The critically ill child

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Chapter 96 The critically ill child

The chapters on paediatric intensive care are intended to help intensivists outside specialised paediatric centres manage common paediatric emergencies. They should be read in conjunction with relevant adult chapters, as there are areas of common interest. Some common neonatal emergencies are also presented.

The differences between neonates and infants from adults render them susceptible to critical illness and alter their response to disease processes. Nevertheless, there are also similarities and many aspects of organ monitoring and support in adult intensive care units (ICUs) have been successfully modified for use in children and are applicable to even the smallest infants.

The major differences between paediatric and adult patients are described below.

CARDIORESPIRATORY EVENTS AT BIRTH

During intrauterine life, 60% of blood returning to the right atrium passes directly through the foramen ovale into the left ventricle and ascending aorta. As most of this blood is from the umbilical arteries, the heart and brain are perfused with better-oxygenated blood. Pulmonary vascular resistance (PVR) is high and most of the blood reaching the right ventricle passes through the ductus arteriosus to the descending aorta. Only 10% of right ventricle output passes to the lungs which, although non-functional, require a blood supply for nutrition, growth and development of the lung vasculature.

At birth, closure of the umbilical vessels increases systemic vascular resistance (SVR) and lung expansion leads to the dramatic fall in PVR. Pulmonary blood flow increases, leading to a rise in left atrial pressure and functional closure of the foramen ovale. The ductus arteriosus subsequently constricts and eventually thromboses.

Following the dramatic fall in PVR at birth, there is a gradual regression in muscularisation of the pulmonary arterioles over the following weeks to months. This regression is prevented if high pulmonary blood flow occurs, due to congenital heart lesions (e.g. ventricular septal defect, large patent ductus arteriosus and truncus arteriosus) or lesions associated with persistent hypoxaemia (e.g. transposition of great vessels). With these lesions, progression to irreversible pulmonary vascular disease may occur at an early age.

TRANSITIONAL CIRCULATION

Haemodynamic adaptation at birth may be delayed or reversed by a number of factors. Persistent pulmonary hypertension and patency of the fetal channels result in right-to-left shunting through the foramen ovale and ductus arteriosus (termed persistent fetal circulation or more correctly transitional circulation). A vicious cycle may develop, with increasing hypoxaemia and acidosis, increased PVR and further shunting. Unless the underlying disturbance is treated and the pulmonary hypertension is corrected, progression to death is likely. Pulmonary circulation pathophysiology is probably related to abnormalities of endogenous nitric oxide production and manipulation of this agent is proving useful in therapy.

THERMOREGULATION IN THE NEWBORN

Human body temperature is maintained within narrow limits. This is achieved most easily in the thermoneutral zone – the range of ambient temperature within which the metabolic rate is at a minimum. Once ambient temperature is outside the thermoneutral zone, heat production (shivering or non-shivering thermogenesis) or evaporative heat loss processes are required to maintain body temperature within normal limits. Regulatory mechanisms are less effective in the neonate (there is no shivering or sweating), who is otherwise disadvantaged by a high surface area to body weight ratio and lack of subcutaneous tissue.

The thermoneutral zone is higher in premature infants and falls with increasing postnatal age. Oxygen consumption is minimal, with an environmental or abdominal skin temperature of 36.5 °C. Oxidation of brown fat found in the interscapular and perirenal areas (non-shivering thermogenesis) is the major source of heat production when ‘cold-stressed’.

Alteration of body temperature above or below normal leads to increased or decreased metabolism respectively. Attempts by the body to maintain body temperature within normal limits are associated with increased metabolism and cardiorespiratory demands. Radiation is a major source of heat loss in the neonate and is effectively minimised by double-walled incubators or by servo-controlled radiant heaters. The latter allows better access to critically ill babies for monitoring and procedures. Cold stress per se increases neonatal mortality. In the presence of respiratory or cardiac disease, it may lead to decompensation.

RESUSCITATION OF THE NEWBORN

Some newborn infants fail to adapt from fetal to extrauterine life and require immediate cardiopulmonary and cerebral resuscitation. The Apgar scoring system (Table 96.1) scored after 1 minute, remains the most widely accepted method of assessment. The best Apgar score is 10 and the worst is 0. There is an inverse relationship between the Apgar score and the degree of hypoxia and acidosis. It has been suggested that the 5-minute score is a guide to ultimate prognosis but this is questioned. Collection of sequential scores must not delay the institution of resuscitation.

MANAGEMENT

The principles of resuscitation are identical to those employed in other situations. Resuscitation must be started immediately after delivery. Although some cerebral insult may have occurred in utero or intrapartum, secondary insults from postpartum asphyxia must be avoided.

Babies suffering mild asphyxia immediately before birth with Apgar scores between 5 and 7 usually respond to stimulation and gentle suction to the nose, mouth and pharynx although oxygen therapy is occasionally required. Babies with moderate asphyxia (Apgar 3–4) usually respond to bag-and-mask ventilation with oxygen. Acid–base status should be determined and sodium bicarbonate administered to restore pH > 7.25. Severely asphyxiated infants (Apgar 0–2) need urgent cardiopulmonary resuscitation (CPR). After airway suction, bag-and-mask ventilation should be followed by rapid orotracheal intubation and positive-pressure ventilation with oxygen. Fear of complications of oxygen therapy must not mitigate against the administration of 100% oxygen at this stage. If the liquor contains thick meconium, it is vital that the pharynx and trachea be suctioned prior to the onset of respiration or application of positive pressure. Meconium aspiration syndrome is a preventable condition that is often difficult to manage.

Venous access via umbilical or peripheral veins must be established immediately and followed by the administration of 1–2 mmol/kg of sodium bicarbonate. Subsequent buffer therapy should be based on arterial acid–base status if available. Rapid or excessive infusions of hypertonic solutions (e.g. sodium bicarbonate or hypertonic dextrose) or volume expanders may precipitate intracranial haemorrhage, particularly in premature infants.

Asphyxiated infants are usually volume-depleted at birth and blood pressure should be immediately restored with colloids (10 ml/kg in the first instance). External cardiac massage and additional drug therapy (see below) should be employed, if necessary, to restore cardiac rhythm. Postresuscitative care to maintain cerebral perfusion pressure, correct abnormal serum biochemistry and control seizures is required to prevent secondary cerebral insults. Myocardial dysfunction may occur secondary to asphyxia. Dopamine or dobutamine (5–10 μg/kg per min) may prove useful.

The orotracheal tube should be changed to nasotracheal to enable secure fixation once a degree of stability is attained. Radiological confirmation of tube position should be made as soon as possible. The trachea is very short in the newborn and endobronchial intubation is a particular risk.

Approximate nose to mid-trachea (T2) distances are:

VASCULAR ACCESS

Venous access may be difficult, particularly in the collapsed, hypovolaemic or hypothermic child. The external jugular vein may be prominent when usual sites are inaccessible. Cannulation of central veins, apart from via the femoral and external jugular veins, is hazardous even in ideal situations and should not be attempted during cardiac arrest in small children and babies. Two may be considered: intraosseous access or endotracheal instillation.

ARTERIAL CANNULATION AND PRESSURE MONITORING

Arterial cannulation is routine practice in paediatric intensive care, even in infants weighing < 1 kg. It is indicated in all critically ill infants for continuous blood pressure monitoring and accurate blood gas sampling. In the neonate, difficult ‘stabs’ may lead to significant errors in PaO2 and PaCO2. Umbilical arterial catheters are commonly used in newborn infants, although users must be aware of the potential vaso-occlusive complications (e.g. lower limb ischaemia, renal thrombosis, necrotising enterocolitis and rarely, paraplegia).

Peripheral arteries used include radial, ulnar, brachial, femoral, posterior tibial and dorsalis pedis. Radial and ulnar or posterior tibial and dorsalis pedis vessels must never be cannulated sequentially in the same limb. The safety of brachial and femoral cannulation lies in the presence of rich collateral vessels around the elbow and hip joints. Arterial lines are kept patent by continuous flushing with 1–2 ml/hour of heparinised normal saline (5 units heparin/ml flushing solution) or 5% dextrose. Complications include distal ischaemia, infection, retrograde embolisation and haemorrhage. Retrograde embolisation occurring with flushing is a particular risk in the small infant, depending on the length and volume of the vessel and volume and speed of injection. In a 1.5 kg infant, as little as 0.5 ml of fluid injected rapidly into the right radial artery will reach the cerebral circulation. Haemorrhage from accidental disconnection can be significant because of the relatively small blood volume. Meticulous fixation is therefore required.

DRUG INFUSIONS

All drugs used in cardiovascular and respiratory support are administered according to body weight; accurate delivery is crucial. Accurate drug infusions require accurate devices, of which syringe pumps are the most useful. Potentially lethal errors in calculating drug dilutions are minimised by the use of dose/dilution/infusion rate guidelines (Table 96.2).9

Table 96.2 Calculation of drug infusion dilutions:

1. Select desired drug dosage to be delivered in μg/kg per min

2. Select infusion rate of syringe pump in ml/h (from centre of table)

3. Calculate number of milligrams of drug to be mixed in 50-ml syringe e.g.: 10-kg child, 0.1–2 μg/kg per min, infusion 1–20 ml/h: put 0.3 ml/kg (= 3 mg) in 50 ml

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PAIN RELIEF AND SEDATION IN CHILDREN

Management of pain and agitation in children has received inadequate attention and has tended to be underestimated and underrated. Infants and children are often unable or unwilling to complain of pain. In the past, some believed that the neonate could not perceive pain. It is now clear that even neonates possess all the anatomical and neurochemical systems necessary for pain perception and exhibit physiological and behavioural responses to pain.10 Stress responses associated with pain and agitation may increase morbidity and mortality in critically ill patients. Analgesia can be provided by narcotic infusions, local blocks and regional techniques in children of all ages. Painful procedures in the ICU must always be accompanied by appropriate analgesia. The addition of sedative agents such as benzodiazepines can reduce agitation, minimise harmful stress responses and result in narcotic sparing.

NEONATAL AND PAEDIATRIC EMERGENCY TRANSPORT

Care of critically ill neonates and children necessitates the use of specialised retrieval services linked to neonatal and paediatric ICUs. Retrieval services should offer facilities for specialist consultation in addition to secondary transport. Careful audit of such services is necessary to improve patient outcome.11 The aim of retrieval services is to extend the intensive care facility to peripheral hospitals, allowing stabilisation by experienced personnel prior to rapid transport to a regional centre in the most appropriate vehicle (see Chapter 4). Special considerations such as thermoregulation and oxygen monitoring must be provided for in neonatal transport. Well-designed neonatal emergency transport services have resulted in significant reductions in morbidity and mortality.

OUTCOME OF PAEDIATRIC INTENSIVE CARE

Depending on admission criteria, mortality in paediatric ICUs ranges from 5 to 15%. If patients with pre-existing severe disabilities are excluded, the majority of survivors have a normal or near-normal life expectancy. A number of scoring systems have been developed or modified for paediatric application to predict ICU mortality. These scoring systems allow comparison between different ICUs, internal audits, stratification of patients for research purposes and analysis of cost benefit. The paediatric risk of mortality (PRISM) score12,13 and the paediatric index of mortality (PIM) score14 are applicable to a wide range of critically ill infants and children. Although PRISM performs marginally better, PIM is easier to collect and hence less prone to errors in data collection. PIM also has the advantage that it predicts mortality based on admission parameters whereas PRISM is based on the worst variables in the first 24hours. As many paediatric ICU deaths occur in the first 24hours, PRISM is often recording the dying process rather than predicting it. Specialised scores have been developed for specific problems, e.g. the modified injury severity scale (MISS) and paediatric trauma score (PTS) for paediatric trauma, and the modified Glasgow Coma Scale (GCS) for neurological insults. Numerous scoring systems have been developed for meningococcaemia, the best validated being the Glasgow meningococcal septicaemia prognostic score (GMSPS).15

Compared with adult intensive care, children with equivalent therapeutic intervention scores (TISS) have a lower in-hospital and 1-month mortality.16 In addition, non-survivors do not consume a disproportionate amount of resources. While multiple organ failure increases mortality, the prognosis is considerably better than for adults.17 There is evidence that mortality is lower in specialist paediatric ICUs,18 and that paediatric ICUs with a larger workload have better outcomes than those looking after fewer children.19 General hospitals should therefore have facilities for urgent resuscitation of children prior to early transport to a specialised paediatric ICU. Unless unavoidable, critically ill children, particularly those requiring mechanical intervention, should not be cared for in an adult ICU for longer than 24 hours. The American Academy of Pediatrics, the Society of Critical Care Medicine, the British Paediatric Association and the Australian National Health and Medical Research Council have all stated that children should receive intensive care in specialist paediatric units.

REFERENCES

1 Kinsella JP, Neish SR, Dunbar ID, et al. Clinical responses to prolonged treatment of persistent pulmonary hypertension of the newborn with low doses of inhaled nitric oxide. J Pediatr. 1993;123:103-108.

2 The International Liaison Committee on Resuscitation. The International Liaison Committee on Resuscitation (ILCOR) Consensus on Science with treatment recommendations for pediatric and neonatal patients: pediatric basic and advanced life support. Pediatrics. 2006;117:955-977.

3 Rosetti VA, Thompson BM, Miller J, et al. Intraosseous infusion: an alternative route of pediatric intravascular access. Ann Emerg Med. 1985;14:885-888.

4 Saccheti AD, Linkenheimer R, Liberman M, et al. Intraosseous drug administration: successful resuscitation from asystole. Pediatr Emerg Care. 1989;5:97-98.

5 Moscati R, Moore GP. Compartment syndrome with resultant amputation following intraosseous infusion. Am J Emerg Med. 1990;8:470-471.

6 Bernholtz SM, Pronovost PJ, Lipsett PA, et al. Eliminating catheter-related bloodstream infection in the intensive care unit. Crit Care Med. 2004;32:2014-2020.

7 McLuckie A, Murdoch IA, Marsh MJ, et al. A comparison of pulmonary and femoral artery thermodilution cardiac indices in paediatric intensive care patients. Acta Paediatr. 1996;85:336-338.

8 Goedje O, Hoeke K, Lichtwarek-Aschoff M, et al. Continuous cardiac output by femoral arterial thermodilution calibrated pulse contour analysis: comparison with pulmonary arterial thermodilution. Crit Care Med. 1999;27:2407-2412.

9 Shann F. Continuous drug infusions in children: a table for simplifying calculations. Crit Care Med. 1983;11:462-463.

10 Anand KJS, Hickey PR. Pain and its effects in the human neonate and fetus. N Engl J Med. 1987;317:1321-1329.

11 Henning R, McNamara V. Difficulties encountered in transport of the critically ill child. Pediatr Emerg Care. 1991;7:133-137.

12 Pollack MM, Ruttimann UE, Getson PR. Pediatric risk of mortality (PRISM) score. Crit Care Med. 1988;16:1110-1116.

13 Pollack MM, Patel KM, Ruttimann UE. PRISM III: an updated pediatric risk of mortality score. Crit Care Med. 1996;24:743-752.

14 Shann F, Pearson G, Slater A, et al. Paediatric index of mortality (PIM): a mortality prediction model for children in intensive care. Intensive Care Med. 1997;23:201-207.

15 Thompson APJ, Sills JA, Hart A. Validation of the Glasgow meningococcal septicaemia prognostic score: a 10 year retrospective survey. Crit Care Med. 1991;19:26-30.

16 Yeh TS, Pollack MM, Holbrook PR, et al. Assessment of pediatric intensive care – application of the Therapeutic Intervention Scoring System. Crit Care Med. 1982;10:497-500.

17 Wilkinson JD, Pollack MM, Ruttimann UE, et al. Outcome of pediatric patients with multiple organ system failure. Crit Care Med. 1986;14:271-274.

18 Pollack MM, Alexander SR, Clarke N, et al. Improved outcomes from tertiary center pediatric intensive care: a statewide comparison of tertiary and nontertiary care facilities. Crit Care Med. 1991;19:150-159.

19 Pearson G, Shann F, Barry P, et al. Should paediatric intensive care be centralized? Trent versus Victoria. Lancet. 1997;349:1214-1217.