SYMPOSIUM: INTENSIVE CARE

Management of severe traumatic brain injury

Helen E Rowlands Kevin P Morris

Abstract
Traumatic brain injury (TBI) causes signicant 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.

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 dened in terms of the characteristics of the injury, level of consciousness or the severity of CT appearances. The level of consciousness at presentation, measured using the Glasgow Coma Scale (GCS), is predictive of neurological outcome.5 Severe TBI is dened as a GCS of 8 or below, moderate TBI as GCS 912, 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 ndings of recent UK studies undertaken by the TBI Subgroup of the Paediatric Intensive Care Society Study Group.2,4,7

Keywords head injury; traumatic brain injury; raised intracranial pressure; cerebral perfusion pressure

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 decit, 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 hypotension and the provision of cervical spine immobilisation. In the emergency department, resuscitation should continue following the APLS guidelines, including cervical spine immobilisation and the treatment of other life-threatening injuries such as intra-abdominal bleeding, pneumothorax and cardiac tamponade. 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 insufciency, loss of protective laryngeal reexes 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-tting uncuffed ETT or a cuffed ETT); rstly, to deliver adequate ventilation to achieve normal PaCO2 (4.55.0 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 difcult to ventilate if there is a large leak around the

Introduction
Traumatic brain injury (TBI) is the leading cause of death in children aged 115 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, 5.67.3 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 trafc accidents involving a pedestrian, falls and bicyclerelated accidents.2 The cause varies with age; non-accidental injury is the most common under 1 year of age, and falls in 14year-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 signicant 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, laceration, 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 Childrens Hospital, Steelhouse Lane, Birmingham, UK. Kevin P Morris MBBS (HONS) MRCP (UK) MD FRCPCH is Consultant in the Paediatric Intensive Care Unit, Birmingham Childrens Hospital, Steelhouse Lane, Birmingham, UK.

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tube. Use of nasal ETT and 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 (dened 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 Childrens Head Injury Algorithm for the

Identication of Important Clinical Events appears to have greater specicity 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 neurointensive 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 rst 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 uids and emergency drugs. Full monitoring is essential, including ECG, invasive arterial blood pressure, oxygen saturation and end-tidal CO2.

Age-related cerebral perfusion pressure targets

In the absence of intracranial pressure monitoring, mean arterial pressure should be targeted Cerebral perfusion pressure targets  02 years 40 mmHg  26 years 50 mmHg  710 years 60 mmHg  1115 years 65 mmHg  416 years 70 mmHg Mean arterial pressure targets  02 years  26 years  710 years  411 years Table 1

6075 mmHg 7085 mmHg 8090 mmHg 8595 mmHg

Selection of patients with a head injury for CT of the head

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 decit Suspected open or depressed skull fracture Any sign of basal skull fracture (haemotympanum, panda eyes, CSF otorrhoea, Battles 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

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

National Institute for Health and Clinical Excellence guidelines GCS, Glasgow Coma Score.

Table 2

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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) Yes No

Request CT of cervical spine

Yes

Presence of neck pain or tenderness? No

No Presence of neurological signs referable to the cervical spine Suspicion of bony injury or ligamentous injury to cervical spine on CT Normal active and passive range of motion of neck?

Yes Cervical spine clear

Yes

MRI of spine recommended

Figure 1

pro-inammatory 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 uids in the form of normal saline. Ventilation using a volume-control mode and endtidal CO2 monitoring should aim for a normal PaCO2. Hypocarbia induces cerebral vasoconstriction, which may induce ischaemia, particularly soon after injury when cerebral blood ow is typically reduced, and should be avoided. The patient should be reviewed by an experienced neurosurgeon, 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 hypertension 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 rst 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 vaccination, 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

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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 greywhite 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 ow (CBF) is constantly maintained by autoregulation in the face of varying MAP. In adults, autoregulation occurs at MAPs of 60160 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).

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 dene these levels by demonstrating increased mortality and worse neurological outcome in children with CPP below 48 mmHg (26 years), 54 mmHg (710 years) or 58 mmHg (1115 years). The recommended MAP and CPP are shown in Table 1. For targeting CPP, invasive arterial pressure monitoring is recommended and intravenous uid boluses or vasoactive drugs may be required. The vasoactive drug most commonly used for this purpose is norepinephrine, which increases MAP predominantly 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, socalled neurogenic pulmonary oedema is related to profound left ventricular dysfunction and therefore has a cardiogenic aetiology. Management of intracranial hypertension Brief increases in ICP that return to normal in less than 5 minutes are probably insignicant. 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, catheter 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, 24 mL/kg (providing serum sodium is less than 150 mmol/L). Mild hyperventilation (PaCO2 4.04.5 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 (3235 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

Intact autoregulation BP Cerebral vasoconstriction to maintain constant CBF CBV ICP

Loss of autoregulation BP No cerebral vasoconstriction CBF CBV ICP

Figure 2 Cerebral autoregulation (ICP, intracranial pressure; CBV, cerebral blood volume; BP, blood pressure; CBF, cerebral blood ow).

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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 4.55.3 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 4.04.5 kPa

Second-tier therapy for raised ICP despite rst-tier therapy and no surgical lesion on CT

 Mild-to-moderate hypothermia (3235 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

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 xed 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 conned to research settings (Table 4).

Outcome predictors
The Glasgow Outcome Score (GOS) classies outcome as death, persistent vegetative state, severe disability, moderate disability or good recovery. The Kings 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 difcult 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 2040 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

Figure 3 Cerebral hypoperfusion caused by reduced PaCO2. Xenon CT images of the same patient taken 20 minutes apart, before and after hyperventilation. (a) PaCO2 36 mmHg (4.8 kPa) with estimated cerebral blood ow of 43 mL/minute/100 g; (b) PaCO2 32 mmHg (4.3 kPa) with estimated reduced cerebral blood ow of 15 mL/minute/100 g. (Normal cerebral blood ow is 425 mL/minute/100 g.)

Multimodality monitoring

 Jugular venous oxygen saturation  Cerebral blood ow 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

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Kings outcome scale for childhood injury

Category 1 2 3 Denition Death Vegetative Severe disability A. Conscious, totally dependant; may be able to communicate B. Limited self-care abilities and predominantly dependant; may have meaningful communication Moderate disability A. Mostly self-caring, but needs support and supervision; problems with behaviour/learning and communication B. Independent daily living; minor neurological decits; residual problems with behaviour/ learning Good recovery A. Full functional recovery, but residual pathology attributable to head injury B. No sequelae identied

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.

REFERENCES
1 West Midlands Public Health Observatory. Health issues: childhood injuries. 2006. /www.wmpho.org.ukS 2 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: 11827. 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: 414. 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: 160612. 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: 4617. 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: 51922. 8 National Institute for Health and Clinical Excellence. Clinical guidelines: head injury 2003. /www.nice.org.ukS. 9 Dunning J, Patrick Daly J, Lomas J P, Lecky F, Batchelor J, MackwayJones K. Derivation of the childrens head injury algorithm for the prediction of important clinical events decision rule for head injury in children. Arch Dis Child 2006; 91: 88591. 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 Association. 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: 647. 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: 23440. 15 OSullivan 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: 4650.

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 mildto-moderate TBI.5,18 Somatosensory evoked potentials (SSEPs) may be helpful in dening 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 difcult. 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 1215 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

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16 Crouchman M, Rossiter L, Colaco T, Forsyth R. A practical outcome scale for paediatric head injury. Arch Dis Child 2001; 84: 1204. 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: 3104. 18 Anderson V, Catroppa C, Morse S, Haritou F, Rosenfeld J. Functional plasticity or vulnerability after early brain injury? Pediatrics 2005; 116: 137483. 19 Carter B G, Butt W. A prospective study of outcome predictors after severe brain injury in children. Intensive Care Med 2005; 31: 8405. 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: 76575.

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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