5. What is the treatment for this condition?

Initial management of cyanide poisoning is largely supportive and includes

supplemental oxygen as well as airway and ventilator support. Activated charcoal
may be considered in conscious patients who present soon after ingestion. Although
adsorption of cyanide to charcoal is poor, binding may be sufficient to avert severe
toxicity in some case. Intravenous crystalloid should be administered initially to
resuscitate hypotensive patients. Patients who are unresponsive of fluid
administration should be given vasopressors. Sodium bicarbonate may be
considered in severely acidemic patients that are refractory to other supportive
measures.
Cyanide toxicity
Acute cyanide toxicity occurs when the cyanide ions bind to tissue cytochrome
oxidase and interfere with normal oxygen utilization. This as a result leads to
metabolic acidosis, cardiac arrhythmias, and increased venous oxygen content (as a
result of the inability to utilize oxygen). Another early sign of cyanide toxicity is the
acute resistance to the hypotensive effects of increasing doses of sodium
nitroprusside (tachyphylaxis). (It should be noted that tachyphylaxis implies acute
tolerance to the drug following multiple rapid injections, as opposed to tolerance,
which is caused by more chronic exposure). Cyanide toxicity can usually be avoided
if the cumulative dose of sodium nitroprusside is less than 0.5 mg/kg/h.
Symptoms: Cyanide toxicity is often associated with the odor of almonds on breath
and can result in acidosis, tachycardia, mental status changes, and death.
How to intervene: Patients with cyanide toxicity should be mechanically
ventilated with 100% oxygen to maximize oxygen availability.
Pharmacological treatment: Treatment of cyanide toxicity depends on increasing
the kinetics of the two reactions by administeringsodium thiosulfate (150 mg/kg
over 15 min) or 3% sodium nitrate (5 mg/kg over 5 min), which oxidizes hemoglobin
to methemoglobin, or by limiting the administration of nitroprusside.
Methemoglobinemia

Methemoglobinemia from excessive doses of sodium nitroprusside or sodium nitrate

can be treated with methylene blue (12 mg/kg of a 1% solution over 5 min), which
reduces methemoglobin to hemoglobin.
Thiocyanate toxicity
Symptoms: Thiocyanate toxicity causes anorexia, fatigue, and mental status
changes, including psychosis, weakness, seizures, tinnitus, and
hyperreflexia. Thiocyanate is usually excreted in the urine. Toxicity can be
minimized by avoiding prolonged administration of nitroprusside and by limiting
drug use in patients with renal insufficiency. If necessary, thiocyanate can be
removed by dialysis.
1. What kind of article?

The article is a controlled clinical trial.