Page 1745 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

1214 PART 11: Special Problems in Critical Care

bowel follow-through contrast study is more sensitive and specific than Clinical manifestations of cyanide poisoning depend upon the
routine abdominal radiographs. Contraindications to whole-bowel amount and rate of cyanide absorption. Patients who are completely
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irrigation include ileus, gastrointestinal hemorrhage, and bowel perfora- asymptomatic after inhalation (which is associated with immediate
tion. Polyethylene glycol electrolyte solutions may also displace cocaine absorption) do not require treatment and can be discharged after brief
from AC. Surgical removal of retained packages may be required, observation. Patients who ingest cyanide orally may develop progressive
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particularly if there is bowel obstruction or package perforation. symptoms over minutes to hours. Oral ingestion on an empty stomach
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Endoscopic approaches risk packet rupture and are not recommended. with low pH results in the rapid generation of HCN from potassium and
Neither dialysis nor hemoperfusion effectively removes cocaine. sodium salts (KCN and NaCN). Oral ingestion into a full and alkaline
Perhaps the most important strategy in cocaine intoxication is rapid stomach delays generation of HCN, resulting in progressive symptoms
treatment of agitation and hyperthermia. Along these lines, cooling, ben- over 1 to 2 hours. Ingestion of plants containing cyanogenic glycosides
zodiazepines, and occasionally muscle relaxation improve outcome. also causes delayed and progressive toxicity because the ingested com-
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Haloperidol has not been shown to be of benefit, and few data are pound is converted in vivo to cyanide.
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available regarding the use of barbiturates. At low concentrations, cyanide acts as a respiratory and central
First-line treatments of cocaine-associated chest pain are nitrates, nervous system stimulant. Clinical manifestations include anxiety, dys-
benzodiazepines, morphine, and aspirin. 2,241,242 Use of an α-adrenergic pnea, headache, confusion, tachycardia, and hypertension. At higher
receptor blocker such as phentolamine is recommended in refractory concentrations, patients may develop stupor or coma, seizures, fixed and
patients. 2,243 The use of nonselective β-blockers in cocaine-associated dilated pupils, hypoventilation, hypotension, bradycardia, heart block,
chest pain has become controversial in recent years with retrospec- and ventricular arrhythmias. Patients with massive ingestion present in
tive analyses emerging that show no increased incidence of morbidity coma and cardiopulmonary collapse. Survival in these cases depends on
or mortality and possibly a reduction in death in patients started on successful cardiopulmonary resuscitation and survivors are at great risk
β-blocker therapy. 11,244 In the light of many previous and current experi- for anoxic brain injury. 250,251
mental animal and human studies contradicting these conclusions, The diagnosis of cyanide poisoning is usually made on clinical
the American Heart Association does not recommend the use of pure grounds, often in the setting of smoke inhalation injury, where com-
β-blockers in the cocaine intoxicated patient with acute chest pain. 2 bined carbon monoxide and cyanide toxicity occurs. Common fea-
In high concentrations, cocaine acts as a class Ic antiarrhythmic tures include coma, seizures, and cardiopulmonary dysfunction. Lactic
leading to wide-complex tachycardia similar to that seen in TCA over- acidosis and elevated venous oxygen saturation provide evidence for
dose. Based on limited data in humans and animals and extensive unpub- the blocking of aerobic oxygen utilization. Elevated venous oxygen is
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lished experience, the expert panel on toxicologic-oriented advanced further demonstrated by arteriolization of retinal veins on funduscopic
life support suggests a primary role for sodium bicarbonate in cocaine- examination or venous blood on routine blood draws. The bitter almond
associated ventricular tachycardia and ventricular fibrillation. Although scent of HCN may also be detected.
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controversial, lidocaine is also likely to be safe in treating cocaine- High-dose sodium nitroprusside therapy (>10 µg/kg per minute)
induced ventricular tachycardia. 2,6,245 may result in acute cyanide poisoning characterized by anxiety, agita-
The role of thrombolytic therapy remains unclear in patients with tion, tachycardia, myocardial ischemia, metabolic acidosis, hyperventi-
cocaine-associated acute myocardial infarction. 6,246 Thrombolytics are lation, seizures, and paradoxical hypertension (or difficulty in lowering
contraindicated in uncontrolled hypertension, aortic dissection, and blood pressure). Cyanide poisoning is uncommon at nitroprusside
intracerebral hemorrhage. infusion rates less than 10 µg/kg per minute; however, toxicity has
Treatment of respiratory complications is supportive. Oxygen is been reported at an infusion rate of 4 µg/kg per minute after 3 hours of
delivered to improve arterial oxygen saturation; continuous positive therapy. Prolonged nitroprusside infusion increases the risk of thiocy-
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airway pressure or positive end-expiratory pressure may decrease anate toxicity. Thiocyanate levels should be followed in these cases, par-
intrapulmonary shunting in patients with diffuse lung disease. Inhaled ticularly in the setting of renal dysfunction. Thiocyanate levels greater
bronchodilators and corticosteroids are indicated for cocaine-associated than 50 to 100 mg/L cause confusion, somnolence, and seizures. 253
bronchospasm. Tube thoracostomy may be required for pneumothorax; When clinical features are present, treatment should proceed without
pneumomediastinum should be watched expectantly. confirmation of the diagnosis by blood cyanide levels, as these levels are
■ CYANIDE not rapidly available. If a level is to be drawn, the laboratory should be
notified prior to drawing the blood, since special instructions may be
Cyanide is found in a variety of synthetic and natural substances: required to measure this unstable compound. Whole blood levels greater
plastics, glue removers, wool, silks, nylons, and various seeds and plants. than 0.5 to 1.0 mg/L are considered toxic. Smokers may have cyanide
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Poisoning occurs through a number of mechanisms including (1) ingestion levels nearing 0.1 mg/mL.
(eg, the cassava-based foodstuff “gari” or tainted over-the-counter Treatment begins by identifying and treating life-threatening problems.
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preparations ); (2) inhalation of hydrogen cyanide gas (HCN), a com- Survival depends on prompt and successful resuscitation. Oxygen therapy
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bustion by-product of cyanide-containing products; (3) sodium nitro- at 100% fraction of inspired oxygen (Fi O 2 ) is effective in cyanide poisoning
prusside infusion; and very rarely (4) absorption of cyanide-containing and should be administered immediately. 255,256 Hyperbaric oxygen is
solutions or gas through skin. likely of no benefit in cyanide poisoning. 257,258
Cyanide is a rapidly acting poison that binds to cellular cytochrome Several antidotes are available. Amyl and sodium nitrite induce for-
oxidase, interfering with the electron transport chain and therefore con- mation of methemoglobin. Cyanide has a high affinity for the ferric iron
verting cellular aerobic oxygen utilization to anaerobic metabolism. contained in methemoglobin, thereby rendering methemoglobin an
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Once ingested, it is detoxified by enzymatic conversion to the less toxic, effective scavenger of unbound cyanide. Amyl nitrite is administered by
renally excreted metabolite thiocyanate. The most important enzyme inhalation of crushable ampules. Ampules are inhaled for 15 to 30 seconds;
for cyanide conversion is rhodanese (a sulfurtransferase), which forms effects last approximately 2 to 3 minutes. This therapy can be used in
thiocyanate in the presence of sulfane sulfur. This reaction occurs in the spontaneously breathing patients and in patients receiving ventilatory
liver, although the kidney also contains high concentrations of rhoda- support by face mask or endotracheal tube until administration of
nese. Serum albumin plays an important role in cyanide detoxification sodium nitrite. Amyl nitrite is usually only used in patients who do not
because it is a readily available source of sulfane sulfur and it has sulfur- have vascular access. Sodium nitrite is administered intravenously at a
transferase activity. A small amount of cyanide is also detoxified by the dose of 300 mg over 3 minutes to convert hemoglobin into methemo-
vitamin B precursor hydroxocobalamin. This agent binds cyanide to globin. Half this dose may be repeated after 2 hours if there is persistent
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form nontoxic cyanocobalamin. toxicity and a tolerable degree of methemoglobinemia (usually less

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