INTRODUCTION:
Road traffic accidents account for the largest number of head injuries in all ages. They cause 50% to 66% of all head injuries in adults and up to 92% of all head injuried 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 or child without a clear history of trauma. Elderly persons may also sustain head injuries due to abuse (7).

THE CLINICAL PICTURE:

Detailed history from relatives and attendants of a head injured person mostly point to the cause of head trauma.
The clinical evaluation of a patient with head-injury 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, 8) and epidural hematomas (3). 
Systemic effects:
The central nervous system (CNS):
Whatever trivial the injury, patients should be observed for at least 24 hours. 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 (9,10).  MRI can be extremely useful to detect lesions not seen on CT scan and to estimate the age of the lesion (11).
The Glasgow Coma Scale (GCS) is widely used in the assessment of head injuries in adults(Table 1)  (7).  

Table (1): Glasgow Coma Scale (GCS) for adults

          This scale has been modified for infants and young children (Table II) to account for their inability to obey commands and for normal developmental variations (4, 12).

Table (II): Glasgow Coma Scale (GCS) for pediatrics (4, 12)

The cardiovascular system (CVS):
Following head injury, hypertension is a common finding, mostly due to increased cardiac output rather than increased SVR (13).  Brain stem compression, medually ischemia and raised ICP may cause severe hypotension. This hyperdynamic response is responsible for dysrhythmias commonly seen with severe head injury. Such changes may cause myocardial necrosis (14). 
The presence of these CVS changes may complicate the management of head injury with cerebral vaso-spasm because the use of inotropes may worsen myocoardial ischemia. On the other hand, the presence of intracranial pathology may prohibit the use of vasodilators because of their cerebral vasodilator effects.
With the exception of children in whom blood loss from scalp laceration may lead to hypotension, low BP in a patient with acute head injury is usually due to causes other than the head injury and requires prompt treatment.
Acute lung Injury (ALI):
Pulmonary dysfunction is a well-described complication after traumatic head injury. The most common cause is neurogenic pulmonary edema, mostly due to the massive release of epinephrine in the first few seconds of the injury. Other causes of ALI are aspiration of oropharyngeal contents, complications of massive blood transfusion, pulmonary contusion and pneumonia.
Endocrine and electrolyte shifts:
Significant stress reponse leads to hyperglycemia which if not treated will worsen the neurological outcome (15).
Damage to the hypothalamic / pituitary axis may lead to lack of ADH secretion and diabetes insipidus which can cause hypernatremia due to massive water loss. However, hyponatremia is common after head injury and may be asociated with extracellular fluid volume changes.
Stress induced beta-adrenergic stimulation, respiratory alkalosis from hyperventilation and diuretic therapy may result in hypokalemia.
Coagulation distrubances:
These may occur in up to 24% of patients with severe head injury and when severe are indicative of poor outcome (16, 17).  The stress response is also associated with an increased risk of gastric ulceration and gastro intestinal bleeding. 
PATHOPHYSIOLOGY: 
Adults have cerebral blood flow (CBF) of 50 ml/100g/min (18). Infants have CBF like 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, 19).
After traumatic brain injury (TBI), more than 90% of adults and children who die from severe head injuries have histological evidence of ischemia (20, 21).  There was a strong correlation between low CBF and poor outcome, with a higher mortality rate for those with than those without ischemia (20). Ischemia after TBI has been confirmed to occur early after injury in a study using the inhaled stable Xe-enhanced CT scan technique (22).  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.  The study showed CBF measurments as early as 3 hours after the injury  where ischemia was found in one third of the patients. Furthermore, all patients with global ischemia and half the patients with focal ischemia died within 48 hours. CBF when decreased to less than 20ml/100g/min was always associated with poor outcome (23).  Low post-traumatic CBF, though more prevalent in adults, is also seen in children (4). This may be due to massive release of epinephrine as a stress response in the first few seconds of the injury(24).
Obrist et al (25) found that 55% of patients with head injury had hyperemia at some point after the injury and 45% had consistently low CBF. Again, Muizelaar et al (19, 20) 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 (19, 20) proved that children with poor outcome had lower CBF in the first 24 hours, compared with children with higher CBF and better outcome. Therefore, low CBF after head injury, although more prevalent in adults, is also seen in children and is a serious finding in any age.
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 (21). So, DBS may be a characteristic marker of severe head injuries in children(21). DBS can be detrimental because it raises ICP, impairs CBF and it represents an ongoing secondary brain injury.
Among patients who talk after head injury and then deteriorate, young patients (20 years or less) had a 39% chance of haing DBS as the apparent aetiology of their detrioration. Patients over 40 years had only 3% chance of having DBS with a nonfocal lesion and were more likely to have a hematoma (31).
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 patients with head injury is the same for any age. 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 secondary 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. Successful early A,B,C basic life support is a must, if improved outcome is aimed at.
 Of utmost importance is to optimize oxygenation, ventilation and circulation of the head-injured patient because hypoxia and hypercarbia cause cerebral vasodilatation increasing CBF and ICP with a negative impact on the patient outcome, mostly due to hypotension and decreased  cerebral perfusion pressure (CPP). 
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 is one of the most reliable and effective measures to reduce ICP, it may induce cerebral vasoconstriction through hypocarbia decreasing CBF and aggravating brain ischemia (22, 26, 33, 34).  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. It should be aimed to raise BP by fluids and inotropes to maintain adequate CPP.
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 patients 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 patients should be nursed with raised upper half of the body at 15-30º without flexing the neck to facilitate cerebral venous drainage (35).
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 (36).
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 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. Osmotic diuretics can be given within limits of normal plasma osmolality. 
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 fluid volume, inotropes or vasopressors.
During management in the ICU, both hyperthermia and seizures should be aggressively treated if they take place, to reduce CMRO2.  The role of ABG optimization for follow up is crucial.
A special attention should be given to subarachnoid haemorrhage (SAH) if suspected. Subarachnoid haemorrhage following head injury should be scheduled according to Hunt and Hess classification (Table III)(37).

Table (III) Neurological grading system for patients with subarachnoid haemorrhage (37)

CT scan is the method of choice for diagnosis of SAH. Some authors recommend lumbar puncture in critical cases because CT scans may be normal in up to 5% of all cases of SAH (38). To detect early vasospasm, transcranial doppler (TCD) sonography can be performed. Head trauma may be the triggering factor of a ruptured cerebral aneurysm which is a common cause of SAH.
Nimodipine, a calcium channel blocker, proved effective in the management of vasopasm accompanying SAH. (38)  It is interesting to note that the deliberate hypertension used to prevent and treat cerebral vasopspasm after subarachnoid haemorrhage does not appear to increase cardiovascular morbidity. (39)
Special anaesthetic considerations should be adopted if surgery is performed for SAH or ruptured cerebral aneurysm.

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 adults and ensuring adequate oxygenation, ventilation and cerebral perfusion are important cornerstones for better outcome.  Resuscitation at the scene of the accident satisfying the ABC principles of basic life support is ideal for decreasing secondary injury. ICU management should follow an algorithm to manage intracranial hypertension, hyperthermia or seizures.  Team work including anaesthetists, physicians, neurosurgeons, radiologists and nurses can achieve good results.

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