Removal of propylene glycol and correction of increased osmolar gap by hemodialysis in a patient on high dose lorazepam infusion therapy

Parker, Mark G.; Fraser, Gilles L.; Watson, Donald M.; Riker, Richard R.

doi:10.1007/s00134-001-1125-1

Cited by 66 publications

(57 citation statements)

References 8 publications

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“…The serum propylene glycol concentration associated with toxicity has ranged from 12 to 520 mg/dl, but toxicity is most likely to occur at blood concentration in excess of 100 mg/dl (19,106,107). Patients with impaired liver or kidney function are said to be at increased risk for developing toxicity (107).…”

Section: Epidemiologymentioning

confidence: 99%

“…Patients with impaired liver or kidney function are said to be at increased risk for developing toxicity (107). In contrast to methanol, ethylene glycol, and diethylene glycol, the mortality of propylene glycol is low, despite its administration to patients with multiple organ dysfunction (19,36,49,100,104 -107).…”

Section: Epidemiologymentioning

confidence: 99%

“…After intravenous administration with benzodiazepines, central nervous system depression may occur, but this is an expected result of the medication rather than due to propylene glycol (29,104,107,109).…”

Section: Clinical Findingsmentioning

confidence: 99%

“…Serum osmolality can be normal or high (26,36,105,107,109,111), and an increased serum osmolality may be the only evidence of abnormal blood concentrations. Because its half-life in blood is short, once the intravenous infusion is discontinued, serum osmolality will return rapidly to baseline.…”

Section: Laboratory Findingsmentioning

confidence: 99%

“…In the face of extremely high blood concentrations, hemodialysis is extremely effective in rapidly reducing serum propylene glycol levels (107). Therefore, in the face of renal failure, extremely high serum propylene glycol levels, or severe metabolic acidosis, early institution of dialysis is warranted (35,107,111).…”

Section: Treatmentmentioning

confidence: 99%

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Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

354

326

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Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Table 1. Methanol, ethylene glycol, diethylene glycol, and propylene glycol intoxication and alcoholic ketoacidosis can produce hyperosmolality and metabolic acidosis (3-9). Isopropanol intoxication is usually associated with hyperosmolality alone (4,5). Importantly, several of these disorders can be fatal or produce irreversible tissue damage if they are not quickly recognized and treated appropriately (4 -15). Effect of Alcohols on Serum Osmolality and the Osmolal GapThe normal serum osmolality of 285 to 290 mOsm/L is due to sodium and its counterbalancing ions, bicarbonate and chloride, and glucose and urea. It can be calculated using the following equation:Serum osmolality (mOsm/L) ϭ 2 ϫ Na ϩ ϩ blood urea nitrogen (mg/dl)/2.8 ϩ glucose (mg/dl)/18. The serum osmolality measured by freezing point depression is usually within 10 mOsm/L of the calculated serum osmolality (16). Accumulation of low molecular weight substances in the serum (such as each of the alcohols) will raise the measured serum osmolality above that of the calculated serum osmolality, producing an osmolal gap (4,5,16 -18). The effect of each of the alcohols on serum osmolality is shown in Table 2. Methanol gives rise to the greatest increment in serum osmolality, followed by ethanol, isopropanol, ethylene glycol, propylene glycol, and diethylene glycol in that...

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Section: Epidemiologymentioning

confidence: 99%

Section: Epidemiologymentioning

confidence: 99%

Section: Clinical Findingsmentioning

confidence: 99%

Section: Laboratory Findingsmentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

See 3 more Smart Citations

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

354

326

View full text Add to dashboard Cite

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User Safety Assessment of Veterinary Medicinal Products

Woodward¹

2009

Veterinary Pharmacovigilance

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Treatment of lactic acidosis: Appropriate confusion

Rachoin

Weisberg

McFadden

2010

Journal of Hospital Medicine

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Lactic acid is a marker of tissue ischemia but it also may accumulate without tissue hypoperfusion. In the latter circumstance, lactic acid accumulation may be an adaptive mechanism-a novel possibility quite in contrast to the traditional view of lactic acid as only a marker of tissue ischemia. Studies on the treatment of LA with sodium bicarbonate or other buffers fail to show consistent clinical benefit. Severe acidemia in the setting of LA is a particularly poorly studied area. In the settings of medication-induced LA, optimal treatment, apart from prompt cessation of the offending agent, is still unclear.

show abstract

Removal of propylene glycol and correction of increased osmolar gap by hemodialysis in a patient on high dose lorazepam infusion therapy

Cited by 66 publications

References 8 publications

Toxic Alcohol Ingestions

Toxic Alcohol Ingestions

User Safety Assessment of Veterinary Medicinal Products

Treatment of lactic acidosis: Appropriate confusion

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