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A Review of Management of Salicylate Intoxication in Children

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A Review of Management of Salicylate Intoxication in Children A review of management of salicylate Salicylates intoxication in children DONALD G. PELINO, D.O. Dolton, Illinois An understanding of the principles of Among all the causes of death due to poison- successful management of salicylate ing in children under the age of 5 years, poisoning is essential for the salicylates are by far the most frequent. The reasons for this are three: (1) the lack of physician with child patients because knowledge of the proper use of aspirin by of their increased susceptibility parents; (2) the lack of knowledge of the dan- to salicylate intoxication. ger of aspirin toxicity; and (3) easy accessi- The first requisite of proper bility of aspirin for children, primarily be- management is early diagnosis. The cause of the first two factors. Children under importance of a good history 2 years of age die from salicylate poisoning because of therapeutic use, but older children is stressed. When faced with possibility are poisoned most frequently from accidental of salicylate poisoning, the ingestion. The increased susceptibility of chil- physician should conduct a thorough dren is related to their age and the concomi- physical examination and a tant tendency toward dehydration. preliminary ferric chloride test. The successful handling of salicylate intoxi- Knowledge of the blood salicylate level cation depends on early diagnosis of the con- dition, prompt treatment adequate for the will not necessarily indicate the degree of intoxication, and carefully planned severity of intoxication. The extent of supportive care. involvement may not be related directly to the amount of aspirin Diagnosis ingested, because of the The diagnosis of salicylate intoxication rests complex mixture of effects of the drug on two cornerstones: (1) a history of ingestion (or absorption from the skin of oil of winter- on many different organ systems green), and (2) an understanding and knowl- and variation in individual response. edge of the mechanisms causing the symptoms. Treatment involves the initiation The first prerequisite for diagnosis is obvious. of emesis or lavage and appropriate It is important to determine the number of fluid and electrolyte therapy, pills taken, the type of pill (baby aspirin, with attention to the likelihood which is 134 grains, or adult aspirin, which is 5 grains), the time since ingestion, whether of potassium depletion. the pills were taken once or several times, When severe intoxication fails whether the salicylate was actually in pills or to respond to the usual treatment, was methyl salicylate (oil of wintergreen), peritoneal dialysis should which is much more toxic, and whether they be considered. were ingested on a full or an empty stomach. An understanding and knowledge of the symp- toms presented in salicylate poisoning are im- perative when a history is not available from the parents or when the child is brought into an emergency room alone and unconscious. 1249/84 The outstanding characteristic of salicylate lem: changes in fluid and electrolyte balance. intoxication is disturbance of acid-base bal- The hyperpnea results in respiratory alkalosis, ance and electrolyte status. The cardinal sign which is characterized by an increase in blood of hyperpnea is well known, but knowledge pH, a decrease in carbon dioxide, and a loss of of the processes involved in its production and extracellular sodium. The renal compensation the production of the fluid and electrolyte im- for this alkalosis is the excretion of bicarbon- balances is also necessary for thorough under- ate ion along with sodium and potassium. standing of the course of the intoxication and Chloride excretion is usually minimal. The the required treatment. What, then, are the result is a compensated respiratory alkalosis mechanisms involved? Salicylates affect res- with resulting low carbon dioxide tension and piration in two ways: indirectly through an bicarbonate, with normal or near normal pH. increase in oxygen consumption with conse- It is the loss of the bicarbonate buffer which quent increase in carbon dioxide production renders the patient susceptible to factors and directly via action on the respiratory cen- which can cause subsequent acidosis. ter in the medulla. The increase in oxygen There are, according to Goodman and Gil- consumption and carbon dioxide production man, three processes which cause the final apparently takes place as a result of salicy- metabolic acidosis. The first is actual salicylic late-induced uncoupling of oxidative phospho- acid dissociation in the blood. The second is rylation, especially in skeletal muscle. The impairment of renal function due to vaso- increase in carbon dioxides affects the medul- motor depression with consequent accumula- lary center and causes much greater increase tion of metabolic acid products. The third is in the depth of respiration than in the rate. the accumulation of organic acids such as This is a direct effect of salicylate on the pyruvic, lactic, and acetoacetic acids accom- medullary respiratory center. Goodman and panying respiratory depression. This is due Gilman stated, "CO2 stimulates depth more to derangements in carbohydrate metabolism than rate of respiration, whereas salicylate and inhibition of synthesis and enhancement stimulates rate more than depth." While stimu- of the breakdown of fatty acids. Thus, bi- lation of both rate and depth may be present carbonate is displaced, and metabolic acidosis during different stages, the clinical picture ensues. The depletion of bicarbonate which is usually of the "panting dog" type of breath- occurs in the initial phase of intoxication in- ing, that is, an increase in respiratory rate. creases the severity of the acidosis. However, Donee pointed out that the subtle To summarize, the direct and indirect ef- increase in depth without an increase in res- fects of salicylate on the respiratory center piratory rate may easily be missed unless it cause respiratory alkalosis. This is compen- is specifically sought, especially when salicylate sated for by the renal secretion of bicarbonate, intoxication is mild. The terminal effect of the effect of which is to lower the pH and salicylate on the medulla occurs with high simultaneously decrease the bloods buffering concentrations of the drug and is one of pro- capacity. The decrease in buffering capacity, found depression of the respiratory center as when challenged by the accumulation of or- well as other areas of the brain. Thus, the hy- ganic and inorganic acids resulting directly perpnea commonly seen is explained. What from salicylate poisoning, causes metabolic follows this, however, is the crux of the prob- acidosis. Journal AOA/vol. 69, August 1970 1250/85 Salicylate intoxication in children Detection in the laboratory of the combina- erythrocytes, and leukocytes in the urine and tion of respiratory alkalosis and metabolic positive tests for reducing substances, such as acidosis rests on the measurement of the blood acetone and diacetic acid, may be observed.2 pH, carbon dioxide tension, or carbon dioxide- For confirmation of the clinical impression combining capacity. The pH will be low; the of salicylate intoxication while the blood is carbon dioxide tension will be low or normal, being analyzed, several screening tests may depending on whether respiratory depression be employed. The ferric chloride test is sensi- has set in, and the carbon dioxide-combining tive to salicylate in the urine, but it is not capacity (measure of bicarbonate) always will quantitative. A few drops of a 10 per cent be low. Although both sodium and potassium solution is added to the urine. In the presence are lost, there is a large water loss from of salicylic acid, a violet to purple color devel- salicylate-induced sweating, from hyperpnea, ops. Reagent strips (Phenistix) also may be and from diuresis, so that relative hyperna- used, and, although not exact, the measure- tremia results. ment is quantitative. A pure tan color indicates Among other signs and symptoms of severe a level of less than 40 mg./100 ml., a darker salicylate poisoning are apathy, confusion, and brown color with some purplish highlights coma. These have been ascribed to cerebrovas- suggests a level of from 40 to 90 mg., and a cular vasodilatation accompanying the respira- pure purple indicates a level of more than 90 tory alkalosis.3 Although therapeutic doses of mg.2 Knowing the blood salicylate level is salicylates cause hypothermia, toxic doses of some aid, but the level is a poor indication cause hyperthermia, ostensibly from the in- of the severity of intoxication. crease in metabolism and dissipation as heat The clinical manifestations of toxicity are of the energy normally used for the conver- related not so much to the blood level of salicy- sion of inorganic phosphate to adenosine tri- late at any given moment as to the level at phosphate in the presence of the uncoupling the peak and the rapidity with which this of oxidative phosphorylation. Intense gastro- level declines. The peak blood level after in- intestinal upset may be present and is a direct gestion of a single dose usually occurs from effect of the salicylate, both locally on the 4 to 6 hours after intake, and blood levels at gastric and enteric mucosa and centrally on this time reveal significant values. Done e has the emetic centera. Large doses of salicylate formulated a nomogram for severity of salicy- reduce the level of prothrombin in the blood late intoxication based on the level of the drug and prolong the prothrombin time. This is after a specified period. If the level is 45 probably related to a decrease in clotting fac- mg./100 ml. or less at this time, the patient tor VII. Hemorrhage may thus occur as a late usually will be asymptomatic and will remain complication. Marked hypoglycemia has been so as the level declines. He may have occa- reported with severe salicyate poisoning in sional subjective, but no objective, manifesta- young children and has been attributed to in- tions at this level.
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