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.

The treatment hospitals use on comatose patients depends on both the severity and cause of the comatose state. Although the best treatment for comatose patients remains unknown, hospitals usually place comatose patients in an Intensive Care Unit (ICU) immediately. Attention must first be directed to maintaining the patient's respiration and circulation, using intubation and ventilation, administration of intravenous fluids or blood and other supportive care as needed. Once a patient is stable and no longer in immediate danger, the medical staff may concentrate on maintaining the health of patient’s physical state. The concentration is directed to preventing infections such as pneumonias, bedsores (decubitus ulcers), and providing balanced nutrition. Infections may appear from the patient not being able to move around, and being confined to the bed. The nursing staff moves the patient every 2–3 hours from side to side and depending on the state of consciousness sometimes to a chair. The goal is to move the patient as much as possible to try to avoid bedsores, atelectasis and pneumonia. Pneumonia can occur from the person’s inability to swallow leading to aspiration, lack of gag reflex or from feeding tube, (aspiration pneumonia). Physical therapy may also be used to prevent contractures and orthopedic deformities that would limit recovery for those patients who awaken from coma.

A person in a coma may become restless, or seize and need special care to prevent them from hurting themselves. Medicine may be given to calm such individuals. Patients who are restless may also try to pull on tubes or dressings so soft cloth wrist restraints may be put on. Side rails on the bed should be kept up to prevent the patient from falling.

Methods to wake comatose patients include reversing the cause of the coma (i.e., glucose shock if low sugar), giving medication to stop brain swelling, or inducing hypothermia. Inducing hypothermia on comatose patients provides one of the main treatments for patients after suffering from cardiac arrest. In this treatment, medical personnel expose patients to “external or intravascular cooling” at 32-34 °C for 24 hours; this treatment cools patients down about 2-3 °C less than normal body temperature. In 2002, Baldursdottir and her coworkers found that in the hospital, more comatose patients survived after induced hypothermia than patients that remained at normal body temperature. For this reason, the hospital chose to continue the induced hypothermia technique for all of its comatose patients that suffered from cardiac arrest.

Coma has a wide variety of emotional reactions from the family members of the affected patients, as well as the primary care givers taking care of the patients. Common reactions, such as desperation, anger, frustration, and denial are possible. The focus of the patient care should be on creating an amicable relationship with the family members or dependents of a comatose patient as well as creating a rapport with the medical staff.

CNS depression is treated within a hospital setting by maintaining breathing and circulation. Individuals with reduced breathing may be given supplemental oxygen, while individuals who are not breathing can be ventilated with bag valve mask ventilation or by mechanical ventilation with a respirator. Sympathomimetic drugs may be used to attempt to stimulate cardiac output in order to maintain circulation. CNS Depression caused by certain drugs may respond to treatment with an antidote.

There are two antidotes that are frequently used in the hospital setting and these are Naloxone and Flumazenil. Naloxone is an opioid antagonist and reverses the central nervous depressive effects seen in opioid overdose. In the setting of a colonoscopy, Naloxone is rarely administered but when it is administered, its half life is shorter than some common opioid agonists. Therefore, the patient may still exhibit central nervous system depression after Naloxone has been cleared. Typically, Naloxone is administered in short intervals with relatively small doses in order to prevent the occurrence of withdrawal, pain, and sympathetic nervous system activation. Flumazenil is a benzodiazepine antagonists and blocks the binding of benzodiazepines to GABAa. Similarly to Naloxone, Flumazenil has a short half life, and this needs to be taken into account because the patient may exhibit central nervous depression after the antidote has been cleared. Benzodiazepines are used in the treatment of seizures and subsequently, the administration of Flumazenil may result in seizures. Therefore, slow administration of Flumazenil is necessary to prevent the occurrence of a seizure. These agents are rarely used in the setting of a colonoscopy as 98.8% of colonoscopies use sedatives but only 0.8% of them result in the administration of one of these antidotes. Even if they are rarely used in colonoscopies they are important in preventing the patient from entering a coma or developing respiratory depression when sedatives are not properly dosed. Outside of the colonoscopy setting, these agents are used for other procedures and in the case of drug overdose.

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.

A pH under 7.1 is an emergency, due to the risk of cardiac arrhythmias, and may warrant treatment with intravenous bicarbonate. Bicarbonate is given at 50-100 mmol at a time under scrupulous monitoring of the arterial blood gas readings. This intervention, however, has some serious complications in lactic acidosis, and in those cases, should be used with great care.

If the acidosis is particularly severe and/or intoxication may be present, consultation with the nephrology team is considered useful, as dialysis may clear both the intoxication and the acidosis.

In closed circuit SCUBA (rebreather) diving, exhaled carbon dioxide must be removed from the breathing system, usually by a scrubber containing a solid chemical compound with a high affinity for CO, such as soda lime. If not removed from the system, it may be re-inhaled, causing an increase in the inhaled concentration.

American and European guidelines come to different conclusions regarding the use of medications. In the United States they are recommended in those with SIADH, cirrhosis, or heart failure who fail limiting fluid intact. In Europe they are not generally recommended.

There is tentative evidence that vasopressin receptor antagonists (vaptans), such as conivaptan, may be slightly more effective than fluid restriction in those with high volume or normal volume hyponatremia. They should not be used in people with low volume. Their use in SIADH is unclear.

Demeclocycline, while sometimes used for SIADH, has significant side effects including potential kidney problems and sun sensitivity. In many people it has no benefit while in others it can result in overcorrection and high blood sodium levels.

Daily use of urea by mouth, while not commonly used due to the taste, has tentative evidence in SIADH. It, however, is not available in many areas of the world.

Options include:

- Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 ml per day of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/day may maintain the person in a symptom free state.

- Moderate and/or symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline.

- Severe hyponatremia or severe symptoms (confusion, convulsions, or coma): consider hypertonic saline (3%) 1–2 ml/kg IV in 3–4 h. Hypertonic saline may lead to a rapid dilute diuresis and fall in the serum sodium. It should not be used in those with an expanded extracellular fluid volume.

Treatment depends upon the underlying cause:

- Hypoglycaemic diabetic coma: administration of the hormone glucagon to reverse the effects of insulin, or glucose given intravenously.

- Ketoacidotic diabetic coma: intravenous fluids, insulin and administration of potassium and sodium.

- Hyperosmolar diabetic coma: plenty of intravenous fluids, insulin, potassium and sodium given as soon as possible.

Hemodialysis can be used to enhance the removal of salicylate from the blood. Hemodialysis is usually used in those who are severely poisoned. Example of severe poisoning include people with high salicylate blood levels: 7.25 mmol/L (100 mg/dL) in acute ingestions or 40 mg/dL in chronic ingestions, significant neurotoxicity (agitation, coma, convulsions), kidney failure, pulmonary edema, or cardiovascular instability. Hemodialysis also has the advantage of restoring electrolyte and acid-base abnormalities while removing salicylate.

The hypercapnic state is routinely used to calibrate blood-oxygen-level dependent functional magnetic resonance imaging (BOLD fMRI), a modality that is sensitive to changes in blood oxygenation. However, this calibration crucially relies on the assumption that hypercapnia has no effect on neuronal function, which is a matter of debate.

Initial treatment of an acute overdose involves resuscitation followed by gastric decontamination by administering activated charcoal, which adsorbs the aspirin in the gastrointestinal tract. Stomach pumping is no longer routinely used in the treatment of poisonings but is sometimes considered if the patient has ingested a potentially lethal amount less than one hour before presentation. Inducing vomiting with syrup of ipecac is not recommended. Repeated doses of charcoal have been proposed to be beneficial in cases of aspirin overdosing, although one study found that they might not be of significant value. Regardless, most clinical toxicologists will administer additional charcoal if serum salicylate levels are increasing.

Supportive measures include observation of vital signs, especially Glasgow Coma Scale and airway patency. IV access with fluid administration and maintenance of the airway with intubation and artificial ventilation may be required if respiratory depression or pulmonary aspiration occurs. Supportive measures should be put in place prior to administration of any benzodiazepine antagonist in order to protect the patient from both the withdrawal effects and possible complications arising from the benzodiazepine. A determination of possible deliberate overdose should be considered with appropriate scrutiny, and precautions taken to prevent any attempt by the patient to commit further bodily harm. Hypotension is corrected with fluid replacement, although catecholamines such as norepinephrine or dopamine may be required to increase blood pressure. Bradycardia is treated with atropine or an infusion of norepinephrine to increase coronary blood flow and heart rate.

Medical observation and supportive care are the mainstay of treatment of benzodiazepine overdose. Although benzodiazepines are absorbed by activated charcoal, gastric decontamination with activated charcoal is not beneficial in pure benzodiazepine overdose as the risk of adverse effects would outweigh any potential benefit from the procedure. It is recommended only if benzodiazepines have been taken in combination with other drugs that may benefit from decontamination. Gastric lavage (stomach pumping) or whole bowel irrigation are also not recommended. Enhancing elimination of the drug with hemodialysis, hemoperfusion, or forced diuresis is unlikely to be beneficial as these procedures have little effect on the clearance of benzodiazepines due to their large volume of distribution and lipid solubility.

Treatment for this condition entails the maintenance of intravascular volume. Additionally, the following can be done as a means of managing FES in an individual:

- Albumin can be used for volume resuscitation

- Long bone fractures should be attended to immediately (surgery)

- Mechanical ventilation

Additional therapy:

- bisphosphonates are pyrophosphate analogues with high affinity for bone, especially areas of high bone-turnover.

- they are taken up by osteoclasts and inhibit osteoclastic bone resorption

- current available drugs include (in order of potency): (1st gen) etidronate, (2nd gen) tiludronate, IV pamidronate, alendronate (3rd gen) zoledronate and risedronate

- all people with cancer-associated hypercalcaemia should receive treatment with bisphosphonates since the 'first line' therapy (above) cannot be continued indefinitely nor is it without risk. Further, even if the 'first line' therapy has been effective, it is a virtual certainty that the hypercalcaemia will recur in the person with hypercalcaemia of malignancy. Use of bisphosphonates in such circumstances, then, becomes both therapeutic and preventative

- people in kidney failure and hypercalcaemia should have a risk-benefit analysis before being given bisphosphonates, since they are relatively contraindicated in kidney failure.

- Calcitonin blocks bone resorption and also increases urinary calcium excretion by inhibiting calcium reabsorption by the kidney

- Usually used in life-threatening hypercalcaemia along with rehydration, diuresis, and bisphosphonates

- Helps prevent recurrence of hypercalcaemia

- Dose is 4 international units per kilogram via subcutaneous or intramuscular route every 12 hours, usually not continued indefinitely due to quick onset of decreased response to calcitonin

Initial therapy:

- hydration, increasing salt intake, and forced diuresis.

- hydration is needed because many patients are dehydrated due to vomiting or kidney defects in concentrating urine.

- increased salt intake also can increase body fluid volume as well as increasing urine sodium excretion, which further increases urinary potassium excretion.

- after rehydration, a loop diuretic such as furosemide can be given to permit continued large volume intravenous salt and water replacement while minimizing the risk of blood volume overload and pulmonary oedema. In addition, loop diuretics tend to depress calcium reabsorption by the kidney thereby helping to lower blood calcium levels

- can usually decrease serum calcium by 1–3 mg/dL within 24 hours

- caution must be taken to prevent potassium or magnesium depletion

The antibiotic rifaximin may be recommended in addition to lactulose for those with recurrent disease. It is a nonabsorbable antibiotic from the rifamycin class. This is thought to work in a similar way to other antibiotics, but without the complications attached to neomycin or metronidazole. Due to the long history and lower cost of lactulose use, rifaximin is generally only used as a second-line treatment if lactulose is poorly tolerated or not effective. When rifaximin is added to lactulose, the combination of the two may be more effective than each component separately. Rifaximin is more expensive than lactulose, but the cost may be offset by reduced hospital admissions for encephalopathy.

The antibiotics neomycin and metronidazole are other antibiotics used to treat hepatic encephalopathy. The rationale of their use was the fact that ammonia and other waste products are generated and converted by intestinal bacteria, and killing these bacteria would reduce the generation of these waste products. Neomycin was chosen because of its low intestinal absorption, as neomycin and similar aminoglycoside antibiotics may cause hearing loss and kidney failure if used by injection. Later studies showed that neomycin was indeed absorbed when taken by mouth, with resultant complications. Metronidazole, similarly, is less commonly used because prolonged use can cause nerve damage, in addition to gastrointestinal side effects.

Lactulose and lactitol are disaccharides that are not absorbed from the digestive tract. They are thought to decrease the generation of ammonia by bacteria, render the ammonia inabsorbable by converting it to ammonium (NH) ions, and increase transit of bowel content through the gut. Doses of 15-30 ml are administered three times a day; the result is aimed to be 3–5 soft stools a day, or (in some settings) a stool pH of <6.0. Lactulose may also be given by enema, especially if encephalopathy is severe. More commonly, phosphate enemas are used. This may relieve constipation, one of the causes of encephalopathy, and increase bowel transit.

Lactulose and lactitol are beneficial for treating hepatic encephalopathy, and are the recommended first-line treatment. Lactulose does not appear to be more effective than lactitol for treating people with hepatic encephalopathy. Side effects of lactulose and lactitol include the possibility of diarrhea, bloating, flatulence, and nausea. In acute liver failure, it is unclear whether lactulose is beneficial. The possible side effect of bloating may interfere with a liver transplant procedure if required.

How to manage SIADH depends on whether symptoms are present, the severity of the hyponatremia, and the duration. Management of SIADH includes:

- Removing the underlying cause when possible.

- Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 ml per day of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/day may maintain the person in a symptom free state.

- Moderate and symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline.

- For people with severe symptoms (severe confusion, convulsions, or coma) hypertonic saline (3%) 1–2 ml/kg IV in 3–4 h should be given.

- Drugs

- Demeclocycline can be used in chronic situations when fluid restrictions are difficult to maintain; demeclocycline is the most potent inhibitor of Vasopressin (ADH/AVP) action. However, demeclocycline has a 2–3 day delay in onset with extensive side effect profile, including skin photosensitivity, and nephrotoxicity.

- Urea: oral daily ingestion has shown favorable long-term results with protective effects in myelinosis and brain damage. Limitations noted to be undesirable taste and is contraindicated in people with cirrhosis to avoid initiation or potentiation of hepatic encephalopathy.

- Conivaptan – an antagonist of both V and V vasopressin receptors.

- Tolvaptan – an antagonist of the V vasopressin receptor.

Raising the serum sodium concentration too rapidly may cause central pontine myelinolysis. Avoid correction by more than 12 mEq/L/day. Initial treatment with hypertonic saline may abruptly lead to a rapid dilute diuresis and fall in ADH.

In a study comparing the central nervous depression due to supra-therapeutic doses of Triazolam (Benzodiazepine), Pentobarbital (Barbiturate) and GHB it appeared as if GHB had the strongest dose-effect function. Since, GHB had a high correlation between its dose and its central nervous system depression it has a high risk of accidental overdose. In the case of accidental overdose of GHB, patients could become drowsy, fall asleep and may enter a coma. Although GHB had higher sedative effects at high doses as compared to Triazolam and Pentobarbital, it had less amnestic effects as compared to Triazolam and Pentobarbital. Arousal of subjects in the GHB group sometimes even required a painful stimulus; this was not seen in the Triazolam or the Pentobarbital group. Fortunately, during this heavy sedation with GHB the subjects maintained normal respiration and blood pressure. This is often not the case with opioids as they will cause respiratory depression.

Inert gas asphyxiation is a form of asphyxiation which results from breathing a physiologically inert gas in the absence of oxygen, or a low amount of oxygen, rather than atmospheric air (which is largely composed of nitrogen and oxygen). Examples of physiologically inert gases, which have caused accidental or deliberate death by this mechanism, are: argon, helium, nitrogen and methane. The term "physiologically inert" is used to indicate a gas which has no toxic or anesthetic properties and does not act upon the heart or hemoglobin. Instead, the gas acts as a simple diluent to reduce oxygen concentration in inspired gas and blood to dangerously low levels, thereby eventually depriving all cells in the body of oxygen.

According to the U.S. Chemical Safety and Hazard Investigation Board, in humans, "breathing an oxygen deficient atmosphere can have serious and immediate effects, including unconsciousness after only one or two breaths. The exposed person has no warning and cannot sense that the oxygen level is too low." In the US, at least 80 people died due to accidental nitrogen asphyxiation between 1992 and 2002. Hazards with inert gases and the risks of asphyxiation are well established.

An occasional cause of accidental death in humans, inert gas asphyxia with gases including helium, nitrogen, methane, and argon, has been used as a suicide method. Inert gas asphyxia has been advocated by proponents of euthanasia, using a gas-retaining plastic hood device colloquially referred to as a suicide bag.

Nitrogen asphyxiation has been suggested by a number of lawmakers and other advocates as a more humane way to carry out capital punishment. In April 2015, the Oklahoma Governor Mary Fallin signed a bill authorizing nitrogen asphyxiation as an alternative execution method in cases where the state's preferred method of lethal injection was not available as an option.

Impaired liver synthesis of clotting factors, low-grade fibrinolysis, and intravascular coagulation are typical of ALF. Thrombocytopenia is common and may also be dysfunctional. Replacement therapy is recommended only in the setting of bleeding or prior to an invasive procedure. Vitamin K can be given to treat an abnormal prothrombin time, regardless of whether there is poor nutritional status. Administration of recombinant factor VIIa has shown promise; however, this treatment approach requires further study. The use of gastrointestinal hemorrhage prophylaxis with a histamine-2 (H2) blocker, proton pump inhibitor, or sucralfate is recommended.

Patients with grade I–II encephalopathy should be transferred to a liver transplant facility and listed for transplantation. Consider a brain computed tomography (CT) scan to rule out other causes of altered or impaired mental status. Stimulation and overhydration can cause elevations in intracranial pressure (ICP) and should be avoided. Unmanageable agitation may be treated with short-acting benzodiazepines in small doses. Lactulose can be considered at this stage. A preliminary report from the ALFSG on 117 patients suggests that use of lactulose in the first 7 days after diagnosis is associated with a small increase in survival time, but with no difference in severity of encephalopathy or in the overall outcome. For patients who progress to grade III–IV encephalopathy, intubation for airway protection is generally required. Many centers use propofol for sedation because it may reduce cerebral blood. The head of the bed should be elevated to 30 degrees, and electrolytes, blood gasses, glucose, and neurologic status monitored frequently.