Head Injury:
The study of the cause of death following head injury focuses attention on the important areas. The major cause of death is primary brain damage followed by multiple injuries, cerebral oedema and airway obstruction. These are the commonly recognized causes, the least common cause being intracranial haematomas .
Figure 17.1(a) CT brain scan showing raised intracranial pressure
Pathophysiology of brain injury :
The classical division of brain injury is into primary and secondary damage . This division is clinically useful. Primary brain damage occurs at the time of the injury, produces its clinical effect immediately and has proved resistant to most treatments. Secondary brain damage, on the other hand, occurs some time after the primary impact and is largely preventable and treatable. The importance of managing a head-injured patient is to recognize and document the primary brain damage and subsequently to prevent and treat secondary damage.
While traumatic brain injury results in an extraordinary cascade of neurochemical events, and there is much speculation as to its importance , most reasearch has focused on injuries to the axon, the neurone and the glia. While axonal injury considered to be irreversible with progressive changes in ultrastructure, the blood-brain barrier and neuronal function over time may provide some potential for treatment. While future treatment, currently the main emphasis remains on secondary brain damage which may begin very soon after the impact, necessitating important early management decisions.
Pressure/volume relationship:
The skull is a rigid compartment within which lies the brain, cerebrospinal flud (CSF), blood and extracellular fluid. The volume within the cranial vault is constant and any increase in volume results in an increase in ICP. The relationship between the pressure and volume is expressed in Figure 17.1. The major intracranial volumes are brain parenchyma (1200-1600ml), blood (100-150ml), and CSF (100-150ml). The latter two constitute about 20% of total intracranial volume and part of each is capable of rapid extracranial displacement. The initial increase in intracranial volume is catered for by the loss of CSF from the intracranial compartment, reduction in the amount of blood in the cerebrum followed by compression of brain tissue with herniation of the brain and a decrease in CBF. The redistribution of the CSF and venous blood have little pathological consenquence but a reduction in CBF and the occurrence of brain herniation results in cerebral ischaemia and secondary cerebral damage.
