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Case Report
2008/07/25
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General Data
51y/o male patient
Mainland China fisherman
Presented to ER on 2008/06/12 18:27pm Smoking: (+)
Drinking: (+)
Denied Hx of major systemic diseases Denied allergy Hx
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Chief complaint
Severe abdominal pain since 12pm,
nausea sensation and vomiting several
times
Vital Signs: (97/06/12)
BP : 140/80mmHg
PR : 88/min
RR : 24/min
BT : 36.40C
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Present Illness
Abdominal pain complained since
afternoon. The pain was colicky and
intermittent. He was initially brought to
LMD and was referred to our ER.
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Physical Examination
Cons: E4V5M6, Clear
Pupils: (2+/2+)
HEENT: Not pale or icteric
Neck: Supple
Chest: Bilateral clear BS
Heart: Regular HB, No murmur
Abdomen: Diffuse tenderness, Voluntarymuscle guarding
Ext: Freely and movable
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Laboratory Findings
Hb 15.9 g/dL WBC 19500/uL N/L 83.6%/11.6%
Glucose 255 mg/dL
Cr 1.8 mg/dL
AST 425 U/L
NA 121.3 mmol/L
K 6.1 mmol/L
Lipase 123 U/L
EKG NSR (90/min)
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Further examination
T Bil 2.8 g/dL
ALK-P 118 U/L
ALT 91 U/L
Blood osmolality 324mOSM/L
BUN 25 mg/dL
Alc 16 mg/dL
Cl 83 mmol/L
Amylase 282 U/L
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ABG and other Data
pH 6.753
pCO2 15.2
pO2 129.1
HCO3 2.1
Anion Gap = Na - (Cl + HCO3-)
Anion Gap 36
Osmolar Gap = Measured Posm Calculated
Posm (Posm = 2(Na) + glucose/18 + BUN/2.8 )
Osmolality Gap 67
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DISCUSSION
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Toxins and disease states associated with
an elevated AG metabolic acidosis
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Drugs and medical conditions not
listed in MUDPILES
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Toxins with elevated Osmol gap
Mannitol
Alcohols: ethanol, ethylene glycol,
isopropanol, methanol, propylene glycol
Diatrizoate
Glycerol
Acetone Sorbitol
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Methanol
Intoxication
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Methanol
Commonly found in automobile windshield
washer solvent, gas line antifreeze, copy
machine fluid, fuel for small stoves, paint
strippers, and as an industrial solvent.
Can be absorbed rapidly from the gut, skin
and lung.
Slowly metabolized first to formaldehyde
(by ADH) ,and then to formic acid
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Metabolic pathway of methanol
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Metabolism and Half life
Methanol is oxidized 10 times more slowly
than ethanol.
Ethanol has a 10 to 20 times greater
affinity for alcohol dehydrogenase than
methanol
The serum half-life of methanol after mild
toxicity is 14 to 20 hours, and, after severe
toxicity, 24 to 30 hours
1mL/kg is considered lethal
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Elimination
Hepatic: 75%~85%
Renal: 2%~5%
Pulmonary: 10%~20%
Alcohol dehydrogenase oxidizes methanolto formaldehyde, which is convertedrapidly to formic acid by formaldehyde
dehydrogenase The folate-dependent pathway oxidizes
formic acid to carbon dioxide
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Time course
Initial symptoms generally occur 12-24 hours
after ingestion.
The interval between ingestion and the
appearance of symptoms is correlated with thevolume of methanol ingested and the amount of
ethanol concomitantly ingested; competitive
inhibition exists between the two.
Methanol blood levels peak at 30-90 minutes
following ingestion and are often not correlated
with time to symptom appearance
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Neurologic effects
Headache
Vertigo
Lethargy
Confusion
Hemorrhagic and nonhemorrhagic damageof the putamen
Coma and seizures may occur in severecases, probably as a result of cerebraledema
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GI effects
Nausea
Vomiting
Abdominal pain Pancreatitis
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Opthalmologic effects
Blurred vision, snow field
Decreased visual acuity
Photophobia
Constricted visual fields
Fixed and dilated pupils
Retinal edema
Visual defects may present in 25% ofsevere cases
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Specific effects due to Formic acid
High anion gap metabolic acidosis
Inhibit cytochrome oxidase chain, leading
to lactate formation
Visual impairment, papilledema
Pancreatitis
High osmol gap
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Treatment
ABCs
GI decontamination( gastric lavage ) +Ativated charcoal
Fluid supply and Thiamine 100mg iv q6h
Correction of metabolic acidosis withbicarbonate
Alcohol dehydrogenase (ADH) blockade Arrange hemodialysis if necessary. Adjuvant therapy folic acid
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ADH competitive inhibitor
Ethanol
Loading dose : 0.8g/kg
Maintain dose : 66-130mg/kg/hr
Alcoholism : 100-154mg/kg/hr
Hemodialysis : 250-350mg/kg/hr
IV with 10% solution
Oral with 20%-30% solution
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Indications and Treatment
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Take Home message
ABG High anion gap metabolic acidosis:
C: CO, CN
A: aspirin, alcohol
T: toluene, theophylline
M: methanol, metformin
D: DKA, AKA, SKA.
U: uremic toxin
P: paraldehyde, phenformin
I : Iron, INH
L: lactic acidosis
E: ethylene glycol
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References
Emergency medicine; A comprehensivestudy guide 6th edition (Oct 2003): JudithE Tintinalli
Differentiating the Causes of MetabolicAcidosis in Poisoned patient : Clin LabMed 26(2006) 31-48 Bryan S. Judge
Emedicine: methanol intoxication
