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Sem 4: Nervous System > 10b.) Intracranial Pressure > Flashcards

10b.) Intracranial Pressure Flashcards

1
Q

What 3 things determine normal intracranial pressure?

A

ICP is determined by volume of:

  • Blood
  • Brain
  • CSF

… all enclosed in a rigid box

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2
Q

State some possible causes of raised intracranial pressure

A
  • Intra-cranial mass lesions
    • Blood
    • Brain
    • Tumour
    • CSF
  • Disorders of CSF
  • Diffuse intracranial pathological processes
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3
Q

Roughly, what volume of each should you have:

  • Brain
  • Blood
  • CSF
A
  • Brain: 1300-1700ml
  • Blood: 100-150ml
  • CSF: 100-150ml

*Main idea is to know normal amounts of blood and CSF

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4
Q

State the normal intracranial pressures for each of the following categories:

  • Children
  • Adults
  • Term infants
A
  • Children: 5-7mmHg
  • Adults: 5-15mmHg
  • Term infants: 1.5-6mmHg

*Good rue of thumb= if >20mmHg then ICP is raised

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5
Q

Describe the Monro-Kellie doctrine

A
  • If there is an increase in volume in any one of the intracranial constituents that contributes to intracranial pressure (brain, blood, CSF) then this must be compensated by a decrease in volume of one of the others
  • The first components to be pushed out of the intracranial space are constituents with the lowest pressure= CSF and venous blood
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6
Q

How do you calculate cerebral perfusion pressure?

A

CPP= MAP - ICP

  • *MAP= mean arterial pressure*
  • *ICP= intracranial pressure*
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7
Q

What is the normal CPP?

A

>70mmHg

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8
Q

What is the normal MAP?

A

~90mmHg

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9
Q

What is normal ICP?

A

~10mmHg

*But remember, it is different for different categories of people and general rule is if it is above 20mmHg it is raised

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10
Q

Describe the cerebral myogenic autoregulation if MAP increases

A
  • MAP increases
  • Increase in MAP causes increase in CPP
  • Vasoconstriction of cerebral vasculature to prevent too much blood going to brain and increasing ICP
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11
Q

Describe the cerebral myogenic autoregulation when ICP increases

A
  • ICP increases
  • Will cause CPP to decrease
  • Hence get vasodilation of cerbral vasculature to ensure adqequete perfusion to brain
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12
Q

Below what pressure does cerebral myogenic autoregulation fail and why?

A

Cerebral myogenic regulation fails below 50mmHg because at a CPP of 50mmHg the cerebral arterioles are maximally dilated

This will consequently lead to imparied perfusion of brain

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13
Q

Can ICP be maintained as an intracranial mass expands?

A

ICP can be maintained up to a cerain point; beyond this point ICP rises very rapidly/exponentially

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14
Q

Can brain damage impair cerebral myogenic autoregulation?

A

Brain damage can impair or even abolish cerebral autoregulation

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15
Q

Describe Cushing’s reflex

A
  • Increase in intracranial pressure
  • Leads to decrease cerebral blood flow
  • Decreased cerebral blood flow means less CO2 is removed hence there is a regional increase in CO2
  • High CO2 sensed by vasomotor centre in brain
  • Activate sympathetic nervous sytem to cause vasoconstriction
  • Vasoconstriction increases MAP which then increases cerebral perfusion pressure (remember CPP= MAP-ICP)
  • Baroreceptors in aortic arch & carotid sinus then detect the increase in MAP
  • Baroreceptors send signals to vasomotor centre to increase vagal activity (parasympathetic) to decrease HR
  • This results in Cushing’s triad: bradycardia, hypertension and irregular breathing
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16
Q

State Cushing’s triad

A
  • Hypertension
  • Bradycardia
  • Irregular respiration/bradypnea
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17
Q

What triad is indicative of raised ICP?

A

Cushing’s triad

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18
Q

The increased vagal activity which is seen in Cushing’s reflex can cause stomach ulcers as a side effect; explain how it can cause stomach ulcers

A

CNX (vagus nerve) can stimulate:

  • G cells to produce gastrin. Gastrin then goes on to stimulate ECL cells which release histamine which causes parietal cells to release HCL
  • ECL cells directly to produce histamine which stimulates parietal cells
  • Parietal cells directly to produce HCL
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19
Q

Why do you get irregular breathing in Cushing’s reflex?

A

Due to continuing compression of brainstem which leads to damage to respiratory centres in brainstem

20
Q

State 6 possible broad causes of raised ICP

A
  • Too much blood in cerebral vessels (RARE)
  • Too much blood outside of cerebral vessels e.g. haemorrhage
  • Too much CSF
  • Acquired e.g. meningitis, tumours
  • Too much brain e.g.cerebral oedema
  • Soemthng else e.g. cerebral abcess, idiopathic
21
Q

Raised ICP can be caused, RARELY, by too much blood in cerebral vessels; state 2 possible reasons for too much blood in cerebral vessels

A
  • Raised arterial pressure
    • Malignant hypertension (very high blood pressure that comes on suddenly)
  • Raised venous pressure
    • SVC obstruction e.g. by lung tumour
22
Q

Raised ICP can be caused by too much blood outside of cerebral vessels a.k.a. a haemorrhage; state 5 possible haemorrhages

A
  • Extradural
  • Subdural
  • Subarachnoid
  • Haemorrhagic stroke
  • Intraventricular stroke
23
Q

Raised ICP can be caused by too much CSF a.k.a hydrocephalus; state some possible causes of hydrocephalus

A

Congenital

  • Obstructive (drainage impaired):
    • Neural tube defects
    • Aqueduct stenosis
    • As part of a larger syndrome
  • Communicating (drainage not impaired):
    • Increased prodution
    • Decreased absorption

Acquired

  • Infection or kinking ofa ventricular shunt which has been put in place
  • Meningitis
  • Trauma
  • Haemorrhage (e.g post subarachnoid)
  • Tumours (which could compress e.g. cerebral aqueduct)
24
Q

Describe the clinical signs of hydrocephalus in infants and young children

A
  • Bulging head with head circumference increasing faster than expected
  • Bulging fontanelles
  • Sunsetting eyes (up-gaze paresis with the eyes appearing driven downward. The lower portion of the pupil may be covered by the lower eyelid, and sclera may be seen between the upper eyelid and the iris. Due to direct compression of the orbit aswell as involvment of occulomotor nerve as it exits midbrain)
25
Q

Describe how we manage hydrocephalus in infants and young children; consider the acute, medium term and long term management

A
  • In acute setting: tap fontanelle with needle (insert needle and allow CSF to drip out)
  • Medium term drainage: external ventricular drain
  • Long term drainage: ventricular (often ventricular peritoneal) shunt
26
Q

Discuss why an external ventricular drain, which is used as medium term drainage, in infants and children with hydrocephalus is not an ideal long term solution

A
  • Infection risk as there is a direct communication between brain & outside world
  • Requires inpatient monitoring

*Used if shunt fails or contraindicated. Allows continous monitoring of pressure

27
Q

A ventricular shunt is a long-term solution for hydrocephalus; state the 2 types of shunt we do and which is most commonly done

A
  • Ventriuclo-peritoneal shunt (most common)
  • Ventriculo-atrial shunt (into RIGHT atrium)
28
Q

Describe how a ventricular shunt works

A
  • Tube tunelled under skin
  • One way valve to prevent backflow into ventricles
  • Extra length of tubing provided to allow fro growth (but ultimately it will require revision at some point)
29
Q

Ventriculo-peritoneal shunts are vulnerable to infection; true or false?

A

True, abdo infection can track back up to brain

30
Q

Raised ICP can be caused by ‘too much brain’; by this we mean there is cerebral oedema. State and explain the 4 major pathophysiologies behind cerebral oedema

A
  • Vasogenic: blood brain barrier interuppted in particular tight junctions are broken down (extracellular oedema)
  • Cytotoxic: damage to brain cells (they swell)
  • Osmotic: if CSF becomes hypotonic so more fluid moves into brain parenchyma (ECF)
  • Interstitial: flow of CSF across ependyma (which lines ventricles) leading to damage to BBB

NOTE: often mutliple mechanisms play a part in disorders such as stroke or trauma

31
Q

Describe idiopathic intracranial hypertension, include:

  • What it is
  • Presentation
  • How we diagnose
  • Treatment
A
  • Benign high blood pressure in cerebral vasculature
  • Headache, visual disturbances and is often obese middle aged females
  • Diagnose via lumbar puncture (raised opening pressure on LP is supportive of diagnosis)
  • Weight loss & blood pressure control
32
Q

What must you always do before you perform a lumbar puncture?

A

Make sure there are no signs of intracranial pathology as doing the LP increases risk of/can precipitate brain herniation

33
Q

State some clinical features of raised ICP

A
  • Headache
    • Constant
    • Worse in morning, when bending or straining
  • Nausea & vomitting
  • Difficulty concentrating or drowsiness
  • Confusion
  • Visual problems
    • Double vision
    • Problems with accomadatin reflex= early sign
    • Pupillary dilation=late sign (i.e. non-reactive pupils)
    • Visual field defects
    • Acuity defects
    • Papilloedema
  • Focal neurological signs
  • Seizures
  • Cushing’s triad
34
Q

State 2 major consequences of raised ICP

A
  • Brain herniations/shifts
  • Brain ischaemia
35
Q

State the 5 types of herniation

A
  • Tonsillar (a.k.a. coning)
  • Subfalcine
  • Uncal
  • Central downward
  • External hernation
36
Q

Describe tonsillar herniation

A

Cerebellar tonsils herniate through foramen magnum compressing medulla

37
Q

Describe subfalcine herniation

A

Cingulate gyrus pushed under free edge of falx cerebri

38
Q

Which artery can be compressed by subfalcine herniation?

A

Anterior cerebral artery as it loops over corpus callosum

39
Q

Describe uncal herniation

A

Uncus of temporal lobe herniates through tentorial notch compressing adjacent midbrain

40
Q

State and explain 2 potential consequences of an uncal herniation

A
  • Cause third nerve palsy if compresses third nerve
  • Contralateral hemiparesis if compresses cerebral peduncle
41
Q

Describe central downward herniation

A

Medial temporal lobe or other midline structures pushed down through tentorial notch

42
Q

State 2 circumstances in which external herniation could occur

A
  • Skull fracture
  • Therapeutic craniectomy
43
Q

Describe the management of raised ICP

  • *7 brain protective measures*
  • *3 others*
A

All managment is centred around brain protection:

  • Airway & breathing:
    • Maintain oxygenation & CO2 removal
  • Circulatory support:
    • Maintain MAP & hence CPP
  • Sedation, analgesia & parlysis:
    • Decrease metabolic demand
    • Prevents cough/shivering etc… as these might increase ICP more
  • Head up tilt:
    • Improves cerebral venous drainage
  • Temperature:
    • Prevent hyperthermia
    • Therapeutic hypothermia may be beneficial
  • Anticonvulsants:
    • Prevent seizures & reduce metabolic demand
  • Nutrition & PPIs:
    • Improved healing of injuries
    • PPIs to prevent stomach ulceration which is a side effect of Cushing’s reflex

Others….

  • Mannitol or hypertonic saline:
    • To cause osmotic diuresis
  • Ventricular drainage
  • Decompressive craiectomy as a last resort
44
Q

What condition did you learn about in H&N that can cause raised ICP?

A

Craniosynostosis

45
Q

Describe the pathphysiology of an anoxic brain injury

A
  • Decreased cerebral flow
  • Decreased oxygen
  • Failure of ATP driven pumps such as Na+/K+ ATPase
  • Efflux of K+, influx of Na+
  • Water follows Na+ into cell causing oedema
  • Depolarisation of neurons
  • Mitochondrial anoxi caused metabolic failure activiating NOS to produce NO
  • Toxic oxygen radicals also produced so oxidative damage can occur

Sem 4: Nervous System (21 decks)

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