Ethylene glycol toxicity: Difference between revisions

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== Treatment ==
== Treatment ==
#ADH enzyme blockade
===ADH enzyme blockade===
#*Fomepizole
'''Fomepizole:'''
#**Indications:
*Indications:
#***Ethylene glycol level >20mg/dL
**Ethylene glycol level >20mg/dL
#***Suspected significant ethylene glycol ingestion w/ ETOH level <100mg/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 osm gap >10
#***Coma or AMS in pt with unclear history and unexplained met acidosis and ETOH level <100
**Coma or AMS in pt with unclear history and unexplained met acidosis and ETOH level <100
#**Dosing
*Dosing
#***15mg/kg IV over 30min; follow by 10mg/kg q12hr until level <20 or acidosis resolves
**15mg/kg IV over 30min; follow by 10mg/kg q12hr until level <20 or acidosis resolves
#*Ethanol
'''Ethanol:'''
#**BAL of 100-150 completely saturates alcohol dehydrogenase
*Ethanol drips are rarely used
#**IV: load 800mg/kg; then give 100mg/kg/hr
*BAL of 100-150 completely saturates alcohol dehydrogenase
#**Oral: 3-4 1-oz "shots" of 80-proof liquor); then give 1-2 "shots" per hour
*Dosing:
#Correction of metabolic acidosis with bicarbonate
**IV: load 800mg/kg; then give 100mg/kg/hr
#* [[Bicarbonate]] 1-2mEq/kg IV bolus to attain pH = 7.45-7.50
**Oral: 3-4 1-oz "shots" of 80-proof liquor); then give 1-2 "shots" per hour
#** Follow by infusion of 150mEq/L in D5 @ 1.5-2 times maintenance fluid rate
===Correction of metabolic acidosis===
#* Monitor for worsening [[hypocalcemia]]
Bicarbonate infusion is an option however the patient will need to compensate with an increased respiratory rate otherwise a concomitant respiratory acidosis will ensure.
#Dialysis
* [[Bicarbonate]] 1-2mEq/kg IV bolus to attain pH = 7.45-7.50
#*Indications:
** Follow by infusion of 150mEq/L in D5 @ 1.5-2 times maintenance fluid rate
#**Refractory metabolic acidosis (pH <7.25) w/ AG >30
* Monitor for worsening [[hypocalcemia]]
#**Renal insufficiency
===Dialysis===
#**Deteriorating vital signs despite aggressive supportive care
*Indications:
#**Electrolyte abnormalities refractory to conventional therapy
**Refractory metabolic acidosis (pH <7.25) w/ AG >30
#**Ethylene glycol level >50mg/dL (controversial)
**Renal insufficiency
#**Glycolic acid level > 8 mmol/L (glycolic acid is metabolite that causes anion gap acidosis)
**Deteriorating vital signs despite aggressive supportive care
#Decrease oxalate production
**Electrolyte abnormalities refractory to conventional therapy
#*[[Thiamine]] 100mg IV q6hr x2d
**Ethylene glycol level >50mg/dL (controversial)
#*[[Pyridoxine]] 50mg q6hr x2d
**Glycolic acid level > 8 mmol/L (glycolic acid is metabolite that causes anion gap acidosis)
#*[[Magnesium]] 2gm IV x1
===Decrease oxalate production===
*[[Thiamine]] 100mg IV q6hr x2d
*[[Pyridoxine]] 50mg q6hr x2d
*[[Magnesium]] 2gm IV x1


==See Also==
==See Also==

Revision as of 00:39, 12 November 2015

Background

  • Characteristics
    • 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

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
    • Anion gap acidosis
      • Will not be present immediately after exposure (only metabolite causes acidosis)
    • Renal failure
  • Serum Osm
    • 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
  • Glucose
  • Alcohol levels
  • UA
    • Hematuria, proteinuria, pyuria
    • Calcium oxalate crystals (late finding; only seen in 50%)
    • Urinary fluorescence (may be seen 6 hours after ingestion)
  • Total CK
  • VBG
  • ECG
  • APAP/ASA levels

Treatment

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

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