Chelation therapy is a medical procedure that involves the administration of chelating agents to remove heavy metals from the body. Chelating agents are molecules that have multiple electron-donating groups, which can form stable coordination complexes with metal ions. Complexation prevents the metal ions from reacting with molecules in the body, and enable them to be dissolved in blood and eliminated in urine. It should only be used in people who have a diagnosis of metal intoxication. That diagnosis should be validated with tests done in appropriate biological samples.

Chelation therapy is administered under very careful medical supervision due to various inherent risks. When the therapy is administered properly, the chelation drugs have significant side effects. Chelation administered inappropriately can cause neurodevelopmental toxicity, increase risk of developing cancer, and cause death; chelation also removes essential metal elements and requires measures to prevent their loss.

It is difficult to differentiate the effects of low level metal poisoning from the environment with other kinds of environmental harms, including nonmetal pollution. Generally, increased exposure to heavy metals in the environment increases risk of developing cancer.

Without a diagnosis of metal toxicity and outside of evidence-based medicine, but perhaps because of worry about metal toxicity, some people seek chelation therapy to treat autism, cardiovascular disease, Alzheimer's disease, or any sort of neurodegeneration. Chelation therapy does not improve outcomes for those diseases.

For precious animals ;

- Repeat screening, case management to abate sources

- Medical and environmental evaluation,

- veterinary evaluation, chelation, case management

- If necessary, veterinary hospitalization, immediate chelation, case management.

The mainstays of treatment are removal from the source of lead and, for precious animals who have significantly high blood lead levels or who have symptoms of poisoning, chelation therapy with a chelating agent.

Withdrawal of the contaminated cooking oil is the most important initial step. Bed rest with leg elevation and a protein-rich diet are useful. Supplements of calcium, antioxidants (vitamin C and E), and thiamine and other B vitamins are commonly used. Corticosteroids and antihistaminics such as promethazine have been advocated by some investigators, but demonstrated efficacy is lacking. Diuretics are used universally but caution must be exercised not to deplete the intravascular volume unless features of frank congestive cardiac failure are present, as oedema is mainly due to increased capillary permeability. Cardiac failure is managed by bed rest, salt restriction, digitalis and diuretics. Pneumonia is treated with appropriate antibiotics. Renal failure may need dialysis therapy and complete clinical recovery is seen. Glaucoma may need operative intervention, but generally responds to medical management.

The standard of care is discontinuation of the environmental exposure, and chelation therapy (with EDTA or maybe better, DMSA).

Treatment is mainly for the symptoms that toxic encephalopathy brings upon victims, varying depending on how severe the case is. Diet changes and nutritional supplements may help some patients. To reduce or halt seizures, anticonvulsants may be prescribed. Dialysis or organ replacement surgery may be needed in some severe cases.

Management of affected individuals consists of immediate removal from exposure to the toxic substance(s), treatment of the common clinical manifestation of depression if present, and counselling for the provision of life strategies to help cope with the potentially debilitating condition.

Those routes include contaminated air, water, soil, and food, and also, for birds ingestion of grit (lead shots, lead bullets).ingestion of paints,materials that are left out from the factories like batteries etc.

On June 30, 2009, an FDA advisory panel recommended that Vicodin and another painkiller, Percocet, be removed from the market because they have allegedly caused over 400 deaths a year. The problem is with paracetamol (acetaminophen/Tylenol for example ) overdose and liver damage. These two drugs, in combination with other drugs like Nyquil and Theraflu, can cause death by multiple drug intake and/or drug overdose. Another solution would be to not include paracetamol with Vicodin or Percocet.

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

Recent research suggests that sulfur amino acids have a protective effect against the toxicity of ODAP.

Eating the chickling pea with grain having high concentrations of sulphur-based amino acids reduces the risk of lathyrism if grain is available. Food preparation is also an important factor. Toxic amino acids are readily soluble in water and can be leached. Bacterial (lactic acid) and fungal (tempeh) fermentation is useful to reduce ODAP content. Moist heat (boiling, steaming) denatures protease inhibitors which otherwise add to the toxic effect of raw grasspea through depletion of protective sulfur amino acids. During times of drought and famine, water for steeping and fuel for boiling is frequently also in short supply. Poor people sometimes know how to reduce the chance of developing lathyrism but face a choice between risking lathyrism or starvation.

The underlying cause for excessive consumption of grasspea is a lack of alternative food sources. This is a consequence of poverty and political conflict. The prevention of lathyrism is therefore a socio-economic challenge.

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

Exposure to cobalt metal dust is most common in the fabrication of tungsten carbide. Another potential source is wear and tear of metal-on-metal hip prostheses; however, this is a relatively uncommon phenomenon with 18 reported cases being documented in the medical literature.

There is no evidence that any treatment for hangovers is very effective.

- Rehydration: Drinking water before going to bed or during hangover may relieve dehydration-associated symptoms such as thirst, dizziness, dry mouth, and headache.

- Non-steroidal anti-inflammatory drugs such as aspirin or ibuprofen have been proposed as a treatment for the headaches associated with a hangover. There however is no evidence to support a benefit, and there are concerns that taking alcohol and aspirin together may increase the risk of stomach bleeding and liver damage.

- Tolfenamic acid, an inhibitor of prostaglandin synthesis, in a 1983 study reduced headache, nausea, vomiting, irritation but had no effect on tiredness in 30 people.

- Pyritinol: A 1973 study found that large doses (several hundred times the recommended daily intake) of Pyritinol, a synthetic Vitamin B6 analog, can help to reduce hangover symptoms. Possible side effects of pyritinol include hepatitis (liver damage) due to cholestasis and acute pancreatitis.

- Yeast-based extracts: The difference in the change for discomfort, restlessness, and impatience were statistically significant but no significant differences on blood chemistry parameters, blood alcohol or acetaldehyde concentrations have been found, and it did not significantly improve general well-being.

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

The values of soluble cobalt salts has been estimated to be between 150 and 500 mg/kg. Thus, for a 100 kg person the LD would be about 20 grams.

Mercury compounds like calomel were historically used for various medical purposes: as laxatives, diuretics, antiseptics or antimicrobial drugs for syphilis, typhus and yellow fever

. Teething powders were a widespread source of mercury poisoning until the recognition of mercury toxicity in the 1940s.

However, mercury poisoning and acrodynia still exist today. Modern sources of mercury intoxication include broken thermometers.

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.

The treatment for auto-brewery syndrome is a change in diet requiring low carbohydrates and high protein. Sugar is fermented into alcohol, and a diet that effectively lowers sugars also lowers the alcohol that can be fermented from it. Anything that causes an imbalance between the beneficial and harmful bacteria in the gut can help increase the chance that fermentation in the gut will develop. This can include not only antibiotics, but also overindulgence in sugars and carbohydrates. Watching what you eat could lower the risk of gut fermentation syndrome, and taking probiotics could further protect you by increasing the number of good bacteria in your system.

Recommendations for foods, drinks and activities to relieve hangover symptoms abound. The ancient Romans, on the authority of Pliny the Elder, favored raw owl's eggs or fried canary, while the "prairie oyster" restorative, introduced at the 1878 Paris World Exposition, calls for raw egg yolk mixed with Worcestershire sauce, Tabasco sauce, salt and pepper. By 1938, the Ritz-Carlton Hotel provided a hangover remedy in the form of a mixture of Coca-Cola and milk (Coca-Cola itself having been invented, by some accounts, as a hangover remedy). Alcoholic writer Ernest Hemingway relied on tomato juice and beer. Other purported hangover cures include cocktails such as Bloody Mary or Black Velvet (consisting of equal parts champagne and stout). A 1957 survey by an American folklorist found widespread belief in the efficacy of heavy fried foods, tomato juice and sexual activity.

Other untested or discredited treatments include:

- Hair of the dog: The belief is that consumption of further alcohol after the onset of a hangover will relieve symptoms, based upon the theory that the hangover represents a form of alcohol withdrawal and that by satiating the body's need for alcohol the symptoms will be relieved. Social drinkers and alcoholics claim that drinking more alcohol gives relief from hangover symptoms, but research shows that the use of alcohol as a hangover cure seems to predict current or future problem drinking and alcohol use disorder, through negative reinforcement and the development of physical dependence. While the practice is popular in tradition and promoted by many sellers of alcoholic beverages, medical opinion holds that the practice merely postpones the symptoms, and courts addiction. Favored choices include Fernet Branca and Bloody Mary.

- Kudzu ("Pueraria montana var. lobata"): The main ingredient in remedies such as kakkonto. A study concluded, "The chronic usage of "Pueraria lobata" at times of high ethanol consumption, such as in hangover remedies, may predispose subjects to an increased risk of acetaldehyde-related neoplasm and pathology. ... Pueraria lobata appears to be an inappropriate herb for use in herbal hangover remedies as it is an inhibitor of ALDH2."

- Artichoke: Research shows that artichoke extract does not prevent the signs and symptoms of alcohol-induced hangover.

- Sauna or steam-bath: Medical opinion holds this may be dangerous, as the combination of alcohol and hyperthermia increases the likelihood of dangerous cardiac arrhythmias.

- Oxygen: There have been anecdotal reports from those with easy access to a breathing oxygen supply – medical staff, and military pilots — that oxygen can also reduce the symptoms of hangovers sometimes caused by alcohol consumption. The theory is that the increased oxygen flow resulting from oxygen therapy improves the metabolic rate, and thus increases the speed at which toxins are broken down. However, one source states that (in an aviation context) oxygen has no effect on physical impairment caused by hangover.

- Fructose and glucose: Glucose and fructose significantly inhibit the metabolic changes produced by alcohol intoxication, nevertheless they have no significant effect on hangover severity.

- Vitamin B: No effects on alcohol metabolism, peak blood alcohol and glucose concentrations have been found and psychomotor function is not significantly improved when using Vitamin B supplements.

- Caffeinated drinks: No significant correlation between caffeine use and hangover severity has been found.

Epidemic dropsy is a form of edema of extremities due to poisoning by "Argemone mexicana" (Mexican prickly poppy).

Epidemic dropsy is a clinical state resulting from use of edible oils adulterated with "Argemone mexicana" seed oil.

Sanguinarine and dihydrosanguinarine are two major toxic alkaloids of argemone oil, which cause widespread capillary dilatation, proliferation and increased capillary permeability. When mustard oil is adulterated deliberately (as in most cases) or accidentally with argemone oil, proteinuria (specifically loss of albumin) occurs, with a resultant edema as would occur in nephrotic syndrome.

Other major symptoms are pitting edema of extremities, headache, nausea, loose bowels, erythema, glaucoma and breathlessness.

Leakage of the protein-rich plasma component into the extracellular compartment leads to the formation of edema. The haemodynamic consequences of this vascular dilatation and permeability lead to a state of relative hypovolemia with a constant stimulus for fluid and salt conservation by the kidneys. Illness begins with gastroenteric symptoms followed by cutaneous erythema and pigmentation. Respiratory symptoms such as cough, shortness of breath and orthopnoea, progressing to frank right-sided congestive cardiac failure, are seen.

Mild to moderate anaemia, hypoproteinaemia, mild to moderate renal azotemia, retinal haemorrhages, and glaucoma are common manifestations. There is no specific therapy. Removal of the adulterated oil and symptomatic treatment of congestive cardiac failure and respiratory symptoms, along with administration of antioxidants and multivitamins, remain the mainstay of treatment.

Epidemic dropsy occurs as an epidemic in places where use of mustard oil, (from the seeds of Brassica "juncea" commonly known as Indian mustard ) as cooking medium is common.

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

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

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

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

Like diagnosis, treating CSE is difficult due to how vaguely defined it is, as well as lack of data on the mechanism of CSE effects on neural tissue. There is no existing treatment that is effective at completely recovering any neurological or physical function lost due to CSE. This is believed to be because of the limited regeneration capabilities in the central nervous system. Furthermore, existing symptoms of CSE can potentially worsen with age. Some symptoms of CSE, such as depression and sleep issues, can be treated separately, and therapy is available to help patients adjust to any disabilities. Current treatment for CSE involves treating accompanying psychopathology, symptoms, and preventing further deterioration.

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.

The most straightforward way to avoid nitrogen narcosis is for a diver to limit the depth of dives. Since narcosis becomes more severe as depth increases, a diver keeping to shallower depths can avoid serious narcosis. Most recreational dive schools will only certify basic divers to depths of , and at these depths narcosis does not present a significant risk. Further training is normally required for certification up to on air, and this training should include a discussion of narcosis, its effects, and cure. Some diver training agencies offer specialized training to prepare recreational divers to go to depths of , often consisting of further theory and some practice in deep dives under close supervision. Scuba organizations that train for diving beyond recreational depths, may forbid diving with gases that cause too much narcosis at depth in the average diver, and strongly encourage the use of other breathing gas mixes containing helium in place of some or all of the nitrogen in air – such as trimix and heliox – because helium has no narcotic effect. The use of these gases forms part of technical diving and requires further training and certification.

While the individual diver cannot predict exactly at what depth the onset of narcosis will occur on a given day, the first symptoms of narcosis for any given diver are often more predictable and personal. For example, one diver may have trouble with eye focus (close accommodation for middle-aged divers), another may experience feelings of euphoria, and another feelings of claustrophobia. Some divers report that they have hearing changes, and that the sound their exhaled bubbles make becomes different. Specialist training may help divers to identify these personal onset signs, which may then be used as a signal to ascend to avoid the narcosis, although severe narcosis may interfere with the judgement necessary to take preventive action.

Deep dives should be made only after a gradual training to test the individual diver's sensitivity to increasing depths, with careful supervision and logging of reactions. Diving organizations such as Global Underwater Explorers (GUE) emphasize that such sessions are for the purpose of gaining experience in recognizing the onset symptoms of narcosis for an individual , which are somewhat more repeatable than for the average group of divers. Scientific evidence does not show that a diver can train to overcome any measure of narcosis at a given depth or become tolerant of it.

Equivalent narcotic depth (END) is a commonly used way of expressing the narcotic effect of different breathing gases. The National Oceanic and Atmospheric Administration (NOAA) Diving Manual now states that oxygen and nitrogen should be considered equally narcotic. Standard tables, based on relative lipid solubilities, list conversion factors for narcotic effect of other gases. For example, hydrogen at a given pressure has a narcotic effect equivalent to nitrogen at 0.55 times that pressure, so in principle it should be usable at more than twice the depth. Argon, however, has 2.33 times the narcotic effect of nitrogen, and is a poor choice as a breathing gas for diving (it is used as a drysuit inflation gas, owing to its low thermal conductivity). Some gases have other dangerous effects when breathed at pressure; for example, high-pressure oxygen can lead to oxygen toxicity. Although helium is the least intoxicating of the breathing gases, at greater depths it can cause high pressure nervous syndrome, a still mysterious but apparently unrelated phenomenon. Inert gas narcosis is only one factor influencing the choice of gas mixture; the risks of decompression sickness and oxygen toxicity, cost, and other factors are also important.

Because of similar and additive effects, divers should avoid sedating medications and drugs, such as marijuana and alcohol before any dive. A hangover, combined with the reduced physical capacity that goes with it, makes nitrogen narcosis more likely. Experts recommend total abstinence from alcohol for at least 12 hours before diving, and longer for other drugs. Abstinence time needed for marijuana is unknown, but owing to the much longer half-life of the active agent of this drug in the body, it is likely to be longer than for alcohol.

Emergency treatment of cocaine-associated hyperthermia consists of administering a benzodiazepine sedation agent, such as diazepam (Valium) or lorazepam (Ativan) to enhance muscle relaxation and decrease sympathetic outflow from the central nervous system. Physical cooling is best accomplished with tepid water misting and cooling with a fan (convection and evaporation), which can be carried out easily in the field or hospital. There is no specific pharmacological antidote for cocaine overdose. The chest pain, high blood pressure, and increased heart rate caused by cocaine may be also treated with a benzodiazepine. Multiple and escalating dose of benzodiazepines may be necessary to achieve effect, which increases risk of over-sedation and respiratory depression. A comprehensive systematic review of all pharmacological treatments of cocaine cardiovascular toxicity revealed benzodiazepines may not always reliably lower heart rate and blood pressure.

Nitric-oxide mediated vasodilators, such as nitroglycerin and nitroprusside, are effective at lowering blood pressure and reversing coronary arterial vasoconstriction, but not heart rate. Nitroglycerin is useful for cocaine-induced chest pain, but the possibility of reflex tachycardia must be considered. Alpha-blockers such as phentolamine have been recommended and may be used to treat cocaine-induced hypertension and coronary arterial vasoconstriction, but these agents do not reduce heart rate. Furthermore, phentolamine is rarely used, not readily available in many emergency departments, and many present-day clinicians are unfamiliar with its use and titratability. Calcium channel blockers may also be used to treat hypertension and coronary arterial vasoconstriction, but fail to lower tachycardia based on all cocaine-related studies. Non-dihydropyridine calcium channels blockers such as diltiazem and verapamil are preferable, as dihydropyridine agents such as nifedipine have much higher risk of reflex tachycardia.

Agitated patients are best treated with benzodiazepines, but antipsychotics such as haloperidol and olanzapine may also be useful. The alpha-2 agonist dexmedetomidine may also be useful for treatment of agitation, but effects on heart rate and blood pressure are variable based on several studies and case reports. Lidocaine and intravenous lipid emulsion have been successfully used for serious ventricular tachyarrhythmias in several case reports.

The use of beta-blockers for cocaine cardiovascular toxicity has been subject to a relative contraindication by many clinicians for several years despite extremely limited evidence. The phenomenon of “unopposed alpha-stimulation,” in which blood pressure increases or coronary artery vasoconstriction worsens after blockade of beta-2 vasodilation in cocaine-abusing patients, is controversial. This rarely-encountered and unpredictable adverse effect has resulted in some clinicians advocating for an absolute contraindication of the use of all beta-blockers, including specific, non-specific, and mixed. Many clinicians have disregarded this dogma and administer beta-blockers for cocaine-related chest pain and acute coronary syndrome, especially when there is demand ischemia from uncontrolled tachycardia. Of the 1,744 total patients identified in the aforementioned systematic review, only 7 adverse events were from putative cases of “unopposed alpha-stimulation” due to propranolol (n=3), esmolol (n=3), and metoprolol (n=1). Some detractors of beta-blockers for cocaine-induced chest pain have cited minimal acute mortality and the short half-life of the drug, making it unnecessary to aggressively treat any associated tachycardia and hypertension. However, the long-term effect of cocaine use and development of heart failure, with early mortality, high morbidity, and tremendous demand on hospital utilization should be taken under consideration.

The mixed beta/alpha blocker labetalol has been shown to be safe and effective for treating concomitant cocaine-induced hypertension and tachycardia, without any “unopposed alpha-stimulation” adverse events recorded. The use of labetalol is approved by a recent AHA/ACC guideline for cocaine and methamphetamine patients with unstable angina/non-STEMI.