Remember, don't kill the messenger.
Here is the Dx ......
Patient was suffering from ASA or Salicylate Toxicity.
Definition of Toxicity
Salicylate toxicity can result from chronic or acute ingestion. Chronic intoxication results from excessive or therapeutic use over a period of 12 hours or longer. Most commonly, this is seen in elderly patients with arthritis or other musculoskeletal problems. Acute intoxication is more likely to be the result of deliberate self-poisoning. Chronic intoxication is seen less frequently and generally has a poorer outcome, because of a low index of suspicion and delay in proper treatment.
In general, the toxic effects of salicylates are seen at serum levels above 30 mg per dL (2.15 mmol per L). Therapeutic levels needed for the anti-inflammatory effects of salicylates range from 15 to 30 mg per dL (1.10 to 2.15 mmol per L). The Food and Drug Administration recommends that the maximum dose of salicylate in a 70-kg person not exceed 3,900 mg in 24 hours for more than ten days.
Pharmacology
Salicylates are weak acids, and thus are rapidly absorbed from the gastrointestinal tract. Peak serum salicylate levels occur within 12 hours of ingestion. Salicylate-induced pylorospasm and the dosage from (effervescent, enteric coated, etc.) can affect the rate of absorption.
Toxic doses of salicylates have a much longer half-life than therapeutic doses. This is due to a shift from first-order to zero-order kinetics as the salicylate metabolic pathways become saturated even at therapeutic levels. When the enzymes are saturated, plasma salicylate concentration rises rapidly, and toxicity occurs.
Clinical Manifestations
Salicylate toxicity should be suspected in any patient with fever, hyperventilation, seizures or coma of uncertain etiology. It is not uncommon for salicylate poisoning to be misdiagnosed initially as diabetic ketoacidosis.
Initial symptoms of salicylate toxicity include tinnitus (followed by hearing loss), vertigo, nausea, vomiting, hyperventilation and agitation. As the serum level rises, metabolic acidosis ensues, resulting in more severe hyperpnea. This is followed by central nervous system deterioration (lethargy, confusion, delirium, convulsions and, eventually, coma). Fever, due to uncoupling of oxidative phosphorylation, is also a common symptom.
Other manifestations of salicylate toxicity include non-cardiogenic pulmonary edema, renal tubular damage, bleeding disorders and hemolysis. The pathophysiology of salicylate damage to the lungs and kidneys is still unclear, but a central factor seems to be a disruption of capillary permeability to protein, producing high concentrations of protein in both pulmonary edema fluid and urine. A similar phenomenon occurs in cerebral membranes and may produce cerebral edema.
INITIAL TREATMENT
As with any acutely ill patient, initial treatment should focus on establishing an adequate airway, breathing and circulation. The history should include the amount of salicylates ingested, the type of preparation and the exact time of ingestion.
Important initial laboratory tests include an arterial blood gas determination and serum salicylate level, as well as serum sodium, potassium, urea nitrogen and glucose levels and coagulation profile. There are rapid screening tests, such as the ferric chloride test, to detect the presence of salicylic acid in the urine.
IPECAC AND GASTRIC LAVAGE
Gastric emptying should be performed as early as possible by either induced emesis should attemtp to prevent drug absorption by gastric emptying and the use of activated charcoal.
Central to the management of these patients is the use of intravenous fluids and bicarbonate to produce alkaline diuresis and to correct acid-base and electrolyte abnormalities. These patients should be monitored closely and treated aggressively; in some patients, hemodialysis may be necessary.
* Unknown what her labs were.
* Unknown if this was a suicide attempt.
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Non Sibi Sed Suis
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