Accidental cyanide poisoning is a potential hazard in some industrial processes and in house and industrial fires.
Which ONE of the following statements is FALSE regarding antidotes used in cyanide toxicity?
Answer: D: Cyanide toxicity is not common. However, when it occurs, and if severe, the majority of patients die before reaching hospital. Patients who reach hospital who show signs of toxicity should be treated emergently with an antidote and provision of supportive care.
Several antidotes are commercially available but dicobalt edetate seems to be the antidote most widely available in Australia. Its efficacy has not been established in cyanide poisoning. There should be definitive clinical evidence of cyanide poisoning including worsening metabolic acidosis (due to lactic acidosis) or impaired consciousness present when administering dicobalt edetate. If administered to a patient without cyanide poisoning it can cause serious direct toxic effects including hypotension, convulsions and oedema of the face and larynx.
Intravenous hydroxycobalamin (vitamin B12) has more evidence for efficacy than other antidotes. It causes minimal adverse effects. Hydroxycobalamin is recommended as the first-line therapy in severely poisoned patients and for a patient in cardiac arrest due to suspected cyanide toxicity. The recommended dose is 5 mg over 15 minutes with repeat dosing up to 15 mg. Hydroxycobalamin is expensive and may not be available widely in EDs.
Sodium thiosulphate is effective in the treatment of mild to moderately poisoned patients and also as a diagnostic trial in suspected cases. Its efficacy has not been proven and as a second line treatment should be used with other cyanide antidotes in severe cases.
References:
Young children often present to the ED following accidental ingestion of household corrosive substances such as oven cleaners and dishwashing powder.
Regarding corrosive ingestion in this age group, which ONE of the following is TRUE?
Answer: B: Widely used household products contain corrosive substances that may result in injury to young children because of poor storage practices. Among those household substances, oven and drain cleaners (potassium hydroxide and sodium hydroxide) have high potential to cause mucosal burns. Household bleaches are relatively safe and generally cause minor injury. Dishwashing powders and tablets are highly alkaline and cause immediate burns. This may be due to the prolonged surface contact expected form powders and tablets.
The absence of oral burns does not exclude oesophageal and gastric burns and therefore does not predict a good outcome. Endoscopy provides the best guide in assessing the early risk of perforation and late sequelae of corrosive burns. About 10–15% of patients with oesophageal burns have no oropharyngeal burns. When there are oral burns one-third of patients have oesophageal burns. Alkalis tend to cause more oesophageal burns than acids do. Acids tend to cause gastric burns.
All symptomatic children should be kept nil by mouth until endoscopic assessment. In children with relatively limited symptoms attempts at neutralization should be avoided but dilution of corrosive with drinking water is acceptable, especially for acids.
Hydrogen peroxide (H2 O2 ) is frequently used in various domestic and industrial products such as disinfectants, bleaches and stain removers. In a patient who has intentionally ingested such products in high concentration, all of the following clinical features may be expected EXCEPT:
Answer: B: Serious toxicity after ingestion of concentrated H2 O2 solutions (>10%) is associated with:
The latter two being the consequence of the release of O2 gas.
The direct corrosive injury to the gastrointestinal tract can cause ulceration of oral mucosa, vomiting, haematemesis and melaena. Also laryngeal oedema and laryngospasm may lead to respiratory distress and airway obstruction. Early airway management is essential in these patients.
Rapid deterioration of neurological function and seizures often occur due to venous and arterial gas embolization. Features of massive distension of hollow viscera due to liberation of large volumes of gas will be evident.
Direct damage to the eye occurs when it is directly exposed to H2 O2 . Visual disturbances and blindness is not a feature of hydrogen peroxide ingestion.
Reference:
When using atropine in the treatment of organophosphate poisoning, all of the following features are end points of treatment EXCEPT:
Answer: B: Organophosphates inhibit acetylcholinesterase, leading to increased acetylcholine levels at cholinergic receptors (both muscarinic and nicotinic).
Along with bradycardia, the muscarinic effects of acetylcholine excess can be remembered by the following mnemonic.
DUMBBELS
The nicotinic effects are:
Atropine is the antidote used as a muscarinic antagonist. It does not act on the nicotinic receptors and therefore there is no improvement of muscle weakness with atropine.
In organophosphate poisoning large doses (up to 100 mg) of atropine may be required. The recommended regime is atropine 1.2 mg IV initially as a bolus, doubling the dose every 5 minutes. The end points of treatment with atropine are drying of airway and oral secretions, resolution of bradycardia and achieving good air entry with resolution of bronchospasm. Fully dilated pupils means excessive anticholinergic toxicity due to over administration of atropine and along with this other anticholinergic toxic features may be found. No further atropine should be administered while these toxic features are present.
Regarding cardiac arrest secondary to cardiotoxic drugs, which ONE of the following statements is TRUE?
Answer: C: The list of drugs that could cause severe cardiotoxicity leading to cardiac arrest is not exhaustive. Cardiac sodium, potassium and calcium channel blockers and beta-blockers are among the major groups of drugs that cause cardiac arrest in a poisoned patient. Advanced life support guidelines applied to a poisoned patient who is in a cardiac arrest are similar to that applied to other patients who are in cardiac arrest. Treatment with specific antidotes in adequate doses should be considered very early. However, the clinical effectiveness of antidotes has not been verified with high level evidence. CPR should be continued for a prolonged period, sometimes up to 4 hours, until the cardiac toxicity of the drug dissipates and the patient recovers. Timely and adequate CPR although prolonged does not seem to adversely affect the neurological outcome in these poisoned patients.
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