Læknaneminn - 01.10.1996, Qupperneq 94

Overdoses and poisonings: physiological responses
C. Acidosis
A metabolic acidosis in the context of an overdose or
poisoning is a clue to the identity of the responsible
drug or toxin, Direct mechanisms for the production
of metabolic acidosis by toxins include:
• Introduction of organic acids from an exogenous
source
• Induction of lactic acidosis by interference with
aerobic respiration
• Impairment of renal reabsorbtion of bicarbonate
It should be kept in mind that metabolic acidosis, can
be produeed indireetly; and thus is not specific to the
presentation of patients poisoned by such toxins, Any
drug which causes a patient to become hypoxemic,
hypotensive, hypoglycemic, to seize, or to have profuse
diarrhoea will produce a metabolic acidosis owing to
the accumulation of lactate.
1. Anion Gap
Further differentiation of the toxic cause of meta-
bolic acidosis can he made on the basis of the presence
of an excess of unmeasured anions as revealed by the
so-called anion gap (AG). A normal anion gap is 12
mEq/L, and is calculated as followed:
(Na+] - ([HC03-] + [Cl-])
This difference is accounted for by a normal excess of
unmeasured anions (proteins, organic acids, phos-
phates, and sulfates) in comparison to unmeasured (or
not included) cations (calcium, magnesium, potassi-
um). Certain toxins, directly and indireetly, and certa-
in disease states will increase the serum concentration
of unmeasured anions.
This list is best remembered by the mnemonic
AT MUD PILES:
• Alcohol
• Toluene
• Methanol
• Uremia
• Diabetic ketoacidosis
• Paraldehyde
• Iron, isoniazid
• Lactic acids
• Ethylene glycol
• Salicylates, Strychnine
2. Osrnolal gap
Another clue to toxin identification which can be
derived from laboratory testing is the so-called osmolal
gap. The osmolal gap is calculated by subtracting a cal-
culated serum osmolality from that measured by freez-
ing point depression. The calculated value is derived
from the concentrations of the major osmotically acti-
ve particles measured in the serum as follows:
2 [Na+] + Glucose/18 + BUN/2.8
A normal gap of 10-12mOsm is accounted for by
unmeasured, osmotically active particles present in the
serum (sulfate, calcium). An elevation of the gap results
from either a decrease in serum water content (as in
hyperlipidemia or hyperproteinemia) or the presence
of additional unmeasured, low-molecular-weight
(<150 daltons) molecules which are osmotically active.
Toxic causes of an elevated osmolal gap can be
recalled using the mnemonic ME DIE:
• Methanol
• Ethanol
• Diuretics
• Isopropanol
• Ethylene glycol
An osmolal gap> 10 mOsm indicates the presence of
a low molecular weight toxin. The serum concentra-
tion of the toxin can be estimated using the osmolal
gap:
• Each 1 mg/dL of methanol
= 0.34 osmolality increase
• Each 1 mg/dL of ethanol
= 0.22 osmolality increase
• Each 1 mg/dL of ethylene glycol
= 0.20 osmolality increase
• Each 1 mg/dL of isopropanol
= 0.17 osmolality increase
3. Saturation gap
Toxins which alter hemoglobin and thus impair its
ability to carry oxygen will cause a so-called saturation
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2. tbl. 1996, 49. árg.