ICP Raised Flashcards
Normal range for CSF pressure ICP and units
Adults <10 - 15 mmHg
Children 3-7 mmHg
Term infants 1.5-6 mmHg
mmHg
H2O
CSF
Use lumbar puncture to measure
What are the immediate compensatory mechanism for raised ICP?
Decreased in CSF volume by movement of fluid into lumbar area
Reduced CSF production
Decrease in blood volume by squeezing blood out of the sinuses
What is the delayed compensatory mechanism for raised ICP?
Decrease in extracellular fluid
What is the Monro-Kellie doctrine?
pressure–volume relationship between ICP, volume of CSF, blood, brain tissue and other components (e.g. tumour, haematoma) and cerebral perfusion pressure (CPP)
cranial compartment is inelastic and volume inside is fixed
Non-linear association between volumes and pressure
Under normal conditions pressure in cranial space in equilibrium, if pressure one constituent increases -> compensation (up to a point) reduction in volume of another constituent and so rise ICP
Through shifts CSF/ venous blood out of cranium
Decompensated phase - pressure increases and Brain shifts may occur and result in herniation
What can raised ICP cause?
Cerebral perfusion pressure = MaP (mean arterial pressure) - ICP
So if ICP increases, CPP decreases -> cerebral autoregulation to mai again blood flow (vasodilation)
Raised ICP final common pathway leads to death or disability in most acute cerebral conditions
Two major consequences:
Brain shifts
Brian ischaemia
Symptoms and signs of raised ICP
Headache Nausea Vomiting Double vision Neurological symptoms
Cushing reflex:
Bradycardia
Systolic hypertension
Irregular respirations
Cheyne strokes respirations Decreased mental abilities Confusion Non-reactive pupils Loss consciousness Pappiloedema
What is Cushing reflex? What’s a possible side effect of this?
Raised ICP (severe and life threatening) -> decreased cerebral blood flow -> increased CO2 -> vasomotor centre of brain (compensation) -> sympathetic response -> vasoconstriction -> increased MAP to increase CPP -> baroreceptors in aortic arch/ carotid arteries -> reflex bradycardia -> high BP and low HR
So three symptoms:
Bradycardia
Systolic hypertension
Irregular respirations (continuing compression Brainstem- damage respiratory centres)
❌ Reflex bradycardia caused via increased vagal activity (can cause stomach ulcers)
Give examples of causes for raised ICP
Localised mass lesions e.g. traumatic haematomas/ abscess/ focal oedema
Disturbances CSF circulation e.g. obstructive hydrocephalus/ communicating hydrocephalus
Obstruction to venous sinuses e.g. depressed fractures overlying, cerebral venous thrombosis
Diffuse brain oedema/ swelling e.g. encephalitis, meningitis, subarachnoid injury
Metabolic encephalopathy e.g. renal failure, diabetic ketoacidosis
Craniosynostosis
Benign intracranial hypertension
What is craniosynostosis?
When the expanding brain of a child lacks space as sutures fused early
(Prominent forehead opp side, prominent temporal region of fused side, deviated nose)
What is the Glasgow coma score?
Eyes open: Spontaneously To speech Pain None
Best verbal response: Orientated Confused Inappropriate words Incomprehensible words Incomprehensible sounds None
Best motor response: Obeys commands Localises to pain Flexes/ withdraws to pain Abnormal flexion Extension None
Also have pupils reactions, limb movements, BP and pulse rate on neuro observation chart
What is an extradural Haemorrhage?
Loss consciousness -> lucid interval -> haematoma enlarges -> raises ICP
Lemon shaped Ct scan
Collection blood between inner surface skull and periosteal dura mater
Most common middle meningeal artery
Sites of brain herniation?
Subfalcine - cingulate gyrus pushed under free edge falx cerebri, can compress anterior cerebral artery as loops over corpus callosum
Transtentorial/ central downward - medial temporal lobe/ other midline structures pushed through tentorial notch
Uncal - of temporal lobes herniated through tentorial notch compressing adjacent midbrain, can cause 3rd nerve palsy/ contralateral hemiparesis (compression cerebral peduncle)
Tonsillar (coning) - cerebellar tonsils through foramen magnum, compressing medulla
External herniation through skull fracture or therapeutic craniecotmy
What’s an acute subarachnoid haemorrhage? Compare to chronic?
Banana shaped Ct
Usually braiding veins torn - older people - minor fall
Chronic - e.g. several weeks - much darker - gradually bigger - less midline shift - abnormalities May not be present immediately
4 tiers of managing raised ICP
Start:
Tier 0 - standard measures
Tier 1 - hyperosmolar therapy and CSF diversion
Tier 2 - sedation and analgesia and paralytic sand normothermia
Tier 3 - decompressive crainectomy and/ or clot evacuation and moderate induced hypothermia and barbiturate coma
What is hydrocephalus?
Communicating:
Impaired CSF reabsorption/ increased production in absence of any obstruction, functional impairment of arachnoid granulations
Non- communicating: CSF-flow obstruction, foramen of monro, aqueduct of sylvius, fourth ventricle obstruction -> dilation of the aqueduct as well as lateral and third ventricles e.g. chiari malformation. Foramina of Luschka and for and of magenide May obstructed due to congenital malformation e.g. Dandy-walker malformation, neural tube defects
