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3 intracranial contents
- brain 1400ml
- blood 150ml
- CSF 150ml
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Vasogenic edema
aka
pathogenesis
extracellular edema
increased capillary permeability
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Cytotoxic Edema
aka
pathogenesis
intracellular edema
cellular swelling (neuronal, glial, endothelial)
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Interstitial Edema
pathogenesis
Increased brain water due to impairment of absorption of cerebrospinal fluid
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location of vasogenic edema
mainly white matter
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location of cytoxic edema
grey and white matter
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location of interstitial edema
- transpendymal flow of CSF
- periventricular white matter in hydrocephalus
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Composition of edema fluid in vasogenic edema
plasma filtrate containing plasma proteins
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Composition of edema fluid in cytotoxic edema
- incresed intracellular water and sodium
- due to failure of membrane transport
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Composition of edema fluid in interstitial edema
cerebrospinal fluid
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Extracellular fluid volume in vasogenic edema
increased
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Extracellular fluid volume in cytotoxic edema
decreased
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Extracellular fluid volume in interstitial edema
increased
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pathologic lesion causing edema in vasogenic edema
- primary or metastatic tumor
- abscess
- late stages of infarction
- trauma
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pathologic lesion causing edema in cytotoxic edema
- early stages of infarction (hypoxia)
- water intoxication
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pathologic lesion causing edema in interstitial edema
obstructive or communicating hydrocephalus
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vasogenic edema
- effect of steroids
- effect of manitol
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cytotoxic edema
- effect of steroids
- effect of manitol
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interstitial edema
- effect of steroids
- effect of manitol
- not effective
- questionable
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Most significant factor determinining cerebral blood flow
Cerebral Profusion Pressure
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CPP
- blood pressure gradient across brain
- MAP - ICP
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3 major factors influencing cerebral blood flow
- systemic blood pressure
- CO2 and H+ concentration in arterial blood
- O2 concentratino
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MAP
diastolic pressure + 1/3 pulse pressure
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autoregulation
ablility to maintain blood flow to brain at a wide range of MAPs, 50 to 160 mmHg
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Autoregulation
Low MAP =
cerebral arteriole dilation --> greater flow at decreased pressure
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Autoregulation
increased systemic BP =
arteriole constriction
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decreased O2 causes
cerebrovascular dilation
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CO2 effects on brain
cerebrovascular dilation
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hyperventilation
decreases CO2, decreases dilation
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Normal ICP
- 10 to 15 mm Hg
- 136 to 204 mm H2O
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two major dural folds
- falx cerebri - sickle shaped in midline
- tentorium cerebelli - tent shaped
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common causes of increased ICP
- Localized masses
- Obstruction of CSF pathways
- Obstruction of major venous sinuses
- Diffuse brain edema or swelling
- Idiopathic
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Localized masses include
- Hematomas
- Neoplasms
- Abscesses
- Focal edema due to trauma
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Obstruction of CSF pathways include
Obstructive and communicating HCP
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Obstruction of major venous sinuses includes
- depressed skull fractures damaging sinus
- thromboembolic desease from contraception
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Diffuse brain swelling and edema occurs with
- Encephalitis, meningitis
- diffuse head injury
- SAH
- Reye's syndrome
- Lead enxephalopathy
- Water intoxication, fluid overload, near drowning
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idiopathic increased ICP
pseudotumor cerebri
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cingulate herniation presentation
no specific clinical signs or symptoms
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cingulate herniation
- due to
- herniation of
- displaces what
- compromisses what
- due to supratentorial mass
- herniation of cingulate gyrus across falx cerebri
- usual displacement of ventricular system
- ACA may be compromissed
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tentorial or uncal herniation
presentation
- impaired consciousness - compressed RAS
- dilated ipsilateral pupil - compressed CNIII
- contralateral hemiplegia - compressed cerebral peduncles
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tentorial or uncal herniation
- prevalence
- due to
- herniation of
- most common
- due to middle cranial fossa mass
- inferomedial temporal lobe herniation between rostoral edge and tentorial edge into posterior fossa
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central herniation
- due to
- displaces
- due to masses far from tentorial hiatus such as frontal, perietal, or occipital
- downward displacement of diencephalon and midbrain throu tentorial incisura
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central herniation
presentation
- not easily recognizable
- bilaterally small reactive pupils
- Cheyne stoke respirations
- obtunded
- loss of vertical gaze
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tonsillar herniation
- due to
- herniation of
- due to acute expansion of posterior fossa lesions or (LP with increase ICP)
- herniation of cerebellum tonsils through foramen magnum in to spinal canal, compressing medulla
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tonsillar herniation
presentation
- Cardiorespiratory impairment
- Hypertension
- High pulse pressue
- Cheyne Stoke respirations
- Neurogenic hyperventilation
- Impaired consciousness
- Stiff neck or in opisthotonic position
- Decorticate or decerebrate posturing
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symptom and signs of increased ICP
- HA with generalized location
- HA worse at night and in recumbant position
- Vomiting without nausea
- Vomiting with neuro sign points to lesion
- Papilledema
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two most common indications for ICP monitoring
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two most common ICP monitoring systems
- intraventricular catheter connected to manometer and drainage system
- fiberoptic transducer tipped catheter system placed within the ventricle, parenchyma, or subdural space.
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advantages to fiberoptic transducer tiped catheters
- zero point does not require recalibration with differences in head position
- not susceptable to blockage
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disadvantages to fiberoptic transducer tiped catheters
- higher cost
- inability to tunnel - thus higher rate of infx
- baseline drift - less reliable over time
- possible inaccuracies
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order of arterial waves reflected in normal ICP wave form
- percussion wave
- tidal wave
- dicrotic notch
- dicrotic wave
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increased ICP is reflected in the wave form as
tidal waves or dicrotic waves of greater amplitude
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type A waves
- due to abrupt elevation in ICP for 5 to 20 minutes
- appear as plateau
- may be marked by decread conciousness, restlessness, increased tone, tonic clonic movements
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B-waves
- frequency of .5-2/min
- related to rhythmic variations in breathing
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C waves
- rhythmic variations related to Traub-Meyer Hering waves of systemic blood pressure
- frequency of 6/min
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B and C waves
have questionable clinicle significance.
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tx of increased ICP
- removal of blood or mass cause
- ventricular drainage
- mannitol
- hyperventilation
- loop diuretics
- steroids
- barbituate coma
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ventricular drainage is particular effective with
cerebral edema
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manitol
- osmotic agent for tx of cerebral edema
- by increasing serum osmolality it cause fluid in brain to be drawn from the parenchyma into the vascular space.
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normal serum osmolality
275 to 290 mOsm/kg
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increase of how much will have significant effect on cerebral edema
10 mOsm/kg
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administration of manitol
- usually small boluses rather then continuous drip
- 0.25g/kg at Q4 or 6
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additional effects of manitol
- decrease in CSF production
- increases in cerebral blood flow
- increases cerebral oxygen consumption
- decreases blood viscosity
- (increases profusion)
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Mannitol's effectiveness
48 to 72 hours then begins to leak from vesels
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hyperventilation
- reduces ICP by reducing intracerebral blood flow and volume through vasoconstriction
- used for acute management only
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in head injuries hyperventilation may not be the best choice because
the brain is often under perfused and hyperventilation will decrease profusion further
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hyperventilation goals for acute condition
pCO2 28 to 32 mm Hg
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loop diuretics
- used in conjuction with manitol has synergistic effect on ICP
- may reduce CSF production
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steroids
dexamethasone is used for treating chronic issues with ICP - for example vasogenic edema from neoplasm
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steroids are ineffective with
vasogenic edema from infarct or trauma
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steroids act by
- stabilizing the cell membrane by inhibiting lysosomal activity
- suppressing polyunsaturated fatty acid production
- decreasing free radical production
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dosing of steroids
- dexamethasone
- loading dose of 10mg IV followed by 4mg Q6H.
- after goal then taper over 3 to 4 days
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barbituate coma
last resort in increased ICP managment
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barbituates decrease ICP by
- scavenging free radicals from mitochondrial respiration
- inhibiting cerebral metabolism and reducing cerebral blood flow
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barbituate dosing
- thiopental
- loading dose 3 to 10 mg/kg over 10min
- maintenance dose of 1-2mg/kg/h
- serum level mantained to 3-4mg/L
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pts under barbitute therapy require
intensive monitoring of hemodynamic function, ICP, and blood gasses
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barbituates are withdrawn when
- ICP normalizes
- there is good intracranial compliance
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administered if pt becomes hypotensive with bartituates
vasopressors
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