A patient who has ingested ethylene glycol will present somewhere along the spectrum of asymptomatic with an increased osmolar gap to very ill with end-organ toxicity and anion gap metabolic acidosis. The evaluation of the ethylene glycol intoxicated patient should follow a diagnostic approach that utilizes historical and objective data. An electrocardiogram, basic metabolic panel, and acetaminophen concentration should be obtained on all toxicology patients with suspected self-harm attempts. Additional tests to be considered when self-harm is a concern are a complete blood count, transaminases, lipase, pregnancy status, serum or urine ketones, lactate, ethanol, and salicylate concentrations. In the case of toxic alcohols, salicylate toxicity is very important to rule out, especially when evaluating a patient with metabolic acidosis. Ethanol concentration is also required in the evaluation of a patient with toxic alcohol ingestion because ethanol inhibits the metabolism of ethylene glycol.
- Natri Sunfit – Na2SO3 – Sodium Sulphite – Sodium Sulfite
- MUỐI NATRI CLORUA LÀ GÌ? CÁC ỨNG DỤNG CỦA NACL NHƯ THẾ NÀO?
- Lương khởi điểm cử nhân ngành Đảm bảo chất lượng và ATTP khoảng 10 triệu/tháng
- SV làm NCKH: Trường chi 800 triệu đồng/năm, trường linh hoạt hỗ trợ vẫn thiếu
- NH4CL (amoni Clorua) LÀ GÌ? ỨNG DỤNG TRONG CUỘC SỐNG ra sao?
Toxic alcohol concentrations are confirmatory and are measured by gas chromatography, which is not readily available in all healthcare facilities. Concentration is reported in milligrams per deciliter (mg/dL) and, since it typically peaks soon after absorption, is expected to decrease by zero-order kinetics as described above. The time of ingestion is also important to consider, as the toxic alcohol concentration may not reflect the level of toxicity if metabolism has already progressed. This is because it is the metabolites that are primarily responsible for the toxic effects. In the case of ethylene glycol, an oxalic acid concentration may be assessed to correlate with end-organ toxicity resulting in nephropathy; however, its upstream precursor, glycolic acid is the primary contributor toward acidosis.
Obtaining toxic alcohol concentrations often requires sending a serum sample to an outside facility, which may take hours to days to result, and diagnosis is usually required sooner. Therefore, a methodological approach to the diagnosis needs to be considered in which the patient is monitored for the anticipated effects of toxicity. Since anion gap acidosis is a later finding, a patient presenting with normal acid-base status early after ingestion should be observed for a minimum of 12 hours with serial basic metabolic panels every 2 to 4 hours to monitor for the development of metabolic acidosis and an elevated anion gap. This observation period can only begin once it is confirmed that the patient’s ethanol concentration is undetectable. It is also important to refrain from administering exogenous bicarbonate or prophylactic fomepizole during this observation period. A 12-hour observation period has been accepted as the standard of care, but it is based on collective experience more than specific data since acidosis is likely to occur earlier than 12 hours.
Many prefer to utilize the measurement of the osmolar gap for further risk stratification in the early-presenting patient. An increased osmolar gap is nonspecific and indicates the presence of any osmotically active agent, such as ethanol. There is an inverse relationship between the osmolar gap and the anion gap in this setting. The osmolar gap should be elevated early after ingestion of alcohol and progressively decrease as anion gap metabolic acidosis develops. This increased osmolality is due to the abundance of the osmotically active parent compound, and the acidosis is due to the production of its metabolites. When calculating the osmolar gap, it is important to include ethanol in the calculation since ethanol is also osmotically active. The equation to measure the osmolar gap is as follows:
The osmolar gap cannot be used to rule out the presence of toxic alcohol but may be useful as an indication to start treatment when the osmolar gap is greater than 25 mOsm/kg. Although, some references cite the use of an osmolar gap of greater than 50 mOsm/kg. Using the above equation, a toxic alcohol concentration can theoretically be extrapolated from the gap using the molar mass of methanol or ethylene glycol, 32 g/mol, and 62 g/mol, respectively. It should be noted that a baseline osmolality gap is believed to be within a range from -9 to 19 mOsm/kg. This should be considered when calculating the osmolar gap, and the true result of the calculation may be +/- 20 compared to the finding. Serial measurements of serum osmolality and osmolar gap calculations are not necessary or indicated in evaluation. 
When ethylene glycol toxicity is being considered in a patient presenting with an anion gap metabolic acidosis, the patient should be evaluated for acute renal injury. In addition, when a serum ethylene glycol concentration cannot be confirmed, it is especially important to rule out salicylate toxicity. An osmolality gap may not be significantly elevated once the patient is acidotic, as the parent compound will have already metabolized to an unknown degree, and if presenting significantly late, the osmolar gap may be normal. A 12-hour observation period should not be pursued if the patient is already acidotic; however, if stable, the patient should be checked for serum or urine ketones and treated with 1 to 2 liters of isotonic, dextrose-containing intravenous fluids. If improvement occurs as evidenced by improved acidosis and a decrease in the anion gap, then toxic alcohol ingestion should be considered less likely, and other etiologies should be more strongly considered. 
Oftentimes, a serum alcohol concentration can also be estimated. (Note, the term “alcohol” does not specifically refer to only ethanol). This approach may be useful in risk stratification of small, inadvertent ingestions with very clear, accurate histories. The estimation is based on the dose or amount ingested in milliliters (D), percent concentration of ingested alcohol, bioavailability (BV), the volume of distribution (V) expressed as liters per kilogram, and patient weight (W) in kilograms. This is most useful when assessing for toxicity in small, accidental ingestions, usually by children. The equation is as follows:
This is performed by first determining the percent concentration of the ingested agent, with 1% being equal to 1 gm/100 mL. The amount ingested is then determined by multiplying the percent concentration by the volume ingested. This product is then multiplied by bioavailability, which is conservatively assumed to be 100%. This is then divided by the product of the volume of distribution (0.7L/kg) and the patient’s weight in kilograms. The result will be in grams per liter which will need to be converted to milligrams per deciliter (or multiplied by 100). The resulting serum concentration assumes that the total ingestion occurred instantaneously with complete absorption. With small mouthfuls, it can be assumed that an adult’s mouthful is approximately 30 mL and a toddler’s mouthful is approximately 10 mL.
Toxic alcohol exposure is confirmed when a serum concentration demonstrates the diagnosis. It should be suspected in a patient with developing metabolic acidosis with an elevated anion gap, preceded by an osmolality gap that is decreasing over time, with associated symptoms as described above. Other findings that may be present in ethylene glycol toxicity may include urinary calcium oxalate crystals, urinary fluorescence of excreted sodium fluorescein – an occasional antifreeze additive, serum hypocalcemia secondary to precipitation of calcium oxalate crystals, QT interval prolongation on electrocardiogram as a result of said hypocalcemia, and elevated or falsely elevated lactate as a result of assay interference from glycolic acid. These findings are nonspecific and can be falsely positive or negative in this setting.