2.4 Specific paediatric resuscitation
Anaphylaxis
Persons receiving β-blocking drugs have a potentiated risk of anaphylaxis. In such patients, it is more resistant to therapy and lasts longer. Hypotension may be refractive to adrenaline. In such cases, glucagon (therapy for β-blocker toxicity) may be required along with infusions of adrenaline and dopamine. See Chapter 22.5 for the detailed account of the treatment of anaphylaxis.
Drowning
Victims of submersion incidents suffer global hypoxaemia and if arrested, global ischaemia. Associated injuries are aspiration pneumonitis and hypothermia. Aspiration of water and gastric contents is common (see Chapter 22.2). In addition, hypothermia (see Chapter 22.4) may be present, but unless the victim was subject to severe environmental hypothermia such as being submersed in ice-cold water (<5°C) or has profound afterdrop after removal from water, this reflects lack of perfusion and is a bad prognostic sign. Hypothermia should be treated but temperature not permitted to rise above 35°C if cardiac arrest has occurred (see Chapter 2.3).
Intubation and mechanical ventilation with 100% oxygen should be instituted immediately. Regurgitation of stomach contents should be anticipated and a rapid sequence intubation technique with cricoid pressure should be used. Sedative drugs with cardiovascular depressive actions should not be used, or in minimally required doses only. The lung compliance is likely to be poor and it may be necessary to insert a larger-than-usual uncuffed or a cuffed endotracheal tube (preferred) to prevent a leak around the tube, to obtain adequate lung inflation in the setting of acute respiratory distress syndrome (ARDS) in order to achieve oxygenation. After restoration of cardiac rhythm myocardial contractility should be measured with echocardiography and optimised with inotropic agents.
During resuscitation, the goal is to provide maximum opportunity for cerebral recovery and this is achieved by restoring cerebral perfusion with well oxygenated blood and the avoidance of factors that decrease cerebral perfusion pressure. It is thus vital to restore cardiac output and blood pressure, to oxygenate blood and to avoid factors that would increase intracranial pressure, such as venous obstruction. Hypocapnia, hypercapnia, hypoglycaemia and hyperglycaemia should be avoided and convulsions treated.
Any pulseless arrhythmia may be encountered and should be managed along standard lines.
There are no important clinical differences between fresh and salt-water immersion. Altered levels of serum electrolytes, especially sodium and potassium, may be detected, but are uncommon and in any case do not influence acute resuscitation.
Toxicological emergencies
The standard resuscitation protocols may be inadequate in some toxicological emergencies, particularly when poisoning has occurred with cardioactive drugs.
Airway and ventilation management
Problems should not be created by treatment. Gastric lavage should not be undertaken unless the patient has ingested a significant toxin in significant amounts within the past hour. There are very few indications for gastric lavage. Gastric lavage should not be performed in the fully conscious or in the less-than-fully conscious patient, without prior securement of the airway with rapid sequence endotracheal intubation. Likewise, activated charcoal should not be administered by oro/nasogastric tube in a patient who is less-than-fully conscious, irrespective of the interval since ingestion. The risk of aspiration pneumonitis in these circumstances is significant. If activated charcoal is to given by naso/orogastruc tube, confirm it is in the stomach, not the lungs, prior to instilling the charcoal.
Drug-induced asystole
Infusions of KCl are hazardous. Molar solutions of KCl are in common use in intensive care units especially after cardiac surgery. They should not be available for regular ward use. An inadvertent IV bolus of potassium can cause asystole. Note that a 1 mL bolus of molar KCl (1 mmol) in a 10 kg child will theoretically raise the serum concentration by 2.5 mmol L–1 and cause immediate asystole.
Immediately acting treatment (within seconds) for hyperkalaemia is either 10% calcium chloride IV 0.2 mL kg–1 (or equivalent) or IV sodium bicarbonate 1 mmol kg–1 or both. Calcium antagonises the cardiac effects of potassium on the heart, while the bicarbonate lowers the serum concentration of potassium by a small amount. Better treatments of rapid onset (within minutes) are glucose 0.5 g kg–1 IV (e.g. 5 mL kg–1 of 10%) plus insulin 0.05 units kg–1 or salbutamol 0.25 mg kg–1 by aerosol or both. Slow treatment (within hours) is by resonium, oral or rectal, 0.5–1 g kg–1.
Drug-induced bradycardia
Organophosphate and carbamate poisoning with bradycardia should be treated with atropine – repeated doses of 20–50 mcg kg–1 every 15 minutes or until secretions are dry and an acceptable heart rate is restored. In organophosphate poisoning (but not carbamate), pralidoxime can reactivate cholinesterase. The dose is 25 mg kg–1 IV over 15–30 minutes then 10–20 mg kg–1 per hour for 18 hours or more.
Bradycardia induced by β-blocker poisoning is treated with glucagon 7 mcg kg–1 IV then 2–7 mcg kg–1 min–1. This is the preferred antidote because it stimulates non-catecholamine cAMP. Isoprenaline 0.05–3 mcg kg–1 min–1 by infusion may be used but it may cause β2-induced hypotension and should not be used if hypotension is pre-existing. Alternatively, an infusion of adrenalin (epinephrine) at 0.05–1 mcg kg–1 min–1 may be used.
Digoxin induced bradycardia may be treated with 1 Digoxin Fab antibody in a dose of 10 vials per 25 of 0.25 mg tablets or per 5 mg elixir ingested. At steady state, the number of vials is calculated as serum digoxin (ng mL–1) × (kg)/100.
Drug-induced tachyarrhythmias
The preferred treatment is a benzodiazepine such as diazepam or midazolam in doses that do not depress CNS function. Other treatments are the ultrashort-acting cardioselective β1 blocker esmolol IV 500 mcg kg–1 over 1 minute and then 25–200 mcg kg–1 min–1 by infusion. Treatments such as intravenous adenosine and DC shock are not likely to be effective because the toxic drug effect will be persistent. Calcium channel blockers such as verapamil may cause severe hypotension and should not be given.
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