The critically ill child

Published on 27/02/2015 by admin

Filed under Anesthesiology

Last modified 27/02/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1250 times

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

Buy Membership for Anesthesiology Category to continue reading. Learn more here