Mini Nurses Clinical Textbook • Neurological Nursing

Head Injury

Classification, Pathophysiology, Assessment, Treatment, Nursing Management and Intracranial Pressure Monitoring

Written by Abbas
An in-depth textbook chapter for nursing and health-science students.

Introduction to Head Injury

Head injury refers to trauma involving the scalp, skull, meninges, brain or associated intracranial structures. The clinical consequences range from a minor scalp injury or uncomplicated concussion to severe traumatic brain injury with intracranial haemorrhage, cerebral oedema, raised intracranial pressure, brain herniation, permanent neurological disability or death.

Definition: A head injury is any traumatic insult to the head that may damage the scalp, skull or intracranial contents. When the trauma produces disruption of normal brain structure or function, the term traumatic brain injury (TBI) is used.

Understanding head injury requires more than memorising the different types of bleeding. The nurse must understand how the skull, meninges, cerebral blood vessels, cerebrospinal fluid and brain tissue interact. The skull is a rigid container. When bleeding or swelling occurs inside it, there is very little space available for expansion. Progressive increases in intracranial volume can therefore compromise cerebral perfusion and eventually compress vital brain structures.

Head injuries may occur after road traffic collisions, falls, sports injuries, occupational accidents, interpersonal trauma and other mechanisms. Assessment must therefore determine not only what happened to the patient but also what physiological consequences the injury has produced.

Learning Objectives

Define head injury and traumatic brain injury.
Describe the anatomy relevant to head trauma.
Classify head injury according to severity, mechanism and pathology.
Differentiate concussion, contusion, skull fracture, epidural haematoma, subdural haematoma and traumatic subarachnoid haemorrhage.
Perform systematic neurological assessment using the Glasgow Coma Scale.
Explain the emergency and definitive management of head injury.
Describe intracranial pressure, cerebral perfusion pressure and the Monro–Kellie principle.
Explain invasive ICP monitoring and nursing care of an external ventricular drain.

Applied Anatomy of the Head and Brain

The head contains several protective layers. From superficial to deep these include the scalp, skull, dura mater, arachnoid mater, subarachnoid space containing cerebrospinal fluid, pia mater and brain tissue. Knowledge of these layers explains the location and appearance of different traumatic intracranial haemorrhages.

Brain, skull, meninges and nearby structures

Figure 2.1 — Brain and surrounding structures. The rigid skull surrounds the brain and its coverings. The ventricular system and cerebrospinal fluid are also important components of intracranial volume. Image: Alan Hoofring / National Cancer Institute, public domain, via Wikimedia Commons.

Figure 2.2 — The meninges. The dura mater is the tough outer covering. The arachnoid lies beneath it, while the pia mater closely follows the surface of the brain. The subarachnoid space lies between the arachnoid and pia and contains cerebrospinal fluid. Image via Wikimedia Commons.

The Scalp

The scalp contains skin, dense connective tissue, the aponeurosis, loose connective tissue and pericranium. Because the scalp is richly vascularised, even relatively small lacerations can bleed considerably. Scalp swelling may be obvious even when intracranial injury is absent, while severe intracranial injury may occur with little external evidence.

The Skull

The skull protects the brain but also creates a rigid closed compartment. Fractures may be linear, depressed, comminuted or involve the base of the skull. A skull fracture is clinically important because it indicates that substantial mechanical force has been transmitted to the head and may coexist with intracranial bleeding or brain injury.

The Meninges

The relationship between the meninges and cerebral vessels determines the location of traumatic haemorrhage. An epidural haematoma develops between the skull and dura. A subdural haematoma occurs between the dura and arachnoid. Subarachnoid haemorrhage occurs within the CSF-containing space beneath the arachnoid.

EXAM CONNECTION If you remember the anatomical layers, the major intracranial haemorrhages become easier to understand: skull → epidural → dura → subdural → arachnoid → subarachnoid space → pia → brain.

Classification of Head Injury

Classification According to Severity

13–15

Mild Traumatic Brain Injury

A Glasgow Coma Scale score of 13–15 falls within the mild range. The patient may have headache, dizziness, amnesia, transient confusion or features of concussion despite appearing relatively well.

9–12

Moderate Traumatic Brain Injury

GCS 9–12 indicates more substantial neurological impairment. These patients require close observation because neurological deterioration, intracranial bleeding and airway compromise may develop.

3–8

Severe Traumatic Brain Injury

A GCS of 8 or below is classified as severe TBI. Airway protection, ventilation, haemodynamic stability, urgent imaging, neurosurgical involvement and intensive neurological monitoring are major priorities.

IMPORTANT GCS should not be documented only as a total number. Record the individual components, for example E3 V4 M6 = 13/15, because deterioration in one component—particularly motor response—may be clinically significant.

Classification According to Mechanism

Closed Head Injury

The skull and overlying tissues remain closed, but energy transmitted through the skull damages the brain. Acceleration, deceleration, rotational forces and direct impact may produce concussion, contusion, diffuse axonal injury or intracranial haemorrhage.

Open / Penetrating Injury

There is disruption of the scalp, skull, dura or deeper structures. Such injuries carry risks of direct tissue destruction, haemorrhage, infection and cerebrospinal fluid leakage and require urgent specialist management.

Primary and Secondary Brain Injury

Primary Injury

Primary brain injury occurs at the moment of trauma. Examples include cerebral contusion, tearing of vessels, diffuse axonal injury and direct structural destruction of neural tissue.

Secondary Injury

Secondary brain injury develops after the initial event. Important mechanisms include hypoxia, hypotension, cerebral oedema, raised ICP, impaired cerebral perfusion, seizures, fever, abnormal glucose, electrolyte disturbance and expanding intracranial haemorrhage.

NURSING SIGNIFICANCE The primary injury has already occurred before the patient reaches hospital. A major objective of emergency and critical-care nursing is therefore to prevent secondary brain injury.

Pathophysiology of Traumatic Brain Injury

Mechanical energy applied to the head produces deformation, stretching, compression and shearing of neural tissue and blood vessels. A direct blow may injure the brain at the site of impact, while rapid movement of the brain within the skull can cause additional injury on the opposite side.

Coup and Contrecoup Injury

A coup injury occurs directly beneath the site of impact. A contrecoup injury develops on the opposite side as the moving brain strikes the inner surface of the skull. Frontal and temporal lobes are particularly susceptible because of their relationship with the irregular bony surfaces of the anterior and middle cranial fossae.

The Secondary Injury Cascade

Initial mechanical trauma

Cellular membranes, axons and blood vessels are disrupted.

Cellular dysfunction

Ionic imbalance, excitotoxicity and disturbed cellular metabolism develop.

Cerebral oedema

Swollen brain tissue increases intracranial volume.

Raised intracranial pressure

Increasing ICP reduces the pressure gradient required to perfuse brain tissue.

Reduced cerebral perfusion

Cerebral ischaemia worsens oedema and neuronal injury, producing a dangerous cycle.

Major Types of Head Injury

5.1 Concussion

Concussion is a mild traumatic brain injury producing transient disturbance of neurological function. Structural abnormalities may not be visible on routine CT. Patients may experience headache, dizziness, temporary confusion, poor concentration, nausea, memory disturbance, sensitivity to light or noise and changes in sleep.

CLINICAL PEARL Loss of consciousness is not required for concussion to occur.

5.2 Cerebral Contusion

A cerebral contusion is bruising of brain tissue. Contusions may involve localised haemorrhage, oedema and tissue damage and commonly affect frontal and temporal regions. Unlike uncomplicated concussion, contusion represents structural injury and may enlarge during the hours following trauma.

5.3 Skull Fracture

Skull fractures may be linear, depressed, comminuted or basilar. Management is determined not simply by the presence of a fracture but by associated intracranial injury, depression of bone fragments, contamination, neurological deficit, CSF leakage and other complications.

$Basilar skull fracture on CT$

Figure 5.1 — Basilar skull fracture demonstrated on CT. Basilar fractures involve the floor of the skull and may be associated with CSF rhinorrhoea or otorrhoea, haemotympanum, periorbital bruising and Battle sign. Image: James Heilman, MD, CC BY-SA 4.0, via Wikimedia Commons.

Clinical Features Suggesting Basal Skull Fracture

Periorbital bruising or “raccoon/panda eyes”.
Battle sign: bruising over the mastoid region.
Blood behind the tympanic membrane.
Clear fluid leaking from the nose or ear.
Cranial nerve abnormalities.

5.4 Epidural Haematoma

Epidural—or extradural—haematoma is accumulation of blood between the inner surface of the skull and dura mater. It is frequently associated with skull fracture and may involve arterial bleeding. Because arterial bleeding can expand rapidly, neurological deterioration can be sudden.

Figure 5.2 — Epidural haematoma. On CT, an acute epidural collection classically appears as a hyperdense biconvex or lens-shaped extra-axial collection. Significant collections can compress the adjacent brain and shift midline structures. Image via Wikimedia Commons, GFDL / CC BY-SA.

CLASSIC EXAM ASSOCIATION Epidural haematoma is often associated with injury to the middle meningeal artery. A patient may initially appear relatively well and later deteriorate as the haematoma expands. The traditional “lucid interval” is useful for examinations but is not present in every patient.

5.5 Subdural Haematoma

A subdural haematoma is blood accumulating between the dura and arachnoid. It commonly results from tearing of bridging veins. Acute subdural haematoma may occur after major trauma and is frequently associated with underlying brain injury.

Figure 5.3 — Traumatic subdural haematoma. Acute subdural blood typically forms a crescent-shaped extra-axial collection extending along the cerebral convexity. Image via Wikimedia Commons.

5.6 Traumatic Subarachnoid Haemorrhage

Traumatic subarachnoid haemorrhage represents bleeding into the subarachnoid space containing cerebrospinal fluid. CT may demonstrate high-density blood within cortical sulci, fissures or basal cisterns.

Figure 5.4 — Subarachnoid haemorrhage on CT. Blood enters the CSF-containing subarachnoid spaces and may be visible within sulci and cisterns. Mirza & Gokhale image, CC BY 4.0, via Wikimedia Commons.

5.7 Diffuse Axonal Injury

Diffuse axonal injury results from rotational and acceleration–deceleration forces that stretch and disrupt axons throughout the brain. Lesions often involve the grey–white matter junction, corpus callosum and deeper structures. Patients may have severe impairment of consciousness even when the initial CT does not appear dramatically abnormal.

Figure 5.5 — Diffuse axonal injury demonstrated on MRI. MRI can demonstrate small lesions that may be difficult to appreciate on routine CT. CC0/public-domain dedication via Wikimedia Commons.

Clinical Assessment of the Patient

Assessment begins immediately. The patient should not undergo a prolonged neurological examination while airway, ventilation or circulation is unstable. Life-threatening physiological abnormalities are treated first because hypoxia and hypotension can significantly worsen secondary brain injury.

Primary Survey

Airway with Cervical Spine Protection

Assess airway patency while maintaining cervical spine precautions when injury is suspected. Look for obstruction, abnormal sounds, facial trauma, blood or vomitus.

Breathing

Assess respiratory rate, chest movement, oxygen saturation and adequacy of ventilation. Hypoxaemia must be corrected promptly.

Circulation

Assess pulse, blood pressure, perfusion and external haemorrhage. Hypotension in a trauma patient should prompt a search for bleeding or other causes rather than automatically being attributed to the head injury.

Disability

Perform rapid neurological assessment: GCS, pupils, limb movement, focal deficits and blood glucose.

Exposure

Examine the patient for associated injuries while preventing hypothermia.

History

Important information includes the mechanism and time of injury, height of a fall, speed of a collision, use of safety devices, loss of consciousness, amnesia, vomiting, seizure, headache, alcohol or medication use, anticoagulant treatment, previous neurological disease and changes in behaviour after the event.

Neurological Examination

Level of Consciousness

Assess using the GCS and document trends rather than relying on one isolated value.

Pupils

Assess size, equality and response to light. New anisocoria or a poorly reactive pupil may indicate worsening intracranial pathology.

Motor Function

Assess spontaneous movement, strength, symmetry and response to stimulation. New weakness or abnormal posturing requires urgent review.

Vital Signs

Monitor blood pressure, pulse, respiratory pattern, temperature and oxygen saturation for evidence of physiological deterioration.

Signs of Neurological Deterioration

Falling GCS score.
Increasing drowsiness or inability to awaken normally.
New pupil asymmetry.
New focal weakness.
Repeated vomiting.
Increasing or severe headache.
New seizure.
Abnormal posturing.
Changes in respiratory pattern.

Glasgow Coma Scale

The Glasgow Coma Scale assesses three components of responsiveness: eye opening, verbal response and motor response. The total ranges from 3 to 15. Each component should be assessed and documented separately.

Eye Opening — E

Spontaneous4

To sound3

To pressure2

None1

Verbal Response — V

Orientated5

Confused4

Words3

Sounds2

None1

Motor Response — M

Obeys commands6

Localises5

Normal flexion4

Abnormal flexion3

Extension2

None1

EXAMPLE A patient who opens the eyes to voice, speaks confused sentences and obeys commands would be documented as E3 V4 M6 = GCS 13/15.

Factors such as sedation, intubation, facial swelling, language barriers, intoxication and paralysis can affect assessment. These limitations should be documented rather than assigning a misleading score.

Investigations

Non-Contrast CT of the Head

CT is the principal initial imaging investigation when clinically important acute traumatic brain injury is suspected. It rapidly identifies intracranial bleeding, mass effect, skull fracture, hydrocephalus, cerebral oedema and other major abnormalities.

Epidural pattern: typically biconvex or lens-shaped.

Subdural pattern: typically crescent shaped.

MRI

MRI is not usually the first investigation in acute unstable trauma, but it can demonstrate abnormalities not easily seen on CT, including certain forms of diffuse axonal injury and smaller parenchymal lesions. It is particularly valuable in selected patients when neurological findings remain unexplained.

Laboratory Studies

Investigations are guided by clinical circumstances and may include full blood count, electrolytes, renal function, glucose, coagulation profile, blood grouping and cross-matching, arterial blood gases and toxicology where relevant. These do not replace neurological examination or imaging.

Emergency Management

The emergency objective is to maintain oxygenation and cerebral perfusion while identifying lesions requiring urgent neurosurgical treatment. Management therefore follows systematic trauma principles.

Airway and Ventilation

The airway must remain patent. Patients with severely reduced consciousness may lose protective airway reflexes and require advanced airway management by appropriately trained clinicians. Oxygenation and ventilation must be carefully controlled because both hypoxaemia and major disturbances in carbon dioxide can alter cerebral physiology.

Circulation

Adequate circulating volume and blood pressure are essential because cerebral perfusion depends partly on systemic arterial pressure. Significant hypotension should be corrected and extracranial bleeding actively sought.

Cervical Spine Protection

A clinically important cervical spine injury may accompany head trauma. Cervical spine protection should therefore be maintained until the cervical spine has been appropriately assessed and cleared.

Control of Secondary Insults

Avoid Hypoxia

Insufficient oxygen delivery worsens neuronal injury.

Avoid Hypotension

Low arterial pressure reduces cerebral perfusion.

Control Seizures

Seizures increase cerebral metabolic demand and may worsen intracranial physiology.

Control Temperature

Fever increases cerebral metabolic requirements.

Correct Glucose Problems

Marked hypo- or hyperglycaemia may complicate neurological assessment and recovery.

Recognise Expanding Bleeding

Neurological deterioration requires urgent reassessment and often repeat imaging.

Definitive Treatment

Treatment depends on the type and severity of injury, neurological status, imaging findings, intracranial pressure, presence of associated injuries and overall physiological stability.

Conservative Management

Selected patients can be managed with neurological observation, symptom control, repeated examination and clear discharge instructions. Observation focuses on identifying deterioration early rather than simply waiting for symptoms to resolve.

Medical Management

Medical treatment may include analgesia, antiemetic therapy, seizure management, measures to reduce intracranial pressure, maintenance of appropriate fluid and electrolyte status, control of fever and other supportive intensive-care interventions. Hyperosmolar therapy may be used in selected patients with raised ICP under specialist management.

IMPORTANT PRINCIPLE Medications used to control pain, agitation or seizures can influence the neurological examination. Nurses should therefore document the drug, timing and clinical response whenever changes in consciousness are assessed.

Surgical Management

Neurosurgical intervention may be required for significant epidural or subdural haematomas, depressed skull fractures, penetrating injuries, refractory intracranial hypertension or other mass lesions. Procedures may include craniotomy, evacuation of haematoma, elevation of depressed bone fragments, decompressive craniectomy or placement of an external ventricular drain.

Nursing Management of Head Injury

Nursing management centres on prevention of secondary brain injury, early recognition of deterioration, maintenance of physiological stability, prevention of complications and support of neurological recovery.

Neurological Observation

Assess and trend the Glasgow Coma Scale, pupil size and reaction, limb movement, behaviour, orientation and other neurological findings. A change from the patient's previous status is often more important than an isolated value.

Respiratory Care

Maintain airway patency and monitor oxygenation. In mechanically ventilated patients, observe ventilator parameters, airway secretions, tube position and clinical evidence of impaired ventilation.

Positioning

Where clinically appropriate and not contraindicated by injuries or haemodynamic status, head elevation and neutral alignment may facilitate cerebral venous drainage. Excessive neck flexion, tight cervical devices or positions that impair venous return should be avoided.

Fluid and Electrolyte Monitoring

Monitor intake, output, serum electrolytes, renal function and fluid balance. Disturbances of sodium and water regulation can occur after brain injury and may produce further neurological deterioration.

Skin, Eye and Mouth Care

Patients with reduced consciousness are at increased risk of pressure injury, corneal injury and oral complications. Regular repositioning, pressure-area assessment, appropriate eye protection and oral hygiene are important components of nursing care.

Nutrition

Severe brain injury produces a significant metabolic response. Nutritional status should therefore be assessed and an appropriate feeding plan established with the multidisciplinary team when oral intake is unsafe or insufficient.

Family Support

Families may be distressed by altered consciousness, neurological deficits and unfamiliar equipment. Explain the purpose of monitoring, changes in the patient's condition and the care being provided using clear, compassionate language.

CORE NURSING OBSERVATIONS Level of consciousness • GCS components • Pupils • Limb movement • Blood pressure • Pulse • Respiratory rate • Oxygen saturation • Temperature • Pain • Fluid balance • Seizure activity • ICP/CPP where monitored.

Raised Intracranial Pressure

Intracranial pressure is the pressure within the cranial cavity. In adults, resting ICP is normally relatively low, commonly around 5–15 mmHg. Persistent elevation becomes clinically important because it can reduce cerebral perfusion and cause displacement of intracranial structures.

The Monro–Kellie Principle

The adult skull is essentially a fixed-volume container containing three major components: brain tissue, blood and cerebrospinal fluid. When the volume of one component rises, another must decrease if intracranial pressure is to remain stable.

Brain

Approximately the largest component of intracranial volume. Oedema increases this volume.

Blood

Haematoma or increased cerebral blood volume can raise intracranial pressure.

CSF

CSF can initially shift into the spinal compartment as a compensatory mechanism.

Compensation is limited. Once compensatory mechanisms are exhausted, a relatively small increase in intracranial volume can cause a substantial rise in ICP.

Cerebral Perfusion Pressure

CPP = MAP − ICP

Cerebral perfusion pressure = Mean arterial pressure − Intracranial pressure

This equation demonstrates why both systemic blood pressure and intracranial pressure matter. A fall in mean arterial pressure or a rise in ICP can reduce the pressure available to perfuse the brain.

SEVERE TBI GUIDANCE In severe traumatic brain injury, the Brain Trauma Foundation recommends treatment when ICP is persistently above approximately 22 mmHg. CPP management is generally aimed within a range of approximately 60–70 mmHg, with individualisation according to the patient's physiology and specialist management plan.

Clinical Features of Raised ICP

Declining level of consciousness.
Increasing headache.
Repeated vomiting.
New pupil abnormalities.
Motor weakness or abnormal posturing.
Seizure.
Changes in respiratory pattern.
Late haemodynamic abnormalities.

CUSHING RESPONSE Hypertension with widening pulse pressure, bradycardia and abnormal respiration is traditionally associated with severe raised intracranial pressure and impending brainstem compromise. It is a late and dangerous sign, not something clinicians should wait to appear before acting.

Intracranial Pressure Monitoring

Invasive ICP monitoring allows continuous or intermittent measurement of intracranial pressure in selected patients with severe brain injury. Monitoring provides information that can be interpreted together with clinical examination, CT findings, haemodynamics and other physiological variables.

Main Methods

Intraventricular Catheter / EVD

A catheter is placed within a cerebral ventricle. It can measure ICP and can also permit drainage of cerebrospinal fluid when clinically indicated.

Intraparenchymal Monitor

A pressure sensor is inserted into brain tissue. It provides continuous ICP measurement but generally does not provide therapeutic CSF drainage.

Figure 13.1 — External ventricular drain system. An EVD provides access to the ventricular system and may be used to monitor pressure and drain CSF. The drainage system must be positioned and levelled correctly according to institutional protocol and the prescribed reference level. Image via Wikimedia Commons, CC BY-SA 3.0.

Why ICP Monitoring Is Useful

Clinical examination alone cannot quantify intracranial pressure, particularly in sedated, paralysed or intubated patients. ICP monitoring helps the clinical team recognise intracranial hypertension, evaluate response to treatment and calculate cerebral perfusion pressure.

Nursing Care of ICP Monitoring

Verify the Reference Level

The drainage or monitoring system must be levelled according to the prescribed anatomical reference point and institutional protocol. Changes in bed height or patient position can alter the apparent pressure or drainage.

Maintain Aseptic Technique

An EVD communicates with the ventricular system and therefore creates an infection risk. Connections should be manipulated only when clinically necessary and according to strict infection-control procedures.

Observe the ICP Trend

Record the value, waveform where applicable and clinical context. A single transient rise during coughing or repositioning is different from sustained intracranial hypertension.

Observe CSF Drainage

When an EVD is being used for drainage, note the amount and appearance of CSF and promptly report unexpected changes according to the care plan.

Maintain Head and Neck Alignment

Avoid unnecessary obstruction of cerebral venous return. Re-level the monitoring system after relevant position changes.

Correlate With the Patient

Never treat a monitor as an isolated number. Interpret ICP together with GCS, pupils, haemodynamics, oxygenation, CT findings and the overall clinical picture.

SAFETY POINT EVD height, drainage limits, clamping and sampling are specialist clinical procedures. They should follow the neurosurgical prescription and the institution's EVD protocol rather than being altered independently.

Measures Used to Control Raised ICP

Treatment is individualised and may include optimisation of airway and ventilation, prevention of hypoxia and hypotension, appropriate head positioning, analgesia and sedation, treatment of fever and seizures, hyperosmolar therapy, CSF drainage, evacuation of intracranial mass lesions and, in selected refractory cases, decompressive surgery.

Complications of Head Injury

Raised ICP and Herniation

Progressive swelling or expanding haemorrhage can shift intracranial structures and compress the brainstem.

Post-Traumatic Seizures

Seizures may occur early or later following significant traumatic brain injury.

CSF Leakage

Disruption of the skull base and dura can allow cerebrospinal fluid to escape through the nose or ear.

Infection

Open fractures, penetrating injury, CSF leakage and invasive devices may increase infection risk.

Neuroendocrine Disturbance

Damage involving hypothalamic or pituitary structures can disturb water, electrolyte and hormonal regulation.

Long-Term Neurological Problems

Survivors may experience weakness, cognitive impairment, mood changes, memory difficulty, speech problems or reduced functional independence.

Brain Herniation

Herniation occurs when pressure gradients force brain tissue from one intracranial compartment into another. This can compress cranial nerves, cerebral vessels and the brainstem and represents a neurological emergency.

EMERGENCY WARNING A rapidly falling GCS, new fixed or poorly reactive pupil, progressive focal deficit or abnormal posturing should trigger immediate medical and neurosurgical reassessment.

Paediatric Considerations

Assessment of head injury in children follows the same fundamental priorities of airway, breathing, circulation and neurological assessment, but important age-related differences exist. Infants and young children may not be able to describe headache, amnesia or visual disturbance, so clinicians rely more heavily on behaviour, feeding, interaction and observations from caregivers.

A paediatric version of the Glasgow Coma Scale may be required in preverbal children. Assessment should also consider scalp swelling, fontanelle findings in infants, safeguarding concerns, mechanism of injury and age-specific CT criteria.

PAEDIATRIC NURSING POINT In young children, subtle changes such as unusual irritability, reduced feeding, decreased interaction, persistent drowsiness or repeated vomiting may be clinically significant even when the child cannot describe symptoms.

High-Yield Examination Points

Remember These Before Your Examination

Mild TBI: GCS 13–15.
Moderate TBI: GCS 9–12.
Severe TBI: GCS 3–8.
Epidural haematoma: blood between skull and dura; classically biconvex on CT.
Subdural haematoma: blood between dura and arachnoid; classically crescent shaped on CT.
Subarachnoid haemorrhage: blood within the subarachnoid CSF space.
Diffuse axonal injury: widespread axonal shearing from acceleration/deceleration and rotational forces.
CT head: primary acute imaging investigation for clinically important TBI.
CPP: MAP − ICP.
Raised ICP: can reduce cerebral perfusion and ultimately produce herniation.
EVD: can measure ICP and provide controlled CSF drainage.
Most important nursing objective: recognise deterioration early and prevent secondary brain injury.

Selected References and Image Credits

Brain Trauma Foundation. Guidelines for the Management of Severe Traumatic Brain Injury, 4th Edition.

National Institute for Health and Care Excellence (NICE). Head injury: assessment and early management. NG232.

Wikimedia Commons. Brain and Nearby Structures — Alan Hoofring / National Cancer Institute.

Wikimedia Commons. Meninges-en.svg.

Wikimedia Commons. Epidural hematoma.png.

Wikimedia Commons. Trauma subdural.jpg and Ct-scan of the brain with an subdural hematoma.jpg.

Wikimedia Commons. CT of subarachnoid hemorrhage.png.

Wikimedia Commons. BasSkullFrac.png — James Heilman, MD.

Wikimedia Commons. Diffuse axonal injury MRI images.

Wikimedia Commons. EVD-ICH.jpg — external ventricular drainage system.