Surgery SC033: Unconscious After An Accident: Head Injury Flashcards
Approach to Unconsciousness
ABC before ICP (ICP is only for managing cerebral perfusion, if circulation (C) is not managed —> no point managing ICP)
- Assume TBI
- Assume extracranial injuries
- Resuscitation first!!!
- CT scan / Neurosurgical intervention only when vital signs stable
ABCDE:
- Airway + C spine protection
- Breathing
- Circulation (not CT scan)
- Disability
- Exposure / Environment
Airway + C spine protection
- Protect airway + prevent aspiration
- Assume C-spine injury and stabilise it
- Normal C-spine X-ray cannot exclude instability
- Remove neck collar only if sure (e.g. after CT)
- Elevate head ~30o for venous drainage
Breathing
- No blind hyperventilation!
- Done occassionally to buy time e.g. on way to OT
Principle:
- ↓ CO2 —> ↑ Vasoconstriction (減少血流到腦) —> ↓ Cerebral blood volume —> ↓ ICP
BUT at the same time
CBF = CPP / CVR
- ↑ Vasoconstriction —> ↑ CPP (∵ ↓ ICP) but ↑↑ CVR (rmb ∵ r^4) —> ↓↓ CBF —> Cerebral Ischaemia
Aim: PaCO2 ~3-3.5 kPa
DO NOT:
- Prophylactic
- Prolonged
- Without ↑ ICP
- Without monitoring
- Stop suddenly —> rebound phenomenon
Circulation
- Identify source + stop bleeding
- Chest drain, limb traction, pelvic binder
- Fluid replacement
-
Post-traumatic coagulopathy
- Packed-cell-only transfusion never inadequate (∵ coagulation profile worsen as bleeding goes on) —> Massive transfusion protocol —> PC:FFP:Plt = 1:1:1 (regardless of normal Plt / INR)
- Hypothermia worsen coagulopathy
Scalp laceration
- Can bleed to shock!
- Use compression —> Finger pressure on wound edges (i.e. compress vessels against bone) (X opening part of wound)
- Big stitches through aponeurosis (X superficial) (continuous running suture) —> Haemostasis before cosmesis! —> can always re-do it later
—> arteries right above aponeurosis of scalp
Suturing purpose:
1. Haemostasis
2. Allow skin to heal
Facilitate haemostasis
- Tranexamic acid
- Anti-fibrinolytic agent —> ↓ Haemorrhage
- Safe + improve outcome on RCT
- Loading 1g over 10 mins —> 1g over next 8 hours IV - Correct bleeding tendency (intrinsic, not trauma-induced coagulopathy)
- Antiplatelet —> Platelet transfusion (no proven benefit, possibly harmful but still done!)
- Warfarin —> Vit K, FFP, 4-factor PCC (Prothrombin complex concentrate, contain Factor 2, 7, 9, 10)
- NOAC —> Idarucizumab for Dabigatran
- Thromboelastometry if feasible (determine which factor the patient is lacking)
Disability: GCS score
- Objective + Reproducible way to assess consciousness
- Quantitative (3-15) but NOT a linear scale
2 purposes:
1. Initial GCS: Prognostic
- Post-resuscitation GCS is highly prognostic
2. Trend reflects deterioration / improvement
Classification of Brain injury:
13-15: Mild, LOC <30 mins
9-12: Moderate, LOC >30 mins, <24 hours
<8: Severe, LOC >24 hours
3 Components:
Eye opening (E1-4) (try to wake up by calling patient by name)
- 4: spontaneous
- 3: to speech
- 2: to pain
- 1: none
Verbal response (V1-5)
- 5: orientated (in person, space, time)
- 4: confused
- 3: inappropriate words
- 2: incomprehensible sounds
- 1: none
Motor response (M1-6) (cortical —> subcortical response) (elicit pain by pricking at Trigeminal region (∵ straight to brainstem))
- 6: obey commands (intact cortical function: able to understand + execute)
- 5: localises to pain (very significant drop, but pyramidal tract still intact, know where the pain is)
- 4: flexion / withdrawal to pain (less precise pyramidal tract function)
- 3: abnormal flexion (extrapyramidal tract response)
- 2: extend
- 1: none
Motor score (M)
- Indicative of extent of injury + prognostic
- Painful stimuli over CNV territory
—> Sternal rub
—> Press on supraorbital ridge
—> Pinch on earlobe - Best response of limbs
M5: UL raised above clavicle
- Unconscious behaviour
- Basal ganglia / Internal capsule level
M4: UL withdraw but not above clavicle
- Unconscious behaviour
- Basal ganglia / Internal capsule level
M3: Decorticate posture, injury to corticospinal tract above midbrain
- Lesion above red nucleus, below cortex (e.g. Diencephalon)
—> Rubrospinal tract intact
—> UL flexion remains
M2: Decerebrate posture, injury to midbrain / upper pons
- Lesion between Red nucleus (midbrain) and Vestibular nucleus (medulla) (More extensive involvement of brainstem: Autonomic functions disrupted which is bad)
—> Rubrospinal tract cut off
—> Un-opposed extensor activities of Reticular (Reticulospinal) and Vestibular nuclei (Vestibulospinal tract) from lower brainstem
—> UL extension (worse prognosis)
Localising + Late signs
Uncal herniation
- Ipsilateral dilated non-reactive pupil (2 DDx: CN3 compressed, Brainstem compressed)
- Contralateral hemiparesis (Ipsilateral hemiparesis: false-localising sign (Kernohan’s notch: indentation of contralateral cerebral peduncle)
- Further drop in conscious level
Late signs:
- Papilloedema
- Cushing triad
CT head
- Only when vital signs stable
- Continuous vital signs monitoring crucial
- If vital signs unstable, skip CT —> straight to theatre (e.g. Laparotomy)
- Skull X-ray not very helpful
- CT brain + C-spine
- Consider whole body CT + contrast
Canadian CT head rule:
High risk (for neurological intervention) (know!!!)
1. GCS <15 at 2 hours after injury
2. Suspected open / depressed skull fracture
3. Any sign of basal skull fracture
4. Vomiting >=2 episodes
5. Age >=65
Medium risk (for brain injury on CT)
6. Amnesia before impact >=30 mins
7. Dangerous mechanism (struck by motor vehicle, ejected from motor vehicle, fall from >=3 feet / 5 stairs)
Rules not applicable (i.e. CT brain always):
- Non-trauma case
- GCS <13
- Age <16
- Warfarin / bleeding disorder
- Obvious open skull fracture
Skull fracture classification
By morphology:
- Linear / Comminuted (in fragments)
- Closed / Compound (“open”)
- Depressed or not
By location:
- Skull vault
- Skull base
Linear skull vault fracture
- Indicates significant energy transfer
- Exclude underlying injury by CT brain (e.g. epidural haematoma, brain contusion) (a cracked helmet does not matter —> what matters is the content inside)
- Otherwise managed conservatively —> if uncomplicated / linear fracture —> fracture will heal itself
- Distinguishable from vessel grooves / sutures
Depressed skull vault fracture
- Depressed —> De-vascularised bone fragments (dead bone)
Complications:
1. Dura tear (CSF leakage)
2. Brain laceration
3. Bleeding
4. Risks of epilepsy and neurological deficits
5. Infection (meningitis, brain abscess) if compound fracture +/- contaminated
Treatment:
1. Irrigation + suture / dress scalp to stop bleed / prevent contamination
2. Do NOT finger-explore
3. Antibiotics
4. Call neurosurgeons
Anterior skull base fracture
Potentially dangerous:
1. Potentially contaminated if connected to paranasal sinuses
2. Numerous nerves + vessels going through
Clinical features:
1. Raccoon eyes (Periorbital ecchymoses)
2. CN1, 2 damage (Loss of smell, vision)
3. CSF rhinorrhoea + meningitis (via frontal sinus / sphenoid sinus)
4. ICA injury —> Life-threatening haemorrhages
5. Traumatic ICA aneurysm
6. Carotico-cavernous fistula (late, when ICA within cavernous sinus injured —> a AV fistula formed —> arterialise ophthalmic vein —> increase pressure within eye —> bulging red eye)
Middle skull base fracture
Connection with mastoid air sinus —> potential contamination causing meningitis
Clinical features:
1. Haemotympanum on otoscopy (blood in middle ear)
2. Battle’s sign (Post-auricular ecchymoses)
3. CSF otorrhoea (CSF in middle ear —> tympanic membrane ruptured)
4. CSF rhinorrhoea (CSF in middle ear —> via Eustachian tube)
5. CN 5, 6, 7, 8 palsies (hearing loss, loss of balance)
Epidural haematoma (EDH)
- Commonly from Skull fracture / Torn meningeal vessels (artery / vein)
- Biconvex hyperdense lesion (∵ clot —> hyperdense)
- May be small initially but can expand quickly
—> ∵ takes time for periosteal dura to split from skull
—> once split then fluid can expand cavity quickly
—> ICP ↑ quickly
—> “talk then die” phenomenon
Treatment:
- Craniotomy for evacuation
Prognosis:
- Relatively good prognosis if treated early
Acute subdural haematoma
- Common rotational injury
- Often brain laceration / contusion —> Brain injury (vs less in EPH)
- Bleeding from bridging veins / cerebral arteries
- Crescent-shaped hyperdense lesion (∵ under dura —> inner surface of subdural conforms to surface of brain)
Treatment:
- Craniotomy for removal
Prognosis:
- High mortality
- Poor functional prognosis
Chronic subdural haematoma (SpC Revision)
- Common in elderly
- History of minor head injury days - weeks before (esp. in elderly)
Clinical features:
- Motor deficit
- Confusion
- Due to brain atrophy, there is potential space allow blood to build up without mass effect —> patient may not have symptoms
Treatment:
- Burr hole drainage
- Craniotomy
Prognosis:
- Very good after drainage
Brain contusion
- Traumatic intracerebral haematoma (massive bruise of brain)
- Deceleration injury
- Focal injury - Coup / Contrecoup (來回彈 —> Polar injury)
- Commonly frontal / temporal poles
- May enlarge with time
- Mass effect + Edema
- Not the worst until at least day 4-5 —> do not discharge the patient early
Post-traumatic brain swelling
- Complex pathology
- Vicious cycle of ↑ ICP, ischaemia —> more swelling
- sometimes reactive hyperaemia
- very difficult to treat + high mortality
Types:
1. Vasogenic edema (disrupted BBB —> capillary leak)
- causes: Trauma
- confined to white matter (white matter is preferentially affected ∵ its lower density with multiple unconnected parallel axonal tracts)
- finger-like projections extending in subcortical white matter
- spares cortical grey matter
- grey white matter interphase is pronounced instead of loss
- Cytotoxic edema (cell membrane failure (ATPase pump fail) due to hypoxia)
- causes: Hypoxia (e.g. ischaemia stroke, post-cardiac arrest causing hypoxic brain injury)
- involves both cortical grey + white matter
- loss of normal grey white interphase
(3. Interstitial edema)
(From JC027:
Vicious cycle of Ischaemia and Brain swelling:
Vicious cycle:
↑ ICP —> ↓ CBF —> Ischaemia —> Swelling —> ↑ ICP
Vasogenic edema (Swelling in extracellular space)
Injury
—> Inflammation, Oxidative stress, Glial activation, Physical impact
—> BBB disruption
—> Extravasation of fluid + serum proteins into extracellular space
Cytotoxic edema (Swelling of brain cells)
Injury
—> ATP depletion, Mitochondrial dysfunction, Oxidative stress
—> Disruption of intra-extracellular ion balance (Failure of Na/K-ATPase pump —> Lose ionic gradient)
—> Astrocytic swelling)
Brain herniation “Coning”
Brain herniates across intracranial compartments
Important signs:
1. Basal cistern obliterated (i.e. CSF space obliterated)
Beware of late deterioration
- Initially normal / mild CT findings do not preclude possibility of subsequent development of life-threatening mass lesion
- Repeat CT if clinically indicated (e.g. drop in GCS, pupil dilatation, seizure, new focal deficit etc.)
ICP and SOL volume:
- ↑ ICP —> Initial compensation by Venous outflow + CSF outflow —> Decompensation
—> GCS can drop quickly (exponentially)
—> “Talk then die” phenomenon
Secondary brain injury
Primary vs Secondary brain injury
Primary:
- At time of trauma
- Fixed
Secondary:
- Develop later
- Potentially avoidable / reversible
Causes of secondary brain injury:
1. Systemic
- Hypotension
- Hypoxia
- Blood glucose!
- Electrolyte!
- Acid/Base!
- Pyrexia
- Infection
- etc.
- Intracranial
- Intracranial haematoma
- Brain swelling
- Hyperaemia (↑ blood flow —> worsen brain swelling)
- Ischaemia
- Epilepsy (↑ blood flow —> worsen brain swelling)
- Hydrocephalus
- etc.
↑ ICP and Cerebral ischaemia
2 equations:
1. CPP = MAP - ICP
2. CBF = CPP / CVR
CBF ∝ CPP
CBF inversely ∝ Cerebral vascular resistance
CBF = CPP / CVR (~50)
ICP ↑ by:
- Intracranial bleeding
- Cerebral edema
- Tumour
ICP ↑ effect:
- Collapses vein
- ↓ Effective CPP
- ↓ CBF
CPP: Cerebral perfusion pressure (Normal: 60-80 mmHg)
MAP: Mean arterial pressure
ICP: Intracranial pressure
CVP: Central venous pressure
CBF: Cerebral bloodflow (Normal: 50 ml / min / 100g tissue)
Aim: CPP ~60-70 mmHg
How to control CPP
CPP = MAP - ICP
Rmb ABC before ICP!
—> Control MAP first (by resuscitation) —> Then control ICP (lowering ICP)
Osmotherapy
- Mannitol (100 ml 20% IV STAT)
- Osmotic effect (need intact BBB), ↓ Blood viscosity (unknown mechanism), ↑ CBF —> vasoconstriction (by autoregulation) —> ↓ CBV
- Foley’s catheter (to monitor output)
- SE (Diuresis): ↓ Vascular volume, Haemoconcentration, Renal failure
- CI: Shock, HyperNa (∵ blood further concentrated by mannitol) - Loop diuretic
- Hypertonic saline (better in multiple injured patients?)
- Osmotic effect but no diuresis effect like Mannitol (i.e. not ↓ Vascular volume)
Steroid
- NO Steroids for TBI
- Only for tumour
ICP Monitoring
Normal (Adults): 10-15 mmHg
Indications:
1. No reliable GCS (e.g. sedation, muscle paralysis for ventilation)
2. GCS <=8 (require intubation)
3. Evolving disease conditions
(4. Abnormal CT scan
5. Normal CT scan with >=2 risk factors:
- Age >40
- SBP <90
- Unilateral / Bilateral motor signs)
Relative contraindications:
- Awake patients
- Bleeding tendency
Methods:
1. Clinical (i.e. GCS score)
2. External Ventricular Drain (EVD) (Gold standard)
3. LP
(4. Subdural
5. Parenchymal (Microsensor))
EVD use:
1. Monitor ICP
2. Drain CSF to ↓ ICP
Rising ICP —> Repeat CT + Escalate treatment
Hierarchy of ICP management
Initial:
1. Head elevation (30o) (facilitate venous drainage)
2. Optimise ventilation (Hyperventilation: PaCO2 ~3-3.5 kPa)
3. Maintain perfusion
- MAP: 80-90 mmHg
- ICP: <20 mmHg
- CPP: ~60-70 mmHg
4. Optimise electrolyte / glucose level
5. Sedation
6. Prevent / Control seizure (first week)
7. Prevent pyrexia
(8. Stress ulcer prophylaxis: H2 blockers)
Intermediate:
1. Osmotherapy: Mannitol 20% 100ml bolus / Furosemide
2. Ventilation therapy
3. Heavy sedation
4. CSF drainage via EVD
Final:
1. Induction of Barbiturate coma
2. Hypothermia
3. Decompressive hemicraniectomy
Surgical treatment
-
External Ventricular Drain (EVD)
- release CSF with / without overt hydrocephalus
- ICP monitoring -
Craniostomy (Burr hole)
- drainage of superficial fluid collection e.g. chronic subdural haematoma (clot has already haemolysed to become fluid)
- not drain solid clot very well -
Craniotomy (Skull flap raised + replaced)
- haematoma / tumour removal -
Decompressive Craniectomy
- for severe brain swelling
- bone flap not replaced
- effective in ↓ ICP + mortality
- massive infarction / post-TBI brain swelling
- but do not correct underlying primary pathology (i.e. swelling)
- quality of survival variable
- ethical + philosophical issues
Barbiturate coma
Advanced level of ICP control
- Done in ICU
- Very very deep anaesthesia —> Switch off brain cells
- Aim at “Burst suppression” —> ↓ Metabolic demand
- Need EEG monitoring
Effect:
1. ↓ Neuronal activities —> ↓ Metabolic demand
2. ↓ CBF (∵ autoregulation to match ↓ metabolic demand) —> ↓ ICP
SE:
- myocardial depression
- hypotension
Therapeutic hypothermia
- Early cooling to 32-34oC
- Neuroprotection by:
—> ↓ Brain metabolic rate
—> ↓ ATP consumption, ↓ O2 demand
—> ↓ Cell death cascades - Established for Post-cardiac arrest brain injury
- Controversial in Stroke / Trauma
- SE: Pneumonia, Coagulopathy (may worsen bleeding in trauma cases)
Example of Algorithm
GCS 15, Normal CT
—> Seizure, fall and cause head injury, GCS 7
—> ABC
—> CT + GCS / ICP monitor
—> ICP 17
—> Mannitol
—> ICP 25 (i.e. not respond to Mannitol)
—> Repeat CT
—> Craniectomy + Clot removal
—> ICU care
—> ICP 10, GCS 15
—> Rehabilitation, Cranioplasty
Summary (Must know)
Potential pitfalls:
1. An unconscious patient is “just drunk”: drunk patient not have protective reflexes like normal people
2. A known epileptic will “wake up later”
3. A drop in GCS “may be nothing and let’s wait”
- ALWAYS significant!!!
4. Sedate an uncooperative / noisy patient without airway protection + monitoring
5. First CT was normal so the patient is ok
Do:
1. ABC first
2. Give Transamin
3. Reverse bleeding tendency
4. Anticipate deterioration
5. Prevent seizure / fever
6. Avoid extreme anything
Do NOT:
1. Give steroids
2. Blindly hyperventilate
3. Blindly lower BP
4. Give mannitol when shocked
5. Use Barbiturates / Propofol outside ICU
SpC Interactive tutorial: Management of head injury
Indications for CT
Indications:
1. Deterioration in consciousness
2. Focal neurological deficit / seizure
3. Penetrating skull injury / skull fracture
4. Mechanism of injury suspicious / high velocity
5. Coagulopathy / On antiplatelet (e.g. aspirin, clopidogrel)
- Low threshold for plain CT brain
Exception:
- Children
Types of damage
- Scalp laceration
- Skull fracture
- Epidural haematoma
- Subdural haematoma
- Traumatic subarachnoid haemorrhage
- Cerebral contusion
- Diffuse axonal injury
Can be a combination of above!
Treatment principles in Head injury
- ICP monitoring
- Control ICP —> help CPP
- Surgical treatment
- Others: seizure prophylaxis, ulcer prophylaxis, nutrition
Basal skull fracture: Management
- Conservative treatment
- Bed rest 5-7 days
- ?Prophylactics antibiotics - Operative repair
- MRI / CT cisternogram
Diffuse axonal injury
- High energy impact / deceleration
- Shearing of axons (white matter tracts)
- Diffuse cerebral edema
- May have normal CT —> MRI for diagnosis
- May have prolong coma (possible vegatative states)
Spine injury
Clear the spine:
1. Clinical examination
- Mechanism of injury
- Focal neurological deficit
- Midline tenderness
- Stepping
- Anal tone
NEXUS criteria:
1. Intoxication (alcohol, drugs)
2. Focal neurological deficit
3. Painful distracting injuries
4. Normal level of alertness
5. Posterior midline tenderness
- If all negative —> clear the spine
- Otherwise —> Imaging
Treatment:
1. ABC
2. DVT prophylaxis
3. Stress ulcer prophylaxis
4. Urinary Catheter (prevent urine retention)
5. Surgical treatment
- Decompress spinal cord
- Fix unstable spinal elements
Complications in C-spine injury
- Airway
- Neck hematoma / soft tissue edema
- Require close monitoring (ICU)
- Consider prophylactic intubation - Breathing
- Diaphragm innervated by C3-5
- Loss of Both diaphragm and intercostal muscles in high C-spine injury
—> inadequate ventilation (intubate and ventilate)
—> aspiration and sputum retention (suction, chest PT) - Circulation
- Neurogenic shock
ASIA impairment scale of Spine injury
ASIA Impairment Scale (American Spinal Injury Association)
A: Complete. No motor or sensory function in the lowest sacral segment
B. Incomplete. Sensory but not motor function is preserved in the lowest sacral segment.
C. Incomplete. Less than 1/2 of the key muscles below the neurological spinal level have grade 3 or better strength.
D. Incomplete. At least 1/2 of the key muscles below the neurological level have grade 3 or better strength.
E. Normal. Sensory and motor functions are normal.
Hypotension in head injury (SpC Revision)
- Blood loss
- Medullary failure
- Spinal cord injury (e.g. Spinal shock)
