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
