poisoning may mimic the systemic inflammatory response
syndrome, and one must consider alternative causes
including sepsis. Obtain salicylate concentrations every
2 hours until a peak value has been obtained. In patients
with salicylate levels <30 mgldL, follow until <20 mgldL
and treat supportively. Initiate urinary alkalinization for
patients with levels >30 mg/dL to facilitate urinary
clearance and limit central nervous system penetration.
One must observe vigilantly for any signs of clinical
deterioration and initiate early hemodialysis, as this may
be a life-saving intervention. Such findings include patients
with altered mental status, seizures, severe acid-base
derangements, pulmonary edema, and renal insufficiency.
Furthermore, patients with salicylate levels >90 mgldL
after an acute ingestion and those with levels >60 mg/dL
with chronic exposures warrant hemodialysis. These
thresholds should be lowered for patients with significant
As with all poisonings, the initial focus should be on
aggressive supportive care. Pay meticulous attention to the
patient's airway, breathing, and circulation. Intubate
patients only if absolutely necessary because of the
difficulty in attaining the required minute ventilation with
mechanical respiration. Because most patients are
significantly dehydrated, initiate aggressive volume
resuscitation with 1-2 L of normal saline to ensure an
adequate urine output ( 1-2 rnL/kg/hr).
There are several available modalities for patient
decontamination. Administer activated charcoal at a dose
of 1 g/kg to awake and alert patients with intact airway
reflexes and no concern for vomiting. This can be repeated
as needed to adsorb salicylates that form a concretion.
Urinary alkalinization is performed by injecting 3 ampules
of sodium bicarbonate into a 1 -L bag of So/o dextrose
solution to create an isotonic solution. Infuse this solution
Suspect significant salicylate
ingestion or evidence of toxicity
Address ABC's, decontaminate with
activated charcoal at 1 gjkg with
intact airway and bowel motility
Figure 57-1. Salicylate toxicity diagnostic algorithm.
at 200 mL/hr. Pay careful attention to potassium levels and
replete as necessary, as hypokalemic patients will excrete
hydrogen ions into the distal renal tubules to retain
potassium, thereby impairing successful alkalinization of
the urine. The goal of alkalinization is to raise the urine
pH > 7 .S-8. Avoid alkalinization in patients with congestive
heart failure and renal failure, as they will be unable to
tolerate the necessary volume load.
All symptomatic patients will require hospitalization.
Patients who require urinary alkalinization or hemodialysis
should be admitted to a critical care setting. All patients
with a suicidal ingestion will require psychiatric evaluation.
Patients with a detectable serum salicylate level require
serial testing to rule out continued absorption. An
asymptomatic patient with an undetectable salicylate con
centration at the 6-hour mark can be safely cleared from a
Bronstein AC, Spyker DA, Canti.lena LR, et al. 2010 Almual report
of the American Association of Poison Control Centers'
National Poison Data system (NPDS): 28th annual report.
Clin Toxicol. 20 11:49:910-941.
management. Clin Toxicol. 2007;45:95-13 1.
O'Malley G. Emergency department management of the
salicylate-poisoned patient. Emerg Med Clin North Am.
Yip L. Aspirin and salicylates. In: Tintinalli JE, Stapczynski JS,
Ma OJ, Cline DM, Cydulka RK, Meckler GD. Tintinalli's
Emergency Medicine: A Comprehensive Study Guide. 7th ed.
New York, NY: McGraw-Hill, 201 1, pp. 1243-1245.
Vinodinee L. Dissa naya ke, MD
• Consider carbon monoxide (CO) poisoning in all patients
with headaches, flu-like symptoms, altered mental
status, or an unexplained anion gap metabolic acidosis.
• Immediately administer supplemental 02 to all patients
with potential co poisoning before any confirmatory studies.
• Pulse oximetry values will be falsely elevated in patients
with CO poisoning as a result of the inabil ity of standard
Carbon monoxide (CO) is an invisible killer; it is an odor
carbon-based fuels (eg, coal, gasoline, natural gas). Faulty
furnaces and vehicle exhaust fumes are common sources for
clinical CO poisoning. Methylene chloride, a substance
found in paint stripper and bubbling holiday lights, is
metabolized in vivo into CO and may account for cases of
delayed poisoning. According to 20 10 US Poison Control
treated in medical facilities, and CO is the leading cause of
toxin-related fatalities in children less than 5 years of age. In
survivors of CO poisoning, it is not uncommon to develop
delayed neurologic sequelae, including recurrent headaches,
cognitive deficits, and motor disorders.
CO exposure produces toxicity by 3 major pathways.
The first of these is an inhibition of systemic 0 2 delivery.
CO binds to hemoglobin (Hb) with an affinity roughly
240 times greater than 0 2• Systemic 0 2 delivery plummets
as the majority of circulating Hb binding sites are now
occupied by CO. In addition, Hb that has bound CO has an
increased affinity for concurrently bound 02, resulting in
oximetry to distinguish between oxyhemoglobin and
• Symptomatology is often more important than the
absol ute carboxyhemoglobin level when determining
the impaired release of 0 2 as it reaches the target tissues.
The ability o f C O t o inhibit normal cellular respiration
accounts for its second mechanism of toxicity. CO binds to
cytochrome aa3 and inhibits normal transit through the
electron transport chain. The resulting shutdown in the
The binding of CO to myoglobin accounts for the third
mechanism of toxicity. Myoglobin binds to CO with an
affected, a global reduction in cardiac contractility occurs.
Of note, CO readily crosses the placenta and binds to fetal
hemoglobin (HbF) with a 10-15% higher affinity than
adult Hb, so fetal toxicity in cases of CO poisoning is often
more severe than is evident on examination of the mother.
The symptoms of CO poisoning are notoriously nonspe
cific, but typically present with some degree of neurologic
and cardiovascular impairment. A vague headache is the
Figure 58-1. Carboxyhemoglobin "shift to the left"
reshaping of the oxyhemoglobin (Hb02) dissociation
curve. Reprinted with permission from Maloney G.
Chapter 217. Carbon monoxide. In: Tintinalli JE,
Stapczynski JS, Ma OJ, Cline OM, Cydulka RK, Meckler GO,
eds. Tintinalli's Emergency Medicine: A Comprehensive
Study Guide. 7th ed. New York: McGraw-Hill, 201 1.
most common complaint, followed by fatigue, malaise,
lethargy. Cardiovascular symptoms include ischemic chest
pain, shortness of breath, and palpitations. Maintain a high
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