Traumatic brain injury: intracranial haemorrhage, diffuse

• Traumatic brain injury is damage to brain tissue caused by an external force; most cases are mild, but a minority become life-threatening, and much of the damage happens after the first blow.
• Severity is graded with the Glasgow Coma Scale: 13 to 15 mild, 9 to 12 moderate, and 3 to 8 severe; a total score of 8 or below is usually treated as coma.
• The dangerous primary lesions are extradural, subdural, subarachnoid and intracerebral haemorrhage and diffuse axonal injury; raised intracranial pressure and brain shifting, not the impact alone, explain most late deterioration.
• The aim of acute care is to stop secondary brain injury by protecting the airway, oxygenation, blood pressure and intracranial pressure, then to evacuate collections that act as a mass.
• Evidence-based imaging rules (NICE NG232 and the Canadian CT head rule) select who needs a CT, and modern therapy targets an intracranial pressure of 22 mm Hg or less and a cerebral perfusion pressure of 60 to 70 mm Hg.

By the end of this page you should be able to:

1. Define traumatic brain injury, grade its severity with the Glasgow Coma Scale, and explain primary versus secondary injury.
2. Recognise extradural, subdural, subarachnoid, intracerebral haemorrhage and diffuse axonal injury on CT and explain their different behaviour.
3. Explain how raised intracranial pressure develops, the Cushing triad, and how brain herniation occurs.
4. Apply the NICE NG232 and Canadian CT head rule criteria to decide who needs a CT head scan.
5. State the intensive care targets for intracranial and cerebral perfusion pressure and the stepwise measures to achieve them.
6. State the indications for neurosurgical discussion and evacuation.
7. Recognise how head and spinal injury assessment and care overlap.
8. Recall the key cautions from the Brain Trauma Foundation 4th edition and ATLS-aligned management.

Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. Injuries may be open (penetrating the skull and meninges) or closed; closed injuries from acceleration and deceleration are the more common and are the focus here. Each year more than 1 million people attend emergency departments in England and Wales with a recent head injury; roughly 200,000 are admitted, about 40,000 have evidence of traumatic brain injury, and about 2,000 die from their injury, so this is both a common and consequential condition.^[2]

Most injuries are mild: a short confusion and headache. A minority are severe, and here the risk shifts over time. Much of the disability and many deaths come not from the blow itself but from what follows it: hypoxia, hypotension, bleeding inside the skull and brain swelling that raise the pressure. The whole acute strategy is therefore aimed at preventing secondary brain injury while the primary injury heals or is removed.^[1] ATLS and its related courses remain the framework for the first hour of assessment.^[2]

This page works within that clinical picture and also links the brain to the injured spine, because head trauma and spinal trauma often occur together and share the same early priorities: airway with cervical spine control, oxygenation, and blood pressure.

TBI is any trauma to the head other than superficial injuries to the face, whether the injury is a closed head injury or a penetrating head injury.^[2]

The useful classification for a clinician is by mechanism and by severity.

• Mechanism. Open (penetrating) injuries breach the skull and meninges; closed injuries are produced by impact, acceleration, deceleration and rotation, with damage at the point of impact (coup), at the opposite pole (contrecoup) and diffusely.^[1]
• Severity on arrival. Graded by the Glasgow Coma Scale: 13 to 15 mild, 9 to 12 moderate, 3 to 8 severe.^[1][2]
• Primary versus secondary. Primary injury is the immediate structural and cellular damage caused by the event itself. Secondary injury is the delayed damage that follows: cerebral oedema, ischaemia, hypoxia, hypotension, hypercapnia or hypocapnia, excitotoxicity and further bleeding. Secondary injury can be prevented or limited, which is why monitoring and targets matter more than the initial scan in severe cases.^[1]

Closed injuries are particularly prone to diffuse axonal injury because rotation and deceleration are harder to control in a rigid skull than in an open injury.

Traumatic brain injury is a leading cause of death and disability worldwide, with road traffic crashes, falls, assault and sport collisions the usual causes.^[1]

The pattern varies with age and setting. Falls dominate in both young children and older adults. Motor vehicle crashes are an important cause across all ages and often produce severe injury. In a trauma system built on road traffic, chest and abdominal injuries often accompany the head injury.^[1][2]

Two groups deserve early recognition. Older adults often have smaller falls than expected for their brain injury because of brain atrophy and often take antiplatelet or anticoagulant drugs; chronic subdural collections can present weeks later with subtle confusion. Children have different physiology, different imaging rules and different cervical injury patterns. Pregnancy is managed by protecting the mother first according to trauma principles, with imaging used when indicated.

Roughly one in three adults in the United States who receives treatment for a severe TBI dies (mortality about 25 to 33 percent).^[1]

There are no simple modifiable risk factors for most TBIs; the causes are largely accidental. The factors that make injury more likely or more severe are practical:

• Falls from height, stairs and ladders, especially in older people.
• Road traffic collisions involving pedestrians, cyclists and ejected passengers, which also figure in imaging criteria as dangerous mechanisms.^[2]
• Contact sport and repeated minor brain injury, which raise concern about long-term change.
• Child abuse, which must be considered in any head injury in an infant or young child.
• Anticoagulation or a bleeding tendency, which converts a minor fall into a serious intracranial haemorrhage.
• Violence and self-harm.^[1][2]

The skull is a rigid box. Its contents - brain, blood and cerebrospinal fluid - occupy a fixed volume, so an increase in one (a haematoma, swollen brain) has to be matched by a decrease in another, mostly cerebrospinal fluid and venous blood.^[1] Once compensation is exhausted, intracranial pressure (ICP) rises and cerebral perfusion falls.

Cerebral perfusion pressure (CPP) is the difference between mean arterial pressure (MAP) and mean intracranial pressure. As ICP rises (or MAP falls), CPP falls. When CPP is below 50 mm Hg the brain becomes ischaemic.^[1]

Primary damage occurs at the moment of impact and includes:

• Fracture of the skull with contusion, laceration or cranial nerve injury.
• Primary axotomy: direct tearing of axons under shear forces. Complete primary axotomy is uncommon; it is a massive, widespread event and is now considered rare.^[6]
• Contusions and the haemorrhages described below.
• Damage to the larger vessels causing epidural, subdural, intracerebral or subarachnoid bleeding.

Diffuse axonal injury (DAI) occurs when rotational deceleration imposes shear-type forces on the brain, producing generalized, widespread disruption of axonal fibres and myelin sheaths. By the current pathological and imaging definition it is multiple scattered small haemorrhagic or non-haemorrhagic lesions concentrated in the white matter, with impaired axoplasmic transport, axonal swelling and disconnection.^[1][6]

Clinically it is suspected when loss of consciousness lasts more than 6 hours, often with a Glasgow Coma Scale score under 9, in the absence of a mass lesion or midline shift. Milder forms produce neurocognitive symptoms that can resemble post-concussion symptoms.^[1][6]

The usual locations are the grey-white junction of the cerebral hemispheres, the corpus callosum, the internal capsule, the cerebral peduncles and the brainstem. Petechial microhaemorrhages in these regions are the CT signature, though early CT is often normal and MRI (SWI, GRE, DWI and DTI) is far more sensitive.^[1][4][6]

The accepted grading of the pathological lesion is that of Adams and colleagues: grade 1 is axonal damage in white matter (cerebral hemispheres, corpus callosum, brainstem and occasionally cerebellum); grade 2 adds a focal lesion in the corpus callosum; grade 3 adds a focal lesion in the dorsolateral quadrant of the rostral brainstem.^[4][6] This grading has never been validated against imaging or outcome and should not be used as a proxy for prognosis.^[6]

Why rotation matters more than a straight blow: the skull turns under the brain, so white matter of different densities rotates at different speeds and shear develops at the grey-white junction. Axonal damage happens in two phases. The mechanical deformation (primary axotomy) is rare in survivable injury; much more important is secondary axotomy, which plays out over hours as microtubules stiffen and break, calcium floods the cell, calpain hydrolyses the cytoskeleton, mitochondrial failure follows, and apoptosis and disconnection occur. This creates a therapeutic window early after injury before the second phase becomes fixed.^[6]

Loss of consciousness and coma can occur from diffuse axonal injury without any raised intracranial pressure, because the lesions involve the thalami and the reticular substance of the brainstem. Brainstem rotation on the transverse axis is particularly associated with coma, whereas the same force in the vertical plane is not.^[6]

After injury the brain swells. Oedema, hyperaemia, haematoma, hydrocephalus from intraventricular blood and seizures all take up volume. As compensation ends, ICP rises and CPP falls. Ischaemia produces further oedema, which raises ICP further - the secondary cascade.^[1]

When ICP is markedly raised at 25 mm Hg or more, the classic Cushing triad appears: hypertension (usually with widened pulse pressure), bradycardia, and slow or irregular breathing. These are late signs and carry a poor prognosis.^[1] A raised ICP can also produce decorticate or decerebrate posturing and autonomic disturbance including sympathetic storms.

Brain herniation is the terminal event. Rising pressure pushes brain tissue across the tentorium or through the foramen magnum (uncal, subfalcine and transtentorial herniation). Clinically this means coma, pupillary change (often a unilaterally dilated fixed pupil in uncal herniation), hemiplegia and the Cushing triad. Many secondary brain injuries are preventable; this is why early targets, osmotherapy and neurosurgery are all directed at intracranial pressure before these signs appear.^[1]

All numbers and appearances below are supported by standard trauma references.^[1]

This is a collection of blood between the skull and the dura mater. The large or rapidly expanding form is usually arterial, classically from the middle meningeal artery damaged by a temporal bone fracture, and without intervention the patient can deteriorate rapidly and die. A smaller venous extradural haematoma is less dangerous. A classic initial lucid interval followed by headache and falling consciousness is common, although not universal, and transtentorial herniation may follow quickly.^[1]

It differs from subdural collection in three ways on CT: the extradural collection is lentiform, does not cross suture lines and usually sits in the temporal region; subdural blood is crescent-shaped and can cross suture lines.

This is bleeding between the dura mater and the arachnoid, usually from lacerated bridging veins during deceleration. Acute subdural haematoma is common with severe trauma, falls and underlying cerebral contusion and produces acute neurological dysfunction, sometimes with focal deficits. It carries a high mortality because the underlying brain is usually more injured than the name suggests. Chronic subdural collections develop over weeks, often in older people, heavy alcohol users and those on anticoagulant or antiplatelet drugs, who may have forgotten a trivial injury. Edema and raised pressure are unusual in the chronic form.^[1]

Intracerebral haematomas in trauma arise from coalescence of contusions, often in the frontal and temporal lobes, and can increase intracranial pressure and cause herniation, particularly when they lie in the temporal lobe.^[1] Traumatic subarachnoid haemorrhage is seen frequently over the cerebral convexities, and in contrast to aneurysmal subarachnoid haemorrhage, which centres deep in the basal cisterns, it is a marker of severe injury and a risk factor for later deterioration.^[1]

See the mechanism above. The clinical signature is prolonged loss of consciousness with altered level of consciousness in the absence of a mass lesion, and CT often shows only microhaemorrhages or nothing at all. Later MRI finds the deeper lesions. Large lesions on susceptibility-weighted MRI may not translate into worse outcome as expected, so imaging grade should not override the clinical examination.^[4][6]

Symptoms overlap across the different lesions. There may be no initial loss of consciousness; minor TBI can follow a concussive insult with confusion and amnesia alone. More severe injury presents with prolonged unconsciousness, seizures (often within the first hour or day), altered level of consciousness from confusion to coma, amnesia, headache, vomiting and focal deficit.

• Extradural haematoma: in the classic course headache, impairment of consciousness and focal deficit develop over minutes to hours, sometimes after a lucid interval, and herniation commonly causes contralateral hemiparesis and ipsilateral pupillary dilatation.^[1]
• Acute subdural haematoma: orientation, arousal and cognition are impaired, with headache, seizures, hemiparesis, signs of raised intracranial pressure and, in severe cases, pupillary asymmetry, abnormal brainstem reflexes and coma from uncal herniation.^[1]
• Intracerebral haemorrhage and contusions: focal deficits such as hemiparesis, progressive decrease in consciousness, or both.^[1]
• Diffuse axonal injury: loss of consciousness for more than 6 hours, altered level of consciousness, speech or memory difficulty without focal motor deficits; milder forms produce headache, dizziness, confusion and concentration problems.^[1]

Signs of raised intracranial pressure include headache, vomiting, altered consciousness and focal deficits; when ICP reaches 25 mm Hg or more, the Cushing triad appears. Vomiting may occur with raised ICP but is not specific.^[1]

Signs of basilar skull fracture, which are highly associated with intracranial haemorrhage, are leakage of cerebrospinal fluid from the nose or ear (rhinorrhoea, otorrhoea), blood behind the tympanic membrane (haemotympanum), Battle sign (bruising behind the ear), raccoon eyes (periorbital ecchymosis), loss of smell or hearing, and facial nerve impairment. Nasogastric and nasotracheal tubes must not be passed through the nose in these patients.^[1]

The differential diagnosis is essentially the differential of an abnormal CT and of impaired consciousness after trauma. The confounders are functional and medical:

• Alcohol or drug intoxication mimicking impaired consciousness. Assuming intoxication as the cause is only justified once important traumatic brain injury has been excluded.^[2]
• Hypoglycaemia, post-ictal state, infection or sepsis, stroke or intracranial tumour unrelated to trauma.
• Cervical spinal cord injury causing apparent paralysis or respiratory depression.
• Hyperglycaemia and metabolic derangement in polytrauma.

On imaging, each collection has the shape and distribution described in the table above, and the CT cannot reliably distinguish a small venous extradural collection from a mass. If a mass is surgically significant, a neurosurgeon decides on evacuation, not the CT report alone.

CT criteria are meaningless without an accurate clinical assessment. The Glasgow Coma Scale (GCS) scores eye opening, verbal and motor responses with a total from 3 to 15, and is used for triage, airway decisions and prognosis. Values measured after resuscitation are more specific for brain dysfunction than the first reading; sedation and hypotension both depress the score.^[1][2]

Severity by total score is defined as 13 to 15 mild, 9 to 12 moderate and 3 to 8 severe, with scores of 8 or below usually regarded as coma.^[1][2] GCS values must be recorded as eye, verbal and motor components as well as the total, because they communicate progress better than a single number.^[2]

Non-contrast CT of the head is the initial investigation of choice in significant head trauma. It is fast, available in most trauma systems, and detects haematomas, contusions, fractures, shift and hydrocephalus.^[1][2] MRI is not used as the primary investigation; it is reserved for later detection of subtle contusions, diffuse axonal injury and brainstem injury, and for prognosis.^[2]

NICE NG232 (published 18 May 2023, with minor updates in July, August and October 2023 and March 2025) standardises early head-injury care. For adults (16 and over) with a head injury, a CT head scan is done within 1 hour if any of the following are identified:

• a GCS score of 12 or less on initial assessment in the emergency department;
• a GCS score below 15 at 2 hours after the injury;
• suspected open or depressed skull fracture; ^[5]
• any sign of basal skull fracture (haemotympanum, "panda" eyes, cerebrospinal fluid leaking from the ear or nose, Battle sign); ^[5]
• post-traumatic seizure;
• focal neurological deficit;
• more than 1 episode of vomiting.^[2]

If there has been some loss of consciousness or amnesia, a CT is done within 8 hours of injury (or within 1 hour if presenting later) when any of these are present: age 65 or over; any current bleeding or clotting disorder; a dangerous mechanism (pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle, or a fall from more than 1 m or 5 stairs); or more than 30 minutes of retrograde amnesia before the injury.^[2]

For people taking anticoagulant or antiplatelet treatment (other than aspirin monotherapy), CT is considered within 8 hours of the injury, or within 1 hour if presenting later, even without other indications.^[2]

NICE advises that a CT scan is not the primary investigation for every trivial injury, that radiation should be minimised, and that plain skull X-rays do not diagnose important brain injury. A provisional written radiology report should be available within 1 hour of the scan.^[2]

The Canadian CT head rule is an externally validated decision rule for patients presenting within 24 hours of injury with a GCS of 13 to 15 and witnessed loss of consciousness, amnesia or disorientation. It excludes patients under 16, those with GCS below 13, those on anticoagulation or with bleeding disorders, pregnant patients, those with obvious open skull fracture, those having a seizure after injury and unstable major trauma patients.^[5]

For eligible patients, CT is indicated if any of the following high-risk (neurosurgical intervention) factors are present:

• GCS below 15 at 2 hours after injury;
• suspected open or depressed skull fracture;
• any sign of basal skull fracture (haemotympanum, "panda" eyes, Battle sign, cerebrospinal fluid otorrhoea or rhinorrhoea);
• vomiting of 2 or more episodes;
• age 65 years or more.^[5]

If no high-risk factor is present, CT is recommended if any medium-risk (brain injury on CT) factor is present:

• retrograde amnesia of 30 minutes or more before the impact;
• a dangerous mechanism: pedestrian struck by a motor vehicle, occupant ejected from a motor vehicle, or a fall from more than three feet or five stairs.^[5]

Clinical comparisons between the Canadian CT head rule and the New Orleans criteria consistently report high sensitivity for clinically important brain injury, with the Canadian rule showing better specificity for CT-requiring lesions.^[5]

ICP monitoring is recommended for patients with severe TBI who cannot follow simple commands, especially those with an abnormal head CT, and for patients with a GCS of 3 to 8 after resuscitation. Ventricular catheters are the gold standard measure and can also drain cerebrospinal fluid; parenchymal monitors measure local pressure and cannot be recalibrated in place. Intracranial pressure monitoring is not routinely indicated in mild or moderate TBI.^[1][3]

The Brain Trauma Foundation 4th edition (2017) advises ICP monitoring for salvageable patients with severe TBI (GCS 3 to 8 after resuscitation) and an abnormal CT (haematoma, contusion, swelling, herniation or compressed basal cisterns); with a normal CT, monitoring is indicated when 2 or more of these are present: age over 40, unilateral or bilateral motor posturing, or systolic blood pressure below 90 mm Hg. Using information from ICP monitoring is recommended to reduce in-hospital and 2-week mortality.^[3]

The principal severity score is the Glasgow Coma Scale, as defined above. TBI severity is also commonly classified pathologically by the Marshall CT classification or the Rotterdam CT score, both of which use CT findings and predict mortality.^[1]

Important severity-linked categories for this page:

• Mild TBI: GCS 13 to 15. Management is observation, or discharge with return precautions when imaging is normal, symptoms are minor and a reliable observer is available.^[1][2]
• Moderate TBI: GCS 9 to 12. Admit and observe; deterioration is common and repeated CT may be needed.^[1][2]
• Severe TBI: GCS 3 to 8. Rapid sequence intubation, critical care, and monitoring and treatment of intracranial pressure as indicated.^[1][2]

Concussion is diagnosed when transient alteration in mental status after mechanical force is not explained by brain injury seen on neuroimaging; loss of consciousness under 30 minutes and post-traumatic amnesia under 24 hours are part of the standard mild TBI definition. CT by definition shows no acute intracranial haemorrhage or contusion, although small linear skull fractures may be present.^[1][2]

Diffuse axonal injury may be suspected when loss of consciousness exceeds 6 hours in the absence of a mass lesion or midline shift, and when microhaemorrhages are seen on MRI, even if the initial CT is normal.^[1]

Initial treatment follows trauma life support principles: airway with cervical spine control, breathing, circulation and disability (Glasgow Coma Scale and pupils).^[1][2]

• People 16 and over with head injury should be assessed and managed initially according to the principles embodied in ATLS, the European Trauma Course, International Trauma Life Support and related courses.^[2]
• For a GCS of 8 or less, arrange a pre-alert call so that experienced staff and imaging are ready on arrival.^[2]
• In the emergency department, assessment within 15 minutes of arrival; stabilise airway, breathing and circulation before other injuries.^[2]
• Pain control matters because pain raises intracranial pressure; fluids must be maintained, limb fractures splinted and the bladder catheterised when needed.^[1][2]
• For patients with a head injury and a GCS of 12 or less, tranexamic acid 2 g intravenously (15 to 30 mg/kg up to a maximum of 2 g in patients under 16) should be considered if there is no active extracranial bleeding, given as soon as possible within 2 hours of injury and before imaging.^[2]
• Hypotonic fluids such as 5 percent dextrose in water are contraindicated because of excess free water, which increases brain oedema and pressure.^[1]

Discussion with a neurosurgeon is mandatory for anyone with new surgically significant imaging abnormalities, with the definition agreed between the neuroscience unit and referring hospitals. Regardless of imaging, a neurosurgeon should be involved if the patient has any of the following: persisting coma with a GCS of 8 or less after resuscitation; unexplained confusion lasting more than 4 hours; deterioration in GCS after admission; progressive focal neurological signs; a seizure without full recovery; a definite or suspected penetrating injury; or a cerebrospinal fluid leak.^[2]

Additional factors that suggest that surgery is needed urgently are a midline brain shift of more than 5 mm, compression of the basal cisterns, worsening neurological examination, large or arterial extradural haematomas, temporal lobe lesions causing swelling, and traumatic intracerebral collections with mass effect or raised pressure. Small intracerebral or subdural collections and small venous extradural collections can often be managed conservatively with close imaging.^[1][2]

The intensity of care should be local and protocol-driven; the following is a physiological summary. When intracranial pressure is clearly threatened or confirmed raised, the goal is to protect perfusion while lowering pressure, using the least invasive step that works.

• Intubate and ventilate patients with a GCS of 8 or less, those needing transfer, and anyone with loss of airway reflexes, ventilatory insufficiency (PaO2 below 13 kPa on oxygen, or PaCO2 above 6 kPa) or irregular respirations.^[2]
• Aim for a normal PaCO2 of 38 to 42 mm Hg in routine severe TBI; oxygen saturation should be maintained above 90 percent and PaO2 above 60 mm Hg, or above 13 kPa in transfer settings.^[1][2]
• Propofol-style sedation is commonly used in adults to prevent agitation and surges in pressure; paralytics, if needed, must be accompanied by adequate sedation.^[1]
• Adequate pain control usually requires opioids.^[1]

• Elevate the head of the bed to 30 degrees and keep the head midline to improve cerebral venous drainage.^[1]
• Drain cerebrospinal fluid through an external ventricular drain when one is in situ. Continuous drainage may lower the intracranial pressure burden more effectively than intermittent drainage.^[1][3]

• Maintain euvolaemia and a serum osmolality of 295 to 320 mOsm/kg (295 to 320 mmol/kg).^[1]
• Hypertonic saline (3 percent or 23.4 percent) is a more effective osmotic agent than mannitol and is given as a bolus or continuous infusion to keep ICP at 20 to 25 mm Hg; serum sodium is monitored and kept at 155 mEq/L or below.^[1]
• 20 percent mannitol is an alternative, rapidly expanding intravascular volume, so it must be used cautiously in coronary, cardiac, renal or pulmonary congestion. Prolonged use can cause water depletion and hypernatraemia. Furosemide helps reduce total body water when the volume load of mannitol is undesirable.^[1]
• Furosemide and fluid and electrolyte balance should be monitored closely when osmotic diuretics are used.^[1]

Sedation can prevent agitation, excessive muscular activity and response to pain, and helps prevent increases in intracranial pressure. Propofol is often used in adults because of quick onset and brief action, although hypotension is common; benzodiazepines and dexmedetomidine are used in children and can be used in adults. Antipsychotics can delay recovery and should be avoided if possible.^[1]

For patients who undergo intracranial pressure monitoring, the usual goal is to keep ICP under 25 mm Hg (some centres use a cut-off of 20 mm Hg) and the cerebral perfusion pressure close to 60 mm Hg.^[1]

Current published targets differ slightly, which is normal in severe TBI practice. The Brain Trauma Foundation 4th edition recommends treating ICP above 22 mm Hg because values beyond that are associated with increased mortality, and a CPP target of 60 to 70 mm Hg, while avoiding aggressive attempts to keep CPP above 70 mm Hg because of the risk of respiratory failure.^[3]

Cerebral perfusion pressure should therefore be kept at 60 to 70 mm Hg in severe TBI, with the minimum threshold (60 or 70 mm Hg) adjusted to the patient's autoregulatory status and local protocol.^[3] The blood pressure thresholds from the same guideline are a systolic blood pressure of at least 100 mm Hg for patients aged 50 to 69 years, and at least 110 mm Hg for patients aged 15 to 49 or over 70 years, to reduce mortality.^[3]

Routine prophylactic hyperventilation to a PaCO2 of 25 to 35 mm Hg is not recommended, because vasoconstriction reduces cerebral perfusion and potentiates ischaemia; it should be avoided completely in the first 24 hours after injury when cerebral blood flow is often critically reduced. It is reserved for the first several hours and for ICP unresponsive to other measures, targeting a PaCO2 of 30 to 35 mm Hg, with an increased inspired oxygen concentration.^[1][2][3]

During transfer of patients with raised ICP, a PaCO2 target of 4.5 to 5.0 kPa is justified, using more aggressive hyperventilation if needed, while maintaining a mean arterial pressure of at least 80 mm Hg.^[2]

Decompressive craniectomy may be considered when increased intracranial pressure is refractory to other measures or as a primary measure with a significant haematoma; whether it improves long-term outcome is uncertain. NICE specifically considers neurosurgery for mass lesions, a midline shift above 5 mm, or ICP refractory to medical treatment.^[1][2]

High-dose barbiturates induce burst suppression and are not recommended prophylactically against intracranial hypertension, but high-dose barbiturate therapy is recommended to control ICP refractory to maximum standard medical and surgical treatment, with hemodynamic stability before and during therapy. Propofol is recommended for ICP control, but not for improved mortality or 6-month outcome, and high-dose propofol can produce significant morbidity.^[3]

Therapeutic systemic hypothermia has not been shown to help in large multicentre trials, and early (within 2.5 hours), short-term (48 hours post-injury) prophylactic hypothermia is not recommended in diffuse injury.^[1][3]

High-dose glucocorticoids are not recommended to decrease cerebral oedema and ICP. In severe TBI, high-dose methylprednisolone is associated with increased mortality and is contraindicated. Glucocorticoids increased mortality and severe disability in a large randomised trial.^[1][3]

Seizure prophylaxis: prophylactic phenytoin or valproate is not recommended for preventing late post-traumatic seizures (after 7 days), and early use is reserved for patients with significant structural injury (larger contusions or haematomas, brain laceration, depressed skull fracture) or a GCS below 10, usually for less than 1 week. Early (within 7 days) phenytoin reduces early post-traumatic seizures when the benefit is felt to outweigh the complications.^[1][3]

The following table summarises the highest-yield differences between older and current teaching, all from the same sources above.

The recognisable complications after traumatic brain injury include:

• Raised intracranial pressure and herniation, cerebral oedema, and hydrocephalus after intraventricular blood.
• Seizures (early and late), infection after skull base fracture, and chronic subdural collection.
• Coagulopathy, which should be corrected.
• Pulmonary, cardiac and renal complications from polytrauma and autonomic disturbance.
• In the longer term, cognitive and emotional deficits, personality change, sleep disturbance and post-traumatic epilepsy; poor smell and vision may persist.

The complications of spinal cord injury that concern the same trauma patient are pneumonia and respiratory failure (especially cervical), deep venous thrombosis (a high risk in the first months without prophylaxis), pressure injury, autonomic dysreflexia (after the acute phase of spinal cord injury), spasticity and urinary sepsis. These overlap so closely with the head-injured patient's care that head and spine are planned together.

Adults with severe TBI who are treated have a mortality of about 25 to 33 percent. Most improvement happens within the first 6 months, and children recover better than adults with a comparable injury. Cognitive deficits (concentration, attention, memory) and personality change are more commonly disabling long-term than focal motor or sensory deficits. Over 40 percent of adults with severe TBI have a good recovery or only moderate disability. A persistent vegetative state lasting 3 months makes recovery of normal function unlikely, and almost none recover after 6 months.^[1]

Prevention is largely public-health rather than clinical: road-traffic safety, helmet use, fall prevention in older adults, child car restraints and abuse recognition. Clinically, early alcohol screening, anticoagulation review in older fallers and identification of repeat minor head injury are the realistic inferences.

Screening tools for intracranial injury after minor head injury are the rules above (NICE NG232, Canadian CT head rule, with local equivalents for children such as the CATCH and PECARN rules). Imaging is not universal after trivial head injury because of cost and radiation.

• Children. Use the paediatric modification of the Glasgow Coma Scale (under 12 suggests severe head injury; 8 or below suggests possible need for intubation and intracranial pressure monitoring). NICE paediatric CT criteria apply (GCS below 14 initially for those under 16, or below 15 at 2 hours, among others, within 1 hour; a single listed risk factor is observed for at least 4 hours before scanning). Cervical injury patterns differ (more often C1 to C4) and MRI is used more readily.^{[1][2] [5]}
• Older adults. Falls dominate and presentation can be delayed; baseline GCS may be below 15 in chronic neurological disease and should be established. Anticoagulation and antiplatelet use raise risk; chronic subdural haematoma presents weeks later.^[1]
• Pregnancy. Manage the mother first according to trauma principles; imaging is used when indicated. Decisions in the individual patient should involve obstetric, trauma and neurosurgical specialists.^[1]

Where advanced imaging or neurosurgery are not available:

• Prioritise the primary survey, cervical spine control, oxygenation and blood pressure. Keep oxygen saturation above 90 percent, avoid hypotension, and keep the head of the bed elevated if there are no spinal concerns.
• Use available CT when possible; if no CT is available after mild injury, observe for 4 to 6 hours and provide clear return precautions.^[2]
• Osmotherapy (hypertonic saline or mannitol, with monitoring of serum sodium and osmolality) can be given with basic nursing. Drainage via an external ventricular drain, where a neurosurgical service and imaging exist, is the single most useful pressure-relieving intervention.
• Prevent the hypoxia, hypotension and hypercapnia or hypocapnia that dominate outcome; the wrong fluid in the wrong patient can worsen brain oedema. Avoid hypotonic fluids.^[1]
• Start venous thromboembolism prophylaxis where possible once bleeding is controlled, and mobilise safely with pressure-injury prevention.
• Mobilise appropriate patients to a higher level of care early.

Because head and spinal injuries are assessed at the same time in the trauma patient, the reader should also recall the spinal cord injury material usually taught alongside:

• Severity. Traumatic brain injury is graded by the Glasgow Coma Scale; spinal cord injury is graded by the ASIA Impairment Scale (A complete, B sensory incomplete, C and D motor incomplete, E normal), with sacral sparing separating complete from incomplete injury.
• Airway. Intubate and protect the cervical spine together in severe brain injury; cervical injuries are often at C1 to C4 in children and can cause diaphragmatic failure.
• Imaging of the neck. Cervical imaging is deferred only in alert, sober patients with no deficit, no midline tenderness and no painful distracting injury; CT is the usual first study and MRI the best study for the cord. The NEXUS criteria (no midline tenderness, no focal deficit, normal alertness, no intoxication, no painful distracting injury) and the Canadian C-spine rule apply to alert, stable adults. High-risk trauma demands CT rather than plain films.
• Shocks. Spinal shock (transient flaccidity and areflexia below the lesion) and neurogenic shock (loss of sympathetic tone with hypotension and often bradycardia, usually with injuries at T6 or above) need different treatment.
• Steroids. High-dose corticosteroids are no longer routine for either spinal cord injury or traumatic brain injury.
• Complications. Spinal injuries carry a high risk of respiratory failure, venous thrombosis, pressure injury and autonomic dysreflexia (following spinal cord injury).

NICE NG232 and NICE's spinal injury guideline are designed to be used together, and many of the same nursing and physiological targets apply.

Trauma primary survey and approach to the trauma patient; increased intracranial pressure; brain herniation; subdural and epidural haematoma; spinal trauma and imaging; coma and brain death; concussion and sports-related head injury; autonomic dysreflexia; penetrating trauma; secondary survey.

• Most of the harm in severe traumatic brain injury is secondary injury: hypoxia, hypotension, hypercapnia or hypocapnia, bleeding and brain swelling, not the first impact.
• Severity is graded by the Glasgow Coma Scale: 13 to 15 mild, 9 to 12 moderate, 3 to 8 severe.
• Raised intracranial pressure becomes clinically dangerous at around 20 to 25 mm Hg; the late Cushing triad is hypertension, bradycardia and slow or irregular breathing, and brain herniation is the terminal event.
• Extradural haematomas are usually arterial and lentiform; subdural collections are venous in origin and crescent-shaped; traumatic subarachnoid haemorrhage over the convexities differs from aneurysmal subarachnoid haemorrhage in the basal cisterns.
• Diffuse axonal injury is rotational shear with lesions at the grey-white junction, corpus callosum and brainstem; early CT is often normal and MRI is far more sensitive.
• NICE NG232 (2023) CT criteria and the Canadian CT head rule are the standard decision rules for minor head injury and they complement one another; dangerous mechanism, anticoagulation, older age and prolonged amnesia drive imaging when GCS is 13 to 15.
• Neurosurgical discussion is mandatory for a midline shift above 5 mm, compression of basal cisterns, surgically significant collections, deteriorating or comatose patients, cerebrospinal fluid leak and penetrating injury.
• Intensive care aims to keep intracranial pressure under about 25 mm Hg (treat above 22 mm Hg), cerebral perfusion pressure at 60 to 70 mm Hg, PaCO2 normal, osmolality at 295 to 320 mOsm/kg and sodium at 155 mEq/L or below.
• Hyperventilation is a temporary bridge only (target PaCO2 30 to 35 mm Hg for refractory ICP), and prophylactic hyperventilation is avoided. ^[1]
• Hypertonic saline is preferred over mannitol for osmotherapy; high-dose corticosteroids are contraindicated and hypothermia is not beneficial in severe diffuse injury.
• High-dose corticosteroids are no longer routine for either traumatic brain injury or spinal cord injury.
• Head and spinal injuries are assessed and stabilised together; imaging of the cervical spine follows validated low-risk rules and high-risk trauma demands CT.