INTRODUCTION:
Road traffic accidents account for the largest number of head injuries in children (1-3).  Falls from heights may be responsible for head injuries in the very young (1-3). It is probable that some alleged falls in infants are due to child abuse (4), as most of the serious head injuries in the very young proved to be non-accidental (5,6).  So, one must be very suspicious when presented with a head injured infant without a clear history of trauma.

THE CLINICAL PICTURE:

Detailed history from relatives and attendants of a head injured child mostly point to the cause of head trauma.
The clinical evaluation of a head-injured child should include assessment of the level of consciousness, motor examination for muscle strength and posturing especially with asymmetry together with pupillary size and reactivity.
In infants, the anterior fontanelle may be tense and bulging if the ICP is raised.
CT scan can diagnose the types of intracranial injury, the most common being an acute inter-hemispheric subdural hematoma in the parieto-occipital region (6). Other CT scan findings include intracerebral and subarachnoid haemorrhages (6, 7) and epidural hematomas (3). 
Seizures may occur in head injured children either early within or late beyond one week of the injury.  In management of acute head injuries, we are more faced with early seizures which occur in children more than in adults after traumatic head injuries (8, 9).  
The Glasgow Coma Scale (GCS) is widely used in the assessment of head injuries in adults (10).   This scale has been modified for infants and young children (Table 1) to account for their inability to obey commands and for normal developmental variations (4, 11).

Table (1): Glasgow Coma Scale for pediatrics

PATHOPHYSIOLOGY: 
Infants have cerebral blood flow (CBF) of 50 ml/100g/min, as adults, which steadily increases during childhood to reach a peak of 70ml/100g/min between the ages of 3 and 8 years, then decreases to adult levels between 15 and 19 years (4, 12).
After traumatic brain injury (TBI), more than 90% of children who die from severe head injuries have histological evidence of ischemia (13).  There was a strong correlation between low CBF and poor outcome, with a higher mortality rate for those with than those without ischemia (13). Ischemia after TBI has been confirmed to occur early after injury in a study using the inhaled stable Xe-enhanced CT scan technique (14).  This technique provides better resolution, has the  ability to measure CBF in deeper brain structures as well as the cortex and can detect regional and global ischemia.  CBF when decreased to less than 20ml/100g/min was always associated with poor outcome (15).  Low post-traumatic CBF, though more prevalent in adults, is also seen in children (4).
However, Muizelaar et al (12, 16) proved that children had relative or absolute hyperemia at some point in their course, as well as very low arterio-juglar venous oxygen difference, suggesting more than adequate CBF for the metabolic needs of the brain. However, those authors (12, 16) proved that children with poor outcome had lower CBF in the first 24 hours, compared with children with higher CBF and better outcome.
Diffuse brain swelling (DBS) after TBI occurs more commonly in children than in adults (17-21), and is most evident in CT scans of children with GCS of 8 or less, caused by hyperemia and vasodilation (18). So, DBS may be a characteristic marker of severe head injuries in children(18). DBS can be detrimental because it raises ICP, impairs CBF and it represents an ongoing secondary brain injury.
It should be clarified here, that TBI is usually classified as primary or secondary. Primary injury is the physical insult caused at the time of traumatic impact.  It causes immediate and permanent destruction to some neural and vascular tissues.
Secondary injury is the biochemical and cellular responses to the primary injury causing loss of tissues not initially damaged.  It also includes physiological derangements causing further systemic insults as hypoxia, hypercerbia, hypotensin and hyperthermia. 
Secondary brain injury induces a complex chain of events involving the release of excitatory amino-acids as aspartate, glutamate and dopamine from the injured neurones (22). These stimulate neuronal membrane receptors causing pathologic excessive ion fluxes, especially calcium and sodium.  Calcium enters the neurones and activates proteases and phopholipases causing loss of cell membrane integrity.
Sodium entery accompanied by water causes intracellular cytotoxic edema.  The breakdown of phospholipids by phospholipases damages the cell membrane and generates arachidonic acid as a byproduct acting as a substrate for production of prostaglandins, thromboxanes and leukotriens. Those inflammatory mediators cause vasodilatation, vasoconstriction and capillary leak with the formation of vasogenic edema and attract inflammatory cells and platelets.  Oxygen free radicles are also produced by arachidonic acid metabolism and by reperfusion injury and cause damage to lipids, proteins and nucleic acid. The interacting processes of ischemia, excitatory amino-acids, ion fluxes, cytotoxic and vasogenic edema and inflammatory mediators compromise the potentially viable cells adjacent to the injured area in a self-perpetuating cascade.  So, the relatively focal primary injury may expand due to unchecked secondary injury.

MANAGEMENT:
The therapeutic approach for children with head injury is analogous to that for adults. It is important not to lose time in the initial attention to physical signs and radiological findings. Golden minutes are saved to concentrate on respiratory and haemodynamic status for prevention of insults and their treatment if they take place.
When an iv access cannot be obtained in a child, central venous access, a venous cutdown and an intra-osseous approach are options depending on the urgency of the situation.
Ensuring adequate perfusion and oxygenation should go on simultaneously.
 Of utmost importance is to optimize oxygenation and ventilation of the head-injured child because hypoxia and hypercarbia cause cerebral vasodilatation increasing CBF and ICP with a negative impact on the child outcome. 
Airway toiletting with a clear patent airway is important to start with.  In severe head injury, orotracheal intubation is done under direct laryngoscopy with an assistant immobilizing the potentially injured cervical spine in a neutral position.  Indications of intubation include inability to maintain a patent airway, clinical signs of elevated ICP, hypoxia and hypercarbia, traumatic coma with GCS of 8 or less, associated severe airway or thoracic trauma precluding effective ventilation and associated respiratory problems.
Although hyperventilation in one of the most reliable and effective measures to reduce ICP, it may induce cerebral vasoconstriction and hypocarbia decreasing CBF and inducing brain ischemia (14, 16,23, 24).  So, hyperventilation should not be used as a first line therapy for raised ICP and should not be used prophylactically. 
Clinical management of severe head injury may show reluctance in volume administration for fear of causing or exacerbating brain edema. However, fluid restriction and dehydration are not beneficial and may cause hypotension which is deleterious. So, one should ensure adequate restoration of intravascular volume by isotonic solution boluses of 10-20ml/kg repeated as needed (4).  Some centres use hypertonic fluids. A study carried out by Luerssen et al (3) found that children with profoundly low blood pressure had a mortality of 33%, compared with 12% for adults with such low blood pressure.
In the ICU, special care should be given in the first 24 hours after head injury because this is the most common period for ischemia to occur.
The meticulous attention given to oxygenation, ventilation and perfusion during resuscitation should continue in the ICU.
All children with severe head injury should be oro-trachealy intubated.  Ventilatory strategy should take into account that raised intrathoracic pressure may impede cerebral venous return and increase ICP. So, the lowest inspiratory and end-expiratory pressures to achieve adequate oxygenation and ventilation should be used.
Isotonic saline is an appropriate fluid for initial volume restoration.  Fluid therapy should maintain adequate intra-vascular volume and perfusion, avoid hyponatremia and hypo-osmolality and provide nutrition.
Head injured children should be nursed with raised upper half of the body at 15-30º without flexing the neck to facilitate cerebral venous drainage (25).
Radiological evaluation should be carried out as soon as possible, once initial respiratory and haemodynamic priorities are addressed.  Evacuation of an intracranial lesion is obviously a must. This decision is taken immediately by the treating team including the neurosurgeon. 
Adequate analgesia by fentanyl and sedation by a benzodiazepine are achieved to prevent patient movement or fighting the ventilator. The use of neuromuscular blockers may prolong the duration of the ICU stay and increase morbidity, and it is suggested not to use these agents routinely, but only when necessary (26).
ICP monitoring is indicated for GCS of  8 or less or if radiological findings suggest raised ICP due to DBS, mass effect or compressed ventricles and cisterns.
If the above mentioned strategy of management do not reduce ICP to 15-20 mmHg to satisfy a cerebral perfusion pressure (CPP) of 50-60 mmHg, other measures are added, including further sedation, osmotic dieuresis, drainage of CSF from ventricles or hyperventilation to PaCo2 of 30 mmHg as advised by the treating physician.
If intracranial hypertension remains refractory, a newly expanding surgical lesion should be ruled out by CT scan.  If this is ruled out or a lesion is evacuated and ICP still remains high, more aggressive hyperventilation to PaCo2 of 25 mmHg, barbiturate coma or hypothermia is induced with management of the expected myocardial depression and hypotension by volume, inotropes or vasopressors.
During management in the ICU, bot hyperthermia or seizures should be aggressively treated if thy take place.

CONCLUSION
Younger child tend to do better than older patiens after comparable head injures and clinical studies do confirm this.  The good understanding of the pathophysiology of head injuries in children and ensuring adequate oxygenation, ventilation and perfusion are important cornerstones for better outcome.  ICU management should follow an algorithm to manage intracranial hypertension, hyperthermia or seizures.  Team work including physicians, neurosurgeons, radiologists and nurses can achieve good results.

REFERENCES

1. Alberico A, Ward J, Choi S, et al: Outcome after severe head injury. J Neurosurg 67: 648-656, 1987.
2. Levin HS, Aldrich EF, Saydjari C, et al: Severe head injury in children: Experience of the Traumatic Coma Data Bank. Neurosurgery 31: 435-444, 1992.
3. Luerssen, T, Klauber M, Marshall L: Outcome from head injury related to patient’s age. J Neurosurg 68: 409-416, 1988.
4. Roberts TM (1997): Head injuries in children and adults, In: Critical Care Clinics, Common issues in pediatric and adult critical care, 13, 3, 611-628, WB Saunders Co.
5. Billmire ME, Myers PA: Serious head injury in infants: Accidents or abuse? Pediatrics 75: 340-342, 1985.
6. Zimmerman R, Bilaniuk L, Bruce D, et al: Computed tomography of craniocerebral injury in the abused child. Radiology 130: 687-690, 1979.
7. Goldstein B, Kelly MM, Bruton D, et al: Inflicted versus accidental head injury in critically injured children. Crit Care Med 21: 1328-1332, 1993.
8. Annegers J, Grabow,J, Groover R, et al: Seizures after head trauma: A population study.  Neurology 30: 683-689, 1980.
9. Hahn Y, Fuchs S, Falnnery A, et al: Factors influencing posttraumatic seizures in children. Neurosurgery 22: 864-867, 1988.
10. Teasdale G, Jennet B: Assessment of coma and impaired consciousness: A practical scale. Lancet 2: 81-84, 1974.
11. Stene JK, Smith CE and Brande C (1998): Evaluation of the trauma patient, In: Principles and Practice of Anaesthesiology, 2nd ed., Editors: longnecker DE, Tinker JH and Morgan GE, Page 588, Mosby.
12. Muizelaar JP, Marmarou A, DeSalles AAF, et al: Cerebral blood flow and metabolism in severely head-injured children, Part 1. J Neurosurg 71: 63-71, 1989.
13. Graham DI. and Adams JH: Ischaemic brain damage in fatal non-missile head injuries. Lancet 1:256-266, 1971.
14. Bouma GJ, Muizelaar Stringer WA, et al: Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. J Neursurg 77: 360-368, 1992.
15. Adelson PD, Clyde B, Kochanek PM, et al: Cerebral blood flow and CO2 vasorespnsivity in children following severe traumatic brain injury. J Neurosurg 84: 357A, 1996.
16. Muizelaar JP, Ward JD, Marmarou A, et al: Cerebrl blood flow and metabolism in severely head-injured children, Part 2. J Neurosurg 71:72-76, 1989.
17. Aldrich EF, Eisenberg HM, Saydjari C, et al: Diffuse brain swelling in severely head injured children. J Neurosurg 76: 450-454, 1992.
18. Bruce DA, Alavi A, Bilaniuk L, et al: Diffuse cerebral swelling following head injuries in children: The syndrome of “malignant brain edema”.  J Neurosurg 54: 170-178, 1981.
19. Graham DI, Ford I, Adams JH, et al: Fatal head injury in children. J Clin Pathol 42: 18-22, 1989.
20. Lang D, Teasdale G, Macpherson P, et al: Diffuse brain swelling after head injury More often malignant in adults than children? J. Neurosurg 80: 675-680, 1994.
21. Zimmerman R, Bilaniuk L, Bruce D, et al: Computed tomography of pediatric head trauma: Acute general cerebral swelling.  Radiology 126: 403-408, 1978.
22. Baker A, Moulton R, MacMillan V, et al: Excitatory amino acids in cerebral spinal fluid following traumatic brain injury in humans.  J Neurosurg 79: 369-372, 1993.
23. Bouma GJ, Muizelaar JP, Choi SC, et al: Cerebral circulation and metabolism after severe traumatic brain injury: The elusive role of ischemia.  J Neurosurg 75: 685-693, 1991.
24. Muizelaar JP, Marmarou A, Ward JD, et al: Adverse effects of prolonged hyperventilation in patients with severe head injury: A randomized clinical trail. J Neurosurg 75: 731-739, 1991.
25. Feldman Z, Kanter MJ, Robertson CS, et al: Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-inured patients. J Neurosurg 76: 207-211, 1992.
26. Hsiang JK, Chesnut RM, Crisp CB, et al: Early, routine paralysis for intracranial pressure control in severe head injury: Is it necessary? Crit Care Med 22: 1471-1476, 1994.