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SYMPOSIUM: INTENSIVE CARE

Management of severetraumatic brain injury

Helen E Rowlands

Kevin P Morris

Abstract

Traumatic brain injury (TBI) causes significant morbidity and mortality in

children. Physiological insults worsen morbidity and mortality and are

particularly common in the pre-hospital setting. Management of severe

TBI in the ICU is largely focused on the management of raised intracranial

pressure and preservation of cerebral perfusion. Few randomised

controlled trials have been undertaken in children with TBI.

Keywords head injury; traumatic brain injury; raised intracranial

pressure; cerebral perfusion pressure

Introduction

Traumatic brain injury (TBI) is the leading cause of death in

children aged 1–15 years. In the West Midlands, for every child

that is killed by an injury, a further 344 are admitted to hospital

and 1522 present to emergency departments.1 In the UK, 5.6–7.3

children per 100,000 population per year require admission to a

paediatric ICU as a result of TBI.2 This equates to approximately

750 ICU admissions per year.

The most common causes of injury in children with severe TBI

are road traffic accidents involving a pedestrian, falls and bicycle-

related accidents.2 The cause varies with age; non-accidental

injury is the most common under 1 year of age, and falls in 1–4-

year-olds. Boys are twice as likely as girls to be injured, and

children from low socioeconomic status groups are at higher risk.

The peak time that injuries occur is late afternoon to early

evening, and there is an increased incidence in the summer.2

A significant proportion of severely injured children die before

they reach hospital. Among those who reach hospital, mortality

varies with the cause of injury, being highest in motor vehicle

occupants and lowest in falls.2 Crude mortality in children with

TBI who are admitted to an ICU is approximately 10%; if multiple

systems are injured, the mortality rises to 20%.2

Primary brain injury occurs at the time of the traumatic

incident and comprises axonal injury, brain contusion, lacera-

tion, haemorrhage and shearing injury. Secondary injury occurs

after the initial traumatic event and may be exacerbated by

Helen E Rowlands MBBS MRCPCH is Specialist Registrar in the Paediatric

Intensive Care Unit, Birmingham Children’s Hospital, Steelhouse Lane,

Birmingham, UK.

Kevin P Morris MBBS (HONS) MRCP (UK) MD FRCPCH is Consultant in the

Paediatric Intensive Care Unit, Birmingham Children’s Hospital,

Steelhouse Lane, Birmingham, UK.

PAEDIATRICS AND CHILD HEALTH 17:3 82

physiological insults such as hypoxaemia, hypotension, seizure

activity, hyperglycaemia and fever.3 Medical intervention aims to

reduce the impact of any potential secondary brain injury and to

limit rises in intracranial pressure (ICP), which, if associated with

reduced cerebral perfusion, may worsen ischaemic injury. There

is little class I evidence to support the management options for

TBI and consequently there is wide variation in practice between

centres in the UK and worldwide.4

Severity of TBI may be defined in terms of the characteristics

of the injury, level of consciousness or the severity of CT

appearances. The level of consciousness at presentation, mea-

sured using the Glasgow Coma Scale (GCS), is predictive of

neurological outcome.5 Severe TBI is defined as a GCS of 8 or

below, moderate TBI as GCS 9–12, and mild TBI as GCS 13 or

above. This review concentrates on the management of severe

TBI in children. The recommendations are based predominantly

on US guidelines published in 20036 and on the findings of recent

UK studies undertaken by the TBI Subgroup of the Paediatric

Intensive Care Society Study Group.2,4,7

Assessment of children with head injuries

All children with a history of high-energy head injury, GCS below

15, loss of consciousness or amnesia, focal neurological deficit,

seizures, abnormal behaviour, or suspicion of skull fracture,

penetrating injury or non-accidental injury should be assessed

and treated in hospital after initial stabilisation at the scene.8

Initial resuscitation at the scene should be in accordance with

advanced paediatric life support (APLS) guidelines, paying

special attention to the avoidance of hypoxaemia and hypoten-

sion and the provision of cervical spine immobilisation.

In the emergency department, resuscitation should continue

following the APLS guidelines, including cervical spine immobi-

lisation and the treatment of other life-threatening injuries such

as intra-abdominal bleeding, pneumothorax and cardiac tampo-

nade. GCS, pupil size and reactivity to light, seizures and any

focal neurological signs should be assessed. The AVPU (alert,

voice, pain, unresponsive) assessment of level of consciousness

should not be used as an alternative to GCS in a child with TBI.

Details of the history should be sought, paying particular

attention to the cause of injury (e.g. pedestrian vs car, cyclist,

motor vehicle occupant, fall from height), speed of impact,

whether ejected from vehicle, use of protective equipment such

as seat belt or helmet, non-accidental injury, the time that the

injury occurred, GCS at the scene, cardiopulmonary resuscitation

at the scene, seizures, loss of consciousness or amnesia, medical

history, drug history and allergies.

Intubation using rapid sequence induction of anaesthesia with

cervical spine immobilisation should be performed in children

with a GCS of 8 or less, ventilatory insufficiency, loss of

protective laryngeal reflexes or severe facial trauma, and in

uncooperative or unsafe children who need CT. It is important to

use an oral endotracheal tube (ETT) with minimal leak (either a

well-fitting uncuffed ETT or a cuffed ETT); firstly, to deliver

adequate ventilation to achieve normal PaCO2 (4.5–5.0 kPa),

which is important for the maintenance of normal ICP and

perfusion, and secondly because patients with head injury may

develop acute lung injury or ‘neurogenic’ pulmonary oedema and

become difficult to ventilate if there is a large leak around the

r 2007 Published by Elsevier Ltd.


tube. Use of nasal ETTand nasogastic tubes is contraindicated, as

there may be a basal skull fracture; an orogastric tube should be

used.

Invasive blood pressure monitoring via an arterial line is

essential to ensure that the blood pressure is adequate to perfuse

the brain. Hypotension (defined as below the 5th centile for age)

must be avoided, but preferably the blood pressure should be

maintained in the higher range of normal until ICP monitoring

can be instituted and cerebral perfusion pressure (CPP) targeted

more accurately (Table 1).

Guidance on who should undergo CT has been produced by

the National Institute for Health and Clinical Excellence (NICE;

Table 2).8 The Children’s Head Injury Algorithm for the

Age-related cerebral perfusion pressure targetsIn the absence of intracranial pressure monitoring, mean arterial

pressure should be targeted

Cerebral perfusion pressure targets

� 0–2 years 40 mmHg




� 416 years 70 mmHg

Mean arterial pressure targets

� 0–2 years 60–75 mmHg

� 2–6 years 70–85 mmHg

� 7–10 years 80–90 mmHg

� 411 years 85–95 mmHg

Table 1

Selection of patients with a head injury for CT of thehead�

CT imaging is recommended in the following situations

� GCS o13 at any time since injury

� GCS 13 or 14 at 2 hours after injury

� Focal neurological deficit

� Suspected open or depressed skull fracture

� Any sign of basal skull fracture (haemotympanum, ‘‘panda’’

eyes, CSF otorrhoea, Battle’s sign)

� Post-traumatic seizure

� More than one episode of vomiting (clinical judgement on

cause of vomiting and need for imaging is required in children

p12 years)

� Any loss of consciousness or amnesia since injury

� Age X65 years

� Coagulopathy

� Dangerous mechanism of injury

� Tense fontanelle in baby

�National Institute for Health and Clinical Excellence guidelines GCS,

Glasgow Coma Score.

Table 2


Identification of Important Clinical Events appears to have

greater specificity than the NICE guidelines.9 Many of these

children are intubated and anaesthetised, and it is consequently

not possible to assess their cervical spine clinically. It is

recommended that these children undergo CT of the spine, but

they should be immobilised after this even if the scan is normal,

because of the risk of SCIWORA (spinal cord injury without

radiological abnormality), until they can be woken and assessed

clinically (Figure 1). In children with cardiovascular instability or

suspected thoracic, intra-abdominal or pelvic trauma, CT of the

chest, abdomen and pelvis may be indicated.

Inter-hospital transfer of children with head injuries

All children requiring urgent life-saving neurosurgery or neuro-

intensive care should be transferred to a unit that can provide

both neurosurgery and paediatric intensive care as soon as

possible. Guidelines from the Royal College of Surgeons state that

‘‘life saving decompressive surgery must be available for all

patients who require it within four hours of injury’’.10,11 This

often involves transfer of the child from a district general hospital

to a neurosurgical centre. A recent study found that this 4 hour

target is often not achieved in the UK, and that transfer by a

paediatric ICU retrieval team adds an additional delay of

approximately 1.5 hours.7 It is therefore recommended that the

referring hospital transfers the child to the neurosurgical centre.

An alternative approach is to take children with severe TBI

directly to a tertiary centre with both neurosurgical and paediatric

ICU facilities, as this is usually achieved in less than 1 hour.7 In

some cases, this model of care would involve increasing the time

from injury to arrival in the first hospital and it would therefore

be best achieved by mobilizing skilled personnel to the scene, to

initiate intensive care. This model of pre-hospital care has been

adopted in countries such as France, and occurs in certain areas

of the UK.

There are important principles to consider when transferring

children with head injuries. The child must be cardiovascularly

stable, and any potential life-threatening injuries (e.g. ruptured

abdominal organs, cardiac tamponade, haemopneumothorax)

should have been dealt with before transfer. Other, less severe

injuries (e.g. fractured long bones) should be immobilised and

dealt with after transfer. The airway must be secure, with

minimal leakage around the ETT, end-tidal CO2 monitoring

should be instituted, and the patient should be on a transport

ventilator. The cervical spine should be stabilised using a hard

collar and sandbags with tape and a spinal board. There should

be at least two large-bore intravenous cannulas for infusion of

fluids and emergency drugs. Full monitoring is essential,

including ECG, invasive arterial blood pressure, oxygen satura-

tion and end-tidal CO2.

Management on the ICU

General management

Cervical spine immobilisation should continue on arrival at the

ICU for all patients who have sustained a severe head injury.

Patients should be nursed in a 301 head-up position, with the

head in the midline position to aid cerebral venous drainage.

Children with TBI often become febrile because of secretion of


• GCS <15• Focal neurological deficit present• Paraesthesia present • Distracting injuries present • Abnormal or inadequate three-view cervical spine radiographs

(anteroposterior, lateral and odontoid peg) or two views in child <10 years(anteroposterior and lateral)

Request CT of cervical spine

Presence of neck pain ortenderness?

Cervical spine clear

Normal active andpassive range of motionof neck?

• Presence of neurological signsreferable to the cervical spine

• Suspicion of bony injury orligamentous injury to cervicalspine on CT

Yes No

No

Yes

Yes

Yes

No

MRI of spine recommended

Figure 1


pro-inflammatory mediators. Fever is associated with a poor

neurological outcome, and the maintenance of normothermia is

essential.6 It is advisable that, on arrival at the paediatric ICU, the

child should be placed on a bed with a cooling blanket so that

active cooling can be undertaken. If active cooling is required, it

is usual for muscle relaxants to be continued to stop the patient

shivering, which may further raise the ICP. It is also important

that a hypothermic patient is not actively rewarmed, but is

allowed to rewarm passively to prevent overshoot and a

consequent rise in ICP.

Patients with severe TBI require analgesia, sedation, paralysis

and isotonic intravenous maintenance fluids in the form of

normal saline. Ventilation using a volume-control mode and end-

tidal CO2 monitoring should aim for a normal PaCO2. Hypocarbia

induces cerebral vasoconstriction, which may induce ischaemia,

particularly soon after injury when cerebral blood flow is

typically reduced, and should be avoided.

The patient should be reviewed by an experienced neurosur-

geon, and should be woken and assessed if no neurosurgical

intervention is required, or should receive full neuro-intensive

care including ICP monitoring.

Neurosurgical intervention may involve insertion of an ICP

monitoring device, craniotomy and removal of haematoma,

elevation of a depressed skull fracture, insertion of a ventricular

catheter or, in severe cases, decompressive craniectomy. The risk

of raised ICP is low following removal of an isolated extradural


haematoma, so the patient is usually allowed to wake for

neurological assessment. When the risk of intracranial hyperten-

sion is high, or the patient does not wake satisfactorily, ICP

monitoring is required. This is most commonly achieved by

placing a catheter into the brain parenchyma through a burr hole,

or by the insertion of a direct ventricular catheter (external

ventricular drain).

Anticonvulsant prophylaxis

Antiseizure prophylaxis with phenytoin has been shown to

reduce the incidence of early post-traumatic seizures. Although

there is no evidence that outcome is improved, it is common to

give phenytoin for the first 7 days following severe TBI.6

Antibiotics

Meningitis is a rare, serious complication of TBI and usually

results from infection with Streptococcus pneumoniae. Children

with chronic CSF leaks should receive pneumococcal vaccina-

tion, but routine use of prophylactic antibiotics in the acute

setting is not recommended. Penetrating head injuries may

be treated by removal of foreign bodies and debridement

(as far as is possible without causing further damage) and

intravenous cefuroxime and metronidazole for 5 days. Antibiotic

prophylaxis is not indicated in children with a base of skull

fracture.12



Chest physiotherapy

Regular chest physiotherapy is essential to maintain the lungs in

a healthy condition, as atelectasis and ventilator-associated

pneumonia are common.

ICP monitoring

ICP monitoring is recommended for all patients who are at risk of

intracranial hypertension, and in those with less severe TBI when

it is not possible to fully assess neurological status because of a

need for sedation and muscle relaxants or a non-neurosurgical

operative procedure. Risk factors for the development of raised

ICP include low GCS and abnormal CT, with features such as

diffuse axonal injury, subdural or subarachnoid haemorrhage, or

features of cerebral oedema such as loss of grey–white

differentiation. Despite their open fontanelle and sutures, infants

are at risk of developing intracranial hypertension and cerebral

herniation (coning). There is no strong evidence to support ICP

monitoring and aggressive treatment of intracranial hypertension

in children, but equally there is no evidence that children should

be treated differently to adults, particularly given the low risks

associated with ICP monitoring.13

Maintenance of ICP within the normal range is needed to

maintain CPP, optimise oxygen and metabolic substrate delivery,

and prevent cerebral herniation and death. High ICP and low CPP

are associated with a poor neurological outcome and higher

mortality. The current consensus is that maintaining the ICP

below 20 mmHg is best practice.6 An external ventricular drain is

the most accurate method for measuring ICP, and has the

advantage of allowing therapeutic drainage of CSF for the

treatment of intracranial hypertension. A parenchymal ICP

monitor or bolt is a commonly used alternative.

Cerebral perfusion pressure

Global or regional cerebral ischaemia results in secondary brain

injury. Perfusion of the brain is dependent on CPP, which is the

difference between the mean arterial pressure (MAP) and the ICP.

In a healthy brain, cerebral blood flow (CBF) is constantly

maintained by autoregulation in the face of varying MAP. In

adults, autoregulation occurs at MAPs of 60–160 mmHg; in

children, autoregulation occurs at lower MAPs depending on age.

In patients with intact autoregulation, an increase in MAP causes

cerebral vasoconstriction to maintain CBF, resulting in decreased

ICP as a result of reduced cerebral blood volume (Figure 2).

Loss of autoregulation↑BP

No cerebralvasoconstriction

↑CBF

↑CBV

↑ICP

↓

↓

↓

↓

Intact autoregulation

Cerebralvasoconstriction to maintain

constant CBF

↑BP↓

↓

↓↓ICP

↓CBV

Figure 2 Cerebral autoregulation (ICP, intracranial pressure; CBV,

cerebral blood volume; BP, blood pressure; CBF, cerebral blood flow).


In an injured brain, autoregulation may be impaired and CBF

may become pressure dependent. In this situation, a decrease in

MAP results in reduced CBF and may lead to cerebral ischaemia.

Conversely, a marked rise in MAP results in excessive CBF, which

further raises ICP (Figure 2).

Recently published US guidelines suggest that ‘‘CPP between

40 and 65 mmHg probably represents an age related continuum

for the optimal treatment threshold’’ and, in adults, a minimum

CPP of 70 mmHg should be maintained.6 Chambers et al.14

attempted to further define these levels by demonstrating

increased mortality and worse neurological outcome in children

with CPP below 48 mmHg (2–6 years), 54 mmHg (7–10 years) or

58 mmHg (11–15 years). The recommended MAP and CPP are

shown in Table 1.

For targeting CPP, invasive arterial pressure monitoring is

recommended and intravenous fluid boluses or vasoactive drugs

may be required. The vasoactive drug most commonly used for

this purpose is norepinephrine, which increases MAP predomi-

nantly by causing systemic vasoconstriction. In cases of reduced

cardiac output, which may occur secondary to myocardial

contusion in the setting of chest trauma, or due to left ventricular

dysfunction in the setting of very severe TBI, it is more

appropriate to use an inotrope or inodilator to improve cardiac

output, rather than a vasoconstrictor. Dopamine, epinephrine and

milrinone may be used in this situation.

Acute left ventricular dysfunction is thought to be secondary

to a ‘catecholamine storm’, which may occur in patients with

severe TBI or subarachnoid haemorrhage. In most cases, so-

called ‘neurogenic’ pulmonary oedema is related to profound left

ventricular dysfunction and therefore has a ‘cardiogenic’ aetiol-

ogy.

Management of intracranial hypertension

Brief increases in ICP that return to normal in less than 5 minutes

are probably insignificant. A sustained rise of more than

20 mmHg for more than 5 minutes should be treated. Events

that can provoke increased ICP are endotracheal suctioning,

inadequate sedation, hyperthermia, hypercarbia, hypoxia, cathe-

ter placement, and expanding intracranial haematoma or mass.

All of these issues must be addressed before therapy to reduce the

ICP is started (Table 3).

First-tier therapy includes drainage of CSF via a ventricular

catheter if present, osmolar therapy in the form of either

mannitol, 0.25 g/kg, or 3% saline, 2–4 mL/kg (providing serum

sodium is less than 150 mmol/L). Mild hyperventilation (PaCO2

4.0–4.5 kPa) can be used to treat raised ICP that is refractory to

CSF drainage and osmolar therapy. Second-tier therapy includes

administration of a barbiturate titrated to ICP and blood pressure,

unilateral or bilateral decompressive craniectomy, insertion of a

lumbar drain and titrated hypothermia (32–35 1C) (Table 3).

Hypothermia has been shown to reduce ICP,6 but was not shown

to improve outcome in a recent randomised paediatric trial

(Hypothermia in Paediatric Head Injury Trial, unpublished data).

Moderate-to-severe hyperventilation to a PaCO2 of less than

4.0 kPa may also be used, but may result in further ischaemia as a

result of cerebral vasoconstriction (Figure 3). In some centres,

jugular venous bulb oximetry (SjvO2) is used as a guide to help

avoid cerebral ischaemia; a reduction in SjvO2 to less than 50%

implies inadequate cerebral oxygen delivery. Brief periods of


Therapy for raised intracranial pressure (ICP)

Raised ICP 420 mmHg for 45 minutes

� Ensure adequate sedation, analgesia and paralysis

� Ensure normothermia (o37.5 1C)

� Ensure PaCO2 4.5–5.3 kPa

� Exclude technical problem with ICP monitor

� Ensure adequate cerebral perfusion pressure

First-tier therapy when above causes excluded

� Drain CSF if external ventricular drain present

� Osmolar therapy (mannitol, 0.25 g/kg i.v., or 3% saline, 3 ml/

kg i.v., if serum Na o150 mmol/L)

� Mild hyperventilation to PaCO2 4.0–4.5 kPa

Second-tier therapy for raised ICP despite first-tier therapy and no

surgical lesion on CT

� Mild-to-moderate hypothermia (32–35 1C)

� Thiopentone coma

� Hyperventilation to PaCO2o4.0 kPa guided by jugular venous

oxygen saturation

� Decompressive craniectomy

� Lumbar drain if external ventricular drain present and working

and open basal cisterns on CT

Table 3

Figure 3 Cerebral hypoperfusion caused by reduced PaCO2. Xenon CT

images of the same patient taken 20 minutes apart, before and after

hyperventilation. (a) PaCO 36 mmHg (4.8 kPa) with estimated cerebral


hand-bagging resulting in PaCO2 below 4.0 kPa may be used as an

emergency treatment when the ICP is persistently greater than

40 mmHg, the pupils become fixed and dilated, and cerebral

herniation is imminent.

Repeat CT of the brain is often useful for identifying any

changes remedial to surgery and showing the progression of any

lesions. CT scans of the brain should be interpreted with caution,

as raised ICP cannot be diagnosed reliably on CT.15

Multi-modality monitoring

A number of additional neuromonitoring techniques can be

used to monitor the brain after TBI. Experience of their use in

children is limited and predominantly confined to research

settings (Table 4).
2
blood flow of 43 mL/minute/100 g; (b) PaCO2 32 mmHg (4.3 kPa) with

estimated reduced cerebral blood flow of 15 mL/minute/100 g. (Normal

cerebral blood flow is 425 mL/minute/100 g.)

Multimodality monitoring

� Jugular venous oxygen saturation

� Cerebral blood flow technique (e.g. transcranial Doppler)

� Cerebral tissue oxygenation measured by near infra-red

spectroscopy

� Microdialysis

� Brain tissue PO2, pH, temperature monitoring

� EEG or cerebral function analysing monitor

Table 4

Outcome predictors

The Glasgow Outcome Score (GOS) classifies outcome as death,

persistent vegetative state, severe disability, moderate disability

or good recovery. The King’s Outcome Scale for Childhood Head

Injury is a paediatric adaptation of the GOS that includes a

number of subcategories (Table 5).16

It can be difficult to predict outcome in children with TBI.

Hypoxia and hypotension are correlated with increased morbidity

and mortality as high as 85%.6,17 Prolonged periods of raised ICP

are also associated with poor outcomes.6 Sustained extremely

high ICP (440 mmHg) is associated with death, ICP 20–40 mmHg

is associated with a moderate outcome, and ICP below 20 mmHg

is associated with a good outcome. In infants with non-accidental

TBI, outcome has been shown to be worse with ICP above

30 mmHg, and it has been suggested that outcome may be

improved by decompressive craniectomy in these patients.6 CPP

PAEDIATRICS AND CHILD HEALTH 17:3 86 r 2007 Published by Elsevier Ltd.

King’s outcome scale for childhood injury

Category Definition

1 Death

2 Vegetative

3 Severe disability

A. Conscious, totally dependant; may be able to

communicate

B. Limited self-care abilities and predominantly

dependant; may have meaningful communication

4 Moderate disability

A. Mostly self-caring, but needs support and

supervision; problems with behaviour/learning

and communication

B. Independent daily living; minor neurological

deficits; residual problems with behaviour/

learning

5 Good recovery

A. Full functional recovery, but residual

pathology attributable to head injury

B. No sequelae identified

Table 5


less than 40 mmHg is strongly correlated with mortality,

independent of age.

In survivors, maximal recovery can take many months.

Children spend a considerable period in hospital during this

time, often-missing months of schooling, and require intensive

neurorehabilitation.

There is evidence that outcome is worse in very young patients

with severe TBI, though this does not seem to be the case in mild-

to-moderate TBI.5,18 Somatosensory evoked potentials (SSEPs)

may be helpful in defining a poor outcome group; bilateral

absence of SSEPs is strongly associated with death or severe

disability.19,20

Death from TBI

Despite maximal neuro-intensive care, some children die from

their injuries, and some of these meet the criteria for brain stem

death. During and after brain herniation with resultant brain stem

death, there is considerable cardiovascular instability, making

management difficult. Vasopressin infusion may be helpful in this

situation. In the setting of brain stem death, the focus of

treatment switches to preservation of organ function with a view

to potential donation of heart, lungs, kidneys, liver and bowel for

transplantation. The maintenance of CPP and the goals for ICP

are no longer important. An approach to the family for their

consent for organ donation is usually made by the consultant

intensivist and/or a transplant coordinator.

Recent UK data suggest that approximately 50% of children

who die in the ICU following TBI meet brain stem death criteria,

but only 50% of these become organ donors,21 equating to

approximately 12–15 donors per year. In the future, the

possibility of non-heart-beating organ donation may increase

the yield of organs from children who do not meet the criteria for


brain stem death but in whom intensive care is withdrawn

because of catastrophic injury. ~

Acknowledgements

The authors thank Dr P. Skippen for providing Figure 3.

REFERENCES1 West Midlands Public Health Observatory. Health issues: childhood

injuries. 2006. /www.wmpho.org.ukS2 Parslow R C, Morris K P, Tasker R C, Forsyth R J, Hawley C A.

Epidemiology of traumatic brain injury in children receiving intensive

care in the UK. Arch Dis Child 2005; 90: 1182–7.

3 Jones P A, Andrews P J, Midgley S et al. Measuring the burden of

secondary insults in head-injured patients during intensive care.

J Neurosurg Anesthesiol 1994; 6: 4–14.

4 Morris K P, Forsyth R J, Parslow R C, Tasker R C, Hawley C. Intracranial

pressure complicating severe traumatic brain injury in children:

monitoring and management. Intensive Care Med 2006; 32:

1606–12.

5 Ducrocq S C, Meyer P G, Orliaguet G A et al. Epidemiology and early

predictive factors of mortality and outcome in children with traumatic

severe brain injury: experience of a French pediatric trauma center.

Pediatr Crit Care Med 2006; 7: 461–7.

6 Adelson D P, Bratton S L, Carney N A et al. Guidelines for the acute

medical management of severe traumatic brain injury in infants,

children and adolescents. Pediatr Crit Care Med 2003; 4(suppl):3.

7 Tasker R C, Morris K P, Forsyth R J, Hawley C A, Parslow R C. Severe

head injury in children: emergency access to neurosurgery in the

United Kingdom. Emerg Med J 2006; 23: 519–22.

8 National Institute for Health and Clinical Excellence. Clinical guide-

lines: head injury 2003. /www.nice.org.ukS.

9 Dunning J, Patrick Daly J, Lomas J P, Lecky F, Batchelor J, Mackway-

Jones K. Derivation of the children’s head injury algorithm for the

prediction of important clinical events decision rule for head injury in

children. Arch Dis Child 2006; 91: 885–91.

10 Royal College of Surgeons of England. Report of the working party on

management of patients with head injuries. London: RCS England,

1999.

11 Royal College of Surgeons of England, British Orthopaedic Associa-

tion. Better care for the severely injured. London: RCS England and

British Orthopaedic Association, 2000.

12 Ritalal B, Costa J, Sampiao C. Antibiotic prophylaxis for preventing

meningitis in patients with basilar skull fractures. Cochrane Database

Syst Rev 2006; 1: CD004884.

13 Pople I K, Muhlbauer M S, Sanford R A, Kirk E. Results and

complications of intracranial pressure monitoring in 303 children.

Pediatr Neurosurg 1995; 23: 64–7.

14 Chambers I R, Jones P A, Lo T Y et al. Critical thresholds of intracranial

pressure and cerebral perfusion pressure related to age in paediatric

head injury. J Neurol Neurosurg Psychiatry 2006; 77: 234–40.

15 O’Sullivan M G, Statham P F, Jones P A et al. Role of intracranial

pressure monitoring in severely head-injured patients without signs

of intracranial hypertension on initial computerized tomography.

J Neurosurg 1994; 80: 46–50.


http://www.wmpho.org.uk

http://www.nice.org.uk


16 Crouchman M, Rossiter L, Colaco T, Forsyth R. A practical outcome

scale for paediatric head injury. Arch Dis Child 2001; 84: 120–4.

17 Pigula F A, Wald S L, Shackford S R, Vane D W. The effect of

hypotension and hypoxia on children with severe head injuries.

J Pediatr Surg 1993; 28: 310–4.

18 Anderson V, Catroppa C, Morse S, Haritou F, Rosenfeld J. Functional

plasticity or vulnerability after early brain injury? Pediatrics 2005;

116: 1374–83.

19 Carter B G, Butt W. A prospective study of outcome predictors after

severe brain injury in children. Intensive Care Med 2005; 31: 840–5.

20 Carter B G, Butt W. Are somatosensory evoked potentials the best

predictor of outcome after severe brain injury? A systematic review.

Intensive Care Med 2005; 31: 765–75.


21 Morris K, Tasker R, Parslow R, Forsyth R, Hawley C. Organ donation

in paediatric traumatic brain injury. Intensive Care Med 2006; 32:

1458.

Practice points

� Prevention and treatment of secondary insults is crucial,

particularly episodes of hypoxia and hypotension

� Targeting age-appropriate CPP or, in the absence of ICP

monitoring, MAP, helps to avoid brain hypoperfusion

� Hyperventilation should be avoided, and used cautiously only

after other treatments have failed


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