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67-year-old man is evaluated in the intensive care unit after ingestion of an unknown quantity of pills. He has a history of alcoholism and rheumatoid arthritis. He was recently hospitalized for severe depression. He is unresponsive to verbal stimuli in the emergency department and is orally intubated for airway protection. No information is available about his home medications. On admission to the intensive care unit, he is tachypneic and his pulse rate is 118/min . Neurologic examination shows no focal deficits, but he remains unresponsive to stimuli. The rest of the physical examination is normal except for diffuse rhonchi on auscultation of the lungs. The chest radiograph shows bilateral interstitial infiltrates.
Laboratory Studies
Sodium
148 meq/L (148 mmol/L)
Potassium
4.5 meq/L (4.5 mmol/L)
Chloride
108 meq/L (108 mmol/L)
Bicarbonate
14 meq/L (14 mmol/L)
Blood urea nitrogen
30 mg/dL (10.71 mmol/L)
Creatinine
1.6 mg/dL (141.47 μmol/L)
Glucose
65 mg/dL (3.61 mmol/L)
Osmolarity
319 mosm/L
Which one of the following is the most likely toxin?
A Ephedrine
B Lithium
C Salicylate
D Ethylene glycol
E Tricyclic antidepressant
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Hi dark horse how u r
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hi Pacemaker...I m fine ...just woke up....getting ready to start a wholdeday of clinic and Theatre...ur qs are brilliant......and getting tougher every day....tx for posting them....they are real brain teasers....
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not sure could it be lithium,,,,,,though looks more like salicylate
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doc,
how abt the anion gap.May be u get any clue from there
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Thanks DH,
yeah , they r tough for me ,but , they r cat walk for u.
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Correct Answer = C)
Key Points
* Metabolic signs of salicylate toxicity include respiratory alkalosis, anion gap metabolic acidosis, and hyperthermia; other signs and symptoms include depressed level of consciousness, noncardiogenic pulmonary edema, prolonged prothrombin time, hepatic toxicity, and hypoglycemia.
* Management of salicylate toxicity includes alkalinization of urine to enhance excretion of salicylates and hemodialysis for severe toxicity.
Salicylates should be considered in this patient with multiple clinical findings consistent with intoxication. The effects of salicylate toxicity include respiratory alkalosis, anion gap metabolic acidosis, and hyperthermia. The increase in insensible water losses and hyperthermia often result in intravascular volume depletion. Salicylates are also associated with a depressed level of consciousness and noncardiogenic pulmonary edema. Other symptoms can include coagulation abnormalities (prolonged prothrombin time), hepatic toxicity, and hypoglycemia.
Chronic salicylate ingestion should be suspected in this patient with a history of degenerative joint disease. Chronic ingestors develop toxicity at lower blood levels than patients with a single acute ingestion. Management includes alkalinization of urine to enhance excretion of salicylates, and hemodialysis for severe toxicity.
Ephedrine can produce a sympathomimetic syndrome with tachycardia, hyperthermia, and altered mental status, but metabolic acidosis and pulmonary edema would not be expected. Lithium can also cause altered mental status and other neurologic findings, as well as tachycardia due to intravascular volume depletion. Lithium would not be expected to cause fever, metabolic acidosis, or pulmonary edema. Ethylene glycol ingestion can produce many of the symptoms this patient is manifesting, including depressed level of consciousness, metabolic acidosis, and pulmonary edema. Ethylene glycol ingestion often results in an osmolar gap, however, and would not be associated with fever. Tricyclic antidepressants can cause neurologic symptoms, including seizures and coma. Anticholinergic features such as hyperthermia, dry mouth, flushing, and dilated pupils associated with tricyclic overdose are not seen in this patient.
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