• TBI is a leading cause of death and disability worldwide, particularly in those aged < 40 years ^[3].
• Road traffic accidents (RTAs) account for only ~25% of all head injuries but contribute to ~60% of head injury mortality — because RTAs involve high-energy mechanisms ^[1][2].
• Bimodal age distribution: peaks in young adults (15–24 years) and elderly (≥65 years) ^[4].

• In Hong Kong specifically, falls are the most common cause across all ages, driven by the ageing population. RTAs remain the leading cause of severe TBI and death.

• High-energy injury: fall from height, RTA ^[4]
• Advanced age ^[4]
• Anticoagulants / antiplatelets / alcohol — all increase bleeding risk and mask deterioration ^[4]
• Signs/symptoms of increased ICP: headache, nausea/vomiting ^[4]
• Signs of herniation: anisocoria, sluggish pupillary response ^[4]
• Lucid interval — suggests expanding mass lesion (classically EDH) ^[4]

The scalp has 5 layers (mnemonic: S-C-A-L-P) ^[2]:

• Skull vault: frontal, parietal, temporal, occipital bones
  • Thinnest at the temporal bone (pterion) — this is where the middle meningeal artery runs → why temporal bone fractures are the classic cause of epidural haematoma (EDH)
• Skull base: anterior, middle, and posterior cranial fossae
  • Contains foramina for cranial nerves and vessels
  • Fractures here → CSF leaks, cranial nerve palsies, vascular injury

Three layers, outside to inside:

1. Dura mater ("tough mother") — two layers:

   • Periosteal layer (endosteum): adherent to inner skull table
   • Meningeal layer: forms dural reflections (falx cerebri, tentorium cerebelli)
   • The two layers separate to form dural venous sinuses (superior sagittal sinus, transverse sinus, etc.)
   • Epidural space: potential space between the periosteal dura and the skull — where epidural haematomas collect
   • The periosteal layer (endosteum) crosses through cranial sutures to become continuous with the outer periosteal layer — this is why EDH does not cross suture lines ^[2][5]

2. Arachnoid mater ("spider-like") — thin, avascular

   • Subdural space: potential space between dura and arachnoid — contains bridging veins that travel from the pial surface to dural venous sinuses
   • These bridging veins are vulnerable to shearing with acceleration-deceleration injuries → subdural haematoma (SDH) ^[5]

3. Pia mater ("tender mother") — adherent to brain surface

   • Subarachnoid space: between arachnoid and pia, contains CSF and major arteries (Circle of Willis)

• Middle meningeal artery (branch of maxillary artery → from external carotid): runs in a groove on the inner skull at the pterion → rupture causes EDH
• Bridging veins: drain cortical surface → dural sinuses; rupture causes SDH
• Circle of Willis: located in subarachnoid space; aneurysms here → SAH
• Internal carotid artery (ICA): passes through the cavernous sinus and foramen lacerum — skull base fractures can injure it → traumatic ICA aneurysm, carotico-cavernous fistula

The skull is a rigid, fixed-volume container. Its contents are:

• Brain parenchyma (~80%)
• Blood (~10%)
• CSF (~10%)

Monro-Kellie Doctrine: The total volume of brain + blood + CSF within the skull is constant. An increase in one component must be compensated by a decrease in another, or ICP will rise.

• Normal ICP: 5–15 mmHg in adults
• Cerebral Perfusion Pressure (CPP) = MAP − ICP
  • If ICP rises (e.g. expanding haematoma), CPP falls → cerebral ischaemia
  • Goal in TBI management: CPP ≥ 60–70 mmHg

• Normally, for mean arterial blood pressure (MABP) 50–150 mmHg, cerebral vascular resistance varies with changing BP, keeping cerebral blood flow (CBF) relatively constant — i.e. "pressure-active" system ^[2]
• In TBI, this system becomes faulty ("pressure-passive" system) → a drop in MABP can directly cause cerebral ischaemia ^[2]
• This is why hypotension is so dangerous in head injury patients — the brain can no longer protect itself from low perfusion

When ICP rises beyond compensatory capacity, brain tissue herniates through rigid dural openings:

The mechanism of injury determines the pattern of brain damage ^[2]:

Why coup and contrecoup? When the moving head hits a stationary object (deceleration), the brain impacts the inner skull at the point of contact (coup). The brain then rebounds and hits the opposite inner skull surface (contrecoup). The contrecoup injury is often worse because the brain accelerates into the opposite skull with less cushioning.

The GCS is the most important clinical tool for assessing severity of head injury ^[1][4].

• Total GCS range: 3 (worst) to 15 (best)
• Mild TBI: GCS 13–15
• Moderate TBI: GCS 9–12
• Severe TBI: GCS ≤8 (this is the threshold for intubation — the patient cannot protect their airway)

For intubated patients, verbal scores are modified ^[4]:

Practical tips for GCS assessment ^[2]:

• Ask patient to stick out tongue to test Motor (M) — this is a higher-level command less likely to be affected by cervical spine injury than limb movements
• Pain stimulation methods: supraorbital pressure, earlobe compression, rubbing knuckles on sternum
• Always record the best response in each category
• The Motor component (M) has the strongest prognostic value

• CN III palsy is the most useful indicator of an expanding intracranial lesion ^[2]
• Ipsilateral dilated, fixed pupil → indicates ipsilateral impending transtentorial (uncal) herniation ^[2]
• Bilateral fixed dilated pupils → brainstem death or severe bilateral herniation
• Anisocoria + sluggish pupillary response → high-risk sign ^[4]

Why? Decorticate = cortex disconnected from brainstem, but red nucleus intact → flexor posturing (red nucleus facilitates flexion). Decerebrate = red nucleus also damaged → loss of flexion facilitation → vestibulospinal and reticulospinal tracts dominate → extension.

• Predicts risk of 14-day mortality and unfavourable outcome at 6 months in TBI
• Variables: country, age, GCS, pupil reactivity, major extracranial injury, CT findings (petechial haemorrhages, obliteration of third ventricle/basal cisterns, subarachnoid bleeding, midline shift, non-evacuated haematoma)

For minor head injury (witnessed LOC or disorientation, definite amnesia, GCS 13–15) ^[2]:

High-risk criteria (for neurological intervention):

1. GCS < 15 at 2 hours post-injury
2. Suspected open or depressed skull fracture
3. Any sign of basal skull fracture
4. ≥ 2 episodes of vomiting
5. Age ≥ 65

Medium-risk criteria (for brain injury on CT):

1. Retrograde amnesia ≥ 30 minutes
2. Dangerous mechanism (pedestrian struck by vehicle, ejection from vehicle, fall from > 3 feet or > 5 stairs)

Key points in history (the "pearls") ^[4]:

1. Mechanism of injury: high-energy (RTA, fall from height) vs. low-energy (standing-height fall)
2. Precipitating factors: convulsion, syncope, stroke — "Did the head injury cause the LOC, or did the LOC cause the head injury?"
3. Events during head injury: duration of LOC, post-traumatic amnesia, lucid interval, convulsions, resuscitations given
4. Neurological symptoms: headache, vomiting, weakness, visual changes
5. Pre-morbid functioning: baseline cognitive status (especially in elderly), medications (anticoagulants!), alcohol use
6. Symptoms of skull base fracture: CSF leakage, blood from ears/nose

Systematic approach ^[1][2]:

1. ABCDE — always before any neurosurgical evaluation
2. GCS — most important
3. External injuries: lacerations, bruising, scalp haematoma
4. Signs of basal skull fracture ^[1][2]:
   • Anterior fossa: CSF rhinorrhoea, raccoon eyes, subconjunctival haemorrhage
   • Middle fossa: CSF otorrhoea, Battle sign
5. Neurological examination:
   • Pupil response — 3rd nerve lesion is the most useful indicator ^[2]
   • Limb weakness — can be falsely localizing (Kernohan's notch) ^[2]
   • Eye movements — ↓GCS + ↓EOM = poor prognosis ^[2]
   • Other cranial nerve lesions
6. Spinal cord assessment: sensory level, motor deficits, anal tone ^[4]
7. Other injuries: chest, abdomen, pelvis, long bones

NECT brain is the single most important investigation in head injury ^[2].

Why NECT?

• Fast (< 5 minutes)
• Widely available
• Excellent at detecting acute blood (hyperdense on CT)
• Can identify fractures, mass effect, midline shift, hydrocephalus
• In acute head trauma, plain CT is appropriate as a first-line study because it can detect acute blood clots ^[3]

Limitations:

• Poor at detecting DAI (→ use MRI with SWI for this)
• Subacute SDH may be isodense and difficult to see → do CT ASAP or use contrast CT ^[5]
• Posterior fossa structures can be obscured by bone artefact

This is the core clinical differential in head injury — you see an abnormal CT, you need to know what you're looking at:

This is the most widely used and validated decision rule ^[2][6]:

Inclusion criteria (i.e., when to apply the rule): patients with minor head injury defined as ^[6]:

• GCS 13–15 after injury
• With any one of: witnessed LOC, amnesia, or confusion/disorientation

Exclusion criteria (do NOT use CCHR — just get a CT) ^[6]:

• ED GCS < 13
• Obvious penetrating skull injury or depressed skull fracture
• Unstable vital signs associated with major trauma
• Focal neurological deficit
• Seizure prior to ED assessment
• Bleeding disorders or use of oral anticoagulants

Why these exclusions? These patients have such a high pre-test probability of significant intracranial pathology that applying a decision rule is pointless — they need CT regardless. A patient on anticoagulants with a head injury can develop a delayed haematoma even from minor trauma.

High-risk criteria (for neurosurgical intervention) — if ANY present → CT is recommended ^[2][6]:

1. GCS < 15 at 2 hours after injury
2. Suspected open or depressed skull fracture
3. Any sign of basal skull fracture (raccoon eyes, Battle sign, CSF otorrhoea/rhinorrhoea, haemotympanum)
4. Vomiting ≥ 2 episodes
5. Age ≥ 65 years

Medium-risk criteria (for brain injury on CT) — if present → CT may be considered ^[2][6]:

1. Retrograde amnesia ≥ 30 minutes before impact
2. Dangerous mechanism:
   • Pedestrian struck by motor vehicle
   • Occupant ejected from motor vehicle
   • Fall from height > 3 feet or > 5 stairs

Logic of high vs. medium risk: The high-risk criteria identify patients who may need neurosurgical intervention (craniotomy, etc.) — these MUST get a CT. The medium-risk criteria identify patients with a significant chance of having a lesion on CT that may not need surgery but needs monitoring.

An alternative rule — CT is indicated in patients with GCS 15/15 (i.e., fully conscious) if any of these 7 criteria are present:

1. Headache
2. Vomiting
3. Age > 60 years
4. Drug or alcohol intoxication
5. Persistent antegrade amnesia
6. Seizure
7. Visible trauma above the clavicle

CCHR vs. NOC: CCHR is more specific (fewer unnecessary scans) while NOC is more sensitive (catches more pathology but leads to more CTs). In practice, CCHR is preferred because it stratifies risk and reduces unnecessary imaging.

Even outside formal decision rules, CT brain is indicated for ^[3][13]:

• Low GCS (any moderate or severe TBI)
• Post-traumatic seizure
• Focal neurological deficit
• Retrograde amnesia
• Suspected open, depressed, or basal skull fracture
• High-energy trauma
• Clotting disorder or on anticoagulation
• Infants with large bruising, swelling, or laceration; suspected non-accidental injury (NAI); tense fontanelle ^[13]

Initially normal/mild CT findings do not preclude the possibility of subsequent development of life-threatening mass lesion ^[1].

Repeat CT if clinically indicated ^[1]:

• Drop in GCS
• Pupil dilation (new or worsening)
• Seizure
• New focal deficit

Why do lesions evolve? Several mechanisms: (1) Contusions accumulate more blood over 24–72 hours through continued microvascular oozing + surrounding oedema. (2) Coagulopathy (traumatic or drug-induced) allows ongoing bleeding. (3) Brain swelling develops over hours to days. The lecture emphasizes that contusions are NOT the worst until at least Day 4–5 ^[1] — this is why serial monitoring is essential.

All significant head injuries should have CT cervical spine — always assume C-spine injury until cleared ^[4].

Why? Because:

• High-energy mechanisms that cause head injury also cause cervical spine injury
• A cervical spine fracture with cord injury can mimic or compound neurological deficits from the head injury
• Failing to immobilize an unstable C-spine can convert a stable injury into paraplegia/quadriplegia

CTA Circle of Willis ^[4]:

• Indicated for skull base fractures involving foramen lacerum — risk of traumatic ICA injury (dissection, pseudoaneurysm)
• Also indicated when SAH pattern suggests aneurysmal rather than traumatic origin

CTA Vertebral arteries ^[4]:

• Indicated for C-spine injury involving vertebral foramen — risk of vertebral artery dissection

CTA generally ^[14]:

• Uses rapid injection of IV contrast bolus → opacifies vessels → reconstructed 3D images
• Can identify: vessel occlusion, dissection, pseudoaneurysm, active extravasation
• Can be used in place of more invasive conventional angiography ^[14]

MRI is inappropriate as first-line study for head trauma ^[13] — too slow (20+ minutes), not widely available in emergency settings, and motion artefact from uncooperative/confused patients is a major problem.

However, MRI is superior to CT for specific indications ^[6][13]:

When to get MRI? Generally 48–72 hours after injury when the acute situation is stabilized ^[6]. It serves as a problem-solving tool rather than a first-line investigation.

MRI vs CT — Summary Comparison [6][14][15]

SXR has very limited use in head injury ^[13]:

• Can detect skull fractures but normal SXR cannot exclude intracranial pathologies (e.g. haemorrhage)
• Main current use: excluding metallic foreign bodies before MRI ^[13]
• Largely replaced by CT, which detects fractures AND intracranial lesions simultaneously
• Do NOT rely on a normal SXR to clear a head injury patient

While imaging is the cornerstone, blood tests are essential for identifying systemic contributors to secondary brain injury and guiding management:

When CSF rhinorrhoea or otorrhoea is suspected ^[4]:

• Beta-2 transferrin: a protein specific to CSF (not found in blood, nasal secretions, or tears) — considered the gold standard for confirming CSF leak
• Halo test (ring sign): drop the fluid onto gauze — if it contains CSF mixed with blood, CSF migrates outward forming a clear ring (halo) around the central blood spot. Simple bedside test but less specific.
• Glucose testing: CSF contains glucose (≈60% of serum); nasal secretions do not. Can be done with a glucometer at bedside — if positive, suggestive but not definitive.

Indications for ICP monitoring ^[12]:

• No reliable GCS (e.g. sedation, muscle paralysis)
• GCS ≤ 8 (requires intubation)
• Evolving disease conditions

Relative contraindications ^[12]:

• Awake patients (clinical exam is more reliable)
• Bleeding tendency (procedure involves placing a catheter into the ventricle or brain parenchyma)

Methods:

• External Ventricular Drain (EVD) ^[12]: gold standard
  • Manometric principle for monitoring intracranial CSF pressure
  • Therapeutic — can drain CSF for decompression
  • Risks: infection, iatrogenic trauma
• Intraparenchymal probe (e.g. Codman): measures pressure directly in brain tissue; cannot drain CSF
• LP is contraindicated if raised ICP (risk of tonsillar herniation — removing CSF from below a pressure gradient can cause the brain to herniate downward through the foramen magnum) ^[12]

• Head injury may result in fatal cerebral oedema or haemorrhage → impede cerebral blood flow
• ↓Cerebral perfusion can be detected by cerebral perfusion study ^[14]
• Also used for confirmation of brain death: "empty light bulb" sign — absence of perfusion to the brain ^[14]
• Causes of coma must be excluded before making diagnosis of brain death ^[14]:
  1. Primary hypothermia
  2. Hypoglycaemia
  3. Electrolytes or endocrine disturbance
  4. Muscle relaxant
  5. Barbiturate overdose
  6. Alcohol intoxication
  7. Sedative overdose

• CXR: in polytrauma — pneumothorax, haemothorax, rib fractures (contribute to hypoxia → secondary brain injury)
• Pelvic XR / CT: if major trauma with haemodynamic instability
• Abdominal imaging: if polytrauma suspected

• Assume C-spine injury in all significant head injuries → maintain in-line immobilization with hard collar ^[2][4]
• Jaw thrust (not head-tilt chin-lift) when C-spine injury is a concern ^[16]
• Indications for intubation ^[2][4]:
  • GCS ≤ 8 — cannot protect airway (lost gag/cough reflexes)
  • Loss of protective laryngeal reflexes
  • Respiratory insufficiency (PaO2 < 60, PaCO2 > 45)
  • Need for controlled ventilation (ICP management)
• Rapid Sequence Induction (RSI): IV induction (e.g. propofol or ketamine) + fast-acting neuromuscular blocker (e.g. suxamethonium or rocuronium) → intubate without prior bag-valve-mask ventilation (to avoid aspiration in unfasted trauma patient) ^[16]
• Early tracheostomy may be considered in severe TBI for better bronchial toileting ^[4]

• Target: SpO2 > 97%, PaO2 > 9 kPa ^[4]
• Supplemental O2 to maintain oxygenation
• Avoid hyperventilation initially (see ICP section below)
• Check for associated chest injuries (pneumothorax, haemothorax, flail chest) — these cause hypoxia → secondary brain injury

• Avoid hypotension at all costs — SBP < 90 mmHg is catastrophic
• Two large-bore IV cannulae, aggressive fluid resuscitation
• Scalp wound: MUST suture to stop bleeding! ^[4] — scalp lacerations can cause haemorrhagic shock
  • Management: haemostasis first → direct compression → wound irrigation ± debridement → primary closure with big stitches through aponeurosis ^[2]
• Identify and treat extracranial sources of blood loss (chest, abdomen, pelvis, long bones)
• Blood products as needed (crossmatch, MTP if massive haemorrhage)

• Head elevation ~30° ^[2][4][12]
• Avoid neck rotation ^[12] — rotation compresses internal jugular veins → impairs venous drainage → ↑ICP
• Remove neck collar if not indicated ^[12] — collar can compress jugular veins. Once C-spine is cleared, remove it
• Maintain vascular volume & BP ^[12]

Why head elevation? Elevating the head uses gravity to promote venous drainage from the brain back to the heart via the internal jugular veins. This reduces intracranial venous blood volume → reduces ICP (Monro-Kellie doctrine: reduce blood component → ICP falls). But you must maintain MAP — if the patient is hypovolaemic, head elevation can drop MAP and worsen CPP.

• IV Tranexamic acid 1g: within 3 hours if mild-moderate TBI + reactive pupils ^[4] — based on the CRASH-3 trial ^[4]
• Dosing: loading dose 1g IV, then maintenance 500 mg Q8H IV ^[2]
• Effect: ↓haemorrhage, might ↓oedema and ischaemic lesions ^[2]

Mechanism of TXA: Tranexamic acid ("trans" = across, "amine" = amino group, "ex" = from, "amic" = related to amino acid) is an antifibrinolytic — it inhibits plasminogen activation → prevents fibrin clot breakdown → stabilizes clots and reduces bleeding. In TBI, ongoing microvascular bleeding worsens contusions and haematomas. TXA helps stop this.

Reverse bleeding tendency ^[1][2]:

• Sedation reduces cerebral metabolic rate → reduces cerebral blood flow → reduces ICP ^[12]
• Also reduces agitation (which increases ICP via Valsalva, fighting the ventilator)
• Common agents: propofol (short-acting, titratable), midazolam, fentanyl
• Use barbiturates or propofol only in ICU ^[1][2] — these can cause profound hypotension

• Avoid hypoglycaemia — glucose is the brain's primary fuel; hypoglycaemia directly causes neuronal death
• Target serum Na > 140 ^[4] — mild hypernatraemia is protective in TBI (reduces cerebral oedema)
• Monitor for post-TBI hyponatraemia: SIADH vs CSWS ^[8] — different volume status → different treatment

• Seizure prophylaxis for 1 week ^[2][4] — only for early post-traumatic seizures (within 7 days)
• Common agents: levetiracetam (Keppra), phenytoin
• No need for prophylaxis if patient is already sedated ^[4]
• No evidence that prophylaxis prevents LATE seizures (> 7 days) — therefore do NOT continue beyond 1 week unless seizures occur
• Why prevent seizures? Seizures cause hyperaemia and exacerbate ↑ICP ^[2]. Seizure activity massively increases cerebral metabolic demand → increases CBF → increases intracranial blood volume → raises ICP. Additionally, prolonged seizures cause excitotoxic neuronal death.

• Fever increases cerebral metabolic rate (~8% per °C) → increases CBF → increases ICP
• Target temperature < 37°C ^[4]
• Identify and treat infectious sources (UTI, pneumonia, line infections)
• Antipyretics (paracetamol), active cooling if needed

• Target: PaCO2 4.5–5 kPa (34–38 mmHg) in routine management ^[4]
• Avoid hypoxia (PaO2 > 9 kPa)
• See hyperventilation section below for ICP emergencies

• Feeding at least by Day 5 ^[4] — early nutrition improves outcomes
• Route: enteral (NG/NJ tube) preferred over parenteral

• Graded compression stockings ^[4]
• Pharmacological prophylaxis (LMWH) when intracranial haemorrhage is stable (typically 48–72h post-injury) — balance bleeding risk vs. VTE risk
• Intermittent pneumatic compression devices

• H2 blockers (ranitidine) or PPIs ^[2]
• TBI patients are at high risk of stress (Cushing) ulcers — the hypothalamic-pituitary axis is disrupted, causing vagal hyperactivation → increased gastric acid secretion

"Do NOT blindly hyperventilate" ^[1]

The physiology: CO2 is a potent cerebral vasodilator. Lowering PaCO2 (by hyperventilating) causes cerebral vasoconstriction → reduces cerebral blood volume → reduces ICP. This works fast (onset ~1 minute).

The danger: Excessive vasoconstriction can cause cerebral ischaemia — you're trading ICP reduction for blood flow reduction. In the first 24 hours after TBI, CBF is already low, so hyperventilation during this period is particularly dangerous.

Guidelines ^[2]:

• Target PaCO2 30–35 mmHg (moderate hyperventilation)
• Short-term measure only — for acute ICP crises (e.g. impending herniation with dilating pupil)
• Not for first 24 hours of head injury (CBF already reduced)
• Must have PaCO2 monitoring (ABG or end-tidal CO2)

• Last-resort medical measure for refractory raised ICP
• Risks: hypotension (barbiturates are vasodilators), infection (immunosuppression), electrolyte derangement ^[2]
• Never use outside ICU ^[1][2] — requires invasive haemodynamic monitoring (arterial line, CVP) and vasopressor support
• Common agent: thiopentone infusion with EEG monitoring (titrate to burst suppression)

Understanding surgical terms is essential:

• Craniotomy = a bone flap is raised and replaced after the procedure ^[6][12]
• Craniectomy = a bone segment is removed and NOT replaced → allows brain to swell outward ^[6]
• Burr hole = a small hole drilled through skull for drainage ^[6][12]
• Cranioplasty = secondary procedure to replace the skull defect (usually months later, using titanium mesh or stored bone)

• Craniotomy + haematoma evacuation ^[1][2]
• Good outcome if timely evacuation ^[4] — because the underlying brain parenchyma is often intact (the problem is the expanding haematoma, not diffuse brain damage)
• Open craniotomy allows complete visualization and haemostasis of the middle meningeal artery

Conservative management of EDH — only if ALL of the following are met ^[6]:

• Haematoma clot volume < 30 cm³
• Maximum thickness < 1.5 cm
• GCS score > 8
• No focal neurological deficits
• Serial CT monitoring with low threshold for surgery if any expansion

Acute SDH ^[1][2]:

• Craniotomy for clot evacuation ^[1] — clotted blood cannot be drained through a small hole
• High mortality ^[1] — because acute SDH is usually associated with significant underlying brain laceration and contusion ^[1]
• Poor functional prognosis ^[1]
• Only consider craniotomy in those who are young with good premorbid status ^[2] — in elderly with severe brain injury, surgery may not improve meaningful outcome

Subacute/Chronic SDH ^[2]:

• Burr hole + drainage ^[2][4][12] — the blood has liquefied over weeks and can be drained through a burr hole
• Good outcome with drainage ^[4]
• Craniotomy if recurrent ^[4]
• Late presentation means most damage is from secondary injury; initial injury was likely mild → good prognosis ^[2]

• May enlarge with time — NOT the worst until at least Day 4–5 ^[1][2] → MUST observe patients + repeat scans even if first scan only shows small haematoma ^[2]
• Surgical evacuation indicated in ^[2]:
  • Posterior fossa when there is evidence of significant mass effect
  • Hemispheric only when very large (> 50 cm³) or GCS 6–8 + frontotemporal ICH > 20 cm³ + midline shift ≥ 5 mm or cisternal compression on CT scan ^[2]

• No surgical management possible — the injury is microscopic and diffuse
• Supportive ICU care: ICP management, prevent secondary insults
• Late sequelae: brain swelling, prolonged coma, poor functional recovery ^[2]

• Surgical removal of a large portion of skull (unilateral or bilateral) without replacing it → allows brain to expand outward
• Indicated for refractory raised ICP with diffuse swelling not responding to medical therapy
• ↓Mortality but poor quality of survival ^[2] — survivors may have severe disability
• Not recommended in all guidelines but still done a lot ^[2]
• A secondary cranioplasty is performed months later to restore skull integrity

Linear vault fractures ^[2]:

• Conservative management unless associated with other lesions (e.g. EDH)
• CT to rule out underlying intracranial pathology

Depressed vault fractures ^[1][6]:

• Irrigation and suture scalp ^[1]
• Do not finger-explore ^[1]
• Antibiotics ^[1]
• Call neurosurgeons ^[1]
• Craniotomy if depression greater than cranial thickness ^[6] — elevate fracture, debridement of fragments and devitalized tissue, repair dural disruption, haemostasis

Skull base fractures ^[4]:

• Nasal packing if bleeding ^[4]
• Antibiotics if open/skull base fractures ^[4]
• Discuss for embolization if life-threatening haemorrhage ^[4]
• CSF fistula: usually heals spontaneously; may require surgical repair if persistent/delayed ^[4]
  • Elevation of head of bed ± lumbar drain to reduce hydrostatic pressure across the defect
  • Incidence of bacterial meningitis rises substantially if leak persists for 7 days ^[6]
  • No proven efficacy of prophylactic antibiotics for preventing meningitis in CSF leaks ^[6] — but antibiotics are often given in practice

• IV Antibiotics — decreases chance of meningitis or abscess formation
• Operative exploration: remove objects extending out of cranium, debridement, irrigation, haemostasis, definitive closure
• Cerebral angiography must be considered if object passes near a major artery or dural venous sinus

• Release CSF with or without overt hydrocephalus ^[12]
• Also for ICP monitoring ^[12]
• Gold standard for ICP measurement ^[12]
• Manometric principle for monitoring intracranial CSF pressure ^[12]
• Therapeutic by draining CSF for decompression ^[12]
• Risk of infection, iatrogenic trauma ^[12]
• LP contraindicated if raised ICP ^[12] — risk of tonsillar herniation

This is the final common pathway by which head injuries kill. Whether the insult is an expanding haematoma, diffuse oedema, or hydrocephalus, the mechanism is the same: ↑ICP → ↓CPP → cerebral ischaemia → herniation → death ^[2].

Causes of ↑ICP after head injury:

• Expanding haematoma (EDH, SDH, ICH)
• Post-traumatic brain swelling (vasogenic + cytotoxic oedema + reactive hyperaemia) ^[2]
• Post-traumatic hydrocephalus (blood in ventricles/subarachnoid space → impaired CSF drainage)
• Contusion expansion (peaks at Day 4–5 — not the worst until at least Day 4–5 ^[1])
• Venous sinus thrombosis (if fracture crosses a sinus groove)

Clinical features of ↑ICP:

• Headache (worse supine, worse early morning — because venous return from brain is reduced when lying flat and PaCO2 rises during sleep)
• Vomiting (may be projectile — area postrema stimulation)
• Deterioration in consciousness (bilateral cerebral compression → impaired reticular activating system)
• Papilloedema (late sign — impaired axoplasmic flow in optic nerve)
• CN VI palsy (abducens nerve has the longest intracranial course → stretched by generalised ↑ICP → "false localizing sign" because it doesn't indicate the location of the lesion)
• Cushing reflex: hypertension + bradycardia + irregular respiration ^[6] — a pre-terminal sign indicating brainstem compression. Mechanism: brainstem ischaemia → massive sympathetic discharge → hypertension → baroreceptor reflex → bradycardia → medullary respiratory centre compression → irregular breathing

Herniation syndromes (detailed in prior sections):

Why is herniation irreversible? Once brain tissue is squeezed through a rigid opening, the blood supply is compressed → tissue infarction. Even if you relieve the pressure later, the infarcted tissue is dead. This is why all of TBI management is about preventing herniation before it happens.

Multifactorial ^[2]:

• Vasogenic oedema: disrupted blood-brain barrier (BBB) → plasma proteins and fluid leak into extracellular space. Why does the BBB break? Direct mechanical injury to capillary endothelial tight junctions + inflammatory mediators (cytokines, free radicals, complement activation)
• Cytotoxic oedema: neuronal and glial cells swell due to energy failure (Na/K-ATPase fails → intracellular Na and water accumulate). Caused by ischaemia, excitotoxicity (glutamate release), direct injury
• Reactive hyperaemia: impaired vascular autoregulation → cerebral vessels dilate inappropriately → increased cerebral blood volume

Vicious cycle: oedema → ↑ICP → ↓CPP → further ischaemia → more oedema → more ↑ICP ^[2] Very difficult to treat because of multifactorial origin ^[2]

• Caused by impaired cerebral vascular autoregulation ^[2]
• Normally, the cerebral vasculature adjusts resistance to maintain constant blood flow across a wide range of blood pressures (MAP 50–150 mmHg, "pressure-active" system) ^[2]
• In TBI, this system is faulty — "pressure-passive" system — a drop in MABP can directly lead to cerebral ischaemia ^[2]
• Features: occurs after severe head injury, risk of neuronal loss ^[2]
• Ischaemia is the single biggest cause of secondary neuronal death in TBI — hence why maintaining MAP/CPP is so critical

Post-traumatic hydrocephalus occurs through two mechanisms:

• Traumatic SAH with intraventricular haemorrhage (IVH) → obstructive hydrocephalus if it obstructs drainage ^[3]
• Clinical: rapid deterioration of consciousness, upgrading of signs of ↑ICP
• Management: EVD (external ventricular drain) for acute hydrocephalus → later VP shunt if chronic

• Brain contusions may enlarge or progress to frank haematoma, particularly in the first 24 hours ^[6]
• Mass effect and oedema develop around contusions ^[1]
• Not the worst until at least Day 4–5 ^[1][2] — this cannot be overemphasized. A "small" contusion on initial CT can evolve into a life-threatening haematoma requiring craniotomy
• Why does contusion expand? Ongoing microvascular oozing + pericontusional oedema + loss of local autoregulation → progressive swelling + more bleeding. Patients on anticoagulants are at especially high risk of delayed expansion
• Repeat CT if clinical deterioration ^[1] — initially normal/mild CT findings do not preclude subsequent development of life-threatening mass lesion ^[1]

• Basal skull fractures indicate risk of meningitis ^[2]
• Mechanism: skull base fracture creates a communication between the subarachnoid space and the external environment (via paranasal sinuses or middle ear) → bacteria enter
• Anterior skull base fracture: breach of cribriform plate → connection with paranasal sinuses → CSF rhinorrhoea → meningitis ^[1]
• Middle skull base fracture: breach of petrous temporal bone → connection with middle ear → CSF otorrhoea → meningitis
• Incidence of bacterial meningitis rises substantially if CSF leak persists for 7 days ^[6]
• Common organisms: Streptococcus pneumoniae (most common in post-traumatic meningitis), Haemophilus influenzae, Gram-negative bacilli
• Risk of infection (meningitis, brain abscess) if compound ± contaminated depressed fracture ^[1]

• Complication of compound depressed fractures, penetrating injuries, or haematogenous spread from wound infection
• Mechanism: bacteria inoculated into brain tissue through contaminated bone fragments or foreign bodies → local infection → encapsulated collection of pus
• Clinical features: headache, fever, focal neurological deficits, seizures, signs of ↑ICP
• Management: IV antibiotics (empirical then targeted) + neurosurgical aspiration or excision
• Prevention: IV antibiotics for penetrating injuries decrease the chance of meningitis or abscess formation ^[6]; debridement of contaminated wounds

• Compound fractures and scalp lacerations in the loose areolar connective tissue layer ("danger zone") of the scalp are at risk because emissary veins from dural venous sinuses pass through this layer → injuries here can lead to osteomyelitis of skull or septic venous thrombosis in dural venous sinuses ^[2]
• Prevention: thorough wound irrigation, debridement, primary closure, antibiotics for compound fractures

• Anterior skull base fracture → injury to internal carotid artery as it passes through the carotid canal/cavernous sinus → pseudoaneurysm formation
• May present with delayed massive epistaxis (carotid blow-out) or with SAH
• Diagnosis: CTA or conventional angiography
• Management: endovascular coiling/stenting or surgical repair

• Late complication of skull base fracture ^[1]
• Mechanism: tear in the ICA wall within the cavernous sinus → abnormal communication between the high-pressure ICA and the low-pressure cavernous sinus
• Clinical features: pulsatile proptosis, chemosis (conjunctival oedema), orbital bruit, ophthalmoplegia (CN III, IV, VI all traverse the cavernous sinus), raised intraocular pressure → visual loss
• Why pulsatile proptosis? Arterial blood at systemic pressure shunts into the cavernous sinus → venous drainage reverses direction → superior ophthalmic vein becomes arterialized → pulsatile orbital congestion
• Management: endovascular embolization of the fistula

• Cervical ICA or vertebral artery dissection from high-energy neck trauma or basal skull fracture
• Can cause delayed ischaemic stroke (hours to days after injury)
• Diagnosis: CTA
• Management: anticoagulation or antiplatelet therapy (controversial in context of traumatic ICH)

• Fractures crossing a dural venous sinus groove may injure the sinus → thrombosis → impaired cerebral venous drainage → raised ICP
• Can also result from infection tracking via emissary veins

• Depressed skull fracture → risks of epilepsy ^[1]
• Cortical contusion (especially frontal/temporal)
• Intracranial haematoma (EDH, SDH, ICH)
• Penetrating injury
• Prolonged post-traumatic amnesia
• Early post-traumatic seizure (increases risk of late PTE by 2–3x)

• Seizure prophylaxis for 1 week (early seizures only) — levetiracetam or phenytoin
• No evidence that prophylaxis prevents late seizures → do NOT continue beyond 1 week unless seizures occur ^[2]
• Early anticonvulsant (usually IV phenytoin) if any seizures occur → wean off (except in delayed seizures) ^[17]
• Long-term anticonvulsants for established post-traumatic epilepsy (levetiracetam, sodium valproate, carbamazepine)

This is a classic exam question — both conditions follow head pathologies and cause hyponatraemia, but the mechanism and treatment are opposite.

Why the treatment is opposite: In SIADH, you have too much water → restrict water. In CSWS, you are losing salt → replace salt and volume. Giving fluid restriction to a CSWS patient will worsen their hypovolaemia and drop their CPP — potentially catastrophic in a head injury patient with impaired autoregulation.

Both can follow head pathologies ^[8]. The key differentiator is volume status — assess clinically (skin turgor, mucous membranes, CVP, urine output) and biochemically.

• Caused by damage to the hypothalamic-pituitary axis (posterior pituitary) → failure of ADH secretion
• Common after skull base fractures involving the sella turcica, or after neurosurgery in this region
• Clinical features: polyuria (dilute urine, urine osm < 300), polydipsia, hypernatraemia, dehydration
• Can be transient (neuronal stunning), triphasic (initial DI → SIADH → permanent DI), or permanent
• Management: IV fluid replacement + desmopressin (DDAVP — synthetic ADH analogue)

• Severe TBI → massive sympathetic surge → systemic vasoconstriction → acute left ventricular overload → transudation of fluid into alveoli
• Rapidly develops after severe head injury, often within minutes to hours
• Clinical: acute respiratory distress, bilateral pulmonary infiltrates, hypoxaemia
• Management: supportive (mechanical ventilation, PEEP), treat the underlying ↑ICP

• GCS ≤ 8 → loss of airway protective reflexes → aspiration of gastric contents/oral secretions
• This is why intubation is mandatory for GCS ≤ 8
• Prevention: early intubation, NGT for gastric decompression, head elevation, careful feeding practice ^[17]

• Head trauma is a recognized indirect cause of ARDS (neurogenic ARDS) ^[19]
• Mechanism: systemic inflammatory response from massive tissue injury + neurogenic catecholamine surge → diffuse alveolar damage
• Part of a broader systemic inflammatory response to severe trauma

• Associated with long bone fractures (which commonly co-exist with head injuries in polytrauma)
• Fat globules from fractured bone marrow enter venous circulation → lodge in pulmonary capillaries → systemic embolization
• Classic triad: respiratory distress, petechial rash, neurological deterioration (24–72h after injury)
• Diagnosis: clinical; no single definitive test
• Management: supportive (O2, mechanical ventilation); prevention by early fracture fixation

• Hallmark: confusion + amnesia (may appear immediately or several minutes later) ^[2]
• LOC not present in the majority of cases ^[2]
• Other early symptoms: headache, dizziness, loss of awareness, N/V ^[2]
• Late symptoms: neuropsychiatric symptoms (mood/cognitive disturbances, sensitivity to light and noise, sleep disturbances), symptomatic seizures ^[2]
• Symptomatic seizures: half ≤ 24h, quarter ≤ 1h, majority ≤ 1 week — NOT regarded as epilepsy ^[2]

• Majority have good prognosis but some develop post-concussion syndrome ^[2]
• Pathogenesis: disputed — may have neurobiological and psychogenic bases ^[2]
• Symptoms ^[2]:
  • Headache (25–78%), dizziness, sleep disturbance
  • Neuropsychiatric (> 50%): personality changes, irritability, anxiety, depression, PTSD
• Diagnosis: often difficult → investigations to rule out more severe pathologies → many psychogenic but don't dismiss ^[2]
• Treatment: generally supportive (little evidence) ^[2]

• Brain remains in a hypermetabolic state for up to 1 week after injury and more susceptible to injury in the first 1–2 weeks after concussion ^[6]
• A second concussive impact during this vulnerable window can cause catastrophic, often fatal, diffuse cerebral swelling
• Patients should be informed that even after mild head injury they might experience memory difficulties or persistent headaches ^[6]
• This is the basis for return-to-play protocols in sports concussion — graded return over days to weeks