CSF + raised ICP Flashcards
medical management of raised ICP
sedation - reduce metabolic demand
maximise venous drainage - head of bed tilt, cervical collars
control CO2
- too low - reduce cerebral blood flow
- too high - too much blood - raised ICP
osmotic diuretics - mannitol
EVD drain - CSF release
(if none of these work - > decompressive craniotomy)
how to calculate cerebral perfusion pressure
CPP = MAP - ICP
- aim for CPP over 70
Cushing’s response = MAP goes up,
- BP goes up, HHR goes down
- ICP is determinant of CPP
intracranial pressure at rest
7-15mmHg
(younger = lower - 3-7ish)
can be negative in vertical position
normal CSF volume
120-150ml
compensatory mechanisms for expanding masses
blood +/- CSF must escpae from cranial vault to avoid rise in pressure
- once this process is exhausted, venous sinuses are flattened + there is little/no CSF
- any further increase result in rapid increase in ICP
venous blood squeezed from sinuses THEN CSF - if CSF squeezing you know bloods already gone
(long horizontal then sharp vertical)
where is CSF secreted
choroid plexus
circulation of CSF
- secreted in choroid plexus
- R+L lateral ventricles
- 3rd ventricle
- then via cerebral aqueduct into..
- 4th ventrical
- mainly into subarachnoid, some into central canal
- then rebsorbed via arachnoid granulations
- into dura venous sinuses
which foramen does CSF pass from lateral ventricles into 3rd?
foramen of Monro
autoregulation of cerebral blood flow
Pressure autoregulation
o Arterioles dilate of constrict in response to changes in BP or ICP
Metabolic autoregulation
o Arterioles dilate in response to chemicals – lactic acid, CO2
CO2 potent vasodilation in brain
o Increased CO2 / increased BP – vasodilation
o Decreased CO2/decreased BP – vasoconstriction
Mechanism unknown
o Myogenic – direct reaction of smooth muscle to stretch
o Humoral – action of metabolic by-products
o Neurogenic – action of perivascular nerves
problems with CSF leading to hydrocephalus
obstructive
- masses, blocked shunt
- Chiari syndrome - tonsils blocking foramen magnum
- outflow obstruction at FM -> rheumatoid arthritis
increased production -> choroid plexus papilloma
decreased absorption -> “communicating hydrocephalus”
causing of communicating hydrocephalus
(decreased absorption or in subarachnoid space)
subarachnoid haemorrhage
meningitis
malignant meningeal disease
arachnoid villi are blocked + not absorbing
presentation of raised ICP
Early signs
o Reduced level of consciousness - GCS
o Headache – can’t look up, photophobic, don’t want to lie down, worse in morning
o Pupillary dysfunction +/-papilloedema
o Changes in vision
o Nausea + vomiting
3rd + 4th ventricle swell pushes on sick centre in brain
Later signs
o Coma
o Fixed, dilated pupils
o CN VI palsy
o Bradycardia – Cushing triad
o Hyperthermia
o Increase urinary output – terminal event
interventions of raised ICP
- Maintain head in midline to facilitate blood flow
- Loosen tube ties, collars – increase blood flow
- HoB 30-45 degrees elevation (head of bed)
- Avoid gagging, coughing – would raise pressure, induced coma
- Decrease environmental stimuli
- Treat hyperthermia
- Maintain fluid balance + normal electrolytes
- Maintain normocarbia
o Acutely hyperventilation – co2 as vasodilator
CSF diversion management
VP shunt into intestine
3rd ventriculostomy - instead of going lateral to 3rd to 4th -> make hole in 3rd to prepontine system
presentation of obstructive hydrocephalus on CT
enlarged frontal horns
temporal tip dilation
rounded 3rd but small or normal 4th ventricle
