ricp 2

Question 1

what is normal icp determined by

Answer 1

Determined by volume of blood, brain and CSF all enclosed within a rigid box

Question 2

What is the range for normal icp? and what is a raise?

Answer 2

Values (wide range, can be difficult to define normality precisely)
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 raise

Question 3

What is teh monro-kellie doctrine?

Answer 3

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), the first components to be pushed out of the intracranialspace are CSF and venous blood, since they are at the lowest pressure

Question 4

What is normal CPP?

Answer 4

Cerebral perfusion pressure 
•CPP = mean arterial pressure (MAP) – ICP
•Normal CPP >70 mmHg 
•Normal MAP ~90mmHg
•Normal ICP ~10 mmHg

Question 5

Describe physiological responses to changes in map and icp

Answer 5

• If MAP increases then CPP increases, triggering cerebral autoregulation to maintain cerebral blood flow (vasoconstriction)
• If ICP increases then CPP decreases, triggering cerebral autoregulation to maintain cerebral blood flow (vasodilatation)

Question 6

When does damage to the brain due to reduced cppoccur?

Answer 6

• If CPP <50 mmHg then cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated
• 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
• Damage to the brain can impair or even abolish cerebral autoregulation

Question 7

What is cushing’s triad?

Answer 7

Cushing’s triad aka Cushing’s response aka Cushing’s reflex
•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 (which can cause stomach ulcers as a dangerous side effect)
•Continuing compression of the brainstem leads to damage to respiratory centres causing irregular breathing

Question 8

What are causes of ricp in terms of “too much blood”

Answer 8

Too much blood within cerebral vessels (rare)
•Raised arterial pressure
oMalignant hypertension
•Raised venous pressure
oSVC obstruction (e.g. external compression by a lung tumour)

Too much blood outside of cerebral vessels (haemorrhage)
•Extradural
•Subdural
•Subarachnoid
•Haemorrhagic stroke
•Intraventricular haemorrhage

Question 9

What can cause raised icp in terms of too much csf?

Answer 9

Hydrocephalus.
Congenital (more common)
or 
Acquired:
- Meningitis
- Trauma
- Haemorrhage (e.g. post subarachnoid haemorrhage)
- Tumours (e.g. compressing cerebral aqueduct)

Question 10

What are types of congenital hydrocephalus

Answer 10

Obstructive
•Neural tube defects
•Aqueduct stenosis
•Frequently part of a larger syndrome

Communicating (i.e. drainage of CSF not impaired)
•Increased CSF production
•Decreased CSF absorption

Question 11

What are the clinical signs of congenital hydrocephalus

Answer 11

Clinical signs
•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)

Question 12

Describe acute management for congenital hydrocephalus

Answer 12

•Can be treated in acute setting by tapping the fontanelle with a needle

Question 13

Describe medium term drainage for congenital hydrocephalus

Answer 13

Medium term drainage can be achieved by external ventricular drain (EVD)
o Allows continuous pressure monitoring
o Can be at risk of infection due to direct communication between brain and outside world
o Requires inpatient monitoring so not good as a long term solution
oUsed if shunt fails or contraindicated

Question 14

Describe long term management of congenital hydrocephalus

Answer 14

Long term drainage by ventricular shunts
o Essentially, a tube is placed from the ventricular system into the peritoneum (V-P) or right atrium (V-A)
o V-P shunts performed most commonly#
o Tube is tunnelled under skin
o A one way valve is incorporated to prevent backflow into ventricle
o Extra length of tubing is provided to allow growth before revision is required
o V-P shunts vulnerable to infection (e.g. if abdominal infection, can track back up to brain) or kinking
o Most shunts will require revision

Question 15

What are causes of ricp in terms of “too much brain”

Answer 15

cerebral oedema

Question 16

Describe the pathophysiology of cerebral oedema

Answer 16

Four major pathophysiologies, but often multiplemechanisms at play 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)

Question 17

What are other causes of ricp

Answer 17

• Tumour
• Cerebral abscess
• Idiopathic e.g iih/bih

Question 18

What is iih?

Answer 18

oIdiopathic intracranial hypertension (IIH)
-Aka benign intracranial hypertension
-May present with headache and visual disturbance
-Usually obese middle aged females
-Poorly understood aetiology
-Diagnosis can be confirmed by raised opening pressure on an LP
•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!
- Treat with weight loss and blood pressure control

Question 19

What are the clinical features/symptoms of ricp

Answer 19

•Headache
oConstant
oWorse in the morning
oWorse on bending / straining

•Nausea and vomiting

•Difficulty concentrating or drowsiness
oEffect on daily life

•Confusion

•Double vision
oProblems with accommodation (early sign, pupillary dilatation a late sign)
oMaybe effects on acuity
oVisual field defects
oPapilloedema (swelling of optic disc)

•Focal neurological signs
oDepends on where lesion is

•Seizures

Question 20

what are types of brain herniation

Answer 20

(when ICP get very high, often preterminal)
tonsillar aka coning
subfalcine
uncal
central downward
external

Question 21

describe tonsillar herniation

Answer 21

Tonsillar herniation aka coning

oCerebellar tonsils herniate through foramen magnum, compressing medulla

Question 22

Describe subfalcine herniation

Answer 22

Subfalcine herniation
oCingulate gyrus is pushed under the free edge of the falx cerebri
oCan compress anterior cerebral artery as it loops over the corpus callosum

Question 23

What is uncal herniation?

Answer 23

Uncal herniation
oUncus of temporal lobe herniates through tentorialnotch compressing adjacent midbrain
oCan cause third nerve palsy and maybe even contralateral hemiparesis (due to compression of cerebral peduncle)

Question 24

What is central downward herniatio

Answer 24

Central downward herniation

oMedial temporal lobe / other midline structures pushed down through tentorial notch

Question 25

What is external herniation

Answer 25

External herniation through skull fracture or therapeutic craniectomy

Question 26

Describe ricp management

Answer 26

Brain protection measures
•Airway and breathing
oMaintain oxygenation and removal of CO2

•Circulatory support
oMaintain MAP and hence CPP

•Sedation, analgesia and paralysis
oDecrease metabolic demand
oPrevents cough / shivering that might increase ICP further

•Head up tiltoImproves cerebral venous drainage

•Temperature
oPrevent hyperthermia
oTherapeutic hypothermia may be beneficial

•Anticonvulsants
oPrevent seizures, reduce metabolic demand

•Nutrition and proton pump inhibitors
oImproved healing of injuries and prevent stomach ulcers due to increased vagal activity

Question 27

What are other treatments for ricp

Answer 27

Other treatments
•Mannitol or hypertonic saline
oOsmotic diuresis  
•Ventricular drainage
•Decompressive craniectomy as a last resort