15. Raised ICP Flashcards
What determines normal ICP?
Determined by volume of blood, brain and CSF all enclosed within a rigid box
What is the normal ICP?
- Adults 5-15 mmHg
- Children 5-7 mmHg
- Term infants 1.5-6mmHg
A good rule of thumb is that a pressure >20 mmHg is raised
What is the Monro-Kellie doctrine?
Any increase in the volume of one of the intracranial constituents (brain, blood or CSF) must be compensated by a decrease in the volume of one of the others.
In the case of an intracranial mass(e.g. brain tumour), what does the monro-kielle doctorine say?
the first components to be pushed out of the intracranial space are CSF and venous blood, since they are at the lowest pressure
How is cerebral perfusion pressure calculated?
CPP = mean arterial pressure (MAP) - ICP
What is the normal value of MAP, ICP and therefore what is the normal CPP?
- Normal CPP >70 mmHg
- Normal MAP ~90mmHg
- Normal ICP ~10 mmHg
What happens to CPP if MAP increases, and what occurs in response?
If MAP increases then CPP increases, triggering cerebral autoregulation to maintain cerebral blood flow (vasoconstriction)
What happens to CPP if ICP increases, and what occurs in response?
If ICP increases then CPP decreases, triggering cerebral autoregulation to maintain cerebral blood flow (vasodilatation)
what would happen if ICP increased without cerebral autoregulation
if ICP increased, perfusion of the brain decreases (without cerebral autoregulation)
Below what CPP can cerebral blood flow not be maintained and why?
If CPP <50 mmHg then cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated
how does expansion of intracranial mass affect ICP?
• ICP can be maintained at a constant level as an
intracranial mass expands, up to a certain point beyond which ICP will rise at a very rapid (exponential) rate
WHat can damage to the brain do to cerebral autoregulation?
can impair or even abolish cerebral autoregulation
CPP explained in numbers
1) Normal: ○ CPP=MAP-ICP ○ CPP=90-10=80 ○ >70 => normal CPP 2) Uncompensated SOL: ○ CPP-MAP-ICP ○ CPP=90-30=60 ○ <70=> abnormal CPP 3) Compensated SOL: ○ CPP=MAP-ICP ○ CPP=110-35=75 ○ >70=> normal CPP
what is the Cushing’s triad?
The three primary signs that indicate raised intracranial pressure:
• hypertension
• bradycardia
• irregular breathing
explain the Cushing’s reflex/triad?
- A rise in ICP will initially lead to hypertension as the body increases MAP to maintain CPP
- The increase in MAP is detected by baroreceptors which stimulate a reflex bradycardia via increased vagal activity
- Continuing compression of the brainstem leads to damage to respiratory centres causing irregular breathing (due to tonsilar herniation)
What may occur as a side effect of increased vagal activity in cushings reflex?
can cause stomach ulcers as a dangerous side effect
What are the causes of raised ICP?
- too much blood within cerebral vessels (rare)
- too much blood outside cerebral vessels (haemorrhage)
- too much CSF
- too much brain
- something else
how can Too much blood within cerebral vessels be split?
- Raised arterial pressure
* Raised venous pressure
What can cause raised arterial pressure within cerbral vessels?
Malignant hypertension
what is Malignant hypertension
○ Systolic >180mmHg or Diastolic >120mmHg ○ Signs of target organ damage ■ Retinal haemorrhages ■ Encephalopathy ■ Left ventricular hypertrophy ■ Reduced renal function
management of malignant hypertension?
○ Urgent referral
○ Goal is to decrease BP gradually in order to avoid
ischaemic events. - hypertension is prothrombotic state - increase risk of MI and strokes - if reduced too quickly can cause hypotension
○ High mortality rate
What can cause raised venous pressure in the skull?
SVC obstruction (e.g. external compression by a lung tumour)
how might patients with SVC obstruction present?
○ localised oedema of face and upper limbs
○ dilated veins over arms chest and face
○ SOB
○ difficulty swallowing
What are the different types of intracranial haemorrhages?
- Extradural
- Subdural
- Subarachnoid
- Haemorrhagic stroke
- Intraventricular haemorrhage
describe Extradural haemorrhage
○ Between skull and dura
○ Most common cause=trauma
○ Unconscious Patient vs Patient with a ‘Lucid Interval’
○ CT-Biconvex shape
describe Subdural haemorrhage
○ Between Dura and Arachnoid mater ○ CT-Concave/Crescent ○ Note: ■ Acute vs Chronic ■ Acute: occurs suddenly, progresses quickly ■ Chronic: Slow progression
describe describe Extradural haemorrhage haemorrhage
○ Between arachnoid and pia mater
○ ‘Thunderclap’ headache
○ 85% rupture of intracranial aneurysm
What can too much CSF cause?
Hydrocephalus
What are the 2 division of hydrocephalus?
- Congenital (more common)
- acquired
What are the 2 causes of congenital hydrocephalus?
Obstructive Communicating (i.e. drainage of CSF not impaired)
What are the clinical signs of congenital hydrocephalus?
- Bulging head with head circumference increasing faster than expected
- Sunsetting eyes (due to direct compression of orbits as well as involvement of oculomotor nerve as it exits midbrain)
effect of genetic on congenital hydrocephalus?
Genetic and non-genetic factors
■ Eg. mutation in L1CAM gene linked to aqueductal stenosis
what are Obstructive causes of congenital hydrocephalus?
● Neural tube defects • Leakage of CSF • Causes fourth ventricle to push downward ● Aqueduct stenosis ● Dandy-Walker Syndrome • Enlargement of fourth ventricle • Outlets of ventricle partially blocked • Cerebellum not fully developed
what are Communicating causes of congenital hydrocephalus?
○ Overproduction of CSF
○ Reduced absorption of CSF
• Choroid plexus papilloma
• Infection and inflammation leading to scarring at subarachnoid space
What is the management of congenital hydrocephalus?
- Can be treated in acute setting by tapping the fontanelle with a needle
- Medium term drainage can be achieved by external ventricular drain (EVD)
- Long term drainage by ventricular shunts
What is an external ventricular drain?
Flexible plastic catheter placed inside ventricle draining the CSF into a collecting bag
What are the good/bad with EVD?
- Allows continuous pressure monitoring
- Can be at risk of infection due to direct communication between brain and outside world
- Requires inpatient monitoring so not good as a long term solution - Used if shunt fails or contraindicated
What is a ventricular shunt?
Tube is placed from the ventricular system into the peritoneum (V-P)(most common) or right atrium (V-A)
- tunnelled under the skin
- one way valve
What are the issues with ventricular shunts?
- V-P shunts vulnerable to infection (e.g. if abdominal infection, can track back up to brain) or kinking
- Most shunts will require revision
What are the causes of acquired hydrocephalus?What are the causes of acquired hydrocephalus?
- Meningitis
- Trauma
- Haemorrhage (e.g. post subarachnoid haemorrhage)
- Tumours (e.g. compressing cerebral aqueduct)
What causes too much brain?
Cerebral oedema (brain swells)
What are the 4 causes of cerebral oedema?
Four major pathophysiologies, which occur in disorders such as stroke or trauma:
- Vasogenic (breakdown of tight junctions)
- Cytotoxic (damage to brain cells)
- Osmotic (e.g. if ECF becomes hypotonic)
- Interstitial (flow of CSF across ependyma and damage to BBB)
describe vasogenic cause of cerebral oedema
● Disruption of blood brain barrier
● Breakdown of tight junctions=increased permeability
describe Cytotoxic cause of cerebral oedema
● Injury to cells of the brain (neurones,
glial cells, axons)
● Derangements in ATP-dependent transmembrane pumps-intracellular accumulation of fluid
describe Osmotic cause of cerebral oedema
● Usually osmolarity of extracellular fluids
is equal on both sides of BBB
● If there is a change-osmotic gradient
describe Interstitial cause of cerebral oedema
● Increased pressure within ventricles, eventual damage to their linings.
● CSF can now be found in brain parenchyma
What else can cause a rise in ICP? (4)
- Tumour
- Cerebral abscess
- Idiopathic
- Craniosynostosis
What is craniosynostosis?
premature closure of cranial sutures
What does idiopathic intracranial hypertension present with?
May present with headache (worse in morning and night and relieves on standing) and visual disturbance
- Usually obese middle aged females
How is a diagnosis of raised idiopathic intracranial hypertension made?
• CT/MRI
• By raised opening pressure on an LP (lumbar puncture)
- Make sure there are no signs of intracranial pathology before doing an LP in a patient with suspected raised ICP as this can precipitate brain herniation! - Contraindicated in raised ICP!
How is idiopathic intracranial hypertension treated?
Treat with weight loss and blood pressure control
what is cerebral abscess and what causes it?
○ Localised pus formation with capsulation within brain parenchyma.
○ Causes: Spread of infection (direct vsdistance), trauma, or unknown
how can brain tumours be classified?
○ Primary
○ Metastatic
○ Intra vs Extra- axial
WHat are the clinical features of raised ICP?
- Headache
- Nausea and vomiting
- Difficulty concentrating or drowsiness (effect on daily life)
- Confusion
- Double vision
- Focal neurological signs
- Seizures
- Non-reactive pupils
- Loss of consciousness
Describe the headaches that occur with raised ICP?
- Constant
- Worse in the morning
- Worse on bending / straining (coughing, sneezing etc)
- precipitated by exercise
vision problems that present with raised ICP?
Problems with accommodation (early sign, pupillary dilatation a late sign)
o Maybe effects on acuity
o Visual field defects
o Papilloedema (swelling of optic disc)
What are the different types of herniations? (5)
- tonsillar (or coning)
- subfalcine
- uncal
- central downward
- external (through skill fracture/therapeutic craniotomy)
WHat is a tonsillar herniation, what is at risk of compression?
Cerebellar tonsils herniate through foramen magnum, compressing medulla
What is a subfalcine herniation, what is at risk of compression?
- Cingulate gyrus is pushed under the free edge of the falx cerebri
- Can compress anterior cerebral artery as it loops over the corpus callosum
What is a uncal herniation, what is at risk of compression?
- Uncus of temporal lobe herniates through tentorial notch compressing adjacent midbrain
- Can cause third nerve palsy and maybe even contralateral hemiparesis (due to compression of cerebral peduncle)
WHat is a central downward herniation?
Medial temporal lobe / other midline structures pushed down through tentorial notch
What is involved in management of raised ICP?
- Airway and breathing: Maintain oxygenation and removal of CO2
- Circulatory support: Maintain MAP and hence CPP
- Sedation, analgesia and paralysis
- Head up tilt: Improves cerebral venous drainage
- Temperature: Prevent hyperthermia, Therapeutic hypothermia may be beneficial
- Anticonvulsants: Prevent seizures, reduce metabolic demand
- Nutrition and proton pump inhibitors - Improved healing of injuries and prevent stomach ulcers due to increased vagal activity
Why may sedation, analgesia and paralysis be useful?
- Decrease metabolic demand
- Prevents cough / shivering that might increase ICP further
What are some other treatments?
- Mannitol or hypertonic saline: Osmotic diuresis
- Ventricular drainage
- Decompressive craniectomy as a last resort
investigations for raised ICP?
● Bedside ○ Vital signs, ECG, fundoscopy ● Bloods: ○ FBC, U+E’s, CRP, Clotting, Group & Save, Crossmatch, Blood culture ● Imaging: ○ CT scan ○ MR
divide management of ICP into simple measures, specific and surgical
Simple measures ● Elevate head of bed ● Avoid pyrexia ● Analgesia Specific medical measures: ● Anticonvulsants ● Sedation or neuromuscular blockade ● Mannitol or hypertonic saline Surgical: ● Ventriculostomy ● Decompressive craniectomy
