Paediatric Anaesthesia 1999

9: 377385

Review article

Paediatric head injury: incidence, aetiology and management

W. HIU LAM BM BS, MRCP, FRCA AND ANGELA MACKERSIE BSc, MB BS, FRCA
Department of Anaesthesia, Great Ormond Street Hospital for Children, NHS Trust, Great Ormond Street, London UK

Summary
Trauma is the commonest cause of hospital admission in children. Head injuries are present in 75% of children with trauma and 70% of all traumatic deaths are due to the head injury. The mechanism of brain injury is examined, resulting from the effects of the primary insult and secondary ischaemic damage. Therapeutic interventions will be discussed with specic emphasis on outcome studies. However, institution of adequate oxygen delivery and haemodynamic stability in the child at the earliest moment remains the most important aspect of the management plan. Keywords: head injury; management

Introduction
Worldwide, trauma is the commonest cause of admission to hospital in children, and it is also a major cause of morbidity and mortality. After the rst year of life, trauma is the most frequent cause of death and remains so until well into adult life, with the incidence increasing throughout childhood. In the rst year of life congenital anomalies, prematurity and sudden infant death syndrome (SIDS) are the major causes of mortality. However, following public campaigns concerning infant sleeping positions, the striking reduction in SIDS in some countries has resulted in trauma deaths relatively increasing in infants, to approximately 10% during the rst half of the 1990s. Three-quarters of all children admitted to hospital with trauma have an associated head injury and 70% of deaths result from the head injury. Overall, 15%
Correspondence to: Angela Mackersie, Department of Anaesthesia, Great Ormond Street Hospital for Children NHS Trust, Great Ormond Street, London WC1N 3JH, UK. 1999 Blackwell Science Ltd

of deaths under 15 years are due to head trauma and, between the ages of 5 and 15 years, the incidence is 25%. In the UK, road trafc accidents (RTAs) are the most common cause of head injuries, with the child pedestrian being the largest subgroup. In the USA, child car passengers have the highest incidence of cranial trauma. Falls and nonaccidental injury are the other major causes of head trauma in children. In the rst year, nonaccident injury is the commonest cause of major head injuries. Following the injury, there is a trimodal pattern to the time of death. Almost half paediatric trauma deaths occur within minutes of the impact where there is usually an overwhelming injury incompatible with life. In the second group (approximately 20%), death occurs within hours due to respiratory failure, circulatory insufciency or raised intracranial pressure (ICP). Death may be avoided if active treatment is timely and effective. The remaining onethird of deaths occur later, days or weeks after the event, and are not only due to raised intracranial pressure, but also to infection and organ failure. 377

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Mechanism of brain injury

The resultant head injury is caused by the so called primary brain injury (PBI) and the effects of the secondary brain injury (SBI) caused by respiratory or circulatory insufciency or raised ICP.

Primary brain injury

The magnitude of the initial impact of the brain in trauma determines the severity of PBI. The injury results from contusions, lacerations, diffuse axonal injury and dural tears which are caused by abrupt acceleration and/or deceleration of the head. In children, the disproportionately larger and heavier head renders them more likely to head injury because the momentum on impact is increased. It is important to bear in mind that even in children, signs of hypovolaemic shock (e.g. hypotension and tachycardia) in head injury should alert the resuscitation team to look for other signs of occult bleeding. It is however, possible to lose signicant circulating blood volume from a scalp wound as the surface area of the head in an infant is 19% of the total body surface area, compared to 9% in adults. Intracranial haemorrhage may also contribute to hypovolaemic shock.

increased with the frequency of hypotensive episodes (5). Cerebral perfusion pressure (CPP) [mean arterial pressure (MAP) ICP]. A reduction in MAP causes a fall in CPP and exacerbates preexisting brain injury. Hypoxia, PaO2 of < 8 kPa (< 60 mmHg) and hypotension impair oxygen delivery to the brain (6). Hypoxia may be caused by a reduced respiratory drive secondary to the brain injury or from airway obstruction accompanying a reduction in conscious level in head injury. It may also be related to direct injury to the lung parenchyma in children with coexisting chest injury. Hypercapnia The arterioles in the brain respond to the local concentration of CO2 by autoregulation. An accumulation of CO2 (e.g. secondary to hypoventilation) increases hydrogen ion concentration which exerts a local vasodilatory effect on these vessels causing an increase in cerebral blood ow which in turn increases the ICP. The raised ICP further exacerbates SBI. Pyrexia For every 1C increase in body temperature, there is a 5% increase in the cerebral metabolic rate which precedes an increase in cerebral blood ow (and ICP) in response to this increased activity (7). In addition, pyrexia also causes an increase in insensible water loss by 12% per degree rise (8), and if not corrected, predisposes to hypovolaemia and a reduction in MAP and CPP. In an animal model, a core temperature rise of as little as 12C may worsen both the neurological signs and the histopathological evidence of ischaemia (9). Electrolyte abnormalities Disturbances in sodium homeostasis are the main abnormality. Hyponatraemia may be caused by inappropriate antidiuretic hormone secretion or cerebral salt wasting; both triggered by an insult to the brain. Although they both present with low serum sodium, the former with normo- or hypervolaemia; whereas the latter is usually with intravascular depletion. Hyponatraemia causes cerebral oedema with devastating morbidity and mortality (1012). Diabetes insipidus (caused by the disruption of antidiuretic hormone secreting cells) is recognized by the presence of serum hypernatraemia,
1999 Blackwell Science Ltd, Paediatric Anaesthesia, 9, 377385

Secondary brain injury

SBI is caused by the complications of PBI. Features of SBI were found in up to 90% of patients with head trauma in a study by Jones (1). Unlike PBI, SBI is largely preventable and its prevention plays a pivotal role in the management of head injury. Brain ischaemia (as a result of oxygen demand and supply mismatch) either locally or globally is the end result of SBI and has been demonstrated in over 80% of fatal head injury (2), but there is a whole range of insults that converge onto a nal common pathway to SBI. Therefore, understanding the mechanism of causation leading to SBI is imperative. Change in blood pressure and hypoxia Hypertension, hypotension and hypoxia have been independently shown to increase morbidity and mortality in severe head injury in both adults (3) and children (4). It has also been demonstrated that the mortality of patients with severe head injury is

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hyperosmolality and inappropriate production of hypotonic urine (urine osmolality < 200 mOsm.l1 and/or urine specicity < 1.002). This is associated with intravascular volume depletion and therefore haemodynamic instability. The depletion should initially be treated with volume replacement using 0.45% saline and 5% dextrose as there is a low sodium content in the urine. The large volume of uid required to restore the decit may cause hyperglycaemia, which can in turn lead to an osmotic diuresis and compound the problem of dehydration. Therefore, in practice, the early and judicial administration of vasopressin or its analogue, 1deamino-8-D-arginine (DDAVP) is usually effective (7,13,14). Hyperglycaemia induces lactic acidosis and subsequent oxygen free radical production which is detrimental to injured brain tissue and is related to poor outcome in head injury (15). Hypoglycaemia, which is more common in premature infants, should be actively sought and treated as glucose is the only substrate for brain metabolism. Careful assessment of the requirement for a glucose containing solution is therefore essential. Intracranial pathology Trauma induced intracranial haematomas such as extradural, subdural and intracerebral all cause disruption of the blood supply to the brain tissue and therefore induce ischaemia and local cerebral oedema. Subdural haemorrhages in infants deserve a special mention as a recent UK study conrms most haemorrhages of this kind are due to nonaccidental injury (16). The outcome in this type of injury is reported to have a poor outcome (17,18). As the brain is enclosed by a bony compartment, the expansion of brain tissue will eventually lead to a rise in ICP when all the compensatory mechanisms are exhausted (MonroKellie doctrine) and is thought to be a poor prognostic index in severe head injury (19). Cellular mechanism Excitatory amino acids (Eaas) are neurotransmitters that are widely distributed in the brain (20), but are neurotoxic in high concentration. It is now evident from animal studies that increased levels of glutamate (one of the excitatory amino acids) are detected in damaged brain (21,22) and in cerobrospinal uid
1999 Blackwell Science Ltd, Paediatric Anaesthesia, 9, 377385

Table 1 Treatment strategies for acute intracranial hypertension Treatment strategy Percentage of intensive care units in USA 83% 64% 57% 29% 44% 33% 28% Percentage of intensive care units in UK 100% 49% 44% 2.5% 5% 6% 6%

Osmotic diuretic Steroid administration Prophylactic hyperventilate CO2 2535 mmHg Prophylactic hyperventilate CO2 < 25 mmHg Cerebrospinal uid drainage Barbiturate administration ICP monitoring

(CSF) after head injury (23). The increase in glutamate appears to initiate an excitotoxic cascade by activating the inotropic and metabotropic glutamate receptors. The former include N-methyl D-aspartate (NMDA) receptors; the latter are associated with G-proteins and are involved in the modulation of intracellular secondary messengers. The net effect is an increase in intracellular calcium which initiates a cascade of intracellular destruction by activation of protein kinase, phospholipases, proteases causing proteolysis, lipid peroxidation, free radical formation and degeneration of the neurone (20).

Management
Almost half the paediatric trauma deaths occur with minutes from the primary injury, so the best way to deal with PBI is to reduce its occurrence by education of children and their families. Government policy and road safety campaigns, in conjunction with the help of schools, motoring organizations and parental education and cooperation, must be the key to success in preventing road accidents. The routine use of helmets for potentially dangerous activities such as cycling and skiing will also reduce the incidence of serious head injuries. In contrast, SBI can be treatable, and its management is the mainstream treatment of head injury, aiming to avoid, anticipate and actively treat the development of intracranial hypertension (ICH). The variability in ICH treatment strategy is well illustrated by surveys of intensive care units from the USA (24) and the UK (25). The variations in treatment strategies from these units are summarized in Table 1. The possible reasons for such different

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approaches to treatment are partly due to scientic weakness, poor education and communication. The UK government is attempting to address the latter by introducing national guidelines for all treatment strategies from the National Institute of Clinical Excellence (NICE), a new statutory body (26,27). At present, there are no universally agreed guidelines for treatment of acute ICH. With this in mind, we set out to review the evidence currently available, looking especially for studies using human clinical outcome as endpoint. There is limited Class I evidence (information derived from large prospective randomized controlled trials) in the adult population of head injury, let alone paediatric subjects. Class II (prospective nonrandomized controlled trials or retrospective studies) and Class III (case series, reports and expert opinions) evidence will also be reviewed. The importance of immediate airway management with oxygen supplementation, cervical spine immobilization, assessment of the adequacy of breathing and optimal circulation at the scene of the accident through to the casualty department and PICU cannot be overemphasized (28). There is evidence for the inuence of hypoxia and hypertension on outcome to support the importance of immediate airway and circulation management (29). Airway management and mechanical ventilatory support have been shown to decrease mortality in various groups of patients with head injury, cerebral tumour, encephalitis and cerebrovascular accident (3033). Initial assessment of the severity of the head injury is needed and, for young children, the Glasgow Coma Scale has been modied to allow for the normal lack of verbal skills. Severe head injuries are dened as those with coma scores of 8 or less, moderate injuries with scores between 9 and 12, and minor between 13 and 15. Rapid assessment can be made whether the child is alert, responds to verbal command, responds to pain, or is unresponsive. Plain skull X-rays are required for initial assessment and the indications for computed tomography (CT) scanning are given in Table 2. Investigations are performed to exclude a surgically treatable lesion, to diagnose hyperaemia or oedema and to delineate fractures. Magnetic resonace imaging scans are not indicated routinely at the initial stage

Table 2 Indications for computed tomography scans in HI Glasgow Coma Scale 8 Skull fracture Onset of neurological signs Cushings response (bradycardia, hypertension, irregular respiration) Fall in Glasgow Coma Scale with normal blood gases Glasgow Coma Scale < 14 for more than 8 h

but may be useful as lesions develop or for planning surgery. Four to ve percent of paediatric head injuries have an associated cervical spinal fracture with or without dislocation., mostly at C1C3, also likely to be caused by the force of the injury on the relatively large head of the child. Unless dynamic images are seen it is impossible to exclude spinal damage or instability and therefore should be assumed to be present and appropriate care taken during intubation or positioning for other procedures.

Evidence to support treatment strategy for intracranial hypertension

Class I Only three aspects of management of acute intracranial hypertension have Class I evidence with human outcome as end point. Unfortunately, they all appear to be negative. Prophylactic hyperventilation. Prophylactic hyperventilation of any magnitude with no intracranial hypertension should be avoided as the vasoconstrictive effect of acute hyperventilation can produce decreases in cerebral blood ow to a potentially detrimental level (34). Most studies on hyperventilation deal with the effect of hypocapnia on cerebral blood ow, but it is demonstrated in one neurological outcome study at 3 and 6 months postinjury that prophylactic hyperventilation is deleterious in head injured patients without proven intracranial hypertension (35). In addition, this is supported by a human observational study that hypocapnia may have made the outcome worse (36). In a recent article by Dexter (37), over 980 articles in a 30-year-period were reviewed to evaluate the effect of hypocapnia and airway protection on cerebral
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outcome and there are no clinical data to support the hypothesis that hypocapnia improves outcome in patients with cerebral disease. Steroid administration. The use of steroids should not be advocated in the management of head injury. Recent studies have not shown a signicant change in mortality and morbidity 6 months after the initial head injured patients were treated with either low or high dose steroid (38,39). Furthermore, high dose steroid has been demonstrated to have no advantage on ICP trend (40). This, in conjunction with the well known complications of exogenous steroid administration have deterred its use. However, a recent systemic review of randomized controlled trials of steroid administration in acute traumatic brain injury shows uncertainty over its use and neither moderate harmful nor moderate benecial effects can be excluded (41). Anti-seizure prophylaxis. Studies dealing with the use of antiseizure drugs such as, phenytoin, carbamazepine or phenobarbitone show no statistically signicant effect in the prevention of late onset posttraumatic seizures (4245). Conversely, with respect to early posttraumatic seizures, data from the same prospective, randomized, controlled trials suggest that prophylactic treatment does have an effect on the incidence of early seizure; but what association this has with the outcome of head injury remains undened. The use of anticonvulsants to treat early posttraumatic seizures remains at the discretion of the clinician. Class II and III Intracranial pressure monitoring. There is no prospective randomized controlled trial examining the inuence of ICP on outcome. Such a study may never be performed due to ethical concerns. There are some data to suggest that denition of treatable intracranial hypertension should be set at 2025 mmHg (5,19). The difculty is the difference in normal ICP in adults (818 mmHg) and children (24 mmHg) (7). It may not be appropriate to extrapolate this data to the paediatric population, the ICP treatment threshold must therefore be assessed in conjunction with clinical status and CPP calculation. It is postulated that ICP monitoring should be initiated in those patients at risk of
1999 Blackwell Science Ltd, Paediatric Anaesthesia, 9, 377385

Table 3 Factors affecting patients at risk of developing intracranial hypertension with normal computed tomography scan Over 40 years old Systolic pressure below 90 mmHg Unilateral or bilateral motor posturing

developing ICH. Adult patients with abnormal CT on admission are associated with a 5363% incidence of ICH compared to 13% in the normal CT group. In those patients with normal CT, the groups at higher risk of developing ICH are summarized in Table 3. There is a 60% risk of developing ICH if two or more of these factors are present compared to 4% if only one factor is present (46). Whether this system can be applied to children with some modication remains to be evaluated. Cerebral perfusion pressure. There are no prospective randomized controlled studies to evaluate the critical CPP management threshold on clinical outcome. A minimal CPP of 50 mmHg is said to be adequate for adult brain perfusion (14) and a CPP of 70 mmHg has been shown retrospectively to be benecial in terms of clinical outcome (47). A reduction of CPP < 70 mmHg is associated with decreased jugular bulb venous oxygen saturation which suggests a failure of cerebral blood ow to meet metabolic demand (48). The minimal required CPP in children has not been dened. Presumably CPP would vary as children in different age groups have different MAP. Although CPP plays an important role in the treatment strategy of head injury, awareness of the class II evidence on which this treatment strategy is based is essential. It is therefore recommended that CPP should be maintained > 70 mmHg during the acute course of head injury (49). Ventricular drainage. Ventricular drainage is recommended by the Brain Trauma Foundation as one of the rst line treatments in acute intracranial hypertension (49). In older children, there is a limited application for this technique as it relies on the presence of surgical access, e.g. extraventricular drain or intraventricular ICP catheter; whereas in infancy, needle aspiration of CSF can be made through the anterior fontanelle. The reduction in cerebrospinal uid volume leads to a fall in ICP.

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Mannitol. Mannitol has a denite place as a rst line treatment of intracranial hypertension provided the blood brain barrier is intact. It has been shown to reduce ICP and improve CPP (50,51). One study also demonstrated that it can simultaneously lower ICP and increase jugular venous oxygen saturation (52). It should not be given repeatedly as this may lead to the accumulation of mannitol in the brain. The mechanism of action is complex. In addition to its osmotic effect in increasing serum osmolality and drawing water from the brain, it also causes an immediate increase in systemic blood pressure and decrease in blood viscosity, both of which increase cerebral blood ow leading to cerebral vasoconstriction and subsequent reduction in ICP. The dosage is in the range of 0.250.5 gkg1 (14). Its use is limited by hyperosmolality, electrolyte disturbances and intravascular volume depletion. Barbiturates. Barbiturates are indicated in the treatment of raised ICP. Thiopentone 24 mgkg1 can be administered to treat an acute rise in ICP as it decreases cerebral metabolism and oxygen consumption Cerebral blood ow, cerebral blood volume and cerebrospinal uid pressure all fall, possibly due to a reduction in the carbon dioxide level (53). In spite of this, prophylactic use of barbiturates against the development of ICH is not recommended (54), nor as a substitute for mannitol in the early management of intracranial hypertension (55). However, the study of Eisenberg et al. (56) showed that barbiturates are highly effective in lowering a raised ICP that was previously refractory to conventional therapy such as CSF drainage, hyperventilation and mannitol administration. No formal association between the lowering of this ICP and clinical outcome has been established. As barbiturates commonly cause myocardial depression and peripheral vasodilatation, which may compromise CPP, the use of thiopentone has to be closely monitored; ideally with invasive arterial and venous pressure monitoring. In practice, these patients may require ionotropic support to maintain adequate circulation whilst in a barbiturate coma. Hypothermia. Pyrexia following acute head injury has a detrimental effect on the outcome (9). Conventional hypothermia (surface cooling to < 30C) decreases ICP, cerebral blood ow and the cerebral metabolic

rate of oxygen consumption (57). In the past decade, conventional hypothermia is less commonly used due to unconvincing clinical outcome as well as complications related to this technique, e.g. cardiac dysrhythmia, haemodynamic instability and coagulation abnormality. Mild to moderate hypothermia (surface cooling to 3234C) is not associated with these complications and may limit SBI by reducing cerebral metabolism, stabilizing cell membranes and suppressing high levels of extracellular excitotoxic amino acids present after severe head injury (58). Both Marion and Shiozakis studies found a signicant reduction of ICP and the latter also demonstrated signicantly improved survival rate in the hypothermic group (50% compared to 18% in the control group) (57,58). More data will become available on completion of the National Acute Brain Injury study on hypothermia. This multicentre trial aims to evaluate if hypothermia to 3234C improves Glasgow Outcome score at 6 months after head injury (49). Hypertonic saline. Recently, the introduction of hypertonic saline in the management of ICH and cerebral oedema has attracted attention (59,60). Effective use of hypertonic saline to treat cerebral oedema and resistant intracranial hypertension has been demonstrated (6163). It acts primarily by creating an osmotic gradient between intra-and extravascular spaces (similar to mannitol), hence drawing water from the brain. A rebound phenomenon occurs with other hypertonic uids, e.g. urea or mannitol as a result of accumulation of these molecules in the brain and hence reversing the osmotic gradient. A possible rebound phenomenon has recently been reported on two patients with cerebral oedema secondary to intracerebral haemorrhage who were treated with hypertonic saline solution (64). The use of this solution requires further evaluation. Surgical treatment. Surgical treatment is either aimed at reducing raised intracranial pressure or for skull and scalp wound repair. Decompressive craniotomy is again popular as part of an aggressive treatment of head injuries but whether this will show improvement in outcome is yet to be demonstrated. Where there is a severe contusion to a functionally
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unimportant area of the brain, it may be an indication for prompt decompression or excision of the contusion. Intracranial bleeds in paediatric head injury have half the incidence of adults, 2025% instead of 4050%, so that less than 1% of children admitted with a head injury require removal of a haematoma. Haematomas can be subdural, the most common and usually associated with a severe injury, extradural or intracerebral. Extradural haematomas, if producing a mass effect need rapid surgical drainage, usually performed through a small craniotomy. More than 85% of children have no history of alteration in consciousness at the time of injury, unlike adults where the classical lucid interval is common. The incidence of extradurals is also much lower in childhood, and accounts for only 25% of all intracranial bleeds in the paediatric age range. Subdural haematomas are associated with a severe head injury and can be caused by cerebral contusions or vessel damage, but are only rarely associated with fractures. It is thought that a bony fracture dissipates the force of the injury making intracranial damage less and reducing the likelihood of subdural haematoma formation. Intracerebral haematomas are also rare. Most develop from cortical contusions in a child with a tremendous head injury with a pathological progression from hyperaemia to a contusion and formation of a collection of blood which eventually progresses to atrophy and the development of cystic areas. If a haematoma is localized, e.g. frontally, excision may be considered. Fractures. Ninety percent of skull fractures in children are linear and are an indication of the force of injury. Most are uncomplicated and provided the child is asymptomatic, no further treatment is required. They tend to be more diastatic than in adults and therefore look more impressive on X-ray. It is important to see whether a large vessel, either middle meningeal artery or dural sinus, crosses the fracture site which could be damaged causing intracranial bleeding and subsequent pressure effect. There are two types of fracture unique to paediatric head injury. Firstly the Ping-Pong Ball fracture which occurs in neonates with a malleable skull and usually results from birth trauma, especially from obstetric forceps. Surgery is indicated for large lesions and for
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frontal fractures for cosmetic reasons. Because of the malleable skull, these fractures can usually be elevated easily through a small incision just lateral to the depressed area. They are not usually associated with any under lying brain injury, but great care needs to be taken to avoid causing secondary damage. The other fracture type that only occurs in children is the growing fracture. This occurs when torn dura or damaged brain is present between the edges of the fracture. A leptomeningeal cyst develops and there is absorption of bone from the edges of the fracture leading to a growing defect. This presents as a soft swelling, usually within weeks of the original injury. Surgical treatment involves removal of gliotic brain, dural closure and bone grafting. This usually done with split calvareal bone and therefore involves an area more than double the size of the original lesion. This increases blood and heat losses because of the large exposure. Compound fractures require wound debridement, dural repair and removal of bone fragments, but great care is taken to prevent additional damage either directly or from haemorrhage. Debridement usually is performed within 624 h. There is however, a surprisingly low infection rate with wounds due to the vascularity of the scalp. Anaesthesia and head injury. Anaesthesia may be required for the investigation and treatment of children with severe head injuries but also for some children who have had less severe cerebral insults. The most severely head injured children will already be receiving intensive care, be heavily sedated and ventilated which needs little supplementation for investigations, but they must be adequately anaesthetized for surgery, to avoid a stress response and its metabolic consequences. Standard neurosurgical anaesthetic technique is appropriate. Invasive monitoring is required if not already in use and vascular access should be appropriate for rapid transfusion. The hyperaemic response to injury may remain for weeks and increased losses can be expected even with delayed surgery.

Conclusions
The management of a head injured child clearly requires a multidisciplinary team approach (6567). This team should consist of paediatricians, surgeons,

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anaesthetists, nurses, operating department assistants who treat children regularly. When the transfer of children to a specialist paediatric centre is necessary, it should be carried out by senior medical personnel or a specialist transport team (68). Undoubtedly, more paediatric trials need to be conducted before further guidelines in paediatric head injury management can be recommended. The institution of adequate oxygen delivery and haemodynamic stability in a child at the earliest possible moment after head injury remains the most important aspect of management strategy. In the presence of established intracranial hypertension, with the evidence currently available from literature, the recommendation for rst line treatment is cerebrospinal uid drainage, hyperventilation and mannitol administration. If ICH remains high, then barbiturate administration may be a useful option and moderate hypothermia may become standard treatment in the future.

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Accepted 26 March 1999

1999 Blackwell Science Ltd, Paediatric Anaesthesia, 9, 377385