Diabetic ketoacidosis (DKA) is a serious and potentially fatal complication that can lead to diabetic coma or death if not treated immediately. It is most common in individuals with type 1 diabetes, but can also occur in those with other types of diabetes. DKA symptoms include excessive thirst, frequent urination, nausea and vomiting, stomach pain, weakness or fatigue, and shortness of breath.
Diabetic acidosis, also known as diabetic ketoacidosis and DKA, develops when substances called ketone bodies build up during uncontrolled diabetes. Metabolic acidosis develops when too much acid is produced in the body or when the kidneys cannot remove enough acid from the body. There are several types of metabolic acidosis, including diabetic acidosis.
Ethylene glycol poisoning is caused by drinking ethylene glycol, with early symptoms including intoxication, vomiting, and abdominal pain. These CNS effects predominate during the first hours after exposure. If undetected or untreated, ethylene glycol ingestion can cause serious or fatal toxicity.
Methanol and ethylene glycol poisonings cause scores of fatal intoxications annually, and even relatively small ingestions of these alcohols can produce severe effects. In another patient, intermittent diarrhea and abdominal pain were attributed to mild colonic ischemia.
Diabetic ketoacidosis is an acute, life-threatening metabolic disturbance characterized by hyperglycemia, metabolic acidosis, and ketonemia.
📹 Metabolic acidosis – causes, symptoms, diagnosis, treatment, pathology
What is metabolic acidosis? Metabolic acidosis is caused by a decreased bicarbonate (HCO3−) concentration in the blood.
What is the diagnostic test for poisoning?
Toxicology test, any of a group of laboratory analyses that are used to determine the presence of poisons and other potentially toxic agents in blood, urine, or other bodily substances. Toxicology is the study of poisons—their action, their detection, and the treatment of conditions they produce. Many substances are toxic only at high concentrations. For example, lithium is used to treat bipolar disorder but can be toxic at high levels. Another example is acetaminophen, which is valuable in controlling fever and discomfort but is toxic in large doses. A single toxicology screen may test for as many as 30 agents at one time.
The concentration of an element in the blood is the usual measure of toxicity. The therapeutic blood range is the concentration of the drug that provides therapeutic benefit, whereas the toxic blood range is the concentration at which toxic manifestations are likely. Some substances such as insecticides are toxic to one individual and not to another. Many environmental substances as well as some encountered in the workplace are toxic in high doses; these include organic solvents, heavy metals, mineral dusts, dyes, and cigarette smoke. Acceptable exposure levels are controlled by government standards.
The nervous system is most sensitive to toxicological damage. Common toxins that cause damage to peripheral nerves are the six-carbon solvents, such as n -hexane, found in glues or solvents and organophosphorus compounds. Carbon disulfide, used in the production of rayon fibres and cellophane, is a potent neurotoxin. Because no specific treatment is available for most of these toxic manifestations, preventing overexposure is important.
What does ethylene glycol do in a reaction?
The Chemical Reaction of Ethylene Glycol. Ethylene glycol is in use as a protecting group for carbonyl groups. Treating a ketone or aldehyde with ethylene glycol in the presence of an acid catalyst gives 1, 3-dioxolane. This is resistant to bases and other nucleophiles. The 1, 3-dioxolane protecting group is thereafter removed by further acid hydrolysis processes. For example, isophorone is protected with the help of ethylene glycol with p-toluenesulfonic acid. Water is removed by an azeotropic distillation process to shift the equilibrium to the right.
Toxicity of Ethylene Glycol. Ethylene glycol is moderately toxic for humans. The major danger is because of its sweet taste, which attracts children and animals. Ethylene glycol upon ingestion is oxidized to glycolic acid. This, in turn, oxidizes to oxalic acid, which is toxic. It and its toxic byproducts first affect the central nervous system of the body, then the heart, and finally the kidneys. Ingestion of sufficient amounts of ethylene glycol is fatal if untreated. Several deaths are recorded annually in the U. S. alone because of ethylene glycol.
Uses of Ethylene Glycol \(C_2H_6O_2)\). It is useful in the following manner:
Does ethylene glycol cause hyperglycemia?
In our series, three EG poisonings have VH glucose concentration >10 mmol/L, thus likely representing a situation of severe and potentially lethal AM hyperglycemia. In one additional case the VH glucose concentration was 8. 6 mmol/L, therefore likely representing a definite case of AM hyperglycemia.
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What are the side effects of ethylene?
* Ethylene gas can affect you when breathed in. * Skin contact with liquid Ethylene can cause frostbite. * Exposure to Ethylene can cause headache, dizziness, fatigue, lightheadedness, confusion and unconsciousness.
What are the effects of ethylene on humans?
* Ethylene gas can affect you when breathed in. * Skin contact with liquid Ethylene can cause frostbite. * Exposure to Ethylene can cause headache, dizziness, fatigue, lightheadedness, confusion and unconsciousness. * Ethylene is a HIGHLY FLAMMABLE and REACTIVE chemical and a DANGEROUS FIRE and EXPLOSION HAZARD.
How does ethylene glycol poisoning affect the kidneys?
Typical renal effects included oxalate crystal deposition and renal tubular dilation, vacuolation, and degeneration. Oxalate, a metabolite of glycolic acid, forms a precipitate in the presence of calcium, and the deposition of these crystals in the renal tubules are hallmarks of ethylene glycol toxicity.
What is the main use of ethylene glycol?
Ethylene glycol is widely used as antifreeze (concentration range: 80%–99%) or de-icing solutions (concentration range: 3%–40%) for cars, boats, and aircraft. It is also used in the chemical synthesis of plastics, films, and solvents.
What are the toxic levels of ethylene glycol?
Reports of fatalities following ingestion of ethylene glycol indicate that a volume of 150–1, 500 mL consumed at one time may cause death. In humans, the lethal dose of ethylene glycol is estimated to be in the range of 1, 400–1, 600 mg/kg.
What causes propylene glycol poisoning?
Propylene glycol is metabolized to compounds that are normal constituents of the citric acid cycle. Propylene glycol toxicity generally is not a factor in environmental or occupational exposures. Iatrogenic propylene glycol overdose is the most common cause of propylene glycol poisoning.
- Learning Objectives
- Definition
- Synonyms
- Uses
- Sources of Exposure
- Who Is at Risk
- Biological Fate
- Toxicological Effects at a Glance
- Clinical Evaluation
- Treatment
- Standards and Regulations
- Key Points
- Progress Check
- Describe the uses of propylene glycol, and
- explain the potential risk for propylene glycol toxicity.
- Clear,
- colorless,
- viscous liquid with a faintly sweet taste.
What is a ethylene glycol poisoning blood test?
A blood or serum ethanol level will establish whether ethanol is contributing to the initial CNS symptoms. If present, ethanol will substantially affect metabolism and influence therapy. Patients who have suspected ethylene glycol exposure also should be assessed with serum methanol tests.
The presence of metabolic acidosis with anion and osmolal gaps is an important clue to the diagnosis (Friedman et al. 1962; Parry and Wallach 1974; Szerlip 1999). Numerous toxic substances are associated with an elevated anion gap ( Table 3 ) (Goldfrank LR FN 1998). An elevated osmolal gap suggests the presence of a low-molecular weight substance.
A measured osmolality by the freezing point depression method is needed to detect an osmolal gap. Results of this test are used to calculate the osmolal gap ( Figure 2 ).
Metabolic acidosis might be inhibited or delayed when large quantities of ethanol and ethylene glycol are ingested concurrently. In such cases, an elevated anion-gap metabolic acidosis will take longer to develop than if ethylene glycol alone were ingested. This is because aldehyde dehydrogenase (ADH) has a higher affinity for ethanol than for ethylene glycol. The presence of ethanol delays the metabolism of ethylene glycol to its acidic metabolites.
How does ethylene glycol cause acidosis?
Ethylene glycol exposure is characterized by an elevated osmolal gap and metabolic acidosis with an elevated anion gap. Onset occurs within 24 hours after ingestion. Acidosis is caused primarily by the accumulation of glycolic and glyoxylic acids.
The initial phase of ethylene glycol poisoning in humans is characterized by inebriation caused by unmetabolized ethylene glycol. The following effects are common in acute poisoning cases (Buell et al. 1998; Hess et al. 2004; Parry and Wallach 1974):
- Ataxia
- Slurred speech
- Drowsiness
- Irritation
- Restlessness
- Disorientation
Possible consequences of neurologic effects in severe poisonings (Froberg et al. 2006; Hantson et al. 2002; Walder and Tyler 1994) include the following:
📹 Causes of metabolic acidosis
Defined as low bicarbonate (less than 21 mEq/L) and academia (pH less than 7.35) Calculate the anion gap (AG) which is …
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