ACCCN's Critical Care Nursing

678 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

151. Abella B, Rhee J, Huang K, Vanden Hoek T, Becker L. Induced hypothermia therapeutic hypothermia in patients after successful resuscitation. trans-
is underused after resuscitation from cardiac arrest: a current practice survey. nasal cooling after cardiac arrest. Circulation 2010; 118(S): 1459.
Resuscitation 2005; 64: 181–6. 158. Castren M, Nordberg P, Svensson L, Taccone F, Vincent J et al. Intra-arrest
152. Merchant R, Soar J, Skrifvars M. Therapeutic hypothermia utilization among transnasal evaporative cooling: a randomized, prehospital, multicenter study
physicians after resuscitation from cardiac arrest. Crit Care Med 2006; 34: (PRINCE: Pre-ROSC IntraNasal Cooling Effectiveness). Circulation 2010;
1935–40. 122(7): 729–36.
153. Kennedy J, Green R, Stenstrom R. The use of induced hypothermia after 159. Oommen S, Menon V. Hypothermia after cardiac arrest: beneficial, but slow
cardiac arrest: a survey of Canadian emergency physicians. CJEM 2008; 10: to be adopted. Cleveland Clin J Med 2011; 78(7): 441–9.
125–30. 160. Insler S, Sessler D. Perioperative thermoregulation and temperature moni-
154. Oksanen T, Pettila V, Hynyen M, Varpula T. Therapeutic hypothermia after toring. Anesthesiology Clinics 2006; 24: 823–37.
cardiac arrest: implementation and outcome in Finnish intensive care units. 161. Tho P, Mordiffi S, Ang E, Chen H. Implementation of the evidence review
Acta Aneaesth Scan 2007; 51: 866–71. on best practice for confirming the correct placement of nasogastric tube in
155. Wolfrum S, Radke P, Pischon T, Willich S, Schunkert H et al. Mild therapeutic patients in an acute care hospital. Int J Evidence-Based Healthcare 2011; 9:
hypothermia after cardiac arrest-a nationwide survey on the implementation 51–60.
of ILCOR guidelines in German intensive care units. Resuscitation 2007; 72: 162. Sunde K, Pytte M, Jacobsen D, Mangschau A, Jensen L et al. Implementation
207–13. of a standardised treatment protocol for post resuscitation care after out-of-
156. Laver S, Padkin A, Atalla A, Nolan J. Therapeutic hypothermia after cardiac hospital cardiac arrest. Resuscitation 2007; 73(1): 29–39.
arrest: a survey of practice in intensive care units in the United Kingdom. 163. Dainty K, Scales D, Brooks S, Needham D, Dorian P et al. A knowledge
Anesthesia 2006; 61: 873–7. translation collaborative to improve the use of therapeutic hypothermia in
157. Busch H, Janata A, Eichwede F, Födisch M, Wöbker G et al. Safety and fea- post-cardiac arrest patients: protocol for a stepped wedge randomized trial.
sibility of a new innovative cooling approach for immediate induction of Implementation Science 2011; 14(6): 4.

Paediatric Considerations


in Critical Care 25





Tina Kendrick
Anne-Sylvie Ramelet


although paediatrics is a specialty defined by age rather
Learning objectives than body systems.

Not only will children experience different patterns of
After reading this chapter, you should be able to: illness and injury compared to adults, their behavioural
l consider and anticipate the specific needs of critically ill and physiological responses to illness differ. It is impor-
infants and children tant that the child’s primary caregiver, who will usually
l describe common conditions that lead to critical illness in be a parent (the term used throughout this chapter), be
infants and children included in planning many aspects of care. While the
l discuss and apply the age-appropriate assessment, critical care team are expert in management of critical
monitoring and management of critically ill infants and illness, parents are generally the experts on their child,
children can provide the child’s health history and know how best
l identify age-appropriate parameters and care required by to settle the child in addition to knowing what their
critically ill infants and children who require ventilation ‘normal’ behaviours are. This child-centred knowledge
l discuss psychological and emotional care required by makes them valuable members of the team.
critically ill infants and children, and their family In mid 2007 the Australian paediatric population was
l consider the child’s family in all interactions estimated to be 4.1 million children aged 0–14 years,
1
with the New Zealand paediatric population 0–15 years
reported at 894,400. Approximately 559,000 children
2
were admitted to Australian public hospitals in 2007–
3
Key words 2008 with over 8300 children in Australia and New
Zealand requiring admission to intensive care units
(ICUs) in 2008. During the same period, there were over
4
paediatrics 145,000 total admissions to Australian and New Zealand
developmental considerations ICUs. Children represent 5.7% of all ICU admissions in
5
upper airway obstruction Australia and New Zealand. Over half of these children
lower airway obstruction required mechanical ventilation, compared with around
4
paediatric ventilation 41% of adults in intensive care. While just over half
5
shock (52.5%) of critically ill children were admitted to special-
neurological dysfunction ist paediatric ICUs, a significant number were managed
4
gastrointestinal tract dysfunction in or retrieved from adult ICUs. Geographical distances
paediatric trauma and the centralised nature of paediatric services can influ-
ence whether a child is nursed in a general or paediatric
ICU. In many circumstances, children will respond effec-
tively to initial resuscitation, particularly support of
INTRODUCTION breathing and fluid resuscitation, and may not require
transfer to a specialist paediatric unit. Paediatric clinical
This chapter focuses on specific considerations for the advice, support and information are available from chil-
care of critically ill infants and children experiencing, or dren’s hospitals and specialist paediatric retrieval services
at risk of experiencing, common life-threatening condi- and should be sought as early as possible in the absence
tions. These include respiratory diseases common in the of paediatric trained staff, or when the need for transfer
paediatric population, major trauma, shock and sepsis. It to a higher level of care becomes apparent.
is aimed at the critical care nurse who encounters paedi-
atric patients occasionally and, while not designed to The age distribution of children in ICUs has remained
meet all the needs of specialist paediatric critical care the same for a number of years, with the figures from
nurses, it provides a summary of the assessment, moni- 2008 showing that children under the age of five years
toring and care required by critically ill children. A systems represent just over 66% of admissions, with almost 59%
approach has been used in this chapter for convenience, of this age group under 12 months of age and 26% under 679

680 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

four weeks of age. Boys make up 58% of children admit-
4
ted to ICUs. The overall ICU mortality rate is 11% for TABLE 25.1 Guide to maintenance water in
4
Australia and 13% for New Zealand, however the paedi- healthy children
5
atric mortality rate is 3%. Over the past 30 years, although
length of stay and severity of illness to the PICUs have For each of the first 10 kg body weight: 100 mL/kg/day or
not essentially changed, mor tality has halved while dis- 4 mL/kg/h
ability has increased. 6 + For each of the second 10 kg of body weight: 50 mL/kg/day or
2 mL/kg/h
ANATOMICAL AND PHYSIOLOGICAL + For every subsequent kg of body weight: 25 mL/kg/day or
CONSIDERATIONS IN CHILDREN 1 mL/kg/h
2
Children require age- and developmentally-appropriate Weight (kg) mL/h mL/kg/day mL/m /day
care. An appropriate range of paediatric equipment is 4 16 100 1600
required to assess, monitor and treat all ages and sizes
of infants and children. The most obvious difference 6 24 100 1800
is the range of weights and sizes across the paediatric 8 32 100 1920
population. General considerations based on differences 10 40 100 2040
between children and adults are described and then a
systems approach is used to identify specific differences. 12 44 88 1960
Children tend to be clustered into one of five stages: 14 48 82 1890
infant, toddler, preschool child, school child and adole- 16 52 78 1860
scent. Developmental considerations for these five stages
are considered later in the chapter. The terms ‘infants’ and 18 56 75 1840
‘children’ are used throughout the remainder of this 20 60 72 1820
chapter. ‘Infants’ includes all children up to the age of 1
year and all other age groups are ‘children’. 30 70 56 1580
40 80 48 1500
A number of general considerations, based on anatomical
and physiological differences from adults, need to be 50 90 43 1460
considered for the critically ill child. 60 100 40 1450
l Children have increased surface area to volume ratio 70 110 38 1470
compared with adults, which leads to increased heat Adapted from (9).
loss and insensible fluid losses, placing infants and
children at increased risk of developing hypothermia
10
and dehydration. Providing an environment that resuscitation. Table 25.1 provides a guide for fluid
maintains the infant and small child’s body tempera- maintenance requirements of children based on body
ture is essential. Avoid exposing infants and children weight.
more than necessary; use warming blankets, open l Excluding the newborn period, normal values for all
care systems for all newborns and infants under 4 kg blood gas and serum electrolyte levels are the same
and overhead heaters when exposure is unavoidable. as adult levels. Creatinine and urea levels will vary
Temperature monitoring is required when using any with age.
heating devices to avoid iatrogenic thermal injury. l Methods of oxygen delivery (humidified if possible)
l Lower glycogen stores and increased metabolic rate for infants include via nasal prongs (maximum rate
predispose infants to hypoglycaemia. There are few 2 L/min) or a head box. A head box can reliably
standard doses in paediatric ICU; rather, medication deliver a required percentage of oxygen, but visualisa-
doses and fluid requirements are calculated on age tion of the infant is often compromised and there
and kilograms of body weight. Weight of infants and is a sense of separation between the parents and
children should therefore be estimated as accurately the infant. Comforting, touching and regular nursing
as possible. The Broselow tape measure is a colour- assessment are more easily achieved when nasal
coded method to estimate weight and is particularly prongs are used. Hudson masks and partial non-
7,8
accurate in children ≤ 25 kg. Some differences may rebreather masks are available in paediatric sizes.
occur in estimated weight of children of different
origin. 7
l Fluid requirements are based on body weight, and Practice tip
aim to ensure adequate hydration while preventing
fluid overload. Maintenance intravenous (IV) fluids Using the Broselow tape measure: (a) place the tape so the red
for infants and young children typically require the arrow is positioned at the top of the child’s head, (b) align the
addition of glucose. Common IV maintenance fluids tape parallel to the side of the child who must be lying in a
used are 0.45% sodium chloride with either 2.5% supine position, (c) Extend the legs straight, and (d) bend the
glucose or 5% glucose and 0.9% sodium chloride with ankle so the toes are pointing straight up. Look at the weight
9
5% glucose. Isotonic sodium chloride is recom- in the coloured areas directly under the bottom of the foot.
mended as the first choice fluid bolus in paediatric

Paediatric Considerations in Critical Care 681

CARDIOVASCULAR SYSTEM
Practice tip In infants, approximately 70% of the haemoglobin is
fetal haemoglobin (HbF), allowing greater amounts of
If paediatric oxygen masks are not available, an adult sized oxygen to be carried for any given PaO 2 . Circulating
mask, including a partial non-rebreather mask, can be used in blood volume per kilogram decreases with age; in the
an emergency. Place the nose section under the child or infant’s infant, circulating volume is approximately 85 mL/kg,
chin in the ‘upside-down’ position.
with total body water accounting for 70% of body mass,
adjusting to the adult values of 65 mL/kg and total
13
CENTRAL NERVOUS SYSTEM body water of 60%. The apex beat is heard at the fourth
intercostal space, mid-clavicle, and by around seven years
Many central nervous system functions, such as locomo- of age the left ventricle has grown and the apex beat can
tion and hand–eye coordination, will take from months be heard at the fifth intercostal space, as in adults. An
to years, to fully develop. Functions of the cerebral cortex infant’s cardiac output is approximately 500 mL/min,
are particularly underdeveloped, with myelination of all which, relative to body weight, is about twice that of an
11
major nerve tracts continuing throughout infancy. Con- adult. Heart rate is a major determinant of cardiac
14
sequently, assessment and management priorities will be output in infants and young children, as there is limited
dictated by the level of neurological maturity of the infant ability to increase stroke volume. Tachycardia is an early
or child. As with adults, neurological dysfunction in sign of distress, but bradycardia is an ominous sign in
infants and children may be primary or secondary. The infants and young children, as they are more dependent
plasticity inherent in the brain of the infant may compen- on a high heart rate to maintain cardiac output. In infants,
sate for injury more readily than older children and bradycardia requires resuscitation. 13
adults in some circumstances, with other areas of the
infant’s brain taking over function. Because the eight Arterial blood pressure should be appropriate for age,
cranial bones are not yet fused, infants’ skulls cope with weight and clinical condition. Mean arterial pressure is
both birth and ongoing growth, which is greatest in the generally used. Monitoring blood pressure using correct
first two years of life. In the first year, the cartilaginous cuff sizes is important because incorrect cuff size is a
sutures fuse at two points to form the posterolateral fon- common cause of inaccurate blood pressure readings in
tanelle. The larger anterior fontanelle closes during the children. Diastolic blood pressure is recorded at Korot-
second year as bone is laid down. By around five years of koff sound 5 (K5); age-related parameters for mean blood
age, the sutures of the child’s skull are completely fused. pressure are displayed in Table 25.3. Tachycardia in the
12
However the thinner skull will provide less protection to absence of fever is a more reliable sign than hypotension,
underlying tissues than the adult skull. as up to 25% of the child’s circulating volume may be
lost before hypotension occurs. Hypotension is thus a
A common misconception is that the Monro-Kellie doc- late sign in children and may indicate late decompen-
trine (see Chapter 16) does not apply to young children sated shock, particularly following fluid delivery. 14
and infants with a more compliant skull. While slow rises
in intracranial volume may be accommodated over time Paediatric Considerations for
in children under three years of age, they will usually be Cardiovascular Assessment
accompanied by growing head circumference, making
routine measurement of head circumference in children Cardiovascular assessment in children includes clinical
under three years of age an important assessment. parameters that are similar to those observed in
However, the less rigid skull of the older child will not adults. The normal values are, however, age and weight
compensate for acute rises in intracranial volume, and the dependent. Urine volume in infants should average
child will display symptoms of neurological compro-
12
mise. Normal ranges of intracranial pressure (ICP) and
cerebral perfusion pressure (CPP) have not been formally TABLE 25.3 Age-related mean blood pressure
studied in infants and children, but are presumed to be
lower than in adults, reaching adult range by adolescence. Age Mean BP (mmHg)
Values that are commonly used to guide treatment are Term 40–60
age-related and are displayed in Table 25.2.
3 months 45–75
6 months 50–90
TABLE 25.2 Target cerebral perfusion pressure (CPP) 1 year 50–90
by age
3 years 50–90
Age Desirable minimum CPP 7 years 60–90
Infants under 1 year 45–55 mmHg 10 years 60–90
Children 1–10 years >55 mmHg 12 years 65–95
Children over 10 years >65 mmHg 14 years 65–95
Adapted from (9). Adapted from (9).

682 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

2 mL/kg/hr, with 1 mL/kg/hr in children and 0.5–1 mL/
kg/hr in adolescents. Other indirect evidence of poor
systemic perfusion in infants may include: 15
l feeding difficulties
l abdominal distension
l fluid imbalances
l temperature instability
l hypoglycaemia
l hypocalcaemia
l apnoea.
Indirect evidence of poor systemic perfusion in children
is irritability, then disorientation or lethargy. Clinical
signs of reduced cardiac output, typically seen in shock,
are similar to adults. 16
RESPIRATORY SYSTEM

The child’s respiratory system, including airways, contin-
ues to mature until at least eight years of age, therefore
the paediatric airway is described and managed differ-
ently from the adult’s. Structural and mechanical differ-
ences predispose infants and young children to respiratory
compromise. Respiratory compromise leading to apnoeas
and even respiratory arrest, is a relatively common occur-
rence in the paediatric population, although specific inci-
dences of occurrence have not been determined. FIGURE 25.1 Adult airway (Courtesy Australian College of Critical Care
Nurses).
The newborn’s larynx is just one-third of the diameter of
17
the adult larynx. Narrow nasal passages, in combination
with being obligatory nose-breathers up to 5–6 months
of age, means that infants may experience respiratory
distress if nasal passages become oedematous or contain
secretions such as mucus or blood. With the airway of an
infant measuring around 6 mm in diameter at the level
of the cricoid, obstruction is more likely. The paediatric
airway is characterised and differentiated from an adult
airway by the following features: 13,17
l short maxilla and mandible
l large tongue
l floppy epiglottis
l shorter trachea
l more acute angle of airway, particularly notable when
attempting to visualise with a laryngoscope
l a more cephalad larynx that moves distally as the neck
grows
l the cricoid ring is the narrowest portion of the airway
l smaller lower airways, less developed with fewer
alveoli
l true alveoli not present until 2 months, with full
complement developed by around eight years of age
l little smooth muscle present in airways
l little collateral ventilation in airways, as the pores of
Kohn are not fully developed until about eight years
of age (see Figures 25.1 and 25.2).

Paediatric Respiratory Assessment
Newborn infants have a respiratory rate of approximately FIGURE 25.2 Paediatric airway (Courtesy Australian College of Critical
40 breaths/min, generating an average tidal volume of Care Nurses).
18
16 mL/kg and minute volume of 0.64 L/min. The tho-
racic cavity of infants and children is characterised by a
thin chest wall that is highly compliant, with poorly

Paediatric Considerations in Critical Care 683

developed intercostal and accessory muscles. The dia- As the infant liver is not completely mature at birth, glu-
phragm is the most important muscle for infants and coneogenesis is deficient, causing low and unstable blood
children in respiration, with abdominal muscles also sugar level in the first weeks of life. The infant is therefore
13
used. The compliant chest wall prevents generation of reliant on fat stores until normal feeding is established.
high intrathoracic pressures, meaning that infants and Formation of plasma proteins and clotting factors are
young children are unable to significantly increase tidal likely to be inadequate in the first weeks of life, thus all
volume; rather, they increase minute volume by breath- newborns in Australasia are given vitamin K shortly after
ing faster. This means that tachypnoea is a normal birth to prevent bleeding. Blood glucose monitoring and
response to illness in infants and children, and a slowing provision of early nutrition are essential aspects of care,
respiratory rate in children may indicate impending especially for infants. Children normally have increased
collapse rather than clinical improvement. 18,19 metabolic demands to achieve growth but have fewer
energy stores than adults.
Assessing airway patency is important. Talking and crying
indicates that the infant or child is maintaining their own
airway. Adventitious airway noises in children include OTHER SYSTEMS AND CONSIDERATIONS
wheeze, stridor and grunting. In infants, grunting may be The following section presents the paediatric consider-
heard and is an attempt by the baby to produce positive ations of the genitourinary, musculoskeletal and integu-
end-expiratory pressure (PEEP). Infants and children who mentary systems.
are grunting, gasping or unconscious need urgent assess-
ment for possible endotracheal intubation. 19 Genitourinary System
Other observed signs of respiratory distress in infants and The small developing pelvic bones of infants and young
children up to about eight years old include head bobbing children cause adult pelvic organs, such as the bladder,
in infants, nasal flaring, and paradoxical chest movement to be located in the lower abdominal cavity. Urine output
observed in several locations on the chest and known in children is calculated in mL/kg bodyweight/hour.
as recessions. Recessions can be observed at the costal In infants with immature kidney function and limited
margin, or subcostal; between the ribs, or intercostal; at ability to conserve water, urine output should be 1–2 mL/
the sternum, or sternal; and at the trachea, called tracheal kg/h. In the first month of life, infants have the capacity
tug. Oral feeding is difficult for infants in moderate to to concentrate urine to only 1.5 times their plasma osmo-
severe respiratory distress due to limitations associated lality, while adults can concentrate their urine to 3–4
with sucking and breathing at the same time. In addition, times their plasma osmolality. The higher metabolic rate
tachypnoea greater than 60–80 breaths/min may lead to of infants means that they produce twice the acid that an
20
vomiting and aspiration. For these reasons, initial adult will, leading to a tendency to acidosis in critical
22
enteral feeding might not be possible or desirable, so illness. By six months of age, normal urine output
nutrients should be given as parenteral nutrition (PN) should be 1 mL/kg/h, and by adolescence 0.5–1 mL/kg/h
until enteral feeding is tolerated. 21 is considered normal. Catheterisation is generally required
in critically ill infants and children for accurate hourly
Diagnosis of an upper or lower respiratory illness may be measurement of urine output. Where this is not possible,
made, using the history of the symptoms from the parent particularly where small sizes of indwelling catheters are
or the child when age-appropriate, in conjunction with not readily available, weighing nappies will provide an
physical assessment of the child. Assessment of the rate, interim estimate of urine output. Inserting feeding tubes
rhythm, effort and pattern of breathing according to age in place of a urinary catheter is not recommended.
as well as colour and agitation should be undertaken.
Similar to how heart rate is used to increase cardiac
output, children compensate to maintain oxygenation for
some time by breathing more rapidly until they become
fatigued, when they are likely to become hypoxic and Practice tip
ultimately apnoeic. Where catheterisation is not possible, nappies can be weighed
to estimate urine output. Use an indelible marker to record
the dry weight of a disposable nappy on the nappy itself. This
GASTROINTESTINAL TRACT weight is then subtracted from the nappy’s wet weight to give
There are few differences between the child’s and adult’s an estimate of volume, with 1 g equivalent to 1 mL.
gastrointestinal tract outside the neonatal period;
although a palpable liver below the costal margin is a
normal finding. It will be up to 3 cm below the costal
margin in normal infants, decreasing to 1 cm by 4–5 Musculoskeletal System
years of age, and should no longer be palpable in adoles- Children have less developed musculature than adults,
cents. In the neonate, a relative pancreatic amylase defi- with less protection from external forces that collide
ciency means utilisation of starches is less effective. Fats with the child. Conversely, a child’s skeleton is more
are also absorbed less well; the reason why higher- cartila ginous than adults and therefore more pliable. As
fat milks such as cow’s milk are not ideal for infants. a result, rib fractures rarely accompany chest trauma in
23
Protein synthesis and storage is however enhanced in children while lung contusions are common. The skel-
the neonate. 13 eton in children changes from less cartilaginous in

684 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

nature at infancy to complete ossification and adult fea- which significantly affect their development and persona-
tures during adolescence, so daily calcium requirements lity. The first five stages are presented below.
increase over childhood and adolescence. 24
INFANTS (STAGE 1)

Integumentary System The first year of life is concerned with developing a sense
of trust, which lays the foundation for all future rela-
Infants have a thinner epidermis, dermis and subcutane- tionships. 38,43 More specifically, the affective exchanges
ous tissue that will continue to mature. This results in a between the infant and the primary caregiver provide a
greater susceptibility to absorption of chemicals, injury foundation for neurological development and lead to the
from adhesive tapes and any shearing force, and loss of creation of neural networks (particularly in the right
22
water and heat, particularly in the newborn period. hemisphere) that will influence the infant’s personality
Critically ill children are more likely to develop pressure and relationships with others throughout life. 44,45 Gener-
areas on the occiput, ear, sacrum, heel, or thigh; 50% of ally, up to the age of six months, infants are able to cope
pressure ulcers in children are associated with equipment with limited separation from their mothers; however,
25
pressing or rubbing on the skin. A commonly used tool changes to usual routine create anxiety and stress. From
43
for assessing risk of development of pressure areas in around 6–18 months of age separation is the major fear,
children is the modified Braden Q scale. This shorter with changes to usual routine and environment resulting
version includes three subscales (mobility, sensory per- in anxiety. Therefore, critically ill infants require paren-
43
ception, tissue perfusion/oxygenation) with a cutoff score tal presence and maintenance of normal routines, includ-
of 7 and has comparable psychometric properties to the ing breastfeeding, as much as is practicable.
26
adult Braden scale (see Chapter 6). However, recent
evidence suggests that the Glamorgan paediatric pressure TODDLERS (STAGE 2)
ulcer risk assessment scale may perform better than the
Braden Q scale. 27,28 The Glamorgan scale includes ten The toddler period, between 12 months and three years
subscales: anaemia, equipment pressing, mobility, poor of age, is a time for establishing autonomy and indepen-
peripheral perfusion, pyrexia, serum albumin, surgery dence. Control over bodily functions, increasing ability
in last 4 weeks, weight < 10th centile, continence, and to communicate, ability to view the self as separate from
nutrition. 27 others, and being able to tolerate brief separation from
the mother are all developmental characteristics during
46
this period. Toddlers tend to be egocentric in how they
DEVELOPMENTAL CONSIDERATIONS view the world, so illness, procedures and separation
43
from parents may be perceived as punishment. Their
29
Admission to ICU is very stressful for paediatric patients thinking processes include transduction, animism and
as well as for their family. 30-33 The stressors, combined ritual. Transductive thinking allows a child to link unre-
39
with the effects of critical illness, can lead to disturbances lated objects or events, such as separation and endotra-
in normal child development and attachment. The psy- cheal suction if suction occurs after the parent leaves the
chological needs of children and families are not always room. Animism attributes lifelike traits to inanimate
34
met. Factors that affect the psychosocial wellbeing of a objects, so the ventilator becomes a hissing monster, or
critically ill child include loss of usual routines and self- monitoring leads may be trying to trap them. Many
control; family presence and role; family and friends’ toddlers have varying levels of ritual or sameness, includ-
visits, comfort and the ICU environment. 29,35-37 ing always eating off the same plate, different foods that
Knowledge and understanding of developmental psycho- should not be touched, or a security toy or blanket.
logy can help nurses assess and plan care for the critically Regression, or loss of recently-acquired skills such as toi-
ill child. 38,39 Identification of internal strengths, external leting, may also occur during critical illness, creating
supports and environmental modification can facilitate further distress. When caring for a critically ill toddler,
40
coping and reduce stress in these children. Parental encourage parental presence and maintain as many of the
47
support is an important coping mechanism of infants usual rituals and routines as possible to facilitate coping.
36
and children during periods of stress. Strategies to faci-
litate coping in children of all ages include: PRESCHOOL CHILDREN (STAGE 3)
Children from 3–5 years of age fall into the preschool
l facilitating parental presence at all times, including
during invasive procedures and resuscitation 41,42 period of development. This period is characterised by
l maintaining normal routines and rituals as much as discovery, inventiveness, curiosity, and the development
38,39,43
possible, including story reading, bedtime routines of culturally- and socially-acceptable behaviour.
and presence of favourite toys Preschoolers can generally verbalise their needs reason-
48
l providing appropriate analgesia and sedation as well ably well. While thought processes become less ritual-
as non-pharmacological interventions istic and negative, they are still egocentric and magical
l providing opportunities for play and activities unre- thinking emerges, thus ideas about causality and linking
lated to treatment. events may be faulty. Fears, both real and imagined, are
39
prevalent during this period. For example, fears of
Erikson’s psychosocial theory is helpful for understand- monsters or being hurt may occur. They may also feel
43
43
ing childhood development. Erikson’s theory asserts guilty as a result of illness. There is, however, greater
that people experience eight ‘psychosocial crisis stages’ understanding of the passage of time, so parents can leave

Paediatric Considerations in Critical Care 685

the preschooler for defined short periods. Hospitalisation critical care nurses need to also consider the developmen-
remains difficult, but preschoolers respond to anticipa- tal level of the child when providing care.
tory preparation and concrete explanations. 38
COMFORT MEASURES
SCHOOL-AGE CHILDREN (STAGE 4)
Children between 6 and 11 years are usually referred to Critically ill infants and children are particularly vulner-
as being of school age. This period represents a widening able to pain. If pain remains unrelieved it may cause
of the sphere of influence from parents/family to include short- and long-term physiological and psychological
39
the school environment and peers. A transition complications, such as increased risk of mortality and
51-53
from egocentric thinking to concrete operations morbidity. The assessment of pain in children is par-
51
occurs, 38,39 with children becoming more independent ticularly challenging, but the use of valid pain and seda-
and achievement-oriented for their sense of self-worth. In tion assessment tools may be useful for the management
54,55
the ICU, school-age children may have a distorted or of pain in critically ill children. Prevention of proce-
fantasy-laden view, and will need concrete explanations. dural pain is important not only to avoid pain-related
Sicker children are less able to cope with the ICU envi- complications and emotional trauma, but also to facili-
56
ronment and are more likely to regress, which can have tate the procedure. Target sedation level according to the
a significant impact on their sense of self-worth. Modesty child’s clinical status may help maintain comfort without
57
49
and privacy is imperative at this age. Preadolescence compromising haemodynamic and respiratory status,
occurs between 10 and 11 years, and represents a time of as well as minimising other undesirable effects of analge-
turmoil and emotional upheaval. 39 sics and sedatives.
ADOLESCENTS (STAGE 5) PAIN AND SEDATION ASSESSMENT
Adolescence is considered a time of transition from child- Recent advances in pain and sedation assessment show
hood to adulthood. It is a developmental stage rather that they remain problematic in paediatric critical care
than an age group, but is typically represented by children and highlight the need for routine assessment, documen-
aged 12–18 years, or teenagers. Internal changes relate to tation and effective communication of the pain and seda-
emotional upheaval, search for autonomy, and transition tion scores. Numerous pain assessment instruments have
of thought process from concrete to abstract. External been developed, but few have been validated for the pae-
43
changes relate to physical changes, such as the emergence diatric critical care population. These latter include the
of secondary sex characteristics with a related preoccupa- PICU-MAPS and the COMFORT behaviour scale. The
tion on bodily functions and image. 38 PICU-MAPS is a multidimensional scale developed for
critically ill children, including five categories of physio-
A goal in adolescence is to develop an integrated sense of logical and behavioural items, providing a possible pain
self, achieved through managing the conflicting demands score between 0 (no pain) and 10 (maximum pain). 58,59
of family and peers. Peer identity is essential to psycho- The COMFORT scale has been validated in several studies
logical growth and development, as is the gradual shift in PICU 60,61 and comprises seven behavioural items,
from family to peer orientation. The peer group provides where only six are rated (alertness, calmness/agitation,
a way for the adolescent to self-evaluate and to bolster respiratory response or crying, physical movement,
self-esteem. Adolescents also target authority figures with muscle tone, and facial tension), generating a possible
retaliation and defiance. Conversely, adolescents will seek score between 6 and 30. In combination with pain,
out non-parental adults, such as a teacher or relative, to assessment of sedation is paramount and the State
50
obtain approval and acceptance. Slote has described a Behavioral Scale (SBS) is particularly relevant to evaluate
50
process associated with adolescent illness. The first is the level of sedation in infants and children in ICU. It
62
hopelessness and helplessness provoked by the equip- consists of a six-level responsiveness continuum, ranging
ment and environment. Adolescents often think they will from −3 (unresponsive) to +2 (agitated), with a neutral
not get better, and need to be given clear information state ‘awake and able to calm’ of 0.
about the expected course of the illness. They also need
to be included as much as possible in decision making PAIN AND SEDATION MANAGEMENT
and encouraged to participate in their own care. Feeling Painful procedures should be minimised when possible.
helpless and defenceless is contrary to their normal feel- Some nonpharmacological therapies have been shown to
ings of invincibility and may result in antisocial behav- be beneficial alone in managing mild pain or in combi-
iours. The adolescent must learn to accept that the quest nation with drug therapy in infants and young children.
for autonomy has been temporarily interrupted. Acknowl- These therapies may include non-nutritive sucking (e.g.
edging his/her feelings and setting clear behavioural finger or pacifier) with or without sucrose (for infants up
50
limits can help an adolescent cope. Adolescents will also to 4 months), swaddling, music therapy, and distraction
63
experience fear and anxiety. This can be offset by clear with or without parental presence. 64
explanations and acknowledgement of feeling through
articulation and reflection. Concerns for body image is Pharmacological treatment of pain and sedation in
also paramount, particularly fear of mutilation and scar- infants and children should be tailored to the child’s
ring. Physical appearance is important for acceptance into need and condition. Continuous opioid (morphine)
50
the peer group and for self-esteem. In summary, in addi- infusions are used at the lowest effective dose and
tion to considering age-related physical characteristics, minimum duration based on regular pain assessment.

686 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Fentanyl boluses are not recommended in neonates as Australia, where the legal age for consent is 14 and 16
65
76
they may cause glottic and chest wall rigidity. Sedation years, respectively. However, a young person with the
management in children is similar to that in adults, emotional maturity and intellectual capacity to agree to
except for the use of propofol, which should be used with medical procedures, in circumstances where he or she is
caution in children. Although there is no strong evidence, not legally authorised or lacks sufficient understanding
propofol infusion in children has been associated with for giving consent competently can provide informed
66
sudden myocardial failure and death. More recent data assent. 77,78 To be considered competent, young people
shows that propofol has an acceptable safety profile and must be able to understand the nature of the decision as
could be used in children for short term deep sedation well as the consequences of making or not making the
78
67
under close monitoring of the airways. Use of dexme- decision. Whenever possible, it is recommended to
detomidine in paediatrics is promising, but additional obtain the child’s assent for treatment or procedures.
safety and efficacy studies need to be carried out before Children, even when deemed not competent, have the
routine use as a sedative agent can be recommended in right to be informed and, when appropriate, to be asked
68
children. Indications for the use of neuromuscular for their permission. However refusal of treatment by a
blocking agents in children, monitoring of the effects and child has no legal bearing when a parent has consented.
management are similar to adult practice. 69 Importantly, parents may also refuse consent, and in that
case national laws and legal mechanisms for resolving
FAMILY ISSUES AND CONSENT disputes may be used. 77,79
When children are admitted to an ICU, the whole family THE CHILD EXPERIENCING UPPER
is affected by the hospitalisation. ‘Family-centred care’
(FCC) provides a framework for the care of children and AIRWAY OBSTRUCTION
their family in hospital. FCC means that during a hospital Upper airway obstruction is common in infants and
stay, nursing care is ‘planned around the whole family, young children for two major reasons: the anatomical
not just the individual child, and in which all the family size of the airway and the frequency of respiratory infec-
members are recognised as care recipients’. 70, p. 1318 Parents tions experienced in early childhood. Congenital struc-
should receive unbiased information at regular times, be tural abnormalities, infections, as well as foreign body
involved in the decision-making process and the care of aspiration are the three categories of causes of upper
their child; this parent–professional collaboration should airway obstruction in children.
be facilitated at all levels of healthcare. 70,71 As the devel-
opmental issues highlight, parents are essential to a
child’s coping with critical illness. Critically ill children GENERAL DESCRIPTION AND CLINICAL
are particularly vulnerable to short- and long-term emo- MANIFESTATIONS
tional and psychological sequelae, but parental presence General indicators of respiratory distress will be present
and participation in care can make a difference. 72 in a child suffering from upper airway obstruction. Spe-
cific clinical signs of upper airway obstruction in children
Parents need to feel involved in their child’s care,
which includes the need for information, communica- include:
tion, understanding the child’s illness and being part l a longer inspiratory phase with unchanged expiratory
of the decision-making process. 31,34,73,74 A partnership phase
between staff and parents is the ideal situation, but l stridor on inspiration
parents often need to be reminded on how to maintain l recessions of the chest wall
the parental role and how they can effectively care for l lower respiratory rate
75
both their child’s and their own psychological health. l in infants, head bobbing and nasal flaring
Parents should be allowed to be present during poten- l hoarseness
tially stre ssful situations such as endotracheal suction, l drooling of saliva. 19
cannulation and resuscitation if they choose to, pro-
viding adequate support from a nurse or another des- Observing and listening to the child’s symptoms without
41
ignated health care worker is given. Being present at disturbing them will provide important clues about the
the end of their child’s life may help them accept the level and degree of obstruction the child is experiencing.
42
death. Not allowing parents to be present during The aim is to assess the child without causing further
procedures is a form of paternalism that goes against distress, as a crying, agitated child can further increase the
the right of the patient. Parents should however be degree of obstruction and work of breathing, leading to
64
80
informed that it is their right to leave if they wish. respiratory collapse. The Paediatric Assessment Triangle
(PAT) is a useful tool to facilitate rapid assessment of the
child’s appearance, work of breathing, and skin circula-
CONSENT AND ASSENT tion. Stridor indicates obstruction in the upper airway,
81
Except for emergency treatment, parents or legal guard- while wheeze is suggestive of lower airway disease. When
ians need to consent to all aspect of medical care, includ- stridor is also associated with a barking cough, it is likely
ing preventive, diagnostic or therapeutic measures for to be croup. A softer stridor in a child who looks systemi-
children. The legal age of consent differs between legis- cally unwell may indicate epiglottitis. When a previously
lations but is 18 years in major European countries and well child presents with a sudden onset of stridor, it is
all Australian states, except New South Wales and South likely to indicate foreign body aspiration, and eliciting

Paediatric Considerations in Critical Care 687

the history of a sudden choking episode can clarify the determined by angiography. Treatment is surgical correc-
diagnosis. 19,80,82 tion of the vascular malformation. 84
MONITORING AND DIAGNOSTICS
CONGENITAL AIRWAY ABNORMALITIES
Congenital structural abnormalities of the airway are Initial monitoring and diagnostic studies for infants and
children with upper airway obstruction are ideally of a
present at birth; depending upon severity of obstruction, non-invasive nature, to avoid distress.
it may take hours to months to become apparent. These
include laryngomalacia, laryngeal web, tracheomalacia
and vascular rings. These infants and children will require
referral to a specialist paediatric centre for ongoing man-
agement and, if they develop respiratory infections, are Practice tip
likely to become compromised much more easily than
children with normal airways. Close direct observation from a short distance away is an ideal
nursing practice, accompanied by non-invasive monitoring.
Laryngomalacia is the most common cause of stridor Ideally, the critical care nurse will be positioned to hear the
in the newborn period. Stridor is produced by flaccid, child’s stridor. Blood sampling, cannulation and other invasive
soft laryngeal cartilage and aryepiglottic folds that procedures should be left until the airway has been secured,
collapse into the glottis on inspiration. An inspiratory the child has been anaesthetised, or airway obstruction is
83
stridor, usually high-pitched, will be present. It may be resolving.
intermittent, may decrease when the patient is placed
prone with the neck extended, may increase with
agitation, and is usually present from birth or the first
weeks of life. The infant’s cry is usually normal. Feeding Pulse oximetry is a non-invasive method of monitoring
problems may be associated with increased respiratory oxygenation. Arterial blood gases are performed only
distress. Laryngoscopy confirms the laryngomalacia when absolutely necessary, as this may increase the child’s
diagnosis. Treatment is supportive, with only a small distress and thus worsen the degree of obstruction. Con-
proportion of infants requiring airway reconstructive tinuous ECG monitoring is also indicated.
surgery unless respiratory distress interferes with feeding
and growth, in which case a tracheostomy may be Lateral airway X-rays are unlikely to be helpful in the
indicated. 84 setting of croup and epiglottitis and, when they are likely
to involve separating the child from a parent, are poten-
A laryngeal web is made of membrane that typically tially harmful and not recommended. When there is a
19
spreads between the vocal cords, with an inspiratory less dramatic presentation of the infant or child, or when
stridor present soon after birth. Diagnosis is confirmed the diagnosis is not clear, as in the case of an inhaled
by laryngoscopy. Treatment involves lysis in the case of foreign body, then a chest X-ray may be diagnostic.
thin membranous webs while a tracheostomy may be
required for a thicker fibrotic web. Laryngeal webs can MANAGING THE PAEDIATRIC AIRWAY
also develop after contracting illnesses such as diphtheria,
and are occasionally reported in otherwise normal adults, A child’s airway may be managed in a number of ways.
typically at intubation for an operative procedure. 85 Simple positioning may be all that is required to manage
an infant’s airway. Children will often assume an upright
Tracheomalacia and tracheobronchomalacia involve sitting position and may become more distressed if placed
malformed cartilage rings, with lack of rigidity and an into the supine position, thus when possible the best
oval shape to the lumen. Secondary tracheomalacia is position for an infant or child with upper airway obstruc-
associated with prolonged intubation and prematurity tion may be sitting on their parent’s lap. Because of the
and presents within the first year of life. Malacias are anatomy and physiology of the respiratory tract, avoid
17
characterised by wheezing and stridor on expiration, with extending the head of infants. Chin-lift and jaw-thrust are
collapse of the tracheal or bronchial lumen. Diagnosis is useful airway adjuncts in children to maintain an airway
confirmed by fluoroscopy and bronchoscopy, which and to facilitate use of a bag–valve–mask. It may be nec-
demonstrate tracheal collapse on expiration. As the infant essary to use an oropharyngeal airway or nasopharyngeal
grows, cartilaginous development improves the airway by airway, laryngeal masks and endotracheal intubation in
about two years of age, but a number of children will an unconscious or sedated infant. 19,80
require airway stenting or reconstructive surgery. 83
Vascular rings result from congenital malformations of Intubation
the intrathoracic great vessels, resulting in compression Intubation may be required to manage airway obstruc-
83
of the airways. Infants present with stridor at birth or tion. Uncuffed endotracheal tubes (ETT) have been
86
within the first few weeks of life. Other symptoms include favoured in paediatric practice over cuffed tubes. Inflating
wheezing, cough, cyanosis, recurrent bronchopulmonary the cuff of a regular ETT can cause damage in prepubes-
infections, and dysphagia. Diagnosis may be confirmed cent children, as the subglottic area is the narrowest
by CT scan, MRI scan or endoscopy, which reveals inden- portion of their airways. The recent availability of a
tations secondary to the extrinsic pressure of the vascu- paediatric-specific ETT with microcuff and markings to
84
lature. The anatomy of the vascular malformations is ensure correct placement below the glottis has facilitated

688 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E
































FIGURE 25.3 Paediatric intubation. (Courtesy Paul de Sensi.)
ventilation when a leak is undesirable, including in the
87
child with facial and airway burns, and when using
inhaled nitric oxide and for high frequency ventilatory
strategies such as oscillation ventilation. Equipment nec-
essary for paediatric intubation are shown in Figure 25.3.
Figure 25.4 shows a range of sizes of uncuffed ETTS:
2.5 mm to 5.5 mm, that should be available in 0.5 mm
increments, while cuffed ETTs are now available in sizes
from 3 mm through to 9 mm. Selecting the correct ETT
size includes having the recommended tube size plus
tubes that are 0.5 mm larger and smaller than that. For
children over 1 year of age, several formulae exist to
calculate appropriate tube sizes, but the age-based and
the fifth fingernail width-based predictions of ETT size
88
are the most accurate. Table 25.4 provides a guide for
ETT sizes, suction catheter size and nasogastric tube size
for different-aged infants and children.


Practice tip
To calculate ETT tube size and length, use the following formula
from the 2010 Australian and New Zealand Resuscitation FIGURE 25.4 Range of ETT sizes. (Courtesy Paul de Sensi.)
Guidelines: 89
l For term newborns ≥3 kg: size 3.0 mm or 3.5 mm (uncuffed
tubes) or 3.0 mm (cuffed tubes) the practically simultaneous administration of hypnotic
l For infant up to 6 months: size 3.5 mm or 4.0 mm (uncuffed medication and a muscle relaxant immediately before
tubes) or 3.5 mm (cuffed tubes) intubation. 92,93 The main advantages of this method
l For infant 7 to 12 months: size 4.0 mm (uncuffed tubes) or include good airway visualisation with a relaxed jaw,
3.5 mm (cuffed tubes) open immobile vocal cords, and the elimination of all
l For children over 1 year: Uncuffed tubes: size (mm) = age movement, including gagging and coughing. 90
(years)/4 + 4 or Cuffed tubes: size (mm) = age (years)/4 + 3.5
SPECIFIC CONDITIONS AFFECTING
The most common method used to intubate children is THE UPPER AIRWAY
the rapid-sequence method. Rapid-sequence intubation Bacterial and viral infections of the upper airway are
is performed where the child may have a full stomach common in children. Croup is the most common infec-
90
and is at risk of aspiration during intubation. It involves tion causing upper airway obstruction in children.

Paediatric Considerations in Critical Care 689



TABLE 25.4 Endotracheal tube (ETT) and nasogastric tube (NG) sizes for infants and children

Age Weight (kg) ETT size (mm ID) At lip (cm) At nose (cm) Suction catheter (FG) NG tube (FG)
0 <3.0 2.5 6 7.5 5 8
0 3.0 3.0 8.5 10.5 6 8
0–3 months 3.5–5 3.5 9 11 6–8 10
3–12 months 6–9 3.5 10 12 6–8 10
1 year 10–12 4.0 11 14 8 10
2 years 13–14 4.5 12 15 8 12
3 years 14–15 4.5 13 16 8 12
4–5 years 16–19 5.0 14 17 8–10 12
6–7 years 20–23 5.5 15 19 10 14
8–9 years 24–29 6.0 16 20 10–12 14
10–11 years 30–37 6.5 17 21 12 14
12–13 years 38–49 7.0 18 22 12 16
14+ years 50–60 7.5 19 23 12 16
Adult >60 8–9 20–21 24–25 12 16
FG = French gauge; ID = internal diameter. Adapted from (91).




Epiglottitis is now rarely seen since immunisation against intubation. Possible complications of croup include
Haemophilus influenzae type b (Hib) was introduced into respiratory failure, respiratory arrest, hypoxic damage,
the immunisation schedule for all Australian and New secondary bacterial infection, acute pulmonary oedema,
Zealand children. However, it is important to distinguish persistence or recurrence. 84
epiglottitis from croup in order to initiate appropriate
management. Other less common infectious causes of Clinical manifestations
upper airway obstruction seen in young children include Croup is characterised by a barking or seal-like cough,
bacterial tracheitis and retropharyngeal abscess, while inspiratory stridor and hoarse voice. The severity of
97
diseases thought to have disappeared, such as Lemierre’s croup is assessed based on increased respiratory rate,
syndrome and diphtheria have not been completely increased heart rate, altered mental state, work of breath-
eradicated. 94 ing and stridor. Stridor at rest is noted in moderate to
Infection of the lymphoid tissue around the nodes drain- severe croup and is often quite loud. If a child’s stridor
ing the nasopharynx, sinuses and eustachian tubes may becomes softer but the work of breathing remains
cause pus to accumulate in the retropharyngeal space, increased, it should be treated as an emergency as the
98
leading to a retropharyngeal abscess. Presenting symp- obstruction may become more severe. The symptoms of
toms include history of upper respiratory tract infection croup are listed and compared with those of epiglottitis
(URTI), sore throat, fever, toxic appearance, meningis- in Table 25.5. Diagnosis is made on physical assessment
mus, stridor, dysphagia, and difficulty handling secre- and the history of the illness.
94
tions. Diagnosis is usually made on bronchoscopy.
Treatment involves surgical drainage and antibiotic Management
administration. Short-term intubation may be required Management of croup depends on the severity of the
until swelling has resolved following surgery. upper airway obstruction and close cardiorespiratory
observation and monitoring is essential. Children with
Croup moderate to severe croup should be given face-mask
Croup (laryngotracheobronchitis) is used to describe a oxygen and allowed to adopt the position which they find
most comfortable. Strategies such as positioning the child
set of symptoms caused by acute swelling causing obstruc- in a parent’s lap and holding the face-mask close to their
tion in the upper airway (larynx, trachea and bronchi) face may limit their distress and can have beneficial effects
from inflammation and oedema, caused mostly by the on oxygenation. 97
parainfluenza or influenza viruses. 84,95 Croup occurs in
approximately 2% of Australian children, generally aged The use of steroids in combination with nebulised adren-
96
1–4 years, and in winter months. Recent advances in aline is responsible for significant improvement of symp-
croup management have been responsible for a fall in toms in children within 12 hours of administration,
the number of children requiring hospitalisation and abating the need for intubation in the vast majority of

690 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

prevalence rate from 22.7 to 3.3 per 100,000 children in
TABLE 25.5 Clinical features of croup and epiglottitis 1998 and 2008, respectively. 101,102 Hib infection can
cause meningitis, septicaemia, septic arthritis and celluli-
Croup Epiglottitis tis as well as epiglottitis. The disease process and devel-
opment of major symptoms progress rapidly over a few
Aetiology Viral Bacterial
hours and an untreated child may become acutely
Age 6 months–3 years Infancy through obstructed. A child will make a full recovery without
adulthood sequelae if diagnosis and treatment are appropriate and
Onset Subacute (over days) Acute (over hours) timely. Supraglottitis has emerged in recent times as a
more accurate description of a similar range of symp-
Fever Mild (±38°C) Severe (>38.5°C)
toms as epiglottitis, and has been linked with the herpes
Cough Present (often barking or Absent virus and other organisms, requiring treatment with aci-
seal-like) clovir and vancomycin. 99
Drooling Absent Present
Activity Distressed Lethargic Clinical manifestations
Colour Pale/sick Toxic The child with epiglottitis presents looking unwell with
a fever, is unable to swallow secretions, drooling saliva
Obstruction +++ + and refusing to talk or swallow. The child may maintain
Stridor Inspiratory, high-pitched Expiratory snore an upright position, usually leaning with the head
extended, supporting a sitting position with the arms
Sore throat Uncommon Common
stretched out behind in what is known as the tripod posi-
Position Any Tripod; sitting up tion. Hypoxaemia is usually present. Sudden respiratory
Course Gradual worsening or Unpredictable; fatal arrest followed by cardiac arrest, can occur unpredictably.
improvement if not treated Cardiac arrest is likely to be asystolic in rhythm due to
either vagal stimulation or hypoxia secondary to airway
Season Autumn–winter Throughout the year
obstruction. 94
Adapted from (95).
Management
The most important aspect in the management of epiglot-
cases. 97,98 Nebulised adrenaline is efficacious to reduce titis is rapid diagnosis and minimal handling of the child
airway inflammation, with effects seen within five minutes until an airway is in place. Children with epiglottitis
and lasting up to two hours. Although inhalations can be require urgent intubation because acute airway obstruc-
repeated, the benefits lessen with subsequent treatments. tion followed by cardiac arrest is a potential hazard. Thus,
Adrenaline does not alter the course of croup. the aim of management at this time is to keep the child
as calm as possible until the airway is secured. 19,99 The
child should be nursed propped up with pillows or on a
parent’s lap while arrangements are made for the inser-
Practice tip tion of an ETT. Procedures such as cannulation and exam-
ination of the throat should be avoided until the child’s
If placement of a facemask to deliver oxygen causes increased 95
agitation and worsens respiratory distress in young children, airway is secure.
have the parent hold the mask near their child’s face and Prophylaxis with antibiotics is required for families and
increase the flow rate. ‘Blow-over’ oxygen will increase oxygen household contacts if there is an infant under 12 months
saturation, and as the child settles, mask or nasal cannulae can of age and/or a child in the household under the age of
be reintroduced. five years who is not fully immunised. Where the infected
child has attended childcare for more than 18 hours each
week, it is recommended that staff and other children at
the centre also receive antibiotic prophylaxis. 82
Epiglottitis
Epiglottitis is inflammation of the epiglottis, frequently
involving surrounding structures, with the classic descrip- FOREIGN BODY ASPIRATION
tion of a swollen, cherry-red, softened and floppy epi- Aspiration of a foreign body into the upper airway is
glottis, which tends to fall backwards, obstructing the another relatively common cause of obstruction in chil-
99
airway. Obstruction also occurs circumferentially, from dren. Infants tend to swallow food items such as nuts and
the oedematous, inflamed aryepiglottic folds surround- seeds, while toddler-aged children tend to swallow coins,
ing the larynx. It is typically caused by Hib and since the teeth, and small toys or toy parts. An inhaled foreign
103
introduction of childhood immunisation programmes body is likely to have a rapid onset with no previous
to protect against Hib infection, the incidence has symptoms. Sometimes the diagnosis is missed for days,
dropped from 23.8 cases per 100,000 children in 1991 weeks or even months, and the child’s symptoms may
100
to 2.81 per 100,000 in 2002 in the UK. A similar be non-specific, such as a cough with or without blood-
pattern was observed in Australia with a drop in stained sputum. 83,103

Paediatric Considerations in Critical Care 691

Clinical Manifestations In temperate regions of Australia and New Zealand, most
Sudden onset of coughing, gagging and an audible stridor cases occur between late autumn and early spring, with
in a previously-well infant or child is suggestive of an sporadic cases throughout the year. There is a paradoxical
83
inhaled foreign body. However, an accurate history – relationship between the incidence of RSV and other viral
such as a recent coughing or choking episode – is the pathogens causing bronchiolitis. RSV epidemics occur
most sensitive factor in making a diagnosis of inhaled when other respiratory pathogen epidemics are diminish-
foreign body. ing, and vice versa. Although there are limited data on
the actual incidence of bronchiolitis, laboratory isolation
Management data in New South Wales estimate that about 1000 infants
are hospitalised with bronchiolitis each year. The major-
Management will depend on the location and level of ity of these are under six months old. There is also a
110
the aspirated foreign body, as it may have lodged in the higher incidence of bronchiolitis in the Indigenous popu-
pharynx, oesophagus, larynx, trachea or bronchial tree. lation of Australia 111,112 and more severe illness when
104
Coughing is encouraged for mild airway obstruction. compared to non-Indigenous. Younger children with
113
Up to five back blows may be successful in dislodging the one or more comorbidities were at higher risk of compli-
foreign body, which may be followed by up to five chest cations. RSV infection occurs throughout the year, with
111
thrusts and back blows. Direct laryngoscopy and removal an annual peak during the winter months. 111,114
of a foreign body using Magill forceps may be required
for an acute episode when back blows and chest thrusts When bronchiolitis occurs, the highest risk for hospita-
have been unsuccessful. When the foreign body has lisation is infants under six months of age, those with
lodged below the carina, for the majority of children exposure to tobacco smoke and underlying conditions
diagnosis and definitive treatment will consist of removal such as congenital heart disease, prematurity and low
20,102,115
of the foreign body via a bronchoscopy under general socioeconomic group. Severe disease, requiring
anaesthesia. 83 admission to a paediatric ICU, is associated with prema-
turity, particularly in infants with chronic lung disease
or a history of ventilation in the newborn period and
THE CHILD EXPERIENCING LOWER congenital heart disease.
AIRWAY DISEASE
Clinical manifestations
Lower airway disease in children is a common reason Bronchiolitis is a clinical diagnosis; non-isolation of a
for admission to ICU. Infants under 12 months usually causative viral agent does not exclude the diagnosis. The
present with bronchiolitis or pneumonia. Asthma is more clinical features of bronchiolitis are variable, and may
common in older children, but infants nearing 12 months include URTI symptoms such as rhinorrhoea (runny
of age may develop asthma and there is often confu- nose) and an irritating cough. Within three days the
105
sion between bronchiolitis and asthma at this age. 106
infant develops tachypnoea and respiratory distress,
which may be mild, moderate or severe. An expiratory
SPECIFIC CONDITIONS wheeze is often present and auscultation usually reveals
Bronchiolitis and asthma are commonly seen in children, fine to coarse crackles. Fever is present in approximately
and the management of each condition is discussed 50% of infants. In very young, premature or low-
below. National and worldwide clinical guidelines for birthweight infants, apnoea is often the presenting
these conditions have been developed and are continu- symptom, which then develops into severe respiratory
ally updated. 107,108 distress. The clinical course of bronchiolitis is usually
116
7–10 days; however, the effects of severe illness may last
Bronchiolitis much longer. Respiratory distress is present. Indications
Viral bronchiolitis in infancy is characterised by obstruc- for intensive care admission include frequent and/or pro-
tion of the small airways, resulting in air trapping and longed apnoeas; hypoxaemia despite administration of
respiratory distress in infants less than 12 months of age. oxygen; haemodynamic instability; an obviously tiring
It is the most common severe respiratory infection in infant or decreased level of consciousness. 20,117
infancy, although the course is usually mild to moderate
and is self-limiting, usually requiring no treatment. Severe Management
infection represents less than 5% of all cases and is A thorough history and assessment are important to
usually associated with prematurity or congenital heart provide a foundation for management of bronchiolitis.
95
disease. Respiratory syncytial virus (RSV) causes 90% of The infant with acute bronchiolitis requires continuous
109
bronchiolitis cases. Other causative agents are parain- cardiorespiratory monitoring and oxygen saturation
fluenza virus types 1, 2 and 3, influenza B, adenovirus monitoring. Treatment and management of infants pre-
types 1, 2 and 5 and Mycoplasma. RSV invades the epithe- senting with bronchiolitis is largely supportive, as most
lial cells of the bronchioles, spreading via cell fusion and pharmacological treatments are unproven. In general,
the creation of syncytia. This results in destruction of management centres on supporting hydration and nutri-
the epithelium and patches of necrosis. The debris associ- tion, oxygenation, and maintaining vigilance for signs of
ated with epithelial shedding and mucus production deterioration that may require mechanical ventilation.
lead to small airway blockage and the clinical features of Minimising the impact of procedures on the infant is also
bronchiolitis. 109 important.

692 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Asthma increasing, 126 is higher in boys 129,130 and in urban areas,
Asthma is a disease of the lower respiratory tract charac- but its mortality has declined over the past two decades,
126
terised by mucosal and immune system dysfunction. from 1–2/100,000 down to 0.8/100,000.
There is a complex interaction between bronchial wall
cells, inflammatory mediators and the nervous system. Clinical manifestations
The chronic inflammatory process causes narrowing of ICU admission is required when children present with
bronchial airways, thus obstructing airflow. This leads to respiratory failure due to an asthma exacerbation. Obesity
episodes of wheezing, breathlessness and chest tighten- and genetic predisposition may be important in reacting
ing that are usually reversible. 106 to β 2 -agonist therapy. These children exhibit clinical
131
Development of childhood asthma results from a com- features associated with respiratory distress. Pulsus para-
bination of genetic, environmental and socioeconomic doxus, a phenomenon of palpable changes in blood pres-
risk factors. 118-122 Increasing prevalence of asthma over sure that occur with respirations, may also be present and
the past 20–30 years may be linked to a higher inci- can also be noted on plethysmography. Arterial blood gas
dence of genetic predisposition, independent of envi- analysis usually reveals initially a mild respiratory alka-
ronmental factors. Some studies have identified links losis and hypoxaemia; however, more severe asthma may
between asthma and various regions of the human show combined respiratory and metabolic acidosis and
genome, but the linkages are not consistent. The CD14 hypercapnia as the child tires and is unable to eliminate
133
gene shows the best promise of linkage, with increased carbon dioxide.
expression or promotion of this gene associated with
123
atopy and asthma in early to late childhood. Certain Assessment and management
racial groups, such as African-Americans, when com- Assessment of asthma severity is based on criteria such as
pared to Americans of European origin, are also more the degree of respiratory failure as evidenced by cyanosis,
likely to develop asthma and have complications, par- length of sentences between breaths, retractions and
ticularly those traditionally from tropical regions. 124 hypoxia, as well as level of consciousness and degree of
Once asthma has developed, there are triggers that may pulsus paradoxus. There are many scores available to
precipitate an attack. These include viral illnesses, par- assist in determining the severity of asthma, including the
ticularly respiratory viruses, tobacco smoke exposure, National Asthma Campaign guidelines, the Pulmonary
house dustmites, exercise, pet hair, food and environ- Index Score, the Respiratory Failure Score and the Modi-
mental allergens. fied Dyspnoea Scale. Whatever method is used, assess-
Asthma is one of the commonest paediatric presentations ments should be frequent and response to treatment
to emergency departments and its worldwide prevalence recorded (see Table 25.6). Severe asthma that worsens
125
is growing with differences between populations. It is and/or does not respond to treatment warrants admis-
130
reported that as many as 20–30% of children in Wester- sion to a paediatric ICU.
nised countries, including Australia and New Zealand, The broad aims of management of severe asthma include
will develop wheeze or asthma symptoms; 126 the current maintaining oxygenation, rapid bronchodilation and
disease rate is between 9.6% in the US, 127 29.7% in the treating any cardiovascular compromise. In children with
UK, 128 and 31% in Australia. Asthma prevalence is severe asthma, hypoxaemia results from ventilation/
1


TABLE 25.6 Asthma severity assessment
Sign* Mild Moderate Severe Life threatening
Altered consciousness no no agitated agitated, confused, drowsy
Accessory muscle use no minimal moderate severe
Oximetry in air >94% 90–94% <90% <90%
Talks in sentences phrases words words
Pulsus paradoxus not present may be palpable palpable palpable
Pulse rate <100 tachycardia marked tachycardia marked tachycardia or bradycardia
Central cyanosis no no likely to be present likely to be present
Wheeze on auscultation variable moderate–loud often quiet often quiet
Physical exhaustion no no yes yes
Initial spirometry (if done; % of >60% 40–60% <40% <40%
best or predicted)
*The child should be assigned to the most severe grade in which any feature occurs. If the child has received treatment prior to arrival, he/she should be managed as
more severe than the clinical signs indicate.
Adapted from (132).

Paediatric Considerations in Critical Care 693

perfusion (V/Q) mismatch due to lower airway obstruc- unresponsive to inhaled bronchodilators and steroids. It
tion, in addition to hypoventilation, hypercarbia, and is a bronchodilator, improving diaphragmatic contractil-
pulmonary vasoconstriction related to acidosis. Hypoxae- ity and a central respiratory stimulant. However, the
mia can result in further bronchoconstriction, hypoten- narrow therapeutic window and side effects of induced
sion, systemically-reduced oxygen availability, increased nausea and/or vomiting represent a non-negligible risk
myocardial oxygen consumption and neurological symp- of complication, thus its use should be limited to manag-
toms such as agitation, confusion or decreased level of ing asthma not responsive to other agents. 138
consciousness. Bronchodilators may worsen hypoxaemia Ventilation may be required when there is profound hy-
through worsening V/Q mismatch or bronchoconstric- poxaemia, severe muscle fatigue or decreased level of
tion, due to the hyperosmolarity of the nebulised solu- consciousness. 130,139 However, as asthmatic children are
tion. In addition, rapid changes to the compliance of the at higher risk of complications such as barotrauma and
airways together with hyperexpanded lungs may result in air trapping, there is a higher risk of death associated
airway collapse.
with ventilation in this group of patients. Non-invasive
Oxygen delivery is achieved by high-flow oxygen mask positive pressure ventilation (NPPV) is the first choice,
with a reservoir bag. All nebuliser therapy should be with some evidence that it rapidly corrects gas exchange
oxygen-driven. However, if hypoxaemia persists despite abnormalities and assists with respiratory muscle
maximal bronchodilator therapy and oxygen administra- fatigue. 140-142 The contraindications for NPPV include
tion, then mask continuous positive airway pressure cardiac/respiratory arrest, severe encephalopathy, haemo-
(CPAP) may be considered. dynamic instability, facial surgery/deformity, high risk for
aspiration, nonrespiratory organ failure, severe upper
β 2 -agonists, anticholinergics and steroids form the foun- gastrointestinal bleeding, unstable arrhythmia and upper
dation of acute severe asthma management, but for chil- airway obstruction. 142
dren over 40 kg and those who have reached puberty it
may be more appropriate to administer IV adrenaline. Intubation may be necessary when signs of deterioration
β 2 -agonists act by relaxing bronchial smooth muscle, are present, such as elevated carbon dioxide levels,
improving mucociliary transport and inhibiting media- exhaustion, alteration of mental status, haemodynamic
tor release. In severe to life-threatening asthma, nebu- instability and refractory hypoxaemia. 142 Because of high
lised salbutamol is preferred. 134 Inhaled salbutamol airway pressures, a cuffed endotracheal tube should
combined with magnesium sulfate improves pulmonary be used.
function. 135 Adverse effects of β 2 -agonists’ administra- Children with acute asthma may have a raised metabolic
tion include hypokalaemia, tachycardia, tremors, agita- rate and increased insensible losses, together with reduced
tion and hyperglycaemia. Mild lactic acidosis may also oral intake. With increased intrathoracic pressure due to
occur. Intravenous salbutamol infusion should be con- air trapping, even mild dehydration may compromise
sidered when there is severe, life-threatening asthma cardiac output. Therefore, adequate fluid replacement is
refractory to inhaled treatment. Inhaled salbutamol may necessary. In addition, pulmonary secretions will thicken
be discontinued once IV infusion has commenced, but and plug the airways if fluid intake is inadequate. Main-
should be reestablished before ceasing the infusion. In tenance fluids should be provided until the child’s con-
acute severe episodes, salbutamol is usually given every dition and oral intake improve. 143
20 minutes; if there is little response, continuous nebu-
liser therapy may be required. In this instance, a feeding
tube is inserted into the nebuliser and the chamber NURSING THE VENTILATED CHILD
replenished as it empties. Anticholinergics, in combina- Principles of mechanical ventilation were covered in
tion with β 2 -agonists, improve lung function by aug- Chapter 15. Issues such as gastric decompression, ade-
menting the action of β 2 -agonists, blocking irritant quate analgesia and sedation and undertaking steps to
receptors and bronchodilation of larger airways. 136 prevent accidental extubation are similar to those for
Corticosteroids decrease airway inflammation, enhancing adults. Specific considerations for ventilating infants and
the β 2 -agonists’ effects, and reduce mucus production. children include:
Oral and intravenous methods of administration are l Most children are oxygenated before, during and after
similarly efficacious. The effects of systemic steroids are suctioning with 100% O 2 . 144 The child’s clinical status
apparent within 3–4 hours of administration, with is monitored throughout the procedure.
maximal benefit achieved within 6–12 hours. There is l Heated humidification is preferred in children as they
little evidence to support giving inhaled steroids during have limited respiratory reserve and are prone to
an acute episode. 137 airway blockage. 145,146
Magnesium sulphate promotes smo3oth muscle relax- l Endotracheal suctioning does not require normal
147-149
ation by inhibiting uptake of calcium. Intravenous mag- saline instillations.
nesium sulfate has demonstrated efficacy in acute severe l To prevent iatrogenic atelectasis, the suction catheter
asthma and inhaled magnesium sulphate combined with size should be less than or equal to two-thirds the
a β 2 -agonist results in improved pulmonary function. 135 internal diameter of the ETT. Suction pressure should
be limited to −60 mmHg (−8 kPa) for infants, and
Aminophylline has shown some benefit in regards to up to −200 mmHg (−27 kPa) for adolescents. A
improved lung function in severe asthma that is suction regulator is useful to monitor the amount of

694 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

applied negative pressure, as too much can result in Non-invasive Ventilation
atelectasis. Non-invasive ventilation (NIV) refers to ventilatory
l Restraints may be required to limit the movement of support without an artificial airway in the trachea (see
the child, with the aim of preventing accidental extu- Chapter 15). In critically ill children with respiratory
bation rather than maintaining the child in an immo- failure, NIV may be used to reduce the need for intuba-
bile state. Restraints may be physical, such as arm tion. However, the evidence for its use in children is
boards or hand ties; or chemical, such as sedation. weak 152 and often extrapolated from adults. 153 Some
Accidental extubation is a medical emergency.
studies showed that NIV decreases the rate of ventilator-
MODES OF VENTILATION associated pneumonia and reduces oxygen requirement
in children with lower airway diseases when compared to
There are many modes of ventilation (see Chapter 15 for conventional ventilation 140,154 and may be recommended
more details). This section includes information specifi- as the first line ventilation strategy. 142
cally related to paediatric ventilation. As with adults, arte-
rial blood gases should be taken about 15–20 minutes High-frequency Oscillatory Ventilation
after initiating mechanical ventilation.
High-frequency oscillatory ventilation (HFOV) uses
Volume Ventilation of Children supra-physiological ventilatory rates and tidal volumes
Typically, volume ventilation is not used in infants under less than anatomical dead space to accomplish gas
exchange. Typical ventilator rates are 3–15 Hz or 180–
5 kg due to the small tidal volumes, which risk being 600 breaths/min (1 Hz = 60 breaths). HFOV is primarily
lost in the distensible tubing and leaking around the used in managing infants and children with diffuse alveo-
ETT. In addition, most volume ventilators do not have lar or interstitial disease requiring high peak distending
a constant fresh gas flow, so the infant has to work pressures. Goals include maximising alveolar recruit-
harder to trigger a breath. Some of the newer models of ment, minimising barotrauma and providing adequate
ventilator have attempted to overcome these problems. alveolar gas exchange.
Steps in beginning volume ventilation for a child are as
follows: 150 HFOV is delivered primarily by the Sensor Medics 3100A
(Mayo Healthcare Australia). This ventilator uses a dia-
1. Set the tidal volume at <8 mL/kg. This is a protec- phragm piston unit to actively move gas into and out of
tive lung strategy approach and can be increased the lung, and requires a non-compliant breathing circuit.
151
if needed. A major difference between HFOV and other forms of
2. Set the rate at 20 breaths/min. This is lower than ventilation is that there is active expiration with oscilla-
physiological norm for infants, but the slightly tion versus passive expiration for conventional ventila-
larger tidal volumes will compensate. tion. 150,155 Unlike conventional ventilation, which uses
3. Set the FiO 2 at <0.6 and titrate according to oxygen bulk flow to deliver gas to the lungs, using smaller-than-
saturation and blood gases. dead-space tidal volumes utilises the mechanisms of pen-
4. Set the PEEP at 5 cm. This is slightly higher than delluft, Taylor dispersion, asymmetrical velocity profiles,
physiological norm. cardiogenic mixing and, to a very limited extent, bulk
5. Set the trigger sensitive enough to allow the infant flow. 155 These are all terms used to describe the distribu-
or child to trigger a breath without working too tion of gas when rapid rates and tiny volumes are used.
hard. If a continuous fresh gas flow is available,
then this is preferable. If autocycling occurs, gradu- Ventilation is dependent on amplitude (a determinant of
ally decrease the trigger-setting sensitivity until the tidal volume) much more than rate. With the Sensor
autocycling stops. Medics oscillator, paradoxically lowering frequency (Hz)
improves CO 2 removal. This is thought to occur because
Pressure Ventilation of Children the oscillating diaphragm is able to move through a
The pressure ventilation mode is most commonly used greater distance, thus increasing tidal volume by provid-
ing more inspiratory time and a longer expiratory time.
155
in infants weighing under 5 kg or with children who have
a large leak around the ETT. Steps in beginning pressure The principal determinants of oxygenation are the same
ventilation for a child are as follows and should be based as those for conventional ventilation. Therefore, as with
on arterial blood gases: 150 conventional ventilation, the alveoli must be opened and
prevented from collapsing if hypoxaemia is to be cor-
1. Set the peak inspiratory pressure (PIP) at rected. HFOV achieves this through delivering a high
18–20 cmH 2 O. mean airway pressure without imposing a large tidal
2. Set the positive end expiratory pressure (PEEP) at volume. It thus avoids overdistension and the risk of
150
5 cmH 2 O. barotrauma.
3. Set the rate at 20 breaths/min.
4. Set the FiO 2 at <0.6 and titrate according to oxygen
saturation and blood gases. Extracorporeal Membrane Oxygenation
5. Set the trigger sensitive enough to trigger a breath. Extracorporeal membrane oxygenation (ECMO) is an
Most pressure ventilators have a constant fresh gas alternative method of providing ventilatory and/or
flow, which allows the child to breathe spontane- cardiac support. When used to support ventilation,
ously without increased effort. ECMO allows the lungs to rest and heal.

Paediatric Considerations in Critical Care 695

Ventilation settings are reduced to minimal to minimise
the iatrogenic effects of positive pressure. 156,157 There are TABLE 25.7 Organisms causing sepsis in newborns,
two main methods of ECMO: veno-venous and venoarte- infants and children
rial. In veno-venous ECMO, large-bore cannulas are
placed in large veins, such as the internal jugular or Age group Common organisms causing sepsis
femoral. 158 The more common form of ECMO in paedi-
atrics, venoarterial, utilises the right internal jugular to Newborns Group B beta-haemolytic streptococci
Enterobacteriaceae (such as E. coli)
drain blood and the right common carotid artery for Listeria monocytogenes
blood return. 158 Alternative placement of cannulas for Herpes simplex virus
venoarterial ECMO after heart surgery is the right atrium Staphylococcus aureus
and aorta. Venoarterial ECMO allows support of both Neisseria meningitidis
circulation and ventilation. Essentially, blood is drained Infants Haemophilus influenzae
from the ‘venous’ line, pumped through a membrane to Streptococcus pneumoniae
oxygenate the blood and remove CO 2 , then returned Staphylococcus aureus
Neisseria meningitidis
through a filter via the ‘arterial’ cannula. 158
Children Staphylococcus aureus
Children are considered for ECMO if they have poten- Neisseria meningitidis
tially reversible lung or cardiac injury, or shock that has Streptococcus pneumoniae
not responded to conventional therapies. 159-161 Contrain- Enterobacteriaceae
dications include irreversible brain or CNS injury, Adapted from (164, 165, 172).
immunodeficiency or severe coagulopathy. Outcomes are
generally positive, but ECMO centres need to maintain
their competence by performing the procedure often.
CLINICAL MANIFESTATIONS
There are many similarities between children and adults
THE CHILD EXPERIENCING SHOCK in the clinical manifestations of shock (see Chapter 21).

Mortality rate for septic shock in children is reported However, there are three major differences: 163
162
at around 9%. A detailed description of shock is 1. Children with systemic inflammatory response
given in Chapter 21, with specific paediatric consider- syndrome have either abnormal temperature or
ations addressed here. Hypovolaemic, cardiogenic and elevated white cell count (or both) plus either
septic shock (also termed distributive shock) are the abnormal heart rate or elevated respiratory rate
most common types of shock in children. Cardiogenic (or both).
shock is rare and is seen mainly after open-heart surgery 2. In addition to the symptoms of cardiovascular
and severe myocarditis or untreated shock. The infant dysfunction seen in adults, children may also
with an undiagnosed congenital heart defect, in par- present with a normal blood pressure with no
ticular lesions that rely on the ductus arteriosis – known inotrope requirements, but have two of the fol-
as duct-dependent lesions – can present in shock. 162 lowing: unexplained metabolic acidosis, increased
As infants and children presenting in hypovolaemic lactate, oliguria, prolonged capillary refill time,
shock are likely to respond to fluid resuscitation alone, or core to peripheral temperature gap >3°C.
they may not require transfer to a specialist paediatric 3. Systemic hypotension is not necessary to make the
centre. However, children presenting with septic shock diagnosis of septic shock.
or cardiogenic shock will require transfer to a specialist
paediatric centre for ongoing management, and contact Other specific factors for children that are not relevant in
should be made to initiate goal-directed therapy as the adult population include a higher risk of sepsis in
soon as possible. Those children who do not respond preterm infants and in infants with cardiac defects or
162
to fluid volume alone will require invasive haemody- chronic lung disease.
namic monitoring and possible pharmacological inter-
vention. The development of shock in a hypovolaemic PATIENT ASSESSMENT AND DIAGNOSTIC
patient is considered to indicate losses of at least Assessment of the child with shock is based on clinical
30 mL/kg. 162 assessment, not on chemical test as recommended in
adult shock. 162 Ideally, shock should be diagnosed
Septic shock was responsible for about 8% of all deaths before hypotension occurs. Hypothermia or hyperther-
of children in Australian and New Zealand ICUs in mia and altered neurological status, which provides
4
2008. Causes of septic shock in infants and children are information about perfusion pressure and peripheral
often different from those in adolescents and adults. The vasodilation (warm shock) or vasoconstriction with
commonest infecting organisms are often age-related in capillary refill >2 sec (cold shock) are clinical signs of
children, and are listed in Table 25.7. Infants and chil- shock in children. 162
dren with either congenital or acquired immunocom-
16
promise are at greater risk of developing septic shock. Careful respiratory and cardiovascular assessment is
Meningococcal sepsis remains the leading cause of septic required, as described in this chapter and Chapters 9 and
shock in developed countries such as Australia and New 13. Monitoring of children experiencing shock is the
Zealand. same as for adults (see Chapter 21). It consists of

696 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

conti nuous monitoring of heart rate, SvO 2 saturation, vasopressors are recommended. 162 Inotropic drugs that
quality of peripheral pulses, capillary refill, level of con- are recommended in children include dopamine, adre-
sciousness, peripheral skin temperature, urine output as naline and noradrenaline. Vasodilators, including sodium
indirect measures of cardiac output (CO) as well as serial nitroprusside or nitroglycerin, are used to recruit micro-
blood gas and electrolyte analysis. 162 circulation; type III phosphodiesterase inhibitors are used
to improve cardiac contractility. If shock persists and
Diagnosis of septic shock can be difficult in children.
When present, non-blanching rash is a specific sign of there is a risk for adrenal insufficiency, hydrocortisone
162
meningococcal septicaemia. 166 therapy is recommended. ECMO may also be consid-
ered for a child who appears to be developing irreversible
shock. 162
Practice tip Monitoring of blood glucose is essential in all critically
ill infants and children. In septic shock hyperglycaemia
As rash may be less visible in dark-skinned children, check soles may be present, which has been linked to higher mortal-
162
of feet, palms of hands and conjunctivae in those children. ity rates in paediatric septic shock. Blood glucose
should be monitored and maintained within normal
ranges (80–150 mg/dL) with appropriate use of insulin
However, a certain proportion of children will present and glucose administration. 104,162
with non-specific symptoms or signs of infection, such as
fever, vomiting, lethargy, irritability, or headache and the THE CHILD EXPERIENCING ACUTE
conditions may be difficult to distinguish from other
infections. 14,15,166 Laboratory testing of samples of blood, NEUROLOGICAL DYSFUNCTION
urine, stool, sputum, cerebrospinal fluid and any obvious There are many reasons why an infant or child can present
wounds or lesions is standard practice in adults and with an acute episode of neurological dysfunction.
children. Common presentations to an ICU include meningi-
tis, 173,174 encephalitis, 174 seizures and encephalopathy 175-177
MANAGEMENT OF SHOCK (see also Chapter 17). Assessment and recognition of the
Early recognition of shock, institution of appropriate clinical features and management of the various causes
goal-directed therapy and targeting the causative agent of neurological dysfunction in children are the keys to
remain the mainstay of managing septic shock in chil- achieving good outcomes.
dren as in adults. Goal-directed therapies such as oxygen
therapy, fluid resuscitation, maintenance of acceptable NEUROLOGICAL ASSESSMENT
blood pressure, and institution of pharmacological treat- To assess a child’s level of consciousness, several different
ment and other supportive treatments to achieve thera- scales can be used. The Glasgow Coma Scale (GCS) is
peutic goals are practised in managing shock in children, commonly used, 178 but the Glasgow Coma Motor sub-
and are linked to better outcomes. 162,163
score is more appropriate for children. 179 Another reliable
Large amounts of fluid may be required by children scale is the Full Outline of Unresponsiveness (FOUR)
16
despite peripheral oedema or absence of overt fluid loss. score; it includes four parameters (eye response, motor
Early aggressive fluid resuscitation will improve survival response, pupil reflexes, and breathing) rated on a 0 to 4
in children with hypovolaemic and septic shock, particu- scale, giving a possible score situated between 0 (com-
larly if received within the first hour, when hypotension pletely unresponsive) and 16. 180 The FOUR score and
19
has not yet developed. Intravascular access in children the GCS are both able to predict in-hospital morbidity
can be difficult and umbilical venous access in newborns and poor outcome at the end of hospitalisation.
and intraosseous access in children can be used before Other neurological assessment parameters include:
®
the placement of central lines. 162,167 The use of the EZ-IO
(Vidacare Corporations, Texas) paediatric intraosseous l Pupils: assess size, reaction and symmetry.
needle set and driver system has become common in l Posture: abnormal flexion posturing, often referred to
practice. 168,169 Other kinds of manually inserted intraos- as decorticate posturing, is a flexion response of the
seous needles are available, and regardless of type, intraos- arms with either flexion or extension of the legs, while
seous needles all allow rapid access to the intramedullary abnormal extension posturing, often referred to as
capillary network, facilitating delivery of fluids, drugs and decerebrate posturing, is an extension response of all
blood products. The site of choice in infants and children limbs, where arms rotate externally. Both abnormal
is the proximal tibia, 2–3 cm below the tibial tuberos- flexion and extension posturing in a previously normal
170
ity. Once sited, a syringe must be attached to aspirate child may indicate raised intracranial pressure.
and ascertain correct placement. Fluid boluses can then l Meningism: this is indicated by neck stiffness in a
be given via syringe into the intramedullary space with child and full/bulging fontanelle in an infant.
the aim of restoring circulating volume which will in turn
facilitate venous access with improvement of peripheral SEIZURES
perfusion. 171
Seizures are covered in Chapter 17. The various aetiolo-
Similarly to adults, after appropriate volume resuscitation gies of seizures in children include febrile convulsions,
has been given and symptoms of shock are not resolving CNS infection such as meningitis or encephalitis, meta-
or hypotension is developing, then inotropes and bolic imbalances, drugs, trauma or epilepsy. Seizures in

Paediatric Considerations in Critical Care 697

189
children are common, with about 4–10% of children 66% of disease. There are two main peaks of disease.
181
having an unprovoked seizure without recurrence. The 0–4-years age group represents 31% of all cases and
Children between the ages of six months and six years are with 17% occurring in the 15–19-years age group. 189 The
more likely to develop seizures. 182 Children, particularly incidence of meningococcal disease in children aged 0–4
those under five years, are at higher risk, as the developing years is 10/100,000. Of children with invasive meningo-
181
brain has a lower threshold for seizures. Febrile convul- coccal disease, 47% have meningitis, with or without
sions occur in 2–5% of children, commonly between the sepsis. 190,191 The mortality rate of meningococcal menin-
183
ages of 6 and 60 months. Non-febrile seizures are typi- gitis in children under five years of age is below 1%; with
cally more common in the neonatal period, with the sepsis present, the rate increases up to 10–15%.
incidence falling with age. 182
The incidence of invasive pneumococcal disease (IPD)
Management has significantly dropped since the introduction of
routine vaccination, with a reported rate of 23.4 cases per
Management of the paediatric patient with seizures is 100,000 children aged less than five years in 2005. The
192
similar to management of the adult (see Chapter 17), but highest peak of IPD is seen in children aged one year with
there are some specific paediatric considerations. The a rate fluctuating between 26.5, 37 and 51/100,000 in
paediatric patient who is suffering seizures is more sus- Australia, North America and Europe, respectively. 193-196
ceptible than an adult to hypoglycaemia. Hypoglycaemia The highest Australian incidence occurs in the Northern
may lead to secondary brain injury during and after sei- Territory, with Indigenous children at highest risk. 197
zures. Blood sugar levels should always be checked in Other risk factors include extreme prematurity, chronic
children suffering from seizures and intravenous fluids lung disease, trisomy 21 (Down syndrome), diabetes and
containing glucose administered. 182,184 cystic fibrosis. Clinical manifestations or symptoms vary
The care of the seizing or post-ictal child is generally sup- with the age of the child, duration of the illness and
portive and includes monitoring for signs of ongoing history of antibiotic use for the current illness. These are
seizures, administration of appropriate anticonvulsants, outlined in Table 25.8.
and regular assessment of neurological function. In young
infants, seizures may be difficult to determine and may Management
include stiffening, staring and lip smacking rather than Initial management of the infant or child with meningitis
obvious clonic activity. 185,186 includes assessment and management of the airway,
breathing, circulation and disability. Once the initial
MENINGITIS resuscitation has been completed, consideration should
Meningitis is an acute inflammation of the meninges be given to correcting any biochemical abnormalities. In
that usually develops over 1–2 days. A fulminant form of particular, blood sugar level should be checked and
meningitis caused by Neisseria meningitidis or meningo- corrected in the early management phase. Once menin-
coccal disease may develop over several hours. Organisms gitis is suspected, a lumbar puncture (LP) is generally
causing bacterial meningitis vary by age group. In infants performed to confirm diagnosis, but if the child is hae-
under three months of age, group b Streptococcus, E. coli, modynamically unstable or has ongoing seizures, prob-
Streptococcus pneumoniae and Listeria are the most likely lems with ventilation or signs of raised intracranial
agents. In children over three months of age meningococ- pressure, the LP should be delayed and blood cultures
166,199
cus, Haemophilus influenzae type b and Streptococcus pneu- obtained.
moniae are more common. 172 The most common causes Steroid use in meningitis has some benefit in reducing
of viral meningitis in infants and children include herpes morbidity in adults, 195 but not in children. However, it
200
simplex virus and the enteroviruses. 187 Tuberculous men- was shown to reduce the risk of severe hearing loss in
ingitis, while still rare, is becoming more common, par- children with bacterial meningitis. 201
ticularly in immigrant families or those with recent travel
to affected areas. Bacterial meningitis continues to have
a poorer outcome than other forms of meningitis, despite TABLE 25.8 Symptoms of meningitis in infants
advances in therapy. 188 and children

Incidence Infants under 3 Infants over 3 months
Data on the incidence of meningitis in Australia is limited months and children
to the major bacterial types, particularly for infants and l Hypothermia or fever l Fever
children over two months of age. Hib, meningococcal l Irritability or lethargy l Headache
and pneumococcal infections are all notifiable. Since the l High-pitched cry l Photophobia
introduction of the Hib vaccine in1993, Hib infection has l Seizures l Kernig’s sign (inability to extend leg)
fallen to 1.2/100,000 in 2005. 189 Of all reports of infec- l Apnoea l Brudzinski’s sign (flexion of hip and
knee in response to neck flexion)
tion only 28% were meningitis, and the majority of infec- l Poor feeding and/or l Lethargy or irritability
vomiting
tions were in children under two years of age. 189 l Nausea and vomiting
l Seizures and neck stiffness
Meningococcus is the main cause of meningitis in chil- l Confusion and coma occurring at a
dren. It occurs seasonally, with the main peak in Australia fairly late stage
between June and October. Serogroups A, B and C account
for 90% of cases in Australia, with serogroup B causing Adapted from (190, 198).

698 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Infants and children with meningitis require intensive is relatively rare in critically ill children, the incidence of
care management when there is a reduced level of con- renal impairment secondary to the underlying illness is
sciousness, respiratory and/or circulatory compromise. recognised increasingly in children, although a paucity
The broad aims of management are to support ventila- of prospective studies remains problematic. The total
tion and circulation, while preventing secondary brain incidence of ARF in PICU is currently between 4.5% and
injury. Regular assessment and monitoring of associated 10%. 210,211 Diagnoses associated with primary ARF in
risks such as seizures, syndrome of inappropriate antidi- children are haemolytic uraemic syndrome, oncological
uretic hormone secretion (SIADH) or cerebral salt wasting diagnoses and following congenital cardiac surgery. 210,212
and sepsis is essential. The RIFLE criteria used to describe kidney injury in
211
adults (see Chapter 18) also applies to children. Both
ENCEPHALITIS primary and acquired kidney injury in children are asso-
The most common type of encephalitis in children is ciated with increased length of stay and increased mor-
acute viral encephalitis, and the causative agent is usually tality. Consequently, continuous renal replacement
202
herpes symplex virus (HSV). Left untreated, HSV is therapy (CRRT) should be considered earlier in manage-
almost uniformly fatal, with over half of survivors expe- ment than has previously been the case. Critically ill
riencing significant long-term morbidity. 174,203-205 Other children experiencing, or at risk of developing, acute
causes of encephalitis in children include: renal failure will benefit from prompt transfer to spe-
cialty PICU.
l enteroviruses (e.g. enterovirus 71, coxsackievirus,
polio and echovirus) The child’s GIT will need protection from developing GIT
l varicella zoster virus ulceration and bleeding in critical illness. A potentially
l Epstein-Barr virus fatal complication, stress ulceration and bleeding, has a
l cytomegalovirus current incidence of around 10% in critically ill chil-
213
l adenovirus dren. Clinically significant bleeding that causes haemo-
l rubella dynamic instability or the need for transfusion is reported
213
l measles in about 1.6% of children in PICU. The same treat-
l Murray Valley encephalitis (MVE) virus ments can be used in both children and adults, with no
l Kunjin virus. one agent, dose or regimen standing out as better for
minimising bleeding and ulceration or leading to fewer
The incidence of acute encephalitis is over 10 cases per complications such as pneumonia. 213
206
100,000 children. Children under one year of age are
at higher risk of developing encephalitis. Other risk NUTRITIONAL CONSIDERATIONS
factors include immune dysfunction and exposure to risk
animals, or specific geographic location. For example, The aims of nutrition in critically ill children are two-fold.
Murray Valley encephalitis and Kunjin viruses are endemic First, children are at particular risk of malnutrition because
in the Kimberley region of the Northern Territory, and they are growing, have greater energy requ irements for
Japanese B virus has been reported on Cape York Penin- their weight and less storage capacity than adults. Second,
sula; it is endemic in southeast Asia. 207 children are at particular risk of developing protein–
calorie malnutrition, which can lead to immunodysfunc-
Encephalitis symptoms are similar to meningitis, but tion, increased risk of infections, morbidity and death in
often with a much slower onset. Progressively worsening those children with organ dysfunction. 214
headache, fever and decreased level of consciousness or
behavioural changes characterise encephalitis. Focal neu- In addition, nutrition is important to maintain gut
rological signs and seizures may indicate involvement of mucosa integrity, prevent the development of hypo- and
the meninges or spinal cord. 208 hyperglycaemia, assist with maintenance of immune
function and in modulating the immune response as well
214
Management as providing energy. One barrier to achieving adequate
nutrition for critically ill children is the fluid restrictions
Prompt administration of aciclovir, if HSV is the sus- that are routine practice in the ICU, so liberalising fluids
pected cause, is warranted due to high mortality and where possible for enteral nutrition to be maximised
morbidity rates. Other viruses are also treated with aci- should be considered.
clovir. Ganciclovir is useful for resistant organisms, but
is more toxic. 208,209 Intensive care management involves When caring for critically ill infants and children, nutri-
supporting ventilation and managing neurological com- tion to support growth needs to be considered. Ideally,
plications such as seizures and cerebral oedema. If the enteral feeding of critically ill children should commence
child is unconscious on presentation, the disease course within 12–24 hours of admission to ICU, but may not
will be more severe. 203 be achievable until the child is transferred to a specialist
centre. It may not be appropriate to commence feeds if
GASTROINTESTINAL AND RENAL the child will require transfer, surgery or intubation. A
CONSIDERATIONS IN CHILDREN dietician should be consulted to advise on appropriate
enteral feeding formulas for children, in addition to orga-
Many critically ill infants and children are also at risk of nising caloric supplementation of feeds. The dietician can
developing complications involving the gastrointestinal advise on handling of human milk while in hospital for
tract (GIT). Although primary acute renal failure (ARF) breastfeeding mothers, who will need to express milk

Paediatric Considerations in Critical Care 699

when the infant is not yet feeding orally or to provide concentration is increased to at least 5% and up to 10%.
milk for tube feeding. In addition, dieticians can assess The addition of potassium chloride into maintenance
the child’s energy requirements and the amount of feed fluids is common, particularly in fasting children, and
required to meet needs. requires serial monitoring of serum potassium. For fluid
resuscitation in infants and children, the use of glucose
Other recent studies have found a reduction in nosoco-
mial infections in children when enteral feeds have been containing IV fluids is contraindicated, and 0.9% sodium
used; transpyloric tube feeding versus gastric feeding and chloride is the resuscitation fluid of choice across the life
nutritional support teams result in improved nutritional span, including in the delivery suite for newborn fluid
delivery and enhanced enteral feeding rates in critically resuscitation.
ill children. 215-218 Glucose Control in Children

Supplements and Feeding Hyperglycaemia is associated with a worse outcome in
221
Whilst promising work has been undertaken in adult infants and children requiring ICU admission, however,
critical care with the supplementation of feeds and total the predisposition to hypoglycaemia in children has
parenteral nutrition (TPN) with supplements including meant that aggressive treatment of hyperglycaemia is not
amino acids such as L-arginine, glutamine, taurine, nucle- yet commonplace in critically ill children as it has been
otides, omega-3 and omega-6 fatty acids, carnitine, anti- in adults in ICU. Hypoglycaemia is documented to occur
oxidants, prebiotics and probiotics, the same outcomes more frequently in two groups of nondiabetic children:
have not been reproduced in children to date. The evi- those requiring mechanical ventilation and those requir-
214
222
dence for additives in enteral feeding is not clearcut in ing inotropic support. In the study cited here, hypogly-
children and therefore routine supplementation for criti- caemia was an independent predictor of increased
cally ill infants and children is not common practice. mortality. While studies are yet to recommend tight
glucose control in the paediatric population, monitoring
Intravenous Therapy for Children for hypoglycaemia continues to be an important assess-
Until enteral feeding is established, critically ill infants ment parameter, particularly in sicker children who
require ventilatory support, inotropic support and where
and children will require maintenance IV fluids. Tradi- enteral feeding may be contraindicated. Hypoglycaemia
tionally, hypotonic fluids – fluids containing a concentra- may be an indicator of worsening organ function, there-
tion of sodium lower than normal serum sodium – have fore further research needs to focus on the safety of
been administered as maintenance fluids. These included insulin therapy in the nondiabetic critically ill child
the hypotonic formulation of 0.225% sodium chloride before aggressive management of hyperglycaemia can be
with 3.75% glucose. Over the past decade this formu- recommended. 222
lation has largely been replaced with 0.45% sodium
chloride and 2.5% glucose as iatragenic hyponatraemia LIVER DISEASE IN CHILDREN
has been observed in otherwise-well children having Liver failure is relatively rare in children. It often arises as
surgery. 219,220 It has been common paediatric practice to a primary problem in children from countries where viral
use only 500 mL IV bags in children for safety reasons. hepatitis is endemic, is associated with paracetamol over-
In the modern era across westernised countries, use of dose, and chronic liver disorders, toxins, autoimmune
volumetric IV pumps and burettes have also been stan- disease, malignancies, vascular and biliary tree malforma-
dard paediatric practice, although changes to larger tions as well as unidentified causes. 223 Chapter 19 con-
volumes of IV formulations for children will need to be tains more detail on liver function and dysfunction. There
closely monitored.
are varying severities and forms of liver failure. Infants
The use of hypotonic fluids is under review in many and children experiencing fulminant hepatic failure and
countries, and changes underway in Australia will see hepatic encephalopathy, regardless of underlying cause,
500 mL bags of IV fluids change to 1000 mL bags in all are critically ill, and require transfer to a specialist PICU
children’s hospitals, with increased level of monitoring for ongoing management and possible liver transplanta-
of weight and serum electrolytes recommended. Hypo- tion. Mortality rate is strongly linked with the develop-
tonic fluids are implicated in hospital-acquired hypona- ment of cerebral oedema and intracranial hypertension,
traemia 219,220 and for critically ill children, the capacity to and is reported to be as high as 50% where cerebral
excrete additional free water is often impaired. In addi- oedema occurs. 224 Many critically ill infants and children
tion, a number of common conditions seen in the ICU are at risk of developing some degree of liver dysfunction;
increase secretion of antidiuretic hormone (ADH), therefore, liver function of all critically ill children requires
including pain, nausea and infections of the CNS, the careful monitoring and management. Clinical manifesta-
GIT, the lung and post surgery, thus promoting the reten- tions and management of infants and children with liver
tion of water. The risk of developing cerebral oedema failure are similar to those of adults.
220
is increased in children, who also have an increased body
tissue water content and studies indicate that there is an In summary, the mainstay of management in children
increased risk of developing acute hyponatraemia leading with fulminant liver failure is liver transplantation. All
to seizures. children with fulminant disease should be transferred
to a paediatric centre as soon as the diagnosis of liver
Infants and children generally require added glucose in failure is made. Children are at particular risk of develop-
IV fluids. In infants under three months, glucose ing protein–calorie malnutrition, which can lead to

700 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

immuno dysfunction, increased risk of infections, mor- Immersions are another leading cause of death in chil-
bidity and death in children with organ dysfunction. 214 dren 0–4 years of age, with around 29% of near-drownings
in Australia in this age group, peaking in the summer
PAEDIATRIC TRAUMA months. Boys outnumber girls, with two-thirds being
boys. Infants are more likely to drown in the bath,
Trauma is the leading cause of death in children and 1–3-year-olds are most likely to drown in a backyard
young adults in all developed countries; in the develop- swimming pool and older children drown in open water-
ing world it is second only to deaths from infections. 4,225 ways such as dams and rivers. In Australia, in 2008–2009
The approach to management of trauma in children is there were a total of 302 deaths from drowning, including
the same as in adults. For further details on trauma 50 children. This figure has increased over the previous
systems and trauma management, see Chapter 23. While five years. 230
there has been some evidence from North America that
specialist paediatric trauma centres produce better out- Homicide and assault of children remains low in Australia
231
comes for children suffering traumatic injuries, the when compared with other developed economies,
23
largely spread-out and relatively small population distri- however it is listed as the third-leading cause of death
bution in Australia and New Zealand means that children from injury in children. 1,231,232 Spinal injury rates for chil-
will often need to be treated initially in adult settings. 4 dren are reportedly low at around 1% but are associated
with significant mortality and disability. Paediatric
233
INCIDENCE AND PATTERNS OF INJURY spinal injury statistics in Australia and New Zealand are
IN CHILDREN not currently reported, as current reporting only captures
3
Across Australia in 2007–2008 almost 68,000 children patients cared for in dedicated adult spinal units,
were hospitalised as the result of injury, accounting for however, the incidence is considered to be low, as it does
12% of all paediatric admissions, with 15% of all chil- not feature in the annual report of the Australian and New
4
dren’s deaths attributable to injury. 3,225 In 2008, injury Zealand Paediatric Intensive Care (ANZPIC) Registry.
accounted for around 7.1% of paediatric admissions to
Australian and New Zealand ICUs, with a 4.8% mortality RISK FACTORS
rate, accounting for 29% of all deaths in ICUs in the The kinetic forces involved in injury are associated with
1–15-years age group. 4 a more diffuse injury pattern and a greater incidence of
multiple trauma in children, as more of the child’s body
Injury patterns in children differ from adults, with 227
traumatic brain injury, blunt trauma and more diffuse is subjected to the traumatic forces. Children generally
injuries more common in children. There is a bimodal have less subcutaneous fat and musculature, providing
injury pattern associated with age, with peak incidence less protection to the liver, kidneys, and spleen, leading
occurring in children aged 1–4 years and a second peak to a higher incidence of lung contusions and abdominal
234
during adolescence and young adulthood, reflecting the trauma. In addition, the relatively large head size of the
different activities associated with each group. 1,226 Infants infant, particularly, and the child leads to a high inci-
227
and young children have a decreased sense of danger and dence of head injury.
reduced ability to protect themselves, while adolescents
have increased exposure to higher risk activities in con- Primary Survey and Resuscitation
junction with exposure to alcohol, drugs and motor vehi- Initial stabilisation of children who have experienced a
cles. 227,228 Children who live in regional and rural areas traumatic injury is likely to have occurred in the field.
have increased rates of traumatic injuries and deaths from Once at the hospital, the primary survey is conducted
trauma, as do children from lower socioeconomic back- to assess for, detect and stabilise the child with life-
grounds. The same pattern is reflected in Australian and threatening injuries. Undertaking a primary survey and
New Zealand statistics. 225,229 Time of day and seasonal resuscitation uses the same structured approach in chil-
factors play a role in childhood injury, with children dren and adults. Chapters 22 and 23 cover emergency
more likely to be injured between 3pm and 5pm, coincid- presentations and trauma management, however, specific
ing with the end of the school day, and during summer paediatric considerations are highlighted below.
months, where the incidence of submersion injuries Children sustaining trauma to the head, just as adults, are
increases. 5,226,230
managed with cervical spine precautions including a
Injury-related deaths in children are highest in the trans- collar, until the spine has been radiologically and clini-
port deaths category, followed by immersion and assault. cally cleared. 9,233 A selection of paediatric hard collars
1
Motor vehicle accidents involving children as passengers, should be available and the measuring guide used to
pedestrians or cyclists are the commonest cause of injury ensure good fit. As the collar can cause neck flexion in
in Australian children, with driveway injuries involving infants and small children, the child’s torso may need to
four-wheel drive or light commercial vehicles more likely be elevated with a folded blanket to maintain a neutral
19
to be fatal. 225 Trauma associated with the use of all terrain neck position. The head and neck are usually immobil-
vehicles such as quad bikes are becoming increasingly ised, with head blocks (e.g. rolled towels) placed either
common, particularly in rural areas. 228,229 For children side of the head to maintain in-line stabilisation and
under 14, falling from one level to another, such as falling tapes applied to the forehead and chin to prevent move-
from a window, was the most common form of falls- ment. The combative, uncooperative child will not toler-
related injury. 231 ate this, and the actions are likely to increase the child’s

Paediatric Considerations in Critical Care 701

23
agitation and movement. The critical care nurse can posi- number of head injuries of any age group. TBI is often
tion themselves to maintain in-line stabilisation while associated with MVA where the child is a vehicle occu-
talking and soothing the child, or ideally where parents pant, a pedestrian or a cyclist, with falls and with near-
are present, seek their assistance to console their child. drowning. TBI is described in detail in Chapter 17.
Specific paediatric trauma boards are available that are In 2008, 273 children were admitted to Australian and
designed to maintain the child’s head in a neutral New Zealand ICUs with a diagnosis of head trauma.
position.
About 10% of all children aged 1–15 years of age who
Fluid resuscitation is a controversial area of practice in died in Australasian ICUs had sustained a traumatic brain
4
paediatric trauma, where therapies have been generally injury. Age and gender are the most significant risk
less-well-studied than in adults. Current recommenda- factors for TBI, with peak incidence in the 0–4-years
tions from the Advanced Paediatric Life Support Group group and in males. 237,238 Other factors to consider in
indicate that fluid boluses should be given initially in children are the increased tendency of the immature
10 mL/kg amounts until uncontrolled bleeding has been brain of children to experience disruption of the blood–
15
assessed for and ruled out. However, in a child with a brain barrier and, unlike adults, for an increased cerebral
traumatic brain injury at risk of secondary brain injury blood volume to lead to cerebral oedema due to higher
from hypotension, this more conservative approach may brain water content. 11
not be appropriate. Where more than 20 mL/kg is
required, immediate surgical assessment for bleeding is In 2003, the Society of Critical Care Medicine published
indicated. 15 guidelines on the management of paediatric brain injury,
however little paediatric research evidence underpinned
Exposure of the child, with temperature control, is neces- these as they were essentially based on extrapolation
sary to assess the child completely for injuries. 234,235 As from adult research evidence and expert opinion. Since
hypothermia can develop quickly in children, overhead the clinical manifestations of TBI in children are very
heating sources and blankets are ideally used to keep the similar to those in adults, management is also very
child warm. Hypothermia in trauma patients is asso- similar. One significant change recommended in the
ciated with increased risk for coagulopathy and mortal- 2003 guidelines was tight control of CO 2 , in recognition
ity, as in adults, so providing warmth is essential of hypocarbia as a major secondary brain injury factor.
236
paediatric trauma nursing care. The child’s right to The practice of hyperventilation should be avoided as it
privacy and dignity should also be considered and expo- is associated with regional cerebral ischaemia. 239
sure minimised.
In terms of assessment, the GCS modified for children
Secondary Survey has previously been described in this book. Indications
for intracranial pressure (ICP) monitoring in children
Undertaking a secondary survey is similar in children and include all infants and children with a severe head injury,
adults and is described in Chapter 22. Specific paediatric which equates to a GCS score of 8 or below that persists
considerations are highlighted below. following adequate cardiopulmonary resusci tation, and
In children, particularly those under one year of age, if those children who present with abnormal motor postur-
237
injuries and the accompanying history do not seem to ing and hypotension. Combined with invasive haemo-
match, non-accidental injury should be considered and dynamic monitoring, targeted therapy to manage both
noted. 226 History should be obtained from the child ICP and CPP remains an important part of treatment.
where possible, from any witnesses to the accident, and While thresholds for treating intracranial hypertension in
ambulance officers if they attended. Parents or caregivers children have not been studied, it has been known since
will provide details of the child’s past medical history, any the 1980s that prolonged intracranial hypertension or
medications and any known allergies. high ICP levels will worsen outcome. An ICP of 20 mmHg
is considered high in children, with 15 mmHg considered
high in infants. ICPs of these values are the usual cut-off
SPECIFIC CONDITIONS points and are likely to be treated with the aim of lower-
Specific injuries that are seen in children are discussed ing ICP while maintaining an adequate CPP. 9,239
briefly under the headings of traumatic brain injury, chest
trauma and abdominal trauma. Obtaining an accurate Diagnostics
history of the accident or events leading up to an injury Diagnostic techniques 240 and clinical management of
is useful in determining the type of injuries that children children with TBI mirror those in adults (see Chapter
241
may have sustained. Regardless of aetiology, where a child 17). The smaller size of children means that diagnostics
has been involved in a motor vehicle accident (MVA) or such as mixed cerebral venous saturation and direct brain
sustained a fall, there are likely to be multiple injuries oxygen saturation are not yet common practice in paedi-
and the situation should be treated as such until other atrics. A high index of suspicion for spinal injuries in
injuries have been considered and excluded. 227 paediatric TBI should be maintained, as spinal cord injury
without radiological abnormality (SCIWORA) on plain
Traumatic Brain Injury X-rays is a feature of paediatric spinal injury. CT scans
233
Traumatic brain injury (TBI) is a leading cause of deaths are available in more centres than MRI, but involves
and injury worldwide in children. In Australia and other radiation exposure to the young spine. Conjecture remains
developed economies, children experience the greatest around CT imaging versus MRI in children. 233

702 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Treatment in children, with less musculature and a more compliant
Several of the therapies used in the treatment of the child ribcage, meaning that there can be injury to underlying
234
with severe head injury are controversial, as they have not organs with no apparent external injury. Blunt trauma
undergone rigorous scientific evaluation. Essentially is common, while penetrating injury is less common,
treatment of TBI in children is identical to adult manage- resulting from gunshot and stab wounds. These injuries
ment: minimising intracranial hypertension, maintaining are associated with older children and adolescents,
optimal CPP while preventing secondary injury from though a thinner body wall may result in greater
hypoxia, hypercarbia, and hypotension while reducing underlying organ damage, particularly if the flank is
234
the risk of iatrogenesis from treatment. Decompressive penetrated.
craniectomy is considered for intractable intracranial During the primary survey, the child’s abdomen should
hypertension to avoid herniation. 235,242 be exposed and may reveal signs such as bruising from
Hypothermia has not yet been shown to make a differ- bicycle handles, tyre marks, abrasions or contusions.
ence in outcome in children, as it has in newborns and Abdominal distension is a less reliable sign in children,
adults with hypoxic-ischaemic brain injury. Moderate as distension may be from air that is swallowed from pain
hypothermia (temperature maintained from 32–34°C) and crying. However, as in adults, the primary survey may
has been studied with disappointing results, 243 thought not include the abdomen if other immediately life-
to be associated with inadequate length of cooling (24 threatening injuries are present, such as thoracic and/or
hours). A multicentre study is planned to commence in head injuries. These injuries will take precedence, so it
the future to provide moderate hypothermia for 76 hours may not be until the secondary survey can be undertaken
with slow controlled rewarming. that abdominal injuries are considered. The monitoring
and management of children sustaining abdominal
Outcomes from traumatic brain injury in children are trauma is very similar to that of adults, 248 and is discussed
associated with the severity of the initial injury and the in Chapter 23.
presence and control of secondary brain injury, as in
adults. Hypotension and hypoxia prehospital admission A number of clinical indicators will determine the
are strongly linked to mortality and poor functional need for a CT scan of the abdomen. These include all
outcome, with some emerging evidence that hyperten- children with multiple injuries, children experiencing
sion in the first 24 hours may also predict poor outcomes pain and tenderness over the abdomen, gross haematuria
at one year post-injury. 244 with a minor injury, children with a haemoglobin
below 100 g/L and children who require fluid resuscita-
Chest Trauma tion with no obvious source of blood loss. Diagnostic
Thoracic injuries in children rarely occur in isolation with peritoneal lavage and FAST sonography are rarely used in
children because of the poor sensitivity of the test to
traumatic injuries and are often accompanied by head and detect the presence of intraabdominal injuries in chil-
neck injuries. There is some evidence that thoracic injuries dren. 249 However, when FAST sonography is combined
are indicative of a more severe injury; they have been with elevated liver transaminases, the sensitivity and
associated with higher mortality. 227 Injury to the heart and specificity of the screening increases to 88% and 98%,
great vessels in particular is associated with higher mortal- respectively. Monitoring of blood in urine is a simple,
250
ity. The combination of head injury and thoracic injury is useful technique to detect bladder and kidney injuries.
also known to have higher mortality. Most chest injuries Management of abdominal trauma generally requires
225
in children are sustained as a consequence of MVAs. The only haemodynamic and laboratory monitoring in con-
pattern of injury in children is predominantly one of junction with supportive therapies such as fluid replace-
blunt trauma. Lung contusions are the commonest tho- ment, monitoring of urine output, and pain management
racic injury seen in children. As the ribcage is much more with the aim of detecting signs of haemorrhage. 14,251
compliant in children, ribs are rarely broken, but they can
damage underlying structures such as the lungs, so pul-
monary contusions, pneumothorax and haemothorax are SUMMARY
often seen. The clinical manifestations, approach to Critically ill infants and children have several anatomical
assessment, monitoring and management of children sus- and physiological differences that predispose them to
taining thoracic trauma is similar to that in adults, and is different types of critical illness when compared to adults.
discussed in Chapter 23. Children with thoracic injuries Children’s relative physiological and psychological imma-
are generally managed in a specialist trauma centre turity means that their needs may be different from adults
equipped to manage children. 245 when critically ill. Family support is important and paren-
tal presence should be allowed at all times. Patterns of
Abdominal Trauma disease may be different from adults; for example, a high
Abdominal trauma in children is a leading cause of death incidence of respiratory illness and a predisposition to
when combined with head injury. 246 Blunt trauma from sustaining multiple trauma, but children have a lower
MVAs is the most common mechanism of injury, but incidence of sepsis, heart failure, liver failure and renal
bicycle handlebars may also inflict a significant injury. 247 failure than adults. The need for specialised nursing and
The liver and spleen are the most commonly injured medical care as well as adapted equipment means that
organs in abdominal trauma and can usually be managed many critically ill children will require transfer to a spe-
non-surgically. The abdominal organs are relatively large cialist paediatric centre.

Paediatric Considerations in Critical Care 703



Case study
Lisa is an eight-year-old girl who was travelling home by car with ventilation para meters, dropping maintenance fluids to half daily
her family at around lunchtime on a Sunday. The car was involved requirements, commencing morphine and midazolam infusions
in a two vehicle high-speed head-on collision at 1:30 pm. Car occu- after ceasing fentanyl and propofol, and commencing transfusion,
pants were Lisa’s uncle (driver), mother (front passenger) Lisa (rear Lisa was transferred by air ambulance to a specialist children’s
driver-side seat) and 10 year old brother (rear passenger side seat). hospital. Lisa’s mother was cleared for discharge, as she had sus-
All passengers were wearing seat belts. The driver was pronounced tained only soft tissue injuries and accompanied Lisa. Lisa’s brother
dead at the scene. required admission to the paediatric ward, with his grandparents
staying with him. The duration of Lisa’s flight was approximately
On arrival in the Emergency Department (ED) of a coastal regional
hospital (located approximately 550 km from the nearest specialist one hour; total time in retrieval almost three hours. Lisa remained
children’s hospitals), the mother was conscious with no obvious stable throughout her retrieval. Her observations on arrival into
−
injuries and the brother had a fractured femur. Lisa had been the PICU were: ABG pH 7.33, PaCO 2 38, PaO 2 225, HCO 3 19.8,
combative in the ambulance in transit, with a decreasing level of BE-5.6, FiO 2 0.48; HR 125, BP 123/54 (MAP 75), SpO 2 100%, T 38.1°C,
consciousness (GCS score dropping to 4), pupils mid-size and BGL 4.0, pupils 3 mm bilaterally and reactive to light; ventilator
non-reactive, possible right-sided focal seizure activity observed respiratory rate 12/min. Lisa was transferred to the operating
in the right arm and hand, a fractured right shaft of femur theatre for placement of two extra ventricular drains (EVD) and
with bruising developing over the right thorax. She was hand- Thomas splint to her right leg. Later that day, she was taken for
ventilated in 100% oxygen by an ambulance officer, with SpO 2 head, spine and abdominal MRIs. Lisa had an inter-spinous liga-
monitor reading 100%. mentous injury at C1–C2 with no cord involvement, but spinal
precautions remained in place.
Lisa was estimated to weigh 30 kg and had a large bore cannula
placed in each antecubetal fossa, was intubated, placed on While in PICU, Lisa’s ICP demonstrated a pattern of slowly increas-
the ventilator, had an orogastric tube inserted, and received two ing pressure at times, rather than sudden sharp spikes. Her cerebral
10 mL/kg intravenous fluid boluses to maintain a mean blood pres- perfusion pressure was rarely compromised at these times. ICP was
sure ≥50 mmHg. Lisa was then given a loading dose of intravenous effectively managed with muscle relaxants, increased sedation,
phenytoin, and a FAST sonography performed to identify intraperi- and infrequent 3% sodium chloride boluses. Temperature control
toneal haemorrhage or pericardial tamponade (result negative). of normothermia was the agreed endpoint for Lisa, with occasional
Once considered to be haemodynamically stable, Lisa was trans- mild rises in temperature (up to 38°C) managed successfully with
ferred for urgent head, neck and chest CT scans. On return to ED, antipyretic therapy.
Lisa had an indwelling catheter (IDC) and a radial arterial line Neurologically, Lisa began responding to painful stimulus prior to
placed. The specialist paediatric retrieval service was then con- retrieval, with pupils becoming equal in size and reacting, thought
tacted to request an urgent transfer to a paediatric trauma centre. to be non-reactive associated with initial seizures on presentation.
ED staff were able to obtain advice from a paediatric surgeon, a Seizures were never observed again, with phenytoin weaned off
paediatric intensivist, and a retrieval consultant via teleconferenc- prior to discharge from hospital. EVD placement facilitated CSF
ing. Advice given was to passively cool Lisa, maintain full spinal drainage, with drains elevated to 5 cm and kept open initially
precautions and provide analgesia. Fentanyl infusion was com- (draining blood-stained CSF for initial 48 hours) with the drain
menced. Lisa had been given stat doses of fentanyl and propofol gradually elevated and then closed, and able to be removed on day
for analgesia and sedation for imaging. 10 post-injury. During her daily sedation and muscle relaxant ‘vaca-
tions’, Lisa’s neurological status was assessed and over the initial
CT scans of Lisa’s head and chest and plain trauma series of limbs,
chest and spine X-rays reveal the following injuries: days in PICU showed responses to pain, then to voice and finally
l diffuse cerebral contusions in frontal, parietal and occipital commands prior to PICU discharge on day 11 post-injury. She had
lobes bilaterally a significant tremor of her right hand.
l diffuse ventricular blood Ventilation was anticipated to be difficult, as Lisa had right-sided
l multiple small bilateral lung contusions of all lobes, nil rib lung contusions. However her ventilation was unremarkable,
fractures though endotracheal secretions remained blood-tinged for some
l comminuted fracture of mid shaft of right femur. days. Lisa was successfully extubated on day 9 post-injury.
A paediatric neurosurgeon reviewed the emailed CT scans. The Lisa’s parents had been separated for some years with shared par-
agreed plan of care while awaiting retrieval to a children’s hospital enting of both children, enjoying an amicable and cooperative
was to transfer Lisa to ICU, maintain full spinal precautions, main- relationship. During a highly stressful time (ICU admission, death
tain serum sodium at 145–150 mmol/L with 3% sodium chloride of Lisa’s uncle), each parent allowed the other time alone with Lisa
(initial serum sodium was 136 mmol/L). The ED team asked whether as well as spending time together. Parents are generally not con-
they should use muscle relaxant agents, but were advised against sidered visitors in PICUs, and Lisa’s parents were able to spend as
this as Lisa’s ICP was not yet able to be monitored. An arterial blood much time at her bedside as they wished. Once Lisa’s brother was
gas, full blood count and electrolytes were performed on admis- discharged from hospital, he was able to rejoin his family at the
sion to adult ICU, revealing dropping haemo globin to 78, sodium paediatric hospital. The multidisciplinary PICU team provided
135, potassium of 4, blood glucose level (BGL) of 5. support for the family during their stay.
Due to bad weather, the retrieval team arrived approximately Lisa was transferred to the ward on day 11, with her management
nine hours after the accident. After reducing the taken over by the brain-injury rehabilitation team. She was fed via

704 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



Case study, Continued
a gastric tube and receiving 1 L/min of O 2 via nasal prongs. Respira- post-injury. At her first review with rehabilitation specialists three
tory physiotherapy continued on the ward. Spinal precautions con- months post-injury she was moving independently, tremor no
tinued until clinical clearance was achieved on the ward, although longer apparent, could recall three of seven elements after 10
she continued to wear a collar for several weeks. Lisa was dis- minutes, was animated and social in her interactions. However,
charged from hospital after eight weeks. ongoing frontal lobe type behaviours of impulsiveness and poor
attention span were also noted. Ongoing formal assessment was
Posttraumatic amnesia lasted for almost eight weeks. Lisa’s neuro- planned semiannually, including review of her first two terms at
logical status improved sufficiently to allow her planned return to school. Returning home has allowed extended family members to
school half-time with a dedicated full-time teacher’s aide and assist the family’s recovery and rehabilitation. Lisa’s parents con-
ongoing speech and occupational therapy to occur at 3 2 months tinue to share parenting and care for both children.
1







Research vignette
Colville G, Darkins J, Hesketh J, Bennett V, Alcock J, Noyes J. The mixed-method study that aims to complement and deepen the
impact on parents of a child’s admission to intensive care: Integra- understanding of the quantitative results. Colville and colleagues
tion of qualitative findings from a cross-sectional study. Intensive justified the mixed-method approach as a strategy that would
and Critical Care Nursing 2009; 25(2): 72–9. best fulfil the objectives and test underlying hypotheses of the
larger study. They described how the qualitative data from inter-
Abstract views was analysed using a framework approach. To meet the
Objectives objective of the study, which was to complement and deepen
In this study, parents were asked which aspects of their experience understanding of the quantitative results, clarification and illustra-
of having a child in intensive care had caused them the most tion of the results from the quantitative data was achieved by
distress and how they continued to be affected by these linking with the descriptive qualitative themes. For instance, recall
experiences. of vivid memories was compared and paired with the high level
of stress associated with witnessing medical procedures. Rigorous
Research methodology
Semi-structured interviews held with 32 mothers and 18 fathers of interpretation of the results was demonstrated with the research-
children admitted to a paediatric intensive care unit 8 months ers’ articulation of the theoretical positioning and the chosen
earlier, were audiotaped, transcribed and subjected to a thematic methodology.
analysis. The findings were clearly stated with emerging themes combined
with the level of distress measured in the quantitative component
Setting of the study. The most striking finding was that the vivid memories
The setting was an eight-bed paediatric intensive care unit in an of parents 8 months post-PICU discharge of their child correlated
inner city teaching hospital.
with the high level of stress experienced at admission. Although
Results they expressed negative emotions, including fear, horror, disorien-
Significant themes included the vividness of parents’ memories of tation and impotence, parents also expressed a great amount of
admission; the intensity of distress associated with times of transi- gratitude and relief. The worst memories were during transition
tion and the lasting impact of their experience, in terms both of times, including retrieval to PICU and transfer to the ward. Mothers
the ongoing need to protect their child and in relation to their reported higher levels of distress than fathers, possibly because
priorities in life. Fathers reported different coping strategies, spent they spent more time at the bedside and were more involved in
less time on the unit and were less likely than mothers to report the care of their child, and also expressed more fear of their child’s
fearing that their child would die. possible death when compared to fathers. This emphasises the
importance and benefits of good communication and support
Conclusions given to parents by nurses and other health professionals, espe-
Parents report significant and persisting distress. Further research cially during transitions from and to PICU.
is needed on how best to support them acutely and in the longer
term. One limitation of this study is the retrospective nature of data col-
lection, as parents were asked to recall their feelings eight months
Critique after their child’s admission to PICU. However, the results of this
This study addresses an important gap highlighted in the litera- longitudinal study add to current knowledge in this area of research
ture, that is, the exploration of the long-term psychological impact and as such should not be discarded. This study’s findings further
of the child’s critical illness on parents, with the targeted inclusion highlight the need for the psychological wellbeing of parents to be
of fathers who are often excluded in studies. As stated by the routinely monitored during PICU stay and after discharge, for
authors, this paper reports the qualitative component of a larger instance in follow-up clinics.

Paediatric Considerations in Critical Care 705



Learning activities
Learning activities are all based on the case study. 4. What is an appropriate ventilation strategy for Lisa, keeping in
1. Consider the information provided in the first paragraph of the mind her lung and head injuries and associated treatment?
case study. What injuries can you predict in children travelling 5. Will permissive hypercapnoea be considered for Lisa? Provide
in a rear car seat? a rationale for your answer.
2. On arrival in the ED, Lisa has a GCS score of 4 and requires 6. The specialist retrieval teams were unable to retrieve Lisa for
immediate intubation. Calculate the ETT size for Lisa. Should some hours due to inclement weather. Consider where Lisa
the ETT be placed orally or nasally? Should a cuffed or uncuffed would be best managed within your own facility, should this
ETT be placed? Justify your answers. situation arise. Imagine your facility is located a minimum of
3. Lisa’s mean blood pressure was initially low, and she required 6-hour drive from a major paediatric trauma centre. Consider
initial fluid resuscitation. What fluids could have been consid- the availability of resources (human and technological) that
ered for Lisa to restore her circulating blood volume while con- would be available in various clinical areas to manage Lisa for
sidering her lung and brain injuries? 12 hours until retrieval could be accomplished.



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Pregnancy and Postpartum


26 Considerations





Wendy Pollock
Clare Fitzpatrick


interaction with pregnancy and describes the major
Learning objectives obstetric conditions that are associated with critical
illness. Additionally, we include guidance on specific
After reading this chapter, you should be able to: practices relating to the care of pregnant and postpartum
l identify the core physiological adaptations of pregnancy women in ICU, for example assessment of fetal wellbeing
pertinent to critical care nursing and establishment of lactation. Further details on these
l describe the antenatal assessment that would be required topics can be found in textbooks that specifically deal
1,2
when caring for a woman 28 weeks pregnant in ICU with critical care obstetrics. Research into critical care
l describe the priorities of management for a postpartum obstetrics is limited and at times the evidence being
woman admitted to ICU with preeclampsia drawn on is dated, but still considered to be valid.
l outline the main causes of obstetric haemorrhage EPIDEMIOLOGY OF CRITICAL ILLNESS
l outline the standard postnatal care required by a woman in
ICU, for the 48 hours following birth IN PREGNANCY
l consider the resources and equipment available in your Most women experience a healthy, normal pregnancy and
workplace that are specifically required for the care of the development of critical illness associated with preg-
pregnant and postpartum women nancy is usually sudden and unexpected. Approximately
1 in 370 births result in a maternal ICU admission,
making up about 1% of the ICU population; more than
three-quarters of admissions occur following the birth of
the baby. Admission of a pregnant woman to ICU is
3,4
Key words infrequent and more likely to be related to a non-obstetric
diagnosis such as pneumonia or a motor vehicle crash.
Conversely, in postpartum women, a condition directly
critical illness in pregnancy associated with pregnancy is more likely, usually
severe maternal morbidity preeclampsia or obstetric haemorrhage. However, preg-
3
fetal wellbeing nant and postpartum women may be admitted to ICU
postpartum care with any diagnosis, which may or may not be associated
antenatal assessment with pregnancy.
severe preeclampsia
severe obstetric haemorrhage Pregnant and postpartum admissions to ICU are usually
short with most lengths of stay less than 24 hours. There
medical disorders in pregnancy is a vast variation in the threshold for admission to ICU
breastfeeding with one European study of severe maternal morbidity
reporting ICU admission proportions of between 0 and
5
50% across different regions. Additionally there are
many women who, when admitted to ICU, do not receive
INTRODUCTION any notable specific ICU intervention (Table 26.1) and
the need for ICU admission for these women has been
6
The admission of a pregnant or postpartum woman to questioned. In general, about a third of women who
ICU often extends ICU staff outside of their comfort experience severe maternal morbidity are admitted to
7
zone. Pregnant and postpartum women undergo substan- ICU. It is feasible that admission to ICU is preventable
6
tial physiological adaptations. Nursing staff also need to by upskilling midwifery services and by early identifica-
consider the fetus and be aware of, and manage, obstetric tion of severe illness resulting in prompt and appropriate
conditions. This chapter provides an overview of the epi- treatment. 6,8,9 There has been limited study of the long
demiology of critical illness in pregnancy, describes the term outcomes for pregnant and postpartum women
physiological adaptations of pregnancy and the puer- admitted to ICU in relation to their ongoing health and
710 perium, outlines some key medical conditions and their wellbeing, partner relationship and infant bonding. In

Pregnancy and Postpartum Considerations 711



TABLE 26.1 ICU interventions required by pregnant and postpartum women in ICU

6
10
ICU intervention Pollock (Australia)* (n = 33) Hazelgrove (UK) (n = 210) Zwart (Netherlands) (n = 837)
#
7
#
Mechanical ventilation 67% 45% 35%
Inotrope infusion 18% 19% 9%
Pulmonary artery catheter 6% 13% 3%
Renal replacement therapy 9% 3% 2%
*Tertiary ICU level only.
# National/regional study, all ICU levels.



developed countries like Australia, the mortality of preg- reduction in all the placental hormonal levels, such as
nant and postpartum women admitted to ICU is rela- progesterone and oestrogens, and thus begins the physi-
tively low at around 3% compared to the 15% mortality ological process for returning the woman’s body to the
observed in the regular ICU population. 3 non-pregnant state.

CARDIOVASCULAR SYSTEM
Practice tip The cardiovascular system undergoes a series of anato-
mical and physiological changes during pregnancy to
Any maternal death, death of a woman during pregnancy or support both the mother and fetus during this period.
within 42 days of having been pregnant, should be reported to
the relevant state authority in Australia and to the Perinatal and Anatomical Changes
Maternal Mortality Review Committee in New Zealand, even if The heart undergoes anatomical change during preg-
the pregnancy is not thought to have contributed to the cause nancy including left ventricular hypertrophy and the
of death.
cross-sectional areas of the aortic, pulmonary and mitral
valves increase by 12–14%. ECG changes include non-
specific ST segment changes, the development of a Q
15
ADAPTED PHYSIOLOGY OF wave in Lead III and a left-axis deviation pattern. These
are evident by the end of the first trimester and remain
PREGNANCY throughout the pregnancy. As with the interpretation
16
Conception results in extensive physiological adaptations of any ECG, consider other information like the
across most body systems (Table 26.2). The physiological patient presentation (signs and symptoms) and blood
adaptations most relevant to critical care nursing include test results to form a complete assessment of the woman’s
cardiovascular, respiratory, renal, gastrointestinal and condition.
coagulation and the role of the placenta as the maternal–
fetal interface. The uterus and breasts obviously undergo Blood Volume
major change in pregnancy and any basic midwifery or Very early in the pregnancy there is generalised vasodila-
obstetric textbook, such as Myles’ Textbook for Midwives or tation resulting in sodium and water retention. The causes
Midwifery: preparation for practice will describe these in of the vasodilatation are likely to include hormonal
detail. 11,12 The physiological adaptations described in this factors (e.g. progesterone), peripheral vasodilators like
chapter refer to a singleton pregnancy only, as women nitric oxide, and potentially, an as-yet unidentified
with a multiple pregnancy (i.e. twins) may undergo pregnancy-specific vasodilatory substance. The end
17
further changes. The physiological changes described result is a 40–50% increase in blood volume as well as
13
refer to a non-labouring pregnant woman. Labour induces reduced normal serum sodium level, from 140 to
further changes to physiology, such as increased cardiac 136 mmol/L and a reduced plasma osmolality from 290
output. 14 to 280 mosmol/kg. These changes persist throughout
pregnancy and the osmoreceptor system resets to accept
The puerperium, also referred to as the postpartum or these values as normal. 18
postnatal period, is the 6 weeks following the end of
pregnancy during which time the woman’s body returns The red cell mass increases 20–40% whilst the plasma
to the pre-pregnant state. The physiology of the puerpe- volume increases 40–50%. The resultant physiological
rium is outlined below for the major body systems, with haemodilution produces a relative anaemia which is
content specific to the uterus and breasts covered later in thought to be beneficial for utero-placental perfusion.
the section on postnatal assessment and lactation. Our Venous haematocrit typically falls from a non-pregnant
19
knowledge of the timing and completeness of the reversal value of 40% to 34% near term. The increase in blood
of the physiological adaptations in pregnancy is incom- volume is evident from seven weeks’ gestation and peaks
plete. Delivery of the placenta results in an abrupt at around 30–32 weeks’ gestation, normally remaining at

712 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Heart Rate, Stroke Volume and
TABLE 26.2 Key physiological changes in pregnancy Cardiac Output
Maternal heart rate increases by 10–15 beats per minute
Change during during pregnancy with an increase noted as early as 5
Parameter pregnancy weeks’ gestation. 16,22 The increase in heart rate may be a
Cardiovascular system: compensatory response related to the generalised vasodi-
Heart rate ↑ 10–15 beats/min latation, although a hormone-related effect cannot be
Blood pressure ruled out. Tachycardia (>100 beats/min) is an abnormal
23
Systolic ↓ 5–9 mmHg 24
Diastolic ↓ 6–17 mmHg sign and warrants further investigation. The stroke
Cardiac output ↑ 30–50% volume is noted to increase between 18 and 32%, begin-
Systemic vascular resistance ↓ up to 35% ning as early as 8 weeks’ gestation. 25,26 An increase in
Central arterial and venous pressures Unchanged cardiac output is detectable from 5 weeks gestation and
Blood and associated components: continues to be 30–50% higher by 32 weeks gestation. 17,26
Blood volume ↑ 40–50% Hence, a normal cardiac output in pregnancy may be as
Plasma volume ↑ 40–50% high as 8 L/min. The increased cardiac output is achieved
Red blood cells ↑ 20–40% by a combination of the increases in heart rate and stroke
White blood cells ↑ 100–300% volume.
Platelets Unchanged
Fibrinogen ↑ 100%
Serum albumin level ↓ 10–15% Systemic Vascular Resistance
Respiratory system The generalised vasodilatation observed in early preg-
Respiratory rate Unchanged nancy reduces systemic vascular resistance by up to 35%,
Tidal volume ↑ 25–40% with some reduction already detectable by 8 weeks’ gesta-
Minute volume ↑ 40–50% 27
Oxygen consumption ↑ 15–20% tion. The development of the low-resistance utero-
Arterial blood gas analysis values placental junction was thought to act as an arteriovenous
80–110 mmHg shunt and contribute to the lowered SVR seen in preg-
PaO 2
28–32 mmHg
PaCO 2 nancy. However, the very-early-observed decrease in SVR
pH 7.40–7.45
− argues against this theory and perhaps circulating sub-
HCO 3 18–21 stances that exert a vasodilatory effect on the vasculature
SaO 2 ≥95%
Vital capacity Unchanged is a more likely proposition.
Functional reserve capacity ↓ 17–20%
Airway compliance and resistance Unchanged Effect of Posture on Maternal
Renal system Haemodynamics
Glomerular filtration rate ↑ 40–50%
Serum urea and creatinine ↓ It is evident that from as early as 5–8 weeks’ gestation,
Urine output Unknown pregnancy is characterised by general vasodilatation,
Proteinuria <300mg/day increased blood volume, increased cardiac output and
is generally a hyperdynamic state. As the pregnancy
advances, the bulk of the uterus begins to have an impact
on maternal haemodynamics. After 20 weeks’ gestation,
a woman lying flat on her back may experience supine
a stable level until delivery. 17,20 Women who do not expe- hypotension, secondary to compression of the inferior
rience this normal increase in blood volume are more vena cava and aorta with subsequent reduction in venous
prone to adverse outcomes such as preeclampsia or small- return, cardiac output and placental flow. A reduction in
21
for-gestational-age infant. The additional blood volume placental flow may occur even without a recorded drop
is also thought to accommodate the normal blood loss in blood pressure. Consequently, it is inadvisable to nurse
associated with birth (<500 mL). Pregnant women are a pregnant woman more than 20 weeks’ gestation, flat on
renowned for being able to maintain stable vital signs, her back. A left lateral lying position results in the best
with blood losses as much as 1500 mL, before acutely cardiac output, although manually displacing the uterus
deteriorating. to the left whilst the woman remains supine is also effec-
28
tive in relieving the aorto-caval compression. Otherwise,
Blood Pressure the use of a wedge or pillows to maintain a left lateral tilt
Blood pressure reduces in pregnancy, with the lowest of at least 15 degrees is recommended to minimise aorto-
29
normal blood pressure recorded during the second tri- caval compression.
mester (16–28 weeks), and returns to pre-pregnancy
levels near term (see Table 26.2). Blood pressure begins Postpartum Cardiovascular Changes
dropping as early as 8 weeks’ gestation, in association Heart rate returns to pre-pregnancy levels by 10 days post-
with the generalised vasodilatation occurring at this time. partum; blood pressure has normally returned to pre-
If a woman does not experience the characteristic lower- pregnancy levels by term and does not change during the
ing of blood pressure, particularly during the second tri- puerperium. 23,27 The first few days of the puerperium are
mester, it is viewed with suspicion and as a potentially associated with a diuresis which reduces the circulating
abnormal sign. volume and results in haemoconcentration of blood.

Pregnancy and Postpartum Considerations 713

Consequently a postpartum haemoglobin level will oestrogen-mediated progesterone response, lower serum
increase over the first few days and the risk of thrombo- osmolality, strong ion difference and increased level of
embolism is higher during the postpartum period than wakefulness that are also present in pregnancy. 33-35
during pregnancy. Due care should be paid to postpartum Increased minute ventilation begins soon after concep-
15
women in ICU to prevent deep vein thrombosis, particu- tion and peaks at 40–50% at term. The increase in
larly as many of these women are in ICU with compli- minute ventilation is achieved by a 30–50% increase in
cations of preeclampsia or severe obstetric haemorrhage, tidal volume (e.g. an increase of 200 ± 50 mL at term),
both of which further increase the likelihood of with no increase in respiratory rate. 15
thromboembolism. 30
Due to the altered respiratory function, normal arterial
Cardiac output increases briefly in the immediate post- blood gas values are different in pregnancy compared to
partum period to compensate for blood losses and tends the non-pregnant values (see Table 26.2). The reduced
to increase by 50% of the pre-delivery value, at this point PaCO 2 level creates the necessary gradient for the fetal
in the post partum phase stroke volume is increased CO 2 to passively cross the placenta for maternal excre-
23
while the maternal heart rate is often slowed. For most tion. PaO 2 normally increases by 10 mmHg, although the
women, the immediate postpartum elevation in cardiac PaO 2 level is affected by posture, particularly as the preg-
36
output only lasts for an hour or so. By 2 weeks postpar- nancy progresses. In advanced pregnancy, the supine
tum, many haemodynamic parameters have returned to position is associated with a reduction in PaO 2 of up to
pre-pregnancy levels for the majority of women, although 10 mmHg when compared with the same woman in the
37
some have been recorded as remaining above pre- sitting position. The kidneys compensate for the lowered
pregnancy levels at 12 months postpartum, including PaCO 2 by increasing bicarbonate excretion, which serves
cardiac output. 14,27 There is increasing acknowledgement to maintain a normal pH. 36,38,39 Normal oxygen satura-
that for many women following childbirth, there is a tion in pregnancy has not been well investigated, however,
permanent modification to the cardiovascular system, it is likely to be 97–100% at sea level, with a healthy
although whether this persists into the menopausal era pregnant woman’s saturation not dropping below 95%
is not known and whether it impacts on cardiovascular during moderate exercise. 40,41
disease risk is also unknown. 27
The notable hyperventilation of pregnancy is associated
RESPIRATORY SYSTEM with a feeling of breathlessness in up to 75% of healthy
pregnant women when attending to activities of daily
Changes to the Upper Airways and Thorax living. Distinguishing what is considered ‘physiological
33
Normal physiological changes of pregnancy include gen- dyspnoea’ from pathological dyspnoea, for example
eralised vasodilatation of the upper airway vasculature, developing cardiomyopathy, can present a challenge in
increased fat deposition around the neck and an increase pregnancy. Dyspnoea at rest is usually an abnormal sign
in mucosal oedema. A combination of hormonal influ- in pregnancy. 42
ences, likely progesterone and oestrogen, are at play.
These physiological changes are thought to be responsi- Postpartum Respiratory Changes
ble for the symptoms of rhinitis, nasal stuffiness and There is complete resolution of the spirometry and arte-
epistaxis that are common in pregnancy. 17 rial blood gas changes by 5 weeks postpartum. Unfor-
36
Changes also occur to the chest wall with relaxation of tunately there has been no study reporting the daily
ligaments resulting in an outwards flaring of the lower transition of these parameters over the first week postpar-
31
ribs and a 50% increase in the subcostal angle. Both the tum – the timing when a postpartum woman is likely to
diameter and the circumference of the thorax increase by be in ICU. One very old study reported that CO 2 levels
2 cm and 5–7 cm respectively. 31,32 These physical changes took between two and five days to return to normal non-
43
are thought to cause the diaphragm to rise by 5 cm, with pregnant values postpartum. Regardless, with the fetus
this occurring early in pregnancy and well before there is delivered, it is probable that no harm will be done to a
32
any pressure from the advancing uterus. Respiratory woman by the titration of her ventilation requirements
muscle function does not change significantly during according to non-pregnant conventions and arterial
31
pregnancy and rib cage compliance is unaltered. The blood gas values.
functional reserve capacity (the amount of air left in
the lungs after expiration) is reduced 17–20% making RENAL SYSTEM
the pregnant woman more vulnerable to hypoxaemia All smooth muscle dilates in early pregnancy, most likely
during any apnoeic period. Chest X-ray interpretation is in response to progesterone. This includes the renal tract,
unchanged during pregnancy, despite the variety of involving the renal pelvis, calyces, ureters and urethra.
changes to cardiovascular and respiratory flows. 23 The placental hormone, relaxin, has also been shown to
44
have an effect on renal tract dilatation. Each kidney
Changes to the Physiology of Breathing lengthens by about 1 cm, which is explained by the dila-
From as early as 5 weeks’ gestation, multiple factors result tation and associated mild hydronephrosis and increased
in an increased respiratory drive. The increase in proges- vascularity of the kidneys, with no hypertrophy of renal
17
terone levels is thought to lower the PaCO 2 threshold in tissue. Another effect of widespread dilatation is urinary
the respiratory centre to stimulate respiration resulting stasis and an increased likelihood of urinary tract infec-
15
in hyperventilation. Other related factors include an tion. Acute pyelonephritis is one of the most common

714 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

renal complications of pregnancy and is associated with Hepatobiliary Changes in Pregnancy
the onset of preterm labour. 45
There is no significant increase in hepatic arterial blood
The kidneys receive a proportion of the additional cardiac flow during pregnancy, despite the 40–50% increased
51
output resulting in a 30% increase in renal blood flow. cardiac output. There is, however, a doubling of blood-
51
The glomerular filtration rate (GFR) increases 40–50% flow to the liver supplied by the portal vein, which may
during the first trimester and then reduces slightly towards have an impact on oral medication metabolism in the
18
the end of the third trimester. The increase in GFR may liver. There are also changes in other hepatic enzymes
result in the tubule active transport systems for both responsible for drug metabolism, resulting in a change
glucose and proteins to be exhausted, with both glycos- in pharmacokinetics of some medications, e.g. higher
uria and proteinuria common in pregnancy. Glycosuria plasma levels of midazolam. Serum albumin levels
is not related to blood sugar levels and is unhelpful in reduce to 30–40 g/L for the majority of pregnancy, with
monitoring diabetes. Proteinuria, up to 300 mg per 24 levels as low as 25 g/L normal during the second post-
46
hours, is considered normal in pregnancy. Conversely, the partum week. This low albumin level reduces colloid
high GFR results in lowered serum levels of both urea and osmotic pressure that contributes to the dependent
creatinine. A plasma urea level exceeding 4.5 mmol/L oedema, for example swollen ankles, that is common in
and plasma creatinine level higher than 75 µmol/L, pregnancy.
should be viewed as abnormal and indicative of potential The general smooth muscle vasodilatation affects the
renal impairment. 18,46 There is conflicting information hepatobiliary ducts, resulting in sluggish bile motility
regarding normal urine output during pregnancy, with and delayed emptying of the gall bladder. These changes
some studies suggesting no difference to that during non- lead to an increased incidence of cholelithiasis and cho-
pregnancy and others reporting an increase in 24-hour lecystitis during pregnancy.
urine volume after 12 weeks’ gestation. 45,47

Postpartum Renal Changes HAEMOSTASIS SYSTEM
The most significant renal change is the diuresis that During pregnancy, the woman’s body prepares for the
occurs in the 1–3 days postpartum. This diuresis serves separation of the placenta, a time of potential large blood
to offload the additional blood volume that the woman loss. The blood flow to the placental bed at term is in the
has had circulating for the duration of the pregnancy. range of 600–800 mL/min. Both elements of the haemo-
There has been little examination of ‘normal urine output’ stasis system are activated during pregnancy (coagulation
with the standard 0.5 mL/kg/hr reported as a minimum and fibrinolysis), with pregnancy and particularly the
acceptable level, however a true ‘normal’ level is likely to postpartum period associated with an increased risk of
be closer to 0.8 mL/kg/hr. Creatinine levels are within thrombus formation. Thromboembolic events remain a
48
the normal non-pregnancy range within 24 hours post- leading cause of maternal death in developed coun-
partum, whilst the lower urea levels remain for at least tries. 24,52 A number of changes to the haemostatic system
46
48 hours. The bladder returns to the pelvis in the early occur during pregnancy (Table 26.3).
postpartum period as the uterus and other organs resume Of note, gestational thrombocytopenia – a platelet level
their pre-pregnancy position. between 80–150 × 10 /L – occurs in 6–8 % of women. 53,54
9
It generally has no negative impact on the woman or fetus
GASTROINTESTINAL SYSTEM AND LIVER at these levels, as there is no pathology associated with
The uterus pushes abdominal organs aside as it advances the low platelet count. 55
making assessment and diagnosis of an acute abdomen
difficult. For example, the appendix is progressively
displaced upwards and laterally from McBurney’s point
at the third month, reaching the level of the iliac crest
by late pregnancy. The bowel and other organs are gen-
49
erally displaced by the enlarging uterus; women with TABLE 26.3 Haemostatic changes during
56-58
prior abdominal surgery and adhesions are predisposed pregnancy
50
to intestinal obstruction as a result. Additionally, there
is an increase in intraabdominal pressure which may Haemostatic component Changes during pregnancy
contribute to another common pregnancy symptom, Platelets:
heartburn. Count Unchanged
Function and lifespan Unchanged
Generalised smooth muscle vasodilatation occurs Clotting factors:
throughout the gastrointestinal tract including sphinc- Factors VII, VIII & IX Increased
ters. Thus there is delayed stomach emptying and a lax Fibrinogen Doubles by term
cardiac sphincter leading to an increased likelihood of Other clotting factors Mainly unchanged
aspiration. The bowel has slowed peristalsis resulting in Fibrinolysis:
constipation, common in many pregnant women. The D-Dimer level Progressively increases
vasodilatation of blood vessels in combination with con- throughout pregnancy
stipation increases the incidence of haemorrhoids during By term, level >0.5 mg/L
pregnancy. common

Pregnancy and Postpartum Considerations 715



Umbilical vein

Umbilical artery





Main villus






Septum




Maternal vein

Decidua
Maternal spiral artery


Uterine muscle


FIGURE 26.1 The maternal–placental interface.
11
CHANGES IN WHITE BLOOD CELLS AND interface whereby maternal blood fills a space in which
THE IMMUNE SYSTEM the nutritive villi float and are bathed in the maternal
There is continued debate on whether the pregnant state blood (Figure 26.1). A few villi are more deeply anchored
increases vulnerability to infection, secondary to some in the decidua and these are referred to as anchoring
61
protective mechanism that prevents the woman’s body villi. The blood drains back into the maternal circula-
17
from reacting to the fetus as a foreign body. Pregnant tion via maternal sinuses and the endometrial veins.
women have increased innate immune system activity Approximately 150 mL of maternal blood, replenished
(non-specific response) and a lowered adaptive immune three to four times per minute, bathes the villi in the
61
system (specific antibody response), with pregnant intervillous space. The chorionic villi maximise the
women more vulnerable to some infections like malaria available surface area to optimise the exchange of prod-
and varicella. 17,59,60 Pregnant women are often in contact ucts across the maternal–placental interface. By term, this
2 62
with small children and potentially have an increased surface area is said to be as large as 13 m . Initially, four
exposure to various infections. The white blood cell layers of cells separate the maternal blood from the fetal
number increases throughout pregnancy, peaking blood, reducing to three after 20 weeks’ gestation; these
around delivery when a normal level may be as high cell layers are collectively referred to as the ‘placental
63
9
as 25 × 10 /L. 46 membrane’ or ‘placental barrier’. Damage to villi, such
as a threatened abortion or blunt trauma, may result in
THE MATERNAL–FETAL INTERFACE mixing of the blood circulations.
The junction of the maternal and fetal circulations is Role of the Placenta
referred to as the maternal–fetal interface. Although, The placenta provides six major functions to sustain the
under normal circumstances the circulations remain sep- pregnancy and fetus: respiration, nutrition, storage, excre-
arated by layers of cells, the maternal–fetal interface is tion, protection and endocrine. Fetal lungs are filled
61
where the maternal and fetal systems interact.
with fluid and all oxygenation and removal of carbon
dioxide must be provided via the placenta. Fetal haemo-
Placenta globin has a slightly different structure to adult haemo-
The placenta develops from the trophoblastic layer of the globin and has a higher affininity for oxygen. Both oxygen
fertilised ovum and is completely formed and function- and carbon dioxide cross the placental membrane by
61
ing ten weeks following fertilisation. The chorionic villi simple diffusion. Nutrients are actively transported across
constitute the undersurface of the placenta and attach to the placental membrane, with the placenta able to select
the uterine wall via the decidua. The end result is an the substances needed by the fetus, even at the expense

716 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

61
of the mother if necessary. The placenta is able to store need to accommodate for, and take into account, the
glucose by converting it to glycogen and reconverting it likely impact of the normal physiology of pregnancy
to glucose as required and is also able to store iron and on common ICU monitoring, interventions and care
some fat-soluble vitamins. (Table 26.4).
The placental membrane operates as a barrier between
the maternal and fetal circulations and provides a limited DISEASES AND CONDITIONS UNIQUE
protective function. Generally, few bacteria can cross the TO PREGNANCY
placenta, although viruses are able to cross fairly readily.
The placenta produces large volumes of hormones includ- There are a number of conditions unique to pregnancy
ing progesterone, oestrogens, placental lactogen, chori- that might cause a woman to become critically ill and
onic gonadotropin, growth factors, cytokine vasoactive result in admission to ICU including preeclampsia,
substances, placental growth hormone, thyrotropin and obstetric haemorrhage, amniotic fluid embolism and
corticotropin. The placenta does not have a nerve supply peripartum cardiomyopathy. These conditions are dis-
so all activities regulated by the placenta must be under- cussed in detail below.
taken by other mechanisms, e.g. chemical, hormonal
changes. PREECLAMPSIA
A full and comprehensive understanding of the placenta The umbrella term ‘hypertension in pregnancy’ is used to
remains elusive. We do know that the placenta is a highly describe a myriad of conditions in pregnancy where
complex organ with the ability to modulate a variety of hypertension is a major feature. These include gestational
metabolic effects in both the woman and the fetus. hypertension, pre-existing essential hypertension and
Disorders of the placenta are thought to be a major preeclampsia which incorporates eclampsia and Haemol-
contri butor to preeclampsia and small-for-gestational- ysis Elevated Liver enzymes and Low Platelets (HELLP)
age neonates. syndrome (Table 26.5). Comprehensive descriptions of
these conditions and their management have been pub-
Impact of Impaired Utero–placental lished by the Australian and New Zealand College of
Gas Exchange Obstetricians and Gynaecologists (RANZCOG) and the
Effective gas exchange across the placental membrane Society of Obstetric Medicine Australia and New Zealand
65,66
depends on sufficient maternal blood pressure and ade- (SOMANZ).
quate O 2 and CO 2 gradients for passive diffusion to occur. Preeclampsia is a condition unique to human pregnancy
In response to hypoxaemia, a fetal brain-sparing mecha- in that, whilst characterised by hypertension and protein-
nism goes into effect that increases fetal arterial pressure uria, it is a multisystem disorder consisting of variable
and redirects blood delivery to the main organs, namely clinical features caused by widespread vasospasm. The
the brain, heart and adrenal glands. This centralisation basis for preeclampsia remains unknown. The indication
64
of fetal blood flow is more apparent in response to mater- for ICU admission is usually related to organ failure,
nal hypoxaemia than to reduced utero–placental blood caused by the widespread vasospasm and reduced organ
flow. It appears that a less mature fetus (i.e. earlier gesta- perfusion that characterises the disease. Preeclampsia
67
tion) may be less susceptible to asphyxia than a fetus can be a very serious condition and remains a leading
at term. 64 cause of maternal death in both developed and develop-
ing countries. 68
Whether the fetus will die in utero or survive, and the
degree of any neurological compromise, depends on the
degree and duration of asphyxia, the recurrent nature of Aetiology
asphyxia, and the degree to which the fetus is able to The placenta is strongly implicated in the cause of pre-
compensate for the asphyxia. Antenatal asphyxia (asphyxia eclampsia; its removal is the only definitive treatment for
during pregnancy, not associated with labour) has been the condition. However, the exact mechanisms of the
linked to the development of cerebral palsy, behaviour aetiology of the disease remain elusive and are likely to
disorders and learning difficulties. The reasons and extent be complex and multifactorial. Theories explaining the
of individual variation in fetal outcome are unknown. pathophysiology of preeclampsia include immune mal-
adaptation, abnormal trophoblast embedding, endothe-
CLINICAL IMPLICATIONS OF lial activation and excessive inflammatory response, and
THE PHYSIOLOGICAL ADAPTATIONS a genetic susceptibility (Box 26.1). The contribution of
71
OF PREGNANCY each component and whether all components are rele-
The beginning point of any nursing practice is an under- vant in all cases of preeclampsia is not known. It is fea-
sible that there are differing types of pathophysiology for
standing of normal anatomy and physiology. The normal mild preeclampsia that occurs at term, compared with
physiological adaptations of pregnancy can be used severe preeclampsia that often occurs prior to 34 weeks’
to explain the so-called ‘minor discomforts’ of pregnancy, gestation.
including constipation, varicose veins, indigestion,
breathlessness and fatigue. For a critically ill pregnant Preeclampsia is associated with impaired remodelling of
woman being nursed in ICU, these normal physiological the uterine spiral arteries and abnormal placental
changes are also highly relevant for her care. ICU nurses implantation. It is thought that maternal–fetal immune

Pregnancy and Postpartum Considerations 717



TABLE 26.4 Clinical relevance of physiological adaptations in pregnancy

Effects of the normal physiology of pregnancy Clinical implications
Cardiovascular system
l Increased likelihood of: l Consider use of thrombophylaxis
l venous stasis
l varicose veins
l deep vein thrombosis
l Increased likelihood of:
l haemorrhoids
l swollen ankles
l Potential for aortal-caval compression from about 20 weeks’ gestation l Avoid nursing the woman flat on her back, e.g. tilt bed if unable to
nurse woman on her side or use pillows/wedges to obtain a lateral
tilt of at least 15° to maintain placental flow, full left lying is best
l CPR and haemodynamic measurements should be done with a
left lateral tilt
l Haemodynamic stability despite large blood loss l Be alert to subtle signs of haemodynamic compromise
l Sudden deterioration
Respiratory system
l Nasal passages more likely to bleed on instrumentation (e.g. nasal l Nasal-tracheal intubation is not usually an option
intubation, nasogastric insertion) l Have a doctor experienced with intubation on hand when a
l More likely to bleed from the gums pregnant woman is being intubated
l More prone to hypoxaemia during apnoea e.g. when being intubated l Ensure that the artificial airway is protected and guard against
l All pregnant women are considered to have a high-risk airway: accidental extubation
l especially if the woman has preeclampsia l Review the ‘failed intubation’ protocol in the ICU
l particularly if the woman is obese l Pre-oxygenate with 100% O 2 prior to intubation or suctioning
l More likely to develop pulmonary oedema unless contraindicated
l Diaphragm raised by about 5 cm l Titrate fluid resuscitation carefully – especially in women with
severe preeclampsia
l Check diaphragm location prior to ICC insertion for haemothorax/
pleural effusion
Gastrointestinal system
l Pregnant woman is more likely to: l Maintain cricoid pressure throughout CPR and intubation until the
l aspirate person obtaining an artificial airway instructs its release
l develop constipation l Chart bowel actions and ensure a bowel management strategy is
l present with advanced signs and symptoms of acute abdomen, implemented
e.g. appendicitis, bowel obstruction l Early consideration of non-obstetric causes of an acute abdomen
l Pregnant women have additional and specific nutritional needs l Consult with a dietician early to ensure that the woman receives
adequate nutrition during ICU admission
Renal system
l Progesterone and relaxin causes relaxation and dilation of smooth l Minimise use of indwelling urinary catheter
muscles l Renal impairment may be signified by lower serum urea and
l Renal calyces and renal pelvis become distended creatinine levels than in non-pregnancy
l Ureters and urethra are elongated, dilated and have reduced l Some glycosuria and proteinuria is normal in pregnancy
peristalsis l The bladder is at risk of traumatic injury in the second and third
l Stasis of urine and increased risk of ascending infection trimesters
l Acute pyelonephritis is associated with preterm labour
l Bladder is displaced into the abdominal cavity after the first trimester




68
maladaptation could be the main cause for this superfi- clinical signs, such as hypertension. Other common
71
cial placentation. Placental flow defects are detected as clinical manifestations in preeclampsia include enhanced
early as 12 weeks in some women who go on to develop endothelial-cell permeability and platelet aggregation,
72
preeclampsia. Placental ischaemia and reperfusion with explaining the increased likelihood for oedema and
subsequent oxidative stress have been regarded as major thrombosis. 71
pathogenetic drivers. It is likely that there is an excessive
or atypical maternal immune response to trophoblasts In summary, preeclampsia presents post 20 weeks’
and the disease represents a failed interaction between gestation, but the foundation for the disease relates to
68
the mother’s and fetus’ genetic make-up. The excessive abnormal placentation early in the first trimester. Whilst
systemic inflammatory response and associated endothe- a number of ‘biomarkers’ attempting to predict the onset
lial dysfunction and enhanced vascular reactivity, results of preeclampsia have been identified, there is no reliable
in widespread vasospasm which precedes the onset of predictive test in clinical use. 68

718 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



TABLE 26.5 Definitions of conditions characterised by BOX 26.1 Theories on the pathophysiology
hypertension in pregnancy of preeclampsia 71

Term Definition Placentation and the immune theory of preeclampsia:
l maternal–fetal (paternal) immune maladaptation
Hypertension in l Systolic BP ≥140 mmHg and/or a diastolic
pregnancy BP ≥90 mmHg 65 l superficial abnormal placentation
l impaired spiral artery remodelling
Essential l Hypertension presenting in the first 20
hypertension weeks or that existed prior to the Placental debris hypothesis: syncytiotrophoblast shedding
pregnancy without an apparent l increased syncytiotrophoblast shedding
underlying cause 65 l placental ischaemia and reperfusion with subsequent oxi-
Gestational l Hypertension arising after 20 weeks’ dative stress
hypertension gestation and resolving by 3 months l increased circulating levels of inflammatory cytokines,
postpartum corticotropin-releasing hormone, free-radical species and
l No evidence of any other feature of the activin A
multisystem disorder preeclampsia 65
Preeclampsia l Hypertension arising after 20 weeks’ Endothelial activation and inflammation:
(Also referred to gestation in combination with one or l enhanced vascular sensitivity to angiotensin II and
as pregnancy more of the following: 65 noradrenaline with subsequent vasoconstriction and
induced l Proteinuria >300 mg/24 hrs hypertension
hypertension l Renal insufficiency: serum/plasma l a fall in production and activity of vasodilator prostaglan-
(PIH), toxaemia) creatinine ≥0.09 mmol/L or oliguria
l Liver disease: raised serum dins, especially prostacyclin and nitric oxide
transaminases and/or severe epigastric/ Genes, the genetic-conflict hypothesis, and genetic imprinting:
right upper quadrant pain
l Neurological problems: convulsions l susceptibility genes, many of which interact with the
(eclampsia), hyperreflexia with clonus, maternal cardiovascular or haemostatic system, or with the
severe headaches with hyperreflexia, regulation of maternal inflammatory responses
persistent visual disturbances
l Haematological disturbances:
thrombocytopenia, DIC, haemolysis
l Fetal growth restriction
Eclampsia l Is a form of severe preeclampsia
l Generalised tonic-clonic seizures, not l family history of preeclampsia, particularly on the
caused by epilepsy or other disease, and maternal side of the family
occurring ≥20 weeks gestation, during
labour or in the postpartum l multiple pregnancy e.g. twins
l body mass index >25 prior to pregnancy
HELLP syndrome l Is a form of severe preeclampsia, although l a new fathering partner for the index pregnancy
hypertension may not be present 69
l Diagnosis of HELLP syndrome is made by l achieving conception using assisted techniques, such
the presence of the following three as in vitro fertilisation.
criteria: 70
l Haemolysis: characteristic peripheral Unfortunately, these known risk factors are not overly
blood smear and serum lactate clinically helpful, as about half of the childbearing popu-
dehydrogenase >600 U/L or serum total lation has at least one. A high priority should be placed
bilirubin ≥1.2 mg/dL on early and accurate diagnosis of preeclampsia in a preg-
l Elevated liver enzymes: serum aspartate
aminotransferase ≥70 U/L nant woman rather than designating a woman as ‘high
9
l Low platelet count: <100 x 10 /L risk’ or ‘low risk’.
DIC – disseminated intravascular coagulopathy; HELLP – haemolysis, Incidence
elevated liver enzymes and low platelets.
The incidence of preeclampsia is reported between 2–8%,
73
with variations based on severity of the disease. The
incidence of eclampsia in developed countries has
Risk Factors reduced since the routine use of magnesium sulphate has
A number of maternal characteristics are associated with been adopted; in the UK, the rate is about 3 cases of
74
an increased likelihood for the development of pre- eclampsia for every 10,000 births. A prospective bina-
eclampsia; these include: 71,73 tional study on the incidence of eclampsia in Australia
and New Zealand is underway by the Australasian Mater-
l nulliparity nity Outcomes Surveillance System (AMOSS), and intends
l age ≥40 years to document Australian and New Zealand population-
75
l preexisting medical conditions including diabetes, based incidences for the first time. The incidence of
chronic hypertension, chronic renal disease, antipho- HELLP syndrome is reported to be between 0.11% and
spholipid antibodies 0.67% of all pregnancies. 76,77 Preeclampsia is one of the
l preeclampsia in a prior pregnancy, particularly if the most common indications for ICU admission at approxi-
previous preeclampsia presented prior to 34 weeks mately one ICU admission for every 1000 deliveries. 3

Pregnancy and Postpartum Considerations 719

Clinical Presentation and Diagnosis specific sign of preeclampsia, though women who develop
The clinical presentation of preeclampsia is often subtle, non-dependent oedema, such as facial oedema, should
66
resulting in delayed diagnosis and treatment. Common be investigated for evidence of preeclampsia. Common
symptoms include feeling ‘generally unwell’, headache, investigations include urea, creatinine and electrolytes,
heartburn, nausea and vomiting, and oedema; all non- full blood examination, liver function tests, serum uric
specific symptoms experienced by many pregnant women acid, spot urine protein/creatinine ratio and 24 hour
who do not have preeclampsia. Severe preeclampsia is urine collection. Additional tests, such as coagulation
associated with severe headache, hypereflexia, vision dis- studies, may be required as indicated by the clinical con-
turbances, severe epigastric pain, right upper quadrant dition. Intra-uterine fetal growth restriction is a sign of
pain and even blindness. There is also evidence of placental involvement (i.e. impairment) and investiga-
impaired systolic and diastolic myocardial function. tion into fetal wellbeing, including an ultrasound for
Diagnosis is made when the woman has hypertension fetal growth estimation and amniotic fluid volume, and
(BP ≥140/90), in association with evidence of multisys- umbilical artery Doppler flow patterns should be done
tem involvement (Box 26.2). Severe preeclampsia is diag- routinely following a diagnosis of severe preeclampsia.
nosed when the BP is ≥160/110, in association with The presentation of preeclampsia is usually restricted to
multisystem involvement. Additionally, eclampsia and women ≥20 weeks’ gestation unless they have a co-existing
HELLP syndrome are considered severe variants of pre- condition that is known to be associated with the <20
eclampsia even if the woman is normotensive. weeks presentation of preeclampsia including hydatidi-
form mole, multiple pregnancy, fetal triploidy, severe
This clinical diagnosis has replaced the traditional triad
of signs of hypertension, proteinuria and oedema, in maternal renal disease or antiphospholipid antibody
66
accordance with the increased understanding of the mul- syndrome.
tisystem nature of the disease. Raised blood pressure is The old adage is that approximately one-third of eclamp-
commonly, but not always, the first sign of the condition. sia occurs during pregnancy, one-third during labour and
Although proteinuria is the most commonly recognised one-third postpartum; the UKOSS study found 45% of
additional feature after hypertension, it is not mandatory first eclamptic fits were during pregnancy, 19% during
to make a clinical diagnosis. Oedema is no longer a labour and 36% postpartum. The majority of post-
74
partum eclampsia occurs in the first 48 hours, although
late-onset eclampsia may occur at two to three weeks
postpartum. Despite the nomenclature, eclampsia can
BOX 26.2 Diagnostic features of occur without any preceding signs and symptoms of pre-
preeclampsia eclampsia. In the UKOSS eclampsia study, only 38% of
women had established hypertension and proteinuria in
Hypertension ≥140/90 accompanied by one or more of the the week preceding the eclamptic fit and 21% of women
74
following: had no sign or symptom prior to the first eclamptic fit.
l Renal involvement: HELLP syndrome commonly presents during pregnancy
l Significant proteinuria: dipstick proteinuria subsequently with about 30% postpartum. 78
confirmed by spot urine protein/creatinine ratio Most women admitted to ICU with a diagnosis of pre-
≥30 mg/mmol or >300 mg protein in a 24 hour urine eclampsia have usually delivered prior to transfer, and
collection require support for complications of preeclampsia, e.g.
l Serum or plasma creatinine >90 µmol/L acute renal failure, disseminated intravascular coagula-
l Oliguria (<500 mL/24 hours) tion (DIC), pulmonary oedema and fluid management.
l Haematological involvement Once the placenta is delivered, most women improve
9
l Thrombocytopenia (<100 × 10 /L) within 24–48 hours, however, women with HELLP syn-
l Haemolysis drome may experience a worsening of condition in the
l Disseminated intravascular coagulation first 48 hours postpartum. Uncontrolled hypertension
l Liver involvement remains a major concern and is associated with cerebral
l Raised serum transaminases haemorrhage, one of the dominant causes of death in
l Severe epigastric or right upper quadrant pain. women with preeclampsia.
l Neurological involvement
l Convulsions (eclampsia) Management Priorities
l Hyperreflexia with sustained clonus
l Severe headache Women with mild preeclampsia at term may be managed
l Persistent visual disturbances (photopsia, scotomata, with induction of labour and delivery and experience few
cortical blindness, retinal vasospasm) complications. The management of women with severe
l Stroke preeclampsia is focused on stablising the woman’s condi-
l Pulmonary oedema tion, optimal timing of delivery of the baby (and pla-
l Fetal growth restriction centa) and preventing complications of the condition.
l Placental abruption Women with eclampsia and HELLP syndrome require
the same treatments as other women with severe pre-
Adapted from (66 and 71). eclampsia, even though they may or may not have the
same degree of hypertension. 69,79

720 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Prevention of eclampsia
Magnesium sulphate has received the most attention as BOX 26.3 Management of women with
an anticonvulsant in preeclampsia, with its mechanism HELLP syndrome using steroids
of action thought to be connected to the release of pros-
tacyclin from the endothelium, reversing the vasocon- The use of steroids has been evaluated in the management
striction that is the basis of the disease. 80,81 Magnesium is of HELLP syndrome in the belief that steroids may mitigate
the anticonvulsant of choice to reduce the incidence of the severity of the disease. However, a Cochrane Review con-
eclampsia. 82,83 A common magnesium regimen is: 68,82 cluded that there was insufficient evidence to determine
whether steroid use as a treatment for HELLP syndrome had
l 4g IV loading dose given over 15–20 minutes a favourable outcome for mothers and babies, although
l an ongoing infusion of 1 g/hr steroids may be beneficial if an increase in platelet count was
l an additional 2–4 g IV loading dose should be admin- imperative. 88
istered over 10 minutes to treat a recurrent eclamptic
seizure
l continue infusion until 24 hours following delivery or
24 hours following the last eclamptic fit; whichever
occurs the later. preeclampsia, to optimise plasma volume and organ per-
87
fusion without the development of pulmonary oedema.
The optimal therapeutic level of magnesium required to Central venous pressure is universally accepted as unhelp-
reduce the risk of fitting is not well understood and many ful to guide fluid management in preeclampsia. See also
advocate against the need to monitor serum magnesium Box 26.3.
levels on the basis that clinical assessment of deep tendon
reflexes, urine output and respiratory rate is adequate to Thrombophylaxis
identify potentially toxic magnesium levels, 68,82 although
evidence is inconsistent. Other opinions suggests a thera- Preeclampsia is an independent risk factor for thrombo-
peutic serum magnesium level of 2 mmol/L but there is embolic disease and when combined with prolonged bed
no rationale provided for this level. 84 rest, as may occur with caesarean section, ICU admission,
obesity and age ≥35 years, due consideration must be
Control hypertension made on the need for thrombophylaxis (in the absence
Obtaining control of high blood pressure remains a pri- of any contraindications). Thus women with severe pre-
ority not only to improve organ perfusion but to mini- eclampsia admitted to ICU may meet the requirements
mise the risk of cerebral haemorrhage, a well-demonstrated for treatment with compression stockings and low mole-
30
24
hazard of hypertension in preeclampsia. Both systolic cular weight heparin for a minimum of 7 days.
and diastolic pressures are important and care should be
taken to ensure a controlled lowering of blood pressure, Betamethasone
as a rapid drop can compromise fetal wellbeing. There is Women in late pregnancy with severe preeclampsia diag-
no evidence for the superiority of any specific antihyper- nosed prior to 34 weeks’ gestation are normally pre-
tensive, although there is some evidence that diazoxide scribed a single dose of betamethasone (11.4 mg IM), to
may result in a potentially-harmful rapid drop in the promote fetal lung maturity and surfactant production. A
woman’s blood pressure, and that ketanserin may not be Cochrane Review has shown that treatment with antena-
83
as effective as hydralazine. Intravenous hydralazine is tal corti costeroids reduces the risk of neonatal death,
the most common drug used to treat very high blood respiratory distress syndrome, cerebroventricular haem-
pressure with IV labetalol increasingly being used. Severe orrhage, necrotising enterocolitis, infectious morbidity,
hypertension may be treated with IV GTN or nitroprus- need for respiratory support and neonatal intensive care
side. The target blood pressure is not well described, other unit admission, with no adverse effects on the mother. 89
than to avoid precipitous drops in BP and to maintain
adequate placental perfusion. Research has used a target Optimal timing of delivery
diastolic BP of 85–95 mmHg. 85 Women with severe preeclampsia can only be definitively
cured by delivery, no matter what the gestation. A number
Optimal fluid management of studies have trialled ‘temporising treatments’, aimed at
Despite being hypertensive, preeclamptic women are prolonging the pregnancy especially when a woman
86
usually plasma-volume depleted. In the past, intrave- develops early onset severe preeclampsia (<34 weeks’ ges-
nous fluid was administered in an attempt to restore the tation). Whilst some have found that treatment with
deficit, with no advantage noted between colloids and vasodilators and fluid administration prolongs pregnancy
crystalloids. More recently, there has been a move towards with no adverse effect, the general belief is that prolong-
more conservative plasma volume expansion due to the ing the pregnancy is associated with an increased chance
risk of pulmonary oedema. In reviews of maternal deaths of the maternal complications of preeclampsia, such as
associated with preeclampsia, it was noticed that some eclampsia, pulmonary oedema and cerebral haemor-
women were dying from complications of fluid overload. rhage. 68,90 Consequently, a woman with severe preeclamp-
Careful titration of intravenous fluid is required with the sia is usually stabilised (magnesium sulphate commenced
use of pulmonary artery catheters advocated by some to and hypertension controlled) and arrangements for
guide the administration of fluid in women with severe delivery are made. Ideally, women <34 weeks’ gestation

Pregnancy and Postpartum Considerations 721

should be transferred to a tertiary obstetric centre prior Antepartum Haemorrhage
to delivery.
Antepartum haemorrhage (APH) is defined as any bleed-
ing from the genital tract occurring between the 20th
week of gestation and the birth of the baby and occurs in
92
2–5% of all pregnancies. Bleeding from the vagina prior
Practice tip
to 20 weeks’ gestation is referred to in terms of miscar-
Many maternity professionals abbreviate preeclampsia to PE. riage (e.g. threatened) and is not classified as an APH. The
This can be very confusing given that in other health care two main causes of APH are placental abruption and
settings, the abbreviation PE usually stands for pulmonary placenta praevia.
embolism. Be clear in any notes that you make, and clarify when
reading notes that have been given to you. Placental abruption (or abruptio placentae)
Placental abruption is premature separation (i.e. before
the birth of the baby) of a normally-sited placenta from
OBSTETRIC HAEMORRHAGE the uterine wall and is responsible for about 25% of
92
APH. Only a portion of the placenta separates with two-
Obstetric haemorrhage is a leading cause of maternal thirds separation considered severe. There are two rele-
mortality across the world and directly accounts for an vant matters to consider with placental abruption: how
estimated 127,000 deaths each year. Postpartum haemor- much blood the woman has lost and how much placenta
rhage (PPH) is responsible for the majority of these remains attached and functionally able to support the
maternal deaths. The past decade has seen an increase in fetus. If the placenta partially separates along an edge of
both the incidence and severity of obstetric haemorrhage, the placenta, blood loss is usually visible via the vagina.
with more women requiring a blood transfusion for post- In some cases the centre part of the placenta detaches,
partum haemorrhage than in the past. Severe bleeding leaving the rim attached all the way around (like the rim
91
in childbirth is estimated to occur once in every 200–250 of a dinner plate) and in these cases, the blood loss is
births, although incidence is highly dependent on how usually not visible via the vagina (i.e. is concealed).
‘severe bleeding’ is defined. Major obstetric haemor- However, the woman may have lost substantial blood
24
rhage is often sudden and unexpected, and is frequently volume and be in hypovolaemic shock. This type of
associated with an acute coagulopathy. Early recognition placental abruption is usually accompanied by severe
and treatment of major obstetric haemorrhage is vital to abdominal pain and DIC commonly develops in response
ensure the best outcome for mother and fetus. A repeated to blood being forced into uterine muscle tissue; referred
finding in maternal death reviews is a delay by obstetric to as a couvelaire uterus. Once half to two-thirds of the
providers in recognising the severity of haemorrhage and placenta is detached, the likelihood of fetal survival is
a consequent deterioration in maternal condition. 24 low, especially if the woman is also hypotensive. In the
majority of cases, only women with severe placental
Obstetric haemorrhage may occur after the 20th week
gestation up to the birth (antepartum haemorrhage) and abruption are admitted to ICU and usually admission
after the birth of the baby (postpartum haemorrhage). occurs following an emergency caesarean section. Under-
Severe obstetric haemorrhage is a common reason standing of the aetiology of placental abruption is not
for postpartum women to be admitted to ICU complete with approximately 20% of cases unexplained.
at 0.7/1000 deliveries, with many women experiencing For most women, placental abruption is associated with
3
haemorrhage before and after the birth of the baby. a known related factor like preeclampsia, blunt trauma
Although not classified technically as an obstetric (e.g. car crash) and sudden reduction in uterine
haemorrhage, ruptured ectopic pregnancy can also volume (e.g. after delivery of the first baby in a twin
result in life-threatening haemorrhage and result in pregnancy).
ICU admission. The common causes of antepartum Placenta praevia
and postpartum haemorrhage are described below with
common management strategies presented at the end of Placenta praevia is when some or the entire placenta is
the section. See also Box 26.4. abnormally sited in the lower segment of the uterus, often
referred to as a low-lying placenta. Placenta praevia is
graded into four categories of severity according to the
location of the placenta in relation to the cervix (Box
26.5). A vaginal birth is not possible with Grades III and
BOX 26.4 What about vaginal bleeding IV as the placenta blocks the passage for the baby, neces-
before the 20th week of gestation? sitating a caesarean section. The lower uterine segment
does not fully form until 28–32 weeks’ gestation and the
Vaginal bleeding before the 20th week of gestation (usually a shearing stress as the lower uterine segment forms may
type of miscarriage, e.g. threatened, incomplete) is considered precipitate detachment of the placenta from the uterine
‘early pregnancy bleeding’ and is not categorised as obstetric wall causing maternal bleeding. However, bleeding can
hae morrhage per se. Septic abortion (or miscarriage) can cause occur at any time, is usually painless and may be massive.
profound bleeding in the days after the event when the infec- Placenta praevia is the main cause of APH accounting for
92
tion has become established. 30% of cases. As with placental abruption, management
is dictated by the size of the blood loss and maternal

722 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



BOX 26.5 Categories of severity of placenta BOX 26.7 Causes of post-partum
praevia haemorrhage characterised by the 4 ‘T’s

l Type I (low-lying placenta): The placenta is located in the Tone:
lower uterine segment but does not impede on the internal l uterine atony
cervical os. l functional or anatomical distortion of the uterus (e.g.
l Type II (marginal): The placenta edge is aligned with the bi-cornuate uterus)
internal cervical os. Tissue:
l Type III (partial): The placenta lies over and partially covers l retained placental products
the internal cervical os. l abnormal placenta
l Type IV (complete): The placenta is centrally located over
the cervix and completely covers it. Trauma:
l cervical and genital tract damage during delivery
l uterine inversion
BOX 26.6 Types of placenta accreta Thrombin:
l Coagulation disorders
l Placenta accreta: the placenta is abnormally adherent to
the uterine lining
l Placenta increta: the placenta invades the uterine muscle
(myometrium)
l Placenta percreta: the placenta grows through the myome- BOX 26.8 Can PPH be prevented?
trium and into adjacent structures, such as the bladder and The most significant intervention shown to reduce the inci-
ureters
dence of PPH is active management of the third stage of labour.
This represents a group of interventions including controlled
cord traction for placental delivery and prophylactic adminis-
condition, how much functioning placenta remains and
fetal wellbeing, and whether bleeding is ongoing. In tration of a uterotonic at delivery: drugs that cause the uterus
severe cases, the woman is usually taken to theatre for an to contract. Active management of the third stage is associated
emergency caesarean section. with a lower incidence of PPH and a reduced need for a blood
transfusion.
Placenta accreta is a serious complicating condition that
may occur in conjunction with placenta praevia. The
attachment of the placenta to the uterine wall is abnor-
mal and is considered morbidly adherent. There are three Postpartum Haemorrhage
levels of severity, although often all three are referred to Postpartum haemorrhage (PPH), a major cause of mater-
as placenta accreta (Box 26.6). Placenta accreta is strongly nal death in developed and developing countries, is
associated with prior caesarean section and a woman defined as ≥500 mL blood loss from the genital tract after
with an anterior placenta praevia and a prior caesarean the birth of the baby. The incidence and severity of PPH
section should be actively screened for placenta accreta is increasing, in both caesarean and vaginal births. 91,94-96
(by ultrasound or MRI) prior to any elective caesarean PPH rates commonly sit at around 10% of all births.
section. Placental tissue can be very invasive and may Severe PPH lacks an agreed definition, with published
infiltrate local structures like the bladder. Many women definitions ranging from ‘≥1000 mL’ to ‘estimated blood
with placenta accreta undergo emergency hysterectomy at loss ≥2500 mL or transfused ≥5 units of blood or received
the time of caesarean section, as a means to remove the treatment for coagulopathy during the acute event’. 12,97
placenta and control bleeding. An alternative manage- Consequently, the incidence of severe PPH varies depend-
ment is to deliver the baby by caesarean section and leave ing on how it has been defined and ranges from 3.7/1000
the placenta in situ. As long as a portion of the placenta deliveries to 4.6/1000 deliveries. 5,97 Additionally, PPH is
93
does not detach, there will be no bleeding and in most also classified according to the timing of the haemorrhage
cases, the placenta will autolyse and be re-absorbed by in relation to the birth. Primary PPH occurs within the
the woman. first 24 hours after birth whilst secondary PPH occurs
from 24 hours up to six weeks following birth. Primary
PPH is often caused by uterine atony, whilst secondary
Practice tip PPH is more likely to be associated with retained prod-
ucts and associated infection.
Read a woman’s operation report if she has a diagnosis of
placenta accreta to identify the extent to which the placental The causes of PPH are varied and have been classified by
tissue has invaded local structures, such as the bladder, ureters the four ‘Ts’: tone, tissue, trauma and thrombin (Box
and bowel. For example, the bladder is often affected and a 26.7). The cause of the PPH should be identified and
cystotomy may have been required to separate the placenta targeted with specific management, in conjunction with
from the bladder. the general principles of haemorrhage management. See
also Box 26.8.

Pregnancy and Postpartum Considerations 723

Severe Obstetric Haemorrhage complicates fluid resuscitation. 100,101 Standard resuscita-
Management Priorities tion fluids, such as normal saline, should be infused
Whilst it is feasible for a pregnant woman in ICU according to routine practice of the non-obstetric haem-
to develop placental abruption, for example, the vast orrhage, remembering that large volumes of blood prod-
majority of women admitted to ICU with obstetric ucts may also be required.
haemorrhage will be transferred following birth, and
are thus postpartum on admission to ICU. These
priorities focus on postpartum management. As with
any major haemorrhage (see Chapter 20), the principles Practice tip
of treatment are:
Keep in mind that:
l restore an adequate circulating volume and maintain
oxygen and perfusion to vital organs l Serum albumin levels are decreased in normal pregnancy,
46
l obtain haemostasis and correct coagulopathy with the lowest levels recorded in the postpartum period.
l prevent complications. l Cardiac output remains elevated postpartum for the first
few days at least.
See Box 26.9 for acute immediate treatment. l CVP and PAP can be interpreted the same as for non-
obstetric patients.
Maintaining circulating volume, oxygenation
and perfusion
Haemodynamic instability following substantial blood
99
loss is a frequent reason for admission to ICU. Accurate Achieving haemostasis and correct coagulopathy
estimation of blood loss is difficult as bleeding can Specific interventions to control haemostasis include
be concealed, and the presence of amniotic fluid makes radiological arterial embolisation or balloon occlusion of
accurate blood volume loss estimation a challenge, the internal iliac arteries and emergency hysterectomy. It
potentially leading to an underestimation of fluid resus- is not uncommon for women to need to return to theatre
citation needs. Furthermore, peripartum women are at an for abdominal packing for ongoing ‘ooze’ that may con-
increased risk of acute pulmonary oedema, which further
tinue after a hysterectomy. Most women with severe
obstetric haemorrhage in ICU have developed DIC that
requires treatment with the appropriate blood prod-
ucts. DIC is particularly common in these women in
102
part because of the normal changes in the clotting factors
during pregnancy and in part due to the potential for
BOX 26.9 Summary of acute immediate an amniotic fluid embolism to have been the triggering
treatment for PPH event for the haemorrhage. 86,103,104
Large volumes of blood products, such as packed red
Resuscitation and immediate management:
l ABC; administer 100% oxygen cells, fresh frozen plasma, platelets and cryoprecipitate
l ‘Rub’ up the uterus are often required. Guidelines recommending the ratio of
l 2 large bore cannulae and send bloods for rapid crossmatch red blood cells:fresh frozen plasma:platelets in acute
l Administer oxytocics e.g. syntocinon 98 major haemorrhage are under development in many
l Fluid resuscitation countries. Increasingly it is thought that more aggressive
l Determine the cause (4 Ts) use of fresh frozen plasma and platelets in line with red
l Transfuse blood (O-negative in the first instance then type blood cell usage is needed to prevent and/or correct
specific) haemorrhage coagulopathy. A recent large trauma study
l Prepare for transfer to theatre found that a 1 : 1 ratio for both red blood cells/fresh
frozen plasma and red blood cells/platelets, if given early
Surgical treatment and other interventions: following a major blood loss, resulted in significantly
105
l Delivery of placenta and uterine pathology, if applicable improved mortality. There has been no similar study
l B-lynch suture conducted in obstetric patients, although it is likely that
l Uterine tamponade, e.g. inflation of uterine balloon for obstetric patients may also benefit from more liberal early
local compression use of fresh frozen plasma and platelet transfusions.
l Surgical ligation Importantly, the large trauma study found the increased
l Hysterectomy ratios of FFPs and platelets were not associated with
l Compression of the aorta an increase in transfusion-related acute lung injury and
l Uterine replacement (if uterine inversion noted) acute respiratory distress syndrome from inflammatory
105
l Radiological arterial embolisation or balloon occlusion mediators. Finally, recombinant Factor VIIa has been
l Consider systemic haemostatic agents used successfully in the management of severe obstetric
l Aprotinin (Trasylol) haemorrhage and should be considered for use early in
l Vitamin K the management of the bleeding woman, with treatment
l Tranexamic acid more likely to be effective if administered before the
woman becomes hypothermic and acidotic. 106

724 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Preventing complications salvage and in practice, there has been no confirmed case
111
Strategies to prevent the following complications should of AFE following use of cell salvage infusion. Regard-
be implemented: less, it is common practice to use a different suction
device from the time of amniotic membrane rupture until
l Complications of major blood transfusion: these are after delivery (which is not re-used) with blood aspirated
similar in the obstetric patient as the non-obstetric from the surgical field collected by the cell salvage
patient and include: acid–base disturbance, trans- device. A leukocyte depletion filter should always be
110
fusion related acute lung injury (TRALI), hypocal- used during the re-infusion of salvaged maternal blood
caemia, hyperkalaemia and hypothermia. Standard to filter any remaining foreign proteins. None of the
109
monitoring and treatment of these complications currently available cell saver equipment is able to discern
should be used. fetal from adult red blood cells and any present fetal cells
l Increased risk of thrombosis: particularly in the early are transfused to the woman. It is important for Rhesus-
postpartum period as the risk is exacerbated by lengthy negative women to have a post-infusion Kleihauer-Betke
theatre procedures, bed rest associated with ICU test to quantify the amount of fetal red cells in the
admission and following major haemorrhage with an maternal circulation to ensure that an adequate dose of
associated massive blood transfusion. Suitable throm- anti-D immunoglobulin can be given to prevent
boprophylaxis should be considered as soon as fea- isoimmunisation.
sible and thromboembolic stockings and/or sequential
compression devices should be applied.
l Acute renal failure: irreversible renal failure has been AMNIOTIC FLUID EMBOLISM
reported as a sequela of acute renal failure following Amniotic fluid embolism (AFE) is a rare and incom-
severe postpartum haemorrhage. Routine monitor- pletely understood obstetric emergency that usually
107
ing and management of renal impairment is required, occurs during labour or pregnancy termination, or shortly
keeping in mind that a pregnant patient has a lower after delivery. Traditional understanding of the condition
urea and creatinine level than non-pregnant patients. was based around the notion that amniotic fluid entered
Careful titration of fluid for renal purposes is needed the maternal blood stream via the endocervical veins or
due to the increased propensity for pulmonary placental bed, with amniotic fluid, fetal cells, hair, or
oedema. other fetal debris functioning as an embolus, and result-
l Rh isoimmunisation: the potential to develop Rh ing in the dramatic cardiorespiratory collapse seen with
isoimmunisation in Rh-negative women who have the condition. However, not all women diagnosed with
experienced antepartum haemorrhage should be con- AFE have evidence of fetal squames/amniotic fluid sub-
108
sidered. A Kleihauer-Betke test should be done to stances in the pulmonary vasculature and many women
quantify the amount of fetal cells in the maternal who do not develop AFE have fetal cells found in the
circulation and determine the dose of anti-D immu- maternal circulation. 112
noglobulin required.
l Sheehan’s syndrome: necrosis of the pituitary gland is More recently, improved understanding of the mechanics
a very rare complication of severe obstetric haemor- of labour and the interaction of amniotic fluid and mater-
rhage. The anterior lobe is most often affected due to nal blood, as well as the striking similarities between
physiological changes that occur during pregnancy. clinical and haemodynamic findings in AFE and both
Whilst the syndrome may go undetected for many anaphylaxis and septic shock, have led to a belief that a
years, one of the earliest symptoms is a failure to common pathophysiological mechanism is likely to be
113
establish lactation, due to the absence of prolactin responsible for all these conditions. As AFE resembles
secretion. Sheehan’s syndrome can be prevented by an anaphylactic reaction to fetal material rather than an
maintaining adequate circulating volume, oxygen- embolic event, the term ‘anaphylactoid syndrome of
113
ation and perfusion. pregnancy’, instead of AFE, has been proposed. AFE has
also been likened to systemic inflammatory response syn-
drome, with the related inappropriate release of endog-
Use of Intra-operative Cell Salvage for enous inflammatory mediators. The trigger for AFE is
112
Obstetric Haemorrhage not well understood, although it is thought to be a fetal
The introduction of cell salvage in obstetrics has been antigen (which may arise from amniotic fluid). It is pos-
sible that all labouring women are exposed to the fetal
delayed compared to other surgeries for two key reasons: antigen, with those affected by AFE exhibiting a rare and
the theoretical risk of amniotic fluid embolism (AFE) and abnormal maternal immune response. One of the dif-
112
109
the risk of rhesus isoimmunisation. New technologies, ficulties blocking improved understanding of AFE is the
combined with an increasing obstetric haemorrhage rate, lack of a diagnostic test.
has seen cell salvage being introduced since the mid-
1990s, now becoming common practice. 109,110 Historical Regardless of the level of understanding, the abnormal
understanding of amniotic fluid embolism argued against mediator release gives rise to acute lung injury, resulting
the risk of infusing blood that potentially contained in acute dyspnoea and hypoxia and often the develop-
amniotic fluid. The more recent understanding that AFE ment of acute respiratory distress syndrome. Within 30
is more aligned with an anaphylactic reaction has less- minutes of the antigen insult, there is evidence of severe
ened these concerns as a woman has already been exposed pulmonary hypertension with acute right ventricular
114
to the contents of the fluid that are infused following cell failure. It is thought that inflammatory mediators are a

Pregnancy and Postpartum Considerations 725

more likely cause of pulmonary vasoconstriction, with quickly leading to fetal demise unless the fetus is deliv-
physical obstruction to the pulmonary vasculature ered swiftly. There is variation in the signs and symptoms,
(embolism) not the main mechanism. 112,115 The left ven- and in the timing of their presentation in individual
tricular failure seen in AFE is considered a secondary women. Premonitory symptoms, shortness of breath and
response due to poor left ventricular filling pressures. fetal distress have been reported as the early signs in a UK
116
Concomitantly, substances in the amniotic fluid trigger a study. Overall, haemorrhage and associated coagulopa-
profound consumptive coagulopathy. thy, hypotension and shortness of breath were the most
116
commonly recorded symptoms. Cardiac arrest was
Incidence and Risk Factors documented in 40% of cases and seizure in 15%. Hae-
The incidence of AFE is thought to be in the range of 2–8 morrhage and coagulopathy may not be immediately
women per 100,000 deliveries making it a very rare apparent, some women die before it develops, however
116
event. However, the lack of a diagnostic test is a serious these clinical features usually develop in women who
limiting factor for accurate determination of incidence, as survive the initial insult.
clinical diagnoses vary and the accuracy of hospital codes Treatment
that may be used to count the incidence are fraught with
116
potential error. There has been geographical variation There is no specific treatment for AFE; all therapy is sup-
in incidence reported, with AFE more common in North portive with the aim to maintain adequate oxygenation
America (1 in 15,200 deliveries) than in Europe (1 in and perfusion, control haemorrhage and correct any
115
53,800 deliveries); this may represent a true difference coagulopathy. Common interventions include: 116
in incidence or reflect differences in clinical diagnosis or l urgent delivery of the fetus
methods of case identification. l emergency hysterectomy to control postpartum
Diagnosis remains one of exclusion and there is a long haemorrhage.
list of differential diagnoses, including air or thrombotic l admission to ICU, with associated support such as
pulmonary emboli, septic shock, cardiomyopathy, acute mechanical ventilation, nitric oxide and extra-
myocardial infarction, anaphylaxis, transfusion reaction, corporeal membrane oxygenation (ECMO)
aspiration, placental abruption, eclampsia, uterine A full range of blood components, including fresh frozen
rupture, local anaesthetic toxicity and primary postpar- plasma, platelets and cryoprecipitate may be required
tum haemorrhage. Older obstetric literature quote to correct the coagulopathy. Adjunct therapies such as
113
mortality rates above 80%. More recent larger studies recombinant Factor VIIa have also been used with effect.
117
have shown that mortality in developed countries is more Transoesophageal echocardiography may be very helpful
likely to be in the range of 13–30%. 115,116,118 However, AFE to guide fluid and inotrope management to optimise
remains a major contributor to maternal death, account- preload and enhance cardiac output.
ing for 5–15% of all maternal deaths in developed
countries. 52,115 Although it is possible for a woman to experience an AFE
in a subsequent pregnancy, repeat AFE is thought to be
Although controversy exists, the factors that have been unlikely as the trigger for AFE is specific to each fetus the
proposed as contributing to an increased likelihood for woman carries. There have been a number of published
AFE include: 112,113,115,116,118 case reports of women having a successful subsequent
l induction of labour pregnancy and none reporting repeat AFE in the same
l caesarean birth woman.
l multiple pregnancy e.g. twins
l maternal age ≥35 years PERIPARTUM CARDIOMYOPATHY
l forceps delivery Peripartum cardiomyopathy, sometimes referred to as
l placenta praevia, preeclampsia and placental postpartum cardiomyopathy, is new onset heart failure in
abruption. association with pregnancy. Diagnosis is usually depen-
dent on all four of the following criteria: (1) the develop-
Given the rarity of AFE and the commonality of these ment of the disease in the last month of pregnancy or
potential risk factors, astute clinical assessment and early within five months of delivery; (2) absence of any other
clinical suspicion based on the clinical presentation of identifiable cause of heart failure; (3) absence of recogni-
the woman should be the focus for early identification sable heart disease before the last month of pregnancy;
and treatment.
119
and (4) left ventricle systolic dysfunction. However,
time of onset outside of the above criteria does occur
Presentation occasionally. Peripartum cardiomyopathy is considered
The symptoms associated with AFE have been well to be a dilated cardiomyopathy, resulting in a dilated left
described and usually comprise premonitory symptoms, atrium and ventricle, and a reduced left ventricular ejec-
120
such as restlessness, agitation and numbness/tingling tion fraction (< 45%). Women commonly present with
121
prior to more severe maternal compromise such as hypo- New York Heart Association Class III or IV heart failure.
tension, dyspnoea, hypoxia, altered mental status and The incidence of peripartum cardiomyopathy varies
115
haemorrhage. Additionally, in pregnant women, col- widely from 1:100 in a small region of sub-Saharan Africa
lapse of the maternal cardiovascular system leads to fetal to 1:4000 in the US, though many studies on peripartum
distress as the placenta is deprived of maternal oxygen, cardiomyopathy were conducted on data that had been

726 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

gathered retrospectively. 119,122 A relatively recent prospec- are required before this specific therapeutic intervention
tive population-based study in the Netherlands found is adopted for routine management.
that 1 in 20,000 pregnancies required ICU admission for For women diagnosed with peripartum cardiomyopathy
peripartum cardiomyopathy. 7
whilst pregnant, timing and mode of delivery are two
The exact cause of peripartum cardiomyopathy is not well other management decisions to be made. A multidisci-
understood and a variety of factors have been implicated, plinary team, including cardiologist, obstetrician, anaes-
including viral infection, autoimmune mechanisms, thetist and nursing/midwifery staff, should consider and
cytokine-mediated inflammation, increased myocyte plan for delivery dependent on maternal and fetal condi-
apoptosis, increased oxidative stress, genetic disposition tion and the woman’s known preferences. Ergometrine-
and/or cultural habits, and abnormal hormonal regula- containing drugs, used to contract the uterus post-delivery,
tion. 121,123 Maternal mortality associated with peripartum are contraindicated because they cause vasoconstriction
cardiomyopathy is around 15%, however, it may be as and the associated increase in afterload may be detrimen-
low as 2% in developed countries. 124 Studies show that tal for maternal heart function. Synthetic preparations,
approximately 20–40% of women recover their left such as oxytocin, are advised instead to prevent post-
ventricular function, usually within six months though partum haemorrhage. Finally, given the postulated role
it may take up to two years. 120,125 Women who never of prolactin in the aetiology of peripartum cardiomyo-
fully recover their cardiac function require ongoing pathy, recent guidelines advise against breastfeeding
medical management; a small proportion of women go in women who have been diagnosed with peripartum
on to require a mechanical-assist device and heart cardiomyopathy. 120
transplantation.
Subsequent Pregnancy
Management and Treatment Priorities Family planning counselling is an important part of the
Women with peripartum cardiomyopathy present with care of women as they recover from peripartum cardio-
varying degrees of left heart failure. Signs and symptoms myopathy. As indicated earlier, left ventricular function
of heart failure including dyspnoea, persistent cough, may take over two years to recover and women, after a
abdominal discomfort, palpitations and oedema may be diagnosis of peripartum cardiomyopathy, are at risk of a
mistaken for ‘discomforts of pregnancy’ and lead to a relapse in any subsequent pregnancy. Generally speaking,
delay in diagnosis. The diagnosis of peripartum cardio- women who become pregnant following a diagnosis
myopathy is one of exclusion requiring systematic of peripartum cardiomyopathy have approximately a
investigation to exclude both cardiac and non-cardiac 30% risk of relapse. 125,131 Peripartum cardiomyopathy
differential diagnoses such as pulmonary embolism, remains an important cause of maternal death and this
acute myocardial infarction, severe preeclampsia and may occur in association with subsequent pregnancies.
pneumonia. 126 Echocardiography is a useful diagnostic
tool with a left ventricular end-diastolic diameter >60 mm EXACERBATION OF MEDICAL DISEASE
120
predictive of poor recovery, as is a LVEF <30%. When ASSOCIATED WITH PREGNANCY
available, a cardiac MRI allows for better chamber volume
and functional assessment and is a more sensitive tool to Women with preexisting medical conditions pose addi-
identify a left ventricular thrombus. 120 tional challenges during pregnancy. In a population-
Management of peripartum cardiomypothy is centred on based prospective study of all pregnant and postpartum
optimising cardiac function and preventing complica- admissions to ICU in the Netherlands, 28% of women
7
tions. The principles of managing acute heart failure in had at lease one chronic disease. However, this preexist-
women with peripartum cardiomyopathy are no different ing medical condition may not have been related to the
to the management of heart failure from any other cause, need for ICU admission. For example, in an Australian
and aims to reduce preload and afterload and to increase study 39% of admissions to ICU had a medical history,
cardiac contractility (see Chapter 10 for a full descrip- but the preexisting illness was related to the ICU admis-
10
tion). Unfortunately, ACE inhibitors and angiotensin sion in 24% of women. Occasionally pregnant and
antagonists are contraindicated in pregnancy, and are postpartum women are admitted to ICU with exacer-
usually not prescribed. bation of an underlying medical condition and two of
the most common conditions, asthma and cardiac
Bromocriptine, a relatively new and novel treatment for disease, are outlined in this section.
peripartum cardiomyopathy, is still undergoing investiga-
tion and as such is not routinely prescribed. Recent ASTHMA
advances in understanding the aetiology of peripartum
cardiomyopathy have suggested that increased oxidative Epidemiology and Course of Asthma
stress plays a significant role and bromocriptine is directly During Pregnancy
able to reduce oxidative stress by blocking the release of Asthma is the most common chronic health disease in
prolactin. 127 Animal and early human studies show pregnant women, affecting 4–8% of all pregnancies in the
promise, with relapse of peripartum cardiomyopathy pre- US. 132 However, the incidence in Australia may be higher
vented in women in a subsequent pregnancy and rapid given the higher prevalence, 12–14%, of ‘current asthma’
recovery in new-onset peripartum cardiomyopathy in women of childbearing age. 133 The course of asthma
observed. 128-130 Larger studies confirming these findings during pregnancy is highly variable and not predictable

Pregnancy and Postpartum Considerations 727


Initial treatment for acute asthma Assess patient Further evaluation and
exacerbation response care
1) Give supplemental inhaled oxygen Good response: PEFR 70%
to keep O 2 saturation >95% or more and sustained for 60
2) Administration of inhaled salbuterol minutes. Normal exam, no Discharge to home
via nebuliser driven by oxygen distress, reassuring fetal
every 20 minutes, up to three status.
doses in the first hour. Incomplete response: PEFR Continue to monitor, add
3) If no improvement (or if severe 50-69%. Continued mild or iprotropium bromide. Continue
exacerbation) give IV or oral moderate symptoms. oxygen and inhaled salbuterol.
corticosteroids. Individualise plan for further
4) Continuous external fetal observation or hospitalisation.
monitoring for those > 24 weeks Consider systemic steroids.
gestation.
Poor response: PEFR less Continue fetal assessment.
than 50%, pCO 2 > 40-42 Consult intensive care unit for
mmHg admission. IV corticosteroids.
FIGURE 26.2 Acute management of exacerbation of asthma in pregnancy.
137


for any individual woman. Approximately one-third of the advice of a thoracic medicine specialist and an obste-
women experience an improvement in asthma symp- trician, who will continue the care of the woman once
toms, one-third report no change and one-third experi- discharged from ICU. Methacholine testing, used as a
ence exacerbation of asthma. 134 Curiously, the fetal gender diagnostic tool for asthma, is contraindicated in preg-
may be a relevant factor with the female fetus associated nancy, and a woman with a clinical picture consistent
with a worsening of asthma symptoms. 135 Generally with new-onset asthma, should be treated as such, until
141
speaking, the more severe asthma symptoms a woman diagnostic testing can be conducted postpartum. Treat-
exhibits pre-pregnancy, the more likely she will experi- ment of severe asthma in pregnancy is no different to the
ence an exacerbation during pregnancy resulting in hos- treatment in non-pregnant patients (see Chapter 14),
pitalisation. 136,137 Very severe exacerbations of asthma apart from the additional needs to monitor fetal wellbe-
during pregnancy requiring ICU admission are rare. A ing and consider the normal respiratory parameters in
persisting problem in pregnant women with asthma is pregnancy (Figure 26.2). Severe hypoxaemia associated
the potential for reluctance to treat (by physicians) and with an exacerbation of asthma places the fetus at risk
decreased medication compliance (by women), based on and should be avoided; maternal SaO 2 should remain
concerns about the safety of medication during preg- ≥95%. Peak flow measures are recommended to be used
nancy, with a substantial number of asthma exacerba- during pregnancy to assess and monitor the woman’s
tions in pregnancy associated with non-adherence to condition, with the normal values unchanged in preg-
prescribed drugs. 138,139 Studies comparing medication use nancy. 137 The risks associated with current asthma
have shown that pregnant women are also less likely to medication use in pregnancy are far less than the risks
be prescribed systemic corticosteroids than non-pregnant associated with uncontrolled asthma, and the regular
asthmatics. 138,140 The second and third trimesters are com- schedule of asthma medications should be prescribed
141
monly the time when a worsening of asthma symptoms in pregnancy according to asthma symptom level.
will develop, although women tend to have an improve- Likewise, none of the common drug categories such as
ment in symptoms for the last four weeks of a term inhaled corticosteroids, long-acting β-agonists and
pregnancy. 138 leukotriene-receptor antagonists, is contraindicated
during lactation. 141
Effect of Asthma on Pregnancy

The relationship between asthma in pregnancy and CARDIAC DISEASE
adverse maternal and neonatal outcomes including pre- Cardiac disease in pregnancy consists of women who
eclampsia, gestational diabetes, small-for-gestational-age have congenital heart disease and women who have
neonates and preterm birth is inconsistent. The general acquired heart disease, such as rheumatic heart disease.
belief is that poor maternal and neonatal outcomes are Congenital heart disease is one of the more common
associated with poor asthma management and not a forms of congenital birth defects with the four most
result of the treatment itself. 137
serious congenital cardiac defects having a combined rate
142
in Australia of 12.4/10,000 births. Increasing numbers
Management and Treatment Priorities of those affected with congenital heart disease are surviv-
A pregnant woman admitted to ICU with asthma may be ing into adulthood with the greatest increase in survival
experiencing new-onset asthma or an exacerbation of pre- benefit seen in people with severe disease. 143 The Cana-
existing asthma. Regardless, the management and treat- dian Cardiovascular Society estimates that in their popu-
ment priorities are the same. Accurate diagnosis and lation of 24 million, 96,000 adults will be living with
evaluation of the disease is necessary and should involve congenital heart disease. 143 The additional load placed on