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
presentation of communicating hydrocephalus on CT
big enlargement of lateral, 3rd, 4th ventricles
normal pressure hydrocephalus
disease of elderly - brain becomes stiffer, decrease brain elastance, even normal pressure is too much for them to absorb at arachnoid villi
can be secondary to head injury, SAH or meningitis
presentation of normal pressure hydrocephalus
abnormal gait
urinary incontinence
dementia
normal pressure hydrocephalus on CT
hydrocephalus with ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement
management of normal pressure hydrocephalus
VP shunt
medium-low or low-pressure valve
ETV - endoscopic third ventriculostomy
-> hole in floor of 3rd
hydrocephalus ex vacuo
Dilation of the ventricular system + compensatory increase in CSF volume secondary to loss of brain parenchyma – Alzheimer’s disease
idiopathic intracranial hypertension
raised ICP of unknown cause - no ventricular dilation
usually young overweight women, western, of child bearing age
presentation of idiopathic intracranial hypertension
headaches
double vision
visual blurring
tinnitus
radicular pain
papilloedema
management of idiopathic intracranial hypertension
weight loss
carbon anhydrase inhibitor - acetazolamide
CSF diversion - LP, VP shunt
ONSF - optic nerve fenestration - reduce swelling of optic nerve to protect eyesight
interventional radiology - intracranial venous sinus plasty/stenting
syringomyelia
fluid filled cyst in spinal cord
strong assoc with chiari malformation
cape like loss of sensation to temp - accidentally burning hands without realising
-> due to crossing of spinothalamic tracts
upgoing platers
MRI
early morning headache & N+V
raised ICP
should always do fundoscopy (papilloedema) + neuro exam
