Complications of head injury

Accelerationdeceleration
 injuries Because the brain floats relatively freely in 'a cushion' of CSF, sudden acceleration or deceleration has an inertia effect, i.e. there is delay between the movement of the head and the corresponding movement of the brain. During this period the brain may be compressed and damaged at the site of impact. In 'contre coup' injuries, brain damage is more severe on the side opposite to the site of impact. Other injuries include: 
• nerve cell damage, usually to the frontal and parietal lobes, due to movement of the brain over the rough surface of bones of the base of the skull
• nerve fibre damage due to stretching, especially following rotational movement 
• haemorrhage due to rupture of blood vessels in the subarachnoid space on the side opposite the impact or more diffuse small haemorrhages, following rotational movement.
Complications of head injury 
If the individual survives the immediate effects, compli-cations may develop hours or days later. Sometimes they are the first indication of serious damage caused by a seemingly trivial injury. Their effects may be to increase ICP, damage brain tissue or provide a route of entry for microbes.

Traumatic intracranial haemorrhage 

Haemorrhage may occur causing secondary brain dam-age at the site of injury, on the opposite side of the brain or diffusely throughout the brain. If bleeding continues, the expanding haematoma increases the ICP, compres-sing the brain. 107.16 Extradural haemorrhage. This may follow a direct blow that may or may not cause a fracture. The individual may recover quickly and indications of increased ICP appear only several hours later as the haematoma grows and the outer layer of dura mater (periosteum) is stripped off the bone. The haematoma grows rapidly when arterial blood vessels are damaged. In children there is rarely a fracture because the skull bones are still soft and the joints have not fused. The haematoma usu-ally remains localised. 
Acute subdural haemorrhage.
 This is due to haemor-rhage from small veins in the dun mater or from larger veins between the layers of dura mater before they enter the venous sinuses. The blood may spread in the sub-dural space over one or both hemispheres . There may be concurrent subarachnoid haemorrhage, especially when there are extensive brain contusions and lacerations. Chronic subdural haemorrhage. This may occur weeks or months after minor injuries and sometimes there is no history of injury. It occurs most commonly in people in whom there is some cerebral atrophy, e.g. older people and in alcoholism. Evidence of increased ICP may bedelayed when brain volume is reduced. The haematoma formed gradually increases in size owing to repeated small haemorrhages and causes mild chronic inflamma. tion and accumulation of inflammatory exudate. In time it is isolated by a wall of fibrous tissue.
Intracerebral haemorrhage and cerebral oedema 

These occur following contusions, lacerations and shearing injuries associated with acceleration and deceleration, especially rotational movements. Cerebral oedema is a common complication' of contusions of the brain, leading to increased ICP hypoxia and further brain damage.
Post-traumatic epilepsy
This is usually characterised by seizures (fits) and may. develop in the first week or several months after injury Early development is most common after severe injuries although in children the injury itself may have appeared trivial. After depressed fractures or large haematomas epilepsy tends to develop later. 
Persistent vegetative state In this condition there is severe brain damage that results in unconsciousness but the vital centres that control homeostasis remain intact, e.g. breathing, blood pressure.
Cerebral hypoxia 
Hypoxia may be due to: 
• disturbances in the autoregulation of blood supply to the brain 
• conditions affecting cerebral blood vessels. When the mean blood pressure falls below about 60 mmHg, the autoregulating mechanisms that control the blood flow to the brain by adjusting the diameter the arterioles fail. The consequent rapid decrease in the cerebral blood supply leads to hypoxia and lack of glutcose. If severe hypoxia is sustained for more than a few minutes there is irreversible brain damage. The neurones are affected first, then the neuroglial cells and later the 

meninges and blood vessels. Conditions in which autoregulation breaks down include: cardiorespiratory arrest 
•. sudden severe hypotension carbon monoxide poisoning hypercapnia (excess blood carbon dioxide) drug overdosage with, e.g., opioid analgesics, hypnotics. Conditions affecting cerebral blood vessels that may ead to hypoxia include: occlusion of a cerebral artery by, e.g., a rapidly expanding intracranial lesion, atheroma, thrombosis or embolism (Ch. 5) 
• arterial stenosis that occurs in arteritis, e.g. polyarteritis — nodosa, syphilis, diabetes mellitus, degenerative . changes in older people. If the individual survives the initial episode of ischaemia, then infarction, necrosis and loss of function of the affected area of brain may occur.