Diferencia entre revisiones de «Ethylene glycol toxicity»
m (moved Ethylene Glycol Poisoning to Ethylene Glycol Toxicity) |
Sin resumen de edición |
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| Línea 1: | Línea 1: | ||
== Background == | == Background == | ||
*Component of antifreeze | *Characteristics | ||
*Lethal dose = 1g/kg | **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 | ||
* | **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 | |||
##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 | #Chemistry | ||
##Anion gap acidosis | ##Anion gap acidosis | ||
###Will not be present immediately after exposure (only metabolite causes acidosis) | |||
##Renal failure | ##Renal failure | ||
##Osm gap | #Serum Osm | ||
###Calculated serum osm = 2Na + BUN/2.8 + glucose/18 + ethanol/4.2) | ##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 | #Glucose | ||
# | #Alcohol levels | ||
#UA | #UA | ||
##Hematuria, proteinuria, pyuria | ##Hematuria, proteinuria, pyuria | ||
##Calcium oxalate crystals (late finding | ##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 | ||
| Línea 27: | Línea 50: | ||
#ECG | #ECG | ||
##QT prolongation ~ hypocalcemia | ##QT prolongation ~ hypocalcemia | ||
# | #APAP/ASA levels | ||
== Treatment == | == 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 | ## 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 | ||
# | #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 | |||
##Indications | ###Ethylene glycol level >50mg/dL (controversial) | ||
### | #Decrease oxalate production | ||
### Renal | ##Thiamine 100mg IV q6hr x2d | ||
### Electrolyte | ##Pyridoxine 50mg q6hr x2d | ||
### | ##Magnesium 2gm IV x1 | ||
# | |||
## Thiamine 100mg IV q6hr | |||
## | |||
== Source == | == Source == | ||
*Rosen's | |||
*Uptodate | |||
[[Category:Tox]] | |||
Revisión del 07:22 4 ene 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
- Component of antifreeze
- Parent compound causes inebriation; metabolite (glycolic acid) causes toxicity
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%)
- 24-72hr after ingestion
Diagnosis
- Chemistry
- Anion gap acidosis
- Will not be present immediately after exposure (only metabolite causes acidosis)
- Renal failure
- Anion gap acidosis
- 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
- Only parent alcohol is osmotically active
- Calculated serum osm - measured serum osm
- Osm gap
- 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
- QT prolongation ~ hypocalcemia
- 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 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
- Indications:
- 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
- Fomepizole
- 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
- Bicarbonate 1-2mEq/kg IV bolus to attain pH = 7.45-7.50
- 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)
- Indications:
- Decrease oxalate production
- Thiamine 100mg IV q6hr x2d
- Pyridoxine 50mg q6hr x2d
- Magnesium 2gm IV x1
Source
- Rosen's
- Uptodate
