S10 L2 Pathophysiology and management of raised intracranial pressure Flashcards
(41 cards)
What is intracranial pressure?
The pressure within the cranium of the skull
What is the normal range for intracranial pressure?
Adults: 5-15mmHg
Young children: 3-7mmHg
Infants: 1.5-6mmHg
Pressure >20mmHg is raised (good rule of thumb)
What contributes to the intracranial pressure?
CSF volume = 150ml (10%)
Blood volume = 150ml (10%)
Brain parenchyma = 1400ml (80%)
What is the Monro-Kellie doctrine?
Proposed that sum of volumes of brain, CSF and intracranial blood is constant
↑volume in any one compensated by ↓in others
e.g. intracranial mass, first components pushed out are the CSF and intracranial venous blood (lowest pressure)
What is important about blood and the brain?
15-20% of CO goes to the brain
- Need oxygenated blood→ neurones need nourishment
- Rising ICP
What is the cerebral perfusion pressure?
Represent the cerebral blood flow
Calculated:
- CPP = Mean Arterial Pressure (MAP) - ICP
Therefore if ↑ICP then ↓CPP unless the MAP decreases - autoregulation
MAP= DBP + 1/3(SBP-DBP)
How does autoregulation in the brain work?
↑MAP the ↑CPP triggering cerebral autoregulation to maintain cerebral blood flow (vasoconstriction)
↑ICP then ↓CPP triggering cerebral autoregulation to maintain cerebral blood flow (vasodilation)
What happens if the ICP too big?
If CPP <50mmHg
Cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated
ICP an be maintained at a constant level up to a point when the ICP will rise at a exponential rate
Damage to the brain can impair or even abolish cerebral autoregulation
What is CSF?
CSF produced by the choroid plexus
Around 500mls produced each day
Homeostasis, protection, buoyancy and waste clearance
What type of brain herniation is there?
- Subfalcine herniation → Cingulate gyrus from cerebral hemisphere, shifts across midline under falx cerebri, can compress anterior cerebral artery as it loops over the corpus callosum
- Tonsillar herniation (aka coning)→ cerebellar tonsils through foramen magnum, compressing medulla
- Uncal herniation → Herniation of uncus, medial temporal lobe through tentorial notch, compressing midbrain, cause third nerve palsy, maybe even contralateral hemiparesis (compression of cerebral peduncle)
What are clinical features of raised ICP?
- Headaches → constant, worse in the morning, worse on bending/straining
- Nausea and vomiting
- Visual disturbances e.g. double vision → problems with accommodation (early signs, pupillary dilation a late sign), visual field defects, papilloedema (swelling of optic disc)
- Confusion
- Seizures
- Amnesia
- Focal neurological signs e.g. CNIII palsy (depend where lesion is)
- Difficulty concentrating or drowsiness → effect on daily life
What is Cushing’s triad?
aka Cushing reflex
- Rise in ICP → Hypertension - compensatory autoregulation mechanism → ↑MAP to maintain CPP
- ↓HR- baroreceptors detect ↑BP ↑vagal activity results in bradycardia
- Irregular breathing → ↑ICP leads to tonsillar herniation resulting in compression of the brainstem leading to damage to respiratory centres resulting in irregular breathing
What are the caused of raised ICP?
- Too much blood
- Too much CSF
- Too much brain tissue
What can cause there to be too much blood?
Too much in the cerebral vessels - Raised arterial pressure → Malignant hypertension - Raised venous pressure → SVC obstruction Too much outside the cerebral vessels (haemorrhage) - Extradural - Subdural - Subarachnoid
What is malignant hypertension?
Accelerated hypertension - Systolic >180mmHg or diastolic >120mmHg - Signs of target organ damage → Retinal haemorrhages → Encephalopathy → Left ventricular hypertrophy → Reduced renal function - Urgent referral is require (same day) - Goal to decrease BP gradually to avoid ischaemic events (hypertension= prothrombotic state, ↑CVS/cerebrovascular events risk) - High mortality rate
What is superior vena cava obstruction?
- Intraluminal obstruction or extrinsic compression
- Reduction in venous return from head and neck and upper limbs
- Most common cause is malignancy (some intravascular devices- clot formation around device)
- Oncology emergency
How would a patient with SVC obstruction present?
Localised oedema of face and upper limbs
Dilated veins over arms, neck, anterior chest wall
SoB, swallowing difficulties
Symptoms worse on lifting of arms
What is an extradural haemotoma?
Between skull and dura
Most common cause= trauma
Unconscious patient vs patient with a ‘Lucid Interval’
CT- biconvex shape
What is a subdural haemorrhage?
Between dura and arachnoid mater CT-concave/crescent Note: - Acute vs chronic - Acute: occurs suddenly, progresses quickly - Chronic: slow progression
What is a subarachnoid haemorrhage?
Between arachnoid and pia mater
Thunderclap headache - worse headache, sudden onset
85% rupture of intracranial aneurysm
What are the reasons for too much CSF?
Congenital
Acquired
Non communicating (flow of CSF block in ventricular system) vs communicating (passageway remains open, increased CSF due to ↑production or ↓removal)
What is congenital hydrocephalus?
- Present a birth
- Genetic and non-genetic factor → e.g. mutation in L1CAM gene linked to aqueduct stenosis
- Fluid build up in the ventricles within the brain
- Present with:
→ Enlargement of head circumference- sutures bot fused
→ Downwards gaze -‘sunsetting gaze’
→ Delay in neurological development
What is obstructive hydrocephalus?
A blockage to the flow of the CSF
- Aqueduct stenosis → most common, blockage/narrowing of the cerebral aqueduct
- Neural tube defects → leakage of CSF, causes fourth ventricle to push downward
- Dandy-Walker syndrome→ enlargement of fourth ventricle, outlets of ventricle partially blocked, cerebellum not fully developed
What is communicating hydrocephalus?
Overproduction of CSF
Reduced absorption of CSF
→ Choroid plexus papilloma - uncommon, intraventricular tumours, cauliflower like appearance on imaging
→ Infection and inflammation leading to scarring at subarachnoid space
