Ethylene glycol toxicity: Difference between revisions
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#**Electrolyte abnormalities refractory to conventional therapy | #**Electrolyte abnormalities refractory to conventional therapy | ||
#**Ethylene glycol level >50mg/dL (controversial) | #**Ethylene glycol level >50mg/dL (controversial) | ||
#**Glycolic acid level > 8 mmol/L (glycolic acid is metabolite that causes anion gap acidosis) | |||
#Decrease oxalate production | #Decrease oxalate production | ||
#*[[Thiamine]] 100mg IV q6hr x2d | #*[[Thiamine]] 100mg IV q6hr x2d |
Revision as of 14:10, 15 October 2015
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 Features
Stage 1 - CNS
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, CVA tenderness
- Hematuria, proteinuria, calcium oxalate crystals (50%)
Differential Diagnosis
Sedative/hypnotic toxicity
- Absinthe
- Barbiturates
- Benzodiazepines
- Chloral hydrate
- Gamma hydroxybutyrate (GHB)
- Baclofen toxicity
- Opioids
- Toxic alcohols
- Xylazine toxicity
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
- 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
- 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)
- Glycolic acid level > 8 mmol/L (glycolic acid is metabolite that causes anion gap acidosis)
- Indications:
- Decrease oxalate production
- Thiamine 100mg IV q6hr x2d
- Pyridoxine 50mg q6hr x2d
- Magnesium 2gm IV x1