Hi there Junior Member,
I think
@nexttime's tough policy helps by making students do the hard work, which is probs more beneficial in the long-term than my tactic of part spoon-feeding, and coaxing millenials to use their brains [which they have been trained from babyhood to allow to decay - sorry
] - I am going to try and push you off the cliff here ["how nasty this guy is!" goes the student!] actually not literally, only metaphorically, with a quick Endnote search and copying of the abstracts therein with the refs list, to get you into 2nd gear [it is now your job to accelerate and go into overdrive [nice & easy - slowly!][have you done your driving test yet? - if you need help I am an MIAM, too - just shout out] Do the searches I recommended with a variety of [separate] keywords to find more + read the full-text articles of the below [agreed these are NOT specific for infants, but you will get an idea esp from the experiment on chicks [no 4] and the one published in the journal
Paediatrics [no 2]].
Best of luck!
Salicylate poisoning remains a major clinical hazard, usually resulting from accidental ingestions in preschool children, suicidal overdoses in adults and teenagers, and therapeutically acquired intoxication in all ages. Alkalemia or acidemia, alkaluria or aciduria, hypoglycemia or hyperglycemia, and water and electrolyte imbalances may occur; nausea, vomiting, tinnitus, hyperpnea, hyperpyrexia, disorientation, coma, and/or convulsions are common. With chronic, therapeutically induced salicylism, these symptoms may be mistaken for symptoms resulting from the illness for which the salicylates were administered. For acute ingestions, the magnitude of the poisoning is clearly dose related. Blood level determinations are good prognostic indicators for acute ingestions but are of limited value in chronic, therapeutically induced salicylism. Fluid and electrolyte management is the mainstay of therapy. Diuresis, hemodialysis, and hemoperfusion are effective, but the latter two rarely are necessary1
The principal pathophysiologic effect of toxic doses of salicylates are characterized by (1) stimulation of the respiratory center of the brain, leading to hyperpnea and respiratory alkalosis; (2) uncoupling of oxidative phosphorylation, leading to increased oxygen utilization and glucose demand, increased oxygen utilization and glucose demand, increased glyconeogenesis, and increased heat production; (3) inhibition of Krebs cycle enzymes, leading to decreased glucose availability and increased organic acids; (4) alterations in lipid metabolism and amino acid metabolism, enhancing metabolic acidosis; and (5) increased fluid and electrolyte losses, leading to dehydration, sodium depletion, potassium depletion, and loss of buffer capacity. The principal toxic manifestations of respiratory alkalosis and metabolic acidosis, altered glucose availability and depletion, fluid and electrolyte losses, and hypermetabolism result in serious morbidity and are potentially fatal. Therapy of salicylate intoxication should be aimed principally at replacement of fluid electrolytes, correction of acidemia, administration of glucose, and prevention of further salicylate absorption and enhancement of salicylate elimination.2
Among 2,391 recipients of plain aspirin tablets, 121 (5.1%) were reported to have adverse reactions. Minor gastrointestinal disturbances, particularly heartburn and nausea, were most common (2.1%). Central nervous system effects were second (1.2%). Among these, tinnitus was reported most often (0.8%); deafness occurred in eight patients (0.3%). Gastrointestinal bleeding, the third major category of adverse reactions, occurred in 1.0% of recipients; it was not considered serious in any of the patients with reactions judged "definitely" or "probably" related to aspirin. The frequency of all adverse reactions increased as the unit dose, daily dose and total dose became larger. Deafness occurred only at high doses. Reactions were more common in females.3
The toxicity of dietary aspirin on growth rate and lipid metabolism was investigated under linoleic acid (LA; 18: 2n-6) deficient conditions. One-week-old chicks were given diets containing 0 or 2% LA with or without 0.4% aspirin, until 4 weeks of age. Growth was severely depressed by dietary aspirin when chicks were given the LA-free diet. The liver was enlarged by both the aspirin and LA deficiency. The aspirin treatment induced a significant increase of 18:0 and arachidonic acid (20: 4n-6) and a decrease of 18: 1n-9 in the liver. In chicks fed LA-free diets, the ratio of 20:3n-9/20: 4n-6, which was used as an indicator of LA deficiency, was suppressed by aspirin treatment. In conclusion, the present results suggest that aspirin toxicity is altered by dietary LA concentrations.4
1. Temple AR. Acute and chronic effects of aspirin toxicity and their treatment. Arch Intern Med. Feb 23 1981;141(3 Spec No):364-369.2. Temple AR. Pathophysiology of aspirin overdosage toxicity, with implications for management. Pediatrics. Nov 1978;62(5 Pt 2 Suppl):873-876.3. Miller RR, Jick H. Acute toxicity of aspirin in hospitalized medical patients. Am J Med Sci. Nov-Dec 1977;274(3):271-279.4. Murai A, Furuse M, Okumura J. Aspirin toxicity in chicks given diets deficient in linoleic acid. Pharmacol Biochem Behav. Aug 1994;48(4):1047-1051.If still stuck PM me - happy to help out!M