JC27 (Surgery) - Raised ICP and hydrocephalus Flashcards
Normal range of ICP for adults, children and infants
Pathological range for intracranial hypertension
Normal range of ICP
• Adults = 10 – 15 mmHg (≤ 15 mmHg)
• Young children: 3 – 7 mmHg
• Infants: 1.5 – 6 mmHg
Intracranial hypertension: ≥ 20 mmHg
Measured via ventricular or lumbar puncture
Symptoms of raised ICP
• Vomiting
• Headache
o Usually early morning headache
o Mediated via the pain fibers of CN V in the dural and blood vessels
• Blurring of vision
o often unilateral and brief (seconds) that clear completely
o spontaneously with postural changes
o Chronic papilledema can lead to progressive visual field loss in the form of peripheral field contraction and even blindness
• ↓ Consciousness
o Mass effect, compression on midbrain reticular formation
Ddx of raised ICP **
Intracranial mass lesions - Brain tumour, hematoma, abscess
Cerebral edema
• Cerebral infarction
• Acute hypoxic ischemic encephalopathy
• Traumatic brain injury
Hydrocephalus
Obstruction of venous outflow
• Venous sinus thrombosis
• Jugular vein compression
• Neck surgery
Seizure
Idiopathic intracranial hypertension
Signs of raised ICP
- Cushing’s triad = Hypertension + Bradycardia + Irregular respiration (late feature)
- Cushing ulcer ( gastro-duodenal ulcer produced by elevated intracranial pressure, causing excess vagal stimulation and gastric acid secretion)
- Papilloedema (late feature)
o Compression of optic nerve and central retinal vein - CN III, IV, VI palsy
o Binocular horizontal diplopia resulting from unilateral or bilateral lateral rectus palsy - Spontaneous periorbital bruising
Explain the Monro-Kellie-Burrows Doctrine on raised ICP
• Brain parenchyma = 80% + CSF = 10% + Blood = 10%
o ICP = function of the volume and compliance of each component
o Pressure-volume relationship that keeps the dynamic equilibrium inside rigid skull
o Decrease in one component should be compensated by increase in the other
Compensatory mechanisms for increased brain parenchyma volume
Compensatory mechanisms allow volume to increase with minimal elevation in ICP
o Displacement of CSF into thecal sac
o ↓ Volume of cerebral venous blood by venoconstriction and extracranial drainage
Formula for cerebral perfusion pressure
CPP = MAP – ICP (if ICP > JVP)
(OR) CPP = MAP – JVP (if JVP > ICP)
o CPP = Cerebral perfusion pressure
o MAP = Mean arterial pressure (MAP)
o ICP = Intracranial pressure
o JVP = Jugular venous pressure
As the ICP increases, the CPP drops. CPP is the force that pushes blood through the cerebral vasculature. Intracranial pathology that increases the ICP reduces blood flow to the brain tissue, and thus, a sympathetically driven compensatory rise in MAP is initiated to increase the CPP
Formula for cerebral blood flow
CBF = CPP/ CVR = (MAP – ICP)/ CVR
o CBF = Cerebral blood flow
o CPP = Cerebral perfusion pressure
o CVR = Cerebrovascular resistance
Describe changes in cerebral blood flow over cerebral perfusion pressure
Changes in CPP regulated by autoregulation of cerebrovascular resistance > maintain relatively constant level of cerebral blood flow
Describe effect of hypertension on cerebral blood flow
Chronic hypertension > high BP > arterial vasoconstriction in brain to prevent damage to distal brain vessels > maintain perfusion
Acute reduction of BP > chronic arterial vasoconstriction fail to react > ischemic symptoms
Pathophysiology of brain cell excitotoxicity from ischemia
Brain cells:
- Obligative aerobic respiration, glucose-dependent
- Decreased cerebral blood flow cause anaerobic respiration and lactic acidosis
- Lactate cannot be recycled
- Decrease ATP formation > Failure of Na-K-ATPase pump > loss ionic gradient
- Deregulated depolarization of presynaptic neurons from Ca influx
- Excessive release of glutamate > excitotoxicity
Levels of decreasing cerebral blood flow and associated cellular changes
Define CBF threshold for ischemia and infarction
CBF:
35-50: decrease protein synthesis
25-35: Anaerobic metabolism, glutamate release
18-25: Lactic acidosis
12-18* Ischemic threshold: Electrolyte deregulation, intracellular edema
<10-12** Infarction threshold: Calcium accumulation, anoxic depolarization, cell death
Define vasogenic and cytotoxic edema in brain parenchyma
Vasogenic: Injury to cerebral blood vessels > extravasation of fluid and serum proteins by BBB disruption
Cytotoxic: injury to astrocytes cause intracellular swelling by disruption of intracellular ionic balance
List 5 types of brain herniation
Uncal transtentorial herniation
Cerebellar tonsillar (coning) herniation
Subfalcine (Cingulate) herniation
Central herniation
Transcalvarial/ fungus/ External herniation
Define uncal transtentorial herniation and associated s/s
Medial part of temporal lobe (uncus) is squeezed to move towards the tentorium cerebelli
Vertical displacement of diencephalon and midbrain
* Ipsilateral pupillary dilatation (CNIII compressed against skull base)**
* Unconsciousness (Midbrain reticular formation compressed)**
* Contralateral hemiplegia (Corticospinal tracts in ipsilateral hemisphere disrupted) or ipsilateral hemiplegia (if contralateral cerebral peduncle is compressed)
* Hemianopia or Cortical Blindness (one or both side posterior cerebral arteries compressed against tentorium)
Define cerebellar tonsillar herniation (coning) and asso. s/s
Space-occupying lesion in cerebellum
Cerebellar tonsils move downwards through foramen magnum
Brainstem and upper cervical spinal cord compression
* Impaired consciousness
* Cardiorespiratory arrest
* Nystagmus
* Midbrain compression = midsized and unreactive pupils; pontine hemorrhage gives pinpoint and unreactive pupils; supratentorial lesion with tentorial herniation occurred first = unequal pupils
Define subfalcine/ cingulate herniation and asso. S/S
Most common herniation, causes midline shift
Innermost part of frontal lobe** is squeezed under part of the falx cerebri**
Displace and insert pressure on the cingulate gyrus
Affects the corpus callosum beneath the falx cerebelli
S/S:
- compress the ipsilateral anterior cerebral artery»infarction of the paramedian cortex»contralateral lower limb weakness
- dominant hemisphere and contralateral arcuate fasciculus involved»conductive aphasia, receptive/sensory aphasia, or expressive/motor aphasia
- Papilloedema
Define central herniation and asso. s/s
Diencephalon and parts of temporal lobes of both cerebral hemispheres squeezed through a notch in tentorium cerebelli
Compression on diencephalon, midbrain, pons and medulla oblongata
S/S:
- Bilateral damage to midbrain: Mid-sized fixed pupils, Decerebrate posture
- Brainstem damage: Loss of all brainstem reflexes, Cheyne- Stokes respiration to apnea, disappearing decrebrate posture, brain dead