Læknaneminn


Læknaneminn - 01.10.1996, Side 94

Læknaneminn - 01.10.1996, Side 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 LÆKNANEMINN 84 2. tbl. 1996, 49. árg.
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