A B C D E F G H I J K L M N O P Q R S T U V W X Y Z # |
Urine Volatile, Qualitative
MessageAll AZ Locations: Order ES or ST the send via ST Courier to BUMCP
Test Code
VLTU
Alias/See Also
Performed at BUMCP
Preferred Specimen
3.0 mL Random Urine
Minimum Volume
1.0 mL Random Urine
Transport Temperature
Refrigerated
Clinical Significance
Ethanol
An estimated 88,000 people die from alcohol-related causes annually, making alcohol (ethanol) the third leading preventable cause of death in the United States. Ethanol belongs in the depressants and sedatives drug classes. It is rapidly absorbed from the GI tract and distributes in body water. Acute toxicity can lead to respiratory depression, vomiting, hypoglycemia, and acidosis. Coma usually occurs at a blood concentration of about 300 mg/dL and death at greater than 400mg/dL.
Methanol
Methanol is a highly toxic substance used extensively in industry and consumer products. It is rapidly absorbed through the skin, respiratory tract, and GI tract. Following ingestion, symptoms may develop between 40 minutes to 72 hours, usually 18-24 hours. Acute toxicity typically exhibits three major types of symptoms: central nervous system depression, severe metabolic acidosis, and ophthalmic changes (reversible and irreversible). Treatment involves initial emesis be performed immediately if the acidosis is marked, is uncorrectable with bicarbonate treatment, or if the blood methanol level is greater than 40mg/dL. Ethanol treatment is indicated in patients with blood levels greater than 20mg/dL to inhibit the formation of the toxic metabolic products by alcoholic dehydrogenase. Ethanol therapy should be continued for 2-3 days or until methanol levels are less than 20 mg/dL or no acidosis is present. A typical blood ethanol level during treatment is 100mg/dL.
Isopropanol
Isopropanol is available in rubbing alcohol, alcohol sponges, etc. Although slightly more toxic than ethanol when ingested, it has no noticeable harmful effects on human skin. It is metabolized in the liver and results in the formation of acetone, which is in turn metabolized to acetate, formate, and carbon dioxide or excreted unchanged or as the glucuronide metabolite. Ingestion may cause hypothermia, lethargy, sleepiness, and coma. Loss of coordination and ataxia may occur if the spinal cord becomes involved. Patients in general have a greater emetic response and gastritis than with ethanol. Hypoglycemia may result, especially in children. Treatment involves emesis (or gastric lavage) and hemodialysis in large ingestions. Toxic effects are generally noted between 50 and 100 mg/dL. Death has been reported at serum concentrations of 150 mg/dL.
Acetone
Acetone is available in pharmaceuticals and cosmetics. At high concentrations, acetone vapor can cause CNS depression, cardiorespiratory failure, and death. In children, blood concentrations of 2 to 3 mL/kg are considered to be toxic. Excessive formation of ketone bodies (acetone) can also occur naturally as a result of ketoacidosis. This condition is associated with a decreased availability of carbohydrates, such as dieting or decreased use of carbohydrates. Diabetes and alcohol consumption are common causes of ketoacidosis. Additionally, acetone is a metabolite of isopropanol. Therefore, ingestion of isopropanol can lead to increased concentrations of acetone.
An estimated 88,000 people die from alcohol-related causes annually, making alcohol (ethanol) the third leading preventable cause of death in the United States. Ethanol belongs in the depressants and sedatives drug classes. It is rapidly absorbed from the GI tract and distributes in body water. Acute toxicity can lead to respiratory depression, vomiting, hypoglycemia, and acidosis. Coma usually occurs at a blood concentration of about 300 mg/dL and death at greater than 400mg/dL.
Methanol
Methanol is a highly toxic substance used extensively in industry and consumer products. It is rapidly absorbed through the skin, respiratory tract, and GI tract. Following ingestion, symptoms may develop between 40 minutes to 72 hours, usually 18-24 hours. Acute toxicity typically exhibits three major types of symptoms: central nervous system depression, severe metabolic acidosis, and ophthalmic changes (reversible and irreversible). Treatment involves initial emesis be performed immediately if the acidosis is marked, is uncorrectable with bicarbonate treatment, or if the blood methanol level is greater than 40mg/dL. Ethanol treatment is indicated in patients with blood levels greater than 20mg/dL to inhibit the formation of the toxic metabolic products by alcoholic dehydrogenase. Ethanol therapy should be continued for 2-3 days or until methanol levels are less than 20 mg/dL or no acidosis is present. A typical blood ethanol level during treatment is 100mg/dL.
Isopropanol
Isopropanol is available in rubbing alcohol, alcohol sponges, etc. Although slightly more toxic than ethanol when ingested, it has no noticeable harmful effects on human skin. It is metabolized in the liver and results in the formation of acetone, which is in turn metabolized to acetate, formate, and carbon dioxide or excreted unchanged or as the glucuronide metabolite. Ingestion may cause hypothermia, lethargy, sleepiness, and coma. Loss of coordination and ataxia may occur if the spinal cord becomes involved. Patients in general have a greater emetic response and gastritis than with ethanol. Hypoglycemia may result, especially in children. Treatment involves emesis (or gastric lavage) and hemodialysis in large ingestions. Toxic effects are generally noted between 50 and 100 mg/dL. Death has been reported at serum concentrations of 150 mg/dL.
Acetone
Acetone is available in pharmaceuticals and cosmetics. At high concentrations, acetone vapor can cause CNS depression, cardiorespiratory failure, and death. In children, blood concentrations of 2 to 3 mL/kg are considered to be toxic. Excessive formation of ketone bodies (acetone) can also occur naturally as a result of ketoacidosis. This condition is associated with a decreased availability of carbohydrates, such as dieting or decreased use of carbohydrates. Diabetes and alcohol consumption are common causes of ketoacidosis. Additionally, acetone is a metabolite of isopropanol. Therefore, ingestion of isopropanol can lead to increased concentrations of acetone.