Pediatric emergency medicine trisk 3087 3087
Bạn đang xem bản rút gọn của tài liệu. Xem và tải ngay bản đầy đủ của tài liệu tại đây (45.81 KB, 1 trang )
aspirin poisoning. However, in cases of chronic therapeutic salicylism, the
clinical picture is the most useful guideline. Because of the nonspecific nature of
symptoms with salicylism, the initial differential diagnosis is broad and may
include diabetic ketoacidosis, iron intoxication, and ethylene glycol ingestion.
Signs and symptoms of salicylism depend on the method and severity of
intoxication. Acute ingestion of amounts of 150 to 300 mg/kg are associated with
mild symptoms, 300 to 500 mg/kg are associated with moderate toxicity, and
more than 500 mg/kg are associated with death. With mild toxicity (serum
concentrations 30 to 50 mg/dL), manifestations may be confined to GI upset,
tinnitus, and mild tachypnea. With moderate salicylate poisoning (serum level 50
to 100 mg/dL), more visible signs of toxicity—fever, diaphoresis, and agitation—
appear. After severe salicylate poisoning (serum concentrations higher than 100
mg/dL), signs and symptoms are primarily neurologic and consist of dysarthria,
coma, and seizures. Pulmonary manifestations, particularly pulmonary edema,
may appear in severe cases. In patients of chronic salicylism, these same
conditions appear at significantly lower serum salicylate concentrations. Death
from salicylism results from severe CNS toxicity with complete loss of function
in cardiorespiratory centers, leading to respiratory and/or cardiac arrest. The
severity of salicylate intoxication is best assessed by physical examination,
electrolytes, and blood gas analyses rather than through use of a nomogram.
Assessment of the patient begins with an accurate history in an attempt to
identify the patient as having acute or chronic poisoning. History of possible
coingestants should also be obtained. Providers should also assess mental status,
temperature, ventilatory function, cardiovascular status, and volume status. IV
access should be obtained if initial assessment points toward clinically significant
salicylate toxicity.
Laboratory assessment includes serum salicylate concentration, electrolytes,
arterial blood gas, liver function tests, CBC, prothrombin and partial
thromboplastin times, urinalysis, and an EKG. In the case of intentional
ingestions by adolescents, attention to a serum acetaminophen measurement is
important (as many OTC analgesics contain aspirin and acetaminophen in
combination). Unless the initial salicylate level is undetectable, given erratic and
delayed absorption after overdose, salicylate levels should be repeated and
monitored q1–2 hours until downtrending.
Because aspirin overdose is associated with delayed gastric emptying and drug
coalescence to form bezoars, consider GI decontamination in patients presenting
within 4 to 6 hours of ingestion. In patients who present more than 6 hours after
ingestion or in those with chronic salicylism, activated charcoal might still be
