11 raised icp and meningitis and subarachnoid haemorrhage Flashcards
what is the rule of thumb for a normal icp?
adults 5-15 mmHg
Children 5-7 mmHg
Term infants 1.5-6mmHg
A good rule of thumb is that a pressure >20 mmHg is raised
outline the monroe kelly doctorine of raised icp
The Monro-Kellie doctrine
• Any increase in the volume of one of the intracranial
constituents (brain, blood or CSF) must be compensated
by a decrease in the volume of one of the others
• In the case of an intracranial mass (e.g. brain tumour),
the first components to be pushed out of the intracranial
space are CSF and venous blood, since they are at the
lowest pressure
it is a compensatory response - fluid would move into the lumbar area
there is a compensatory phase and then a decomp phase
outline the concept of a cerebral perfusion pressure,
use the equation - CPP=MAP-ICP to do so
a raised ICP will cause brain ischemia and a brain shit, then damage and death
Cerebral perfusion pressure
• CPP = mean arterial pressure (MAP) – ICP
• Normal CPP >70 mmHg
• Normal MAP ~90mmHg
• Normal ICP ~10 mmHg
• If MAP increases then CPP increases, triggering cerebral autoregulation to maintain cerebral blood flow
(vasoconstriction)
• If ICP increases then CPP decreases, triggering cerebral autoregulation to maintain cerebral blood flow
(vasodilatation)
• If CPP <50 mmHg then cerebral blood flow cannot be
maintained as cerebral arterioles are maximally dilated
• ICP can be maintained at a constant level as an
intracranial mass expands, up to a certain point beyond
which ICP will rise at a very rapid (exponential) rate
• Damage to the brain can impair or even abolish cerebralautoregulation
outline cushings reflex
Cushing’s triad aka Cushing’s response aka Cushing’s reflex
• A rise in ICP will initially lead to hypertension as the
body increases MAP to maintain CPP
• The increase in MAP is detected by baroreceptors which stimulate a reflex bradycardia via increased vagal
activity
• Continuing compression of the brainstem leads to
damage to respiratory centres causing irregular breathing
so see a HIGH BP and LOW HR
symtoms of rICP
Signs or rICP
symptoms - headache, nausea, vomiting, double vision
signs - bradycardia, systolic hypertension, irregular respiration, confusion and decreased mental ability, non reactive pupils, loss of consciousness, pappilodema
common causes of raised icp to do with blood
Raised venous pressure (rare)
o SVC obstruction (e.g. external compression by a
lung tumour)
Too much blood outside of cerebral vessels (haemorrhage) • Extradural • Subdural • Subarachnoid • Haemorrhagic stroke • Intraventricular haemorrhage
outline hydrocephalus
some congential causes
other causes
what are the clinical signs
managment
- Too much CSF
• Hydrocephalus - too much fluid in brain
o Congenital (more common than acquired types) Obstructive • Neural tube defects • Aqueduct stenosis
- Communicating (i.e. drainage of CSF not
impaired)
• Increased CSF production
• Decreased CSF absorption
Clinical signs • Bulging head with head circumference increasing faster than expected • Sunsetting eyes (due to direct compression of orbits as well as involvement of oculomotor nerve as it exits midbrain)
Management • Can be treated in acute setting by tapping the fontanelle with a needle • Medium term drainage can be achieved by external ventricular drain (EVD) o Allows continuous pressure monitoring o Can be at risk of infection due to direct communication between brain and outside world
• Long term drainage by ventricular shunts o Essentially, a tube is placed from the ventricular system into the peritoneum (V-P) or right atrium (V-A) o V-P shunts performed most commonly o Tube is tunnelled under skin
o V-P shunts vulnerable to
infection (e.g. if abdominal
infection, can track back up to
brain) or kinking
aquired causes of a ricp by too much csf
Acquired Meningitis Trauma Haemorrhage (e.g. post subarachnoid haemorrhage) Tumours (e.g. compressing cerebral aqueduct)
causes of a ricp due to too much brain
Too much brain
• Cerebral oedema
o Four major pathophysiologies, but often multiple
mechanisms at play in disorders such as stroke or
trauma
Vasogenic (breakdown of tight junctions)
Cytotoxic (damage to brain cells)
Osmotic (e.g. if ECF becomes hypotonic)
Interstitial (flow of CSF across ependyma
and damage to BBB)
Something else • Tumour • Cerebral abscess • Idiopathic o Idiopathic intracranial hypertension (IIH) May present with headache and visual disturbance Usually obese middle aged females
• Make sure there are no signs of intracranial pathology before doing an LP in a patient with suspected raised ICP as this can precipitate brain herniation! - KEY
Treat with weight loss and blood pressure
control
consequences of a raised icp
Consequences Clinical features • Headache o Constant o Worse in the morning o Worse on bending / straining
- Nausea and vomiting
- Difficulty concentrating or drowsiness
• Confusion • Double vision o Problems with accommodation (early sign, pupillary dilatation a late sign) o Maybe effects on acuity o Visual field defects o Papilloedema (swelling of optic disc) • Focal neurological sign- Depends on where lesion is • Seizures
herniations
outline the types of brain herniation
Brain herniation (when ICP get very high, often preterminal)
• Tonsillar herniation aka coning
o Cerebellar tonsils herniate through foramen
magnum, compressing medulla
• Subfalcine herniation
o Cingulate gyrus is pushed under the free edge of
the falx cerebri
o Can compress anterior cerebral artery as it loops
over the corpus callosum
• Uncal herniation
o Uncus of temporal lobe herniates through tentorial
notch compressing adjacent midbrain
o Can cause third nerve palsy and maybe even
contralateral hemiparesis (due to compression of
cerebral peduncle)
• Central downward herniation
o Medial temporal lobe / other midline structures
pushed down through tentorial notch
• External herniation through skull fracture or therapeutic craniectomy
how do we manage raised icp ?
A B D-Analgesia T Meds
Management Brain protection measures • Airway and breathing o Maintain oxygenation and removal of CO2 • Circulatory support o Maintain MAP and hence CPP • Sedation, analgesia and paralysis o Decrease metabolic demand o Prevents cough / shivering that might increase ICP further • Head up tilt o Improves cerebral venous drainage • Temperature o Prevent hyperthermia o Therapeutic hypothermia may be beneficial • Anticonvulsants o Prevent seizures, reduce metabolic demand • Nutrition and proton pump inhibitors o Improved healing of injuries and prevent stomach ulcers due to increased vagal activity
• Decompressive craniectomy as a last resort
subarachnoid haemorrhage - risk factors
• Hypertension • Smoking • Excess alcohol consumption • Predisposition to aneurysm formation • Family history • Associated conditions o Chronic kidney disease (resultant effect on vessel wall) o Marfan’s syndrome (effect on connective tissues of vessels) o Neurofibromatosis (unclear mechanism, if any link) • Trauma • Cocaine use
subarachnoid haemorrhage - Pathophys
you do not need to know all the details of this
Pathophysiology
▪ Usually occur following rupture of an aneurysm in the circle of Willis
• Most are berry aneurysms (as they look like berries) weakness in vessel wall.
Common sites, making up 75% of all aneursyms:
o Anterior communicating artery / proximal anterior
cerebral artery (30%)
▪ Can compress the nearby optic chiasm and
may affect frontal lobe or even pituitary
o Posterior communicating artery (25%)
▪ Can compress the adjacent oculomotor
nerve causing an ipsilateral third nerve
palsy
o Bifurcation of the middle cerebral artery as it splits
into superior and inferior divisions (20%)
▪ Bleeding into the subarachnoid space causes the following • Early brain injury o Microthrombi ▪ These may occlude more distal branches o Vasoconstriction
▪ As a result of blood in the CSF ‘irritating’
cerebral arteries
o Cerebral oedema
▪ General inflammatory response to tissue hypoxia and extravasated blood
o Apoptosis of brain cells
• Cellular changes o Oxidative stress o Release of inflammatory mediators o Platelet activation ▪ Formation of thrombi
• Systemic complications
o Sympathetic activation
▪ Early Cushing response
o Myocardial necrosis
o Systemic inflammatory response
▪ Can affect multiple systems
subarachnoid haemorrhage - clinical signs and symptoms
Thunderclap headache
• Explosive in onset and severe, often reported as worst
headache ever or even ‘like being hit on the head with a
cricket bat’
• Diffuse pain
▪ Frequently loss of consciousness and confusion
▪ Meningism
• Neck stiffness
• Photophobia
▪ May be focal neurology
▪ May present as cardiac arrest (if intracranial pressure rises rapidly following bleed leading to profound Cushing response)
