GC208 Unconscious After An Accident Head Injury
Unconsciousness following traumatic head injury is a state of impaired awareness resulting from brain damage due to external force, often involving concussion, intracranial hemorrhage, or diffuse axonal injury requiring urgent neurological assessment and management.
Unconscious After an Accident: Head Injury
Lecture Map
This lecture by Professor Gilberto Leung is one of the highest-yield neurosurgery sessions for the Fourth Summative. It covers the pathophysiology, clinical assessment, and management of traumatic brain injury (TBI) — a topic that has appeared in MCQ, SAQ, and Minicase formats repeatedly across multiple exam years.
- Understand the pathophysiology & complications of traumatic brain injury (TBI)
- Understand the clinical presentation of raised intracranial pressure (ICP)
- Apply the principles of management of TBI and raised ICP
A patient who arrives unconscious after trauma needs simultaneous consideration of three possibilities: (1) unconsciousness from TBI itself, (2) unconsciousness from shock due to extracranial injuries, and (3) unconsciousness that preceded the accident (e.g. cardiac arrhythmia, seizure, stroke) and caused the trauma in the first place. The management hierarchy is ABC before ICP — you resuscitate first, stabilise vital signs, and only then proceed to CT and neurosurgical intervention. [1]
- MCQs: GCS calculation, ICP physiology (CPP formula, normal values), which intervention is correct/contraindicated
- SAQs: Common exam scenario is a patient with GCS breakdown → calculate score, fixed dilated pupil → explain mechanism, CT findings → name pathology, management steps
- Minicases: Multi-system trauma with evolving neurological deterioration
Core Concepts and Mechanisms (First Principles)
Assumed TBI. Assume extracranial injuries. Resuscitation first. CT scan & neurosurgical intervention only when vital signs stable. ABC before ICP!! [1]
The brain cannot survive if the body is dying. A patient with BP 65/20 and SpO2 82% is in haemorrhagic shock and hypoxic — these systemic insults cause secondary brain injury that compounds whatever primary injury the brain has already sustained. Fixing the brain first while the patient bleeds out from a pelvic fracture is fatal. Hence: Airway → Breathing → Circulation (not CT scan!) → Disability → Exposure. [1]
| Primary Brain Injury | Secondary Brain Injury | |
|---|---|---|
| Timing | At time of trauma | Develops later |
| Nature | Fixed, irreversible | Potentially avoidable/reversible |
| Examples | Cortical contusion, diffuse axonal injury, skull fracture | Hypotension, hypoxia, expanding haematoma, brain swelling, seizures, infection, electrolyte disturbance |
Why this matters: Everything we do in TBI management is aimed at preventing or treating secondary injury. The primary injury is done — you cannot undo the moment of impact. But you CAN prevent the cascade of hypotension → cerebral ischaemia → oedema → raised ICP → herniation → death. [1]
The skull is a rigid box containing three compartments: brain tissue (~80%), blood (~10%), and CSF (~10%). Total intracranial volume is constant. If one compartment expands (e.g. haematoma, swelling), the others must decrease to compensate:
- Venous blood is displaced outward (through jugular veins)
- CSF is displaced into the spinal canal
This is the compensatory phase (ICP remains normal despite growing mass). Once compensation is exhausted, ICP rises exponentially with even small volume increases — this is the decompensation phase. [1]
"Talk… and die" — the exponential ICP-volume curve [1]
This is why a patient with an epidural haematoma can be lucid initially (compensating) and then suddenly deteriorate catastrophically (decompensation). The ICP-volume curve is not linear.
CPP = MAP – ICP [1]
- Normal ICP = 10–15 mmHg [1]
- Normal CPP = 60–80 mmHg [1]
- Normal CBF = 45–65 ml/min/100g tissue [1]
- Aim: CPP ~60–70 mmHg [1]
Why CPP matters: The brain has no energy stores. It requires continuous perfusion. If ICP rises or MAP drops, CPP falls → cerebral ischaemia → more oedema → higher ICP → vicious cycle.
Why you must not "blindly lower BP": Lowering MAP in a head-injured patient drops CPP and worsens ischaemia. Conversely, you must not let severe hypertension go unchecked either (worsens vasogenic oedema). The lecture says "Avoid extreme anything". [1]
CBF = CPP / CVR [1]
CO₂ is a potent cerebral vasodilator. Hyperventilation lowers PaCO₂ → vasoconstriction → decreased cerebral blood volume → decreased ICP. Sounds great — but:
- Excessive vasoconstriction → increased CVR → decreased CBF → cerebral ischaemia [1]
- Aim: PaCO₂ ~3.0–3.5 kPa (≈22.5–26.3 mmHg) [1]
High-Yield: Do NOT Blindly Hyperventilate
Hyperventilation should NOT be: prophylactic, prolonged, without evidence of raised ICP, without ICP monitoring, or stopped suddenly (rebound ICP rise). It may be used briefly to "buy time" (e.g. on the way to OT). [1]
The ABCDE Approach in Head Injury (Slide-by-Slide)
- Protect airway & prevent aspiration while simultaneously assuming C-spine injury and stabilising it
- Normal C-spine X-rays do NOT exclude instability — only remove the collar after CT confirmation
- Then elevate head ~30° for venous drainage (improves jugular outflow → lowers ICP)
Why 30° head elevation? The brain drains venously through the jugular veins. If the head is flat or turned/flexed, jugular venous outflow is impeded → venous congestion → raised ICP. Elevating to 30° optimises venous drainage without excessively reducing MAP (which would happen with extreme elevation). [5]
Why assume C-spine injury? Up to 10% of patients with significant head injury have a concomitant C-spine injury. An unconscious patient cannot report neck pain. Moving an unstable C-spine risks quadriplegia. [2]
Airway management in suspected C-spine injury: Use jaw thrust (not head-tilt/chin-lift, which extends the neck). [10]
- Ensure adequate ventilation and oxygenation
- Controlled ventilation targeting PaCO₂ 3.0–3.5 kPa
- No blind hyperventilation (see above)
C — Circulation [1]
"C is for Circulation, not CT scan!" [1]
- Fluid replacement
- Identify source and stop bleeding: chest drain, limb traction, pelvic binder
- Post-traumatic coagulopathy: packed-cell-only transfusion is inadequate
- Massive Transfusion Protocol: PC:FFP:PLT = 1:1:1 [1]
- Hypothermia worsens coagulopathy → actively warm the patient
Why 1:1:1 ratio? In massive haemorrhage, you lose all blood components. If you transfuse only packed cells, you dilute out clotting factors and platelets → dilutional coagulopathy → more bleeding → more transfusion needed (vicious cycle). The balanced 1:1:1 approach mimics whole blood and breaks this cycle. [1]
Can bleed to shock! [1]
- Use compression first
- Big stitches through the aponeurosis (the galea aponeurotica carries the blood supply; stitching through it controls arterial bleeding)
- Haemostasis before cosmesis — you can always redo it later
- Do NOT attempt fine cosmetic repair in the resuscitation room
Tranexamic Acid (TXA):
- Anti-fibrinolytic agent → decreases haemorrhage
- Safe & improves outcome on RCT (CRASH-2 / CRASH-3)
- Loading: 1g over 10 min, then 1g over 8 hours IV [1]
Correct Bleeding Tendency: [1]
| Anticoagulant/Antiplatelet | Reversal |
|---|---|
| Antiplatelet agents | Platelet transfusion (no proven benefit; possibly harmful but still done) |
| Warfarin | Vitamin K + FFP + 4-factor PCC (prothrombin complex concentrate) |
| NOAC (dabigatran) | Idarucizumab |
| Any | Thromboelastometry (ROTEM) if feasible for guided therapy |
Exam Scenario
The lecture's common clinical scenario features a patient on warfarin for AF. Exam Q: "He was taking warfarin. What should be done?" → Answer: Reverse with Vitamin K, FFP, and 4-factor PCC. [1]
This is where the Glasgow Coma Scale (GCS) comes in.
Full exposure to identify all injuries, but prevent hypothermia.
Glasgow Coma Scale (GCS)
Objective & reproducible way to assess consciousness. Post-resuscitation GCS is highly prognostic. Trend reflects deterioration/improvement. Quantitative (3–15) but not a linear scale. [1]
| Component | Score | Response |
|---|---|---|
| Eye Opening (E) | 4 | Spontaneous |
| 3 | To speech | |
| 2 | To pain | |
| 1 | None | |
| Verbal Response (V) | 5 | Orientated (person, place, time) |
| 4 | Confused (sentences but disoriented) | |
| 3 | Inappropriate words | |
| 2 | Incomprehensible sounds (moaning/groaning) | |
| 1 | None | |
| Motor Response (M) | 6 | Obeys commands |
| 5 | Localises pain (hand raised above clavicle) | |
| 4 | Flexion withdrawal (hand does NOT rise above clavicle) | |
| 3 | Abnormal flexion (decorticate posture) | |
| 2 | Extension (decerebrate posture) | |
| 1 | None |
Motor score is indicative of extent of injury & prognostic [1]
- Apply painful stimuli over CN V territory (supraorbital pressure)
- Record the best response of any limb
- M5 (localise): UL raised above clavicle
- M4 (withdrawal): UL withdraws but NOT above clavicle
- M3 (abnormal flexion / decorticate): injury to corticospinal tract above midbrain
- M2 (extension / decerebrate): injury to midbrain or upper pons [1]
Why decorticate vs decerebrate matters anatomically:
- Decorticate (M3): The corticospinal tract (from cortex) is damaged, but the rubrospinal tract (from red nucleus in midbrain) is intact → red nucleus drives UL flexion while LL extends
- Decerebrate (M2): Damage extends to/below midbrain → both rubrospinal and corticospinal tracts are out → vestibulospinal/reticulospinal pathways dominate → extension of all limbs
| Severity | GCS | Disability rate |
|---|---|---|
| Mild | 13–15 | 30% become disabled |
| Moderate | 9–12 | 40% become disabled |
| Severe | ≤8 | Variable; predictors: post-resuscitation GCS & age |
"He could open eyes and flex his upper limbs upon painful stimulation but had no verbal response"
- E2 (eyes open to pain)
- M4 (flexion to pain — "flex upper limbs" without mention of going above clavicle = withdrawal = M4)
- V1 (no verbal response)
- GCS = E2M4V1 = 7 [1]
Localising & Late Signs of Raised ICP [1]
Uncal herniation → ipsilateral dilated non-reactive pupil (CN III compression) + contralateral hemiparesis + further drop in conscious level [1]
Why ipsilateral pupil? The uncus of the temporal lobe herniates over the tentorial edge and compresses CN III on the same side. CN III carries parasympathetic fibres to the pupillary sphincter (constriction). Compression of these fibres → loss of constriction → mydriasis (dilation). The pupil becomes "fixed and dilated."
Why contralateral hemiparesis? The herniating uncus compresses the ipsilateral cerebral peduncle (containing the corticospinal tract), which has not yet decussated → contralateral weakness.
(Exception: Kernohan's notch — the contralateral cerebral peduncle is compressed against the opposite tentorial edge → ipsilateral hemiparesis, a "false localising sign")
Late signs: Papilloedema, Cushing Triad [1]
Cushing Triad = Hypertension + Bradycardia + Irregular respirations
- This is a brainstem reflex — the brain detects falling CPP and triggers massive sympathetic outflow to raise BP. The baroreceptors then respond to the high BP with reflex bradycardia. Irregular breathing reflects brainstem compression affecting respiratory centres.
- Cushing reflex is a pre-terminal sign — by the time you see it, the patient is near death.
Obliteration of basal cisterns indicates "coning" (brain herniation) — The lecture shows a CT comparison: patent basal cisterns = "brain is smiling" vs obliterated cisterns = "not smiling" = brainstem compressed. [1]
Only when vital signs stabilised. Continuous monitoring during transport. If unstable, skip CT and go straight to theatre (e.g. laparotomy). [1]
- SXR (skull X-ray) is NOT very helpful (low sensitivity for intracranial pathology)
- CT Brain + C-spine is the standard
- Consider whole-body CT with contrast in polytrauma
The Donut of Death
The CT scanner has been called the "Donut of Death" because unstable patients die in the scanner when they should be in the operating theatre. Never send an unstable patient for CT. [1]
Indications for CT Brain [1]
The lecture explicitly says "Know these indications" — indications include:
- GCS < 15 (any reduction in consciousness)
- Suspected skull fracture (depressed, open, or base of skull signs)
- Post-traumatic seizure
- Focal neurological deficit
-
1 episode of vomiting
- Amnesia for events > 30 minutes before impact
- Dangerous mechanism of injury
- On anticoagulants / coagulopathy
- Age ≥ 65
Skull Fracture Classification [1]
- Linear / Comminuted (in fragments)
- Closed or Compound ("open")
- Depressed or not
- Skull vault
- Skull base (anterior, middle, posterior fossa)
Indicates significant energy transfer. Exclude underlying injury (CT Brain) — e.g. epidural haematoma, brain contusion. Otherwise managed conservatively. Distinguishable from vessel grooves or sutures. [1]
- De-vascularized bone fragments
- Complications: dura tear (CSF leakage), brain laceration, bleeding, risks of epilepsy and neurological deficits
- If compound +/- contaminated → risk of infection (meningitis, brain abscess)
- Management: Irrigation & suture scalp. Do NOT finger-explore. Antibiotics. Call neurosurgeons. [1]
| Feature | Explanation |
|---|---|
| Periorbital ecchymoses (raccoon eyes) | Blood tracks along anterior cranial fossa to orbits |
| Olfactory / optic nerve injury | CN I and II pass through anterior fossa |
| CSF rhinorrhoea → meningitis risk | Fracture connects subarachnoid space to paranasal sinuses |
| Life-threatening haemorrhages | Internal carotid artery runs through cavernous sinus nearby |
| Traumatic ICA aneurysm | Vessel wall damage from fracture |
| Carotico-cavernous fistula (late) | Abnormal communication between ICA and cavernous sinus |
| Feature | Explanation |
|---|---|
| Haemotympanum | Blood behind tympanic membrane (seen on otoscopy) |
| Post-auricular ecchymoses (Battle's sign) | Blood tracks along mastoid |
| CSF otorrhoea | If TM is ruptured |
| CSF rhinorrhoea via Eustachian tube | If TM is intact, CSF drains anteriorly |
| CN V, VI, VII, VIII palsies | These nerves traverse the middle cranial fossa/petrous bone |
Intracranial Haematomas [1]
Commonly from skull fracture & torn meningeal vessels (middle meningeal artery in 75–85%). Biconvex (lentiform) hyperdense lesion on CT. May be small initially but can expand quickly. Craniotomy for evacuation. Relatively good prognosis if treated early. [1]
"Talk then die!" [1] — The classic lucid interval: patient is initially conscious (before haematoma reaches critical volume), then rapidly deteriorates as ICP spikes during decompensation.
| Feature | EDH | Acute SDH |
|---|---|---|
| Source | Middle meningeal artery (arterial, 85%) | Bridging veins (venous) / cerebral arteries |
| CT shape | Biconvex / lentiform | Crescent-shaped |
| Crosses sutures? | No (dura is adherent to bone at sutures) | Yes |
| Crosses midline? | Yes | No (falx cerebri stops it) |
| Associated skull fracture | 75–90% | Usually no |
| Clinical course | Lucid interval → rapid deterioration | Fluctuating consciousness |
| Prognosis | Relatively good if treated early | High mortality, poor functional outcome |
| Surgery | Craniotomy | Craniotomy |
Commonly rotational injury. Bleeding from bridging veins/cerebral arteries. Crescent-shaped hyperdense lesion. Often associated with brain laceration & contusion. Craniotomy for removal. High mortality. Poor functional prognosis. [1]
Why worse prognosis than EDH? Because SDH is usually associated with underlying brain parenchymal damage (contusion, laceration). The haematoma itself is just the tip of the iceberg — the brain beneath is badly injured. EDH, by contrast, often has minimal underlying brain injury — it's purely an arterial bleed between skull and dura. [1][3]
SDH density changes over time [8]:
- Acute ( < 1 week): Hyperdense
- Subacute (1–3 weeks): Isodense (hard to see!)
- Chronic ( > 3 weeks): Hypodense
Traumatic intracerebral haematoma. Deceleration injury. Focal injury — Coup / Contrecoup. Commonly frontal & temporal poles. May enlarge with time. Mass effect & oedema. Not the worst until at least Day 4–5. [1]
Why frontal and temporal poles? These areas sit on rough, irregular bone (orbital roof, sphenoid wing). During deceleration, the brain impacts these surfaces. Coup = injury directly under the impact site. Contrecoup = injury on the opposite side (brain rebounds against the opposite skull wall).
Why "not the worst until Day 4–5"? Contusions evolve — surrounding oedema and secondary ischaemic injury peak at 4–5 days post-injury. Serial CT is essential.
Complex pathology: disrupted BBB (vasogenic oedema), membrane failure (cytotoxic oedema), vicious cycle of raised ICP → ischaemia → more swelling. Sometimes reactive hyperaemia. Very difficult to treat & high mortality. [1]
Initially normal/mild CT findings do NOT preclude subsequent development of life-threatening mass lesion. Repeat CT if clinically indicated (e.g. drop in GCS, pupil dilatation, seizure, new focal deficit). [1]
| Systemic | Intracranial |
|---|---|
| Hypotension | Intracranial haematoma |
| Hypoxia | Brain swelling |
| Blood glucose abnormalities | Hyperaemia |
| Electrolyte disturbances | Ischaemia |
| Acid-base disturbances | Epilepsy |
| Pyrexia | Hydrocephalus |
| Infection |
Why Fever and Seizures Matter
Fever increases cerebral metabolic rate → increased oxygen demand in already compromised brain. Seizures massively increase neuronal metabolic demand and can worsen ischaemia. Both must be aggressively prevented/treated. [1]
Management of Raised ICP [1]
Mannitol (e.g. 100ml 20% IV):
- Osmotic effect (needs intact BBB to work — draws water from brain into intravascular space)
- Decreases blood viscosity → increases CBF → decreases CBV
- Decreases vascular volume → decreases systemic BP
- Requires Foley's catheter (massive diuresis)
- NOT IF SHOCKED! (it will drop BP further and worsen CPP) [1]
Hypertonic saline:
- Probably better for multiple trauma (does not drop BP as much as mannitol; may actually expand intravascular volume) [1]
Loop diuretics (e.g. frusemide):
- Can be used as adjunct
NO STEROIDS for TBI [1]
Why no steroids? The CRASH trial showed that corticosteroids (methylprednisolone) increased mortality in TBI patients. This is different from brain tumours or spinal cord injury where steroids may have a role. For TBI, steroids are HARMFUL. [1]
- Normal adult ICP = 10–15 mmHg
- Indications: no reliable clinical monitoring (sedated/paralysed), GCS ≤ 8, evolving disease
- Relative contraindications: awake patients, coagulopathy
- Rising ICP: repeat CT & escalate treatment [1]
External Ventricular Drain (EVD):
- Simultaneously monitors ICP AND drains CSF to reduce ICP
- Therapeutic and diagnostic
| Procedure | Indication |
|---|---|
| External Ventricular Drain (EVD) | Release CSF ± hydrocephalus; ICP monitoring |
| Craniostomy (burr hole) | Drainage of superficial fluid collection (e.g. chronic SDH) |
| Craniotomy | Haematoma/tumour removal (bone flap raised and replaced) |
| Decompressive craniectomy | Severe brain swelling — bone flap NOT replaced. Effective in lowering ICP & mortality. Also for massive infarction. Primary pathology/deficit unaltered. Quality of survival variable. Ethical/philosophical issues. |
Aim at "burst suppression." Need EEG monitoring. Decreases neuronal activities → decreases CBF & ICP. Side effects: hypotension, myocardial depression. [1]
Early cooling to 32–34°C. Neuroprotection by: decreased brain metabolic rate, decreased ATP consumption & O₂ demand, decreased cell death cascades. Established therapy for post-cardiac-arrest brain injury. Controversial in stroke & trauma. Side effects: pneumonia, coagulopathy. [1]
Brain "herniates" across intracranial compartments. Basal cistern patent = brainstem happy ("smiling"). Basal cistern obliterated = brainstem compressed ("not smiling"). [1]
Types of brain herniation (from GC 111 and past papers) [4]:
- Subfalcine (cingulate) herniation — cingulate gyrus herniates under falx cerebri
- Transtentorial (uncal) herniation — medial temporal lobe herniates through tentorial notch
- Tonsillar herniation — cerebellar tonsils herniate through foramen magnum → brainstem compression → death
- Upward (ascending) herniation — posterior fossa contents herniate upward through tentorium
- Transcalvarial herniation — brain herniates through skull defect
What MBBS Candidates Must Know:
| DO | DO NOT |
|---|---|
| ABC first | Give steroids |
| Give Transamin (TXA) | Blindly hyperventilate |
| Reverse bleeding tendency | Blindly lower BP |
| Anticipate/Manage deterioration | Give mannitol when shocked |
| Prevent seizure/fever | Use barbiturates or Propofol outside ICU |
| Avoid extreme anything |
An unconscious patient is "just drunk." A known epileptic will "wake up later." A drop in GCS "may be nothing & let's wait." Sedate an uncooperative/noisy patient without airway protection and monitoring. First CT was normal so the patient is OK. [1]
Every one of these is a potential medicolegal disaster. Always assume the worst and prove yourself wrong with investigation.
From Chemical Pathology teaching [9]: After skull base fracture, patients may develop:
- Diabetes insipidus (DI): Damage to pituitary stalk → loss of ADH → massive dilute polyuria → hypernatraemia (Na 164 in the lecture case)
- SIADH: Excess ADH → water retention → hyponatraemia
- Cerebral Salt Wasting Syndrome (CSWS): Natriuresis + diuresis → hypovolaemic hyponatraemia (vs SIADH which is euvolaemic)
SIADH vs CSWS
Both can follow head pathology and both cause hyponatraemia. The key discriminator is volume status: SIADH = euvolaemic, CSWS = hypovolaemic. Treatment differs: SIADH = fluid restriction, CSWS = fluid + sodium replacement. [9]
Exam Intelligence
- "Intracranial pressure is increased by hyperventilation" — FALSE. Hyperventilation decreases ICP (by causing vasoconstriction). But excessive hyperventilation decreases CBF. [1]
- "Normal ICP is 15–20 mmHg" — FALSE in adults (it's 10–15 mmHg). May be trick answer in neonates (lower). [1]
- "CPP should be maintained at 50 mmHg" — FALSE. Aim is 60–70 mmHg. [1]
- CBF is directly proportional to systolic BP — FALSE. CBF = CPP/CVR, and CPP = MAP – ICP (not SBP). Also, autoregulation means CBF is relatively constant over a range of MAPs. [1]
- "CBF is inversely proportional to CVR" — TRUE. This is from CBF = CPP/CVR. [1]
- GCS calculation: Always break down E, M, V separately. The exam loves M4 vs M5.
- Fixed dilated pupil: Always say "ipsilateral CN III compression due to uncal herniation" — not just "raised ICP."
- Three non-surgical treatments for raised ICP: Head elevation 30°, osmotherapy (mannitol/hypertonic saline), controlled hyperventilation, seizure prophylaxis, temperature control, sedation, barbiturate coma. Pick three. [1]
- Appropriate surgical treatment: Depends on pathology. EDH/SDH → craniotomy. Diffuse swelling → decompressive craniectomy. Hydrocephalus → EVD.
Past Paper Questions
Stem: "A 68-year-old woman presented with a sudden onset of right-sided weakness. CT showed a left basal ganglion haemorrhage. She could open eyes and flex her limbs to painful stimuli, and utter inappropriate words."
- (a) What was her GCS? → E2 M4 V3 = 9 (Eyes to pain = 2, Flexion to pain = 4, Inappropriate words = 3)
- (b) She developed a left dilated non-reactive pupil. Mechanism? → Left uncal (transtentorial) herniation compressing the ipsilateral CN III (2 marks)
- (c) Name three types of brain herniation → Subfalcine, transtentorial (uncal), tonsillar (accept also: upward/transcalvarial)
- (d) Commonest cause? → Hypertension (hypertensive intracerebral haemorrhage)
- (e) Three other causes → Cerebral amyloid angiopathy, AVM/aneurysm, coagulopathy/anticoagulant use, brain tumour
(Identical question stem to 2018 Q8 — note this is a repeat/near-identical question)
- Same answers apply
Stem: "Maintaining normal intracranial pressure and adequate cerebral perfusion is crucial in head injury management. Which of the following statements is correct?"
Stem: "A 40-year-old man sustained a whiplash injury in a car crash. Which of the following findings suggests a high risk of respiratory compromise?"
- A. Bilateral hand numbness and clumsiness → Central cord syndrome
- B. Loss of cervical lordosis → Common post-whiplash but not respiratory compromise per se
- C. Raised diaphragm on chest radiograph → CORRECT ✓ (phrenic nerve C3-4-5 palsy → diaphragmatic paralysis → respiratory compromise)
- D. Systemic hypotension and bradycardia → Neurogenic shock (spinal shock), cardiovascular not respiratory
- Answer: C [14]
Stem: "A head-injured patient could open eyes to painful stimulation, show abnormal flexion of his upper limbs, and make incomprehensible sound. What was his GCS?"
Stem: "Maintaining normal intracranial pressure and adequate cerebral perfusion is crucial in head injury management. Which of the following statements is CORRECT?"
- A. CBF is directly proportional to systolic BP → Incorrect (CPP/CVR, not SBP)
- B. CPP should be maintained at around 70 mmHg → CORRECT ✓ (lecture says aim 60–70 mmHg; 70 is within range)
- C. ICP is increased by hyperventilation → Incorrect
- D. ICP is normally around 15–20 mmHg in neonates → Incorrect (lower in neonates)
- Answer: B [1][15]
(Note: This is essentially the same question as 2020 Q63 but with different answer options. The examiners clearly love this topic.)
Stem: "An elderly woman fell at home... During transport, she started snoring and gurgling when taking a breath. What is the MOST APPROPRIATE method to immediately manage this problem?"
- A. Salbutamol → No (not airway obstruction from bronchospasm)
- B. Head-tilt/chin-lift → Risky with neck pain (possible C-spine injury)
- C. Jaw thrust → CORRECT ✓ (maintains C-spine neutrality while opening airway)
- D. Recovery position → Not ideal with possible C-spine injury
- Answer: C [10]
Stem: "A 23-year-old man is carried in after diving head first into a river. He is speaking and his airway is open but he cannot walk or move his arms or legs. What is the first thing you must do?"
- C. Immobilise the cervical spine → CORRECT ✓
- Answer: C — Diving injury with quadriplegia = assume C-spine fracture until proven otherwise [10]
High Yield Summary
TBI Management Framework:
- ABC before ICP — resuscitate first, CT only when stable
- Assume C-spine injury in all unconscious trauma patients; normal X-rays don't exclude instability
- GCS: Motor score is most prognostic; M5 = localise (above clavicle), M4 = withdraw (below clavicle), M3 = decorticate (above midbrain), M2 = decerebrate (midbrain/pons)
- Post-resuscitation GCS is the prognostic GCS
- CPP = MAP – ICP; Aim CPP 60–70 mmHg; Normal ICP 10–15 mmHg
- Hyperventilation: PaCO₂ 3.0–3.5 kPa; NOT prophylactic/prolonged/without monitoring
- TXA: 1g IV over 10 min then 1g over 8 hours
- Warfarin reversal: Vit K + FFP + 4-factor PCC
- Mannitol: Osmotic diuresis for raised ICP — NOT if shocked
- No steroids in TBI
- EDH: Biconvex, doesn't cross sutures, "talk and die," good prognosis if treated early
- Acute SDH: Crescent, crosses sutures, high mortality, poor prognosis
- Contusion: Peaks Day 4–5, coup/contrecoup, frontal & temporal poles
- Uncal herniation: Ipsilateral dilated pupil (CN III) + contralateral hemiparesis
- Obliterated basal cisterns on CT = coning
- Repeat CT if GCS drops, new pupil changes, seizure, or new focal deficit
Active Recall - Lecture Notes
[1] Lecture slides: GC 208. Unconscious after an accident Head injury.pdf [2] Senior notes: Maksim Surgery Notes.pdf (Section 5.1 Traumatic brain injury) [3] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (Neurosurgery Diseases - EDH/SDH) [4] Lecture slides: GC 111. Raised intracranial pressure and hydrocephalus.pdf [5] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Management of increased ICP) [6] Senior notes: Ryan Ho Fundamentals.pdf (Level of Consciousness - GCS) [7] Senior notes: Ryan Ho Neurology.pdf (Level of Consciousness - GCS) [8] Senior notes: Ryan Ho Diagnostic Radiology.pdf (EDH and SDH imaging) [9] Senior notes: Ryan Ho Chemical Path.pdf (SIADH and CSWS); Chemical Pathology Seminar 1_Sodium and water.pdf (Case 3 - skull base fracture with hypernatraemia) [10] Past papers: 2024 Fourth Summative MCQ.pdf (Q2, Q74) [11] Past papers: 2018 Fourth Summative SAQ.pdf (Q8) [12] Past papers: 2019 Fourth Summative SAQ.pdf (Q8) [13] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q63) [14] Past papers: 2022 Fourth Summative MCQ.pdf (Q62, Q67) [15] Past papers: 2023 Fourth Summative MCQ.pdf (Q58)
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