Ethylene glycol toxicity: Difference between revisions

Revision as of 07:22, 4 January 2012

Background

Characteristics
- Component of antifreeze
  - 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 Manifestations

Stage 1 - CNS
1. 30min-12hr after ingestion
2. Pt appears intoxicated (slurred speech, ataxia, stupor, seizure, coma)
Stage 2 - Cardiopulmonary
1. 12-24hr after ingestion
2. Most deaths occur during this stage
  1. Hypertension, tachycardia, CHF
  2. ARDS, pulmonary infiltrates
  3. Hypocalcemia (chelation by oxalate)
  4. Myositis & CK elevation
Stage 3 - Renal
1. 24-72hr after ingestion
  1. Flank pain, CVAT
  2. Hematuria, proteinuria, calcium oxalate crystals (50%)

Diagnosis

Chemistry
1. Anion gap acidosis
  1. Will not be present immediately after exposure (only metabolite causes acidosis)
2. Renal failure
Serum Osm
1. Osm gap
  1. Calculated serum osm - measured serum osm
    1. Calculated serum osm = 2Na + BUN/2.8 + glucose/18 + ethanol/4.2)
  2. Normal < 10
  3. >50 highly suggestive of toxic alcohol poisoning)
  4. Note: Cannot rule out toxic ingestion with a "normal" osmol gap
    1. Only parent alcohol is osmotically active
      1. Delayed presentation may mean that much of it is already metabolized
Glucose
Alcohol levels
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)
Total CK
VBG
ECG
1. QT prolongation ~ hypocalcemia
APAP/ASA levels

Treatment

ADH enzyme blockade
1. Fomepizole
  1. Indications:
    1. Ethylene glycol level >20mg/dL
    2. Suspected significant ethylene glycol ingestion w/ ETOH level <100mg/dL
    3. Coma or AMS in pt w/ unclear history and osm gap >10
    4. Coma or AMS in pt w/ unclear history and unexplained met acidosis and ETOH level <100
  2. Dosing
    1. 15mg/kg IV over 30min; follow by 10mg/kg q12hr until level <20 or acidosis resolves
2. Ethanol
  1. BAL of 100-150 completely saturates alcohol dehydrogenase
  2. IV: load 800mg/kg; then give 100mg/kg/hr
  3. Oral: 3-4 1-oz "shots" of 80-proof liquor); then give 1-2 "shots" per hour
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
Dialysis
1. Indications:
  1. Refractory metabolic acidosis (pH <7.25) w/ AG >30
  2. Renal insufficiency
  3. Deteriorating vital signs despite aggressive supportive care
  4. Electrolyte abnormalities refractory to conventional therapy
  5. Ethylene glycol level >50mg/dL (controversial)
Decrease oxalate production
1. Thiamine 100mg IV q6hr x2d
2. Pyridoxine 50mg q6hr x2d
3. Magnesium 2gm IV x1

Source

Rosen's
Uptodate

Authors:

@@ Line 1: / Line 1: @@
 == Background ==
-*Component of antifreeze
+*Characteristics
-*Lethal dose = 1g/kg of ethylene glycol
+**Component of antifreeze
-**Volume depends on percentage of ethylene glycol in solution, typically 0.6 g/mL
+***Fluoresces yellow/green under Wood's lamp (neither Sn nor Sp)
-**60 kg patient lethal dose ~ 100 mL
+**Sweet taste
-*Sweet taste
+**Lethal dose = 1g/kg
-*Fluoresces yellow/green under Wood's lamp
+***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
-== Pathophysiology ==
-*Ethylene glycol + alcohol/aldehyde dehydrogenase > oxalate + glycolic acid
-== Work-Up ==
+== Clinical Manifestations ==
+#Stage 1 - CNS
+##30min-12hr after ingestion
+##Pt appears intoxicated (slurred speech, ataxia, stupor, seizure, coma)
+#Stage 2 - Cardiopulmonary
+##12-24hr after ingestion
+##Most deaths occur during this stage
+###Hypertension, tachycardia, CHF
+###ARDS, pulmonary infiltrates
+###Hypocalcemia (chelation by oxalate)
+###Myositis & CK elevation
+#Stage 3 - Renal
+##24-72hr after ingestion
+###Flank pain, CVAT
+###Hematuria, proteinuria, calcium oxalate crystals (50%)
+== Diagnosis ==
 #Chemistry
 ##Anion gap acidosis
+###Will not be present immediately after exposure (only metabolite causes acidosis)
 ##Renal failure
-##Osm gap (Calculated serum osm - measured serum osm): normal < 10
+#Serum Osm
-###Calculated serum osm = 2Na + BUN/2.8 + glucose/18 + ethanol/4.2)
+##Osm gap
-##Serum Osm
+###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
-#Ethanol level
+#Alcohol levels
 #UA
 ##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)
 #Total CK
@@ Line 27: / Line 50: @@
 #ECG
 ##QT prolongation ~ hypocalcemia
-#Tylenol/Aspirin levels
+#APAP/ASA levels
-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 ==
-# Correction of metabolic acidosis with bicarbonate
+#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 w/ unclear history and osm gap >10
+####Coma or AMS in pt w/ 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
+###BAL of 100-150 completely saturates alcohol dehydrogenase
+###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 with bicarbonate
 ## 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
-# ADH enzyme blockade
+#Dialysis
-##Fomepizole (4-MP)
+##Indications:
-### 15mg/kg followed by 10mg/kg q12hr x 4 doses
+###Refractory metabolic acidosis (pH <7.25) w/ AG >30
-##Ethyl alcohol
+###Renal insufficiency
-###BAL of 100-150 completely saturates alcohol dehydrogenase
+###Deteriorating vital signs despite aggressive supportive care
-# Removal of parent alcohol and metabolites via dialysis
+###Electrolyte abnormalities refractory to conventional therapy
-##Indications (controversial):
+###Ethylene glycol level >50mg/dL (controversial)
-### Severe acidosis (pH <7.30)
+#Decrease oxalate production
-### Renal compromise
+##Thiamine 100mg IV q6hr x2d
-### Electrolyte imbalances unreponsive to conventional therapy
+##Pyridoxine 50mg q6hr x2d
-### Anion gap > 20
+##Magnesium 2gm IV x1
-# Other
-## 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 ==
+*Rosen's
+*Uptodate
-Rosen's
+[[Category:Tox]]
-Uptodate
-<br/>[[Category:Tox]] <br/><br/>