Lecture 17- Pathophysiology and management of raised intracranial pressure Flashcards
1
Q
Normal ICP
A
‘The pressure within the cranium of the skull’
2
Q
Ways of measuring pressure:
A
3
Q
What is contained within the cranium of the skull?
*
A
-
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
4
Q
Intracranial elastance curve
- As intracranial volume increases initially ICP stays the same due to compensatory mechanisms
- After mechanisms exhausted the ICP will increase
A
5
Q
Blood within the cranium
A
Need constant blood supply to supply neurones and brain tissue. Incredibly sensitive to low oxygen.
6
Q
Cerebral perfusion pressure (CCP)
A
- Represents cerebral blood flow.*
- If ICP increased, perfusion of the brain decreases (without cerebral autoregulation)- BV will vasodilate
7
Q
Cerebral autoregulation
A
- 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
8
Q
- If MAP increases then CPP
A
increases, triggering cerebral autoregulation to maintain cerebral blood flow (vasoconstriction)
9
Q
- If ICP increases then CPP
A
decreases, triggering cerebral autoregulation to maintain cerebral blood flow (vasodilatation) –> will result in having to increase MAP- therefore hypertension
10
Q
- Damage to the brain can impair or even abolish
A
cerebral autoregulation
11
Q
CSF
A
- CSF produced by the choroid plexus into the lateral ventricles
- Around 500mls produced each day
- Homeostasis, protection, buoyancy and waste clearance
12
Q
(3) Brain
A
- If herniating, usually high pressure inside
- Types of herniation
- Subfalcine herniation (commonest)
- Tonsillar herniation (aka coning)
- Uncalherniation
13
Q
clincal featues of RICP
A
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
14
Q
papilloedema on a fundocscopy
A
15
Q
Cushing’s triad
A
3 primary signs that indicate raised ICP
16
Q
Causes of increase ICP
A
- Too much blood
- Too much CSF
- Too much brain
17
Q
Too much blood
A
-
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
18
Q
Too much blood outside the cerebral vessels
(1) Extradural
A
- Between skull and dura
- Most common cause=trauma
- Unconscious Patient vs Patient with a ‘Lucid Interval’
- CT-Biconvex shape
19
Q
Too much blood outside the cerebral vessels
(2) Subdural haematoma
A
- 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
20
Q
Too much blood outside the cerebral vessels
(3) Subarachnoid
A
- Between arachnoid and pia mater
- ‘Thunderclap’ headache
- 85% rupture of intracranial aneurysm – berry aneurysm within circle of willis
21
Q
Too much blood within cerebral vessels
(1) Malignant (accelerated) hypertension
A
- Systolic >180mmHg or Diastolic >120mmHg
- High mortality rate
- Signs of target organ damage
- Retinal haemorrhages
- Encephalopathy
- Left ventricular hypertrophy
- Reduced renal function
- Urgent referral
- Goal is to decrease BP gradually in order to avoid ischaemic events.
22
Q
Too much blood within cerebral vessels
(2) Superior vena cava (SVC) obstruction
A
- 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
23
Q
Too much CSF
A
- Congenital
- Acquired
- Non communicating (obstructive) vs communicating
24
Q
Too much CSF - Congenital
A
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
25
**Too much CSF- Acquired causes**
* Intraventricular haematoma
* Tumour
* Infection
* Trauma
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**Too much CSF- Obstructive (non-communicating)**
A blockage to the flow of CSF
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**Too much CSF- Communicating hydrocephalus**
* Overproduction of CSF or
* Reduced absorption of CSF
* Examples of cause
* Choroid plexus papilloma
* Infection and inflammation leading to scarring at subarachnoid space
28
**Too much brain**
* Usually causes by **cerebral oedema**= swelling of the brain
* 4 types
* other types
* brain tumour
* cerebral abscess
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* Hypoxic brain injury
* Generalised cerebral oedema
* Loss of differentiation between grey and white matter
* Sulci are efaced
* Small ventricles
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* Left brain metastasises surrounded by oedema (darker)
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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)
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Cerebral abscess
* Localised pus formation with capsulation within brain parenchyma
* Causes: spread of infection (direct (mastoiditis) vs distance), trauma or unknown
33
**Idiopathic Intracranial Hypertension**
* Present with headache (relieved on standing, worse at night)and visual disturbances
* Unknown cause
34
Idiopathic Intracranial Hypertension associations and RF
* Hypoparathyroidism
* Hypothyroidism
* Hyperthyroidisms
* Iron deficient anaemia
* Risk factors:
* Gender F\>M
* Increased BMI
35
**Idiopathic Intracranial Hypertension diagnosis**
* CT/MRI, Raised opening pressure on an LP (lumbar puncture)\*
* LP contraindicated with RICP due to risk of herniation
36
**Idiopathic Intracranial Hypertension** treatment
* weight loss and blood pressure control
37
**Establishing a diagnosis of RICP**
**1) History and examination**
**2) Investigations**
38
investigations fro RICP
39
CT head scan indication
40
**Management** of RICP
41
management fo hydrocephalus
**Management**
42
example case
1. **12**
2. **YES**
3. **GCS 15 --\>****12**
43
next part of the case- just read
with GCS trend is key--\> decrease in GCS bad signs
