Ethylene glycol toxicity: Difference between revisions

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== Background ==
== Background ==
*Component of antifreeze
*Component of antifreeze
*Toxic dose = 0.2mL/kg
*Toxic dose = 0.2mL/kg
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== Pathophysiology ==
== Pathophysiology ==
*Ethylene glycol + alcohol/aldehyde dehydrogenase > oxalate + glycolic acid
*Ethylene glycol + alcohol/aldehyde dehydrogenase > oxalate + glycolic acid


== Work-Up ==
== Work-Up ==
 
#Chemistry
*Chemistry
##Anion gap acidosis
**Anion gap acidosis
##Renal failure
**Renal failure
##Osm gap
**Osm gap
###Calculated serum osm = 2Na + BUN/2.8 + glucose/18 + ethanol/4.2)
***Calculated serum osm = 2Na + BUN/2.8 + glucose/18 + ethanol/4.2)
##Serum Osm
**Serum Osm
#Glucose
*Glucose
#Ethanol level
*Ethanol level
#UA
*UA
##Hematuria, proteinuria, pyuria
**Hematuria, proteinuria, pyuria
##Calcium oxalate crystals (late finding, only seen in 50%)
**Calcium oxalate crystals (late finding, only seen in 50%)
##Urinary fluorescence (may be seen 6 hours after ingestion)
**Urinary fluorescence (may be seen 6 hours after ingestion)
#Total CK
*Total CK
#VBG
*VBG
#ECG
*ECG
##QT prolongation ~ hypocalcemia
**QT prolongation ~ hypocalcemia


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


== Clinical Manifestations ==
== Clinical Manifestations ==
*Patients may die in any stage!
*Patients may die in any stage!


*Stage 1 - CNS
*Stage 1 - CNS
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== Treatment ==
== Treatment ==
 
# Correction of metabolic acidosis with bicarbonate
1. Correction of metabolic acidosis with bicarbonate
## Bicarbonate 1-2mEq/kg IV bolus to attain pH = 7.45-7.50
* 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
** Follow by infusion of 150mEq/L in D5 @ 1.5-2 times maintenance fluid rate
## Monitor for worsening hypocalcemia
* Monitor for worsening hypocalcemia
# ADH enzyme blockade
 
##Fomepizole (4-MP)
 
### 15mg/kg followed by 10mg/kg q12hr x 4 doses
2. ADH enzyme blockade
##Ethyl alcohol
*Fomepizole (4-MP)
###BAL of 100-150 completely saturates alcohol dehydrogenase
** 15mg/kg followed by 10mg/kg q12hr x 4 doses
# Removal of parent alcohol and metabolites via dialysis
*Ethyl alcohol
##Indications (controversial):
**BAL of 100-150 completely saturates alcohol dehydrogenase
### Severe acidosis (pH <7.30)
 
### Renal compromise
 
### Electrolyte imbalances unreponsive to conventional therapy
3. Removal of parent alcohol and metabolites via dialysis
### Anion gap > 20
*Indications (controversial):
# Other
** Severe acidosis (pH <7.30)
## Thiamine 100mg IV q6hr and Pyridoxine 50mg q6hr
** Renal compromise
###Theoretically decreases oxalate production
** Electrolyte imbalances unreponsive to conventional therapy
## Replace Magnesium
** Anion gap > 20
##Hypercalcemia
 
### Symptomatic - treat cautiously (avoid further precipitation)
4. Other
### Asymptomatic - do not treat
* Thiamine 100mg IV q6hr and Pyridoxine 50mg q6hr
**Theoretically decreases oxalate production
* Replace Magnesium
*Hypercalcemia
** Symptomatic - treat cautiously (avoid further precipitation)
** Asymptomatic - do not treat
 


== Source ==
== Source ==

Revision as of 23:37, 11 June 2011

Background

  • Component of antifreeze
  • Toxic dose = 0.2mL/kg
  • Lethal dose = 1.4mL/kg
  • Sweet taste
  • Fluoresces yellow/green under Wood's lamp

Pathophysiology

  • Ethylene glycol + alcohol/aldehyde dehydrogenase > oxalate + glycolic acid

Work-Up

  1. Chemistry
    1. Anion gap acidosis
    2. Renal failure
    3. Osm gap
      1. Calculated serum osm = 2Na + BUN/2.8 + glucose/18 + ethanol/4.2)
    4. Serum Osm
  2. Glucose
  3. Ethanol level
  4. UA
    1. Hematuria, proteinuria, pyuria
    2. Calcium oxalate crystals (late finding, only seen in 50%)
    3. Urinary fluorescence (may be seen 6 hours after ingestion)
  5. Total CK
  6. VBG
  7. ECG
    1. QT prolongation ~ hypocalcemia

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

Clinical Manifestations

  • Patients may die in any stage!
  • Stage 1 - CNS
    • 30min to 12h
    • Pt appears intoxicated (slurred speech, ataxia, stupor, sz, coma)
  • Stage 2 - Cardiopulmonary
    • 12- 24h
    • Hypertension, tachycardia, CHF
    • ARDS, pulmonary infiltrates
    • Hypocalcemia (chelation by oxalate)
    • Myositis & CK elevation
  • Stage 3 - Renal
    • 24- 72h
    • Flank pain, CVAT
    • Hematuria, proteinuria, calcium oxalate crystals (50%)
  • Stage 4 - Delayed CNS
    • 6-12days
    • Cranial neuropathy

Treatment

  1. Correction of metabolic acidosis with bicarbonate
    1. Bicarbonate 1-2mEq/kg IV bolus to attain pH = 7.45-7.50
      1. Follow by infusion of 150mEq/L in D5 @ 1.5-2 times maintenance fluid rate
    2. Monitor for worsening hypocalcemia
  2. ADH enzyme blockade
    1. Fomepizole (4-MP)
      1. 15mg/kg followed by 10mg/kg q12hr x 4 doses
    2. Ethyl alcohol
      1. BAL of 100-150 completely saturates alcohol dehydrogenase
  3. Removal of parent alcohol and metabolites via dialysis
    1. Indications (controversial):
      1. Severe acidosis (pH <7.30)
      2. Renal compromise
      3. Electrolyte imbalances unreponsive to conventional therapy
      4. Anion gap > 20
  4. Other
    1. Thiamine 100mg IV q6hr and Pyridoxine 50mg q6hr
      1. Theoretically decreases oxalate production
    2. Replace Magnesium
    3. Hypercalcemia
      1. Symptomatic - treat cautiously (avoid further precipitation)
      2. Asymptomatic - do not treat

Source

Rosen's




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