Head injury is the most common cause of death in children between the ages of 1 and 15. Those who survive severe head injuries suffer enormous problems: although the ability to walk and talk may suggest a satisfactory outcome, changes of personality and blunting of subtle (‘higher’) intellectual activities responsible for tact and judgement may render such patients unemployable and difficult to live with. Those who suffer less severe injuries may develop post-concussion syndrome. They require proper informed counselling, which they often fail to receive.

Head injuries can be somewhat imprecisely divided into penetrating injuries due to missiles and non-penetrating injuries from other causes. A careful history must be taken to ensure that conditions such as diabetic coma, subarachnoid haemorrhage, or epilepsy have not caused the patient to fall, the head injury being a secondary event in these circumstances.

The management of head injuries is easier if the pathology and mechanism are understood. Complications can often be anticipated if the cause and pattern of an injury are known.

Examination of the scalp often reveals the site and type of injury. In general, blunt injuries cause bruising: a sharp object causes a ragged laceration, often localized, and the presence of an underlying depressed skull fracture needs to be excluded.

Blunt injuries to the skull, caused by the head hitting the road, for example, result in linear fractures. Considerable distortion of the skull without fracturing may occur in infant because of the elasticity of the skull; the sutures may, however, spring apart.

Linear fractures often radiate to the skull base, guided by the greater wing of the sphenoid and the petrous bone. Thus linear fractures in the anterior cranial fossa may open into the frontal or ethmoid air sinuses, or may run across the cribriform plate, causing anosmia. The fracture then becomes compound to the nose or paranasal sinuses and cerebrospinal fluid rhinorrhoea occurs. If the nasal pressure is increased by nose blowing or if the intracranial pressure falls after excessive drainage of cerebrospinal fluid by lumber puncture, reversal of flow in this fistula may cause air or bacteria to enter the intracranial cavity. Brain tissue often plugs the fracture, and the rise of intranasal pressure caused by nose blowing forces air into the brain, producing an aerocele, or occasionally into the ventricle, producing a spontaneous air ventriculogram which is apparent on radiographs. Meningitis or brain abscess may occur in such circumstances. Fractures of the anterior cranial fossa may also involve the optic foramen, causing damage to the optic nerve and permanent blindness.

Linear fractures radiating into the middle fossa may cross the middle meningeal vessels and cause an extradural haematoma (Fig. 1) 2268. Other fractures may involve cranial nerves (third, fifth, and sixth), the sphenoid air sinus, the pituitary gland, and the internal carotid artery.

Fractures situated more posteriorly may run along the petrous bone, affecting the middle and inner ear. If the ear drum is ruptured blood or cerebrospinal fluid may leak out (otorrhoea). Facial palsy may result from bruising of the facial nerve in its canal; auditory nerve damage commonly causes permanent deafness. Fractures radiating into the posterior fossa may rupture the large venous sinuses and cause a venous extradural haematoma (Fig. 2) 2269.

Sharp injuries exert their force over a small area and the skull is ‘pushed in’. The inner table of the skull is more extensively affected than the outer table. Often the dura is not penetrated and the component pieces of the depressed fracture are interlocked, with hair firmly wedged between the bones. In more severe injuries the dura is penetrated by fragments of bone which may pierce the brain.

Such injuries may be missed, for the scalp wound is small and apparently insignificant. An inexperienced doctor may fail to associate an innocent looking injury in an alert patient with a depressed or even penetrating skull fracture.

Blunt injuries are usually associated with acceleration and deceleration of the brain resulting in diffuse brain damage and, at the very least, concussion. If such acceleration and deceleration of the brain does not occur, for example in a crush injury, there is no loss of memory or consciousness, no concussion and little brain damage, but the skull damage is severe. Any acceleration force will cause the brain to impinge on the skull at the point of impact, while cerebrospinal fluid is displaced to the opposite pole. The reverse occurs during deceleration, when the head comes to rest. Frontal or occipital blows cause the brain to shift in an anteroposterior direction, but lateral movement is limited by the falx. More glancing blows will cause rotatory movements of the skull and brain. Acceleration–deceleration may therefore cause two types of brain damage: diffuse and local.

Diffuse neuronal damage to the cerebral white matter is due to rotatory shearing movements. When mild this is the pathological basis of concussion. When severe the patient is left demented with a spastic diplegia, reflecting the diffuse nature of severe brain damage. Less often the brain-stem and the cerebellum or both bears the brunt of the damage.

Local brain damage usually occurs when the frontal or temporal poles accelerate or decelerate into the roof of the orbit or wing of the sphenoid. Local damage usually occurs at the site of impact or at the opposite pole (‘contrecoup’). Bruising and laceration of the brain is associated with intracerebral, subarachnoid, and subdural bleeding, and brain swelling.

Sharp injuries cause local brain damage without concussion, because no acceleration or deceleration occurs. The brain damage is adjacent to the depressed fracture and consists of bleeding and swelling of the brain. A compound fracture, in which the overlying scalp is lacerated may be followed by infection. These injuries produce similar problems to penetrating missile injuries.

It is not possible to describe the myriad of possible clinical features following a head injury. Care of patients with head injury consists of recognizing concussion and any other complicating factors. Major complications cause a deterioration in level of consciousness, preventing the expected improvement of an uncomplicated head injury. A thorough appreciation of pathology of head injuries allows the possible effects of a head injury including concussion, extradural haematoma, subdural haematoma, brain swelling, other traumatic complications, and traumatic epilepsy, to be considered.

The attending doctor has four duties when faced with head-injured patients. These are known as the ABCD of head injuries.

An unconscious patient must be treated immediately, even before full assessment has been undertaken. The most important duty is to clear and maintain the airway. Loose teeth, blood, and vomit must be removed and the airway maintained by laying the patient semiprone, with the foot of the bed raised and an airway inserted. In the absence of a cough reflex a cuffed endotracheal tube is required.

Baseline observations must be made as soon as possible so that any change of intracranial pressure can be appreciated. Ideally these observations should be assessed by the ambulance crew, who must report them to the receiving doctor.

The conscious level is determined by the response of the patient to various stimuli defined by the Glasgow coma scale (Section 38.1, Table 2 590). These parameters should be used rather than ill-defined levels of consciousness which mean different things to different people. If the patient is conscious then the length of amnesia before and after the accident must, if possible, be assessed.

The pulse, blood pressure, respiratory rate and temperature, must be measured at half-hourly intervals, or more frequently.

Fixed dilated pupils may not only be due to severely raised intracranial pressure. A blind eye will have a dilated pupil unreactive to direct light but reactive to consensual light in the opposite eye. A patient may have dilated pupils following an epileptic fit; this may cause confusion if the epilepsy was not witnessed. Morphine should not be given, not only because it causes small and fixed pupils but because it affects the level of consciousness. Direct trauma to the third cranial nerve will cause an immediate fixed dilated pupil which bears no relation to the patient's conscious level.

These must be anticipated by reconstructing the site, type, and force of injury from the scalp and skull damage. A skull radiograph must be obtained before the patient leaves the casualty department. An extradural haematoma is most likely to occur in patients with a combination of a skull fracture and impaired conscious level when seen in the accident department.

This must include details of the accident, the injuries sustained, and the level of consciousness when first seen.

Complete examination of the patient must be performed, including a neurological examination to establish the baseline observations and to determine whether there are focal neurological signs or meningeal irritation. Careful examination of the scalp, ears, and nose will disclose bruising, bleeding, or leakage of cerebrospinal fluid. If a neck injury is suspected neck stiffness should not be assessed until after radiographs of the cervical spine have been examined.

A low blood pressure suggests bleeding elsewhere (abdomen, chest, or a fractured pelvis); head injuries, except in children, do not cause hypotension unless scalp bleeding is severe.

It may be difficult to diagnose paraplegia or tetraplegia due to spinal injury in an unconscious head-injured patient. Features which are useful indicators of spinal injury are:

1.Flaccid weakness of the limbs.

2.Retention of urine (incontinence being usual in head injuries).

3.Measurement of sweat level (or sensory level if the patient is conscious).

4.A low blood pressure with warm limbs (warm shock due to a traumatic sympathectomy).

It is particularly important to recognize extradural haematoma. This may occur in the presence of little or no primary brain injury, but if unrecognized causes death or brain damage. Early removal of the haematoma allows full or nearly full recovery because of the small amount of brain injury at the time of the blow. Patients most at risk of this complication have impaired consciousness and a skull fracture.

The importance of maintaining a clear airway in any severely head-injured patient has already been emphasized. Blood must be taken for grouping and cross-matching, intravenous fluids must be administered, and long limb fractures splinted; this is undertaken before full assessment of the injuries, and certainly before any radiographs are taken.

Most scalp lacerations should be sutured under local anaesthesia after the more important complications of the injury have been treated. Treatment of severe wounds may require general anaesthesia. It is important that an underlying depressed fracture is not missed; this should be avoided if a proper history is taken, the skull radiograph is carefully examined, and the wound is carefully inspected. If there is doubt the wound can be gently palpated with a gloved finger.

The edges of a scalp laceration should be excised after adequate shaving and cleaning. Approximation can usually be achieved with or without undermining the adjacent scalp. A large scalp defect will need to be covered by a formal rotation flap. The scalp should be repaired in two layers; the deep layer in the galea takes the tension, while the skin sutures stop the bleeding. These can be removed after 3 days. Extreme care should be taken in the treatment of scalp wounds to prevent infection. Antitetanus immunization and antibiotics should be given. An infected scalp wound is usually a sign of inadequate primary treatment.

Vault fractures may be linear or depressed, compound or penetrating, depending on whether the force applied was blunt or sharp. Linear fractures require no treatment, apart from proper treatment of any scalp wound that is present. The importance of this fracture lies in the possible complications associated with it.

Depressed fractures of the skull may be non-compound or compound (when the overlying scalp is breached). These are best treated in a neurosurgical unit. The fracture is exposed and hair is removed from between the bone fragments, which are then elevated. Thorough debridement is performed and if the dura has been penetrated, the brain is inspected. The dura must be closed, using a free graft of pericranium if necessary. Any clean bone fragments can be replaced, but if the wound is seriously contaminated the bone fragments should be removed and the defect closed 6 months later with an acrylic prothesis. Attempts at primary repair of the skull with acrylic have been most disappointing because of a high incidence of infection. Prophylactic antibiotics should be administered.

Closed depressed fractures do not need treatment unless there is associated intracranial bleeding or unless the depression is obvious and constitutes a cosmetic disability. The latter need not be corrected urgently; such a depression in a young child almost always corrects itself in time.

These may be produced either by radiation from the vault or by fractures of the middle third of the face extending upwards to the cribriform plate and ethmoid air sinuses. Complications of such fractures have already been described; cerebrospinal fluid rhinorrhoea is the most important. When this occurs clear salty fluid is noticed dripping from one or both nostrils, usually in the first week after the injury, but sometimes some months later. Patients with ‘a cold in one side of the nose’ should be consider to have cerebrospinal fluid rhinorrhoea until proved otherwise. The best way of demonstrating this is to lie the patient face down over the bed and gently squeeze the jugular veins. Fluid should be collected and tested for sugar, or even better, acetylcholinesterase, the presence of which confirms the origin of the fluid. Patients should be given prophylactic antibiotics and told not to blow their nose.

Rhinorrhoea usually stops spontaneously, but if there is doubt about its persistence, or if meningitis occurs, fascial repair of the anterior cranial fossa should be performed. Rhinorrhoea associated with a middle third fracture of the face almost always stops when the fracture is reduced. Cerebrospinal fluid otorrhoea almost always subsides spontaneously, but it must be remembered that rhinorrhoea may arise from the middle ear via the eustachian tube if the ear drum is intact.

The essential feature of concussion is amnesia for the blow: a patient who can clearly recollect the blow has no concussion. The length of time the patient is amnesic after the blow is called post-traumatic amnesia, and this is the best biological marker of the severity of concussion. ‘Islands’ of memory may occur but should be discounted; post-traumatic amnesia extends until the patient has continuous memory for who he is, what time it is, and where he is, i.e. ‘for person, time and place’. Only an observer can assess the length of time in coma which will be shorter than the period of post-traumatic amnesia. Post-traumatic amnesia is constant and does not recede with time, unlike retrograde amnesia.

The pathological basis for the impaired brain function associated with concussion has recently been demonstrated by MRI. This impairment of brain function is difficult for patients to describe, but it is essentially a difficulty with holding several facts in mind, and with making correlations and deductions, especially at speed. Judgement and decision taking therefore become very difficult. Concussion with post-traumatic amnesia lasting only 30 min may produce such difficulties for several weeks.

Many patients suffer from remarkably consistent ‘post-concussional syndrome’, consisting of headache, irritability, depression, and vertigo. The consistent nature suggest an organic basis, rather than the previously suggested functional basis, for this condition. It seems more common following minor concussion, perhaps because patients return to work too soon, feeling that little damage was done. The best treatment is prevention by adequate counselling and explanation, but this is often not carried out. Patients may also complain of rotatory vertigo which is probably due to disruption of the delicate otoliths in the ear. This subsides slowly, but explanation and reassurance is equally important.

A concussive blow, by definition and tradition, is associated with full recovery. More severe deceleration/acceleration injuries can cause severe concussion which merges with the permanent brain damage that, at its most profound, is called a persistent vegetative state. Repeated concussive blows may lead to permanent brain damage, as is seen in ‘boxer's encephalopathy’.

The criteria governing admission of this group of patients to hospital are shown in Table 2 592. Patients no longer suffering from post-traumatic amnesia (and careful questioning may be needed to determine this) do not require admission if they have someone to care for them at home. A ‘head injury card’ explaining when to return to hospital should be given to the patient's relatives on discharge. If a patient is confused or has a skull fracture, or if it is difficult to assess the patient in the accident department or there is no one to care for the patient in the home, admission is necessary.

The speed with which the patient can resume normal activities and return to work depends on the severity of headache; reassurance and explanation concerning the impaired higher intellectual functioning of the brain is essential. Too early a return to work causes depression, anxiety, and the post-concussional syndrome.

Intracranial complications of head injury are shown in Table 4 594; of these, extradural haematoma is the most important. Suspected meningitis is the only indication for lumber puncture after a head injury. Diabetes insipidus may occur after basal fractures that tear the pituitary from the hypothalamus. Inappropriate secretion of antidiuretic hormone may also occur, resulting in low sodium levels. These may cause coma and epilepsy.

Extradural haematoma may be associated with an insignificant brain injury, being essentially caused by a skull fracture crossing and rupturing the middle meningeal artery or a large venous sinus (Figs 1, 2) 2268,2269. The patient suffers little or no concussion, or may have completely recovered consciousness on arrival at hospital. Extradural haematoma may also be superimposed on a more severe brain injury. In such patients the conscious level may not improve as would be expected if damage was due solely to concussion. Extradural haematomata usually present in the first 24 h after injury, but they may present later. This is particularly the case if an atypical extradural haematoma develops due to a fracture rupturing the venous sinus and causing a more slowly developing ‘venous’ bleed (Fig. 3) 2270,2271. The dura is stripped from the bone at the site of the blow; knowledge of this will lead to the site of the haematoma and to the site at which the skull has to be opened.

Bruising of the scalp at the site of the injury is classically in the temporal region and causes a ‘boggy’ swelling, due to a haematoma in the temporalis muscle. There is often a skull fracture across the middle meningeal artery or a large venous sinus. Rarely, particularly in children, there may be no such fracture. A conscious patient may experience severe and increasing headache and restlessness due to distortion of the pain-sensitive dura. Other causes of restlessness include a painful distended bladder or a fracture elsewhere. Other features of raised intracranial pressure may also be present. Deterioration of the conscious level is the most important sign of increasing intracranial pressure.

Dilatation of a pupil is a late sign signifying severe brain-stem distortion. The diagnosis must be made before this stage. Once both pupils become dilated and fixed, decerebrate rigidity develops and is followed shortly by respiratory failure and death,

An extradural haematoma adjacent to the motor cortex may cause contralateral weakness with an extensor plantar response. Tentorial coning may occasionally cause such signs on the side of the clot. Focal or generalized epilepsy may also occur.

An extradural haematoma must be treated as soon as possible. The best recovery is seen in patients treated before the development of coma and severe brain-stem distortion. There is little to gain in transferring a patient with a rapidly expanding haematoma to a neurosurgical unit some distance away. Now that CT scanning is able to reveal the exact location of the haematoma, any surgeon can make a burr hole to release the clot; a 3 cm incision is made over the extradural haematoma (at the site of the blow) down to the skull bone (Fig. 1) 2268. The pericranium is scraped to one side and a self-retaining retractor is inserted. Severe bleeding occurs in patients with raised intracranial pressure, but this can easily be controlled if a self-retaining retractor is left in place during the subsequent transfer of the patient to the neurosurgical unit. The haematoma immediately exudes from a burr hole: the dura and brain are already pushed away from the skull. The burr hole can be enlarged to allow more of the haematoma to be removed. The condition of the patient will improve immediately, allowing safe transfer to a neurosurgeon who can then perform a formal craniotomy flap. If the haematoma develops more slowly the patient can be transferred without the need for a prior emergency burr hole.

A delayed or missed diagnosis of extradural haematoma is an important cause of preventable mortality and morbidity after head injury (Fig. 2) 2269. This is particularly tragic since the primary injury is often slight and the brain damage minimal. Diagnosing intracranial bleeding can be difficult, but if the two major risk factors of a depressed conscious level and a skull fracture are considered and all accident and emergency units are equipped with CT scanners, mortality and morbidity should improve.

Acute subdural haematomata usually follow damage to the frontal or temporal poles of the brain and are associated with considerable brain swelling, bruising, and subarachnoid bleeding (Fig. 4) 2272. They are often bilateral and arise some distance from the site of the blow, which is usually in the occipital or frontal region, allowing the brain to move anteroposteriorly. A skull fracture may or may not be present.

Acute subdural haematoma may occasionally be caused by rupture of the draining, bridging vein in the presence of minimal primary brain damage. These patients present with features similar to those of an extradural haematoma, but without scalp or skull damage.

The initial brain injury is usually severe, and the patient often remains unconscious for hours or weeks. Evidence of raised intracranial pressure is present, with deterioration of the conscious level or failure to improve. Headache and restlessness are important features. Focal neurological signs, usually contralateral pyramidal signs or epilepsy, may also occur, as can meningeal irritation due to subarachnoid bleeding.

A CT scan will reveal the site and nature of the haematoma and allow evacuation, either through a burr hole (enlarged to a craniectomy) or a formal craniotomy flap. The prognosis depends on the degree of primary brain injury (Fig. 4) 2272.

Cerebral ischaemia may cause deterioration in conscious level. The most important cause is respiratory insufficiency due to failure to maintain the airway. Attention to this may produce a dramatic improvement in the conscious level of the patient, and should always be considered before an emergency burr hole is created. The airway may also be compromised during an unobserved epileptic fit.

Other causes of cerebral ischaemia are rare. Carotid artery thrombosis is uncommon but may be associated with fractures of the sternum. It is characterized by a sudden hemiplegia with relatively little impairment of the conscious level. The diagnosis is confirmed by angiography.

Fat embolism causes coma 2 or 3 days after the injury. A rapid pulse, petechial haemorrhages in the skin and conjunctiva, together with exudates and haemorrhages in the retina is suggestive of the diagnosis. The blood oxygen level is low.

Caroticocavernous fistula is the least common complication of a head injury and is characterized by pulsating exophthalmus and a bruit. The patient often describes this sensation as ‘crows crowing’; the doctor will hear a machinery murmur throughout systole and diastole when the eyeball is auscultated (Fig. 5) 2273.

Brain swelling increases intracranial pressure in the absence of an intracranial haematoma (Fig. 6) 2274. The swelling usually occurs several hours after the injury, and may develop rapidly in children. CT scanning is the best way to differentiate this condition from an intracranial haematoma. The precise pathophysiological mechanism and the reasons for its alarming presentation in children are unknown.

Treatment is unsatisfactory. Dexamethasone is of no value and the value of hyperventilation to reduce the carbon dioxide level of the blood is uncertain. Intracranial pressure monitoring is particularly appropriate for this condition: any elevation of pressure beyond 25 to 30 mmHg should be treated by an intravenous bolus of 20 per cent mannitol. The fluid balance has to be carefully monitored: renal failure due to excessive dehydration can complicate this treatment, but those patients who survive seem to appear better than those given other treatments.

Cranial nerve damage is not rare. Anosmia commonly follows frontal or occipital blows to the head which cause avulsion of the olfactory nerve fibres passing through the cribriform plate. Delayed facial palsy follows petrous fractures, but recovery always occurs. Deafness may be perceptive or conductive; occasionally it is due to dislocation of the auditory ossicles, and may be remediable.

‘Immediate epilepsy’ at the time of blow has no prognostic importance. Epilepsy occurring within 1 week of the injury is particularly common in patients with an intracranial haematoma, focal neurological signs, or with a skull fracture, especially if post-traumatic amnesia lasts longer than 24 h. Such early epilepsy may indicate the presence of an extradural or subdural haematoma, and may presage late epilepsy.

‘Late epilepsy’, occurring after the first week following injury occurs particularly in patients who have had ‘early epilepsy’ and in those who have developed an intracranial haematoma. Other risk factors are a depressed fracture, especially in association with penetration of the dura, early epilepsy, or post-traumatic amnesia of over 24 h. About 50 per cent of patients who develop late epilepsy do so in the first year after an injury but onset is delayed for more than 4 years in 25 per cent of those affected. Once late epilepsy develops it usually persists. Risk factors should be considered when advising patients whether they can drive following injury, and when advising about the use of prophylactic anticonvulsants.

Missiles cause penetrating injury and localized brain damage. The exit wound is larger than the entry wound. The speed of the missile is the most crucial factor determining the amount of brain damage (the energy dissipated equals MV&sub2; where M is the mass and V the velocity of the missile). Death occurs from overwhelming brain damage; those who survive may suffer devastating impairment of brain function. There is a 40 per cent chance of epilepsy developing after such injuries.

These injuries are treated in the same way as compound depressed penetrating fractures, the brain being debrided gently after the entry and exit wounds have been excised. The dura and scalp should be closed.

Chronic subdural haematoma in infancy usually occurs in the first 6 months of life. The haematoma consists of liquefied brown blood collected between the dura and arachnoid and extending laterally over the cerebral hemisphere. The condition is often bilateral.

The majority of patients have a history of injury, with rupture of a bridging vein between the cerebral hemisphere and superior sagittal sinus following an occipital or frontal blow. Blood collects in the subdural space and accumulates due to recurrent bleeding from the vascular subdural membrane produced by the initial bleed.

The liquefied blood is bound on the dural aspect by a thick membrane of granulation and fibrous tissue that can be peeled away from the dura. The deep aspect is limited by a thinner membrane, which can be stripped from the arachnoid. In some patients, clear or faintly yellow fluid may be found rather than altered blood. Such a subdural hygroma is thought to arise from a tear in the arachnoid causing a valvular leak of CSF into the subdural space. Subdural hygromas are not associated with a well-defined membrane: the whole extent of the subdural space on both sides of the falx may be distended with fluid.

Occasionally a subdural hygroma may occur secondary to meningitis, particularly that caused by Haemophilus. Children with blood coagulation disorders are at risk of subdural haematoma, and this should be considered if there is no obvious traumatic history.

These are due to raised intracranial pressure, but seizures may also be a presenting feature. The child is usually brought to hospital with a history of vomiting, drowsiness, or restlessness, or because of enlargement of the head or bulging of the anterior fontanelle. A large head with retinal or subhyloid haemorrhages are characteristic signs of intracranial bleeding in an infant.

The CT scan confirms the diagnosis. Bleeding and clotting times should be checked, and if meningitis may be causing the subdural effusion, a lumbar puncture should be performed. This is particularly important if seizures are the presenting feature.

Percutaneous aspiration of the (liquefied) subdural haematoma may be carried out by passing a needle through the lateral extremity of the anterior fontanelle. Aspirations may be repeated two or three times, but if refilling occurs, as is usually the case with a hygroma, shunts need to be introduced. Two ordinary silastic tubes can be inserted between the subdural space and the pleural cavities: expensive shunt systems are not required since long-term shunting is not necessary. Once the subdural space is empty the subdural space becomes obliterated by adhesions (sealing the arachnoid tear), and recurrence is unusual.

Chronic subdural haematoma usually occurs in patients over the age of 60. Prompt treatment may result in complete recovery. A history of a mild head injury is sometimes obtained, but the injury is often not serious enough to render the patient recumbent. Bleeding arises from ruptured bridging veins from the brain to the superior sagittal sinus, and the haematoma enlarges by recurrent bleeding from the vascular subdural membrane. The (liquefied) haematoma usually takes several weeks to accumulate, and it may be bilateral. Underlying cerebral atrophy makes raised intracranial pressure less obvious, but brain-stem distortion and tentorial coning occurs early and is responsible for many of the features (Fig. 7) 2275.

Clinical features typically fluctuate because of the ‘cystic’ nature of the haematoma. Occasionally a subdural haematoma may be due to bleeding from a dural metastatic deposit; more commonly patients are taking anticoagulants.

Headache and fluctuating drowsiness are the two most important features of a chronic subdural haematoma. Seizures are rare. Other signs which occur, such as ptosis of the eyelids and limitation of upward gaze are due to midbrain distortion. Papilloedema is not common except in younger patients.

Dementia is not a feature of a subdural haematoma: an alert demented patient who happens to have a subdural collection will not be helped by its evacuation. In many cases subdural blood will leak out slowly, its presence being secondary to underlying cerebral atrophy, and surgical removal will only produce a further collection. Patients who do well are those in whom the subdural fluid shoots out under considerable pressure, with rapid obliteration of the subdural space by the expanding brain.

Frontal and parietal burr holes are made, opening the dura and then the outer membrane of the subdural haematoma to release the liquefied clot. It is important to identify the subdural membrane to be certain that a dural venous lacuna is not being mistakenly opened. Warm Ringer's solution is then irrigated from one burr hole to the other to wash out the haematoma fluid. The brain should expand fairly rapidly to meet the dura and obliterate the subdural space, especially at the posterior burr hole. This process can be encouraged by tilting the operating table head down. Seizures are rare in these patients and they do not need prophylactic anticonvulsants. They should be advised against driving for at least 6 months.

Jennett WB, Teasdale G. Management of Head Injuries. Philadelphia: Davis, 1981.