Neurosurgery JC030: Headache And Loss Of Consciousness: Acute Stroke, Subarachnoid Haemorrhage And Vascular Malformation Flashcards
Causes of headache
- ***TMJ disease
- Sinus disease
- Cluster headchae
- Tension headache
- Cervical spine pathology
- Migraine
- ***↑ ICP (concern of neurosurgery)
Consciousness
2 components:
1. Brainstem reticular activating system —> provide **Arousal (keep cortex awake)
2. Cerebral cortex —> provide **Awareness
LOC = Failure of either / both
- A gradation
- when GCS <=8 —> Coma
—> Unarousable
—> **Cannot protect airway
—> **Inadequate breathing
Common causes of Coma
Intracranial
- **Vascular
- Trauma
- **Tumour
- ***Hydrocephalus
- Infection / Inflammation
Extracranial
- **Cardiac insufficiency
- **Respiratory insufficiency
- Metabolic
- Drug, Toxins
A sudden onset of **headache + **deterioration in consciousness is a ***Cerebrovascular event (唔係淨係指stroke) until proven otherwise
Cerebrovascular events
- **Ischaemic / **Haemorrhagic
- Typically abrupt onset
- Severely disabling / fatal but potentially reversible
- Distinct types with different prognoses
Clinical features:
1. **Headache (∵ ↑ ICP / Meningeal irritation / Infarction)
2. **LOC (if brainstem / cortical failure)
3. ***Focal deficits (depending on location)
***Types of Brain haemorrhages: Traumatic vs Spontaneous
Traumatic mostly:
- Epidural haemorrhage
- Subdural haemorrhage
Spontaneous mostly:
- Intraventricular haemorrhage (IVH)
- Deep intracerebral haemorrhage
Traumatic / Spontaneous:
- Subarachnoid haemorrhage (SAH)
- Lobar intracerebral haemorrhage
- Haemorrhagic Stroke (i.e. Intracerebral Haemorrhage)
- Often refers to ***Spontaneous Intraparenchymal haemorrhage (e.g. lenticulostriate arteries of MCA —> Basal ganglia)
- Primary destruction of brain tissue
- Haematoma causes ***↑ ICP —> affect other regions by compression
- ***Rebleeding occurs (aka Haemotoma expansion)
Causes:
1. **Systemic HT
2. **Cerebral amyloid angiopathy (common in elderly)
3. **Haemorrhagic transformation of infarction
4. **Bleeding tendency
5. Tumour bleeding
6. **AVM / Cavernoma
7. Venous sinus thrombosis
8. Moyamoya disease
9. Arterial dissection
10. **Vasculitis
11. ***Sympathomimetic abuse
Etc.
***Treatment of Haemorrhagic Stroke
ABC + ICP control:
1. **Mannitol
2. Surgical decompression
- **CSF drainage
- **Clot evacuation
3. **NO role for steroids
4. **Tranexamic acid might help —> ↓ rate of haematoma expansion
5. **Reverse bleeding tendency (e.g. in Warfarin patients)
6. Principles of maintaining Cerebral perfusion (pressure + bloodflow) apply
Patient selection:
- Age
- Co-morbidities
- Location of haematoma
- Neurological status
- Etiology
**Clot evacuation:
- Craniotomy to take out clot
- Decompress brain, ↓ ICP, Life-saving but does **NOT affect primary injury
- Functional prognosis depends on location + extent of haemorrhage (usually poor)
Haemorrhage location
Superficial lobes (Lobar / Subcortical haemorrhage)
1. Frontal lobe
2. Parietal lobe
3. Occipital lobe
4. Temporal lobe
- Involves superficial lobe
- Deep nuclei / brainstem may be compressed but **not primarily injured
- Commonly due to **HT, other pathology (e.g. **tumour, **bleeding tendency, **vasculitis, **AVM)
- Surgery has better outcome / prognosis (can operate to decompress brain) —> even may lose some functions (e.g. limb movements), usually recover well in terms of consciousness
Deep nuclei
1. Basal ganglion
2. Internal capsule
3. Thalamus
4. Intraventricular
5. Brainstem
- Damage usually **severe + Hard to reverse
- **Poor functional outcome / prognosis (tend not to treat)
- Managed conservatively unless young
- Commonly due to ***systemic HT
(Basal ganglion more prone to HT since less branching off from main artery —> sustain higher BP)
- Cerebellar haemorrhage
- ***Distinct entity
- **IVH + **Direct brainstem compression —> **Respiratory distress + **Obstructive hydrocephalus
- ***Rapidly fatal if large size
- ***Good prognosis if timely surgery (more dispensable than other regions of brain)
Treatment:
1. ***Evacuation of haematoma +/- Suboccipital craniectomy (SpC Revision)
Indications:
- Brainstem compression
- Obliteration of cistern
- Haematoma >3cm
- ***External ventricular drainage (EVD)
- Hydrocephalus
- Small haematoma
- Acute ischaemic stroke
Causes:
1. **Cardioembolism
2. **Critical arterial stenosis (complicated by **hypotension) (Large + Small vessel disease)
3. **Arterial dissection
- Can be painful without ↑ ICP
- ***+/- LOC depending on location / extent
- Acute cell death + Loss of function —> cannot salvage
- Cells in ***penumbra potentially salvageable (∵ only ischaemic, injured / potentially injured) —> aim at timely **restoration of perfusion
- Act **FAST + Treat like **heart attack (2 million brain cells die every minute)
—> Face drooping
—> Arm weakness
—> Speech difficulty
—> Time to call 999
CBF:
- Ischaemic threshold ~20 ml/min/100g
- Infarction threshold ~10 ml/min/100g
Management of Acute ischaemic stroke
-
**IV tPA thrombolysis
- standard treatment (but not yet available 24/7 in HK)
- converts plasminogen —> plasmin —> lyse clot in **small vessels
- therapeutic window of **3-4.5 hours from **symptom onset (or ***last seen well time (SC teaching clinic)) (x admission) (UpToDate: if exact onset time unknown —> use last seen well time)
- can completely reverse deficit (quite effective) - Acute Large Vessel Occlusion (LVO)
- **Large vessel branch blocked by thrombus (e.g. circle of Willis, ICA, CCA) —> potential large infarction
- Plain CT: appear **hyperdense elongated structure (thrombus)
- Does **NOT respond well to IV tPA
- Confirm LVO with urgent CT **angiography
- Standard treatment: Endovascular mechanical thrombectomy (EMT) within ***6 hours of symptom onset - Established infarction (beyond 4.5 / 6 hour window)
**Decompressive Craniectomy
- large infarct can swell with mass effect + ↑ ICP
—> maybe initially conscious but deteriorate in next 24-48 hours
—> may die ∵ brainstem compression / brain herniation
- dead brain does not respond well to medical therapy
- surgical decompression saves lives but does **not reverse deficits
- for young + fit patient
- ethical issues
Haemorrhagic Transformation: Complications of Ischaemic stroke
- Ischaemic brain has **disturbed BBB + **vascular reactivity
- Reperfusion of dead brain —> ***Haemorrhagic transformation (aka Reperfusion haemorrhage) —> worsens outcome
- Particularly delayed perfusion hence limit EMT within ***6 hours
Pathophysiology:
- preserved collateral perfusion (from adjacent vessels/territories)
- reperfusion of infarcted tissues which have weakened vessels (i.e. from extravasation or diapedesis)
However, reperfusion of penumbra —> ↓ risk of haemorrhagic transformation
- size of salvageable penumbra varies with collateral vascular supply
- routine CT / MRI cannot tell
- advanced imaging can delineate a “mismatch” between truly dead brain and salvageable penumbra tissue
- identify who may benefit from treatment >6 hours post-onset
- Subarachnoid haemorrhage (+ SpC Revision)
Causes:
1. **Trauma (commonest)
2. Spontaneous (i.e. Non-traumatic)
- **Saccular / Dissecting aneurysm
- “Mycotic” aneurysm (due to infection but not necessarily fungus, usually infective embolus lodged in distal artery —> forming aneurysm)
- ***Vascular malformation
- Cocaine
Risk factors:
1. Smoking
2. Hypertension (Haemodynamic stress)
3. Genetic predisposition
4. Connective tissue diseases
Clinical features:
- Amount of SAH varies (can be very minor (25-50%))
- High index of suspicion
If no history of trauma —> SAH is **aneurysmal until proven otherwise
- beware spontaneous SAH —> LOC —> fall and head injury
- need to ask patient headache **before / after LOC (before: SAH)
WFNS subarachnoid hemorrhage grading system:
- Grade 1: GCS 15, No neurological deficit
- Grade 2: GCS 13-14, No neurological deficit
- Grade 3: GCS 13-14, Have neurological deficit
- Grade 4: GCS 7-12, +/- neurological deficit
- Grade 5: GCS 3-6, +/- neurological deficit
—> Grade 1-3: Good prognosis —> Early surgery
—> Grade 4-5: Poor prognosis —> Control ICP by CSF drainage
Cerebral aneurysm
- Outpouches of arterial tree in brain
- Commonly in ***Circle of Willis
—> AComA
—> ICA
—> PComA
—> MCA
Predisposing factors:
- **Smoking
- **HT
- **Age >40
- Family history
- Female
- **Connective tissue disease: Ehlers-Danlos syndrome, ***AD polycystic kidney disease, Marfan syndrome, Fibromuscular dysplasia
- Can be forever asymptomatic
- ***Unpredictable spontaneous rupture
- ↑ Size —> ↑ Risk of rupture
- Unstable aneurysms: **Pseudoaneurysm due to arterial dissection (∵ outer wall is thin), **Mycotic aneurysm (∵ thin wall made up of inflammatory tissue)
- Large aneurysms: cause **Mass effect (e.g. CN palsy) / **Thromboembolism (∵ stagnant bloodflow)
Impending aneurysmal rupture
Can have symptoms before a rupture
- e.g. an enlarging **PComA aneurysm compresses on CN3 (run below PComA)
—> “Surgical” CN3 palsy
—> **Peripheral parasympathetic fibres affected (run peripheral of CN3) —> **Dilated pupils + **Ptosis
—> Central motor fibres intact (preserved eye movement)
- ***Urgent angiogram before rupture!
Medical vs Surgical CN3 palsy
Medical:
- Ophthalmoplegia with Pupillary sparing
Surgical:
- Pupillary involvement with EOM sparing
Aneurysmal rupture and SAH
Clinical features
1. **Sudden severe headache
- worst headache in life
- like being clubbed on head
2. **Signs of Meningism (Kernig’s sign, Brudzinski’s neck sign)
3. **Photophobia
4. **+/- LOC
5. ***Focal neurological deficit
6. Cardiac arrest and out-of-hospital death
7. Fundi: Subhyaloid haemorrhage
DDx: Meningitis (difference: SAH usually sudden onset)
***Diagnosis of SAH (+ SpC Revision)
- Clinical suspicion
- History
- P/E -
**CT
- can be subtle / even normal
- **“Star” sign on brain base -
**Lumbar puncture
- **ONLY if CT negative
- blood-stained CSF
- SAH vs Traumatic tap
—> **3-bottle test (genuine SAH: **uniform cell count / redness in all 3 bottles, traumatic: less red in last bottle)
—> **Xanthochromia after **several hours (breakdown of blood products —> redness turn ***yellow (haemosiderin) —> yellowish CSF tapped out) - MRI
- can be ***false-negative at acute stage - CT angiogram / DSA
Potential pitfalls in diagnosis:
1. No / Substandard History + P/E + poor documentation
- Onset, Severity, Meningism, Photophobia
- Head injury + SAH on CT
- maybe SAH first —> LOC —> TBI
- maybe LOC / TBI first —> Traumatic SAH - Dismiss headache as
- migraine, stress, psychological etc.
- part of other conditions e.g. URTI - Leave till tomorrow / grand round
- Radiologist refuses angiogram
Principles of management of SAH (+ SpC Revision)
Cannot undo injury caused by initial haemorrhage
1. ABC
2. Optimise ICP + CBF
3. ***Prevent secondary injury
4. Angiogram
Once diagnosed SAH:
1. **Tranexamic acid (Stop bleeding)
2. **Anticonvulsant
3. Call neurosurgeon
Complications:
1. **Rebleeding of aneurysm (Day 14: **20%) —> Need to identify + obliterate aneurysm
2. **Vasospasm
3. **Hydrocephalus
Angiography to identify Cerebral aneurysm:
1. CT Angiogram
- non-invasive but can be false-negative
- ***proceed to DSA if CTA negative
- ***Digital Subtraction Angiogram (DSA, gold standard)
- direct injection of contrast into ICA / Vertebral artery
- invasive
- 1% stroke risk - MR angiogram
- hard to get one acutely
Obliteration of Cerebral aneurysm
- ***Microsurgical clipping (open surgery)
- apply small aneurysm clip at neck of aneurysm without obstructing parent artery
- risk of intra-operative rupture / occlusion of parent artery - ***Endovascular embolisation (endovascular surgery)
- Guglielmi detachable coil —> induce thrombosis —> close off aneurysm - ***Flow diverter (endovascular surgery)
- stenting at base of aneurysm —> cut off bloodflow into aneurysm
Aim:
- Complete obliteration to prevent re-rupture “as soon as is feasible”
Method, Patient selection, Timing depends on:
- age
- premorbid status
- neurological prognosis
- technical feasibility
Post-SAH Vasospasm (+ SpC Revision)
- Delayed complication of SAH
- Delayed cerebral ischaemia (aka Delayed ischaemic neurological deficit (DIND))
- Starts ***~day 4, peaks day 7-10
- High mortality / morbidity
Pathophysiology (web):
- Breakdown products of blood —> Ca-dependent and Ca-independent vasoconstriction
Investigation:
- Transcranial cranial doppler (TCD)
Treatment:
1. **Maintain good perfusion
2. **Nimodipine (act selectively to dilate cerebral vessel, do NOT give Nifedipine —> ∵ ↓ systemic BP)
3. ***Chemical / Mechanical angioplasty
SpC Revision:
1. Triple H therapy
- Hypertensive (Inotrope)
- Haemodilution
- Hypervolaemia (Give fluid)
2. Endovascular intervention: Mechanical angioplasty / Chemical (e.g. Verapamil)
Post-SAH Hydrocephalus
- ∵ Blockage of CSF flow + absorption
- Acute ↑ in ICP
- CSF drainage helps but might ***provoke re-bleeding if aneurysm not yet secured
- Delayed: Poor absorption and usually communicating
- Beware of new symptoms several months post-SAH
Treatment:
- ***CSF shunting
***Summary of management of Aneurysmal SAH
Clinical suspicion
—> **CT scan (Star sign) / **LP (Blood-stained)
—> **Diagnosis of SAH
—> Identify Aneurysm by **DSA / CTA / MRA
—> Secure aneurysm by **Clip / Coil / Flow diverter
—> ICU Care + **Angioplasty / **Nimodipine for Vasospasm + **CSF shunting for Hydrocephalus
- Cerebral Vascular Malformation
4 types:
1. Arteriovenous (AVM)
2. Cavernous angioma (CA)
3. Venous angioma (VA)
4. Capillary telangiectasia (CT)
- most likely ***congenital
- different bleeding risk: ***AVM highest
- AVM, CA: whether to treat depend on balance between treatment / harm
- VA, CT: Conservative management
Cerebral AVM (+ SpC Revision)
Abnormal development of arteries and vein
—> Direct connection between artery and vein (i.e. no intervening capillary)
—> AV shunting and arterialisation of cerebral veins (under high pressure)
—> ***Unstable high-pressure system
—> Prone to rupture + Associated with aneurysm (esp. on feeding artery)
—> Disturbs normal cerebral perfusion
Spetzler and Martin classification (1986):
- Based on Size, Eloquence (Location), Venous drainage
- Higher score —> Higher risk of surgery
Clinical features:
1. **Haemorrhage (3% / year)
- Deep, IVH, Lobar
2. **Seizure (if microbleed)
3. **Ischaemia (“vascular steal”: shunt blood away from adjacent normal brain)
4. **Headache (∵ high pressure)
5. Others
- Bruit
- Hydrocephalus
- Heart failure (∵ high haemodynamic stress)
Treatment:
- Mainly to prevent bleeding
- Risk-Benefit balance
1. ***Surgical excision
- cure is immediate if a total resection is achieved
- recommended for grade 1, 2, and 3 lesions
- ***Endovascular embolisation
- less invasive than surgery and can reach lesions that are inaccessible surgically
- risk of embolic stroke
- rarely achieves complete eradication - ***Stereotactic Radiosurgery
- non-invasive
- access all anatomic locations of brain
- only small lesions
- may require 2 years for a full destructive effect - ***Combination
- total eradication of lesion often requires >1 modality
