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The Clinical Picturetypical of Salicylate Poison

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The Clinical Picturetypical of Salicylate Poison THE EFFECT OF SALICYLATES ON THE ELECTROLYTE STRUCTURE OF THE BLOOD PLASMA.1 I. RESPIRATORY ALKALOSIS IN MONKEYS AND DOGS AFTER SODIUM AND METHYL SALICYLATE; THE INFLU- ENCE OF HYPNOTIC DRUGS AND OF SODIUM BI- CARBONATE ON SALICYLATE POISONING BY S. RAPOPORT AND GEORGE M. GUEST (From the Children's Hospital Research Foundation and the Department of Pediatries, College of Medicine, University of Cincinnati, Cincinnati) (Received for publication May 23, 1945) The clinical picture typical of salicylate poison- view that the hyperpnea is of central origin and ing has often been described: hyperpnea appears that changes in the blood are secondary. In a to be the most prominent symptom; other symp- study of salicylate poisoning in man the finding toms are vomiting, thirst, sweating, diuresis, fever, of insignificant changes in the blood pH in the and various signs of irritation of the central nerv- presence of lowered concentrations of bicarbonate ous system, including convulsions followed by de- suggested that the hyperpnea must result from pression and coma. Albumen, casts, and red and central stimulation by the drug (9). Others (10, white cells are often found in the urine. The 11) came to the same conclusion on the basis of physiologic mechanism underlying the hyperpnea short-time experiments with small doses of so- of salicylism has been the subject of much discus- dium salicylate in man, in which lowered CO2 sion. As the dyspnea of salicylate poisoning was tensions and alkaline urines were observed co- noted to resemble the Kussmaul type of breath- incidentally with unchanged values for the alkali ing of diabetic coma, ketone bodies were suggested reserve of the blood. A critical evaluation of the as a common cause for the acidosis and hyper- literature led to the conclusion that the cause of ventilation in both conditions (1). This hypothe- the hyperpnea was both central and metabolic sis was not borne out in later studies, which did (12). In a recent study dealing experimentally not reveal increased ketonemia in man or rabbits with the effects of toxic doses on the composition receiving large doses of salicylates (2). In more of the blood of dogs (13), a pH of 7.61 con- recent times the theory of a primary metabolic comitant with a CO2 content of 13 m.eq. per liter acidosis, accepted by many clinical observers, ap- was reported in 1 dog and mention was made of peared to be supported by the finding of a de- unpublished experiments, which also indicated creased bicarbonate content of the blood, but the the presence of at least transient alkalosis follow- origin of this presumed acidosis has remained ing the administration of salicylates. In this obscure (3 to 5). Increased amounts of lactate study, changes in the heat regulation were stressed found in the blood of rabbits following sodium as an explanation for the hyperpnea of salicylism. salicylate administration were thought to be partly In all, it would appear that the data available at responsible for the presumed acidosis (6). The present are insufficient to permit a satisfactory significance of this observation appears uncertain, description of the electrolyte structure of the since the increases varied widely, and the muscu- blood in salicylate poisoning. lar effort involved in hyperventilation may have The observation of a case of aspirin poisoning accounted for them. A renal mechanism for the in a 3-year-old child, with the plasma pH ele- metabolic acidosis has been suggested (7, 8) but vated and the CO2 content and tension decreased, the rapidity of the onset of the hyperpnea and led us to investigate the effects of salicylates in the inconstancy and mildness of the renal changes monkeys and dogs. Sodium and methyl salicylate appear difficult to reconcile with such an hypothe- were administered to the animals by parenteral sis. Another group of observers has favored the routes and blood analyses were performed for pH, 1 A preliminary report was presented before the Ameri- CO2, chloride, sodium, and potassium. The can Pediatric Society, May 1, 1942 (Am. J. Dis. Child., serum protein and the distribution of the acid- 1942, 64, 200). soluble phosphorus in the blood of several ani- 759 760 S. RAPOPORT AND GEORGE M. GUEST mals were determined. The effects of 'several phorus, and protein values were determined by methods hypnotic drugs and of sodium bicarbonate on the previously described (14), sodium by the method of Leva (15), and potassium according to the slightly-modi- hyperpnea of salicylism were also studied. fied method of Consolazio and Talbott (16). The CO2 tension was calculated from the values for pH and bi- METHODS carbonate. Data on the hemoglobin, the red count, and the packed volume of red cells of several animals did not Rhesus monkeys weighing 3 to 5 kgm., and male mon- reveal any significant change, and, therefore, are not re- grel dogs weighing 14 to 20 kgm. were used. The ani- ported here. mals were fasted 24 hours before and during the experi- mental periods but were allowed free access to water at EXPERIMENTATION WITH SODIUM SALICYLATE all times. Weight, temperature, and respiratory rate were recorded in all, and urinary output in some of the In Table I are shown representative experiments on dogs. The dogs lost on the average 1.5 kgm. of weight the effect of sodium salicylate on monkeys and dogs: during the experiments. The respirations of all animals increased greatly in frequency and depth following the Rhesus monkey number 400, weighing 3.6 kgm., re- administration of salicylates. Two types of hyperventila- ceived repeated intravenous injections of sodium salicy- tion were observed occurring in the same animals alter- late. The animal presented signs of poisoning closely nately within short periods of time: (1) deep labored resembling those seen in man, including hyperpnea, breathing reaching frequencies as high as 150 per minute; flushing of the face, weakness, and profuse diuresis. The and (2) panting, much more shallow in character, at chemical data on the blood taken 1 hour after the last rates of 250 or more respirations per minute. During the dose of sodium salicylate, when the animal appeared very later stages of fatal intoxication or under the influence weak, showed an extraordinarily elevated pH, a moder- of hypnotic drugs, the first type of breathing predomi- ately reduced CO2 content, and a greatly decreased ten- nated and panting was observed only occasionally. The sion of CO2. temperature of the animals rose in a few instances to Dog S1 received a total of 1.0 gram per kgm. of sodium values as high as 410 C., but often remained at 390 C. salicylate intraperitoneally in divided doses over a period The urinary output was greatly increased in the begin- of 24 hours. Extreme hyperpnea developed shortly after ning of the intoxication, and diminished during the later the first dose of 0.2 gram per kgm. had been adminis- stages. tered and continued until the dog died. Diuresis, great Blood samples from the femoral artery were drawn weakness, and hyper-reflexia were noticed among the with a tightly-fitting syringe and needle and were de- signs of intoxication. livered under paraffin oil. The serum pH values were The dogs 839 and 840 were studied with the purpose determined with a glass electrode at 380 C. with precau- of following the effect of single intravenous doses of tions against exposure to air. Serum CO2, chloride, phos- sodium salicylate on the electrolyte equilibrium. Dog 840 TABLE I Effect of sodium salicylate on the ionic equilibrium of blood plasma Animal Number pH CO2 pCOs Chloride Comment m. eq. per mm. Hg m. eq. per liter liter Monkey 400 7.85 16.5 9 97.3 Received 1.1 grams per kgm. intravenously in 5 divided doses over a period of 30 hours. Sample 1 hour after last dose. Panting, flushed face, weak. Sacrificed. Dog S1 7.44 25.7 38 102.2 Preliminary sample, followed by intraperitoneal injections of 0.2 gram doses of sodium salicylate. Wt. 14 kgm. 7.49 24.2 32 105.3 4 hours later; total dose 0.4 gram per kgm.; breathing fast. 7.66 23.1 20 110.9 24 hours later; total dose 1.0 gram per kgm.; panting hard, weak. Died 1 hour after sample. Dog 840 7.42 20.5 31 112.9 Preliminary sample, followed by intravenous injection of sodium salicylate, 0.6 gram per kgm. Weight 17 kgm. 7.62 17.9 17 111.3 45 minutes later; panting hard. 7.50 19.2 24 108.4 3 hours later; very weak; died i hour later. Dog 839 7.48 22.3 30 113.4 Preliminary sample, followed by intravenous injection of sodium salicylate, 0.3 gram per kgm. Weight 15 kgm. 7.49 22.2 29 109.2 20 minutes later; breathing rapidly. 7.58 22.5 24 109.6 1.5 hours later; panting. 7.54 22.9 27 107.2 5 hours later; hyperpnea diminished. 7.43 22.0 33 103.9 23 hours later; appears normal. RESPIRATORY ALKALOSIS AFTER SODIUM AND METHYL SALICYLATE 761 TABLE II Effects of methyl salicylak on plasma electrolytes Dog pH C02 pCO, Chloride Sodium Comment m. eq. per mm. Hg m. eq. per m. eq. Per liter liter Lite Pr. 7.42 25.4 40 111.4 150.3 Preliminary sample, followed by intramuscular injection of 2 ml. doses of methyl salicylate. Weight 15 kgm. 7.41 18.6 28 106.6 30 hours later; total dose 14 ml. 7.41 12.9 19 102.6 129.6 53 hours- later; total dose 18 ml.; panting, weak; died 8 hours later.
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