262 Emergency Medicine
(a)NAC is used in the treatment of hepatic failure secondary to APAP
overdose. (c and d)IV NAC is not known to cause these side effects.
(e)Amitriptyline,indomethacin, doxorubicin, phenazopyridine, and rifampin
are some medications known to cause urine to change color.
239.The answer is b.(Rosen, pp 2151-2152.)Deferoxamineis a specific
chelator of ferric iron (Fe3+). It binds with iron to form a water-soluble
compound, ferrioxamine, which can be excreted by the kidneys. Deferoxamine
has a half-life of 1 hour, so continuous infusion is the preferred method of
administration.
The patient’s clinical presentation is consistent with acute iron poi-
soning.Initial presentation reflects the corrosive effects of iron on the gut
and includes nausea, vomiting, diarrhea, and sometimes GI bleeding. Patients
with severe overdose may present with shock or coma.
(a)The treatment for organophosphate toxicity is atropine and prali-
doxime. Physostigmine is an antidote for the anticholinergic syndrome.
(c)Aspirinoverdose is treated with decontamination, urine alkalinization, and
sometimes dialysis. NAC is the antidote for APAP overdose. (d)Acute benzo-
diazepine overdose is treated with flumazenil. Narcan is the antidote for opioid
overdose. (e)Anticholinergic overdose can be treated with physostigmine.
Fomepizole is the treatment for toxic alcohol ingestion (ie, ethylene glycol).
240.The answer is b.(Rosen, pp 2087-2093.)Overdose of TCAresults in
toxicity by a number of different mechanisms. The anticholinergic properties
of TCAs result in the toxidrome “blind as a bat (mydriasis), red as a beet
(flushed skin), hot as a hare (hyperthermia secondary to lack of sweating),
dry as a bone (dry mucous membranes), mad as a hatter (mental status
changes).” This is secondary to muscarinic receptor blockade.The cardi-
nal signs of TCA overdose include ventricular dysrhythmias, hypotension,
and decreased mental status. Sodium bicarbonateis a potentially life-
savingintervention in TCA overdose because an alkaline pH combined with
a sodium load increases conductance through cardiac fast sodium channels
and prevents ventricular dysrhythmias as evidenced by narrowing of the
QRS complex on an ECG.
(a)The most worrisome effect is sodium channel blockade causing
conduction delays and dysrhythmias as evidenced by QRS widening, QT
prolongation, and wide-complex tachycardias. (c)Inhibition of serotonin
and norepinephrine reuptake results in catecholamine depletion and con-
tributes to hypotension. (d)Histamine receptor blockade is associated with