CHAPTER 18 Neurosurgery
Head injuries
In the UK, head injuries account for annual attendance rates at A&E departments of almost 1 million people. Head injuries account for nine deaths per 100 000 population and in young males, account for 15–20% of all deaths. Some 20% of all patients attending A&E departments with head injuries are admitted, and over 25% of these have alcohol-related head injuries. More than 50% of all patients admitted with head injuries are discharged within 24 h. Head injuries, therefore, cause a considerable workload and bed occupancy. It is therefore necessary to have a protocol to decide which patients need admission and which patients need further investigation.
It is recommended that all patients are monitored using the Glasgow Coma Scale after initial resuscitation (→ Table 4.1, in Ch. 4). In all cases, the diagnosis and initial treatment of serious extracranial injuries takes priority over investigations of head injury, or transfer to a neurosurgical unit.
Criteria for urgent CT scan and consultation with a neurosurgical unit
The presence of one or more of the following:
Criteria for hospital admission after recent head injury
The presence of one or more of the following:
Skull radiography after recent head injury
CT scan is the preferred option. A skull radiograph images the skull but provides no information about the brain and therefore is of little use. All patients suffering a significant head injury should have a CT scan, which in most cases will identify any skull fracture.
Simple scalp laceration is not a criterion for skull radiography if the history can exclude a significant impact.Types of brain injury
Primary
This is the damage caused as an immediate result of trauma. It results in contusions, lacerations or diffuse brain damage. Treatment cannot reverse primary brain injury.
Assessment of head injury
Emergency
Evaluate CNS injury
Assess the level of consciousness as this is the most significant factor after head injury. Use GCS (→ Table 4.1) and check pupillary reactions. Pupillary changes may indicate brain swelling or compression. Pressure on a cerebral hemisphere causes the third nerve on that side to be stretched over the edge of the tentorium. The resultant paralysis of the nerve allows unopposed action of the dilator pupillae under the control of the sympathetic nervous system and the pupils dilate. There is also loss of light reaction of the pupil on the affected side. If compression continues, the contralateral third nerve is compressed and the opposite pupil also dilates and is fixed to light. Bilateral fixed dilated pupils in a patient with a head injury are a grave prognostic sign and recovery is rare. Pupillary changes are always late signs (‘undertaker signs’), and are always preceded by an alteration in conscious level caused by raised intracranial pressure. Direct blows to the eyes can cause dilated pupils in patients without severe brain injury.
CNS examination
This may be difficult in the unconscious patient. Observe the pattern of limb movement in response to painful stimuli. Progressive unilateral weakness or focal epilepsy may be helpful localizing signs. Obtain a history from witnesses to the event, e.g. speed of impact, height of fall, state of crash helmet.
Check for CSF rhinorrhoea or otorrhoea
Check for these signs. Periorbital bruising and retromastoid bruising imply basal skull fracture.
Scalp lacerations or depressed fractures
Check these using a gloved finger. If in doubt, perform a CT scan.
Assess amnesia
Post-traumatic amnesia (loss from time of the injury) gives an assessment of the severity of the injury. Retrograde amnesia correlates poorly with the severity of the injury. Post-traumatic amnesia of >1 week signifies severe damage. Patients seen initially may appear fully conscious and orientated. Do not make allowances when assessing. They are often amnesic of events in A&E when asked at a later date.
CT and MRI brain scanning
Computerized tomography (CT) and magnetic resonance imaging (MRI) provide very rapid and highly accurate detail of the brain. CT also provides excellent bone detail and should be performed if a significant brain injury is suspected. Resuscitation must always precede any form of imaging, however sophisticated. MRI is not at present necessary for management of acute head injury but may provide important prognostic data. A cervical spine X-ray or CT scan of the cervical spine is mandatory for all significant head injuries and must include C7/T1.
Skull fractures
A skull fracture is an indication for hospital admission. Patients with skull fractures are more likely to suffer secondary brain damage. Skull fractures are classified as closed, i.e. the skin over the underlying fracture is intact, or open (compound) where the skin overlying the fracture is broken, or the fracture connects with an air sinus or the external auditory canal.
They may be further classified as follows:
Linear, stellate or comminuted non-depressed
These fractures are serious if they cross major vascular channels, e.g. the groove for the middle meningeal artery.
Depressed fracture
A portion of the vault of the skull is depressed inwards. Surgery may be required to elevate the fracture.
Compound comminuted fractures with damage to the underlying brain
These are treated by removing all bony fragments, debridement and closure. Failure to remove all bony fragments may lead to development of cerebral abscess. They are associated with epilepsy.
Fractures of the base of the skull
They usually involve the anterior or middle cranial fossa. Those affecting the anterior fossa may cause nasal bleeding, periorbital haematoma, subconjunctival haemorrhage, CSF rhinorrhoea and cranial nerve injuries (I–V). Middle cranial fossa fractures involving the petrous temporal bone may cause bleeding from the ear, CSF otorrhoea, bruising over the ear and over the mastoid, and cranial nerve injuries (VII and VIII).
Summary
The emphasis in the management of head injuries is on damage to the underlying structures rather than on any skull fracture per se. CT scanning is the investigation of choice for patients with head injury and no patient with a significant head injury should be admitted to a hospital A&E department that does not have immediate 24-hour access to CT scanning.
Management of CSF leakage
It may be difficult to distinguish bleeding from blood mixed with CSF. Place a drop of the blood-stained discharge on a clean white gauze. If CSF is present there will be a spreading yellowish ring around a central stain of blood (halo sign). CSF leakage implies that the dura and arachnoid are torn and therefore there is a potential pathway allowing infection to spread to the meninges and brain. The head of the bed should be elevated 30°. The patient should be advised not to blow their nose. In many cases, the leakage settles spontaneously but all CSF leaks should be referred for a neurosurgical opinion. Where CSF rhinorrhoea occurs do not pass a nasogastric tube. Do not pack the nose or ears.
Intracranial bleeding
This may be extradural, subdural (acute or chronic) and intracerebral. Subarachnoid haemorrhage commonly follows trauma.
Extradural
This results from bleeding between the bone and the dura. It is most likely to occur when a fracture occurs in the temporal region crossing the middle meningeal artery. It may occasionally occur without a fracture. Usually low-speed injury.
Symptoms and signs
History of head injury (may be relatively minor). Temporary concussion. Recovery (‘lucid interval’), then increasing headache, decreased conscious level, coma. There may be no lucid period or the patient may have the signs when admitted unconscious. Falling pulse rate. Rising BP. Reduced and irregular respiration. Dilated ipsilateral pupil. Contralateral hemiparesis or focal fits. May be boggy swelling overlying the site of the fracture as extradural blood may track through the fracture and into the subcutaneous tissues.
Treatment
This is a true emergency and requires neurosurgical assistance. If none is immediately available and the patient’s condition is critical despite resuscitation, i.v. mannitol should be given and ventilation commenced. A burr hole should be made over the suspected site of clot. Enlarge the hole with bone-nibbling forceps. Gently evacuate the clot. Clip or diathermy the bleeding vessel.
Subdural
Acute
This results from tearing of small bridging veins that bleed into the subdural space and is usually associated with a lacerated brain resulting from high-speed injuries. The haematoma spreads over a large area. The patient usually has marked brain injury at the outset and is comatose but the condition deteriorates further. Can rarely be caused by a ruptured aneurysm, which can cause the patient’s collapse and a secondary head injury. The history of the event should distinguish from primary trauma.
Symptoms and signs
Severe head injury. May be rapid deterioration. Signs of raised ICP. Localizing signs. Pupillary inequality.
Chronic
Usually in the elderly. Brain shrinkage makes the bridging veins between cortex and venous sinuses vulnerable. May have only been a trivial and forgotten head injury. It may occur weeks or months after the injury, presenting with neurological signs, headache or coma, confusion or personality change. A brain tumour may be suspected in the differential diagnosis. There may be fluctuating level of consciousness.
Intracerebral
This occurs as a result of primary brain injury but may expand causing secondary brain damage. It may extend into the ventricles. A discrete haematoma may require craniotomy if the patient’s condition deteriorates. Always consider other primary causes for the intracerebral haematoma causing collapse and secondary head injury.
Complications
Meningitis
Organisms enter via compound skull fractures. Prophylactic antibiotics should be used for all compound fractures. Current prophylaxis includes cefuroxime given for a minimum of 1 week. It is not necessary for the drug to cross the blood–brain barrier if given for prophylaxis but it is necessary for it to cross the blood–brain barrier if given for specific treatment of meningitis.
Cerebral hypoxia
This is a major and preventable cause of secondary brain injury. Respiratory failure after head injury may be peripheral or central. Peripheral causes include upper airway obstruction, e.g. tongue; vomit; chest injuries; pneumothorax; pneumonitis; shock lung. Central causes include primary brainstem injury or depressant drugs, e.g. alcohol. Hypertension may also contribute.
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