cerebral oedema Flashcards
what is intracranial pressure
normal = 5-15mmHg
brain + blood V + CSF
what is cerebral perfusion pressure
and what is the equation
how much blood is the brain getting?
CPP = MABP - ICP
when IC > MABP, CPP is 0 (no cerebral blood flow = death)
factors that can increase ICP
non-neoplastic lesions (haem, abscess, swollen infarct)
benign or malignant tumours
general swelling
inc vascular V (high pCO2)
inc CSF (hydrocephalus)
what is vasogenic oedema and its causes
accumulation of EC fluid bc inc bp/permeability of vasculature
bc tumours, traumatic brain injury, stroke
open BBB, plasma proteins enter EC space + incrase osmotic pressure = water enters brain
what is cytotoxic oedema and its causes + effects
accumulatio of IC fluid associated with energy failure
stroke, hypoxia, cardiac arrest
energy failure -> loss ATP -> reduced Na/K pump -> Na accumulates in cell -> water enters cell -> swelling and explosion
how can cytotoxic oedema lead to vasogenic oedema
stroke cuts off o2/blood supply -> reduced energy -> reduced Na/Kt pump -> cytotoxic oedema -> cells exploding + downstream cascades = BBB damage = vasogenic
what happens with uncontrolled elevated ICP
hypercapnia = vasodilator = inc brain V -> further in IC
dec consciousness, bradycardia, hyperventilation, fixed pupils, herniation, loss of autoregulation
further ICP = further hypoxia + lactic acidosis = further vasodilation = cycle
what mechanisms does brain have to compensate for inc ICP
shunt of csf
venous vasoconstriction
arterial vasoconstriction (low blood)
arterial vasodilation bc needed more blood and inc ICP
describe the 3 trypes of brain herniation
subfalcine/cingulate = midline shift, lobe pushed under falx cerebri, symptoms not well defined
uncal = pressure on brain stem = fixed pupils
tonsillar = compress lower brain stem = dec resp + cardiac function
how can we manage inc ICP
hypersomotic agents, ventricular drain for CSF, hypothermia, steroids, decompressive craniectomy
optimise head and neck position to facilitate intracranial venous outflow
mannitol = osmotherapeutic agent, dec blood viscosity, eastablished osmotic gradient between pasma and brain parenchyma => comp vasocon, dec bv, dec icp.
mannitol = less effective with repeat dosing, rebound icp, many side effects
what are clinical signs of elevated ICP (early vs late)
early = low consciousness, headache, nausea, douvle vision +pupillary changes
late = speech impairment, enlarged +fixed pupils, abnormal reflexes + motor posture + cushings triad (hypertension, bradycardia, respiratory depression)
consequences of elevated ICP
compress bv -> cerebral ischaemia
reduce perfusion ->
loss function brain tissue -> neuro dysfunction
displace brain tissue -> herniation
brain stem omcpression -> intermittenet resp/HR => death
