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Thursday, 30 April 2020

CRAB CRITERIA AT THE EMERGENCY LABORATORY DEPARTMENT

Written by María Francesca Font Picó | Xavier Gabaldó Barrios | Josep María Simó i Sisó

Figure. Atypical crystals of calcium oxalate monohydrate in urine caused by ethylene glycol poisoning.

A 52-year-old female is admitted to intensive care unit (ICU) after being found on her floor's home, she presents decreased level of consciousness. Her blood profile performed at admission shows a severe metabolic acidosis with pH <7 and lactic acid >20_mmol/L. Crystals of calcium oxalate monohydrate are observed in the urine sediment. Osmolal gap is determined (88 mOsm/kg), so that treatment with intravenous ethanol and hemodialysis is initiated. Sample is sent to an outside laboratory to determinate levels of methanol, ethylene glycol and salicylates; ethylene glycol was positive with 2,68 g/L.
The toxic levels are then normalized and the intravenous treatment with ethanol can be discontinued on day 3 (table 1). After extubation, the patient reports voluntary and premeditated intake of the toxic.

tablaTable 1. Evolution of the analytical parameters of the patient in the ICU.

Ethylene glycol is a highly dangerous substance that is metabolized by the liver enzyme alcohol dehydrogenase in glycoaldehyde, glycolic acid, glyoxylic acid and oxalic acid. These substances inhibit cellular oxidative metabolism causing depression of the central nervous system, cardiopulmonary and renal failure. Glycolic acid accumulated in blood is related to metabolic acidosis and mortality. Oxalic acid binds to circulating calcium by precipitating calcium oxalate crystals in the kidney and other tissues (Figure).

This intoxication usually occurs by autolytic attempt as is the case of this patient. It can also happening accidentally. Ethylene glycol is found in different household products such as antifreeze forvehicles. Ethylene glycol poisoning is rare but extremely serious, survivors may suffer neurological sequelae such as blindness, parkinsionan syndrome and axonal sensory polyneuropathy. Prevention of sequelae is dependent upon early treatment is established.

The diagnosis is based on suspision, clinic and laboratory test results.

Treatment with antidote (ethanol or fomepizol) is effective, selectively and competitively binding to the enzyme alcohol dehydrogenase.

In these cases, the calculation of the osmolal gap can provide preliminary real-time and low-cost information to rule out or confirm the presence of osmotically active substances in plasma. Studies point out a high negative predictive value with a cut-off point <10 mOsm / kg H2O to start treatment with antidotes. However, there are other causes of increased osmolal gap such as lactic acidosis, ketoacidosis, critical patients and chronic renal failure.

The calculation of the osmolal gap is obtained from the difference between the measured plasma osmolarity and the calculated osmolarity:

tabla2
REFERENCES

  1. Singh R., Arain E., Buth A., Kado J., Soubani A., Imran N. Ethylene glycol poisoning: an unusual cause of altered mental status and the lessons learned from management of the disease in the acute setting. Case Rep Crit Case 2016; 9157393.
  2. Zaldíbar E., Aguilera L., Aguayo F. J. Severe acute ethylene glicol poisoning: diagnostic utility of osmolar gap monitoring. Rev Esp Anestesiol Reanim 2011; 58:183-185.


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