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Topics Revised 11/3/03 2:13 PM Page 466 topics revised 11/3/03 2:13 PM Page 466 MAIN TOPIC Disturbances of water, electrolyte and acid-base metabolism in acute poisoning Disturbances of water, electrolyte and acid-base metabolism may develop as a result of a direct effect of poisons on metabolic systems, or indirectly as a result of an effect of the poison on cardiorespiratory, gastrointestinal, hepatic, or renal function. 1 bicarbonate concentration of 8 ACID-BASE DISORDERS The anion gap can be calculated mmol/l or lower. Major adverse A low pH is referred to as aci- as follows:2 consequences of severe acidaemia daemia, and for practical purposes Anion gap = [Na+] - ([HCO -]+ include decreased cardiac output, 3 severe acidaemia may be defined as [Cl-]) a pH < 7.2 (normal range: 7.35 - decreased arterial blood pressure, Normal range: 8 to 16 mmol/l 7.45). reduction in the threshold for cardiac dysrhythmias, and a E.g.: Anion gap = 140 - (26 + decrease in hepatic and renal blood 106) = 8 mmol/l flow. Acidaemia causes potassium Acidaemia causes (Note: Clinicians should con- to leave cells, resulting in hyper- sult their particular laboratory’s potassium to leave kalaemia. Brain metabolism and reference ranges when assessing cells, resulting in the regulation of its volume are the anion gap, as some may impaired, resulting in progressive include the [K+] in the above hyperkalaemia. central nervous system depression formula.) Brain metabolism and coma.1 and the regulation The anion gap (unmeasured Causes of a high anion gap metabolic acidosis3,4 of its volume are anions) is a valuable calculation in the differential diagnosis of meta- • Renal failure. impaired, resulting bolic acidosis. This gap (some- • Diabetic ketoacidosis and alco- thing of a misnomer) refers to the in progressive cen- holic ketoacidosis. difference between the concentra- tral nervous system • Profuse fluid losses leading to loss tion of cations other than Na+, and of bicarbonate from the digestive depression and the concentration of anions other tract (as in severe diarrhoea). than Cl- and HCO -, in the plasma. coma. 3 Usually, the unmeasured anions • Lactic acidosis. Two types are exceed the unmeasured cations. recognised, i.e. type A, where The normal anion gap is there is evidence of impaired tis- Metabolic acidosis -8 - 16 mmol/l (since the pH of the sue oxygenation, and type B, where no such evidence is Metabolic acidosis is a condition serum is 7.4). It is increased when apparent. Most cases of type A characterised by a low arterial pH the plasma concentration of organic lactic acidosis are caused by tis- and a reduced plasma HCO - con- anions, such as lactate or foreign 3 sue hypoxia arising from circula- centration, and is usually accompa- ions, accumulates in blood. The tory failure. In poisoned nied by compensatory alveolar anion gap is increased in cases of patients type A lactic acidosis hyperventilation, resulting in a ketoacidosis, lactic acidosis, and may occur nonspecifically owing decreased PaCO . Severe metabol- other forms of acidosis in which 2 to impairment of cardiorespira- ic acidosis also implies a plasma organic anions are increased. 466 CME August 2003 Vol.21 No.8 topics revised 11/3/03 2:13 PM Page 467 MAIN TOPIC tory function (e.g. as a result of Using sodium bicarbonate in severe metabolic acidosis seizures), or more specifically where the oxygen-carrying NaHCO3 may be given undiluted as a 4.2% solution. However, some capacity of blood is impaired prefer diluting it in 5% dextrose in water or hypotonic (0.45%) saline (e.g. as in carboxyhaemoglobi- solution, depending on the clinical setting. The goal of bicarbonate naemia or methaemoglobi- therapy is to raise the blood pH to 7.3 and the plasma bicarbonate to 12 naemia). Type B lactic acidosis - 15 mmol/l. The amount necessary can be calculated using the formu- occurs with poisons that directly la: base excess x 0.3 x body weight (kg), expressed in mmol bicarbonate. inhibit mitochondrial enzymes (One ml 8.5 % NaHCO3 = 1 mmol, or 1 ml of 4.2% = 0.5 mmol.) It is (as in cyanide poisoning). wise to give only two-thirds of the calculated amount initially, and then Therapy should focus primarily reassess the situation. To raise the plasma bicarbonate concentration on securing adequate tissue oxy- from 4 to 8 mmol/l in a 70 kg patient, one should administer 4 x 70 x genation and on identifying and 0.5, or 140 mmol of sodium bicarbonate. An average dose is 1 - 2 treating the underlying cause. mmol/kg (2 - 4 ml) of a 4.2% solution over 15 minutes. (Several formu- Improvement of tissue oxygena- lae exist to calculate the dose of NaHCO3.) If acid-base data are not tion may require ventilatory available 1 - 2 mmol/kg body weight may be given. About 30 minutes support, maintenance of a high must elapse after the administration of NaHCO3 before its effect can be inspired oxygen fraction, reple- judged. It is important to consider the serum calcium level when treat- tion of extracellular fluid, after- ing metabolic acidosis, especially in children. Metabolic acidosis load reducing agents and increases the ionised fraction of total calcium. Treatment of acidosis inotropic support. In severe aci- decreases the amount of ionised calcium, an effect which may precipi- daemia (pH < 7.2 and/or base tate tetany and/or seizures. The administration of calcium gluconate, excess > -12), the abovemen- therefore, is sometimes indicated.1,3,5,6 tioned measures may be supple- mented by cautious administra- controversial. Bicarbonate given in urine. Administration of 250 - 500 tion of intravenous sodium large quantities may lead to sodium mg of acetazolamide increases both bicarbonate, initially at doses of and fluid overload, to hypokalaemia, urinary pH and urine flow. Urine no more than 1 - 2 mmol/kg of and to ‘alkalosis overshoot’. Regard- pH values may increase to 7.8. body weight (see information less of whether or not sodium bicar- This procedure is, however, not below). bonate is given, the underlying cause recommended in salicylate poison- • Acute poisonings. These of the acidaemia must be identified ing, since it may worsen the central include methanol, ethylene gly- and treated where possible (e.g. man- nervous system effects of poison- col, and salicylate poisoning. agement of ethylene glycol or ing. In tricyclic antidepressant Both methanol and ethylene gly- methanol poisoning with fomepizole overdose, NaHCO3 is given pri- col are substrates for hepatic or ethanol, etc.). alcohol dehydrogenase and are metabolised to formic and gly- Despite the above reservations, most colic acids, respectively. experts still recommend the judicious Exposure to toluene, by sniffing use of intravenous NaHCO3 in the glue, may also cause severe management of severe metabolic aci- metabolic acidosis resulting dosis (pH < 7.2). from the stepwise metabolism of In salicylate poisoning NaHCO3 is toluene to benzoic and hippuric given to alkalinise the urine to acid. Other poisons known to enhance excretion of salicylate (ion cause metabolic acidosis include trapping) and is usually not admin- ethanol, iron, isoniazid and istered to correct the acidosis. strychnine. Although alkaline diuresis increases Management of the abovemen- the elimination of salicylates and tioned acute poisonings may phenobarbitone, it is clinically dif- require large amounts of sodium ficult to achieve a urinary pH bicarbonate to combat severe aci- above 8 with NaHCO3. In pheno- daemia. The role of sodium bicar- barbitone poisoning parenteral bonate in the management of high acetazolamide (Diamox) has been anion gap acidaemia, however, is recommended to alkalinise the CME August 2003 Vol.21 No.8 467 topics revised 11/3/03 2:13 PM Page 468 MAIN TOPIC marily to prevent the development vomiting and diarrhoea. Hypokalaemia of cardiac dysrhythmias. Plasma osmolarity Hypokalaemia (< 3 mmol/l) is often caused by excessive losses of Respiratory acidosis The osmolal concentration of a K+ from the gastrointestinal tract, Respiratory acidosis is a condition solution is called osmolality when as in diarrhoea. Hypokalaemia is caused by decreased ventilation, the concentration is expressed as almost invariably present in meta- resulting in a low arterial pH, an osmoles per kilogram of water; it is bolic alkalosis. Hypokalaemia is elevated PaCO and, usually, a called osmolarity when it is 2 also a complication of theophylline compensatory increase in plasma expressed as osmoles per litre of and beta -agonist poisoning. This HCO - concentration. Causes solution.8 The major intracellular 2 3 is caused by the movement of include upper or lower airway cation is potassium, with a concen- potassium from the extracellular obstruction, status asthmaticus, tration range of 3.3 - 5.3 mmol/l. fluid into the cell. severe alveolar defects, ventilatory The major extracellular cation is restriction, central nervous system sodium, with a concentration range Intravenous potassium should be depression and neuromuscular of 135 - 147 mmol/l. Normally, given slowly, preferably through a impairment. The two last-men- the osmolarity of the extracellular central line, while monitoring the tioned entities are often complica- fluid (280 - 295 mmol/l) approxi- amplitude of the T-wave of the tions of overdoses with sedative- mates that of the intracellular fluid. ECG (10 ml of a 15% KCl solu- hypnotics (e.g. barbiturates), opi- Therefore, the plasma osmolarity is tion contains 1.5 g potassium chlo- oids, tricyclic antidepressants, bot- a convenient guide to intracellular ride, or 20 mmol of KCl). The ulism and paralytic mussel poison- osmolarity. maximum concentration of KCl in ing, to mention a few. In patients an intravenous solution should The body fluid or plasma osmolar- breathing room air a rise in PaCO2 generally not exceed 40 mmol/l. If ity can be calculated from routine will cause a fall in PaO2, which in higher concentrations are required, electrolyte measurements by the severe cases, may cause hypoxia.
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