Ethylene glycol poisoning is poisoning caused by drinking ethylene glycol. Early symptoms include poisoning, vomiting and abdominal pain. Further symptoms may include decreased level of consciousness, headache, and seizures. Long-term outcomes may include kidney failure and brain damage. Toxicity and death can occur even after drinking small amounts.
Ethylene glycol is a colorless, odorless, sweet liquid, commonly found in antifreeze. It may be taken by accident or by accident in an attempt to cause death. When broken down by the body it produces glycolic acid and oxalic acid which causes most toxicity. Diagnosis can be suspected when calcium oxalate crystals are seen in the urine or when acidosis or an increase in osmole clearance is present in the blood. Diagnosis can be confirmed by measuring the levels of ethylene glycol in the blood; However, many hospitals do not have the ability to perform these tests.
Early treatment increases the likelihood of good results. Treatment consists of stabilizing people, followed by the use of antidote. The preferred bidder is fomepizole with ethanol used if this is not available. Hemodialysis can also be used in those with high levels of organ damage or acidosis. Other treatments may include sodium bicarbonate, thiamine, and magnesium.
More than 5000 cases of poisoning occur in the United States each year. Those affected are often adults and men. Deaths due to ethylene glycol have been reported since 1930. An outbreak of death in 1937 due to drugs mixed in the same compound, diethylene glycol, produced the Food, Drug, and Cosmetic Act of 1938 in the United States mandated evidence. safety before new drugs can be sold. Antifreeze products sometimes have substances to make them more bitter to prevent drinking by children and other animals but these have not yet been found to be effective.
Video Ethylene glycol poisoning
Signs and symptoms
Signs of ethylene glycol poisoning depend on the time after consumption. Symptoms usually follow a three-step development, even if the poisoned individual will not always develop each stage.
- Stage 1 (30 minutes to 12 hours) consists of neurological and gastrointestinal symptoms and looks similar to alcohol poisoning. Individuals who are poisoned may appear to be drunk, dizzy, lacking coordination of muscle movements, drooling, depression, and having slurred speech, seizures, abnormal eye movements, headaches, and confusion. Stomach irritation can cause nausea and vomiting. Also notice excessive thirst and urination. Over time, the body metabolizes ethylene glycol into another poison.
- Stage 2 (12 to 36 h) in which signs of "alcoholic" toxicity appear to be improving, severe internal damage still occurs. Increased heart rate, hyperventilation or increased respiratory effort, and dehydration may begin to develop, along with high blood pressure and metabolic acidosis. These symptoms are the result of the accumulation of organic acids formed by the metabolism of ethylene glycol. In addition, low blood calcium concentrations, overactive muscle reflexes, muscle spasms, QT interval prolongation, and congestive heart failure may occur. If left untreated, death most often occurs during this period. <3> Stage 3 (24 to 72 hours) of renal failure is the result of ethylene glycol poisoning. In cats, this stage occurs 12-24 hours after entry into antifreeze; in dogs, at 36-72 hours after entry into antifreeze. During this stage, severe kidney failure develops due to the formation of calcium oxalate crystals that form in the kidneys. Severe lethargy, coma, depression, vomiting, seizures, drooling, and insensitivity can be seen. Other symptoms include acute tubular necrosis, red blood cells in the urine, excess protein in the urine, lower back pain, decreased or absent urine production, increased blood potassium concentration, and acute renal failure. If renal failure occurs it is usually reversible, although weeks or months of supportive care including hemodialysis may be necessary before renal function returns.
Maps Ethylene glycol poisoning
Source
The most common source of ethylene glycol is the antifreeze or radiator coolant, where the concentration is high. Other sources of ethylene glycol include windshield deicing agents, brake fluid, motor oil, developing solutions for hobby photographers, wood stains, solvents, and paints. Some people insert antifreeze into their cabin toilets to prevent it freezing during the winter, which results in toxins when animals drink from the toilet. Small amounts of ethylene glycol can be contained in holiday ornaments such as snowballs.
The most significant source of ethylene glycol comes from air and anti-ice drainage operations, which are released into land and eventually into waterways near airports experiencing cold winter climates. It is also used in the manufacture of polyester products. In 2006, about 1540 kilotons of ethylene glycol were produced in Canada by three companies in Alberta, with most of the production destined for export.
Pathophysiology
The three main systems that are affected by ethylene glycol poisoning are the central nervous system, metabolic processes, and kidneys. The central nervous system is affected early in the poisoning process as a result of the direct action of ethylene glycol. Similar to ethanol, it causes poisoning, followed by drowsiness or coma. Seizures can occur due to direct effects. The toxic mechanism of ethylene glycol poisoning is primarily due to the metabolite of ethylene glycol. Initially metabolized by alcohol dehydrogenase to glycolaldehyde, which is then oxidized to glycolic acid by aldehyde dehydrogenase. Increased metabolites may cause encephalopathy or cerebral edema. Metabolic effects occur 12 to 36 hours after swallowing, causing metabolic acidosis mainly due to the accumulation of glycolic acid. In addition, as a side effect of the first two steps of metabolism, elevated blood concentrations of lactic acid occur to contribute to lactic acidosis. The formation of acid metabolites also causes inhibition of other metabolic pathways, such as oxidative phosphorylation.
Renal toxicity of ethylene glycol occurs 24 to 72 hours after consumption and is caused by direct cytotoxic effects of glycolic acid. Glycolic acid is then metabolised into glyoxylic acid and eventually becomes oxalic acid. Oxalic acid binds with calcium to form calcium oxalate crystals that can store and cause damage to many areas of the body including the brain, heart, kidneys, and lungs. The most significant effect is the accumulation of calcium oxalate crystals in the kidney causing kidney damage that causes acute or olural acute kidney failure. The rate-limiting step in this cascade is the conversion of glycolic acid to glyoxylic acid. The accumulation of glycolic acid in the body is primarily responsible for toxicity.
Toxicity
Ethylene glycol has been shown to be toxic to humans and also toxic to pet pets such as cats and dogs. Toxic doses requiring medical care vary but are considered to be more than 0.1 mL per kg body weight (mL/kg) of pure substance. That's about 16 mL of ethylene glycol 50% for adults 80 kg and 4 mL for 20 kg children. Toxic control centers often use more than one or more flavors in children or more than a mouthful in adults as doses requiring hospital assessment.
The deadly oral dose in humans has been reported to be about 1.4 mL/kg of pure ethylene glycol. That's about 224 ml (7.6 oz.) Of 50% ethylene glycol for adults 80Ã,® and 56 mL (2 oz.) For children 20 kg. Although survival with medical care has occurred with much higher doses than this, death has occurred with 30 mL concentrate in adults. In the EU classification hazardous substances are 'dangerous' (Xn) while more toxic substances are classified as 'toxic' (T) or 'highly toxic' (T). The US Environmental Protection Agency generally places lethal substances at more than 30 g for adults in Class III Toxicity.
Ethylene glycol has a low vapor pressure; it does not evaporate easily at normal temperatures and therefore high concentrations in air or poisoning are unlikely to occur after inhalation exposures. There may be little risk of poisoning where fog or fog is produced, although this rarely causes toxicity because ethylene glycol causes irritation and coughing when exhaled, warning the victim of its existence. Ethylene glycol is not well absorbed through the skin which means poisoning after skin exposure is also uncommon.
Diagnosis
Because many clinical signs and symptoms of ethylene glycol poisoning are not specific and occur in many toxicities, diagnosis is often difficult. It is most reliably diagnosed by the measurement of blood ethylene glycol concentration. Ethylene glycol in biological fluids can be determined by gas chromatography. Many hospital labs do not have the ability to perform this blood test and in the absence of these tests the diagnosis should be made based on the patient's clinical presentation. In this situation, the test that helps to diagnose poisoning is the measurement of the osmolal gap. The patient's serum osmolality is measured by freezing depression and then compared with predicted osmolality based on measurements of sodium, glucose, blood urea nitrogen of the patient, and any ethanol that may have been digested. The presence of a large osmolal cleft supports the diagnosis of ethylene glycol poisoning. However, normal osmolar gaps do not rule out ethylene glycol exposure due to wide individual variability.
Increased osmolal gap is caused by ethylene glycol itself. When ethylene glycol metabolism takes place there will be less ethylene glycol and this will decrease the concentration of ethylene glycol blood and osmolal gap that makes this test less useful. In addition, the presence of other alcohols such as ethanol, isopropanol, or methanol or conditions such as alcoholic ketoacidosis or diabetes, lactic acidosis, or renal failure may also produce high osmolal gaps leading to incorrect diagnosis.
Other laboratory abnormalities may indicate toxicity, particularly the presence of metabolic acidosis, especially if characterized by large anion disparities. A large anion gap acidosis usually occurs during the early stages of poisoning. However, acidosis has a large number of differential diagnoses, including poisoning from methanol, salicylates, iron, isoniazid, paracetamol, theophylline, or from conditions such as uremia or diabetic ketoacidosis and alcohol. Diagnosis of ethylene glycol toxicity should be considered in patients with severe acidosis. Urine microscopy may reveal needle-shaped calcium oxalate crystals or envelopes in the urine that can show poisoning; although these crystals may not be present until the final stages of poisoning. Finally, many commercial antifreeze radiator products have added fluorescein to allow radiator leakage to be detected using Wood lamps. After consuming antifreeze products containing ethylene glycol and fluorescein, Wood's lamps can reveal fluorescence in the mouth area, clothing, vomit, or urine of the patient that can help diagnose poisoning.
Prevention
Anti-freeze products for automotive use containing propylene glycol as a substitute for ethylene glycol are available, and are generally considered to be safer to use, as they have a distinctly unpleasant taste with the perceived "sweet" flavor of a toxic ethylene glycol-based refrigerant, and only produce lactic acid in the animal body, like their muscles while exercising.
When using antifreeze products containing ethylene glycol, the recommended safety measures include:
- Clean up any spills immediately and thoroughly. Spills can be cleaned by sprinkling cat litter, sand or other absorbent material directly on the spill. After fully absorbed, when wearing protective gloves, the material can be inserted into a plastic bag, sealed and disposed of. The spill area can be rubbed with a stiff brush and warm soapy water. Soap water is not recommended for drying in storm drains.
- Check the vehicle regularly for leaks.
- Store antifreeze in clear, clearly marked packets, in areas not accessible by pets or small children.
- Keeping pets and small children away from the area while draining the car radiator.
- Dispose of used antifreeze just by taking it to the service station.
- If the antifreeze is placed in the toilet, make sure the lid is down and the door is closed.
Treatment
Stabilization and decontamination
The most important initial treatment for ethylene glycol poisoning is to stabilize the patient. Because ethylene glycol is rapidly absorbed, gastric decontamination will not be useful unless it is done within 60 minutes after consumption. Traditionally, gastric rinse or nasogastric aspiration of gastric contents is the most commonly used method of ethylene glycol poisoning. However, the use of gastric lavage has been questioned, and is now no longer used routinely in poisoning situations. Ipecac-induced vomiting is not recommended. Since activated charcoal does not absorb glycol, it is not recommended because it will not be effective in preventing absorption. This is only used in the presence of toxic poison doses or other drugs. Patients with significant poisoning are often present in critical conditions. In this situation patient stabilization including airway management with intubation should be done in preference for gastrointestinal decontamination. Patients with metabolic acidosis or seizures require treatment with sodium bicarbonate and anticonvulsivity such as benzodiazepines. Sodium bicarbonate should be used with caution as it may aggravate hypocalcemia by increasing the binding of calcium plasma proteins. If hypocalcemia occurs it can be treated with calcium replacement although calcium supplementation may increase the precipitation of calcium oxalate crystals that cause tissue damage. Respiratory intubation and support may be necessary in highly intoxicated patients; patients with hypotension require treatment with intravenous fluids and possibly vasopressors.
Antidote
After decontamination and institutional support measures, the next priority is inhibition of further ethylene glycol metabolism using antidotes. Antidotes for ethylene glycol poisoning are ethanol and fomepizole. This unusual treatment forms the mainstay of the management of ethylene glycol poisoning. The toxicity of ethylene glycol derives from metabolism for glycolic acid and oxalic acid. The purpose of pharmacotherapy is to prevent the formation of these metabolites. Ethanol acts by competing with ethylene glycol for alcohol dehydrogenase, the first enzyme in the degradation pathway. Because ethanol has a much higher affinity for alcohol dehydrogenase, about 100 times greater affinity, it successfully blocks the breakdown of ethylene glycol into glycolaldehyde, which prevents further degradation. Without the formation of oxalic acid, nephrotoxic effects can be avoided, but ethylene glycol still exists in the body. This is ultimately excreted in the urine, but supportive therapy for CNS depression and metabolic acidosis will be required until the concentration of ethylene glycol falls below the toxic limit. Ethanol pharmaceutical grade is usually given intravenously as a 5 or 10% solution in 5% dextrose, but is sometimes given orally in the form of strong spirits such as whiskey, vodka, or gin.
Fomepizole is a potent alcohol dehydrogenase inhibitor; similar to ethanol, it serves to block the formation of toxic metabolites. Fomepizole has been shown to be very effective as an antidote to ethylene glycol poisoning. This is the only antidote approved by the US Food and Drug Administration for the treatment of ethylene glycol poisoning. Both antidotes have advantages and disadvantages. Ethanol is available in most hospitals, inexpensive, and can be administered orally or intravenously. Side effects include intoxication, hypoglycemia in children, and possibly liver toxicity. Patients receiving ethanol therapy also require measurement of blood ethanol concentrations and dose adjustments to maintain therapeutic ethanol concentrations. Therefore patients should be monitored in the intensive care unit. Alternatively, the adverse side effects of fomepizole are minimal and an approved dose regimen maintains therapeutic concentrations without the need to monitor blood concentrations of the drug. The disadvantage of fomepizole is its expensive price. At a cost of US $ 1,000 per gram, the average course used in adult poisoning would cost about $ 3,500 to $ 4,000. Despite the cost, fomepizole gradually replaces ethanol as the preferred antidote in ethylene glycol poisoning. Additional agents including thiamine and pyridoxine are often given, as they can help prevent oxalic acid formation. The use of these agents is based on theoretical observations and there is limited evidence to support their use in medicine; they may be of particular benefit to people with vitamin deficiency such as malnourished or alcoholic patients.
hemodialysis
In addition to the antidote, an important treatment for poisoning is the use of hemodialysis. Hemodialysis is used to increase the removal of ethylene glycol that is not metabolized, and its metabolites from the body. It has been shown to be very effective in removing ethylene glycol and its metabolites from the blood. Hemodialysis also has the added benefit of repairing other metabolic damage or supporting deteriorating renal function. Hemodialysis is usually indicated in patients with severe metabolic acidosis (blood pH less than 7.3), renal failure, severe electrolyte imbalance, or if the patient's condition worsens despite treatment. Often both antidotal and hemodialysis treatments are used together in the treatment of poisoning. Because hemodialysis will also remove antidotes from the blood, the dose of antidote needs to be increased to compensate. If hemodialysis is not available, peritoneal dialysis also removes ethylene glycol, although it is less efficient.
Prognosis
Treatment for antifreeze toxicity needs to begin as soon as consumption is likely to be effective; Previous treatments begin, the greater the chance of survival. Cats should be treated within 3 hours after consuming antifreeze to be effective, while the dog should be treated within 8-12 hours after consumption. After renal failure develops, the prognosis is poor.
Generally, if the patient is treated and persisted then full recovery is expected. Patients who arrive early to a medical facility and have quick medical care will usually get a favorable outcome. Alternatively, patients who come late with signs and symptoms of coma, hyperkalemia, convulsions, or severe acidosis have a poor prognosis. Patients who develop severe central nervous system manifestations or survival strokes may have long-term neurological dysfunction; in some cases they can recover, although recovery can be extended. The most significant long-term complications associated with the kidney. Cases of permanent renal damage, often requiring chronic dialysis or kidney transplant, have been reported after severe poisoning.
Epidemiology
Ethylene glycol poisoning is a relatively common occurrence worldwide. Human poisoning often occurs in isolated cases, but may also occur in epidemics. Many cases of poisoning are the result of the use of ethylene glycol as a substitute for alcohol or intentional consumption in suicide attempts. Less common has been used as a killing tool. Children or animals may be exposed to unintentional consumption; children and animals often consume large amounts because ethylene glycol has a sweet taste. In the United States there were 5816 cases reported to poison centers in 2002. In addition, ethylene glycol was the most common chemical responsible for deaths reported by the US poison center in 2003. In Australia there were 17 cases reported to the center Victorian toxins and 30 cases were reported to the New South Wales poison center in 2007. However, these figures may underestimate the true number because not all cases caused by ethylene glycol are reported to poison the control center. Most deaths from ethylene glycol are intentional suicide; deaths in children due to unintentional consumption are very rare.
In an effort to prevent toxicity, it is often a bitter agent called denatonium benzoate, known by the trade name Bitrex, added to the preparation of ethylene glycol as opposed to preventing accidental or intentional intake. The bitter agent considered to stop swallowing as part of the human defense against the consumption of harmful substances is the rejection of bitter tasting substances. In the United States, eight states (Oregon, California, New Mexico, Virginia, Arizona, Maine, Tennessee, Washington) have made the addition of bitter agents into mandatory antifreeze. Three follow-up studies targeting a limited population or suicidal person to assess the effectiveness of bitter agents in preventing toxicity or death, however, show limited benefits from the preparation of bitter ethylene glycol in these two populations. Specifically, Mullins found that the bitterness of antifreeze did not reduce the cases of poisoning preschool children reported in the US state of Oregon. Similarly, White found that adding bitter substances did not reduce the frequency or level of antifreeze toxicity in children under 5 years of age. In addition, another study by White found that people who wanted to commit suicide were not hindered by the bitterness of antifreeze in their attempts to kill. self. These studies do not focus on domestic pet or domestic poultry poisoning, for example, or unintentional exposure to bitter antifreeze among large populations (children of non-preschool ages).
Raccoon poisoning was diagnosed in 2002 in Prince Edward Island, Canada. An online veterinarian's guide provides information on the lethal dose of ethylene glycol for chickens, cows, as well as cats and dogs, adding that younger animals may be more vulnerable.
History
Ethylene glycol was once considered harmless; in 1931 it was suggested to be used as a vehicle or solvent for injectable pharmaceutical preparations. Many cases of poisoning have been reported since then, and have been shown to be toxic to humans.
Environmental effects
Ethylene glycol is involved in air-clearing operations and anti-ice plane is released to the ground and finally to the waterway. A report prepared for the World Health Organization in 2000 states that laboratory tests showing aquatic organisms to drain the water receiving runoff from airports have shown toxic effects and death (page 12). Field studies around airports have reported toxic signs consistent with ethylene glycol poisoning, fish killing, and reduced biodiversity, although the effect can not be definitively thought to be derived from ethylene glycol (page 12). The process of biodegrading glycol also increases the risk to the organism, as the oxygen content becomes exhausted on the water surface (page 13). Other studies found the toxicity for aquatic and other organisms is relatively low, but the oxygen depletion effect of biodegradation is more serious (p.a, 245). Furthermore, "Anaerobic biodegradation may also release relatively toxic byproducts such as acetaldehyde, ethanol, acetate, and methane (p 245)."
In Canada, Environment Canada reports that "in recent years, management practices at major Canadian airports have increased with the installation of new ethylene glycol applications and mitigation or repair facilities for existing ones." Since 1994, federal airports must comply with Canada's Environmental Protection Act Glikol Guidelines, monitoring and reporting of water glycol concentrations. Detailed mitigation plans include storage and handling issues (page 27), spill response procedures, and actions taken to reduce fluid volume (page 28). Considering factors such as "the seasonality of release, ambient temperature, metabolic rate and duration of exposure", Environment Canada states in 2014 that "it is proposed that ethylene glycol does not enter the environment in quantity or concentration or in conditions that have or may have a long- short or long term environmental or biological diversity ".
In the US, airports are required to obtain stormwater disposal permits and ensure that waste from deicing operations is collected and treated properly. Large new airports may be needed to collect 60 percent of deicing aircraft fluid after deicing. Airports that empty aircraft fluids collected directly into US waters must also meet numerical disposal requirements for chemical oxygen demand. A report in 2000 stated that ethylene glycol became less popular for deicing aircraft in the US, due to reporting requirements and adverse environmental impacts (p.Ã, 213), and noted a shift to the use of propylene glycol (p.Ã, I-3).
Other animals
After kidney failure develops in dogs and cats, the results are poor.
See also
- Methylmalonic acidemia - an autosomal recessive metabolic disorder that resembles the effects of ethylene glycol poisoning.
- wine scandal diethylene glycol 1985
- Elixir sulfanilamide where diethylene glycol is used as a solvent for the drug
References
External links
- "Antifreeze Poisoning in Dogs & Cats (Ethylene Glycol Poisoning)" - Pet Poison Helpline
- "Antifreeze Poisoning" - Washington University Medical Information Sheet, College of Veterinary Medicine
- "Overview of Ethylene Glycol Poisoning" - Veterans Veteran Merck Information.
Source of the article : Wikipedia
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