• Chest radiograph
  
• Arterial or central venous blood gasses
  
• Haemoglobin, haematocrit and platelets
  
• Group and save serum for cross-match
  
• Sodium, potassium, calcium, urea and creatinine
  
• Clotting screen
  
• Blood glucose
  
• Liver function tests
  
• Urinalysis, microscopy and culture
  
• Culture of blood and, if indicated, cerebrospinal fluid
  
• C-reactive protein or procalcitonin

Children who have been resuscitated from cardiorespiratory arrest may die hours or days later from multiple organ failure. In addition, to the cellular and homeostatic abnormalities that occur during the preceding illness, and during the arrest itself, cellular damage continues after spontaneous circulation has been restored. This is called reperfusion injury and is caused by the following:

• Depletion of adenosine triphosphate (ATP).
  
• Entry of calcium into cells.
  
• Free fatty acid metabolism activation.
  
• Free-radical oxygen production.

Similarly, children resuscitated with serious illness or injury may suffer multisystem dysfunction as a result of hypoxia or ischaemia. Ongoing activation of inflammatory mediators, as occurs in serious sepsis, also contributes to multisystem organ failure. Post-resuscitation management aims to achieve and maintain homeostasis in order to optimise the chances of recovery. Management should be directed in a systematic way.

Airway and Breathing

Seriously ill children often exhibit an impaired conscious level and a depressed gag reflex. Intubation should always be considered and will usually have occurred during resuscitation.

• The endotracheal tube should have a minimal leak, be appropriately secured and ventilation should be monitored by continuous capnography.
  
• Ventilation settings should be maintained to keep blood gases normal, at a PCO₂ of 35–40 mmHg (4.7–5.3 kPa). Children with intracranial injuries should have their PCO₂ maintained as close to 35 mmHg (4.7 kPa) as possible. The rational for this is to minimise cerebral oedema and minimise any increase in intracranial pressure. If this is difficult because of airway or lung pathology, urgent advice should be obtained from a paediatric intensivist.
  
• In all non-cardiac cases, sufficient inspired oxygen should be given to maintain SpO₂ at between 94% and 98%. If anaemia or carbon monoxide poisoning is suspected, inspired oxygen should be delivered at the highest possible concentration irrespective of the SpO₂ value. Specialist advice regarding target saturations should be sought from a paediatric intensivist or cardiologist for all children where a cardiac abnormality is either known or suspected.

Circulation

Following resuscitation, there will often be a poor cardiac output. This may be due to any combination of the following factors:

• An underlying cardiac abnormality.
  
• The effects on the myocardium of hypoxia, acidosis and toxins, preceding and during any arrest.
  
• Continuing acid–base or electrolyte disturbance.
  
• Hypovolaemia.

The following steps should be taken if there are signs of poor perfusion:

• Assess cardiac output clinically.
  
• Infuse crystalloid or colloid in aliquots of 10 mL/kg and reassess cardiac output clinically.
  
• Aim for a normal arterial pH (>7.3) and good oxygenation. This may require the use of inotropic drug support with or without further fluid boluses.
  
• Monitor ventilation and intervene with support when inadequate.
  
• Identify and correct hypoglycaemia and electrolyte abnormalities.

A central venous pressure (CVP) line will give useful information about the preload to the heart. This may assist in decisions about fluid infusion and inotropic support. A target value for the CVP should be discussed and established with an expert team.

The CVP is best used in assessing the response to a fluid challenge. In hypovolaemic children, CVP alters little with a fluid bolus, but in euvolaemia or hypervolaemia it usually shows a sustained rise.

Drugs Used to Maintain Perfusion Following Cardiac Arrest or Treatment of Shock

There are no research data comparing one drug with another that show an advantage of any specific drug on outcome. In addition, the pharmacokinetics of these drugs vary from patient to patient and even from hour to hour in the same child. Factors that influence, in an unmeasurable manner, the effects of these drugs include the child’s age and maturity, underlying disease process, metabolic state, acid–base balance, the patient’s autonomic and endocrine response, and liver and renal function. Therefore, the recommended infusion doses are starting points; the infusions must be adjusted according to patient response.

Dopamine

Dopamine is an endogenous catecholamine with complex cardiovascular effects. At low infusion rates (5 micrograms/kg/min) dopamine may increase renal perfusion and has little effect on systemic haemodynamics. At infusion rates greater than 5 micrograms/kg/min, dopamine directly stimulates cardiac β-adrenergic receptors and releases noradrenaline from cardiac sympathetic nerves. Myocardial noradrenaline stores may be low in chronic congestive heart failure and in infants, so the drug may be less effective in these groups.

Dopamine is generally used in preference to dobutamine (see below) in the treatment of circulatory shock following resuscitation.

Dopamine infusions may produce tachycardia, vasoconstriction and ventricular ectopy. Infiltration of dopamine into tissues can produce local tissue necrosis. Dopamine and other catecholamines are partially inactivated in alkaline solutions and therefore should not be mixed with sodium bicarbonate.

• Infusion concentration: 15 mg/kg in 50 mL of 5% glucose or 0.9% saline will give 5 micrograms/kg/min if run at 1 mL/h.
  
• For a dose of 5–20 micrograms/kg/min, give 1–4 mL/h of the above dilution.

Dobutamine

Dobutamine increases the heart rate and myocardial contractility and has some vasodilating effect by decreasing peripheral vascular tone. It is potentially useful in the treatment of low cardiac output secondary to poor myocardial function. It is infused in a dose range of 5–20 micrograms/kg/min. Higher infusion rates often produce tachycardia or ventricular ectopy. Pharmacokinetics and clinical response vary widely, so the drug must be titrated according to individual patient response.

• Infusion concentration: 15 mg/kg in 50 mL of 5% glucose or 0.9% saline will give 5 micrograms/kg/min if run at 1 mL/h.
  
• For a dose of 5–20 micrograms/kg/min give 1–4 mL/h of the above dilution.

Adrenaline

An adrenaline infusion is a good first-line treatment for shock with poor systemic perfusion from any cause that is unresponsive to fluid resuscitation. Adrenaline may be preferable to dopamine or dobutamine in children with severe hypotensive shock and in very young infants in whom other inotropes may be ineffectual. The infusion is started at 0.05–0.1 micrograms/kg/min and may be incrementally increased to 1 microgram/kg/min or higher depending on clinical response. Wherever possible, adrenaline should be infused into a central intravenous or intraosseous line. Peripheral lines should only be used if there is no alternative because tissue infiltration can cause local ischaemia and ulceration.

• Infusion concentration: 0.3 mg/kg in 50 mL of 5% glucose or 0.9% saline will give 0.1 micrograms/kg/min if run at a rate of 1 mL/h.
  
• For a dose of 0.05–2.0 micrograms/kg/min, give 0.5–20 mL/h of the above dilution.

Kidneys

It is important both to maximise renal blood flow and to maintain renal tubular patency by maintaining urine flow. To achieve this, the following are necessary:

• Maintenance of an adequate blood pressure to drive renal perfusion.
  
• Maintenance of adequate filling and a good cardiac output using inotropes and fluids as required.
  
• Maintenance of good oxygenation.
  
• Diuretics (e.g. frusemide (furosemide) 0.5–1 mg/kg) may be utilised in children with a good cardiac output to maintain urine output at or above 1 mL/kg/h. However, great care must be exercised as excessive diuretics can cause further damage to the failing kidney. Wherever possible seek specialist advice before administration.
  
• Monitoring and normalisation of electrolytes (sodium, potassium, calcium, magnesium) and the acid–base balance in blood should be undertaken as a supporting measure. Sodium bicarbonate should not usually be given to non-intubated patients. Potassium should be given slowly and cautiously and only be given in small aliquots in oliguric or anuric children.

Liver

Hepatic cellular damage can become manifest up to 24 hours following an arrest. Coagulation factors can become depleted, and bleeding may be worsened by concomitant, ischaemia-induced intravascular coagulopathy. The patient’s clotting profile and platelets should be monitored and corrected, as indicated, with fresh frozen plasma, cryoprecipitate or platelets.

Brain

The aim of therapy is to protect the brain from further (secondary) damage. To achieve this, the cerebral blood flow must be maintained, normal cellular homeostasis must be achieved and cerebral metabolic needs must be reduced.

When intracranial pathology is present, cerebral autoregulation may not function correctly. In these circumstances adequate cerebral blood flow may be achieved if the cerebral perfusion pressure (mean arterial pressure minus intracranial pressure) is kept above 50 mmHg (6.5 kPa). Maintenance of cellular homeostasis is helped by normalisation of the acid–base and electrolyte balances. Cerebral metabolic needs can be reduced by sedating and paralysing the child. Convulsions should prompt an investigation into their cause. They should be swiftly controlled and anticonvulsant medication, such as phenytoin, should be used if recurrent. Although a barbiturate coma reduces both cerebral metabolism and intracranial pressure, it has not been shown to improve neurological outcome.

Practical steps to minimise secondary brain injury are:

• Maintenance of good oxygenation.
  
• Protection of cerebral perfusion through:
  
  
  
  • maintenance of adequate blood pressure using inotropes and fluids,
    
  • intubation and maintenance of normal blood gases, and
    
  • nursing head-up at 20° and in midline.
  
  
• Using osmotic agents for acutely raised intracranial pressure such as:
  
  
  
  • IV infusion with mannitol 0.5–1.0 g/kg (2.5–5 mL/kg of mannitol 20%) over 20–30 minutes (repeated once or twice after an interval of 4–8 hours if necessary, if serum osmolality remains below 325 mOsm/L), or
    
  • hypertonic saline 3 mL/kg of 3% solution IV over 15 minutes.
  
  
• Control of blood glucose avoiding both hypoglycaemia and hyperglycaemia.
  
• Maintenance of good analgesia, sedation and paralysis (where indicated).
  
• Monitoring and normalisation of electrolytes and acid–base balance.
  
• Control of seizures.

Although there is some evidence that post-arrest hypothermia (core temperatures of 32–34°C) has beneficial effects on neurological recovery in adults, the evidence does not support the use of hypothermia in children outside the newborn period. Harm may occur, however, with raised core temperature, which increases metabolic demand by 10–13% for each degree centigrade increase in temperature above normal. Therefore, in the post-arrest child with compromised cardiac output, hyperthermia should be treated with active cooling to achieve a normal core temperature. Shivering should be prevented since it will increase metabolic demand. Sedation may be adequate to control shivering, but neuromuscular blockade is usually needed.

24.2 ASSESSMENT AFTER STABILISATION

After resuscitation and emergency treatment have been provided, consideration will need to be given to the best place to continue the child’s care, which may be a paediatric intensive care unit (PICU). This may involve a transfer to another unit, often another hospital. Critically ill children transferred by untrained personnel have been shown to be subjected to an excess of adverse events. Often a child needs to be transported from the emergency department to another department within the same hospital. These transfers have also been associated with a high incidence of serious transport-related adverse events. The impact of these events on long-term outcome is unknown. Nevertheless, international practice has focused on minimising adverse events during transfer.

Where possible it is recommended that these are undertaken by specialised paediatric intensive care transfer teams. These teams can be contacted in the event of requests for transfer of a child to a PICU or a specialised facility such as a neurosurgical or burns unit. Paediatric and Neonatal Safe Transfer and Retrieval: the Practical Approach (ALSG, 2008) is a sister publication to this manual that supports a practical course in the UK of the same name. Although the interested reader should consider reviewing this text in detail, a summary of the principles described are detailed below.

24.3 PRINCIPLES OF SAFE TRANSFER AND RETRIEVAL

Transfers are undertaken to ensure that the child’s care is of the highest possible standard at all times. To achieve this, the right child has to be taken at the right time, by the right people, to the right place, by the right form of transport, and receive the right care throughout. This requires a systematic approach that incorporates a high level of planning and preparation before the child is moved. One such approach is the ACCEPT method, which is described in detail in Paediatric and Neonatal Safe Transfer and Retrieval: the Practical Approach (ALSG, 2008).

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