Trauma is the leading cause of death in youth and early middle age, and death is often associated with major head trauma. Head injury contributes significantly to the outcome in more than half of trauma-related deaths. There are approximately 2.5 deaths from head injury per 10 000 population in Australia each year and road traffic accidents are responsible for about 65% of all fatal head injuries.
Head injury may vary from mild concussion to severe brain injury resulting in death. Management of patients requires careful identification of the pathological processes that have occurred.
Pathophysiology of head injury
Most head injuries result from blunt trauma, as distinct from a penetrating wound of the skull and brain caused by missiles or sharp objects. The pathological processes involved in a head injury are:
- direct trauma
- cerebral contusion
- intracerebral shearing
- cerebral swelling (oedema)
- intracranial haemorrhage
In addition, it is likely that following the initial injury there is a ‘secondary injury’ leading to further tissue damage, involving a complex series of destructive biochemical events. These include the possible release of excitotoxic neurotransmitters, such as glutamate, and lipid peroxidation initiated by free oxygen radicals originating from the injured tissue, which leads to a cascade of oxidative damage.
In penetrating injuries the direct trauma to the brain produces most of the damage, but in blunt injuries the energy from the impact has a widespread effect on the brain.
Cerebral contusion may occur locally, under the position of the impact, but often occurs at a distance from the area of impact as a result of a ‘contra-coup’ injury. As the brain is mobile within the cranial cavity a sudden acceleration/deceleration force will result in the opposite ‘poles’ of the brain being jammed against the cranial vault. A sudden blow to the back of the head will cause the temporal and frontal lobes to slide across the skull base, causing contusion to the undersurface of the brain, and to the temporal and frontal poles of the brain as they are jammed against the sphenoid ridge and frontal bones, respectively.
Intracerebral shearing forces result from the differential brain movement following blunt trauma, causing petechial haemorrhages, and tearing of axons and myelin sheaths.
Cerebral swelling occurs either focally around an intracerebral haematoma or diffusely throughout the brain. The process involves a disturbance of vasomotor tone causing vasodilatation and cerebral oedema.
Intracranial haemorrhage following trauma may be intracerebral, subdural or extradural. Intracranial haematoma or cerebral swelling may cause cerebral herniation. The medial surface of the hemisphere may be pushed under the falx (subfalcine), the uncus and parahippocampal gyrus of the temporal lobe herniate through the tentorium, causing pressure on the third nerve and mid-brain (Brain herniation. 1, subfalcine; 2, herniation of the uncus and hippocampal gyrus of the temporal lobe into the tentorial notch, causing pressure on the third nerve and mid-brain; 3, brainstem caudally; 4, cerebellar tonsils through foramen magnum. (Adapted from Kaye AH. Essential Neurosurgery. Oxford: Blackwell Publishing 2005. Reproduced with permission.)), or there may be a caudal displacement of the brainstem and/or cerebellum herniating into the foramen magnum.
Hydrocephalus occurs occasionally early after a head injury and may be due to obstruction of the fourth ventricle by blood or swelling in the posterior fossa, or a result of a traumatic subarachnoid haemorrhage causing a communicating hydrocephalus. This is also an uncommon but important cause of delayed neurological deterioration.
Concussion usually involves an instantaneous loss of consciousness as a result of trauma. The term concussion is not strictly defined in respect to the severity of the injury. However, a minimum criterion is that the patient will have had a period of amnesia. The retrograde amnesia of most cerebral concussion is usually short-term, lasting less than 1 day. The initial retrograde amnesia may extend over a much longer period but gradually diminishes. A more reliable assessment of the severity of the head injury is the post-traumatic amnesia. The concussion is regarded as being severe if the amnesia following the head injury lasts more than 1 day.
The exact definition of concussion remains a contentious issue. The American National Football League established a Committee on Mild Traumatic Brain Injury (MTBI) who have established a much broader definition for concussion which includes an alteration of awareness or consciousness including being ‘dazed’, ‘stunned’, and with features of a ‘post-concussion syndrome’ that include headache, vertigo, light-headedness, loss of balance, blurred vision, drowsiness and lethargy.
The cranial nerves may be injured either as a result of direct trauma by the skull fracture, cerebral swelling, brain herniation or the movement of the brain. The olfactory nerves are most commonly affected.
Eighth nerve damage is often associated with a fracture of the petrous temporal bone and deafness may be conductive, due to a haemotympanum, or sensorineural, as a result of injury to the inner ear or nerve itself.
Facial paralysis is usually associated with a fracture through the petrous temporal bone. It may be either immediate, as a result of direct compression of the nerve, or delayed, due to bleeding and/or swelling around the nerve.
The sixth cranial nerve has a long subarachnoid course and is easily damaged by torsion or herniation of the brain.
The third nerve may also be damaged by direct trauma or by brain herniation, with the herniated uncus of the temporal lobe either impinging on the mid-brain or directly stretching the nerve.
Trauma may result in skull fractures that are classified as simple (a linear fracture of the skull vault), depressed (when bone fragments are depressed beneath the vault; Depressed skull fracture.) or compound (when there is a communication with the external environment, usually from a laceration over the fracture). A fracture of the base of the skull may have a direct connection outside the vault, via the air sinuses.
The extent of the scalp laceration does not necessarily indicate the degree of trauma to the underlying brain.
Traumatic intracranial haematomas
Intracranial haematoma formation following head injury is the major cause of fatal injuries in which death may potentially have been avoidable. Delay in the evacuation of the haematoma may also increase morbidity in survivors.
The general classification of traumatic intracranial haematoma depends on the relationship of the haematoma to the dura and brain. They are classified as extradural, subdural or intracerebral.
Extradural haematomas are more likely to occur in the younger age group because the dura is able to strip more readily off the underlying bone. Although an extradural haematoma may occur in the presence of a severe head injury and coexist with a severe primary brain injury, its important feature is that it may occur when the injury to the underlying brain is either trivial or negligible.
The most common sites of the extradural haematoma are the temporal region followed by the frontal area. Posterior fossa and parasagittal extradural haematomas are relatively uncommon. In most cases the haemorrhage is from a torn middle meningeal artery or its branches, but haematomas may also develop from haemorrhage from extradural veins or the venous sinuses. A fracture overlies the haematoma in nearly all (95%) adults and most (75%) children.
Frequently, extradural haematoma occurs following a head injury that has resulted in only a transient loss of consciousness, and in approximately 25% of cases there has been no initial loss of consciousness. In these patients the most important symptoms are:
- deteriorating conscious state
- focal neurological signs (dilating pupil, hemiparesis)
- change in vital signs (hypertension, bradycardia).
Headache is the main initial symptom in patients who have either not lost consciousness or who have regained consciousness. The headache is often followed by vomiting.
A deteriorating conscious state is the most important neurological sign, particularly when it develops after a ‘lucid’ interval. It is essential that the drowsiness that occurs in a patient following a head injury is not misinterpreted as just the patient wishing to sleep.
Focal neurological signs will depend upon the position of the haematoma. In general, a temporal haematoma will produce a progressive contralateral spastic hemiparesis and an ipsilateral dilated pupil. Further progression will result in bilateral spastic limbs in a decerebrate posture and dilated pupils related to uncal herniation. Occasionally, the hemiparesis may initially be ipsilateral due to compression of the contralateral crus cerebri of the tentorial edge, but only rarely is the opposite pupil involved first.
A change in vital signs shows the classical Cushing response to increased intracranial pressure, that is, bradycardia accompanied by an increase in blood pressure. Disturbances in respiration will develop into a Cheyne—Stokes pattern of breathing.
A computed tomography (CT) scan will show the typical hyperdense biconvex haematoma with compression of the underlying brain and distortion of the lateral ventricle (Extradural haematoma with typical biconvex configuration.).
The treatment of extradural haematoma is urgent craniotomy with evacuation of the clot.
As soon as an extradural haematoma is suspected clinically, the patient should have an urgent CT scan. In some cases the rate of neurological deterioration may be so rapid that there is not sufficient time for a CT scan and the patient should be transferred immediately to the operating theatre. Infusion of mannitol (25% solution, 1 g/kg) or frusemide (20 mg i.v.) may temporarily reduce the intracranial pressure during the transfer to the operating theatre. If unconscious, the patient should be intubated and hyperventilated during the transfer. It is essential that there should be no delay in evacuating the haematoma. An extradural haematoma is a surgical emergency because the haematoma will result in death if not removed promptly.
Subdural haematomas are classified depending on the time at which they become clinically evident following injury: acute (<3 days), subacute (4–21 days) and chronic (>21 days).
A CT scan enables a further classification depending on the density of the haematoma relative to the adjacent brain. An acute subdural haematoma is hyperdense (white) and a chronic subdural haematoma is hypodense. Between the end of the first week and the third week the subdural haematoma will be isodense with the adjacent brain.
Acute subdural haematoma
The acute subdural haematoma frequently results from severe trauma to the head and commonly arises from cortical lacerations.
An acute subdural haematoma usually presents in the context of a patient with a severe head injury whose neurological state is either failing to improve or deteriorating. The features of a deteriorating neurological state (decrease in conscious state and/or increase in lateralising signs) should raise the possibility of a subdural haematoma.
A CT scan will show the characteristic hyperdense haematoma, which is concave towards the brain with compression of the underlying brain and distortion of the lateral ventricles (Acute subdural haematoma with compression of ventricles.). More than 80% of patients with acute subdural haematomas have a fracture of either the cranial vault or base of skull.
Chronic subdural haematoma
Chronic subdural haematoma may follow a significant and often severe head injury, but in approximately onethird of patients there is no definite history of preceding head trauma. The aetiology of the subdural haematoma in this non-traumatic group is probably related to rupture of a fragile bridging vein in a relatively atrophic ‘mobile’ brain. A relatively trivial injury may result in movement of the brain, like a walnut inside its shell, with tearing of the bridging vein. The majority of patients in this group are more than 50 years of age.
If the patient is being treated in hospital for a head injury the presence of a chronic subdural haematoma should be considered if the neurological state deteriorates. Alternatively a patient may present without the history of a significant head injury in one of three characteristic ways:
- Raised intracranial pressure without significant localising signs. Headache, vomiting and drowsiness and the absence of focal neurological signs indicate the possible differential diagnosis of a cerebral neoplasm or chronic subdural haematoma.
- Fluctuating drowsiness.
- Progressive dementia.
Chronic subdural haematoma will be diagnosed on CT scan as a hypodense extracerebral collection causing compression of the underlying brain (Acute subdural haematoma with compression of ventricles.). In 25% of cases the haematoma is bilateral. The chronic subdural haematoma can usually be drained through burr holes.
Intracerebral haematomas occur as a result of a penetrating injury (e.g. a missile injury), a depressed skull fracture or following a severe head injury. They are frequently associated with a subdural haematoma.
An intracerebral haematoma should be suspected in any patient with a severe head injury or a patient whose neurological state is deteriorating. A CT scan will show the size and position of the haematomas (Chronic subdural haematoma.).
A large intracerebral haematoma usually needs to be evacuated. Small intracerebral haematomas are not removed but should be monitored because the haematoma may expand and require evacuation.
The key aspects in the management of patients following head injury are:
- clinical assessment of the neurological and other injuries
- determination of the pathological process involved
- recognition that a change in the neurological signs indicates a progression or change in the pathological processes.
Immediate treatment at the site of the accident involves rapid restoration of an adequate airway and ventilation, circulatory resuscitation, first-aid treatment of other injuries, and the urgent transfer of the patient to hospital. It is essential to avoid hypoxia and hypotension because both will cause further brain injury.
In the management of head injury it is essential to know the type of accident that caused the head inujury and whether the neurological condition is deteriorating. An assessment of the patient's initial neurological condition can be obtained from bystanders at the site of the accident or from the ambulance officers.
Neurological examination will help to determine the type and position of the pathological process and provide a baseline for comparison with subsequent examinations. Although a full neurological examination should be undertaken special emphasis should be given to:
- the conscious state
- pupillary size and reaction
- focal neurological signs in the limbs.
An assessment should be made of the retrograde amnesia and post-traumatic amnesia, if possible.
There is a continuum of altered consciousness from the patient being alert and responding appropriately to verbal command to those who are deeply unconscious. Drowsiness is the first sign of a depressed conscious state. As the level of consciousness deteriorates, the patient will become confused. The use of the words ‘coma’, ‘semi-coma’ or ‘stuporose’ should be avoided because they convey different meanings to different observers. The assessment is more accurate and reproducible if the Glasgow Coma Scale (GCS) is used (Table 48, “The Glasgow Coma Scale”). This scale gives a numerical value to the three most important parameters of the level of consciousness: eye opening, best verbal response and best motor response. The exact response can be shown on a chart or the level of consciousness can be given as a numerical score (the sum of the three parameters of the GCS). A score of 8 or less indicates a severe injury.
|Best verbal response||Oriented||5|
|Best motor response to painful stimulus||Obeys commands||6|
|Localise to pain||5|
|Flexion to pain (withdrawal)||4|
|Extension to pain||2|
Careful evaluation of the pupil size and response to light is essential at the initial clinical assessment and during further observation. Raised intracranial pressure causing temporal lobe herniation will cause compression of the third nerve, resulting in pupillary dilatation that nearly always occurs initially on the side of the raised pressure. The pupil will initially remain reactive to light but will subsequently fail to respond at all to light. As the intracranial pressure increases, this same process commences on the opposite side.
Neurological examination of the limbs will assess the tone, power and sensation. A hemiparesis will result from an injury of the corticospinal tract at any point from the motor cortex to the spinal cord. Following a severe brain injury the limbs may adopt an abnormal ‘posturing’ attitude. The decerebrate posture consists of the upper limbs adducted and internally rotated against the trunk, extended at the elbow and flexed at the wrist and fingers, with the lower limbs adducted, extended at the hip and knee with the feet plantar flexed. Less frequently the upper limbs may be flexed, probably due to an injury predominantly involving the cerebral white matter and basal ganglia, corresponding to a posture of decortication.
Particular attention must be given to the patient's ventilation, blood pressure and pulse. At all times it is essential to ensure the patient's ventilation is adequate. Respiratory problems may result either as a direct manifestation of the severity of the head injury or due to an associated chest injury.
Pyrexia frequently occurs following a head injury. A raised temperature lasting more than 2 days is usually due to traumatic subarachnoid haemorrhage or may occur in patients with a severe brainstem injury.
Careful assessment must be made of any other injuries. Chest, skeletal, cardiovascular or intra-abdominal injury must be diagnosed and the appropriate management instituted. Hypotension or hypoxia may severely aggravate the brain injury.
Radiological assessment following the clinical evaluation will be essential unless the injury has been minor. A CT scan will show the macroscopic intracranial injury and should be performed if:
- the patient is persistently drowsy or has a more seriously depressed conscious state
- there are lateralising neurological signs
- there is neurological deterioration
- there is cerebrospinal fluid (CSF) rhinorrhoea
- there are associated injuries that will entail prolonged ventilation so that ongoing neurological assessment will be difficult.
The indications for a skull X-ray have diminished since the introduction of the CT scan, especially as the bony vault can be assessed by the CT scan using the bone ‘windows’.
It is important to note that radiological assessment of the cervical spine is essential in all patients who have sustained a significant head injury, particularly if there are associated facial injuries.
Following the clinical and radiological assessments, subsequent management will depend on the severity of the injury and the intracranial pathology.
Minor head injury
Any patient who has suffered a head injury must be observed for at least 4 hours. The minimum criteria for obligatory admission to hospital are given in Minimum criteria for obligatory admission to hospital after head injury.
Further management of these patients will be by careful observation, and neurological observations should be recorded on a chart displaying the GCS scores.
Should the patient's neurological state deteriorate, an immediate CT scan is essential to re-evaluate the intracranial pathology. Further treatment will depend on the outcome of the scan.
Severe head injury
The management of a patient following a severe head injury depends on the patient's neurological state and the intracranial pathology resulting from the trauma. In general, the following applies.
The patient has a clinical assessment and CT scan as described previously. If the CT scan shows an intracranial haematoma causing shift of the underlying brain structures then this is evacuated immediately.
Following the operation, or if there is no surgical lesion, the patient should be carefully observed and the neurological observations recorded on a chart with the GCS scores. Measures to decrease brain swelling should be implemented, including management of the airway to ensure adequate oxygenation and ventilation (hypercapnia will cause cerebral vasodilatation and so exacerbate brain swelling), elevation of the head of the bed to 20 degrees, and maintenance of fluid and electrolyte balance. Normal fluid maintenance with an intake of 3000 mL per 24 hours is optimum for the average adult. Blood loss from other injuries should be replaced with colloid or blood, not with crystalloid solutions. Pyrexia may be due to hypothalamic damage or traumatic subarachnoid haemorrhage, but infection as a cause of the fever must be excluded. The temperature must be controlled because hyperthermia can elevate the intracranial pressure, will increase brain and body metabolism, and predisposes to seizure activity. Adequate nutrition must be maintained as well as routine care of the unconscious patient, including bowel and bladder care, and pressure care.
More aggressive methods to control intracranial pressure are advisable if the patient's neurological state continues to deteriorate and the CT scan shows evidence of cerebral swelling without an intracranial haematoma, there is posturing (decerebrate) response to stimuli, or the GCS score is less than 8.
An intracranial pressure monitor will also be useful in patients requiring prolonged sedation and ventilation as a result of other injuries. Measurement of the intracranial pressure will provide another useful monitoring parameter, and any sustained rise in the pressure will be an indication for careful reassessment and, if necessary, CT scan.
The techniques used to control intracranial pressure include controlled ventilation maintaining PaCO2 at 33–38 mm Hg, CSF drainage from a ventricular catheter and diuretic therapy, using intermittent administration of mannitol or frusemide. Mild hypothermia, achieved by cooling the patient to 34°C is possibly of benefit. Other techniques such as barbiturate administration, to reduce cerebral metabolism and intracranial pressure, and hyperbaric oxygen have been advocated in the past but have not been shown to have any proven benefit. Steroid medication is of no proven benefit in head injury.
Management of associated conditions
A large scalp laceration may result in considerable blood loss. When the patient arrives in the emergency department, ‘spurting’ arteries should be controlled with haemostatic clips prior to a sterile bandage being applied to the head. After initial assessment and stabilisation the wound should be closed without delay. The hair should be shaved widely around the wound, which should be meticulously cleaned and debrided. The closure should be performed in two layers if possible, with careful apposition of the galea prior to closing the skin.
If the scalp wound has resulted in loss of soft tissue the wound may need to be extended to provide an extra ‘flap’ of healthy tissue so that the skin edges can be approximated without tension.
There is no specific management for a simple skull fracture without an overlying skin injury, although it is an indication that the trauma was not trivial and it should provide a warning that a haematoma may develop beneath the fracture.
A skull fracture may be compound because of an overlying scalp laceration or if it involves an air sinus. The scalp wound should be debrided and closed. A short course of prophylactic antibiotics should be administered to reduce the risk of infection.
Depressed skull fracture
If the depressed skull fracture is compound, prophylactic antibiotics and tetanus prophylaxis should be administered. Surgery, usually requiring a general anaesthetic, should be performed as soon as possible.
Cerebrospinal fluid rhinorrhoea
A fracture involving the base of the anterior cranial fossa may cause tearing of the dura, resulting in a fistula into the air sinuses. This type of fistulous connection should also be suspected if the patient suffers an episode of meningitis or if the radiological investigations show a fracture in the appropriate site. An intracranial aerocele is proof of a fistulous connection. Cerebrospinal fluid rhinorrhoea may also occur as a result of a fistula through the tegmen tympani into the cavity of the middle ear and leakage via the Eustachian tube.
Surgery should be performed if CSF leakage persists, if there is an intracranial aerocele, or if there has been an episode of meningitis in a patient with a fracture of the anterior cranial fossa.
Some form of rehabilitation is essential following any significant head injury. If the injury has been relatively minor, then the rehabilitation necessary may involve only advice and reassurance to the patient and family. Following a severe head injury, rehabilitation will also usually involve a team of paramedical personnel, including physiotherapists, occupational therapists, speech therapists and social workers.
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