Dear Editor,
Accidental overdose or suicide by salicylates provokes metabolic alterations and organ failure that can be fatal. 1,2 Haemodialysis must be used appropriately in these cases.3,4 We present a case where haemodialysis was used in a potentially lethal overdose of Acetylsalicylic Acid (ASA).
We describe the case of a 24 year old female patient, with no morbid history, that presented in the Emergency Room 18 hours after having ingested 50 pills of ASAof 500mg, 25g total or 400mg per kilogram of weight, with suicidal intention. When hospitalized, she presented lethargy, confusion, vomiting, hypoacusia and tinnitus. Vital signs were normal and there were no positive findings in the physical examination. Laboratory tests on admission included: arterial gasometry: pH: 7.42, PO2 115mmHg, PCO2 14mmHg, HCO3 9.2mmol/l. Creatininaemia: 0.89mg/dl, kalaemia: 2.1mEq/l, natraemia: 138mEq/l. The anion gap was 18. There were no alterations in liver function tests or in cardiac enzymes. A gastric lavage was performed, saline solution and sodium bicarbonate were administered. She was transferred to the Intermediate Care Unit with a salycilate level of 682mg/l.
Haemodialysis was carried out for four hours, with a polysulphone filter, and 39mEq/l bicarbonate, 3.5mEq/l of potassium and 140mEq/l of sodium bath. Fluid balance during haemodialysis was positive at 2,500cc. The patient was stable with progressive improvement of state of consciousness and slow correction of acidbase alterations. Salycilate levels of 99 and 1mg/l were obtained 12 to 20 hours after dialysis, respectively.
The ASA is absorbed in the stomach and small intestine as salicylic acid. It is conjugated in the liver and excreted in bile and urine. Therapeutic levels are of 100 to 300mg/l. The classic triad of intoxication by salicylate is hyperventilation, gastric irritation and tinnitus.1 There may be liver, kidney, central nervous system and cardiovascular organ damage. Salicylate, above therapeutic levels, stimulates the respiratory centre and causes respiratory alkalosis.5
The toxic levels also produce a separation in the oxidative phosphorylation and accumulation of lactic acid, resulting in metabolic acidosis.6 This mixed acid-base syndrome, with an increased anion gap, should lead one to suspect an intoxication by ASAin a patient where the antecedents of what has been ingested is unknown. The treatment of salycilate poisoning includes vital support, gastric lavage, the use of activated charcoal and alcalinization of the urine to encourage the excretion of the drug.3 Salicylate has a distribution volume of 150ml/k, a protein binding rate between 50 and 80% (which decreases when levels are high), and a molecular weight of 138.3 These properties favour its elimination by haemodialysis, which is the indicated treatment in serious cases.
