• Aspirin overdose pathophysiology and treatment

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o Decontamination via activated charcoal
o Supplemental glucose — Aspirin intoxication may decrease cerebral
glucose concentrations despite a normal serum glucose [19,42]. Thus,
supplemental glucose should be given to patients with an altered mental
status regardless of the serum glucose concentration.
• Causes of metabolic acidosis w/ anion gap
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• DKA: pathophysiology, diagnosis, treatment
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o Presentation:
§ Early: marked hyperglycemia are polyuria, polydipsia, and weight
loss
§ Neurologic: stupor/coma
§ Abdominal pain, nausea, vomiting
§ PEx:
• Signs of volume depletion are common in both DKA and
HHS and include decreased skin turgor, dry axillae and oral
mucosa, low jugular venous pressure, tachycardia, and, if
severe, hypotension
• Patients with DKA may have a fruity odor (due to exhaled
acetone; this is similar to the scent of nail polish remover)
and deep respirations reflecting the compensatory
hyperventilation (called Kussmaul respirations).
o Diagnosis
§ Serum ketones — Three ketone bodies are produced and
accumulate in DKA: acetoacetic acid, which is the only one that is a
true ketoacid; beta-hydroxybutyric acid, and acetone. Testing for
 serum ketones is generally performed if urine testing is positive.
Urine ketone bodies are detected with nitroprusside tests, while
serum ketones can be detected with either a nitroprusside test or
by direct assay of beta-hydroxybutyrate levels
§ Glucose 350-800
§ Anion gap metabolic acidosis
§ DKA is characterized by the triad of hyperglycemia, anion gap
metabolic acidosis, and ketonemia.
o Treatment
§ Administer insulin, correct fluid/electrolyte imbalances

§
• Lactic acidosis

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• Ethylene glycol poisoning
o Pathology
§ The "parent alcohols" methanol and ethylene glycol are relatively
nontoxic, and cause mainly central nervous system (CNS)
sedation. However, profound toxicity can ensue when these parent
 alcohols are metabolized in vivo (ie, oxidized, primarily by alcohol
dehydrogenase and aldehyde dehydrogenase)

§ the ethylene glycol metabolites glycolate, glyoxylate, and oxalate

accumulate following large ingestions. Above plasma levels of
approximately 20 mg/dL (approximately 6 mmol/L of methanol or 3
mmol/L of ethylene glycol), these metabolites can cause specific
end-organ damage

§ metabolites target the kidney and lead to reversible oliguric or

anuric acute kidney injury (acute renal failure), which in turn slows
elimination of ethylene glycol [12]. The renal failure is primarily due
to glycolate-induced damage to tubules, although tubule obstruction
from precipitated oxalate crystals may contribute [13,14].
Hypocalcemia in ethylene glycol overdose results from calcium
oxalate formation.

o Presentation

§Complaints of visual blurring, central scotomata, and blindness

suggest methanol poisoning. Flank pain, hematuria, and oliguria
suggest ethylene glycol poisoning.
o Treatment

•
• Metabolic acidosis compensation
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