ICU - Paediatric

FLUIDS & ELECTROLYTES

Total Body Water

a. TBW is higher ECF ICF

i. prem ~ 85% 45% 40%
ii. term ~ 75% 40% 35%
iii. 12/12 ~ 60% 27% 33%
iv. adult ~ 60% 20% 40%
b. both fat and muscle content increase with age
c. decreases in TBW are predominantly due to ECF decreases
d. as ECF decreases, ICF increases ~ 35% → ~ 43% @ 3 mth
e. predicted body weight < 9 yrs ~ (2 x age) + 9
> 9 yrs ~ 3 x age

higher proportion of TBW in younger children cf. adults is due to their relatively larger ECF
organs with more ECF (skin and brain) are a higher proportion of body weight, and those with
more ICF (muscle and viscera) are a lower proportion
obligatory water loss in urine depends on,
1. endogenous renal solute load
proportional to caloric expenditure and VO2, which are higher in infants
2. renal concentrating ability
limited ability to dilute / concentrate urine cf. adult,
i. infant ~ 200-800 mosm/l
ii. adult ~ 80-1200 mosm/l

this, combined with a higher solute load (VO2) and higher insensible losses, makes infants more
prone to develop water deficits

Daily Water Requirement

Day 1 ~ 2 ml/kg/hr1
Day 2 ~ 3 ml/kg/hr
Day 3 - 12 Months ~ 4 ml/kg/hr2
10 - 20 kg ~ 40 + 2 ml/(kg>10)/hr
> 20 kg ~ 60 + 1 ml/(kg>20)/hr
1
kcal/kg/hr can be substituted for ml/kg/hr

2
some say 120 ml/kg/day for day 4 and over
 ICU - Paediatric

Sodium Requirement

a. days 1 & 2 - low urinary Na + loss & high insensible water losses
→ risk of hypernatraemia
→ use 5-10% dextrose
b. ≥ 3 days → 2-4 mmol Na+/kg/day

Potassium Requirement

NB: similar to Na+ → ~ 2-4 mmol K +/kg/day

≤0.5 mmol/kg/hr
* absence of anuria / severe oliguria

therefore, example of maintenance fluids might be,

a. day 1 → 5% or 10% dextrose at 2 ml/kg/hr
b. ≥ day 2 → 5% dextrose + Na+ 40 mmol/l
K+ 20 mmol/l

@ 4 ml/kg/hr

Elemental Requirements
sodium 2-6 mmol/kg/d
potassium 2-4 mmol/kg/d
calcium 0.5-1 mmol/kg/d
magnesium 0.5-1 mmol/kg/d
phosphate 0.4-1 mmol/kg/d
glucose 10-15 g/kg/d
neonates1 ~ 20 g/kg/d
1
glucose 20 g/kg/d ~ 80 kcal/kg/d
~ 80% of energy requirement

NB: glucose requirement → ~ 4-6 mg/kg/min S.K.

~ 6-8 g/kg/day

~ 6-8 mg/kg/min N.M. for neonates

2
 ICU - Paediatric

Replacement Solutions and Composition

Solution % mmol/ml Infusion rate
NaCl 20 % 3.4 ~ 0.6 x TBW x (125-[Na+])
KCl 7.5 % 1 0.5 mmol/kg/hr
NaHCO3 8.4 % 1 ~ 0.5-2.0 ml/kg
∝ BE & pH
CaCl2 10 % 0.68 0.1-0.2 mmol/kg/hr
Ca-gluconate 10 % 0.22 as above
MgSO4 49.3% 2 0.4 mmol/kg/hr

Clinical Assessment

a. mild dehydration ~ 5% loss of body water

- thirsty, irritable
- poor tissue turgor
- dry mucous membranes
b. moderate dehydration ~ 10% loss of body fluid
as 5% plus, - tachycardia, oliguria
- sunken fontanelles
- poor capillary refill
c. severe dehydration ≥ 15% loss of body water
as 10% plus, - hypotension, anuria
- tachypnoea
- sunken eyeballs
- skin mottled, cold peripheries
- diminished / absent peripheral pulses
NB: ≥ 20% may result in coma

Investigation

a. body weight = best guide

+
b. serum [Na ] ~ water balance
i. urine Na+ < 20 mmol/l = hypovolaemia
ii. urine Na+ > 40 mmol/l
+ oliguria = ATN, renal failure, etc.

3
 ICU - Paediatric

Adjustment Factors for Fluid Requirements

Decreased
hypothermia - 12% / °C
high ambient humidity

head injury
IPPV (ADH) x 0.7
high ADH
paralysis (decreased BMR)

inactivity

IPPV with humidified gases x 0.75

renal failure x 0.3 + urine output

SIADH

Increased
hyperthermia + 12% / °C

ambient temperature > 31°C + 30% / °C

radiant heater, phototherapy x 1.3

motor activity
air currents
low ambient humidity

age (preterm infant ~ 1.0-1.5kg) x 1.2

hyperventilation x 1.2

dry or cool inspired gases

burns - day 1 + (4x %SAburn)%

- day 2 & after + (2x %SAburn)%

4
 ICU - Paediatric

Management - Hypovolaemia/Dehydration

a. give adequate volume of colloid/crystalloid to restore circulatory status

NSA-5% ~ 10-20 ml/kg
SPPS used to cause vasodilatation (diluted HSA-conc to 5% OK)
if no response to 20 ml/kg then presume other cause for hypotension & consider
insertion of a CVC line
b. IVT = deficit + maintenance + ongoing losses
c. replace deficit over next 24 hrs
~ ½ deficit over 8 hrs, remainder over 16 hrs
if hypernatraemic, then replace over 48 hrs

Hyponatraemia

a. renal loss - poor renal conservation

b. breast milk - low Na+ content
c. inappropriate ADH - IPPV /CPAP
- head injury or CNS disease
- respiratory disease
d. excess water intake
e. hypotonic IV fluids
NB: → ileus
hypotension
listlessness
± convulsions

RX H2O excess - water restriction ± Na+/frusemide

Na+ deficit - hypertonic saline (20% = 3.4 mmol/ml)
- correct to [Na+] ~ 125 mmol/l
at ≤2 mmol/l/hr
mmol Na+ ~ 0.6 x (125 - [Na+]) x weight

5
 ICU - Paediatric

Hypernatraemia

a. dehydration
b. inadequate fluid intake
c. diarrhoea
d. radiant heaters
e. osmotic diuresis
f. NaHCO3
NB: ± can be associated with hyperglycaemia & hypocalcaemia

RX normal saline ~ 10-20 ml/kg to correct volume deficit,

then correct water deficit over 48 + hrs (rapid → cerebral oedema)
→ fall in [Na ] ≤2 mmol/l/hr
+

Oedema

a. premature
b. excess fluid intake
c. inappropriate ADH - CNS or lung disease
- IPPV
- serum osmolality ≤270 mosm/l
- urine osmolality > 270 mosm/l
d. capillary leak - hypoxia, acidosis
- ischaemia, sepsis
e. heart failure
f. renal failure
g. hypoalbuminaemia
h. multiple of above
NB: RX fluid restriction ± diuretics
albumin / blood volume replacement
dialysis

6
 ICU - Paediatric

Hypocalcaemia ± Hypomagnesaemia

a. "sick neonates" within first few days of life

b. neonate of diabetic mother
c. large volume IV fluids
d. exchange transfusion with citrated blood (transient)
e. diarrhoea
f. cows milk feeding * high phosphate content
→ jitters, tetany, cardiac arrhythmias & convulsions
g. normal daily requirement,
i. Ca++ ~ 1.0 mmol/kg/day
++
ii. Mg ~ 0.3 mmol/kg/day
iii. RX - maximum rate of 0.1 mmol/kg
- CaCl2 = 0.68 mmol/ml
- Ca gluconate = 0.22 mmol/ml
NB: * rickets is not uncommon in small preterm neonates

Rx Hyperkalaemia

a. calcium ~ 0.1 mmol/kg

-
b. HCO 3 ~ 1.0-2.0 mmol/kg
c. glucose ~ 0.5-1.0 g/kg
insulin ~ 0.1 U/kg
d. cation exchange resins - Resonium 1 g/kg
± sorbitol 1.5 mg/kg
e. dialysis

Pyloric Stenosis

a. gastric fluid composition Na+ ~ 80 mmol/l

K+ ~ 20 mmol/l
H+ ~ 30-120 mmol/l
Cl- ~ 150 mmol/l
b. methods of assessment
i. body weight change
ii. clinical assessment of % dehydration
iii. Cl- deficit = 0.5 x body weight x (110-[Cl -])/110
iv. urinary Cl- excretion

7
 ICU - Paediatric

Nutrition
a survey of hospitalised paediatric patients demonstrated evidence of acute malnutrition in 30%
the critically ill child has problems of decreased intake and increased metabolic demands →
a. poor wound healing
b. reduced immune response
c. lack of growth
d. reduced energy and protein stores

the metabolic requirements of children are higher and the stress response results in a drain of
energy and protein stores
→ increased utilization of glucose, glycogen and fat
except in sepsis where this utilization is impaired

the aim of nutritional support is to provide ordinary caloric requirements, as well as those needed
for growth and development, without fluid retention
assessment of appropriate caloric assimilation is difficult,
a. body size - weight, height, & head circumference
b. tissue composition - skinfold thickness
c. biochemical & immunological parameters
creatinine/height index
albumin, transferrin
CMI by skin testing and lymphocyte count

however, a simple nutritional assessment system is required because those suggested for adults
have not proved useful in paediatrics
fat administration prevents essential fatty acid deficiency and when metabolised produces less
CO2 , which may be important in patients with respiratory distress
there are recommended daily allowances for vitamins and minerals in children
daily monitoring of caloric intake is important
the choice of caloric administration (enteral or parenteral) depends on disease processes and
adequacy of gut function

8
 ICU - Paediatric

Daily Nutritional Requirements

Carbohydrate 10-15 g/kg/d 4.1 kcal/g
≤20 neonates

Protein 2-3 g/kg/d 5.3 kcal/g

Fat 1-3 g/kg/d 9.3 kcal/g

Newborn 120 kcal/kg

1 year 90 kcal/kg CHO ~ 65%
7 years 75 kcal/kg Protein ~ 10%
12 years 60 kcal/kg Fat ~ 25%
18 years 30 kcal/kg

Synthamin 17 (g-N) is 10% = 100g protein/1000ml

~ 0.5 kcal/ml
→ 2.0 g/kg/day = 20 ml/kg/day

disease processes requiring increased caloric expenditure are,

a. fever
b. surgery
c. sepsis
d. cardiac failure
e. respiratory failure
f. burns
g. malnutrition

Enteral Nutrition
enteral feeding maintains better gut function and has less complications
diets include,
a. homogenised food - causes less diarrhoea and abdominal distension
b. formula - with added calories (as CHO) if volume is limited
c. elemental diets - simple sugars, AA's, elements
- where digestive ability is limited
± abdominal distension / diarrhoea

nasal tubes are difficult to maintain long term, and obstruct the nares resulting in an increase in
work of breathing which is important in the presence of respiratory failure

9
 ICU - Paediatric

Parenteral Nutrition
parenteral nutrition is required where enteral feeds are precluded because of disease or surgery
most common indications are for,
a. primary gastrointestinal diseases - short bowel syndrome
- inflammatory bowel disease
b. supportive therapy for prematurity
c. necrotizing enterocolitis
d. neoplasia
e. burns
f. pre- / postoperatively - small bowel atresia
- TOF
- gastroschisis ± omphalocole
- diaphragmatic hernia

long term central venous administration is via percutaneous or surgically inserted small bore
silicone catheters
peripheral administration has fewer complications and is technically easier, but has limitations in
the amount of calories that can be delivered
also, problems with long-term IV maintenance in children
when given intravenously, glucose, protein and fat should be introduced slowly over 3-4 days
monitoring is aimed at assessing the effects of therapy and avoiding complications,
a. daily - weight, temperature, ? fluid overload
- catheter related problems
- glycosuria
b. 3x / week - electrolytes and glucose
c. 2x / week - urea, creatinine, Ca++, Mg ++, phosphate
d. 1x / week - LFT's, Hb, triglyceride levels (when fat emulsion is used)
- head circumference and length

technical, infectious, metabolic and psychiatric complications are similar to those in adult patients
decreased fat clearance reduces capillary blood flow and affects white cell and platelet function
thus, lipid is relatively contraindicated in,
a. liver disease
b. bleeding disorders
c. pulmonary hypertension
d. premature neonates
e. sepsis

serum lipaemia and triglyceride levels should be frequently monitored when fat is commenced or
clinical conditions change

10
 ICU - Paediatric

Caloric Requirement TPN

a. 5% dextrose (100 ml/kg/day) ~ 20 kcal/kg/day

~ 1/5th of the basal requirement
b. many ill neonates/small children are unable to absorb adequate nutrients from the GIT
→ institute TPN early
c. nutrient solutions for paediatric use have high concentrations of Ca ++, Mg++ & PO4=
→ incompatible with fat emulsion
d. dislodged canulae / unavailable solution should be supplemented immediately to
prevent rebound hypoglycaemia
e. complications include
i. line related problems
ii. hyperglycaemia / glycosuria
iii. rebound hypoglycaemia
iv. extravasation, tissue necrosis
v. hypoproteinaemia, hyperlipidaemia
vi. electrolyte imbalance, acidaemia
vii. uraemia, cholestatic jaundice
viii. sepsis

11
 ICU - Paediatric

CONGENITAL HEART DISEASE

1. incidence ~ 6-8:1000 live births

2. acyanotic ~ 25% VSD (30)
~ 17% PDA (10)
~ 7% ASD (7)
3. cyanotic ~ 11% Fallot's tetralogy (5)
~ 8% transposition (5)
~ 3% tricuspid atresia
4. obstructive ~ 7% PS (7)
~ 6% coarctation (6)
~ 4% AS (5)

Classification

1. obstructive - aortic stenosis

- pulmonary stenosis
- coarctation of the aorta
- interrupted aortic arch
- aortic atresia
- mitral atresia & stenosis
- cor triatriatum (accessory LA)
2. increased pulmonary blood flow - ventricular septal defect
- patent ductus arteriosus
acyanotic - ASD, ostium secundum / primum type
- total anomalous pulmonary venous connection
- complete atrioventricular canal
- truncus arteriosus
- aortic pulmonary window
- ruptured sinus of valsalva
- LV to RA shunt
- coronary arterial fistula
3. decreased pulmonary blood flow - tetralogy of Fallot
- pulmonary atresia with intact ventricular septum
cyanotic - tricuspid atresia
- Ebstein's anomaly
- hypoplastic right ventricle
- transposition of the great arteries
- "corrected" transposition of the great arteries
- double outlet right/left ventricle
- single ventricle
- cardiac malposition

12
 ICU - Paediatric

4. miscellaneous cardiac lesions - congenital heart block

- congenital mitral insufficiency
- anomalous left coronary artery
- pulmonary arteriovenous fistula
- endocardial fibroelastosis
- cardiac tumours

Initial Management

NB: treatment is aimed at improving oxygenation and cardiac output

to enable stabilisation and transfer to a tertiary unit

marked cyanosis presenting in a newborn is usually caused by CHD

a. PaO2 ~ 40-60 mmHg is well tolerated
b. commonly P aO2 ~ 30 mmHg

acidosis reflects failure of oxygen transport

however, oxygen is only helpful where there is,
1. an element of ventilation/perfusion mismatch, or
2. pulmonary hypertension

positive pressure ventilation, muscle relaxation and sedation reduce work of breathing and help
left ventricular performance, provided venous return is not reduced or the lungs overdistended

where a patent ductus arteriosus is required for maintenance of,

a. pulmonary blood flow - right to left shunts, or
b. systemic blood flow - coarctation
- hypoplastic left heart syndrome

intravenous PGE1 (~ 0.01 µg/kg/min) can be life-saving

13
 ICU - Paediatric

OBSTRUCTIVE CONGENITAL HEART DISEASE

Pulmonary Stenosis

a. incidence ~ 7% of CHD
- males ~ females
b. pathology ~ 95% = valvular stenosis
- most have a patent foramen ovale
- few have a true ASD
- some have a hypoplastic RV
c. clinical symptoms - usually none and normal growth
severe lesions - dizziness, hypoxic spells
- cyanosis and right sided failure
- anterior chest pain ± angina
- sudden death
d. signs - high pitched SEM ± click
- RV heave
- delayed and soft S2
e. ECG ~ 50% RVH ± strain, RAD
f. CXR - RVH
- oligaemic lung fields
g. operative indications - gradient ≥ 50 mmHg
→ open pulmonary valvotomy + closure of foramen ovale
- if hypoplastic RV leave FO open
h. complications - RVF
- cyanosis, respiratory failure
~ 50% of deaths occur in the 1st year

Aortic Stenosis
four types of aortic stenosis are recognised,
a. valvular aortic stenosis * most common
b. subvalvular aortic stenosis
c. supravalvular aortic stenosis
d. asymmetrical septal hypertrophy

14
 ICU - Paediatric

Valvular Aortic Stenosis

a. incidence ~ 7% of CHD
- predominantly in males
b. pathology - the valve is frequently bicuspid
- aorta and aortic annulus are small
~ 20% → associated CHD
c. clinical symptoms - usually none, with normal growth
severe lesions - LVF or syncope
- anterior chest pain ± angina
- sudden death
infants - cyanosis with severe LVF
- respiratory distress
- poor ventricular function 2° to,
i. subendocardial ischaemia
ii. endocardial fibroelastosis
d. signs - SEM at LSE ± click
- may be absent in severe LVF
- LV heave
e. ECG - LVH ± LV strain, ischaemic changes
f. CXR - usually normal or show only LVH
- the ascending aorta may be dilated
infant - the cardiac outline is large
- pulmonary venous congestion present
g. operative indications → commissurotomy
≥ 50 mmHg gradient
- symptoms of syncope, LVF
- ECG changes of ischaemia
unless associated AI it is rarely necessary to insert a prosthetic valve in a child
thus, they suffer from progressive thickening and calcification of the valves,
requiring continued follow-up ± repeat operations
h. complications - LVF, pulmonary oedema
- angina, IHD ± MI
- respiratory failure
- sudden death
- re-stenosis postoperatively

Subvalvular Aortic Stenosis

is caused by a discrete fibromuscular segment of the LV outflow tract
this is seldom seen in infants
it has a good prognosis as operative resection of the band is possible and recurrence is
uncommon

15
 ICU - Paediatric

Supravalvular Aortic Stenosis

this is usually an isolated lesion, not associated with mental retardation or genetic defect
however, ~ 20% of patients known to have supravalvular stenosis, also show,
a. mental retardation
b. "elfin facies"
c. strabismus
d. dental anomalies
e. narrowing of the pulmonary & peripheral systemic arteries
f. many with hypercalcaemia

the aorta has an "hour-glass" deformity just above the valve, which may be improved with a
prosthetic patch

Asymmetrical Septal Hypertrophy

disease of cardiac muscle and results in disproportionate thickening of the ventricular septum
autosomal dominant inheritance ~ 50% familial
the muscle mass may, or may not result in outflow obstruction
the severity of any obstruction increases during systole and is proportionate to,
a. the inverse of the LVES volume
b. the force of contraction
c. the cross sectional area of the LV outflow tract

physiological events associated with increased catecholamines or SNS activity worsen

obstruction, as do pharmacological agents with sympathomimetic action
the common symptoms are,
a. chronic fatigue
b. episodes of syncope and angina
c. dyspnoea on exertion

operative resection is frequently difficult due to the diffuse nature of the muscle disease
LBBB frequently follows operative resection

16
 ICU - Paediatric

Coarctation of The Aorta

a. incidence ~ 10% of CHD

* males ~ 2x females
b. associated with - Marfan's syndrome
- Turner's syndrome
- berry aneurysms
~ 25-50% have bicuspid valve (ie. develop AS later)
c. site ~ 98% distal to the left subclavian artery
~ 2% proximal (ie. to isthmus)
d. clinical symptoms - headaches, epistaxis
- lower limb weakness, cramps, claudication
- congestive failure
e. signs - upper limb hypertension, LV thrust
- weak femoral pulses
- radio-femoral delay
- collateral circulation - scapulae, post. intercostals
- axillae, epigastrium
- hypertensive retinopathy
f. murmurs - collateral bruits
- crescendo/decrescendo ESM
- AS/ESM ∝ bicuspid valve
- S3, S4 with loud S2 & LVH
g. ECG ~ 50% LVH ± strain
h. CXR - LAH, LVH
- prominent left subclavian
- "3 sign" ≡t pre/post-dilatation
- notching of ribs 3-7
i. complications - malignant hypertension
- CVA / SAH
- LVF
- endocarditis

in most patients, blood flow to the lower extremities is not reduced at rest
however, pulse pressure and exercise tolerance are significantly reduced
in infants, coarctation may produce severe LVF and there is a high incidence of associated
anomalies, particularly PDA and VSD
untreated, the first year mortality ~ 75%
many children are asymptomatic and undergo normal development
operative repair is indicated as soon as practicable, before hypertension & secondary vessel
changes occur
residual hypertension after operative frequently remains a problem
re-stenosis & re-operation is less common after patch repair than end-to-end anastomosis

17
 ICU - Paediatric

CHD WITH INCREASED PULMONARY BLOOD FLOW

~ 50% of all CHD shunt blood from the systemic to the pulmonary circulation
the most common in this group include VSD, PDA, atrial defects and atrioventricular canal
factors which contribute to this include,
a. thicker walled, less compliant LV
b. SVR ~ 10 x PVR
c. mean LV & systemic pressures are ~ 8x RV & pulmonary

the increased pulmonary blood flow results in,

a. vascular congestion
b. ↑ RV work load ± RV failure
c. ↑ frequency of respiratory infections & growth retardation
d. ↑ pulmonary vascular pressures & PVR

→ ↑ mean PAP ~ 2x with a 3x increase in flow

e. ↑ LAP & LVEDP *ventricular interdependence
f. ↑ lung water

the rise in PVR is at first passive, hyperkinetic pulmonary hypertension

later this progresses to pulmonary vascular disease & progressive hypertension,
1. stage 1 - muscular hypertrophy of the media of arterioles
2. stage 2 - proliferation of the intima
3. stage 3 - hyalinization & fibrosis of the media and adventitia

these changes are more likely with lesions associated with large increases in flow and pressure,
a. VSD
b. complete AV canal
c. truncus arteriosus

residence at high altitude and chronic hypoxaemia also favour its development
patients with advanced pulmonary disease and reversal of shunt flow, Eisenmenger's syndrome,
cannot be helped by operation
pulmonary banding is a palliative technique to reduce pulmonary flow
however, the addition of a fixed resistance,
1. is detrimental under any physiological condition which would increase flow
2. becomes inadequate with growth

18
 ICU - Paediatric

ASD - Ostium Secundum

a. incidence - secundum defects are the commonest ASD

~ 2% of CHD (~ 95% of total ASD's)
b. pathology - defects in the region of the fossa ovalis
- may be single or multiple
- usually largest of the atrial defects
c. signs/symptoms - usually asymptomatic and acyanotic
- normal growth & development
- RV lift
- S2 widely split and fixed
- grade 1-3/6 pulmonary ESM (murmur is not from ASD flow)
- diastolic flow murmur at lower LSE
- CCF rare in children but occurs in adults
d. complications - infective endocarditis
- paradoxical embolism
- arrhythmias, increasing with age
- progressive PVD and RV failure are relatively rare

ASD - Ostium Primum

a. incidence - uncommon
b. pathology - defect occurs during development of the AV canal
~ incomplete AV canal
- defect is located low in the atrial septum
- aortic leaflet of the mitral valve is usually cleft
± MR
c. signs/symptoms - usually asymptomatic and acyanotic
± dyspnoea on exertion
- S2 widely split and fixed
- frequently apical SEM
- diastolic flow murmur at lower LSE
- CCF more common than with secundum defect
d. ECG * characteristic
→ LAD with frontal QRS ∼ 0 to -60°
e. complications - mitral regurgitation & progressive CCF
→ major determinant of long term prognosis
- infective endocarditis
- paradoxical embolism
- arrhythmias, increasing with age
- progressive PVD and RV failure > ostium secundum

19
 ICU - Paediatric

Complete Atrioventricular Canal

a. pathology - deficient atrial & ventricular septa

- also deficient mitral & tricuspid valves
- major shunting of blood at ventricular & atrial levels
- usually with mitral regurgitation ± tricuspid regurgitation
b. signs/symptoms - biventricular heart failure common in infancy
- loud S2 with fixed splitting
- blowing, pansystolic murmur ± other bruits
- cardiomegally on CXR & examination
c. catheter - "gooseneck" deformity of mitral valve and LV outflow tract
d. ECG - LAD with frontal QRS ~ 0 to -60°
e. complications - progressive PVD, LV & RV failure are very common
- severe CCF early requiring therapy
- infective endocarditis, paradoxical embolism
- arrhythmias, increasing with age
f. postoperatively ~ 5% develop CHB
- result depends upon AV valve tissue present
- many with residual MI
- late pulmonary vascular disease
± requiring mitral valve replacement

Ventricular Septal Defect

a. incidence ~ 25% of CHD

b. pathology ~ 85% occur in the membranous septum
- conduction bundle is close to these
~ 10% are defects of the muscular septum
- occasionally may have associated AI
c. signs/symptoms = those of pulmonary overcirculation
± dyspnoea on exertion, fatigue & poor weight gain
± CCF, frequent respiratory infections
- often asymptomatic and acyanotic (small)
- loud S2 with fixed splitting
- grade 2-6/6 pansystolic murmur → LSE
- apical diastolic flow murmur
- biventricular enlargement if large defect & hyperaemic lung fields
d. ECG ± LBBB
e. complications - biventricular CCF
- frequent respiratory infections
- progressive PVD → operate earlier
- infective endocarditis & arrhythmias

20
 ICU - Paediatric

Patent Ductus Arteriosus

a. incidence ~ 17% of CHD

b. pathology - failure of normal ductal closure
- prematurity ≡t persistent foetal circulation
± hypoxia, hypercarbia, acidosis
c. signs/symptoms ± those of pulmonary overcirculation
- often asymptomatic
infants → ± dyspnoea on exertion, fatigue & poor weight gain
± CCF, frequent respiratory infections
- loud S2 with fixed splitting
- bounding peripheral pulses (↓ SVR)
- systolic ± continuous murmur at base
- hyperaemic lung fields
d. complications - infants may → biventricular CCF
- frequent respiratory infections
* a large ductus & progressive PVD are unusual
e. risk of SBE - lesions more common on the pulmonary side of the ductus
f. RX - most close spontaneously without RX
- indomethacin inhibits synthesis of PGE1 , works in ~ 1/52
- surgical ligation
* no requirement for AB prophylaxis post-ligation

21
 ICU - Paediatric

CHD WITH DECREASED PULMONARY BLOOD FLOW

the combination of obstruction to RV outflow and a septal defect results in reduced pulmonary
blood flow and R→ L shunt
the degree of shunt flow is inversely proportional to pulmonary blood flow
common causative lesions include,
1. tetralogy of Fallot
2. pulmonary atresia
3. tricuspid atresia
4. Ebstein's anomaly
NB: less commonly this results from reversal of a left-right shunt,
2° to progressive PVD → Eisenmenger's syndrome

severe cyanosis stimulates red cell production, with polycythaemia

this may result in elevation of the Hct ≤80%
up to ~ 60% this increases DO2, however, increases in viscosity above this level result in
decreased organ perfusion
this also results in the reduction of fibrinogen & platelets
despite this, dehydration may lead to systemic and pulmonary venous thrombosis
clubbing of the fingers and toes develops due to proliferation of capillaries and small
arteriovenous fistulae ? mechanism → PDGF
hypoxic spells are due to acute cerebral hypoxia, 2° to decreased pulmonary blood flow
spasm of the infundibular region is the most likely cause
factors which lead to alterations of SVR/PVR are likely to precipitate spells, including,
1. physical exercise → ↓ SVR
2. hypoxia, hypercarbia, acidosis
3. hyperthermia, sepsis
4. drugs - vasodilators

the reduction in pulmonary blood flow stimulates enlargement of bronchial and mediastinal
arteries, which may provide the majority of blood flow
at birth, the patent ductus provides a large contribution to PBF
administration of PGE1, may prolong patency for up to days in some infants, allowing correction
of the metabolic derangements prior to operation
there are a number of anastomotic procedures to increase PBF,
a. Blalok-Taussig = subclavian to ipsilateral PA (end to side anastomosis)
* now often done with a vascular patch to preserve the artery
b. Waterson = ascending aorta to right PA
c. Potts = descending aorta to left PA (Potts → Posterior)

injection of the wall of the ductus with formalin 10% can delay closure for up to months in some
infants

22
 ICU - Paediatric

Tetralogy of Fallot

Def'n: pulmonary stenosis - with outflow obstruction

VSD - large, non-restrictive with R→ L shunt
dextroposition of the aorta - over-ridding the septum
right ventricular hypertrophy ± failure

→ 10% of CHD and the commonest form of cyanotic CHD

plus atrial septal defect = pentalogy of Fallot

Clinical Features

a. symptoms - syncope ~ 20%

- dyspnoea, exercise intolerance
- growth retardation
b. signs - cyanosis, finger clubbing
- grade 1-3/6 PS bruit
* no VSD murmur
- prominent RV impulse, single S2
- murmur often absent during spell
c. ECG - RAH, LVH
? RVH
d. CXR - large aorta, small heart "boot shaped"
- small PA's, oligaemic lungs
e. complications - cerebral abscess (~ 10%)
- other systemic emboli
- endocarditis
- thrombotic stroke (polycythaemia)
- epilepsy
- growth retardation
- increased risk/severity of "tet" spells if uncorrected

Treatment
treatment varies with age and the severity of disease,
a. neonate - maintain oxygenation
- maintain PDA, high SVR until shunt
b. severe infant - Blalok-Taussig shunt
c. child without shunt but increasing "spells" * β-blockers
NB: increasing trend toward primary repair

23
 ICU - Paediatric

cyanotic spells are associated with self-perpetuating,

1. cyanosis
2. R→ L shunt
3. hypoxic pulmonary vasoconstriction
4. subvalvular obstruction & spasm
5. RV ischaemia ± failure

mild to moderate attack,

1. 100% O2
2. knee-chest position → ↑ SVR & reverse shunt
3. morphine 0.1 mg/kg → ↓ sympathetic drive

severe attack,
1. 100% O2
2. morphine 0.1 mg/kg - ↓ sympathetic drive
3. IPPV - ↑ PaO2 / DO2
- ↓ VO2
4. paralysis - ↓ VO2
5. hypocapnia - pulmonary vasodilator
6. maintain RV perfusion pressure
7. peripheral vasopressors - metaraminol
- ↑ SVR
* avoid β-agonists
8. pulmonary vasodilators - PGI2 ~ 0.1-0.2 µg/kg/min
but, - also a systemic vasodilator
- closes PDA (cf. PGE 1 maintains PDA)
- fever
- decreased platelet adhesiveness
? nitric oxide

β-agonists may increase infundibular dynamic obstruction, reduce RV coronary perfusion and
increase cardiac VO2 (tachycardia)
propranolol may therefore be used for prophylaxis
providing the pulmonary vessels are of a reasonable size a corrective procedure is attempted
the pulmonary outflow and annulus are frequently small, requiring insertion of a patch
post surgery, greater volume work is required as PA flow is now normal, or often there is some
incompetence of the valve
therefore, these patients frequently have elevated heart rates and mild degrees of RV
hypertrophy/failure postoperatively (↑ RBBB, sudden death)
the overall success rate for surgical correction ~ 90-95%
~ 50% of these have near normal exercise tolerance

24
 ICU - Paediatric

Transposition of The Great Vessels

major diagnostic criteria,
a. situs solitus, levocardia
b. cyanosis from birth ± hypoxic spells
c. frequently in heart failure
d. cardiac enlargement and small PA segment on CXR *narrow vascular pedicle
e. the presence of some pulmonary/systemic shunt,
→ VSD (~ 30%), ASD, or PDA

the lesion is more common in males

the aorta arises from the normally situated RV, and gives rise to the coronary vessels
the atria and ventricles are concordant
the systemic and pulmonary circulations are functionally separated, therefore, some abnormal
shunt is required for existence
patients with an intact ventricular septum and absent patent ductus have the worse clinical
picture, as mixing occurs only at the atrial level
however, these are the best candidates for surgery
patients with large VSD's may die from excessive PBF and CCF from progressive PVD
management includes,
a. maintain high PVR
maintain RAP ~ LAP so that adequate mixing occurs, cf. one-way shunt flow
if LAP decreases (venous return / pulmonary afterload),
then flow from RA → LA increases, with increased PBF and 2° LVF
b. septostomy - ASAP
c. vascular switch - 2 to 3 months

corrected transposition is a rare anomaly where systemic venous blood reaches the lungs despite
the presence of transposition
commonly associated defects,
1. pulmonary stenosis - ie. systemic inlet obstruction
2. VSD

25
 ICU - Paediatric

Cardiac Malposition
situs inversus totalis is a rare anomaly where the stomach and other abdominal organs also
occupy the mirror image of normal position
except in asplenia, or polysplenia, the position of the abdominal organs determines the position of
the atria
thus, in situs inversus, the atria are reversed and the heart is right sided
the morphologic left ventricle is on the right and the atria and ventricles are concordant
severe anomalies may occur with situs inversus, dextrocardia and transposition of the great
vessels,
a. the atria and ventricles are discordant
b. transposition of the great vessels is always present

isolated levocardia is the remaining anomaly which may accompany situs inversus
the heart is located in the left chest, there are severe cardiac anomalies and agenesis of the left
lung
in isolated dextrocardia the heart is in the right chest, the abdominal organs normal and there is
agenesis of the right lung

asplenia, midline position of the stomach & liver (situs intermedius), distinct middle lobes of
both lungs and Howell-Jolly bodies within RBC's are associated with severe cardiac anomalies

Miscellaneous Congenital Heart Lesions

a. congenital heart block

may be an isolated lesion, or with certain anomalies
especially - corrected transposition
- 1º ASD or endocardial fibroelastosis
b. congenital mitral insufficiency
c. anomalous left coronary artery
d. pulmonary arterio-venous fistula
~ 50% have Rendu-Osler-Weber syndrome (multiple telangectasia)
e. pulmonary artery stenosis
f. persistent left SVC (connects LIJ & SC to coronary sinus)
g. endocardial fibroelastosis
~ 1-2% of patients with CHD but may be sole anomaly
involves predominantly the left side
? secondary to subendocardial ischaemia in utero
almost all die within the first year 2° to CCF

26
 ICU - Paediatric

CHD - GA Considerations

1. prophylaxis for endocarditis

* all patient, ? except ligated PDA & secundum ASD without patch
2. air filters and meticulous removal of air from IV lines
* all patients with intracardiac shunts, irrespective of the direction of the shunt
3. minimise myocardial VO2
i. adequate premedication & a (? rapid) smooth induction
ii. adequate analgesia
iii. avoid hypertension / tachycardia
iv. maintain normocarbia
v. maintain NMJ paralysis
vi. LV or RV afterload reduction
4. optimise cardiac output
i. avoid depressant agents
ii. maintain filling pressures - minimise preoperative dehydration
iii. avoid / manage arrhythmias
iv. avoid hypocarbia - reduces CO, increases SVR
- shifts HbO2 curve left
- decreases myocardial & cerebral blood flow
- decreases K+
- increases arrhythmias
5. avoid alteration of shunt flow
i. avoid agents which alter SVR or PVR
ii. be aware of the possible effects of IPPV/PEEP
iii. factors which alter dynamic outflow obstruction
- positive inotropes, sympathetic stimulation
iv. avoid hypotension if dependent on systemic-pulmonary shunt flow for
oxygenation
6. heparin has a larger volume of distribution and a more rapid plasma clearance in
infants - larger loading doses and monitoring are often required
7. myocardial protection, during CPB,
i. cardioplegic solutions - different opinions
- high K+, Mg++
- high dextrose
ii. hypothermia - repeated PRN
iii. pre-CPB steroids ? controversial
iv. optimal reperfusate solution - cool & alkaline
- low ionised Ca++
- slightly high K+

27
 ICU - Paediatric

Post-operative Management Cardiac Surgery

postoperative respiratory function is altered by,
a. anaesthesia - hypoventilation, atelectasis
- reduced clearance of secretions
b. surgical incision - midline sternotomy or thoracotomy
- poor cough and reduced FRC
c. effects of CP bypass - capillary leak and pulmonary oedema
- damaged pulmonary capillary endothelium
? from endotoxin release
- mechanical red cell damage
- C' activation from exposure to oxygenator membrane
the effects of CPB on C', platelets etc. are greater than adults, due to the relatively
greater SA of the circuit cf. body endothelial SA
d. ↑ LAP - left ventricular failure
- mitral incompetence or stenosis
- residual VSD
e. phrenic nerve palsy
f. pneumothorax

postoperative cardiovascular function is altered by,

a. direct damage to myocardium from ventriculotomy
b. ischaemic damage because of hypoxia
c. effects of cardiopulmonary bypass
d. excision of hypertrophic muscle
e. changes to flow/load patterns, especially from central shunts, where repeat surgery
may be necessary
f. hypovolaemia from insufficient venous filling from the bypass pump or haemorrhage
g. increased PVR - operative L→ R shunts acutely increasing PBF
- high PBF preoperatively
h. cardiac tamponade - bleeding
- pericardial effusion
- tension pneumothorax
i. HR abnormalities - surgical damage to conductive tissue
- SA node with intra-atrial repairs
(atrial baffles, patch closure ASD, repair A-V canal)
- interruption of atrial pathways
- distortion from atrial dilatation

28
 ICU - Paediatric

non-surgical postoperative bleeding results from,

a. consumption of platelets and clotting factors - bypass circuit
- intracardiac patches
b. residual heparinisation
c. citrate toxicity from large blood transfusion
d. preoperative hepatic insufficiency (2° to congestion)

renal failure following cardiac surgery is caused by low cardiac output, and reduced renal
perfusion while on bypass

Persistent Foetal Circulation

a. low lung volume states - hyaline membrane disease

- perinatal asphyxia
b. pulmonary hypoplasia
diaphragmatic hernia
Potter's syndrome - renal agenesis
→ - lack of amniotic fluid
- secondary failure of pulmonary development
c. meconium aspiration syndrome
d. chronic placental insufficiency
e. hypoxia or acidosis - any cause
f. sepsis - any cause
g. hyperviscosity syndrome
h. any increase in PVR → cyclic effect → ↓ PaO2 & pH

Clinical Features

a. hypoxaemia >> the degree of respiratory distress

b. cyanosis - suggesting CHD
- may be differential with PDA
c. acidosis ± hypercarbia

29
 ICU - Paediatric

Management

a. maintain a high FIO2

b. correct low lung volume with CPAP
c. correct metabolic and respiratory acidosis
d. NMJ blockade + IPPV + deliberate hyperventilation
→ generate a respiratory alkalosis (pulmonary vasodilation)
e. maintain systemic volume & pressure = plasma volume expanders ± inotropes
→ reduce the pressure gradient for shunting
f. isovolaemic haemodilution if hyperviscosity present
g. pulmonary vasodilators
i. inhaled nitric oxide
ii. others - isoprenaline
- tolazoline
- SNP, GTN
- phenoxybenzamine
- PGE 1
→ variable response depending on underlying pathology
h. surfactant therapy
i. animal (bovine) surfactant
ii. recombinant human

30
 ICU - Paediatric

CARDIAC ARREST IN CHILDREN

the majority lack intrinsic cardiac disease, arrest being the end result of hypoxaemia & acidosis
→ biochemistry is grossly abnormal prior to arrest

~ 70% or more of paediatric arrests occur < 1 yr of age

Most Common Causes

1. rapidly progressive upper airway obstruction

2. SIDS
3. severe systemic illness
i. pneumonia
ii. gastroenteritis
iii. septicaemia
4. major trauma / accidents
i. MVA's
ii. fire/smoke inhalation
iii. near-drowning
iv. NAI / abuse
5. congenital disorders
i. heart disease
ii. respiratory disease

children invariably arrest in asystole (96% in one series) and this should be suspected if an ECG
is unavailable
ventricular fibrillation may be anticipated in the following situations,
1. congenital heart disease
2. cardiomyopathies / myocarditis
3. drug poisoning - TCA's
4. hereditary long QT - Romano-Ward syndrome
- Jervelle-Lange-Neilsen

EMD may occur from hypovolaemia but is rare from other causes
presence of a pulse is best determined at the carotid

31
 ICU - Paediatric

Management

a. airway
i. obstruction is more likely
ii. gastric distension is almost invariable → early ETT & NG tubes
b. cardiac massage
relative organomegaly etc. in the infant → used to advocate mid-sternal massage
risks of trauma unfounded & lower sternal massage → more effective
conventional CPR is more effective than simultaneous compression / ventilation
i. < 1 year 2 fingers 100+ bpm 1-2.5 cm
ii. 1-8 years 1 hand 80-100 bpm ~ 2.5 cm
iii. adult 2 hands 80 bpm ~ 5.0 cm
c. drug access- best by CVC lines, proximity to heart
- technically difficult, interferes with CPR
- percutaneous cut-down ± intraosseous needle
d. asystole
SR can often be restored ≤45-60 min but high incidence of hypoxic brain damage
CPR alone is often successful
in absence of AGA's → NaHCO3 ~ 2 ml/kg stat
adrenaline 1:10,000 → ~ 0.1 ml/kg stat (0.01 mg/kg) & repeat 3 minutely
≤2 ml/kg if required
VF is uncommon & tachycardia well tolerated
Ca++ should only be used for hyperkalaemia, hypocalcaemia & CEB toxicity due to
role of Ca++ in reperfusion injury
e. intracardiac injection
endotracheal administration of adrenaline, but ? effectiveness (use ~ 5x dose)
HCO3- cannot be given via ETT
thus, intracardiac injection may be justified in children
either left ant. 4th ICS or sub-xiphisternal (beware the liver)
potential complications include,
i. intramyocardial injection & VF
ii. coronary vessel laceration
iii. pericardial tamponade
iv. pneumothorax - always with parasternal injection
v. interruption of CPR
f. ventricular fibrillation
spontaneous reversion may occur with CPR
~ 3-5 J/kg DC shock + repeat x1
± lignocaine 1 mg/kg IV ± 0.5 mg/kg
adrenaline to improve coronary perfusion
phenytoin 15 mg/kg if TCA overdosage & early HCO3-

32
 ICU - Paediatric

Outcome
important complications of paediatric cardiac arrest are,
1. brain failure
2. disseminated intravascular coagulation
3. splanchnic ischaemia mucosal sloughing
NB: in one study, patients who were resuscitated from absence of pulse or electrical
activity showed no neurologically intact survivors

neurologically intact survival is only seen in those paediatric patients who receive immediate
resuscitation and respond promptly
results are poor where cardiac arrest occurs in hospital wards or in paediatric and neonatal ICU's
→ ~ 9% long term survival
outcome from near-drowning episodes may be good if the patient receives effective resuscitation
at the scene and is gasping soon after
where cardiac arrest occurs in the community, physician-staffed mobile intensive care units do
not improve outcome

Arrhythmias in Children

Causes

a. hypoxia, hypercarbia, acidosis

b. electrolyte disturbance
c. hypotension
d. hypothermia
e. excessive vagal stimulation
f. cardiomyopathies, myocarditis
g. long QT syndrome
h. congenital - aberrant pathways
- complex CHD
i. surgery - transplantation
- cardiothoracic surgery
- cardiac catheterization
j. drugs - TCA's
- digoxin
- organophosphates
- suxamethonium
k. malignant hyperthermia

33
 ICU - Paediatric

Clinical Features

a. sinus bradycardia - hypoxia, hypotension, acidosis

- raised ICP
- vagal stimulation, SCh
- post cardiac surgery (Mustard)
b. bradycardia-tachycardia - cardiomyopathy
- post cardiac surgery
(Mustard, Fontan & Senning operations)
c. A-V block - congenital
- cardiomyopathy
- post cardiac surgery
- myocarditis
- vascular disorders
d. SVT - WPW syndrome
- post cardiac surgery
- myocarditis, sepsis
- drugs, idiopathic causes
RX infant - DC shock, overdrive pacing
- neostigmine ~ 10 µg/kg ( ≤50 µg, atropine readily available)
- digoxin ~ 15 µg/kg
- amiodarone ~ 5 mg/kg/1 hr, then 5-15µg/kg/min
* avoid Ca ++-entry blockers
RX child - vagal stimulation
- neostigmine
- verapamil 0.1 mg/kg IV
- DC shock, overdrive pacing
- digoxin, amiodarone
adenosine ? no controlled trials in children, but ? similar efficacy to adults
~ 0.0375-0.25 mg/kg
e. VEB's / VT - aortic stenosis
- other CHD
- myocarditis
- digitalis toxicity
- long QT syndrome
- TCA overdosage
RX acute - lignocaine ~ 1.0 mg/kg IV, then 20-50 µg/kg/min
++
- Mg ~ 0.05 mmol/kg/10 mins, then 0.2 mmol/kg/6 hrs
- bretylium ~ 5.0 mg/kg IV, then 5-15 µg/kg/min
* vasopressors for AS
RX maintenance - quinidine ~ 6.0 mg/kg q6h
- phenytoin ~ 4.0 mg/kg q8h

34
 ICU - Paediatric

f. long QT syndromes
i. pause dependent - drugs: TCA's, phenothiazines
- metabolic: ↓ Mg++ | ↓ Ca++
↓ K+ = "apparent long QT"
RX - correct cause
- DC shock & overdrive @ 120 bpm
± isoprenaline infusion
ii. adrenergic - hereditary
- following SAH
RX - β-blockade
± phenytoin
g. TCA overdosage - multifocal VEB's
- VT / VF, torsade de pointes
- SVT
- CHB
RX - hyperventilate
- alkalinise blood to pH ~ 7.45-7.5
- NaHCO3 ~ 1-3 mmol/kg
- phenytoin ~ 15 mg/kg slow IV
± lignocaine, Mg++, or bretylium

Invasive Monitoring in Children

excessive flushing of arterial lines may cause retrograde flow into cerebral vessels (especially
temporal artery lines)
normal saline is used as the fluid column to allow accurate glucose measurement from sampled
blood
central venous lines and pulmonary artery catheters are inserted as for adults
cardiac output is described in terms of cardiac index (N ~ 3-3.5 l/min/m 2) to account for changes
with weight and size, and is measured by,
a. thermodilution via PA catheter
use limited in small patients
not accurate where intracardiac shunts are present
(systemic and pulmonary blood flows not equal)
volume load in small patients
b. dye dilution
CVC injection of dye and peripheral artery sampling
not easily performed but demonstrates intracardiac shunts

pulse oximetry monitoring is routine, and suitable probes are available for all age groups
with end-tidal CO2 , in line sampling may be superior to side arm sampling techniques, especially
with small tidal volumes at rapid rates, however, added dead space may be significant
core-peripheral temperature gradients do not accurately trend changes in cardiac output

35
 ICU - Paediatric

Circulatory Failure in Children

the causes differ from the adult due to,
a. smaller fluid compartments → % changes are greater
b. immature immune system ≤2 years of age
i. ↓ IgG, C', opsonins (fibronectin)
→ susceptibility to bacterial infection
ii. ↓ interferon, lymphocyte cytotoxicity
→ susceptibility to viral infection
c. heart rate dependent CO - little alteration of SV
- greater Ca++ dependency,
i. fewer sarcomeres/myofilaments per unit mass
ii. fewer mitochondria/myosin ATP'ase →
higher diastolic volume, limited diastolic reserve
less responsive to increases in preload
augmentation of contraction is limited
afterload induced increases in contraction are small
VO2 and CI are high with limited systolic reserve

→ less compliant ventricle & easily volume overloaded

d. autonomic immaturity - SNS << PNS innervation
- basal PNS tone is low
- insensitivity to β-agonists
- low myocardial NA stores
∴ stress response → bradycardia & less vasoconstriction
e. ischaemic tolerance - greater than the adult
- cerebral plasticity
- cardiac glycogen stores
f. factors peculiar to infancy - SIDS
- haemorrhagic shock & encephalopathy syndrome
g. congenital abnormalities - cardiac, metabolic
h. dependency / inexperience

36
 ICU - Paediatric

Causes of Shock in Childhood

Hypovolaemic

1. bleeding - bowel, body cavity, haematoma, external

* scalp, intracranial
2. fluid/electrolyte loss
i. bowel - V&D, obstruction, 3rd spacing
ii. renal - diuretic use
- diabetes insipidus
iii. skin - burns, heat stroke
3. plasma loss - sepsis, burns
- pancreatitis
- nephrotic syndrome
Distributive

1. septic
2. anaphylactic
3. drug induced - barbiturates, phenothiazines
4. neurogenic - brainstem, high Cx spine
5. ↑ intrathoracic press. - IPPV, CPAP, PEEP
- tension pneumothorax
- pericardial effusion/tamponade
Cardiogenic

1. congenital heart disease

2. hypoxia/ischaemia - global, near drowning
- Kawasaki disease, anomalous LCA
3. cardiomyopathy - metabolic, glycogen storage diseases
- muscular dystrophies
- endocardial fibroelastosis
- infective, Echo & Coxsackie
4. drug intoxication - barbiturate, chloramphenacol
5. loss of atrioventricular coordination
6. rate induced - bradycardia / tachycardia
7. sepsis
Mixed
eg. septis, drug, pancreatitis

37
 ICU - Paediatric

Clinical Signs of Shock in Children

Hypovolaemic signs of dehydration if severe H2O loss

tachycardia, hypotension, narrow pulse
pallor, mottled & cyanosed skin
slow capillary refill
cool extremities
tachypnoea early, later hypoventilation
lethargy ± coma
oliguria

Cardiogenic tachycardia, hypotension, narrow pulse

pallor, mottled & cyanosed skin
cardiomegaly, hepatomegaly
faint heart sounds, gallop rhythm
pulmonary crepitations

Septic tachycardia, hypotension, oliguria

early: warm extremities, bounding pulse, lethargy
later: cool, cyanosed extremities
narrow pulse, tachypnoea, coma

Other distributive tachycardia, hypotension, oliguria

bounding pulse, warm pink extremities
lethargy, stupor, coma

septic neonates and infants ≤6 months generally present with a hypodynamic rather than
hyperdynamic circulatory picture
in hypovolaemia, BP is maintained until ~ 15-20% of blood volume is lost
subsequent signs of cellular injury include,
a. metabolic acidosis & hyponatraemia ∝ decrease Na+/K+-ATPase
b. increased catechols, tachycardia, glucose intolerance
c. falling platelet count & fibrinogen, increased clotting time
d. late: coagulopathy, bloody diarrhoea, fitting & coma

Age Related BP (mmHg) HR (bpm) RR

birth 75 / 40 100-200 40-60
1-2 years 95 / 60 100-180 20-30
6 years 98 / 60 70-120 15-20
10 years 110 / 70
14 years 118 / 75

38
 ICU - Paediatric

Investigation

a. biochemistry - U&E's, LFT's, BSL

- AGA's
b. haematology - FBE, differential WCC, platelets
- coagulation screen
- group & hold serum
c. microbiology - blood cultures x 3
- M,C&S: sputum, pus, CSF, urine
- viral studies: urine, stool, nasal
- urinary bacterial Ag's
d. imaging - CXR ± AXR
- ECG ± echocardiography
e. drug screen - urine, blood, gastric aspirate
f. metabolic screen - urinary amino acids/organic acids
- serum ammonia

Monitoring

a. HR, BP - NIBP/intra-arterial, RR
b. urine output
c. AGA's & pulse oximetry
d. CVP ± PAWP -δ P/δV (compliance) better guide than absolute values
- normal values ~ adults
e. cardiac output - signs/clinical examination
- doppler
- bioimpaedance
- dye/thermodilution
f. derived data (PA) - PVR/SVR ≡t afterload
- CI, DO2, VO2
g. core-toe temperature gradient * does not correlate with CI
h. clinical examination - GCS

Management - Priorities

a. brain and heart perfusion ~ 80% "normal" BP

b. gas exchange ± IPPV
c. renal & GIT perfusion - adequate BP/CO
? low dose dopamine
d. peripheral perfusion

39
 ICU - Paediatric

Methods of Treatment

a. optimise
i. preload ~ 10 ml/kg colloid "challenges"
- monitor as above
* hypotension ~ 30 ml/kg deficit !
* at 30 ml/kg consider rbc transfusion
ii. afterload - short acting systemic agents, SNP
~ selective pulmonary agents (NO, PGE 1, GTN, tolazoline)
iii. contractility - inotropic support
- often need higher doses (per kg) than adults
- myocardial NA stores easily depleted
- receptor down-regulation
± try 10% Ca-gluconate (0.2-0.5 ml/hr)
b. correct metabolic acidosis with NaHCO3
c. treat sepsis - antibiotics, drainage
d. supportive measures
i. peptic ulcer prophylaxis ?what
ii. platelets/FFP in coagulopathy
iii. steroids in Waterhouse-Friderichsen syndrome
iv. accurate fluid balance
v. thermal environment
e. controversial RX
i. high dose steroids of no benefit in large trials
ii. plasma exchange
- positive animal work
? anecdotal human reports
iii. granulocyte transfusion/exchange
positive case reports - esp. newborns
iv. immunotherapy
E.coli J5 immune serum
anti-lipopolysacharrhide serum
phase III trials → no benefit
v. acute phase reactant inhibitors: anti - phospholipase A2
- lipogenase
- leukotrienes
- PAF
vi. continuous haemofiltration ? middle molecule removal
vii. balloon counterpulsation - effective but technically difficult

40
 ICU - Paediatric

Heart Failure in Children

a. congenital heart disease

i. presenting at birth - obstructive lesions
- systemic AVM
ii. presenting 1st 4 months - large left or right shunts
b. post-cardiac surgery
c. asphyxia - perinatal
- near drowning
- upper airway obstruction
d. metabolic
e. arrhythmia
f. cardiomyopathy - infective
- infiltrative
- metabolic
g. endocarditis
h. rheumatic heart disease
i. severe anaemia - eg. hydrops foetalis
j. acute hypertension - acute GN
k. cor pulmonale - cystic fibrosis
- pulmonary vascular disease 1°/2°

Sepsis - Common Organisms

a. neonates - group B, beta haemolytic streptococci

- Enterobacteriaciae
- Listeria monocytogenes
- Staphylococcus aureus
b. infants/children - H. influenzae
- Strep. pneumoniae
- N. meningitidis
- Staph. aureus
- Enterobacteriaciae
c. immunocompromised - Enterobacteriaciae
- Staph. aureus
- pseudomonas species
- Candida albicans

41
 ICU - Paediatric

Haemorrhagic Shock & Encephalopathy

syndrome described in infants and children,
a. high mortality
b. shock, hyperthermia, watery diarrhoea, coagulopathy
c. impaired renal and hepatic function
d. cause has yet to be determined

Evaluation of the Cyanotic Neonate & Infant

difficult to differentiate between pulmonary and cardiac causes of respiratory distress and
cyanosis in neonates and infants because,
a. typical cardiac findings may be absent or obscured
b. central cyanosis, crackles and wheezes are caused by both intracardiac or
intrapulmonary right to left shunting
c. noisy breathing interferes with auscultation
d. murmurs may not initially be present during transitional foetal/newborn circulation

other causes of cyanosis are,

a. 2° to hypoventilation / apnoea - prematurity
- hypothermia
- hypocalcaemia
- hypoglycaemia
- sepsis
b. circulatory shock - sepsis
- obstructive cardiac lesions
- hypoplastic left heart
c. persistent foetal circulation - elevated PVR

cyanosis is clinically evident when SpO2 ≤88%

in neonates this corresponds to a P aO2 ~ 30-85 mmHg
depending on foetal haemoglobin, pH, temperature and 2,3-DPG
pulse oximetry is not reliable in this range of saturation

42
 ICU - Paediatric

Intracardiac vs. Extracardiac Causes of Cyanosis

blood gas with intracardiac shunts,
a. no significant improvement in PaO2 with increase in FIO2
b. PaO2 < 160 mmHg with FIO2 = 1.0 (N: ~ 20-50 mmHg)
c. no improvement in PaO2 with positive airway pressure
d. PaCO2 is usually normal

note that PaO2 may also not rise when FIO2 is increased with intrapulmonary shunting, when,
a. the pulmonary lesion is severe, or
b. where shunting occurs through foetal pathways
i. patent ductus and foramen ovale
ii. raised pulmonary vascular resistance

CXR may help exclude non-cardiac causes but differentiation may be difficult,
a. an enlarged heart equals cardiac disease
however, heart size may be normal with some cardiac conditions
b. heart shape shows chamber enlargement and abnormally placed vessels
c. lung fields show increased, reduced or normal pulmonary blood flow & vasculature
d. classical appearances,
i. transposition - cardiomegaly
- increased vascular markings
- narrow vascular pedicle
ii. Fallot's - normal heart size
- reduced pulmonary vascular markings
- "boot-shaped" heart

ECG may show increase in size of cardiac chambers (note that normal newborn ECG has right
ventricular dominance) and arrhythmias
other investigations for cyanosis include,
a. FBE - Hb, *chronic cyanosis → polycythaemia
- white cell count
b. biochemistry - K+, Na+, HCO3-, Ca++, glucose
- ABG's
c. temperature
d. microbiology - MC&S: blood, urine, tracheal aspirate
- CSF if no coagulopathy
e. echocardiogram - in the presence of CHD
± cardiac catheter

43
 ICU - Paediatric

Hypertension

1. elevated diastolic blood pressure,

i. ≥ 90 mmHg < 6 years age N: 95 / 60
ii. ≥ 95 mmHg ~ 6-12 years age N: 100 / 60
iii. ≥ 100 mmHg > 12 years age N: 110 / 70
2. ECG or echocardiogram evidence of ventricular hypertrophy
3. hypertensive encephalopathy
i. headaches, dizziness
ii. seizures
iii. hypertensive retinopathy / papilloedema

causes in the paediatric age group are,

a. essential hypertension
b. renal disease
PSGN
GN - other causes
HUS
nephrotic syndrome
c. coarctation of the aorta
d. adrenal disease
phaeochromocytoma
Cushing's
Conn's

Barrter's syndrome are usually normotensive

44
 ICU - Paediatric

RESPIRATORY DISORDERS

Respiratory Mechanics
a number of factors make respiration less efficient in the neonate,
a. large V/Q mismatch
i. large shunt fraction ~ 10%
ii. similar dead space but ~ 2-3x VO2 of adults
iii. small FRC
↑ VO2 :: FRC ratio → rapid desaturation
↓ FRC :: CC ratio → gas trapping & ↑ V/Q mismatch
loss of laryngeal brake with ETT & further ↓ FRC
b. small airway diameter RAW ∝ 1/r4
compliant airways & increased narrowing 2° venturi (Bernoulli) effect
most resistance in the upper respiratory tract ~ 25% in the nasal passages,
cf. ~ 60% in the adult
c. highly compliant/flexible airways & chest wall
i. functional airway closure
ii. inability to sustain a high negative PIP
iii. high compliance of chest wall / horizontal ribs
iv. abdominal organomegaly/stomach
d. ↓ type I muscle fibre (oxidative phosphorylation) → less resistant to fatigue
i. neonate ~ 25% diaphragm / 45% intercostal
ii. adult ~ 60% in both
but, fast type II fibres are better suited to the neonates rapid respiratory rates
however, these are more prone to fatigue under conditions of increased load

in the premature infant the basal work of breathing ~ 3x that of adults without disease
the pulmonary circulation at birth is characterised by the muscularity of the pulmonary arteries
the response to hypoxia/stress is vasoconstriction and this may worsen the situation
work of breathing is given by the volume of gas moved against respiratory compliance, and the
work to overcome resistance to airflow,
W = V/CRS + RAW.Q

lungs of neonates with HMD or bronchitis may markedly differ from the above,
a. deficient surfactant
b. ↑ ventilation/perfusion mismatch
c. ↓↓ compliance ~ 0.00025-0.001 l/cmH2O ↓ 5-20x
d. ↑↑ resistance ~ 100-250 cmH2O/l/s ↑ 5-10x
e. ↑ work of breathing
f. ↑ propensity to pneumothorax / barotrauma

45
 ICU - Paediatric

Respiratory Control Centres

during infancy, central responsiveness to,
a. ↑ stimulatory inputs - hypoxia | hypercarbia | acidosis
b. ↓ inhibitory inputs - chest wall deformation | laryngeal stimulation
NB: → newborns have a biphasic response to hypoxia
initial ~ 30% ↑ VM, then ~ 30% ↓ VM below baseline ± apnoea

response depends upon the thermal environment

→ hypothermic neonates responds only with respiratory depression
the ventilatory response to hypoxia becomes "adult-like" at ~ 3 weeks
the ventilatory response to CO 2 increases with gestational & postnatal age
this response is ~ 3x greater in 2-3 day term infants cf. 2-3 day prem's
by ~ 1 month the response of a term infant is ~ adult
→ thus, both hypoxic & hypercapnic drives → adult at ~ 1 month

in young infants, the increased apnoeic,

a. incidence ∝ ↑ sensitivity to inhibitory inputs that trigger apnoea
b. duration ∝ ↓ central responsiveness to stimulatory afferents,
which promote recovery from apnoea

Anaesthetic Considerations - Respiratory

Laylock (1988) found the incidence of hypoxaemia (SpO 2 < 80%) during induction to be,
a. infants ≤1 year ~ 28%
b. children 2-5 yrs ~ 2%
c. children 4-10 yrs ~ 4%
NB: the most commonly associated factor was a delay in intubation

recommendations for neonate/young infant,

1. set time sampling interval on oximeter to 2-3 cycles
2. intubate all infants ≤1 year unless procedure is very brief
3. pre-O2 for 2-3 minutes prior to laryngoscopy
4. use the pulse oximeter to limit the duration of laryngoscopy
5. ?? assist ventilation during induction/emergence
6. control ventilation during maintenance (preserves FRC)

46
 ICU - Paediatric

Neonatal Intubation
differences which make the neonate more difficult to intubate,
1. poor tone of the neck muscles and the large head → "floppy"
2. large size of tongue cf. oropharynx
3. the larynx is located higher in the neck C3-4 vs C4-5
4. "V-shaped", short, stubby, highly mobile epiglottis
adult is parallel to trachea cf. infant angled over
5. vocal cords are angled infero-anteriorly
blind ETT passage may lodge in the anterior commissure, rather than the trachea
6. the larynx is funnel shaped, being narrowest at the cricoid
tubes easily passing the cords may result in subglottic oedema
→ use uncuffed tubes for ages < 10 years
7. the trachea only 4 cm long
∴ ΕΤΤ easily dislodged, or positioned in RMB, especially with head movement

Mechanical Ventilation
most neonates breathe at 30-60 bpm, I:E ratio of ~ 1:1, 5x the mean time constant being ~ 0.6s
as the respiratory rate increases there is the potential for gas trapping
this may be beneficial at low lung volumes but detrimental in the face of increased airways
resistance or high lung volumes

majority of neonatal ventilation is with pressure-limited, time cycled ventilators

these are used due to a reduced incidence of barotrauma and bronchopulmonary dysplasia
the major disadvantage is the lack of compensation for alterations in pulmonary mechanics, with
subsequent changes in VM
NB: oxygenation is predominantly determined by the mean airway pressure,
normocapnia by alveolar ventilation

Boros (1979) showed that the ratio PaO 2:F IO2 is proportional to the mean airway pressure
however, at some point this becomes excessive and is detrimental (analogous to "best-PEEP")
approximate guidelines are,
a. PaO2 ~ 50-70 mmHg
b. SaO2 ~ 87-93 % *this is oximeter dependent
c. PaCO2 ~ 35-50 mmHg
d. pH ≥ 7.28
e. peak PAW ≤30 cmH2O
NB: by accepting these values the incidence of barotrauma is reduced

47
 ICU - Paediatric

PEEP increases mean PAW and improves FRC at low lung volumes
increasing PEEP without increasing the peak P AW decreases the tidal volume & minute ventilation
at rapid respiratory rates (> 60 bpm) significant gas trapping occurs
time-cycled flow ventilators tend to more reliably deliver a constant tidal volume when the
inspiratory time is ≤0.4 sec

oxygen should only be administered to achieve a PaO2 in the above range

excessive administration is associated with an increased incidence of,
a. retrolental fibroplasia
b. bronchopulmonary dysplasia

the aim should be to reduce the F IO2 to ≤0.6 ASAP

there are few studies on the effects of gas flow rates
the general aims of weaning should be to,
a. ↓ FIO2 ≤0.6 prior to other reductions
b. ↓ peak Pinsp ≤20 cmH2O
c. ↓ IMV rate
d. ↓ PEEP ≤5 cmH2O
NB: most are extubatable at IMV ~ 5 bpm / PEEP ~ 3 cmH 2O

if infants have periodic breathing or apnoeic spells, weaning may be facilitated with theophylline

exogenous surfactant often has a dramatic effect upon neonatal respiratory function
within 2-3 hours ventilation on room air with peak P AW ≤20 cmH2O is often seen
changes may occur so rapidly that alteration of ventilatory parameters fails to keep pace with
alterations in pulmonary mechanics
this effect tends to be worse with bovine surfactant, as changes occur more rapidly than with
synthetic surfactants
despite this, these patients frequently require ventilation for several days
early extubation is associated with a high incidence of re-intubation and deterioration of
respiratory function
occasionally 2-3 doses of surfactant are required

48
 ICU - Paediatric

other forms of ventilation, high frequency jet/oscillatory ventilation, have not been shown to be
of any advantage in reducing,
a. the incidence of barotrauma or chronic respiratory disease
b. mortality
c. persistent PDA

initial studies with these forms of ventilation were associated with,

a. a higher incidence of intraventricular haemorrhage
b. higher requirements for vasopressors to maintain MAP
NB: 2° to interference with - cerebral autoregulation
- the baroreceptor reflex

HIFI study group, NEJM 1989 → widespread condemnation

since then, improved knowledge of optimal lung volume strategies have resulted in improved
outcomes in paediatric use of HFOV Review by Froese, Current Opinion in CC 1996
aim is to institute ventilatory strategies maintaining open lung units, while preventing
overdistension, early and thus preventing lung injury
numerous neonatal/paediatric studies now support this view

chronic lung disease, bronchopulmonary dysplasia, is managed with a combination of diuretics

(frusemide) and steroids (dexamethasone)
infants frequently relapse following response to steroids and multiple courses may be required

Postoperative Apnoea
postoperative apnoea occurs predominantly in former premature infants, and rarely in term
infants ≤1 month of age
in prem's the incidence is inversely proportional to the postconceptual age
incidence is very low ≥ 50-60 weeks postconception
the apnoeic episodes usually commence within 2 hours of surgery and may be,
a. brief ~ 5-15 s
b. prolonged ≥ 15 s

~ 1/3 will have onset of apnoea at 4-6 hours, very rarely the onset may be at 8-12 hours
the duration of apnoeic episodes also varies with postconceptual age,
a. ≤45 weeks - episodes may occur for up to 24-48 hours
b. > 45 weeks - episodes usually disappear within 12 hours
NB: most will admit ex-prem's < 60 weeks PCA for overnight monitoring

49
 ICU - Paediatric

Upper Airway Obstruction

Neonate Infant & Child

Nasal choanal atresia

Oropharyngeal Pierre-Robin syndrome macroglossia

Treacher-Collins retropharyngeal abscess
thyroglossal atresia tonsillitis ± abscess
vallecular cyst obstructive sleep apnoea

Laryngeal "infantile larynx" croup & spasmodic croup

vocal cord palsy epiglottitis
subglottic haemangioma post-extubation oedema
laryngeal cysts teratoma / papilloma
(cystic hygroma, teratoma) haem/lymph-angioma
laryngeal web reflex (laryngospasm)
laryngomalacia burns / smoke inhalation
laryngeal spasm caustic ingestion

Tracheal tracheomalacia foreign body

vascular ring tracheal stenosis
meconium aspiration vascular ring
bacterial tracheitis
obstruction of ETT burns / smoke inhalation

Progression of Obstruction

1. Early
i. stridor on exertion
ii. stridor at rest
iii. retraction on exertion → intercostal & suprasternal

2. Late = indications for intubation

i. retraction at rest → tachycardia/tachypnoea
ii. exhaustion & tiredness
iii. cyanosis & bradycardia
iv. cardiorespiratory failure
v. cardiac arrest

50
 ICU - Paediatric

Upper Airway Obstruction Adult

a. foreign body / aspiration

b. infections - adult epiglottitis
- nectrotising fasciitis
- Ludwig's angina
- pharyngeal abscess, quinsy
- infected epiglottic cyst
c. neck / facial trauma - gunshot wounds
- burns
- postoperative
- acid/caustic ingestion
- laryngeal fracture
d. tumour - tongue
- larynx, trachea
- thyroid
- oesophagus
- 2° nodes, mediastinal masses
e. oedema - angioneurotic oedema
- pre-eclampsia
- anaphylaxis
f. neurological - bulbar/pseudobulbar palsy
- GBS, CIP
- myasthenia
- CNS depressants, drug overdose
- CVA
g. endocrine - hypocalcaemia, acute hypoparathyroidism
- goitre, myxoedema
h. tracheal stenosis / tracheomalacia
i. post-surgical - oedema
- haemorrhage
- throat packs
- vocal cord palsy
j. instrumentation - ETT kinking
- cuff overinflation
- Minnesota tube
- tracheostomy false passage

51
 ICU - Paediatric

Respiratory Failure

Predisposing Factors: Neonate

a. structural immaturity of the thorax - high chest wall compliance

- diaphragm fatigue
- horizontal ribs
- relative abdominal organomegaly
b. immaturity of the respiratory system - surfactant
- alveolar instability
- central drive
c. airway size / resistance
d. high VO2
e. high shunt fraction
f. relative immunoparetic state
g. the presence of developmental defects
h. perinatal asphyxia or other injuries

Clinical Presentation

a. young infants - lethargy, pallor, apnoea

- bradycardia, hypotension
≡t CNS / CVS depression
b. older child - tachypnoea, tachycardia, hypertension
- restlessness, confusion
- prior to CNS / CVS depression (≡t adult)
c. respiratory signs - tachypnoea / apnoea
- flaring alar nasi
- chest wall retractions
- expiratory grunting ± stridor
- prolonged expiration ± wheezing
- decreased or absent breath sounds
- cyanosis
d. cardiac signs - tachycardia / bradycardia
- hypertension / hypotension
- cardiac arrest
e. cerebral signs - confusion, irritability, restlessness, combativeness
- lethargy
- seizures ± coma
f. general signs - sweating, pallor
- fatigue

52
 ICU - Paediatric

Causes of Acute Respiratory Failure

Neonate Small Child

Airways meconium aspiration bronchiolitis

obstruction gastric aspiration status asthmaticus
congenital abnormalities cystic fibrosis
(see preceding table) tracheomalacia foreign body
croup/epiglottitis

Alveolar disease HMD, BPD trauma/contusion

CHD + high PBF/HT CHD & pulmonary HT
pneumonia pneumonia
aspiration near drowning
pulmonary oedema chemical pneumonitis
2° diaphragmatic hernia pulmonary fibrosis
interstitial emphysema
congenital lobar emphysema
congenital lung cysts

External pneumothorax pneumothorax

compression diaphragmatic hernia haemo/chylothorax
abdominal distension pleural effusion
abdominal wall defects "TPN/IVT" thorax
(post repair) thoracic trauma
burns

Neuromuscular birth asphyxia trauma

disorders apnoea of prematurity drugs/poisons (OP's)
IC haemorrhage IC haemorrhage
convulsions meningo-encephalitis
sepsis / meningitis tumour
drugs ± maternal status epilepticus
kyphoscoliosis
Guillain-Barré
poliomyelitis
botulinism

53
 ICU - Paediatric

Neonate: General Causes

1. respiratory disease - HMD, aspiration, etc.

2. neurological disease - birth asphyxia, ICH
- seizures
- phrenic nerve palsy, etc.
3. cardiac disease - CHD, PFC
4. abdominal disorders - diaphragmatic hernia
- TOF
- gastric distension, SBO
NB: RX → controlled O 2 therapy
posture and physiotherapy
microbiology - NP swab, skin, NG tube, urine, blood
penicillin & gentamicin
thermoneutral environment
fluid monitoring and restriction
± intubation and IPPV
monitoring - clinical, SpO2, AGA's, CXR

Infant: General Causes

1. respiratory disease - bronchiolitis, asthma

- cystic fibrosis
- pneumonia
- airway obstruction
2. cardiac disease - CHD, myocarditis
3. neurological disease - GBS
- meningitis, encephalitis
- epilepsy
- poisoning
4. trauma - head, chest, abdomen
- Cx spine
- drowning

54
 ICU - Paediatric

Causes - Specific

a. transient tachypnoea - common, especially LSCS

b. hyaline membrane disorders - surfactant deficiency
prematurity, maternal diabetes, intrauterine asphyxia, LSCS
alveolar instability, atelectasis, increased shunt & WOB
tachypnoea, retraction, expiratory grunting
CXR: bilateral interstitial pattern & air bronchogram
complications: severe respiratory failure, BPD
CPAP → improved PaO2 , breathing pattern
reduced disease progression, lower morbidity
c. acute viral bronchiolitis
cough, wheeze, low temp., tachypnoea, wheeze ± apnoeas
RX = O2, IVT ± CPAP
no benefit from steroids or bronchodilators
d. aspiration pneumonitis
meconium / gastric contents
prematurity, birth asphyxia
oesophageal atresia ± tracheo-oesophageal fistula
oesophageal reflux
intracranial haemorrhage
gastric pH > 2.5, therefore ≠ Mendelsonn's syndrome
e. apnoea of prematurity > 20 sec apnoeic spells
- immaturity of brainstem
- chemoreceptor dysfunction
- diaphragmatic fatigue
- ↑ REM sleep component
NB: exclude - hypoglycaemia
- HMD, aspiration
- sepsis, anaemia
- IC haemorrhage
RX - CPAP, IMV
- theophylline
f. spontaneous pneumothorax
barotrauma in the presence of HMD
IPPV with aspiration syndrome, pneumonia
especially lung hypoplasia (including diaphragmatic hernia), Staph. pneumonia,
bronchiolitis, asthma, pre-existing PIE
abdominal distension, unilateral chest hyperexpansion, transillumination of the chest

55
 ICU - Paediatric

g. pneumonia
prolonged rupture of the membranes
infected birth canal
immunoparetic state, invasive procedures
difficult to differentiate from HMD
most are viral: RSV, influenza, parainfluenza
* beware group B haemolytic streptococci
* empyema, bronchopleural fistula, haematogenous spread
h. congenital diaphragmatic hernia
associated bilateral lung hypoplasia
~ 50% mortality if present within 4 hrs of birth
> 4 hrs almost all survive
IPPV may → BPF or pneumothorax on either side
pulmonary hypertension & persistent foetal circulation
sample pre/post-ductal P aO2
respiratory alkalosis, high FIO2, avoid acidaemia
i. acute severe asthma - see below
j. congenital heart disease
i. obstructive lesions
ii. lesions with increased pulmonary blood flow
iii. lesions with decreased PBF
iv. intercurrent infection - especially (ii)
v. post-surgical
k. near drowning
2° to either aspiration pneumonitis or hypoxic/ischaemic encephalopathy
pulmonary oedema ± necrotizing pneumonia may develop
both fresh & salt water are usually hypovolaemic, hypoxic and acidotic on
presentation
thus, they require volume expansion, oxygen, inotropic support and correction of
acidaemia
associated hypothermia may afford some brain protection and should not be
actively treated before volume resuscitation

56
 ICU - Paediatric

l. convulsions
i. newborn - birth asphyxia
- trauma
- IC haemorrhage
- hypoglycaemia
- hypo-Ca++/Mg++
- pyridoxine deficiency, inborn errors of metabolism
ii. children - fever
- idiopathic epilepsy
- meningitis, encephalitis
- drugs, poisoning
respiratory failure 2° to airway obstruction, aspiration, apnoea & respiratory
depression
associated ↑ VO2 and CO2 production
m. trauma
majority are 2° to bicycle and motor vehicle accidents
isolated CHI is common
in the very young (< 2 yrs → open sutures), head injury alone may result in
hypotension from hypovolaemia
high cord lesions are difficult to detect with severe CHI
(NB: rhythmical flaring of the alae nasi without respiration)
major damage to the thoracic structures may occur without significant chest wall
injury → CXR is mandatory
acute gastric dilatation occurs almost invariably and may exacerbate failure
→ RX nasogastric tube
n. poisoning
o. Guillain Barré → IPPV if vital capacity is < 15 ml/kg
± early tracheostomy (children tolerate long-term ETT)
± management for muscle pains
p. acute respiratory distress syndrome
can occur at any age
most common precipitating causes in children are,
i. shock, sepsis
ii. pneumonia, near drowning, aspiration pneumonia
iii. trauma
iv. ingestion
management is similar to that for adults
mortality in paediatric series is high (28-90%)
this relates to the severity of the disease, secondary infection, or MOSF

57
 ICU - Paediatric

Croup - Acute Laryngotracheobronchitis

Def'n: inflammation of the glottic & subglottic region (narrowest)

1. viral croup - parainfluenzae viruses

- occasionally RSV, rhinoviruses, or measles
- coryzal prodrome, low grade fever
- rare < 6/12, ? underlying lesion
- commonest obstruction 6/12 to 6 yrs
- median age of presentation 18/12
- more common in autumn & winter
≤5% require intubation
2. spasmodic croup - children with an allergic nature
? spectrum of asthmatic population
- no coryzal prodrome / fever
3. bacterial tracheitis - usually Staph. aureus ± H. influenzae
group A Strep.
- high fever, WCC, purulent secretions
* risk of sudden obstruction

Clinical Presentation

a. signs of mild croup - URTI preceding 2-3 days

- loud barking "croupy" cough
- gradual onset inspiratory stridor which is high pitched
- hoarse voice
- no postural preference
- mild fever
- often a past history of croup
b. moderate - stridor on inspiration & expiration
- tachypnoea
- flaring alar nasae
- suprasternal/intercostal retractions
c. severe - restlessness caused by hypoxia
- exhaustion & listlessness
- deteriorating conscious state
- cyanosis on air
d. differential diagnosis - epiglottitis
- aspiration of foreign body
- bacterial tracheitis
- retropharyngeal abscess
- peritonsillar abscess

58
 ICU - Paediatric

e. diagnosis
i. history and examination * mainstay of diagnosis
ii. radiology of the larynx (ESS or ICU) →
"steeple" sign - AP view
widened hypopharynx - lat. view, only ~ 40-50% of cases
iii. direct laryngoscopy under GA

Management

a. minimal disturbance - ↓ VM & VO2

- nursed by parent
b. adequate hydration
but propensity for pulmonary oedema
hypo-Na + & convulsions have occurred 2° to SIADH with airway obstruction
c. oxygen therapy → SpO 2 > 90%
hypoxia from parenchymal infection ± increased interstitial water
d. humidification
mainstay for years but studies showing efficacy are lacking
now abandoned by many centres but anecdotal evidence ? otherwise
e. steroids
dexamethasone ~ 0.6 mg/kg (≤12 mg) stat., then 0.15 mg/kg q6h
given on admission → ↓ intubation rate & duration of stay
↓ failed extubation rate
administer 24 hrs pre & 12 hrs post-extubation
may also be of use in spasmodic croup
f. nebulized adrenaline
1:1,000 ~ 0.5 ml/kg ≤5 ml of 0.1% solution, nebulised 2 hrly
this dose is effective, has little systemic effect, and is less than the recommended
dose for the racemic solution
subsequent doses → less effective
obstruction may be more severe after the effect has worn-off
→ rebound phenomenon ? progression of the disease process
i. acute LTB - lasts ~ 1-2 hrs
- doesn't alter course
- may allow secretion expectoration
- prior to intubation, enhances induction
ii. spasmodic croup - may obviate need for intubation
iii. post ETT / endoscopy oedema where effect is often dramatic
iv. prior to transfer if not for intubation
v. prior to anaesthesia & intubation if tolerated

59
 ICU - Paediatric

g. antibiotics - only for proven bacterial infection

h. intubation ~ 2-5% of cases, nasotracheal
- use 1 mm less than "size for age"

Indications for Intubation

NB: essentially subjective assessment

a. ↑ respiratory rate, HR, and chest wall retractions

b. cyanosis not responsive to oxygen
c. exhaustion and/or confusion
d. increased use of, and failure to respond to, nebulised adrenaline
e. need for transport to another hospital

Method
spontaneously breathing, inhalational anaesthetic
induction is prolonged ∝ ↓ tidal volume
↑ V/Q mismatch
ETT ~ 1 size smaller for age to minimise trauma
most safely passed orally, then changed to a nasal
small tubes are shorter and may be difficult to secure
sedation ± arm splints to prevent self extubation
stomach should be emptied with a nasogastric tube
CPAP or IPPV with PEEP to maintain oxygenation

Extubation
extubation can be attempted when a leak is present with positive pressure or coughing, or when
the disease has run its course at 5 to 7 days
size limited to > 3.0 mm, due to requirement to pass a suction catheter to clear secretions
reintubation may be required, but the incidence is reduced by administration of steroids prior to
extubation → prednisolone ~ 2 mg/kg/day
prior to steroid therapy intubation duration average 5 days, but now reduced to 2-3 days

60
 ICU - Paediatric

Bacterial Tracheitis
results in purulent secretions, pseudomembranes and ulceration of epithelium within the trachea
death can result from upper airway obstruction, endotracheal tube blockage, and toxic shock
either a primary bacterial infection or a superinfection on primary viral illness
the causative organisms are,
a. Staphylococcus aureus
b. Haemophilus influenza type B
c. Streptococcus pneumoniae
d. Branhamella catarrhalis

Clinical Presentation

a. fever & toxaemia

b. respiratory distress
c. similar to epiglottitis except for
i. the presence of a cough
ii. a subjective difference in quality of the stridor
d. diagnosis
i. CXR - may show tracheal membranes
- narrowing & "fuzziness" are variable
ii. ETT - absence of epiglotitis
- suction following intubation
→ pus and membranes in the trachea

Management
similar to that for epiglottitis (see over)
if intubation is required, the ETT may block acutely with secretions
→ aggressive tracheal suction ± reintubation

bronchoscopy to clear tracheal pus should be considered where the airway remains compromised
after intubation, suction and reintubation
initially, there may not be a leak around an appropriately sized endotracheal tube
sputum should be sent for gram stain and culture, and urine for rapid antigen identification
extubation is best performed when,
a. the fever and secretions have settled, and
b. a leak is present around the endotracheal tube

initial antibiotic therapy → cefotaxime ~ 50 mg/kg q6h for 10/7

then by MC&S

61
 ICU - Paediatric

Epiglottitis

Def'n: supraglottic, infective inflammatory lesion,

caused almost exclusively by Haemophilus influenzae - type B
± occasionally streptococci, staphlococci, or pneumococci

a. acute onset - short history (hrs)

- no preceding URTI
b. high fever & toxaemia
c. stridor - low pitched, inspiratory ± expiratory snore
- usually constant in nature
d. absence of cough and reluctance to talk
e. characteristic posture - sitting forward
- mouth open
- drooling & dysphagia
f. diagnosis
i. direct laryngoscopy
ii. urine latex antigen agglutination
iii. ~ 80% blood culture (+)'ve
iv. lateral XRay → "thumb print"

most commonly children from 2 to 7 years but the disease can involve adults and infants
due to septicaemia, the severity of the illness is often out of proportion to the airway obstruction
children less than 2 years of age may present with airway obstruction atypically accompanied by
apnoea, URTI, low grade fever, and/or cough
sudden total obstruction may be precipitated by,
a. instrumentation of the pharynx
b. painful stimuli - eg. IV insertion
c. supine posture

Management

a. minimal disturbance - nurse in mothers arms, etc.

- ready access to intubation equipment
b. oxygenation - mask or nasal canulae
- if obstructs → CPAP/assist by bag
c. antibiotics
i. cefotaxime ~ 50 mg/kg q6h
± chloramphenacol ~ 25 mg/kg q6h
ii. ampicillin was used but high percentage of resistant strains

62
 ICU - Paediatric

d. intubation - all but the mildest cases

- average duration ~ 18 hours
may be required for longer in cases with,
i. pulmonary oedema
ii. pneumonia
iii. cerebral hypoxia
e. racemic adrenaline is of no use in this condition and can precipitate obstruction

Epiglottitis - Intubation Indications

1. severe or progressive respiratory distress

2. prior to transportation to a tertiary centre
3. following diagnosis by direct laryngoscopy under GA

patients can be managed without intubation if they remain in an area where appropriate
personnel, equipment and supervision is available
such patients are generally older, co-operative and are seen early in the day with minimal signs of
obstruction
diagnosis in these cases is made by lateral neck XRay
an IV line can be inserted before anaesthesia, but should be delayed until after induction when the
patient is distressed or obstruction is severe, in order to avoid sudden obstruction
spontaneously breathing, inhalational GA is best tolerated in the sitting position
agitation and distress at induction may be due to acute hypoxia
the patient can be laid flat on loss of awareness, and airway obstruction overcome by application
of CPAP or assisted ventilation
induction is prolonged, and laryngospasm may be precipitated if laryngeal stimulation occurs
prior to surgical anaesthesia being achieved
copious and persistent pulmonary oedema fluid may obscure the larynx, making intubation
difficult
an ETT of normal size for age or one size smaller should be inserted orally then changed to the
nasal route once the child has settled
positive pressure should demonstrate a leak around the tube
the patient can be sedated ± restrained to prevent self-extubation
muscle relaxants are not routinely required unless IPPV/PEEP is required to overcome hypoxia
and hypoventilation from pulmonary oedema

63
 ICU - Paediatric

Complications

a. respiratory failure / obstruction

b. pulmonary oedema ~ 7-10% of cases
- precipitated by intubation
i. hypoxia & SNS discharge - ↑ PAP
ii. vascular - endothelial injury & capillary permeability
iii. decreased intrathoracic pressure after intubation
augmenting venous return, and increasing transmural pulmonary vascular
hydrostatic pressure gradients
c. barotrauma
i. pulmonary interstitial emphysema (PIE)
ii. pneumothorax
iii. pneumomediastinum
d. septicaemia / pneumonia

Extubation Criteria

a. when the fever has settled

b. signs of inflammation subside → usually ~ 18 hours
i. pain subsided
ii. able to swallow
iii. free movement of the larynx
NB: exceptions are where hypoxia and reduced lung compliance persist
direct laryngoscopy prior to extubation is not required

64
 ICU - Paediatric

Croup vs. Epiglottitis

Parameter Croup Epiglottitis
Age 6-24 months 3-7 years
Aetiology parainfluenza Haemophilus infleunzae type B
RSV, rhinovirus Group B Strep., Pneumococcus
Seasonal autumn, winter none
Onset few days rapid
preceding URTI
Cough present, barking absent
Dysphagia no yes ± drooling
Appearance pale toxic, flushed, febrile
Temperature variable, ≤39°C high, often ≥ 39°C
Posture variable sitting-up / forward
Stridor inspiratory expiratory snore ± inspiratory
high pitched low-pitched
WCC usually normal often > 15,000
Neck X-Ray tracheal narrowing "thumbprint sign"
"steeple sign"
Treatment nebulized adrenaline Cefotaxime 50mg/kg q6h, or
Chloramphenacol 25mg/kg q6h
Intubation
frequency ~ 1-5% majority
duration days ~ 1 day
Complications obstruction obstruction
pneumonitis pulmonary oedema
"asthma" septicaemia
meningitis

65
 ICU - Paediatric

Supraglottic Obstruction - Other Causes

NB: these may all present in a similar fashion,

i. retropharyngeal abscess
ii. tonsillitis, peritonsillar abscess
iii. infectious mononucleosis
iv. Ludwig's angina

airway management is essentially the same ± antibiotics

± surgical drainage

the conservative approach to tonsillectomy & adenoidectomy has led to an increased frequency
of hypertrophy and chronic upper airway obstruction
these children may present with an acute exacerbation with intercurrent infection
removal is generally contraindicated in the acute setting due to the risk of haemorrhage

Foreign Body
most common between 6 months and 3 years age
clinical presentation depends on the site of lodgement,
1. pharynx / larynx - respiratory distress
- gagging, persistent cough
- stridor, dysphonia
- sudden total obstruction
2. tracheal / bronchial - cough, stridor, wheeze
- persistent pneumonia, lobar collapse
3. oesophageal - dysphagia, drooling
- stridor from tracheal compression

diagnosis is best made from the history, usually choking while eating, and examination
AP and lateral XRays only demonstrate radiopaque objects
inspiratory and expiratory films may show localised air trapping
management for respiratory arrest includes,
1. holding the child upside down while supporting the airway
2. backblows
3. finger sweep of the pharynx
4. chest thrusts, and abdominal thrusts (Heimlich manoeuvre) in the older child
5. direct laryngoscopy, bronchoscopy, and emergency intubation.

66
 ICU - Paediatric

Obstructive Sleep Apnoea

characterized by intermittent upper airway obstruction during sleep, with,
a. heavy snoring & stertorous breathing
b. an abnormal, irregular respiratory pattern
c. hypopnoea → chest wall motion with inadequate airflow
d. obstructive apnoea → chest wall motion with no airflow

these episodes occur most frequently in REM sleep, which constitutes,

a. pre-term infant ~ 65%
b. 6 months ~ 20%

the episodes are accompanied by varying degrees of arterial desaturation

these may be accompanied by cardiorespiratory decompensation
chronic hypoxia/hypercarbia may lead to progressive pulmonary vascular disease, hypertension
and cor pulmonale

Associated Findings

a. obesity
b. enlarged tonsils/adenoids
c. a large uvula or long soft palate
d. macroglossia
e. retrognathia
f. various neurological abnormalities
NB: severely affected children may be growth retarded

Surgical Management

a. tonsillectomy & adenoidectomy - even if normal size

b. ± uvulopalatopharyngoplasty
c. ± tracheostomy
NB: long term nasopharyngeal intubation or nocturnal nasal CPAP is not feasible in the
young child

67
 ICU - Paediatric

Pierre-Robin Syndrome

Def'n: congenital syndrome associated with,

1. posterior cleft palate
2. retrognathia & relative macroglossia
3. chronic upper airway obstruction
4. feeding difficulties & failure to thrive in the newborn

differential growth generally reduces the significance of the deformity

acute obstruction may be managed by nursing prone or the passage of a naso-pharyngeal tube
intubation is rarely required
tongue/lip anastomosis is sometimes beneficial

Other Subglottic Lesions

a. burns
b. subglottic stenosis
c. subglottic haemangioma
d. foreign body

68
 ICU - Paediatric

Anaesthetic Considerations - Airway Obstruction

NB: → inhalational induction with halothane & 100% O2

+ skilled assistance if available

a. adequate preparation - reliable suction, tube sizes, stylets, etc.

b. inhalational induction is slow with obstruction
small tidal volumes
parenchymal lung disease - infection, increased lung water
if oxygen saturation is adequate, N2O reduces induction time
c. use the sitting position ± the parent with epiglottitis
d. CPAP / assisted ventilation will aid induction, but may result in abdominal distension
e. laryngoscopy should only be attempted once a deep plane of anaesthesia is reached
f. orotracheal intubation is safest & may be performed first
replacement with nasotracheal intubation following adequate tracheal toilet
g. placement should be at ~ T2 , or the aortic arch/medial claviclular heads on CXR
~ 13 cm + age for children ≥ 1 year (at the naris)
~ (age + 17)/4 ETT size
h. humidification is difficult → lightweight heat/moisture exchangers
i. require regular toileting due to inspissated secretions
j. sedation is rarely required once the obstruction is relieved
arm restraints may be required to prevent self-extubation
incidence of spontaneous extubation is 8% to 12%

if obstruction occurs prior to anaesthesia, immediate oral intubation should be performed

emergency cricothyroidotomy and tracheostomy are rarely indicated, except for failure of oral or
nasal intubation
cricothyroidotomy can be performed using a 14G intravenous cannula, with ventilation
performed via a 15 mm standard connector from a 3.5 mm ETT
percutaneous tracheal ventilation requires short inspiratory times and long expiratory times to
minimize the risk of barotrauma
nasal intubation allows secure fixation and greater comfort
subglottic stenosis may result from too large a tube,
a. incidence ~ 2% ventilated neonates
b. may be related to duration, reintubation rate, infection and age

low lung compliance may produce an excessive leak

this can be overcome by placing the endotracheal tube tip lower in trachea (not endobronchial),
inserting a larger endotracheal tube, or considering a low pressure cuffed tube (the smallest is 4.5
mm ID)
problems with cuffed tubes include larger outside diameter, trauma and tracheomalacia

69
 ICU - Paediatric

Severe Acute Asthma

Def'n: severe asthma unresponsive to conventional therapy

incidence is increasing, frequently triggered by viral infection

patients presenting with one episode of acute respiratory failure are at higher risk of presenting
with another

Clinical Features

a. air hunger, tachypnoea, wheeze ± silent chest, cyanosis

→ unreliable for assessment, use AGA's
b. PaCO2 - hypocarbia 2° hypoxic drive is usually present
- normocarbia/hypercarbia ≡t fatigue & failure
c. pulse paradox - should be < 20 mmHg
- may be low with severe disease & fatigue
d. best assessment of need to intubate → clinical picture

Management

a. supplemental O2 - hypoxia presumed on presentation

b. IVT - hydration is important for inspissated secretions
- beware SIADH & oedema
- total lung water is increased
c. nebulized salbutamol
0.5% solution, 0.05 ml/kg q2-4h
can be given neat (undilute) continuously with less side effects of tremor,
tachycardia, hyperglycaemia, and hypokalaemia cf. IV administration
< 2 yrs little airway muscle & relatively unresponsive to bronchodilators
d. steroids
hydrocortisone 2-4 mg/kg q4h
significant benefit at 12 hrs
e. IV salbutamol
may obviate need for intubation ~ 1.0 µg/kg/min
increment ≥ 20 minutely to 14 µg/kg/min maximum → ↓ PaCO2 ≥ 10%
equally effective & less side-effects cf. adrenaline
indications,
i. progressive deterioration
ii. O2 flows too high for effective nebulisation
iii. no response to nebulised salbutamol
iv. patients in extremis

70
 ICU - Paediatric

f. aminophylline
bronchodilator also improves respiratory muscle function and stimulates the
respiratory centre
increased clearance of theophylline < 9 years
loading dose ~ 10 mg/kg - less if recent administration
infusion ~ 1.1 mg/kg/hr - cf. adults ~ 0.5-0.7 mg/kg/hr
serum levels must be monitored, especially when symptomatic
→ vomiting, tremors, convulsions
* isoprenaline & theophylline may override HPV
→ ↑ shunt, ∴ salbutamol is preferable
* salbutamol & aminophylline precipitate, use separate IV's
g. intubation / ventilation
i. progressive exhaustion and hypercapnia despite aggressive therapy
ii. where the patient presents in a terminal state
usually not required, and morbidity from IPPV is low
intubation technique should be rapid
use either a large uncuffed, or a cuffed ETT to minimise leak with high inflation
pressures
IPPV → low rates with prolonged expiratory times
minimal peak airway pressures
volume cycling
± adequate VM *lesser requirement
ventilation is aimed at correcting hypoxia, not normocapnia
PEEP may minimise hypoxia, but the use of PEEP for reversal of airway
obstruction is not proven
paralysis and sedation → maximise compliance & ↓ VO2
drugs which release histamine are best avoided (eg. morphine, but no evidence)
complications include barotrauma and muscle weakness
h. bronchoalveolar lavage
indicated where hypoxia is associated with persistent lobar collapse or localised
hyperexpansion
requires a fibreoptic bronchoscope with a suction channel, and it's use is limited by
endotracheal tube size

mortality is low and thus extraordinary measures such as anaesthesia (inhalational agents,
ketamine) and extracorporeal CO 2 removal are rarely indicated
there is a high incidence metabolic acidosis in severe asthma, and HCO3- has been advocated to
improve bronchodilator responsiveness (ie. adrenergic function), however,
a. ↑ morbidity from untreated acidosis is not proven
b. HCO3- does not significantly change pH in asthma unless large doses
c. HCO3- → ↑ CO2 production
d. some don't believe improves adrenergic response anyway - eg M. Fisher

71
 ICU - Paediatric

Bronchiolitis

Def'n: acute lower respiratory tract infection of infants

effects ~ 2% of all infants
the most common severe lower respiratory infection
more frequent in winter months

age distribution from 6 months to 2 years age (same as croup) is attributed to,
a. loss of protective maternal antibodies
b. aspiration of infected nasopharyngeal secretions
c. small calibre of peripheral airways

Aetiology

a. respiratory syncitial virus (RSV) ~ 70%

b. influenza, parainfluenza types I and III
c. rhinovirus
d. adenovirus
e. mycoplasma

Pathology

a. lymphocytosis in peribronchiolar spaces

b. inflammation & oedema of submucosa and adventitia in small airways
c. necrosis and desquamation of small airways epithelium
d. airway obstruction from oedema, cellular debris, and secretions in small airways
e. hyperinflation, atelectasis, ventilation/perfusion inequality
f. ↑ resistance, ↓ compliance and ↑ work of breathing

ventilation is a compromise between the work required to breathe at high lung volumes and the
required minute volume
this results in hypercapnia which is tolerated in order to minimise work of breathing
further progressive increases in PaCO2 denote decompensation
mortality (≤1%) is associated with other serious disease,
a. congenital heart disease
b. bronchopulmonary dysplasia
c. cystic fibrosis
d. congenital lung disease
e. immunosuppressive disorders

72
 ICU - Paediatric

Clinical Presentation

NB: broad clinical spectrum,

from mild URTI → severe pneumonia and respiratory distress

a. preceding URTI
b. symptoms usually last ~ 5-10 days
c. acute onset with rhinorrhoea, cough, dyspnoea, and wheezing
copious thick nasal & pharyngeal secretions
may have high fever
d. occasional progression to severe respiratory distress
e. infants present with tachypnoea, hyperinflation, and fine crepitations
f. premature infants & neonates may present with apnoeic spells, 2° to,
hypoxia
respiratory muscle fatigue
immaturity of respiratory muscle control
g. immunofluorescent techniques of nasopharyngeal secretions allow rapid virus
identification

Complications

1. acute respiratory failure

2. pneumonia
3. interstitial emphysema, pneumothorax
4. obliterative bronchiolitis < 1% of cases
chronic hyperinflation, collapse, and abnormal small airways
usually results from adenovirus infection
5. RSV bronchiolitis can lead to asthma in older children,
~ 75% have symptoms of wheezing in the subsequent 2 years
~ 22% in the next 10 years

Investigations

a. CXR - hyperinflation ± diffuse patchy infiltrates

- flat diaphragms, horizontal ribs, 'air under heart', etc
- increased abdominal gas ∝ air swallowing
b. AGA's - hypoxia
- frequently hypercarbic
c. immunofluorescence of nasopharyngeal swab
d. serology - 4x rise in RSV titre

73
 ICU - Paediatric

Management

a. supplemental O2 - head box, nasal cannula or face mask

monitor by SpO 2 ± arterial cannula for serial AGA's
? warmed, humidified gases
mist inhalations may induce bronchospasm
physiotherapy and handling may increase respiratory distress
b. IVT ± mild fluid restriction
c. warmed, thermoneutral environment
d. steroids are of no benefit
e. antibiotics are of no benefit
infiltrates on CXR are common
there is no increased incidence of bacterial infection
f. bronchodilator therapy
trials assessing the effect of bronchodilator therapy have been unpredictable
→ either no response, or improvement
a trial of nebulized salbutamol, or IV aminophylline may prove beneficial
(especially if apnoea is associated)
g. respiratory stimulation ? aminophylline, caffeine
h. riboviron
antiviral agent, limits RSV replication within cells
aerosol (~ 1.3 µm) for 3-7 days
increases elimination of the virus and resolution of symptoms, and improves
oxygenation
given orally it is teratogenic in pregnant rodents
it precipitates in ventilator circuits
no evidence for earlier discharge or effects on mortality
expensive & disease has low morbidity, therefore only considered early in the
infection and where there is severe pre-existing cardiorespiratory disease
i. nasopharyngeal CPAP
proved helpful in one series but not in another
if commenced early, it may reduce incidence of tracheal intubation
j. intubation / ventilation
tend to be younger, smaller, and more premature
endotracheal CPAP may correct apnoea
IPPV is required - bradycardia
- persistent hypoxia, rising PaCO2
- exhaustion
IPPV is well tolerated few require paralysis
sedation may aid synchronisation, and does not prolong weaning provided dose is
adjusted to clinical response
potential problems - air trapping, barotrauma, ETT obstruction

74
 ICU - Paediatric

Cystic Fibrosis
autosomal recessive disorder, most common genetic abnormality in Caucasians,
a. gene frequency ~ 1:25
b. incidence ~ 1:2500 live births
~ ¼ of 1/252

median survival (1990) ~ 28 years

most common molecular basis is deletion of 3 base pairs from long arm of chromosome 7
eliminates phenylalanine from membrane protein, cystic fibrosis transmembrane conductance
regulator CFTR, which permits apical membrane conductance of water
major organ systems affected,
1. respiratory
i. upper airway - chronic sinusitis, polyposis
ii. lower airways
bronchial hyper-reactivity
inflammatory cell activation and tissue destruction
bronchiectasis, abscess formation, empyema
colonisation - H.influenzae, S.aureus, P.aeuroginosa, P.cepacia
pneumothorax
haemoptysis - bronchial artery errosion/rupture
2. pancreatic insufficiency
i. exocrine - malabsorption syndromes
ii. endocrine ~ 75% have glucose intolerance
~ 15% → diabetes mellitus
3. gastrointestinal
i. meconium ileus ~ 12% of presentations at birth
ii. gastro-oesophageal reflux
iii. recurrent constipation
iv. rectal prolapse
4. hepatobiliary
i. fatty liver ~ 40%
ii. focal cirrhosis ~ 25%
iii. cholelithiasis ~ 12%
5. malnutrition - multifactorial
6. immune suppression

75
 ICU - Paediatric

Respiratory Failure - General Management

1. thermoneutral environment - humidicrib

- overhead heater
- room temperature control
→ minimise VO2
2. diaphragmatic movement - abdominal contents
- prone or head-up position
- NG tube
3. cease feeding - diaphragmatic movement
- microaspiration
4. minimal handling - dynamic airways collapse
- reduces VO2
5. monitoring - HR, RR, SpO2, PaO2 and PaCO2
- routine CXR's

Complications of Oxygen Therapy

a. retrolental fibroplasia ? absolute duration

(retinopathy of prematurity) ? level of hyperoxia
→ P aO2 ~ 50-80 mmHg
retinal receptors mature from the centre to the periphery of the retina
pattern results from high O2 consumption during development, ∴ ordered formation
from centre → out
hyperoxia allows proliferation in multiple regions simultaneously, ∴ results in a
disorganised vascular pattern
? frequency reduced by vit.E and other antioxidants
b. bronchopulmonary dysplasia ∝ peak inspiratory pressures
+ other evidence of barotrauma
c. resorption atelectasis
d. ? acute lung injury / O2 toxicity

76
 ICU - Paediatric

Intubation - Disadvantages

a. risks / complications of intubation procedure

b. bypasses the humidifying action of the nose
c. increases total airway resistance
d. risk of subglottic stenosis
e. interference with cough reflex
f. loss of physiological PEEP - "laryngeal braking"
g. impairment of pulmonary defence mechanisms
increased incidence of nosocomial pneumonia

the subglottic area is relatively narrow, and an ET tube small enough to be passed through the
larynx may be too large to be inserted into the trachea
the ETT is easily malpositioned because,
a. the trachea is short ~ 4-5 cm in neonates
b. the tube changes position with head and neck movement
→ in with flexion
out with extension

the smaller airways and endotracheal tubes are easily blocked with secretions
→ patients require frequent suctioning and constant humidification,
by servo-controlled humidifiers or moisture exchangers

the correct size tube is one which allows a small leak with IPPV ~ 25 cmH2O
exceptions to this rule are,
a. neonates - absence of a leak rarely causes problems
- problems correlate with duration & re-intubation frequency
b. croup - the appearance of a leak ∝ disease resolution
c. IPPV with low compliance lung disease
d. Down's synd. - often have subglottic narrowing & require a smaller tube

77
 ICU - Paediatric

CPAP

Benefits

1. increases FRC, stabilises alveoli, reduces shunt fraction

→ allows a reduction of FIO2

2. promotes both small and large airways stability
airway obstruction
bronchomalacia, tracheomalacia
croup, bronchiolitis, asthma
3. decreases the work of breathing
4. reduces auto-PEEP
5. may abolish apnoeic spells in neonates & improves the respiratory pattern
→ small (physiological) levels should be applied wherever possible
≤3-5 cmH2O, to prevent airway closure

requires a fresh gas flow,

a. ~ 2-3x minute ventilation
b. ≥ peak inspiratory flow rate
c. or requires use of a reservoir bag

nasotracheal intubation is the safest means of administration

however, a nasal mask or a single nasopharyngeal tube may be used

Complications

1. ↑ incidence of barotrauma *potentially

2. ↓ cardiac output
3. ↓ GFR
4. ↑ secretion of ADH → fluid retention
5. ↑ PVR and RV afterload
this is balanced against the ↓ PVR which follows opening of small airways and
expansion of areas of atelectasis

78
 ICU - Paediatric

Indications for Mechanical Ventilation

1. general anaesthesia with muscle relaxation

2. cardiopulmonary resuscitation
i. respiratory / cardiac arrest
ii. severe LV failure / acute pulmonary oedema
as a form of circulatory support
3. acute / chronic respiratory failure
i. maintenance of adequate gas exchange → parenchymal failure
to maximise DO2 - reduce work of breathing
- paralysis, reducing VO2
ii. minimise work of breathing → pump failure
4. manipulation of CO2 excretion
i. induced hypocapnia - metabolic / respiratory acidosis
- raised ICP, acute head injury
ii. ∝ ↑ CO2 production - MH, thyroid storm
iii. manipulation of PVR - pulmonary hypertension ± cor pulmonale
- CHD with R→ L shunt
- transitional circulation in the newborn
5. "prophylactic" ventilation - severe flail chest
- major, chest & upper abdominal surgery
- unstable patients for transport

time-cycled, pressure limited ventilation is used for neonates and infants less than 10 kg weight
this compensates for leak around the ETT and overcomes the problem of a relatively large circuit
compliance and compressible volume compared to the small tidal volume
however, this form of ventilation has problems,
a. the inspiratory waveform pattern is dependent on,
i. the flow through the circuit
ii. the resistance of the circuit
iii. the performance of the expiratory valve
b. tidal volume varies with pulmonary compliance & resistance
c. in patients spontaneously breathing or receiving IMV, stability of inspiratory and
expiratory pressures is not maintained with varying flows in the respiratory cycle,
resulting in suboptimal work of breathing
d. on older ventilators there is no ability to synchronise ventilation, or calibrate PEEP and
CPAP → these problems have been overcome in modern ventilators with acceptable
flow heads at the patient T-piece and digitally controlled valves

79
 ICU - Paediatric

Mechanical Ventilation - Complications

a. airway trauma
i. nasal passages
ii. mouth & pharynx
iii. tracheal trauma - subglottic stenosis
- ulceration
b. barotrauma
i. pulmonary interstitial emphysema (PIE)
ii. pneumothorax
iii. pneumopericardium, pneumomediastinum
iv. pneumoperitoneum
c. raised mean intrathoracic pressure
i. ↓ cardiac output
ii. ↓ GFR
iii. fluid retention - ↑ ADH / ↓ ANF
d. equipment related
i. disconnection
ii. ETT obstruction
iii. ventilator malfunction
e. nosocomial infection
f. microaspiration / macroaspiration

Indications for Tracheostomy

a. failure to achieve intubation by the oral or nasal route

b. congenital or traumatic upper airway obstruction
c. following craniofacial surgery
d. long term ventilation in children - GBS
- quadriplegia
- neuromuscular diseases

paediatric patients can be managed for long periods with nasotracheal tubes without long term
sequelae and tracheostomies are rarely performed
percutaneous tracheostomy has not been described
cricothyroidotomy is preferable in emergencies for small children and infants

80
 ICU - Paediatric

Extracorporeal Membrane Oxygenation (ECMO)

pulmonary bypass procedures for neonates has been used in the U.S.A.
limited to those patients with acute, potentially reversible pulmonary failure, who fail to respond
to conventional therapy
attempts to identify this group remain difficult
a. neonates - need to fulfil the following criteria:
i. acute reversible disease - eg. meconium aspiration
ii. ≥ 80% predicted mortality by statistical analysis
iii. no other abnormality incompatible with life
iv. body weight > 2.5 kg
limitations in body size and the risk of haemorrhage
b. children
attempts have been made to identify those with predictably high mortality,
and it's use has been extended to include,
i. bypass dependence following cardiac surgery
ii. catastrophic post cardiac surgical events
iii. reversible lung disease - aspiration pneumonia
- uncontrolled air leak

the advantages of ECMO are,

a. lost lung function is directly replaced
b. technical success is independent of disease severity
c. further lung damage is limited

complications include,
1. bleeding from heparinisation, as completely heparin bonded circuits are yet to be
developed
2. the effects of large vessel cannulation and ligation (EJV & ICA)
3. platelet & WBC activation

side effects of vessel ligation appear acceptable and reconstruction techniques are now available
outcome from ECMO for neonates is good, with impressive survival figures
~ 75 to 80% survival in those patients with 80% predicted mortality

however, no adequate controlled trials have been performed

81
 ICU - Paediatric

Surfactant
a phospholipid produced by alveolar type II cells
trials of surfactant administered via the trachea have shown improved outcome in neonates
susceptible to hyaline membrane disease
sources of exogenous surfactant are,
a. modified natural surfactant
lipid extract of animal lung - bovine most commonly used
b. human surfactant recovered from amniotic fluid
c. synthetic dipalmitoylphosphatidylcholine

indications have not been standardised but are based on,

a. age
b. PA-aO2 gradient
c. positive inflation pressure
d. duration of ventilation

results, when given prophylactically, show significant decreases in acute complications of

neonatal respiratory distress syndrome,
a. mortality 30% → ~ 12%
b. barotrauma 40% → ~ 8%

82
 ICU - Paediatric

RENAL SUPPORTIVE THERAPY

renal failure in the critically ill patient is prevented by,

a. maintaining or improving RBF despite other organ failure
b. careful monitoring/avoidance of nephrotoxic drugs
± vigorous use of loop diuretics (frusemide) and inotropes (dopamine)
→ normal or high output failure

high output ARF being easier to manage than oliguria, and may not require renal replacement
therapy
the choice between peritoneal dialysis (PD), haemodialysis (HD), or continuous arteriovenous
haemofiltration (CAVH) is governed by a number of factors,
a. no modality has been demonstrated superior in outcome in ARF
b. HD is more effective than PD in highly catabolic patients
c. PD clearance is impaired in - microangiopathies
- heatstroke
d. advantages of PD include - technically simpler
- widespread availability
- useful for infants
- useful post CPB

83
 ICU - Paediatric

Continuous Haemofiltration
haemofiltration is either arterio-venous (CAVH) with flow from the arterio-venous pressure
difference, or veno-venous (CVVH) requiring flow from an extrinsic pump
the ultrafiltrate formed is proportional to,
a. the hydrostatic pressure gradient
b. the membrane area & mean pore size

this UF is then replaced IV with a solution of desired composition

haemodiafiltration is where dialysate is perfused across the filter
indications for haemofiltration are,
a. acute renal failure
b. fluid overload / pulmonary oedema
c. metabolic derangements - hepatic failure
- severe electrolyte or acid-base imbalance
d. fluid volume limitations that restrict nutrition
e. drug and poison removal

haemofiltration is most useful for fluid removal in cardiovascularly unstable patients, but is less
rapid and effective than haemodialysis
it removes middle molecular weight vasoactive peptides that may lead to capillary leakage &
contribute to the "sepsis syndrome"

problems of continuous haemofiltration in children are,

a. additional arterial ± venous lines
b. blood flow and UF flow are dependent on,
i. arterial blood pressure (which is lower in children),
or, blood flow through the pump (CVVH)
ii. haematocrit
iii. position, size and length of catheters - greater dead space
c. greater circuit::blood volume ratio
i. dilution
ii. heat loss
iii. hypo / hypervolaemia with pump failure
d. regional heparinisation may cause bleeding
e. platelet sequestration, especially at low blood flows in paediatric patients
f. microaggregates are flushed into the venous circulation

84
 ICU - Paediatric

CAVH is simpler because the A-V pressure gradient drives blood through the filter
→ this provides safety and haemodynamic stability

however, with small paediatric cannulae and lower blood pressure, blood flow rates are low urea
clearance is reduced
blood flow can be improved by,
a. correcting hypovolaemia
b. increasing blood pressure
c. reducing blood flow resistance
i. reducing cannula length
ii. increasing cannula size
iii. changing cannula position

continuous arterio-venous diafiltration improves urea clearance

CVVH via a central venous dialysis catheter must be pump driven, but provides higher blood
flow and ultrafiltration rates, with better urea clearance
CVVH is technically more difficult than CAVH in infants
haemodialysis allows controlled ultrafiltration and dialysis
it requires relatively large central vascular access, specialised personnel and regional
heparinisation, and is expensive
it may cause rapid osmotic shifts and haemodynamic instability

Peritoneal Dialysis PD
peritoneal dialysis is inexpensive and provides smooth changes in fluid volume
a soft, purpose-designed catheter is inserted into the peritoneal cavity using a Seldinger technique
respiratory function may be affected in infants because raised intra-peritoneal pressure impairs
diaphragm function
complications include,
a. infection
b. catheter blockage
c. leakage of dialysate fluid and bowel perforation

it is contraindicated where abdominal pathology is present or recent surgery has been performed

85
 ICU - Paediatric

NEUROLOGICAL EMERGENCIES IN CHILDREN

these are the most common causes of life-threatening injury & death in children
SIDS outranks all other causes of death in infants by ~ 10x
after the first year, trauma accounts of ~ 50% of all deaths
primary brain injury results from,
a. trauma
b. ischaemia
c. infection
d. metabolic disturbance

secondary injury results from,

a. oedema - acute vasogenic cerebral oedema
b. altered cerebral autoregulation
c. tissue hypoxia, reperfusion injury
d. other cytotoxic events

factors pertinent to the paediatric population include,

a. diffuse cerebral swelling
occurs commonly and early in severe CHI
may be progressive with development of vasogenic oedema
b. cerebral blood flow
ICP & MAP vary with age
autoregulation is easily disrupted
with vasogenic oedema, hypertension may worsen ICP
c. hypovolaemia
commonly occurs 2° to scalp or intracranial bleeding
d. anatomical differences
large head, weak neck muscles, short stature
→ isolated severe head injury is common
under 2 years the sutures are open and the vault may expand
high cervical cord damage may occur without bony damage (SCIWORA)

86
 ICU - Paediatric

Causes of Coma in Children

Structural Metabolic

trauma infection
accidental meningitis
child abuse encephalitis

hydrocephalus hypoxia / ischaemia

blocked CSF shunts circulatory shock / arrest

tumours drugs / toxins

intracranial haemorrhage postictal / status epilepticus

infection biochemical - Na+/H2O

meningitis - Mg++/Ca++
encephalitis - pH
abscess - hypoglycaemia

hyper / hypothermia
diabetic ketoacidosis
hepatic failure
Reye's syndrome
complication of haemodialysis
haemolytic uraemic syndrome
hypertensive encephalopathy
inborn errors of metabolism

87
 ICU - Paediatric

Intracranial Pressure

a. 2 years of age ≤5 mmHg

b. 5 years of age ≤10 mmHg
c. > 10 yrs / adults ≤15 mmHg

elevation per se is not an indicator of poor outcome, unless persistently > 40 mmHg
symptoms and signs of raised ICP are,
a. depressed conscious level
b. vomiting, headache and papilloedema
c. strabismus
d. changes in blood pressure, heart rate and respiratory pattern
e. in infants with open sutures,
i. the fontanelle is full
ii. head circumference increases
iii. papilloedema is uncommon

physiological compensations for raised ICP are,

a. displacement of CSF → spinal canal
b. ↑ CSF resorption | ↓ CSF production
c. compression of intracranial veins → may worsen ICP
d. increase in head size

in the infant, gradual increases in volume of intracranial contents are accommodated by an

increase in head circumference, and this can delay clinical signs and diagnosis
the limiting factor on whether the ICP rises quickly or there is an increase in head size is the
elasticity of the dura
acute increases in head circumference is limited to children ≤ 18 months
over this age, any additional intracranial volume must be accommodated by displacement of
blood, CSF and brain
signs of cerebral herniation are,
a. abrupt changes in level of consciousness ± coma
b. irregular respiratory pattern
c. peripheral weakness / focal neurological signs
d. cranial nerve palsies - including pupillary dilatation
e. decorticate or decerebrate posturing
f. cardiorespiratory failure

88
 ICU - Paediatric

Cerebral Perfusion Pressure

CPP = MAP - ICP (when ICP > CVP)

dependence on blood pressure is important in the younger age group because physiological blood
pressures are low and autoregulation is disturbed
normal systolic blood pressure, 50th percentiles,
a. 1-6 months ~ 85 mmHg
b. 2 years ~ 95 mmHg
c. 7 years ~ 100 mmHg

in younger age groups, CPP is more easily encroached upon, and relative hypotension has a
significant effect on CPP and outcome
hypotension may be the principle cause of cerebral circulatory failure and infarction, resulting in
complete cessation of CBF
CPP < 40 mmHg reduces the likelihood of good outcome, and is critical for a range of paediatric
management
if vasogenic oedema is present (trauma, hypoxia/ischaemia, infection), hypertension may worsen
oedema

Cerebral Blood Flow

metabolism requires constant supply of oxygen ~ 3.3 ml.O2/100g/min
CBF is maintained at 50-60 ml/100g/min over a range of MAP by autoregulation
→ 50 ml/100g/min ~ 10 ml.O2/100g/min → O2 ER ~ 35%

abnormal CBF is caused by,

a. gross changes in PaCO2 and PaO2
b. convulsions
c. head injury
d. drugs - eg vasodilators
e. ↑ temperature

regional pressure, regional perfusion and total blood flow are not absolutely linked, and focal
oedema can effect local cerebral blood flow despite an adequate CPP
attempts to improve monitoring have led to measurement of cerebral blood flow as a clinical
indicator of changes in regional perfusion, but this is technically difficult and subject to significant
errors

89
 ICU - Paediatric

Management
the aims of therapy are to,
1. reverse the 1° disease processes
2. maintain CBF to prevent 2° ischaemic injury
3. prevent herniation from raised ICP
NB: there is no evidence that therapies aimed at reducing ICP, maintaining cerebral
blood flow, and improving cerebral perfusion pressure (CPP) improve outcome

however, monitoring these parameters allows for assessment of effects of therapy and routine
clinical interventions, and for outcome prognostication
a. initial - assessment/management of ABC
- venous access, blood for routine tests
- 0.5 ml/kg 50% dextrose if ? hypoglycaemia
- history & examination
b. controlled ventilation
i. apnoea, respiratory failure, or poor airway control
ii. rapidly worsening coma GCS < 9
iii. evidence of advancing IC hypertension
following this the stomach should be drained via NG tube
hyperventilation ± 15-30° head up (?? CPP better flat)
± mannitol 0.25 g/kg
± frusemide 1 mg/kg
± NMJ blockade
beware excessive diuresis → hypovolaemia
c. circulation - frequently hypotensive / hypovolaemic
- support MAP for age
- non-hypoosmotic fluids
d. CT scan - coma & localizing signs
- no diagnosis
e. LP - suspicion of meningitis, encephalitis
- no evidence of raised ICP
- defer until after CT scan if in doubt
- IC haemorrhage better defined by CT
f. ultrasound - when the fontanelle is open
- ventricular size & IC haemorrhage
g. EEG - focal or non-specific global abnormalities
h. other IX - U&E's, AGA's
- metabolic screen (LFT's, NH3 , amino and organic acids)
- blood, urine & gastric fluid for toxicology
- blood cultures and urine antigen screen
- virology for HSV, enteric viruses, CMV, measles, and rubella

90
 ICU - Paediatric

Head Injury
majority are from road trauma (MVA, pedestrian, cyclist)
a. age < 1 yr → 3rd leading cause behind SIDS & congenital anomalies
b. age > 1 yr → leading cause of death

presence of early hypoxia, hypercarbia or hypotension with severe CHI confers a bad prognosis
factors in initial assessment peculiar to paediatric patients,
a. GCS modified for age
b. acute gastric distension → NG tube
c. significant liver, lung, spleen & kidney trauma may occur without bony trauma
d. major blood loss with hypotension may be concealed
e. higher incidence of
i. seizure activity
ii. mass lesions
iii. white matter tears - frontal and temporal lobes
- especially infants < 6 months
iv. subdural haematomas - especially NAI

indications for further monitoring include,

a. CT scan
all children with modified GCS ≤ 8
presence of focal neurological deficit
less severe injuries prior to prolonged anaesthesia / procedures for other injuries
b. ICP monitoring
GCS ≤8 with cerebral swelling on CT scan
following drainage of cerebral collections
? best method but intraventricular catheter allows CSF removal
where NMJ blockade obscures signs of ICP

91
 ICU - Paediatric

Modified Glasgow Coma Scale

≤1 year > 1 year Score
Motor Response obeys 6
1
localises pain localises pain 5
withdrawal withdrawal 4
decorticate2 decorticate 3
decerebrate3 decerebrate 2
flaccid flaccid 1
Eye Opening spontaneous spontaneous 4
to voice / noise to command 3
to pain to pain 2
nil nil 1
Verbal Response
0-2 years 2-5 years > 5 yrs
appropriate appropriate oriented/converses 5
smile/cry smile/cry
crying inappropriate words disoriented 4
irritable crying irritable crying inappropriate words 3
grunts grunts incomprehensible 2
nil nil nil 1
Total Score 3-15
1
some score GCS/14 for ages < 1 year
2
decorticate = abnormal flexion, flexion/extension & crossed patterns
3
decerebrate = extension ± clonus

Prognosis - Coma

a. in large series - variable figures

~ 3% mortality
~ 2% severe disability
~ 95% normal
b. severe CHI (GCS ≤8) ~ 20-40% mortality cf adults ~ 40-50%
c. poor prognostic factors
i. initial GCS ≤4
ii. apnoea
iii. absent pupillary/vestibular reflexes
iv. subdural or multiple IC haematomas
v. intractable high ICP

92
 ICU - Paediatric

Management - Head Injury

NB: maintain CBF, DO2 & avoid hypercarbia

a. IPPV + muscle relaxation & sedation

→ PaO2 ≥ 100 mmHg / PaCO2 ~ 35 mmHg
b. prevent rises in ICP - head-up ~ 30° & neutral position
~ 30% of maintenance fluids
(no evidence that this works)
c. treatment of ICH > 20 mmHg ICP persistently
? RX at > 15 mmHg better prognosis
i. hyperventilation → PaCO2 ~ 25-30 mmHg
- effect wanes over hours
- excessive may decrease CBF
* RAH study in adults showing ↓ SjbO2 ∝ ↓ PaCO2
- rebound on cessation
ii. diuretic therapy - mannitol 0.25 g/kg
may be repeated 1-2 hrly
≤ 325 mOsm/l maximum effect ? also decreases viscosity
frusemide 0.5 mg/kg IV ? also decreases CSF formation
synergistic with mannitol
iii. CSF removal - situate drain at set height above the tragus
iv. barbiturate therapy
decrease CMRO2, blood volume and ICP with bolus injection
no studies show morbidity or mortality reduced with infusions
v. surgical decompression → bifrontal craniectomy
rarely used for high ICP
some American centres use this in adults
d. hypovolaemia - occurs more commonly in children
- especially scalp & intracranial
- associated intra-abdominal
e. seizure prophylaxis ~ 7.2% risk with severe CHI in child
phenytoin ~ 20 mg/kg IV + 3 mg/kg q8h
f. steroids??
g. surgery for mass lesions

93
 ICU - Paediatric

Prolonged Seizures
the common causes of prolonged seizures are,
a. known epilepsy + - withdrawal of anticonvulsants
- intercurrent infection & fever
b. CNS infection - meningitis
- encephalitis
c. febrile convulsion *atypical
usually → short duration ≤15 minutes
absence of focal signs
absence of post-ictal features
d. metabolic disturbance - hyponatraemia
- hypocalcaemia
- hypoglycaemia
e. trauma
f. NAI

Management

a. ABC
b. diazepam ~ 0.1-0.2 mg/kg IV/PR, up to 0.5 mg/kg
c. phenytoin ~ 20 mg/kg IV then 3-4 mg/kg q8h (minimal sedation), or,
phenobarbitone ~ 20 mg/kg IV
d. thiopentone ~ 2-5 mg/kg IV, then 1-5 mg/kg/hr by infusion
seizures are only controlled by anaesthetic doses
intubation and IPPV are therefore mandatory
e. management of metabolic / respiratory acidaemia
f. LP / CT scan

in neonates, seizures may be subtle and difficult to diagnose, with signs being irregular breathing,
apnoea, nystagmus and "bicycling" movements

NB: HSV encephalitis is frequently atypical in children, thus the early use of acyclovir
in febrile patients with unknown cause is justified

→ early therapy is associated with a markedly reduced morbidity & mortality

94
 ICU - Paediatric

Bacterial Meningitis
the major route of spread is haematogenous from the nasopharynx
it may result as a local complication of,
a. head trauma involving the paranasal sinuses
b. neural tube defect
c. dermoid sinus
d. middle ear infection

the causative organisms are usually,

a. Haemophilus influenzae - type B
b. Neisseria meningitidis
c. Streptococcus pneumoniae - sickle cell anaemia
- post splenectomy

the classical clinical findings,

a. fever
b. headache, painful stiff neck
c. photophobia
d. altered conscious state
NB: these may be absent in young children or following seizures, and
may be obscured by partial treatment

there may be over-ridding features of septic shock

petechiae / pupura fulminans may be seen not only associated with meningococcus, but also
with pneumococcus and Haemophilus
an atypical history with lower cranial nerve signs may represent TB
NB: the common pathogens can frequently be discerned using latex agglutination
antigen testing of the CSF or urine

pathophysiology includes,
a. early transient ventricular dilatation
b. cerebral oedema - cytotoxic and vasogenic
c. vasculitis - resulting in thrombosis/infarction
d. arterial spasm
e. cortical vein thrombosis

95
 ICU - Paediatric

Differential Diagnosis

a. infection - viral encephalitis

- fungal / tuberculous meningitis
- cerebral abscess
b. tumour - cerebral neoplasm, meningeal carcinomatosis
- leukaemic infiltration of meninges
c. subarachnoid haemorrhage (uncommon in children)

Investigation

a. FBE - ↑ WCC, ↑ ESR

± anaemia, thrombocytopaenia
b. INR / APTT ± DIC screen
c. E,C+U, CaP, LFT, BSL
d. urine antigen screen
e. blood cultures ± fluid from other suppurative foci
f. CXR ± SXR if sinisitis / otitis are origin
g. lumbar puncture - ↑ WCC - usually > 1000/ml
- ↑ protein - marked rise in TB
- ↓ glucose
organisms on gram stain ± bacterial antigen determination
increased lactate > 4 mmol/l → ↑ morbidity
LP should not be performed when,
i. the diagnosis of meningitis is clear
ii. the patient is seriously ill, or
iii. there is evidence of raised ICP

Complications

a. profound coma → - 2° complications

b. uncontrolled seizures
c. persistent focal signs - hemiparesis
- hearing loss (esp. pneumococcus)
d. suppurative lesions - pericarditis
- septic arthritis
- pneumonia
e. immune complex disease - arthritis
- glomerulonephritis
f. SIADH & hyponatraemia

96
 ICU - Paediatric

these complications may occur in the presence of,

a. infarction
b. cerebral oedema
c. subdural effusion - persistent fever & signs
d. cerebral abscess
e. venous sinus thrombosis

Management

a. ABC
b. IVT
~ 1/3 normal maintenance H 2O, once normovolaemic
SIADH almost always occurs
hypotonic fluids may → hyponatraemia & cerebral oedema
coma, fitting ± death
c. ABx
for community acquired → 3rd generation cephalosporin
cefotaxime ~ 50 mg/kg tds
once sensitivities known continue R X for 10 days
d. prophylaxis
every case of Strep. pneumoniae
H. influenzae with another child ≤5 years
i. infants/children → rifampicin ~ 20 mg/kg/day (max 600) for 4 days
ii. neonates → rifampicin ~ 10 mg/kg/day for 4 days
iii. pregnant women → ceftriaxone ~ 25 mg/kg stat
e. dexamethasone
0.15 mg/kg q6h for 4 days → ↓ deafness with H. influenzae
given with the first dose of antibiotics when the diagnosis is proven or strongly
suspected

97
 ICU - Paediatric

Neonatal Meningitis
typically present with a paucity of clinical findings,
a. poor feeding
b. weight loss, failure to thrive
c. loss of thermoregulation
d. respiratory distress, apnoea
e. metabolic disturbances - hypoglycaemia
- hypocalcaemia

causative agents include,

a. group B haemolytic streptococci
most common, often associated with fulminant sepsis
b. E. coli & gram negative rods
c. Listeria monocytogenes
NB: (a + b) were the causative agents in > 70% of cases in one large review
(c) responsible for ~ 5%

ventriculitis, with surrounding cerebral oedema and communicating hydrocephalus occurs more
commonly in neonates
therapy is similar to that for older children, initial ABX cover,
a. amoxicillin ~ 100-200 mg/kg/day, plus
b. cefotaxime ~ 150-200 mg/kg/day, or
gentamicin ~ 2.5 mg/kg q12h
NB: although aminoglycosides have poor penetration into CSF,
direct instillation SA or intraventricular in neonates is of no benefit

3rd generation cephalosporins have good activity against most GN enteric organisms
but not against Pseudomonas spp., or against L. monocytogenes

98
 ICU - Paediatric

Herpes Simplex Virus Encephalitis

NB: the most common cause of severe, often fatal encephalitis

a. wide range of symptoms from mild illness to sudden deterioration and death
b. usually a non-specific acute systemic illness
→ fever, headache, nasopharyngitis, & screaming spells in infants
c. progressive symptoms
i. nausea and vomiting
ii. lethargy, stupor
iii. neck stiffness, photophobia
iv. bizarre movements
v. focal neurological signs
vi. convulsions ± coma

Investigations

a. CT Scan - localised or generalized changes

- may be normal in the first 2-3 days
b. LP
i. ICP - universally raised in encephalitis
ii. CSF - ↑ WBC (predominantly lymphocytes)
- ↑ protein & ↓ glucose
- often blood stained
c. EEG - focal changes
* the most common abnormal neuroradiological test
d. viral studies - isolation from peripheral sites is unhelpful
- Ab responses are not always positive at time of infection
- the virus is rarely isolated from CSF (PCR takes 2 weeks)
→ these may be normal early in the disease

Management

a. acyclovir ~ 10 mg/kg 8 hrly IV reduces mortality

commence empirically without brain biopsy
phosphorylated by viral thymidine kinase
→ inhibition of HSV DNA polymerase
side effects - nephrotoxicity
- encephalopathy, agitation, seizures & coma
b. general - maintenance of cerebral blood flow
- monitoring and reduction of ICP

99
 ICU - Paediatric

Hypoxic-Ischaemic Encephalopathy
the commonest causes in children are,
1. SIDS
2. immersion - salt/fresh water
3. accidents - drug ingestion
- child abuse
- strangulation

anaerobic glycolysis produces 1/19th the ATP and requires the conversion of pyruvate to lactate
to provide NAD+ for ongoing glycolysis
if ischaemia accompanies hypoxia, there is also a failure of substrate removal which amplifies the
cellular insult
ischaemia produces coma in ~ 10 seconds and cellular injury in as little as 2 minutes

Management
same principles of ABC as for other arrest/brain injury scenarios
large volumes of air/water may be in the stomach after immersion & resuscitation
in 10-15% of immersion, early laryngospasm prevents aspiration → dry drowning
common problems after prolonged arrest,
1. cardiac dysfunction requiring inotropic support
2. hypovolaemia from GIT fluid loss & ischaemic diarrhoea

comatose patients with a GCS < 8 should be ventilated for several days, though, this is of
unproven benefit in outcome
barbiturate coma & induced hypothermia are of no proven value and increase the risk of sepsis
hyperglycaemia should be actively treated as this has been shown experimentally to worsen
prognosis

Prognosis
the onset of ischaemia may be delayed by bradycardia with preferential cerebral blood flow, the
diving reflex, in young children
survival from out-of-hospital arrest presenting in asystole is poor
the exception is hypothermia following immersion, where prolonged resuscitation is justified
recovery is likely in comatose patients who respond to pain → flexion or extension
normothermic patients who are flaccid & apnoeic are unlikely to survive
in contrast to isolated head injuries, defects present at the end of 1 week are unlikely to recover
further

100
 ICU - Paediatric

Guillain-Barré Syndrome
the most common cause of acute motor paralysis in children, the usual presentation being,
→ ascending symmetrical areflexic weakness

may present insidiously with apparent lethargy and failure of motor milestones in young children
sensory loss is usually minimal or transient
muscular back & leg pain, presumably neurogenic in origin, is common
papilloedema and encephalopathy occasionally occur
DVT and thromboembolism are not as significant a problem in children
admission criteria to ICU include,
1. respiratory failure ≤30% of patients will require mechanical ventilation
2. severe autonomic disturbance
3. bulbar palsy
4. rapidly progressive weakness

early indications for elective ventilation include,

1. ↑ work of breathing
2. fatigue with a poor cough
3. arterial hypoxaemia - SpO2 ≤ 90%
4. progressive bulbar palsy

hypercarbia is a late sign and should be avoided

FVC is difficult to assess in children but successful weaning is unlikely unless,
1. vital capacity ≥ 12 ml/kg , or
2. peak inspiratory pressure ≥ -20 cmH2O

Differential Diagnosis

a. botulism - clostridium toxin in blood

b. tick toxin - presence of a tick bite
c. OP poisoning - reduced serum cholinesterase levels
d. myasthenia gravis - deep tendon reflexes present
e. transverse myelitis - presence a sensory level
f. motor neurone disease - weakness is asymmetrical
g. dermatomyositis - presence of rash, muscle pain and increased CPK
h. periodic paralysis - history of previous episodes
- increased or reduced potassium
i. posterior fossa tumour - spinal long tract signs

101
 ICU - Paediatric

CSF findings,
1. normal pressure & clear
2. ≥ 90% have increased protein ≥ 400 mg/l → mainly albumin
3
3. cell count / mm < 50 lymphocytes
< 2 PMN's
≤10% have mild lymhpocytosis

nerve conduction studies show

a. normal, slow or non-existent nerve conduction
b. reduced amplitude of motor potentials

autonomic dysfunction may be a serious problem, especially with airway manipulation or other
procedures,
a. cardiac arrhythmias
b. hyper / hypotension
c. urinary retention
d. GIT dysfunction

however, autonomic dysfunction is uncommon in children

plasmapheresis within 7 days of onset may reduce the period of ventilation and reduce the time
to recovery (no controlled trials - only adults)

gammaglobulin may be of benefit in severe cases and in cases of relapsing polyneuropathy

steroids and other immunosuppressives are of no proven benefit
other problems peculiar to long-term IPPV in the paediatric patient include,
a. emotional immaturity
b. speech failure
c. fear of procedures
d. family disruption
NB: the prognosis for GBS is better in the paediatric group

full recovery is likely if the time from maximal deficit to start of recovery
is less than 18 days

102
 ICU - Paediatric

Reye's Syndrome

Def'n: severe metabolic encephalopathy with cerebral oedema

and fatty degeneration of the viscera, especially the liver

occurs almost exclusively children, usually ≤15 years

the aetiology is unknown, however,
a. incidence is higher during epidemics of influenza or varicella
b. relationship to salicylates is controversial
c. children with juvenile RA taking salicylates are at risk →
i. ? viral
ii. ? drugs (aspirin) / toxins cf. post-vaccination encephalitis
d. abnormal mitochondrial function in hepatocytes
→ disturbed carnitine / coenzyme-A metabolism

liver histology shows non-inflammatory microvesicular fat deposition

EM studies show swollen and disrupted mitochondria

the toxic encephalopathy is characterised by,

a. progressive, generalized CNS damage
b. severe, refractory cerebral oedema (usual cause of death)
c. neuronal damage

Clinical Picture

a. prodromal URTI ± exanthem

b. intractable vomiting is often the first symptom
c. encephalopathy - progressing over hours to days
- personality change / agitation
± convulsions / coma
- normal CSF (if no coagulopathy)
d. hepatic failure - from mild to fulminant
- hepatocellular enzyme elevation
- hyperammonaemia
- coagulopathy & prolongation of PT
- hypoglycaemia rare unless ≤2 yrs
* mild jaundice, bilirubin seldom > 50 µmol/l
e. MOSF - cardiac failure
- pancreatic failure
f. mortality ~ 50% (T.OH states ~ 25% overall)
~ 100% for stages ≥ 4 (see below)

103
 ICU - Paediatric

Treatment

a. control of raised ICP

b. manage liver failure
i. coagulopathy
ii. prevention of hypoglycaemia
iii. minimise ammonia load
c. support renal function
d. high dose l-carnitine ? may prevent progression in stage 2

Staging in Reye's Syndrome - Lovejoy

Stage Coma Pain response Reflexes
1 lethargy normal normal
2 combative variable pupils slow
3 coma decorticate pupils slow
4 coma decerebrate pupils slow
5 coma flaccid no δpupils
no occulo-cephalic

Differential Diagnosis

a. meningitis
b. encephalitis
c. fulminant hepatic failure
d. pancreatitis
e. inborn errors of metabolism
f. drugs or poisons

104
 ICU - Paediatric

SPINAL TRAUMA

paediatric spinal trauma is relatively rare → ~ 5% of all spinal injuries

of children with severe trauma ~ 5% will have a cervical spine injury
injuries will occur at more than one spinal level in ~ 16% of cases
the commonest causes are,
a. road trauma - MVA, pedestrian, cyclist
b. falls - especially diving

anatomical differences include,

a. interspinous ligaments & joint capsules are more flexible
b. uncinate articulations are poorly developed & slide forward
c. the facet joints are flat
d. the vertebral bodies are wedged anteriorly & slide forward with flexion
e. the head is relatively large
→ greater angular momentum can be generated with flexion / extension

normal radiological variations include,

a. anterior displacement of C2 on C3 ~ 40% < 7 yrs
~ 20% ≤16 yrs
± ≥ 3mm movement
b. increased distance between the dens and anterior arch of C1 ~ 20% of children
c. skeletal growth centres may resemble fractures
d. basilar odontoid synchondrosis appears as a radiolucent line at the base of the dens
(especially ≤ 5 years)

spinal cord injury without radiographic abnormality, SCIWORA is almost unique to the
paediatric age group
a. ~ 20-60% of all SCI
b. ~ 30-50% of these the lesion is complete

SCI in the first decade of life is,

a. almost exclusively high cervical ~ C1/2
b. either subluxation or SCIWORA and severe cord injury
c. rarely associated with fractures

105
 ICU - Paediatric

a high proportion of children who die in MVA's, or suffer cardiorespiratory arrest prior to
reaching hospital have cord trauma above C 3 , particularly at the cervico-medullary junction
this is difficult to diagnose in the unconscious patient, signs including,
a. flaccid immobility & areflexia
b. hypoventilation with paradoxical chest movement
c. apnoea and rhythmic flaring of the alae nasi (above C3)
d. hypotension with - inappropriate bradycardia
- peripheral vasodilatation
± priapism

Spinal Shock
the syndrome of spinal shock occurs more commonly in children,
a. SCI lesion resolves after 2-3 days
b. progressive return of reflexes → bulbocavernous & anal first
c. incomplete lesions may then become apparent
i. Brown-Sequard hemisection
ii. anterior cord lesion
iii. central cord lesion

106
 ICU - Paediatric

Non-Accidental Injury

a. physical
b. sexual and emotional abuse
c. deprivation of medical care and nutrition

children are also intentionally poisoned, and endure the consequences of inadequate supervision
diagnosis of children who suffer from abuse or neglect is difficult
NAI should be suspected where,
a. an injury is unexplained
b. the history is not consistent with the type of injury
c. it is alleged that the injury was self-inflicted
d. relatives delay in seeking medical aid
e. there are repeated suspicious injuries

the history is rarely volunteered by the child

the pattern of physical findings can be helpful,
a. bruises and scars on the back and buttocks in different stages of development and of
unusual shapes
b. burns from cigarettes or forced immersion in hot water
c. retinal haemorrhages occur with head shaking, but also have other causes
d. head injury - skull fractures
- subdural haematomas
e. overt bone fractures or healing fractures

when non-accidental injury is suspected, referral to a specialised child protection unit to enable
appropriate counselling and intervention is helpful
safety of siblings must be considered

107