Page 1724 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 124: Toxicology in Adults 1193

• Patients presenting with cocaine-associated chest pain need to be Methemoglobinemia
evaluated for myocardial infarction. Acute coronary syndromes • Hereditary methemoglobinemia (eg, hemoglobin M or cytochrome
should be treated with nitrates and benzodiazepines. b5 reductase deficiency) is generally insignificant and does not
Cyanide require treatment. Acquired and potentially life-threatening met-
• Features of cyanide poisoning depend on the amount and rate hemoglobinemia can occur after oxidant drug or toxin exposure.
of cyanide absorption. Patients who are asymptomatic after • Methemoglobinemia decreases oxyhemoglobin saturation and
inhalation generally do not require treatment. Oral ingestion blood oxygen-carrying capacity by decreasing available hemoglo-
causes progressive symptoms over minutes to hours. bin and shifting the oxyhemoglobin dissociation curve to the left.
• Sodium nitroprusside infusions can cause cyanide and thiocyanate • Symptoms of moderate methemoglobinemia include dyspnea,
poisoning. headache, and weakness. Confusion, seizures, and death can occur
• Symptoms include anxiety, dyspnea, headache, confusion, tachy- with levels >60%.
cardia, and hypertension. High concentrations of cyanide cause • Cooximetry measures methemoglobin saturation. Standard pulse
stupor or coma, seizures, fixed and dilated pupils, hypoventilation, oximetry registers falsely high in patients with methemoglobinemia.
hypotension, arrhythmias, and cardiopulmonary collapse. Arterial blood gases typically demonstrate a normal Pa O 2 and a
• In addition to supportive measures and oxygen, several antidotes normal calculated oxygen saturation.
are available: amyl and sodium nitrite, sodium thiosulfate, and • Routine treatment of methemoglobinemia consists of oxygen and
hydroxycobalamine. methylene blue.
Cyclic Antidepressants Opioids
• Neurologic deterioration is often abrupt and has been associated • The triad of miosis, respiratory depression, and coma suggests
with QRS prolongation >0.10 second. opioid intoxication.
• Acidemia potentiates toxicity. Therapeutic alkalemia with sodium • Naloxone reverses sedation, hypotension, and respiratory depression.
bicarbonate is beneficial. The initial dose is 0.4 mg IV or 0.8 mg IM or SC. Lower doses
• Lidocaine should be used for ventricular arrhythmias resistant to should be given when there is a concurrent stimulant overdose.
sodium bicarbonate. Procainamide is contraindicated. Larger initial doses may be required when there is abuse of
• Physostigmine should be avoided as it has been associated with naloxone-resistant opioids. Lack of response to 6 to 10 mg of
death. Flumazenil should be avoided because of risk of increased naloxone generally excludes opioid toxicity.
seizure activity.
Organophosphate and Carbamate Insecticides
Digoxin
• Features of digitalis intoxication include fatigue, gastrointestinal • Organophosphates are irreversible inhibitors of acetylcholinesterase
(AChE); carbamates reversibly inhibit AChE.
symptoms, neurologic disturbances such as blurred vision, visual
color changes, headache, dizziness, delirium, and cardiac arrhyth- • Signs of cholinergic poisoning include salivation, lacrima-
mias. Significant overdose may cause hyperkalemia. tion, urination, diarrhea, gastrointestinal cramping, and emesis
• Supportive therapy includes rapid correction of arrhythmogenic (SLUDGE). Muscle fasciculations, coma, and seizures also occur.
metabolic disturbances, particularly hypokalemia if present. • Respiratory failure results from muscle weakness, bronchorrhea,
Hyperkalemia requires treatment unless Fab therapy is immediately depressed respiratory drive, and bronchoconstriction.
available. • The level of red blood cell cholinesterase helps diagnose organo-
• Immunotherapy with digoxin-specific antibody Fab fragments is phosphate poisoning.
indicated for severe intoxications. • Treatment includes supportive measures, atropine, and oximes. Large
• Gastrointestinal decontamination measures include gastric lavage doses of atropine may be needed to decrease pulmonary secretions.
and activated charcoal. Hemodialysis removes only small amounts of Salicylates
total body digitalis, but may be indicated for correction of hyperka-
lemia or other acid-base derangements in renally impaired patients. • The Done nomogram for predicting salicylate toxicity is of limited
• Electrical cardioversion of a digitalis toxicity–induced arrhythmia use in current practice.
should be reserved as a last resort, using the minimum effective • Salicylate poisoning causes respiratory alkalosis and metabolic
energy level. acidosis; the latter is more prominent in children.
• Manifestations of chronic ingestion may be subtle and occur at
γ-Hydroxybutyrate relatively low serum salicylate levels.
• Depressed mental status, emesis, bradycardia, hypotension, and • Acidemia favors tissue penetration of salicylates. Urinary alkalini-
respiratory depression are features of GHB overdose. zation enhances renal clearance of salicylates. Hypokalemia must
• Treatment is supportive. be corrected to succeed in urinary alkalinization.
Lithium • Seizures, coma, refractory acidosis, and high serum salicylate
• Most cases of intoxication, associated with levels above 1.5 mEq/L, levels are indications for hemodialysis.
are caused by unintentional overdose during chronic therapy. • Alkalemia should be maintained in mechanically ventilated
• High levels of lithium decrease the anion gap. patients with salicylate poisoning
• Severe poisoning causes coma, seizures, and cardiovascular instability. Selective Serotonin Reuptake Inhibitors
• Treatment includes seizure control and vasopressors for • In combination with a number of drugs, SSRIs may cause serotonin
hypotension refractory to fluids. Gastric emptying should be syndrome. Toxic combinations may not be evident for days to weeks.
performed initially. Oral charcoal is of little benefit. Whole-bowel • Serotonin syndrome is characterized by combinations of specific
irrigation is important with sustained-release preparations. neurologic and autonomic abnormalities best outlined in diagnostic
• Lithium is the prototypical dialyzable intoxicant. criteria.

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