Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (619 page)

   Indicates acute hypoperfusion and tissue hypoxia.

   Should be considered in any metabolic acidosis with increased AG (>15 mmol/L).

   Diagnosis is confirmed by exclusion of other causes of metabolic acidosis and serum lactate ≥5 mmol/L (upper limit of normal = 1.6 for plasma and 1.4 for whole blood). There is considerable variation in the literature in limits of serum lactate and pH to define lactic acidosis.

   In lactic acidosis, the increase in AG is usually greater than the decrease in HCO
₃
⁻
, in contrast to DKA, in which the increase in AG is identical to the decrease in HCO
₃
⁻
.

   Exclusion of other causes by

   Normal serum creatinine and BUN (increased acetoacetic acid [but not betahydroxybutyric acid] will cause false increase of creatinine by colorimetric assay).

   Osmolar gap <10 mOsm/L.

   Negative nitroprusside reaction (nitroprusside test for ketoacidosis measures acetoacetic acid but not β-hydroxybutyric acid; thus, the blood ketone test may be negative in DKA).

   Urine negative for calcium oxalate crystals.

   No known ingestion of toxic substances.

   Laboratory findings due to underlying diseases (e.g., DM, renal insufficiency).

   Laboratory tests for monitoring therapy:

   Arterial pH, pCO
₂
, HCO
₃
⁻
, serum electrolytes every 1–2 hours until the patient is stable