exhaustive testing and a customary 12 months of observation, a medical diagnosis that it is "impossible" by any informed medical expectations that the mental condition will ever improve. Hence, a "continuous vegetative state" in the UK may remain the diagnosis in cases that would be called "persistent" in the US or elsewhere.

While the actual testing criteria for a diagnosis of "permanent" in the UK are quite similar to the criteria for a diagnosis of "persistent" in the US, the semantic difference imparts in the UK a "legal" presumption that is commonly used in court applications for ending life support. The UK diagnosis is generally only made after 12 months of observing a static vegetative state. A diagnosis of a persistent vegetative state in the US usually still requires a petitioner to prove in court that recovery is impossible by informed medical opinion, while in the UK the "permanent" diagnosis already gives the petitioner this presumption and may make the legal process less time-consuming.

In common usage, the "permanent" and "persistent" definitions are sometimes conflated and used interchangeably. However, the acronym "PVS" is intended to define a "persistent vegetative state", without necessarily the connotations of permanence, and is used as such throughout this article.

Bryan Jennett, who originally coined the term "persistent vegetative state", has now recommended using the UK division between continuous and permanent in his most recent book "The Vegetative State". This is one for purposes of precision, on the grounds that "the 'persistent' component of this term ... may seem to suggest irreversibility".

The Australian National Health and Medical Research Council has suggested "post coma unresponsiveness" as an alternative term for "vegetative state" in general.

In medical parlance, cardiac arrest is referred to as a "code" or a "crash". This typically refers to "code blue" on the hospital emergency codes. A dramatic drop in vital sign measurements is referred to as "coding" or "crashing", though coding is usually used when it results in cardiac arrest, while crashing might not. Treatment for cardiac arrest is sometimes referred to as "calling a code".

People in general wards often deteriorate for several hours or even days before a cardiac arrest occurs. This has been attributed to a lack of knowledge and skill amongst ward-based staff, in particular a failure to carry out measurement of the respiratory rate, which is often the major predictor of a deterioration and can often change up to 48 hours prior to a cardiac arrest. In response to this, many hospitals now have increased training for ward-based staff. A number of "early warning" systems also exist which aim to quantify the risk which patients are at of deterioration based on their vital signs and thus provide a guide to staff. In addition, specialist staff are being used more effectively in order to augment the work already being done at ward level. These include:

- Crash teams (or code teams) – These are designated staff members with particular expertise in resuscitation who are called to the scene of all arrests within the hospital. This usually involves a specialized cart of equipment (including defibrillator) and drugs called a "crash cart" or "crash trolley".

- Medical emergency teams – These teams respond to all emergencies, with the aim of treating the people in the acute phase of their illness in order to prevent a cardiac arrest. These teams have been found to decrease the rates of in hospital cardiac arrest and improve survival.

- Critical care outreach – As well as providing the services of the other two types of team, these teams are also responsible for educating non-specialist staff. In addition, they help to facilitate transfers between intensive care/high dependency units and the general hospital wards. This is particularly important, as many studies have shown that a significant percentage of patients discharged from critical care environments quickly deteriorate and are re-admitted; the outreach team offers support to ward staff to prevent this from happening.

The diagnosis of benzodiazepine overdose may be difficult, but is usually made based on the clinical presentation of the patient along with a history of overdose. Obtaining a laboratory test for benzodiazepine blood concentrations can be useful in patients presenting with CNS depression or coma of unknown origin. Techniques available to measure blood concentrations include thin layer chromatography, gas liquid chromatography with or without a mass spectrometer, and radioimmunoassay. Blood benzodiazepine concentrations, however, do not appear to be related to any toxicological effect or predictive of clinical outcome. Blood concentrations are, therefore, used mainly to confirm the diagnosis rather than being useful for the clinical management of the patient.

The lack of generally recognized clinical recommendations available are a reflection of the dearth of data on the effectiveness of any particular clinical strategy, but on the basis of present evidence, the following may be relevant:

- Epileptic seizure control with the appropriate use of medication and lifestyle counseling is the focus of prevention.

- Reduction of stress, participation in physical exercises, and night supervision might minimize the risk of SUDEP.

- Knowledge of how to perform the appropriate first-aid responses to seizure by persons who live with epileptic people may prevent death.

- People associated with arrhythmias during seizures should be submitted to extensive cardiac investigation with a view to determining the indication for on-demand cardiac pacing.

- Successful epilepsy surgery may reduce the risk of SUDEP, but this depends on the outcome in terms of seizure control.

- The use of anti suffocation pillows have been advocated by some practitioners to improve respiration while sleeping, but their effectiveness remain unproven because experimental studies are lacking.

- Providing information to individuals and relatives about SUDEP is beneficial.

Therapeutic hypothermia has been attempted to improve results post brain ischemia . This procedure was suggested to be beneficial based on its effects post cardiac arrest. Evidence supporting the use of therapeutic hypothermia after brain ischemia, however, is limited.

A closely related disease to brain ischemia is brain hypoxia. Brain hypoxia is the condition in which there is a decrease in the oxygen supply to the brain even in the presence of adequate blood flow. If hypoxia lasts for long periods of time, coma, seizures, and even brain death may occur. Symptoms of brain hypoxia are similar to ischemia and include inattentiveness, poor judgment, memory loss, and a decrease in motor coordination. Potential causes of brain hypoxia are suffocation, carbon monoxide poisoning, severe anemia, and use of drugs such as cocaine and other amphetamines. Other causes associated with brain hypoxia include drowning, strangling, choking, cardiac arrest, head trauma, and complications during general anesthesia. Treatment strategies for brain hypoxia vary depending on the original cause of injury, primary and/or secondary.