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SC WCS > Surgery SC033: Unconscious After An Accident: Head Injury > Flashcards

Surgery SC033: Unconscious After An Accident: Head Injury Flashcards

1
Q

Approach to Unconsciousness

A

ABC before ICP (ICP is only for managing cerebral perfusion, if circulation (C) is not managed —> no point managing ICP)

  1. Assume TBI
  2. Assume extracranial injuries
  3. Resuscitation first!!!
  4. CT scan / Neurosurgical intervention only when vital signs stable

ABCDE:
- Airway + C spine protection
- Breathing
- Circulation (not CT scan)
- Disability
- Exposure / Environment

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2
Q

Airway + C spine protection

A
  1. Protect airway + prevent aspiration
  2. Assume C-spine injury and stabilise it
  3. Normal C-spine X-ray cannot exclude instability
  4. Remove neck collar only if sure (e.g. after CT)
  5. Elevate head ~30o for venous drainage
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3
Q

Breathing

A
  • 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

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4
Q

Circulation

A
  1. Identify source + stop bleeding
  2. Chest drain, limb traction, pelvic binder
  3. Fluid replacement
  4. 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
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5
Q

Scalp laceration

A
  • 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

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6
Q

Facilitate haemostasis

A
  1. Tranexamic acid
    - Anti-fibrinolytic agent —> ↓ Haemorrhage
    - Safe + improve outcome on RCT
    - Loading 1g over 10 mins —> 1g over next 8 hours IV
  2. 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)
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7
Q

Disability: GCS score

A
  • 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

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8
Q

Motor score (M)

A
  • 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)

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9
Q

Localising + Late signs

A

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

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10
Q

CT head

A
  • 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

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11
Q

Skull fracture classification

A

By morphology:
- Linear / Comminuted (in fragments)
- Closed / Compound (“open”)
- Depressed or not

By location:
- Skull vault
- Skull base

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12
Q

Linear skull vault fracture

A
  • 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
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13
Q

Depressed skull vault fracture

A
  • 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

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14
Q

Anterior skull base fracture

A

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)

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15
Q

Middle skull base fracture

A

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)

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16
Q

Epidural haematoma (EDH)

A
  • 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

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17
Q

Acute subdural haematoma

A
  • 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

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18
Q

Chronic subdural haematoma (SpC Revision)

A
  • 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

19
Q

Brain contusion

A
  • 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
20
Q

Post-traumatic brain swelling

A
  • 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

  1. 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)

21
Q

Brain herniation “Coning”

A

Brain herniates across intracranial compartments

Important signs:
1. Basal cistern obliterated (i.e. CSF space obliterated)

22
Q

Beware of late deterioration

A
  • 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

23
Q

Secondary brain injury

A

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.

  1. Intracranial
    - Intracranial haematoma
    - Brain swelling
    - Hyperaemia (↑ blood flow —> worsen brain swelling)
    - Ischaemia
    - Epilepsy (↑ blood flow —> worsen brain swelling)
    - Hydrocephalus
    - etc.
24
Q

↑ ICP and Cerebral ischaemia

A

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

25
Q

How to control CPP

A

CPP = MAP - ICP

Rmb ABC before ICP!
—> Control MAP first (by resuscitation) —> Then control ICP (lowering ICP)

26
Q

Osmotherapy

A
  1. 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)
  2. Loop diuretic
  3. Hypertonic saline (better in multiple injured patients?)
    - Osmotic effect but no diuresis effect like Mannitol (i.e. not ↓ Vascular volume)
27
Q

Steroid

A
  • NO Steroids for TBI
  • Only for tumour
28
Q

ICP Monitoring

A

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

29
Q

Hierarchy of ICP management

A

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

30
Q

Surgical treatment

A
  1. External Ventricular Drain (EVD)
    - release CSF with / without overt hydrocephalus
    - ICP monitoring
  2. 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
  3. Craniotomy (Skull flap raised + replaced)
    - haematoma / tumour removal
  4. 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
31
Q

Barbiturate coma

A

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

32
Q

Therapeutic hypothermia

A
  • 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)
33
Q

Example of Algorithm

A

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

34
Q

Summary (Must know)

A

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

35
Q

SpC Interactive tutorial: Management of head injury
Indications for CT

A

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

36
Q

Types of damage

A
  1. Scalp laceration
  2. Skull fracture
  3. Epidural haematoma
  4. Subdural haematoma
  5. Traumatic subarachnoid haemorrhage
  6. Cerebral contusion
  7. Diffuse axonal injury

Can be a combination of above!

37
Q

Treatment principles in Head injury

A
  1. ICP monitoring
  2. Control ICP —> help CPP
  3. Surgical treatment
  4. Others: seizure prophylaxis, ulcer prophylaxis, nutrition
38
Q

Basal skull fracture: Management

A
  1. Conservative treatment
    - Bed rest 5-7 days
    - ?Prophylactics antibiotics
  2. Operative repair
    - MRI / CT cisternogram
39
Q

Diffuse axonal injury

A
  • 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)
40
Q

Spine injury

A

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

41
Q

Complications in C-spine injury

A
  1. Airway
    - Neck hematoma / soft tissue edema
    - Require close monitoring (ICU)
    - Consider prophylactic intubation
  2. 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)
  3. Circulation
    - Neurogenic shock
42
Q

ASIA impairment scale of Spine injury

A

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.

43
Q

Hypotension in head injury (SpC Revision)

A
  1. Blood loss
  2. Medullary failure
  3. Spinal cord injury (e.g. Spinal shock)

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