Week 5 Flashcards
what percentage of the skull does the brain take up
80-85%
how many mls of blood in the skull
100-150ml
how many mls of CSF in the skull
100-150mls
monroe-kellie doctrine
total volume in skull is constant. Made up of brain, blood and CSF.
According to the monroe-kellie doctrine, if there is an increase in the volume in one of these components, one or both of the others need to decrease. Otherwise increased ICP can occur.
what is the normal ICP
adults: 7-15mmHG
newborn: 1.5-6, often <0
young children: 3-7
older children: 10-15
usually by age 15 it’s reached adult level
what are the immediate compensatory mechanisms for expanding masses in the skull (to maintain ICP)
- decrease in CSF volume by moving it out of foramen magnum
- decrease in blood volume by squeezing sinuses
what is a delayed compensatory mechanism for expanding masses in the skull (to maintain ICP)
- decrease in extracellular fluid
how much CSF is secreted in 24 hours
around 500mls
flow of CSF
- choroid plexus (lat ventricles) –> ventricular system —> subarachnoid space (come through from 4th ventricle via Magendie and Luschka) —> venous system (absorbed into bloodstream by arachnoid granulations)
what will any obstruction in CSF flow will lead to?
hydrocephalus (and increased intracranial pressure)
what is hydrocephalus
a neurological disorder caused by an abnormal build up of CSF in the ventricles
what is CBF
cerebral blood flow
how is cerebral blood flow autoregulated
- pressure autoregulation (arterioles dilate or constrict in response to changes in BP or ICP
- metabolic autoregulation (arterioles dilate in response to chemicals e.g. lactic acid and CO2)
- CO2 is a potent dilator
problems with CSF
- obstruction
- increased production
- decreased absorption (“communicating hydrocephalus”)
causes of obstructive hydrocephalus
- masses
- Chiari Syndrome
- Outflow obstruction at foramen magnum
name a cause of increased CSF production
choroid plexus papilloma
causes of decreased absorption of CSF
- subarachnoid haemorrhage
- meningitis
- malignant meningeal disease
- increased CSF protein
Early signs of raised ICP
- headache
- pupillary dysfunction +/- papilloedema
- changes in vision
- nausea and vomiting
- decreased level of consciousness
later signs of raised ICP
- coma
- fixed, dilated pupils
- hemiplegia
- bradycardia –> cushings triad
- hyperthermia
- increased urinary output
goals of therapy for patients with a raised ICP
- maintain cerebral perfusion pressure (CPP)
- prevent ischaemia and brain compression
raised ICP management
- maintain head in midline to facilitate blood flow
- loosen tube ties, collars etc
- head 30-45 degree elevation
- avoid gagging, coughing etc
- decrease environmental stimuli
- treat hyperthermia
- maintain fluid balance and normal electrolytes
- maintain normocarbia
to do all this sometimes patients are put in coma
volume pressure curve
patients can compensate for a while then suddenly reach a point when ICP goes up suddenly exponentially
medical management of raised ICP
- diuretics (mannitol, hypertonic saline, furosemide, urea)
- barbiturate coma
- antiepileptics
surgical management of raised ICP
- surgical decompression
- other surgical treatment like remove mass lesions, CSF diversion
types of hydrocephalus
- obstruction
- increased production of CSF
- decreased absorption
hydrocephalus classifications
communicating vs non-communicating
congenital vs acquired
aetiology
what is chiari
cerebellum pushes down through foramen magnum into spinal cord
there are 4 main types
what age group does normal pressure hydrocephalus usually affect
elderly