The early symptoms of acute salicylism are the triad of gastrointestinal distress, tinnitus or altered hearing, and hyperventilation.

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1 POISONING SALICYLATES (ASPIRIN) Management Guidelines Emergency Department Princess Margaret Hospital for Children Perth, Western Australia Last reviewed: January 2007 Page 1 of 5 Dr Gary Geelhoed Dr Frank Daly INTRODUCTION The early symptoms of acute salicylism are the triad of gastrointestinal distress, tinnitus or altered hearing, and hyperventilation. Severe salicylate poisoning may be complicated by mixed acid-base abnormalities (respiratory alkalosis and metabolic acidosis), altered mental status, seizures, fever and pulmonary oedema. Salicylate poisoning is rarely associated with significant coagulopathy. Chronic salicylism usually occurs in the elderly due to small increases in dose, or decreased renal function. Reyes syndrome is the rare constellation of fatty infiltration of the liver, raised hepatic transaminases, hypoglycemia, nausea, vomiting and coma following therapeutic doses of salicylates in children with viral illnesses. Reyes syndrome has also been reported in adults. RISK ASSESSMENT DOSE INGESTED: Accidental paediatric ingestions of less than 150 mg/kg of aspirin are considered non-toxic and do not require decontamination or referral to hospital. Accidental paediatric ingestions of greater than 150 mg/kg are potentially toxic and require referral to hospital for evaluation. Moderate to severe symptoms may be seen with doses exceeding 300 mg/kg. Children may ingest other forms of salicylate that are potentially toxic. For example, methylsalicylate or oil of wintergreen contains a high concentration of salicylate. Consultation with a clinical toxicologist is recommended. DRUG LEVEL: The therapeutic range for aspirin is mg/l. Symptoms of mild intoxication are associated with serum levels of mg/l. Mixed metabolic and respiratory acidosis with acidaemia (ph less than 7.35) indicates severe poisoning with a grave prognosis and requires urgent intermittent haemodialysis. COMMON EFFECTS Acute ingestion of greater than 150 mg/kg may be associated with nausea, vomiting, hearing loss and tinnitus (at levels mg/l). Direct stimulation of the respiratory center leads to hyperpnoea, hyperventilation and primary respiratory alkalosis. In pediatric patients this respiratory alkalosis may be early and relatively transient. Anion gap metabolic acidosis occurs with moderate intoxication, but acidaemia (ph less than 7.35) is a late and ominous sign. (Anion gap is defined as the difference between the measured serum cations and anions, and is calculated using the formula AG = Na + - (Cl - + HCO 3 - ). Normal AG is 8-12 mmol/l. Salicylates are one of the few things which cause a metabolic acidosis associated with an increased AG. Poisoning Salicylates (Aspirin) DPMS No 1521 Page 1

2 LIFE-THREATENING EFFECTS Mixed metabolic and respiratory acidosis with acidaemia (ph less than 7.35) indicates very severe poisoning with a grave prognosis and requires urgent intermittent haemodialysis. Manifestations of severe intoxication include agitation, altered mental state, coma, seizures and cerebral oedema, rhabdomyolysis, hepatitis, and hypoglycemia. Hyperpyrexia may occur and is also a marker of grave poisoning. Coagulopathy is not usually a complication of salicylate poisoning. TYPICAL COURSE After accidental pediatric ingestions, peak serum levels usually occur within 6 hours. Most accidental paediatric ingestions are not associated with significant complications and do not require observation longer than 6-8 hours. After deliberate self-poisoning, peak serum concentrations may not be reached for up to 12 hours, and up to hours for enteric-coated preparations. With appropriate management severe symptoms usually resolve within 24 hours. MANAGEMENT a) RESUSCITATION Airway, Breathing, Circulation. NB: If a patient with severe salicylism requires intubation and ventilation, extreme care is required to ensure that hyperventilation is maintained to prevent sudden loss of respiratory alkalosis, as respiratory acidosis causes worsening cerebral edema and sudden death. Monitor vital signs (temperature, pulse, blood pressure, respiratory rate, pulse oximetry). IV access is required in all symptomatic patients and patients suspected of taking large overdoses (greater than 300 mg/kg). Treat seizures with benzodiazepines and urgent intubation and hyperventilation. A bedside blood glucose level should be checked in all patients with altered mental status. b) DECONTAMINATION Activated charcoal (1 gram/kg) should be administered to all patients suspected of taking large ingestions (greater than 150 mg/kg) up to six hours after the ingestion. Activated charcoal is also indicated in any symptomatic patient, regardless of the time after the ingestion. The reasoning behind these recommendations is that aspirin causes pylorospasm and significantly delayed gastric emptying. Irrespective of which aspirin preparation is swallowed, aspirin forms a sludge in the stomach. The result is that aspirin is very slow absorbed from the GIT following overdose. Since there is no antidote to aspirin, and since massive overdose often results in death despite aggressive haemodialysis, the usual 1 hour limit on using activated charcoal is stretched to 6 hours post-ingestion. However, the risks of forced activated charcoal administration (e.g. via nasogastric tube) usually outweigh the benefits when a pediatric patient is unable / unwilling to drink the activated charcoal solution. Gastric lavage is technically extremely difficult in young children and not routinely recommended. The risks associated with the procedure usually outweigh any benefit. Gastric lavage is probably no more effective than spontaneous emesis, which is common in salicylate poisoning. Poisoning Salicylates (Aspirin) DPMS No 1521 Page 2

3 There is no role for syrup of ipecac, except perhaps in rare situations where patients in remote areas are unlikely to be able to get to a medical centre for hours / days. In such a situation, consultation with a toxicologist is recommended prior to use of ipecac. Whole bowel irrigation with polyethylene glycol might be considered if a massive ingestion (e.g. 300 mg/kg) is suspected, especially if an enteric-coated preparation is involved or serial aspirin levels continue to rise over 500 mg/l despite activated charcoal and urinary alkalinization. Consultation with a toxicologist is recommended. c) LABORATORY TESTING If an ingestion of greater than 150 mg/kg is suspected, a serum salicylate level should be performed. A level less than 10 mg/l more than one hour after the ingestion excludes a significant ingestion and the patient may be discharged. The exact timing of salicylate levels in salicylate poisoning is not important. The Done nomogram is no longer used to manage patients. It is the trend in levels that is important rather than an absolute level at a given time. The therapeutic range for aspirin is mg/l. Symptoms of mild intoxication are associated with serum levels of mg/l. Severe acute salicylate poisoning is associated with levels greater than 500 mg/l. A level exceeding 1000 mg/l has been the traditional threshold for haemodialysis, but it should be considered much earlier. Serum salicylate levels should be performed every 2-4 hours until the patient is clinically well, has normal acid-base status, and serum salicylate level is less than 300 mg/l. Obtain arterial gases if the patient looks unwell (nausea, vomiting, sweating, tachycardia), manifests evidence of severe metabolic acidosis (serum bicarbonate <16 meq/l), serum salicylate levels exceed 500 mg/l, or there is hyperthermia, confusion, seizures, coma or non-cardiac pulmonary edema. Patients with mild to moderate intoxication manifest alkalaemia (ph greater than 7.45). A serum ph that is normal or low actually indicates severe intoxication and represents an indication for dialysis. Screening tests for patients with deliberate self-poisoning: Serum paracetamol level ECG d) ENHANCED ELIMINATION i. Urinary alkalinisation At levels greater than 200 mg/l, hepatic metabolism of aspirin is saturated and renal elimination becomes more important. However, in acid urine, aspirin is unionized and is rapidly reabsorbed by the proximal tubule. Alkalinisation of the urine traps ionized aspirin in the renal tubule and markedly increases its elimination. For every 1.0 increase in urine ph (e.g. from 5 to 6) the elimination of aspirin by the kidney theoretically increases 10-fold. Alkalinisation of the urine is indicated in the following circumstances: Patient is symptomatic. Serum salicylate level exceeds 300 mg/l. History of ingestion of greater than 300 mg/kg. Alkalinisation of the urine is often confused with forced diuresis and forced alkaline diuresis, which are now discouraged. Poisoning Salicylates (Aspirin) DPMS No 1521 Page 3

4 Alkalinisation of the urine has been shown to improve salicylate renal clearance better than the other techniques and has fewer adverse effects. Forced diuresis may lead to electrolyte abnormalities or precipitate cerebral or non-cardiac pulmonary oedema. The use of frusemide to enhance diuresis actually decreases urinary excretion of aspirin. To alkalinize the urine: 1. Give 2 meq/kg of sodium bicarbonate as an initial intravenous bolus over 5 minutes. 2. Then start a bicarbonate infusion. Place 150 meq of sodium bicarbonate in 1000 ml of 5% dextrose, and infuse at 2-4 ml/kg/hr. A burette or infusion pump may be required to prevent accidental volume overload in small children. Check the urine ph and titrate the infusion to maintain a urinary ph greater than Check serum potassium every 2-4 hours (along with salicylate level). Hypokalaemia is common with urinary alkalinisation and intravenous potassium supplementation is often required. Urinary alkalinisation may be ceased when: Patient is clinically well. Serum salicylate level is below 300 mg/l Normal acid-base status (if monitored). ii. Haemodialysis Haemodialysis is the definitive therapy for severe salicylate intoxication. It rapidly removes aspirin from the serum and extracellular space, assists rapid movement of salicylate out of the brain, and assists correction of metabolic disorders. Unfortunately no prospective controlled clinical studies have been performed to delineate indications. Most texts list indications for dialysis (included below), which define critically ill patients. However, as resuscitation of patients with grave salicylate intoxication is extremely difficult, even with dialysis, the aim should be to perform dialysis early, before grave intoxication is manifest. Thus, the following are suggested as indications for haemodialysis (any of the following): 1. Evidence of impending severe intoxication: Rising serum salicylate levels above 500 mg/l beyond 6 hours after ingestion, despite aggressive decontamination and urinary alkalinisation. Mixed respiratory alkalosis/metabolic acidosis on arterial blood gases but ph in the normal range (i.e. patient no longer has alkalotic serum ph). Patient acidaemic (ph less than 7.35) with mixed respiratory and metabolic acidosis. Serum level greater than 1000 mg/l at any time. 2. Failure of elimination: Renal failure. 3. Evidence of severe intoxication: Altered mental status. Seizures. Cardiovascular instability. Hyperthermia. Pulmonary oedema (rare in children and young adults). e) ANTIDOTES There is no specific antidote for salicylate poisoning. Poisoning Salicylates (Aspirin) DPMS No 1521 Page 4

5 DISPOSTION PATIENTS WHO CAN USUALLY BE MANAGED AT HOME Asymptomatic paediatric patients with accidental potential ingestion of less than or equal to 150 mg/kg. Abdominal pain or vomiting should prompt assessment in a health care facility. PATIENTS WHO SHOULD USUALLY BE EVALUATED IN A HEALTHCARE FACILITY Asymptomatic patients with a history of ingestion of potentially greater than 150 mg/kg. All patients with abdominal pain, nausea, vomiting or altered hearing (usually tinnitus) should be referred to a health care facility for evaluation. All patients with deliberate self-poisoning should be referred to a hospital for evaluation. PATIENTS WHO SHOULD USUALLY BE OBSERVED FOR AT LEAST 8 HOURS AFTER INGESTION Asymptomatic patients with history of ingestion of potentially greater than 150 mg/kg. Patients with a history of deliberate self-poisoning of non-enteric coated tablets should be observed for at least eight hours. Patients may be discharged from the emergency department if they are clinically well and serum salicylate levels have not increased over a period of 8 hours. If salicylate levels rise above the therapeutic range (200 mg/l), then two consecutive decreasing salicylate levels are required before discharge. PATIENTS WHO SHOULD USUALLY BE ADMITTED Patients requiring urinary alkalinisation or observation for periods greater than 8 hours will require admission. Poisoning Salicylates (Aspirin) DPMS No 1521 Page 5

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