Lecture 17- Pathophysiology and management of raised intracranial pressure Flashcards
Normal ICP
‘The pressure within the cranium of the skull’
Ways of measuring pressure:
What is contained within the cranium of the skull?
*
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Monroe Kellie docrine = sum of volumes of brain, CSF and intracranial blood is constant
- Skull is a rigid box
- If one of these components is lost e.g. a bleed or tumour (SOL) , other components of this volume will need to reduce to make sure the sum of volume stays constant
Intracranial elastance curve
- As intracranial volume increases initially ICP stays the same due to compensatory mechanisms
- After mechanisms exhausted the ICP will increase
Blood within the cranium
Need constant blood supply to supply neurones and brain tissue. Incredibly sensitive to low oxygen.
Cerebral perfusion pressure (CCP)
- Represents cerebral blood flow.*
- If ICP increased, perfusion of the brain decreases (without cerebral autoregulation)- BV will vasodilate
Cerebral autoregulation
- 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) à will result in having to increase MAP- therefore hypertension
- 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
- 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) –> will result in having to increase MAP- therefore hypertension
- Damage to the brain can impair or even abolish
cerebral autoregulation
CSF
- CSF produced by the choroid plexus into the lateral ventricles
- Around 500mls produced each day
- Homeostasis, protection, buoyancy and waste clearance
(3) Brain
- If herniating, usually high pressure inside
- Types of herniation
- Subfalcine herniation (commonest)
- Tonsillar herniation (aka coning)
- Uncalherniation
clincal featues of RICP
Clinical features
- Headaches
- At night time, waking and bending over
- Nausea + vomiting
- Visual disturbances e.g. double vision
- Confusion
- Seizures
- Amnesia
- Papilloedema
- Focal neurological signs
- E.g. CN3 palsy
papilloedema on a fundocscopy
Cushing’s triad
3 primary signs that indicate raised ICP
Causes of increase ICP
- Too much blood
- Too much CSF
- Too much brain
Too much blood
-
Too much blood within cerebral vessels (rare)
- Raised arterial pressure- malignant hypertension
- Raised venous pressure- SVC obstruction
-
Too much blood outside the cerebral vessels (haemorrhage)
- Extradural
- Subdural
- Subarachnoid
Too much blood outside the cerebral vessels
(1) Extradural
- Between skull and dura
- Most common cause=trauma
- Unconscious Patient vs Patient with a ‘Lucid Interval’
- CT-Biconvex shape
Too much blood outside the cerebral vessels
(2) Subdural haematoma
- Between Dura and Arachnoid mater
- CT-Concave/Crescent
- Rupture of bridging veins usually in the elderly
- Note:
- Acute vs Chronic
- Acute: occurs suddenly, progresses quickly
- Chronic: Slow progression
Too much blood outside the cerebral vessels
(3) Subarachnoid
- Between arachnoid and pia mater
- ‘Thunderclap’ headache
- 85% rupture of intracranial aneurysm – berry aneurysm within circle of willis
Too much blood within cerebral vessels
(2) Superior vena cava (SVC) obstruction
- Reduction in venous return from head & neck & upper limbs
- Most common cause is malignancy (note- some causes due to intravascular devices)
- Oncology Emergency
- Presentation
- Local oedema of the face and upper limbs
- Dilated veins in the arm and neck and anterior chest wall
- SoB
- Difficulty swallowing
- After lifting arms the signs will get worse
Too much CSF - Congenital
Congenital hydrocephalus
- Present at birth
- Genetic and non-genetic factors
- Eg. mutation in L1CAM gene linked to aqueductal stenosis
- Present with:
- Enlargement of head circumference- sutures not fused
- Downward gaze
- Delay in neurological development
Too much CSF- Obstructive (non-communicating)
A blockage to the flow of CSF
Too much brain
- Usually causes by cerebral oedema= swelling of the brain
- 4 types
- other types
- brain tumour
- cerebral abscess
- Hypoxic brain injury
- Generalised cerebral oedema
- Loss of differentiation between grey and white matter
- Sulci are efaced
- Small ventricles
- Left brain metastasises surrounded by oedema (darker)
Brain tumour
- Primary
- Metastatic (1/3) – lung, breast, renal carcinomas
- Intra (if mass is within brain tissue) vs extra-axial (outside brain tissue e.g. meningioma)
Cerebral abscess
- Localised pus formation with capsulation within brain parenchyma
- Causes: spread of infection (direct (mastoiditis) vs distance), trauma or unknown
investigations fro RICP
CT head scan indication
Management of RICP
management fo hydrocephalus
Management
example case
- 12
- YES
- GCS 15 –>12
next part of the case- just read
with GCS trend is key–> decrease in GCS bad signs
