Ethylene glycol toxicity: Difference between revisions

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== Background ==
== Background ==
*Characteristics
*Component of antifreeze, automobile coolants, de-icing agents, industrial solvents and hydraulic brake fluid.
**Component of antifreeze, automobile coolants, de-icing agents, industrial solvents and hydraulic brake fluid.
**Fluoresces yellow/green under Wood's lamp (neither Sn nor Sp)
***Fluoresces yellow/green under Wood's lamp (neither Sn nor Sp)
*Sweet taste
**Sweet taste
*Lethal dose = 1g/kg
**Lethal dose = 1g/kg
**Volume depends on percentage of ethylene glycol in solution, typically 0.6 g/mL
***Volume depends on percentage of ethylene glycol in solution, typically 0.6 g/mL
**60 kg patient lethal dose ~ 100 mL
***60 kg patient lethal dose ~ 100 mL
*Parent compound causes inebriation; metabolite (glycolic acid) causes toxicity
*Parent compound causes inebriation; metabolite (glycolic acid) causes toxicity
[[File:toxic alcohol ingestion - ethylene glycol.JPG|thumbnail]]
[[File:toxic alcohol ingestion - ethylene glycol.JPG|thumbnail]]


== Clinical Features ==
==Clinical Features==
===Stage 1 - CNS===
===Stage 1 - CNS===
*30min-12hr after ingestion
*30min-12hr after ingestion
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{{Sedatve/hypnotic toxicity types}}
{{Sedatve/hypnotic toxicity types}}


== Diagnosis ==
==Diagnosis==
===Chemistry===
===Chemistry===
May see:
May see:
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*Useful to discern the cause of the anion gap as well as assess for other toxic ingestion
*Useful to discern the cause of the anion gap as well as assess for other toxic ingestion


== Treatment ==
==Management==
===ADH enzyme blockade===
===ADH enzyme blockade===
'''Fomepizole:'''
'''Fomepizole:'''
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*[[Sedative/hypnotic toxicity]]
*[[Sedative/hypnotic toxicity]]


== References ==
==References==
<references/>
<references/>


[[Category:Tox]]
[[Category:Tox]]

Revision as of 06:10, 23 February 2016

Background

  • Component of antifreeze, automobile coolants, de-icing agents, industrial solvents and hydraulic brake fluid.
    • Fluoresces yellow/green under Wood's lamp (neither Sn nor Sp)
  • Sweet taste
  • Lethal dose = 1g/kg
    • Volume depends on percentage of ethylene glycol in solution, typically 0.6 g/mL
    • 60 kg patient lethal dose ~ 100 mL
  • Parent compound causes inebriation; metabolite (glycolic acid) causes toxicity
Toxic alcohol ingestion - ethylene glycol.JPG

Clinical Features

Stage 1 - CNS

  • 30min-12hr after ingestion
  • Appears intoxicated (slurred speech, ataxia, stupor, seizure, coma)

Stage 2 - Cardiopulmonary

Stage 3 - Renal

  • 24-72hr after ingestion

Differential Diagnosis

Sedative/hypnotic toxicity

Diagnosis

Chemistry

May see:

  • Anion gap acidosis
    • Will not be present immediately after exposure (only metabolite causes acidosis)
  • Renal failure
  • Glucose - may be low in setting of decreased caloric intake

Serum osmolality

Osm gap:

  • Calculated serum osm - measured serum osm
  • Calculated serum osm = 2Na + BUN/2.8 + glucose/18 + ethanol/4.2)
  • Normal < 10
  • >50 highly suggestive of toxic alcohol poisoning)

Note: Cannot rule out toxic ingestion with a "normal" osmol gap

  • Only parent alcohol is osmotically active
  • Delayed presentation may mean that much of it is already metabolized

Alcohol levels

May be useful however even if elevated, patients can still have ingested a toxic alcohol

Urinalysis

  • Hematuria, proteinuria, pyuria
  • Calcium oxalate crystals (late finding; only seen in 50%)
  • Urinary fluorescence (may be seen 6 hours after ingestion)

Total CK

Useful to assess for signs of rhabdomyolysis especially if the patient was found laying down

Venous blood gas

Needed to assess degree of acidosis. An ABG is not necessary since pH can be approximated with a clinical degree via a VBG

ECG

Acetaminophen or Aspirin levels

  • Useful to discern the cause of the anion gap as well as assess for other toxic ingestion

Management

ADH enzyme blockade

Fomepizole:

  • Indications:
    • Ethylene glycol level >20mg/dL
    • Suspected significant ethylene glycol ingestion w/ ETOH level <100mg/dL
    • Coma or AMS in pt with unclear history and osm gap >10
    • Coma or AMS in pt with unclear history and unexplained met acidosis and ETOH level <100
  • Dosing
    • 15mg/kg IV over 30min; follow by 10mg/kg q12hr until level <20 or acidosis resolves

Ethanol:

  • Ethanol drips are rarely used
  • BAL of 100-150 completely saturates alcohol dehydrogenase
  • Dosing:
    • IV: load 800mg/kg; then give 100mg/kg/hr
    • Oral: 3-4 1-oz "shots" of 80-proof liquor); then give 1-2 "shots" per hour

Correction of metabolic acidosis

Bicarbonate infusion is an option however the patient will need to compensate with an increased respiratory rate otherwise a concomitant respiratory acidosis will ensure.

  • Bicarbonate 1-2mEq/kg IV bolus to attain pH = 7.45-7.50
    • Follow by infusion of 150mEq/L in D5 @ 1.5-2 times maintenance fluid rate
  • Monitor for worsening hypocalcemia

Dialysis

  • Indications:
    • Refractory metabolic acidosis (pH <7.25) w/ AG >30
    • Renal insufficiency
    • Deteriorating vital signs despite aggressive supportive care
    • Electrolyte abnormalities refractory to conventional therapy
    • Ethylene glycol level >50mg/dL (controversial)
    • Glycolic acid level > 8 mmol/L (glycolic acid is metabolite that causes anion gap acidosis)

Decrease oxalate production

See Also

References