Page 1723 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

1192 PART 11: Special Problems in Critical Care

CHAPTER Toxicology in Adults • Isopropanol causes hemorrhagic gastritis, ketonemia, and ketonuria,
124 Patrick McCafferty Lank but not acidosis. Fomepizole and ethanol are not indicated because
metabolites are nontoxic. Dialysis is effective in severe cases.
Thomas Corbridge
Patrick T. Murray Barbiturates
• Hypothermia, hypotension, bradycardia, flaccidity, hyporeflexia,
coma, and apnea are features of barbiturate overdose. Severe over-
KEY POINTS
dose can mimic death.
General Measures • Supportive measures include gastric emptying and activated
• Supportive measures supersede other considerations in the charcoal. Alkalinization of the urine increases elimination of phe-
management of the poisoned patient. After addressing the ABCDs nobarbital, but not other barbiturates, and may aggravate pulmo-
of life support, the focus can switch to confirmation of intoxication nary edema. Hemodialysis should be considered in severe cases.
and targeted therapy. Benzodiazepines
• Administer a “cocktail” of oxygen, dextrose, thiamine, and • Supportive measures, gastric emptying, activated charcoal, and
naloxone to patients with depressed mental status. flumazenil treat benzodiazepine overdose.
• An increase in anion gap, osmol gap, or arterial saturation gap • Flumazenil reverses sedation but may increase the toxicity of coin-
should raise the suspicion of intoxication. gested drugs. Flumazenil should be avoided in patients taking benzo-
• An osmol gap of large magnitude (>25 mOsm/kg) suggests diazepines therapeutically and in benzodiazepine-addicted patients.
methanol or ethylene glycol poisoning; however, serious intoxica- • There is no role for forced diuresis, dialysis, or hemoperfusion in
tion with either agent can occur without increasing the osmol gap, benzodiazepine overdose.
particularly in the later stages of intoxication.
• Carbon monoxide and methemoglobin elevate the arterial oxygen β-Blockers
saturation gap. These toxins interfere with oxygen binding to hemo- • Cardiovascular manifestations of overdose are treated with fluids,
. Oxygen vasopressors, atropine, glucagon, and hyperinsulinemia/euglycemia
globin and decrease oxygen content without lowering Pa O 2
saturation measured by pulse oximetry is falsely high in this setting. (HIE) therapy.
• Toxicology screening can provide direct evidence of intoxication, Calcium-Channel Blockers
but it rarely impacts initial management. • Hypotension is treated with fluids, calcium chloride, and vasopressors.
• Poison control center consultation is advised to determine appro- Glucagon and HIE therapy may decrease vasopressor requirements.
priate laboratory testing and patient disposition and treatment. • Intravenous lipid emulsion should be considered in the poisoned
The emergency phone number is 1-800-222-1222. patient with cardiac arrest, terminal arrhythmia, or refractory severe
• Gastric lavage only improves outcome in patients if performed hypotension.
within 1 hour of ingestion, although this time may be extended in Carbon Monoxide
poisonings that delay gastric emptying. Risks of lavage preclude its
use in nontoxic ingestions, subtoxic amounts of a toxic ingestion, • Exposure to smoke, poorly ventilated charcoal or gas heaters, and
ingestion of caustic liquids, and when the toxin is no longer expected automobile exhaust are responsible for most poisonings.
to be in the stomach. The airway must be protected prior to lavage. • Carbon monoxide poisoning can present with myocardial ischemia,
• Activated charcoal should be administered for most acute oral arrhythmias, mental status changes, headache, and generalized
ingestions if the airway is protected. weakness.
• Whole-bowel irrigation with a polyethylene glycol electrolyte • Prompt oxygen therapy is crucial.
solution is only indicated for iron overdose, ingestion of sustained- • Pulse oximetry is unreliable in detecting carboxyhemoglobin;
release tablets, and “body packing” with illicit drugs. pulse oximetry overestimates oxyhemoglobin by the amount of
• Urinary alkalinization enhances excretion of nonpolar weak acids carboxyhemoglobin present; saturation by pulse oximetry may be
normal despite elevated carboxyhemoglobin.
and is most commonly used in salicylate toxicity.
• The use of hyperbaric oxygen is controversial. Patients with poten-
Acetaminophen tially life-threatening exposures should receive hyperbaric therapy
• All overdose cases should be screened for acetaminophen poisoning. if it is readily available and other life-threatening conditions do not
• The antidote, N-acetylcysteine (NAC), should be started within preclude its use.
8 hours of ingestion to decrease the risk of hepatotoxicity. The • Delayed neurologic sequelae may occur in survivors.
Rumack-Matthew nomogram allows for stratification of selected Cocaine
patients into categories of probable, possible, and no hepatic toxicity.
• Cocaine is often mixed with other substances of abuse.
Alcohols • Cocaine causes acute coronary syndromes, hypertensive crisis,
• Metabolic acidosis with an elevated anion gap and/or the presence of seizures, rhabdomyolysis, intracranial hemorrhage, pneumomedi-
an osmol gap are classic in methanol and ethylene glycol poisoning. astinum, and respiratory failure.
• Features of methanol poisoning include inebriation, optic papillitis, • Agitation and hyperthermia should be treated rapidly with
and pancreatitis. benzodiazepines and cooling strategies.
• Features of ethylene glycol poisoning include inebriation, acute • Benzodiazepines are first-line therapy for hypertensive crisis.
renal failure, crystalluria, and myocardial dysfunction. Refractory patients should receive an α-adrenergic antagonist.
• Treatment of methanol and ethylene glycol poisoning with fomepi- Nonselective β-blockers (eg, propranolol) should not be used
zole or ethanol inhibits metabolism by alcohol dehydrogenase to alone to treat hypertension because of the potential for unopposed
toxic metabolites. Dialytic removal of toxic metabolites is indicated α-adrenergic stimulation. Labetalol is controversial. Selective
in severe poisonings. β-blockers do not aggravate hypertension but may cause hypotension.

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