Iron
The child with iron poisoning presents with shock, which may be due to gut haemorrhage. If over 20 mg/kg of elemental iron has been taken, toxicity is likely. Over 150 mg/kg may be fatal. Intubation, ventilation, and circulatory support are necessary in the severely affected child.
Initial symptoms of toxicity are vomiting, diarrhoea and abdominal pain. These may lead on to drowsiness, fits and circulatory collapse.
Gastric lavage should be performed once the airway is secured and circulatory access has been gained. Charcoal is not helpful. Desferrioxamine can be left in the stomach, but the main treatment is to infuse desferrioxamine at a dose of 15 mg/kg/h. This treatment should be given immediately to children with serious symptoms such as shock, coma or fits and to all with a serum iron level (4 hours or more after ingestion) of 3 mg/l and GI symptoms, leucocytosis or hyperglycaemia
Radiography of the abdomen can help to show how much iron remains within. Whole bowel irrigation with polyethylene glycol-electrolyte solutions may have a place in severe cases.
Tricyclic antidepressant (TCA) poisoning
The toxic effects of these agents results from their inhibition of fast sodium channels in the brain and myocardium. This action is known as “quinidine-like”. With serious
THE POISONED CHILD
intoxication, the cardiac problems are due to intraventricular conduction delay. This results in QRS prolongation (a QRS of more than 4 little squares on the ECG paper is predictive of serious effects).
TCA poisoning causes anticholinergic effects (tachycardia, dilated pupils, convulsions) and cardiac effects (conduction delay, any arrhythmia). Convulsions should be treated as described in Chapter 13.
Additionally, alkalinisation up to an arterial pH of at least 7·45 and preferable 7·5 has been shown to reduce the toxic effects on the heart. This can be achieved by hyperventilation (PCO2 no lower than 3·33 kPa (25 mmHg)) and by infusing sodium bicarbonate (1–2 mmol/kg). Hypotension should be treated with volume expansion and if an inotrope is necessary, norepinephrine (noradrenaline) is superior to dopamine, dobutamine and epinephrine (adrenaline). Glucagon has an inotropic effect and can be used in this circumstance.
The use of antiarrhythmics should be guided from a Poisons Centre. Lignocaine and phenytoin may be helpful. Quinidine, procainamide and disopyramide are contraindicated.
Opiates (including methadone)
Following stabilisation of airway, breathing and circulation, the specific antidote is naloxone. An initial bolus dose of 100 micrograms/kg up to a maximum of 2 mg should be given. Naloxone has a short half-life, relapse often occurring after 20 minutes.
Further boluses, or an infusion of 10–20 micrograms/kg/min may be required.
It is important to normalise CO2before the naloxone is given as adverse events such as ventricular arrhythmias, acute pulmonary oedema, asystole or seizures may otherwise occur. This is because the opioid system and adrenergic system are interrelated. Opioid antagonists and hypercapnia stimulate sympathetic nervous system activity. Therefore if ventilation is not provided to normalise carbon dioxide prior to naloxone administration, the sudden rise in epinephrine concentration can cause arrhythmias.
Paracetamol
Significant paracetamol poisoning in childhood is almost always intentional: the accidental ingestion of paediatric paracetamol elixir preparations by the toddler very rarely achieves toxicity. Doses of less than 150 mg/kg will not cause toxicity except in a child with hepatic or renal disease. Current treatment of paracetamol poisoning includes oral charcoal and a paracetamol blood level to be taken at 4 hours or later.
Figure 14.1 shows a nomogram indicating the level of blood paracetamol at which acetylcysteine should be given intravenously. A total dose of 300 mg/kg is given over approximately 24 hours. Contact a Poisons Centre for individual details.
Salicylates
Aspirin slows stomach emptying so gastric lavage can be undertaken up to 4 hours after ingestion. Repeated charcoal doses should be given for patients who have ingested sustained release preparations. The salicylate level can be measured initially at 2 hours.
However, repeated measurements are necessary and no reliance should be placed on a single salicylate level.The levels will usually rise significantly over the first 6 hours (longer if an enteric coated preparation is used). Salicylate poisoning causes a respiratory alkalosis and metabolic acidosis. Arterial blood gas estimation is necessary to manage the patient. Alkalinisation of the patient improves excretion of salicylate: 1 mmol/kg of sodium bicarbonate should be infused over 4 hours. Forced diuresis is no longer used.
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Ethylene glycol
This sweet-tasting substance is available as an antifreeze and de-icer fluid for vehicles.
It produces a clinical appearance of inebriation accompanied by metabolic acidosis and causes widespread cellular damage, especially to the kidneys. In unwitnessed ingestions the clue is in the metabolic acidosis with an inexplicable anion gap. Activated charcoal is ineffective. Ethanol is a competitive inhibitor of alcohol dehydrogenase and can block metabolism of the ethylene glycol to its poisonous metabolic byproducts. An oral loading dose of 2·5 ml/kg of 40% ethanol (the strength of most spirits) should be started. The aim is to have a blood ethanol concentration of 100 mg/dl. Haemodialysis may be necessary. Cofactors, thiamine, and pyridoxine are also recommended.
Cocaine
Cocaine poisoning leads to local accumulation of the neurotransmitters norepinephrine (noradrenaline), dopamine, epinephrine (adrenaline) and serotonin.
Accumulation of norepinephrine and epinephrine leads to tachycardia which increases myocardial oxygen demand while reducing the time for diastolic coronary perfusion.
Vasoconstriction causing hypertension results from the accumulation of neurotransmitter at peripheral ß-adrenergic receptors and peripheral 5-HT receptor stimulation causes coronary artery vasospasm. In addition, cocaine stimulates platelet aggregation. Together, these changes can produce what is effectively a coronary event in a child or adolescent.
Acute coronary syndrome producing chest pain and varying types of cardiac rhythm disturbances is the most frequent complication of cocaine use which leads to hospitalisation.
Cocaine is also a sodium channel inhibitor, similar to a type I anti-arrhythmic agent so can prolong the QRS duration and impair myocardial contractility.Through the combination of adrenergic and sodium channel effects, cocaine use may cause various tachyarrhythmias including ventricular tachycardia and ventricular fibrillation.Treatment should be guided by a Poisons Centre.
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Figure 14.1. Nomogram showing level of blood paracetamol
Initial treatment of acute coronary syndrome consists of oxygen administration, continuous ECG monitoring, administration of a benzodiazepine (e.g., diazepam or lorazepam) aspirin and heparin. Hyperthermia should be treated with cooling. ß-adrenergic blockers are contraindicated in the setting of cocaine intoxication.
Ventricular tachycardia should be treated with DC shock as anti-arrhythmic drugs may cause further pro-arrhythmic effects
Since cocaine is a sodium channel blocker, administration of sodium bicarbonate in a dose of 1–2 meq/kg should be considered in the treatment of ventricular arrhythmias Ecstasy
Most ecstasy tablets contain 30–150 mg of 3,4-methylenedioxymethamphetamine (MDMA). This drug, which has a half-life of around 8 hours, most probably stimulates both peripheral and central alpha- and beta-adrenergic receptors. Early deaths are usually due to cardiac dysrhythmias while deaths after 24 hours occur from a neuroleptic malignant-like syndrome.
Mild adverse effects occur at low doses and include increased muscle tone, agitation, anxiety and tachycardia. Mild elevation of temperature may also occur. At higher doses, hypertonia with hyperreflexia, tachycardia, tachypnoea and visual disturbance can be seen. In the worst affected children, coma, convulsions and cardiac dysrhythmias can occur. Hyperpyrexia with increased muscle tone can lead to rhabdomyolysis, metabolic acidosis with acute renal failure and disseminated intravascular coagulation.
Activated charcoal should be given to conscious patients. Blood pressure and temperature must be monitored. Diazepam can be used to control anxiety – major tranquilisers should not be used as they exacerbate symptoms. If core temperature exceeds 39ºC then active cooling should be commenced and the use of dantrolene sodium (1 mg/kg over 10–15 min) should be considered. Some children may require ventilation.
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TELEPHONE NUMBER OF POISONS CENTRES IN THE UK THERE IS NOW A SINGLE NATIONAL ENQUIRY NUMBER 0870 600 6266
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