Neurosurgery JC027: Raised Intracranial Pressure And Hydrocephalus Flashcards
Intracranial pressure (ICP)
- 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
Common causes of ↑ ICP
- ***Space-occupying mass lesion
- Haematoma (e.g. ICH)
- Tumour
- Abscess - ***Hydrocephalus
- ∵ excessive accumulation of CSF
- communicating / non-communicating - ***Brain swelling (∵ injury e.g. infarction)
- focal / diffuse - Hyperaemia
- Venous congestion
Clinical features of ↑ ICP
-
**Headache
- worse on **supine > erect (∵ ↑ arterial pressure going into head, ↓ venous drainage from brain)
- worse early morning (can wake patient up) - ***Vomiting
- might transiently relieve headache (∵ hyperventilation) - ***Blurring of vision + diplopia (CN6)
- brainstem compression, CN palsy - Deterioration in consciousness
- ***Papilloedema (late)
- ∵ extension of CSF space into CN2 —> inhibit axoplasmic flow, venous congestion
Monro-Kellie-Burrows Doctrine
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)
↑ 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
Brain cell don’t like Ischaemia
- ***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
Effects of Cerebral Ischaemia
Threshold exist for CBF
- Ischaemic threshold
- CBF: 12-18
- EEG changes: Increasingly **Slower frequency (1-4 Hz))
- **Na/K-ATPase failure
- ↑ Intracellular H2O - Infarction threshold
- CBF: <12
- EEG changes: **Suppressed
- **Ca accumulation
- ***Anoxic (uncontrollable) depolarisation
- Cell death
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
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
Terminal stage of ↑ ICP: Cushing reflex
- 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
Glasgow Coma Score (GCS)
- 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
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)
Pitfalls of GCS
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)
- Total score can mean many things
- Effect of ***shock (impair brain function)
- use Post-resuscitation GCS - Effect of ***sedative drugs e.g. for mechanical ventilation
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
External Ventricular Drain (EVD) vs Lumbar puncture
- 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
Clinical management of ↑ ICP
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
***Treatment of ↑ ICP
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
Enhance Cerebral Venous Drainage
- Head elevation ~30o (angle too large will compromise MAP, CPP)
- Avoid neck rotation
- Remove neck collar if not indicated
- Maintain vascular volume + BP
BP control can be tricky
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
Hyperventilation
- 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
Other Preventions
- Hypoglycaemia
- seizure
- brain injury - Hyperglycaemia
- lactic acidosis - Seizure
- ↑ metabolic demand —> Hyperaemia —> ↑ brain swelling
- Treatment: ***Phenytoin (loading + infusion) - Electrolyte imbalance
- Fever
- 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) - 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 -
**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 - 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)
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
CSF
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
Common causes of Hydrocephalus
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
Clinical presentation of Hydrocephalus
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
Normal Pressure Hydrocephalus (NPH)
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
Diagnosis of Hydrocephalus
- Clinical suspicion
- Imaging
- ***Ventricular dilatation (Evans ratio: Diameter of frontal horn / Biparietal diameter >=0.3)
- Change in morphology, periventricular edema - MRI CSF studies
- ***LP
- measures CSF pressure
- trial drainage but be careful! - EVD (rarely)
Communicating vs Non-communicating Hydrocephalus
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))
***Treatment of Hydrocephalus
- ABC (always first)
- Temporising measures
- **LP if communicating
- **EVD if doubt / unstable / evolving condition - Definitive measures
- **CSF shunting (e.g. ventriculo-peritoneal VP, ventriculo-atrial VA)
- **Endoscopic third ventriculostomy (ETV)
- ***Treat underlying cause (e.g. haematoma, tumour removal)
CSF Shunting
- 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
- ↑ ICP symptom +/- Focal deficit
- CSDH (e.g. elderly on aspirin) - Postural headache (worse when erect)
- Intracranial hypotension (e.g. over-shunting without CSDH) - Fever + abdominal pain
- Shunt infection causing peritonitis?
- Peritonitis causing shunt infection?
- Externalise shunt + Antibiotics
Programmable CSF shunt
- 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
Endoscopic Third Ventriculostomy (ETV)
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
Summary of Key messages
- ↑ 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
