Specific Issues

The Done nomogram was created to assist in clarifying the level of salicylate intoxication that should prompt intervention: "This (nomogram) provides only a rough guide to a single criterion of severity in previously well patients ... it obviously does not supplant clinical judgement." 23 Although widely taught and used for almost 40 years, the Done nomogram is typically misunderstood and often misused. Thus, it is strongly recommended that the patient's clinical condition and early course, rather than the nomogram, guide clinical therapy. The nomogram was based primarily on previously healthy pediatric patients with acute single salicylate ingestion. 23 The patients' presentations were clinically graded. The initial serum salicylate concentration was extrapolated based on toxicokinetic data. The clinical grade was then correlated to the extrapolated initial salicylate concentration. The potential usefulness of the nomogram is to assist in predicting the degree of toxicity after an acute, single ingestion of ASA in patients who have not been taking salicylate recently. However, there are severe limitations to the usefulness of the Done nomogram. The nomogram is not useful when (1) salicylate has been ingested over several hours or days, (2) the preparation is an enteric-coated or a sustained-release tablet, (3) the compound is oil of wintergreen, which is rapidly absorbed, (4) the patient has renal insufficiency or failure, (5) the time of ingestion is unknown or uncertain, (6) the patient is acidemic, or (7) a salicylate level drawn before 6 h after ingestion returns nontoxic. In such situations, the clinical condition of the patient should be considered paramount and not the salicylate level. The degree of toxicity is determined by serial evaluation of a patient's clinical condition and serial salicylate levels. Evolution of a "nontoxic" salicylate level into severe salicylate intoxication has surprised many physicians. Failure to anticipate worsening intoxication is generally due to reliance on a single salicylate level, without regard to the formulation or the time of ingestion. If the level was drawn before 6 h, it may underestimate the severity. It is prudent in most patients to draw serial serum salicylate levels every 1 to 2 h until the levels are declining and the patient's clinical status stabilizes. Acidemia must alter estimation of the severity of the intoxication. Due to its limitations and deceptive utility, use of the Done nomogram is not recommended and, as such, a description of its use is not provided in this text.

The presence of salicylate may be determined with the ferric chloride test, which uses several drops of 10% ferric chloride added to 1 mL of urine. A purple color will be seen in the presence of salicylic acid, acetoacetic acid, or phenylpyruvic acid. This test is very sensitive to small quantities of salicylic acid, and a positive test result does not indicate salicylate poisoning or toxicity. False-negative results have not been reported. However, false-positive results may occur when a small quantity of urine that has been used for dipstick analysis with the N-multistix or Bili Labstix is then used for ferric chloride testing. Presumably, some impregnated chemical from the dipstick dissolves in the urine and causes a false-positive reaction. Another bedside test for salicylic acid utilizes the Ames Phenistix, which turns brown when either salicylic acid or phenothiazines are present in the urine or serum. Adding one drop of 20 N sulfuric acid to the strip bleaches out the color in the case of phenothiazines but not in the case of salicylic acid. The color change is often difficult to interpret. Both the ferric chloride and Ames Phenistix tests are qualitative tests. All positive urine results must be confirmed with serum salicylate level. There are severe limitations associated with bedside detection techniques for salicylic acid, and we do not advocate their use in the clinical setting.

Assessing the condition of patients who have ingested enteric-coated or a sustained-release aspirin preparation is difficult. These products are formulated to remain intact in the acidic gastric environment, but to dissolve in the alkaline intestinal fluids. Drug release is therefore primarily a function of gastric emptying, and peak levels may not be apparent until 10 to 60 h after ingestion.2

Another problem with enteric-coated and sustained-release tablets is their large size, which makes them difficult to remove from the stomach even through a 40-French gastric lavage tube. A plain radiograph of the abdomen has been recommended for enteric-coated medications, but not all are radiopaque. 24 Thus, a positive radiograph can confirm that pills are present, but a negative radiograph does not rule out an enteric-coated or sustained-release ASA in the GI tract. If a potentially lethal number of enteric-coated or sustained-release tablets have been ingested, the patient should be observed for a minimum of 24 h and serial serum salicylate levels obtained until a declining level is assured. 2

Many standard texts assert that urinary alkalinization is impossible until hypokalemia has been corrected. 1,25,26. The kidneys will attempt to excrete H+ in order to retain potassium, leading to paradoxical aciduria despite alkalemia. However, there seem to be little or no clinical data specifically regarding the role of potassium replacement in alkalinization of urine during salicylate intoxication. In one human study, no correlation was found between serum potassium levels and urinary pH, and the patients' urines remained acidic in spite of alkalemia and normokalemia.27 Although it is important to administer supplemental potassium to hypokalemic patients, it is inappropriate to delay the administration of sodium bicarbonate until normokalemia is achieved. Potassium and sodium bicarbonate should be administered simultaneously.

When aggressive management for ARDS with endotracheal intubation, mechanical ventilation, and sedation becomes necessary, hyperventilation must be maintained or acute deterioration may occur as a result of iatrogenic respiratory acidosis, causing a rapid shift of salicylate into the CNS.

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Getting to Know Anxiety

Getting to Know Anxiety

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