The critically ill child

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Chapter 96 The critically ill child

Alan W. Duncan

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.

ADAPTATION

Dramatic physiological adaptation takes place as the fetus adjusts to extrauterine life. Many changes are incomplete until some time after birth and, until then, reversion to fetal physiology may occur. Classically, this applies to the cardiorespiratory events at birth and the subsequent development of a transitional pattern of circulation (see below).

GROWTH AND DEVELOPMENT

There is progressive growth and development of all organ systems throughout childhood. ‘Small-body technology’ has evolved to cope with the technical aspects of paediatric critical care. Some aspects of growth are non-linear and contribute to the reduced cardiorespiratory reserve of the infant. Physiological differences that influence disease processes and their management are discussed in respective chapters in this section.

MATURATION

At birth, the immaturity of many systems and biochemical processes alters the response to pathophysiological stress and drugs. Thermoregulation, immune function and renal function are immature at birth, even in the full-term infant. Such immaturity is magnified in the premature infant; for example, surfactant deficiency in the lung causing hyaline membrane disease and liver glucuronyl transferase deficiency causing jaundice.

DIVERSE PATHOPHYSIOLOGICAL STATES

Developmental anomalies, inborn errors of metabolism, susceptibility to infection and various accidents and trauma provide a wide spectrum of paediatric critical illnesses. The response to these illnesses is modified by various aspects of adaptation, growth and development and maturation.

PAEDIATRIC INTENSIVE CARE

The development of separate paediatric ICUs recognised the unique problems and requirements of critically ill children. The paediatric ICU (PICU) should not be seen in isolation, but as part of a tertiary paediatric centre, with well-defined prehospital care, emergency medical services and retrieval teams. Minimum standards should be adopted. In general, a PICU should provide:

• a specialist trained in paediatric intensive care available at short notice
• a range of paediatric subspecialty support
• immediately available junior medical staff with advanced life support skills
• nursing staff with experience in paediatric intensive care
• allied health professionals and ancillary support staff
• specialised advanced life support equipment for children ranging in age from neonates to adolescents
• 24-hour laboratory, radiological and pharmacy services
• purpose-built PICU, recognising the special physical and emotional needs of critically ill children and their families
• a programme for teaching, continuing education, research and quality assurance

Neonatal ICUs have their own particular requirements.

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.

CAUSES OF TRANSITIONAL CIRCULATION

A ‘fetal’ pattern may persist due to:

• low lung volume states (e.g. hyaline membrane disease and perinatal asphyxia)
• pulmonary hypoplasia (e.g. diaphragmatic hernia and Potter’s syndrome)
• meconium aspiration syndrome
• chronic placental insufficiency
• perinatal hypoxia and acidosis from any cause
• sepsis (e.g. group B streptococcal infection)
• hyperviscosity syndrome

CLINICAL FEATURES

Hypoxaemia disproportional to the degree of respiratory distress is typical of transitional circulation and suggests the possibility of congenital cyanotic heart disease. In cases without significant lung disease, echocardiography may be necessary to exclude a structural cardiac lesion. Severe respiratory distress is present in cases secondary to pulmonary disease. Differential cyanosis (i.e. increased cyanosis affecting the lower limbs when compared with the head, neck and right arm) may be seen with the right-to-left shunting at ductal level. This may be confirmed by simultaneous pre- and postductal arterial blood sampling, transcutaneous PO2 monitoring or oximetry.

TREATMENT

It is important to treat the underlying cause (e.g. surfactant therapy for hyaline membrane disease) in addition to therapy to reduce PVR. The main steps employed are:

• maintenance of high inspired oxygen. Alveolar oxygen tension is an important determinant of pulmonary arteriolar resistance. Sudden reductions in inspired oxygen may increase shunting through fetal channels (so-called flip-flop phenomenon)
• correction of low lung volume states with continuous positive airway pressure (CPAP) or positive-pressure ventilation with positive end-expiratory pressure (PEEP)
• correction of both metabolic and respiratory acidosis
• deliberate hyperventilation using muscle relaxants to lower PaCO2 and generate a respiratory alkalosis. This manoeuvre is limited by lung immaturity and risk of barotrauma. Rapid rates of ventilation (> 60 breaths/min) may prove beneficial
• maintenance of systemic arterial pressure with volume expanders and inotropic agents to reduce the pressure gradient favouring ductal shunting
• isovolaemic haemodilution with colloid, if indicated, to reduce hyperviscosity
• administration of pulmonary vasodilators, e.g. inhaled nitric oxide1

Many centres successfully employ extracorporeal membrane oxygenation (ECMO) in this situation.

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.

IMMUNOLOGY OF THE INFANT

The immunological system consists of:

• non-specific mechanisms, including phagocytosis and the inflammatory response
• specific immune responses, consisting of cell-mediated (T-cell) and humoral (B-cell) systems (see Chapter 59). These two components are intimately related and both may be abnormal in the newborn infant

The inflammatory response of the newborn is attenuated. Febrile response to infection may be lacking and both cellular (chemotaxis and phagocytosis) and humoral (complement activity and opsonisation) responses may be impaired. Cell-mediated immunity is completely absent in infants born without thymic function (DiGeorge syndrome). In the normal newborn, however, T-cell function appears to be quite well developed. Rejection of skin allografts is slower in the newborn but this seems to be related mainly to the attenuated inflammatory response.

The B-cell system, responsible for antibody production, is immature at birth. The neonate has passive immunity against some infections because of transplacental transfer of maternal antibodies. Natural immunity is acquired as a result of immunoglobulin A (IgA) in breast milk and protects against some acquired gastrointestinal infections. Overall, the immaturity and inexperience of the immune system result in a markedly increased susceptibility to infection in the first 6 months of life.

RESUSCITATION OF THE NEWBORN

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