Neurosurgery JC027: Raised Intracranial Pressure And Hydrocephalus

Question 1

Intracranial pressure (ICP)

Answer 1

• Created by Arterial inflow to brain
• Measured at External auditory meatus (~ same level with Foramen Monro)
• Measured by Ventricular / Lumbar puncture
• Adult: ***10-15 mmHg
• Infant: 1-6 mmHg (∵ unfused fontanelle / skull sutures —> ICP subject to atm pressure)

ICP waveform (no need to know):
- Follows arterial pulsation
- P1: Arterial pulse
- P2: Vaguely related cerebral compliance
- P3: Aortic valve closure, Dicrotic notch

Question 2

Common causes of ↑ ICP

Answer 2

1. ***Space-occupying mass lesion
   - Haematoma (e.g. ICH)
   - Tumour
   - Abscess
2. ***Hydrocephalus
   - ∵ excessive accumulation of CSF
   - communicating / non-communicating
3. ***Brain swelling (∵ injury e.g. infarction)
   - focal / diffuse
4. Hyperaemia
5. Venous congestion

Question 3

Clinical features of ↑ ICP

Answer 3

1. **Headache
   - worse on **supine > erect (∵ ↑ arterial pressure going into head, ↓ venous drainage from brain)
   - worse early morning (can wake patient up)
2. ***Vomiting
   - might transiently relieve headache (∵ hyperventilation)
3. ***Blurring of vision + diplopia (CN6)
   - brainstem compression, CN palsy
4. Deterioration in consciousness
5. ***Papilloedema (late)
   - ∵ extension of CSF space into CN2 —> inhibit axoplasmic flow, venous congestion

Question 4

Monro-Kellie-Burrows Doctrine

Answer 4

Adult skull:
- a rigid box with Brain + Blood + CSF
- mass lesion initially displaces Venous blood + CSF —> leave skull to accommodate Brain —> when exhaust (no more buffer) —> ICP ↑ rapidly

ICP vs Space-occupying lesion volume curve:
- High —> Low —> No compliance
- Initial SOL ↑ —> ICP not ↑ much (∵ Compensation by Venous + CSF outflow)
- SOL continue to ↑ (exhaust buffer) —> ICP ↑ rapidly (∵ Decompensation —> Death)

Question 5

↑ ICP and Cerebral ischaemia

Answer 5

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

Question 6

Brain cell don’t like Ischaemia

Answer 6

• ***Obligatory aerobic respiration
• Can only use glucose (ketones in emergency but not efficient)
• Injured neurons can’t recycle lactate —> Lactic acidosis (harmful to brain cells)
• Vicious cycles of **Biochemical + **Cellular responses (e.g. inflammatory cells infiltration)
• **Glutamate release (Excitotoxicity), **Ca influx, Energy failure, DNA damage —> Rapid cell death

Pathophysiology:
↓ CBF
—> ↓ ATP formation —> Failure of Na/K-ATPase pump —> Lose ionic gradient
—> Dysregulated depolarisation of presynaptic neurons **↑ Ca
—> **Excessive release of neurotransmitter Glutamate
—> Excitotoxicity

Question 7

Effects of Cerebral Ischaemia

Answer 7

Threshold exist for CBF

1. Ischaemic threshold
   - CBF: 12-18
   - EEG changes: Increasingly **Slower frequency (1-4 Hz))
   - **Na/K-ATPase failure
   - ↑ Intracellular H2O
2. Infarction threshold
   - CBF: <12
   - EEG changes: **Suppressed
   - **Ca accumulation
   - ***Anoxic (uncontrollable) depolarisation
   - Cell death

Question 8

Vicious cycle of Ischaemia and Brain swelling

Answer 8

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

Question 9

Brain herniation / Coning

Answer 9

Normal: Basal cistern is patent (“smiling”) (pocket of CSF: space between brainstem and skull base)

Herniation: Basal cistern obliterated

Types:
1. Subfalcine (Cingulate)
2. **Central (Tentorial) (成個大腦落小腦 via Tentorial hiatus —> Brainstem compression)
3. Transcalvarial (External)
4. **Uncal (Transtentorial) (Temporal lobe downward via Tentorial hiatus —> Brainstem compression)
5. ***Tonsillar (Downward cerebellar via Foramen Magnum —> Medulla compression: Respiratory centre)
6. Upward

Central + Tonsillar type most important —> Respiratory centre compressed

Question 10

Terminal stage of ↑ ICP: Cushing reflex

Answer 10

• Combination of Sympathetic + Parasympathetic activation
• ***Cushing Triad:
  1. HT (∵ peripheral vasoconstriction)
  2. Bradycardia (reflex to HT) (initially tachycardic ∵ sympathetic activation)
  3. Irregular respiration (rapid + shallow + ineffective)
• ***Cushing ulcer (∵ excessive gastric acid production by uncontrolled activation of parietal cells ∵ parasympathetic activation)
• Other focal signs: Fixed dilated pupil (CN3 palsy due to Uncal herniation) etc.

End result:
Cardiac arrest —> Death

Question 11

Glasgow Coma Score (GCS)

Answer 11

• Objective + Reproducible way to assess consciousness
• Initial GCS: ***Prognostic
• Post-resuscitation GCS is highly prognostic
• ***Trend reflects deterioration / improvement
• Quantitative (3-15) but ***NOT a linear scale

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

Question 12

Motor score (M)

Answer 12

• 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)

Question 13

Pitfalls of GCS

Answer 13

1.
E: **Swollen eyes, Loss of eye post-trauma
M: **Spinal cord injury, Limb injury, Muscle relaxant (Alternative: Tongue protrusion)
V: Language barrier, ***Intubation, Tracheostomy (VT)

2. Total score can mean many things
3. Effect of ***shock (impair brain function)
   - use Post-resuscitation GCS
4. Effect of ***sedative drugs e.g. for mechanical ventilation

Question 14

ICP Monitoring

Answer 14

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

Question 15

External Ventricular Drain (EVD) vs Lumbar puncture

Answer 15

• Manometric principle for monitoring Intracranial CSF pressure
  —> Drainage of ***Lateral ventricle
  —> Manometer at external auditory meatus level
• ***Therapeutic by draining CSF for decompression
• Risk of **infection, iatrogenic **trauma

Lumbar puncture:
- CI if **↑ ICP (with exception: **Communicating Hydrocephalus) —> Pressure gradient push brain downward

Question 16

Clinical management of ↑ ICP

Answer 16

Fundamentals:
1. Protect uninjured brain
2. Salvage injured brain
3. Treat underlying cause

Rule:
1. Always resuscitate first
- Airway, Breathing (protect C-spine), Circulation (IV volume), Disability, Exposure / Environment
- **ABC before ICP!!!
2. Clinical / ICP monitoring
3. **Control ICP + Maintain cerebral perfusion
4. Neuroprotective therapies

Question 17

***Treatment of ↑ ICP

Answer 17

Any doctor:
1. **Head elevation (30o) (facilitate venous drainage)
2. **Optimise ventilation (Hyperventilation: PaCO2 ~3-3.5 kPa)
3. **Maintain MAP (CPP ~60-70 mmHg)
4. **Osmotherapy (Mannitol, Loop diuretic, Hypertonic saline)
5. **Sedation
6. Optimise electrolyte / glucose level
7. **Prevent / Control seizure
8. Prevent pyrexia

By neurosurgeon / ICU:
1. **EVD: ICP monitoring + CSF drainage
2. **Controlled hyperventilation
3. Barbiturate coma
4. **Craniostomy
5. **Surgical removal of SOL (Craniotomy)
6. ***Decompressive craniectomy

Question 18

Enhance Cerebral Venous Drainage

Answer 18

1. Head elevation ~30o (angle too large will compromise MAP, CPP)
2. Avoid neck rotation
3. Remove neck collar if not indicated
4. Maintain vascular volume + BP

Question 19

BP control can be tricky

Answer 19

Normally: Vasoreactivity will maintain stable CBF (even if BP ↑)
- Pressure active: ↑ MAP —> Vasoconstriction (to maintain stable CBF) —> ↓ Cerebral blood volume —> ↓ ICP
- 太多血會收縮減少血流

Brain injury: impaired Vasoreactivity
- Pressure passive: ↑ MAP —> ↑ Cerebral blood volume —> ↑ ICP
- 太多血但唔識收縮減少血流

Aim: CPP ***~60-70 mmHg

Question 20

Hyperventilation

Answer 20

• No blind hyperventilation!
• 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

Question 21

Other Preventions

Answer 21

1. Hypoglycaemia
   - seizure
   - brain injury
2. Hyperglycaemia
   - lactic acidosis
3. Seizure
   - ↑ metabolic demand —> Hyperaemia —> ↑ brain swelling
   - Treatment: ***Phenytoin (loading + infusion)
4. Electrolyte imbalance
5. Fever
6. 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)
7. Glucocorticoids
   - Anti-inflammatory effect
   - Effective for **Vasogenic edema (e.g. Peri-tumoural edema)
   - **Absolute CI in Traumatic brain injury (TBI)
   —> Complex heterogenous pathophysiology
   —> ↑ Mortality
   - ***Questionable in Stroke
8. **Barbiturate coma
   - Done in ICU
   - Very very deep anaesthesia —> Switch off brain cells
   - Aim at “Burst suppression” —> **↓ Metabolic demand
   - Need EEG monitoring
   - ↓ Neuronal activities —> ↓ Metabolic demand
   - ↓ CBF —> ↓ ICP
   - SE: **myocardial depression, **hypotension
9. 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)

Question 22

Surgical treatment

Answer 22

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

Question 23

CSF

Answer 23

Production:
- Choroid plexus in ventricles
- ***450 ml/day in adults

Absorption:
- Arachnoid granulations at Dura venous sinuses

Flow:
Lateral ventricles
—> Foramen Monro
—> 3rd Ventricle
—> ***Aqueduct
—> 4th Ventricle
—> Foramen Luschka, Magendie
—> Subarachnoid space (spinal cord, around brain)
—> reabsorbed at Arachnoid villi

Hydrocephalus occurs if:
1. ↑ Production
2. Flow obstruction
3. ↓ Absorption

Question 24

Common causes of Hydrocephalus

Answer 24

3 causes:
1. ↑ Production
2. Flow obstruction
3. ↓ Absorption

Congenital
- **Aqueductal stenosis
- **Atresia of various foramina
- Arnold-Chiari malformation
- Dandy-Walker syndrome
- Neural tube defect
- Congenital infection
- Congenital mass lesions

Acquired
- ↑ CSF production (e.g. choroidal plexus papilloma (rare))
- **Flow obstruction (e.g. tumour, haematoma)
- **↓ Absorption (e.g. meningitis, SAH —> inflammation of arachnoid villi)
- Idiopathic

Question 25

Clinical presentation of Hydrocephalus

Answer 25

Depends on:
- age
- cause
- chronicity
- brain compliance
- etc.

***Progression:
- Insidious onset / Rapidly fatal

Infants:
1. **Large head
2. **Sunset eyes
3. **Dilated scalp veins
4. **Tense fontanelle
5. Irritability
6. Developmental delay

Adults:
1. **↑ ICP symptoms (Headache, Vomiting)
2. **Motor deficit
3. ***Cognitive dysfunction
4. Urinary incontinence
5. Drowsiness
6. Coma

Question 26

Normal Pressure Hydrocephalus (NPH)

Answer 26

ICP **not high despite large ventricles (i.e. CSF accumulation)
- Complex pathophysiology of **abnormal brain compliance
- ***NO ↑ ICP symptoms (e.g. headache, vomit)

Classic clinical triad:
1. **Gait disturbance (∵ descending pyramidal tracts of lower limb go around frontal horn of lateral ventricles got stretched)
2. **Cognitive decline (∵ frontal lobe affected)
3. **Urinary incontinence (∵ frontal lobe affected)
—> Look like **Alzheimer’s disease (enlarged ventricles as well)

• ***Responds well to CSF diversion / shunting
• Need to distinguish from other causes of dementia e.g. AD, Cerebral atrophy which do NOT respond to shunting

Question 27

Diagnosis of Hydrocephalus

Answer 27

1. Clinical suspicion
2. Imaging
   - ***Ventricular dilatation (Evans ratio: Diameter of frontal horn / Biparietal diameter >=0.3)
   - Change in morphology, periventricular edema
3. MRI CSF studies
4. ***LP
   - measures CSF pressure
   - trial drainage but be careful!
5. EVD (rarely)

Question 28

Communicating vs Non-communicating Hydrocephalus

Answer 28

Communicating Hydrocephalus:
e.g. SAH
—> Damaged subarachnoid villi (Ventricles still communicating with Subarachnoid space)
—> LP also drains CSF in ventricles
—> do not create pressure gradient between skull / spine
—> LP is diagnostic + therapeutic
(***Both 4th + 3rd ventricles are dilated (SpC Revision))

Non-communicating Hydrocephalus
e.g. Colloid cyst in 3th Ventricle / Cerebellar tumour / 4th ventricular obstruction
Blockage of CSF flow between Ventricles / Subarachnoid space
—> If decompress spine CSF space
—> Ventricular pressure remain high
—> Pressure gradient created between skull / spine
—> Coning
—> LP absolutely contraindicated + lethal
(***Only 3rd ventricles is dilated, 4th ventricle is small (SpC Revision))

Question 29

***Treatment of Hydrocephalus

Answer 29

1. ABC (always first)
2. Temporising measures
   - **LP if communicating
   - **EVD if doubt / unstable / evolving condition
3. Definitive measures
   - **CSF shunting (e.g. ventriculo-peritoneal VP, ventriculo-atrial VA)
   - **Endoscopic third ventriculostomy (ETV)
   - ***Treat underlying cause (e.g. haematoma, tumour removal)

Question 30

CSF Shunting

Answer 30

• VP / VA shunt
• one-way valve to control CSF flow

Complications:
1. **Infection (primary / secondary)
2. Blockage —> recurrent hydrocephalus
3. Dislodgement / Fracture —> recurrent hydrocephalus
4. **Over-shunting (drainage too quick)
- **Intracranial hypotension: worse headache when sitting up
- **CSDH (Chronic subdural haemorrhage: veins being torn by negative pressure)
5. Abdominal pseudocyst
6. **Slit ventricle syndrome (in children)
- skull do not grow (∵ brain not expanding) —> once shunt blocked —> ICP ↑
- ventricular wall is stiff also —> do not expand adequately
7. **Nephritis (VA, ∵ immune complex)
8. ***Bowel perforation (VP)

Key message: Avoid shunting if possible!

Common scenarios:
1. Recurrent hydrocephalus symptom
- consider blocked shunt —> test shunt

2. ↑ ICP symptom +/- Focal deficit
   - CSDH (e.g. elderly on aspirin)
3. Postural headache (worse when erect)
   - Intracranial hypotension (e.g. over-shunting without CSDH)
4. Fever + abdominal pain
   - Shunt infection causing peritonitis?
   - Peritonitis causing shunt infection?
   - Externalise shunt + Antibiotics

Question 31

Programmable CSF shunt

Answer 31

• Allows post-op transcutaneous adjustment of shunt valve setting using magnets
• Tailored to individual patients’ needs
• Affected by external magnetic field —> check before / after MRI

Question 32

Endoscopic Third Ventriculostomy (ETV)

Answer 32

Fenestrate floor of 3rd ventricle
—> CSF flow directly from 3rd ventricle into Subarachnoid space
—> bypass obstruction and restore CSF flow
—> avoid permanent shunting
—> enable tumour biopsy

Question 33

Summary of Key messages

Answer 33

• ↑ ICP can have insidious onset / rapidly fatal
• CPP = MAP - ICP (~60-80)
• CBF = CPP / CVR (~50)
• GCS = E(4) + V(5) + M(6) (3-15)
• ICP monitoring when GCS unreliable / evolving condition (GCS <=8 as intubation / sedation required)
• ABC before ICP
• Steroids for tumour but ***NOT TBI / stroke
• ***No prophylactic / prolonged / uncontrolled hyperventilation
• ***No mannitol when shocked
• No LP if ↑ ICP unless absolutely sure Communicating hydrocephalus