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SA Clinical Neuroscience > S10) Pathophysiology and Management of Raised Intracranial Pressure > Flashcards

S10) Pathophysiology and Management of Raised Intracranial Pressure Flashcards

1
Q

What is normal intracranial pressure?

A

Normal ICP = 5–15 mm Hg (7–20 cm H2O)

5-7 in children

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2
Q

which two components normally change to maintain the Brain Vol

A

CSF and venous blood since they are at the lowest pressure

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3
Q

What are the occupants of intracranial space?

A
  • CSF (10%)
  • Blood (10%)
  • Neural tissue (brain + spinal cord) (80%)
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4
Q

In a healthy individual, the blood flow to the brain is regulated.

Explain how this occurs by autoregulation and chemo-regulation?

A
  • Autoregulation – vasoconstriction, vasodilation
  • Chemo-regulation – vasodilation in response to low cerebral pH e.g. high pCO2
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5
Q

Illustrate the intracranial compensation for an expanding mass

A
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6
Q

In four steps, illustrate the pathophysiology of a brain injury

A
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7
Q

Identify four signs of symptoms of raised intracranial pressure

A
  • Headache
  • Vomiting
  • Visual disturbances
  • Depression of conscious level
  • seizures
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8
Q

Describe five characteristics of a headache due to raised ICP

A
  • Generalised ache
  • Worst on awakening in the morning
  • May awaken patient from sleep (due to hypoventilation in sleep)
  • Aggravated by bending, stooping, coughing or sneezing
  • Severity gradually progresses
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9
Q

Describe four characteristics of visual disturbances due to raised ICP

A
  • Blurring
  • Obscurations – transient blindness upon bending or posture changes
  • Papilloedema (some patients)
  • Retinal haemorrhages (if rapid ICP rise)
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10
Q

Identify two red flag signs of raised ICP

A
  • Papilloedema
  • CN VI palsy – false localising sign

and blown dilated pupil due to compression of oculomotor nerve

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11
Q

Describe the occurrence and presentation of a subfalcine herniation

A
  • Most common
  • May be asymptomatic
  • Symptoms incl. headache, contralateral leg weakness (if, ACA affected)
  • Midline shift on CT

→ cingulate gyrus is pushed under the free edge of the falcs cerebri which can compress the anterior cerebral artery as it loops over the corpus callosum

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12
Q

What is an uncal herniation?

A

An uncal herniation is when the uncus, the medial part of the temporal lobe, is displaced across the tentorial opening

→ Uncus of temporal Lobe herniates through tentorial notch compressing adjacent midbrain = 3rd nerve palsy → contralateral hemiparesis

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13
Q

As the herniation progresses, the uncus puts pressure on the midbrain.

Describe the different possible presentations of uncal herniations

A
  • Decreased level of consciousness
  • Compressed ipsilateral oculomotor nerve – ipsilateral dilated pupil
  • Compressed cerebral peduncle – contralateral leg weakness
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14
Q

What is a tonsillar herniation?

A

A tonsillar herniation is when the cerebellar tonsils herniate through the foramen magnum compressing medulla

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15
Q

Explain the presentations of tonsillar herniations?

A

Compression of medulla and upper spinal cord:

  • Brainstem affected – cardiac and respiratory dysfunction
  • Decreased level of consciousness
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16
Q

what is a central downward herniation

A

→ medial temoral lobe / other midline structures pushed through the tentorial notch

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17
Q

What is Cushing’s reflex?

A

- Cushing reflex is a physiological nervous system response to untreated raised ICP

  • It is a poor prognostic sign consisting of the following triad: high BP, bradycardia, low RR
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18
Q

In five steps, explain how bradycardia and hypertension occur due to raised ICP

A

⇒ Ischaemia at medulla

⇒ Sympathetic activation

⇒ Rise in blood pressure & tachycardia

⇒ Baroreceptors react

⇒ Bradycardia

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19
Q

In two steps, explain how hypoventilation occur due to raised ICP

A

⇒ Ischaemia at pons/medulla at respiratory centres

⇒ Low respiratory rate

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20
Q

Identify and describe the four causes of raised intracranial pressure

A
  • Increased cerebral blood volume – venous outflow obstruction, venous sinus thrombosis
  • Cerebral oedema – meningitis, encephalitis, diffuse head injury, infarction
  • Increased CSF – impaired absorption (hydrocephalus), excessive secretion (choroid plexus papilloma)
  • Expanding mass / SOL – abscess, tumour, haematoma
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21
Q

What leads to the clinical suspicion of raised ICP?

A
  • Traumatic brain injury (haemorrhages, anticoagulants)
  • Severe meningitis encephalitis
  • Risk factors, signs and symptoms of cancer
  • CVS risk factors
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22
Q

Describe the composition and appearance of cerebrospinal fluid

A
  • Normal CSF is clear and colourless
  • It contains very little protein (15 to 45 mg/dL), little immunoglobulin, and only 1-5 cells (leukocytes) per ml
  • It is hyperosmolar compared to plasma
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23
Q

Where is CSF produced?

A

The choroid plexus

24
Q

Briefly describe the pathway of CSF flow

A
25
Q

what are clinical signs of hydrocephalus

A

→ bulging head with head circumference increasing faster than expected

→ sunsetting eyes (direct compression of orbits as well involvement of oculomotor nerve

26
Q

What is hydrocephalus?

A

Hydrocephalus is the accumulation of CSF due to an imbalance between the production and absorption of CSF with subsequent enlargement of brain ventricles

→ due to neural tube defects

→ aqueduct stenosis

→ or part of a larger syndrome

27
Q

Identify and describe the two types of hydrocephalus

A
  • Non-communicating/obstructive – CSF is obstructed within the ventricles or between the ventricles
  • Communicating – there is communication between the ventricles and the subarachnoid space

( increased CSF production and reduced CSF absorption)

28
Q

A communicating hydrocephalus occurs when there is communication between the ventricles and the subarachnoid space.

Discuss the possible causes

A

Problem lies outside of the ventricular system:

  • Due to reduced absorption or blockage of the venous drainage system
  • May also be due to increased CSF production the subarachnoid space
  • Mostly due to post-meningitis (bacterial, fungal, TB)
  • Also due to trauma + neoplastic infiltration of subarachnoid space
29
Q

A non-communicating/obstructive hydrocephalus occurs when the CSF is obstructed within the ventricles or between the ventricles and the subarachnoid space.

Discuss its possible causes

A
  • Most commonly due to aqueduct blockade
  • Can be congenital or acquired
  • May be due to tumours e.g. meningioma
30
Q

What are the two age peaks for brain tumours?

A
  • In children
  • In late middle age
31
Q

how can a hydrocephalus be treated

A

tapping fontanelle with a needle

→ medium term drainage achieved by external ventricular drain = continuous monitoring BUT risk of infection as direct communication between brain and outside world

32
Q

when is an external ventricular drain used

A

if a shunt fails

requires inpatient frequent monitoring so not really long term solution

33
Q

how does a V-P Shunt work

A

Tube tunneled under the skin, prevents back flow of ventricle, extra length of tubing given for growth but these are vulnerable to infection

34
Q

What are the most common types of brain tumours in children?

A
  • Astrocytomas from astrocytes
  • Medulloblastomas from neuroectodermal cells
35
Q

What are the most common types of brain tumours for adults?

A
  • Gliomas
  • Meningiomas
  • Metastases from lung, breast and kidneys
36
Q

What is idiopathic intracranial hypertension?

A
  • Idiopathic intracranial hypertension is raised intracranial pressure without evidence of hydrocephalus or mass lesion
  • This usually occurs in obese young women after weight gain
37
Q

What are the treatment options for idiopathic intracranial hypertension?

A
  • Weight loss
  • Drugs e.g. carbonic anhydrase inhibitors, CSF drainage and shunts
38
Q

What are the principles of management of raised ICP due to increased cerebral blood volume?

A

Varies:

  • Anticoagulation
  • Rarely, tenting of venous sinuses
39
Q

What are the principles of management of raised ICP due to cerebral oedema?

A

Treat the cause:

  • Mannitol
  • Hypertonic saline
40
Q

What are the principles of management of raised ICP due to increased CSF?

A
  • Shunts
  • Tumour resection
  • Use diuretics whilst awaiting intervention e.g. furosemide, carbonic anhydrase inhibitors
41
Q

What are the principles of management of raised ICP due to space occupying lesions?

A
  • Surgical resection e.g. craniotomy
  • Steroids of high value of brain tumours
42
Q

what is the Monro Kellie doctrine

A

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

43
Q

what are the values for normal

  1. CPP
  2. MAP
  3. ICP
A

CPP = mean arterial pressure (MAP) – ICP

Normal CPP >70 mmHg

Normal MAP ~90mmHg

Normal ICP ~10 mmHg

44
Q

What happens to CPP if MAP increases

A

If MAP increases then CPP increases, triggering cerebral

autoregulation to maintain cerebral blood flow

(vasoconstriction)

45
Q

what happens if ICP increases to CPP

A

If ICP increases then CPP decreases, triggering cerebral

autoregulation to maintain cerebral blood flow

(vasodilatation)

46
Q

what is the equation for CPP

A

CPP = MAP - ICP

47
Q

If CPP <50mmHg then what happens to cerebral blood flow

A

it can’t be maintained as cerebral arterioles maximally dilated

48
Q

what can damage to the brain do to the cerebral auto regulation

A

impair or abolish

49
Q

Diagram explaining how cerebral autoregulation maintains CPP and cerebral blood flow over a range of MAP

A

there is a limitation to constriction and dilation, after a

50
Q

what Is cushings response aka cushings reflex

A

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 (which can cause stomach ulcers as a dangerous

side effect
• Continuing compression of the brainstem leads to damage to respiratory centres causing irregular breathing

51
Q

what is the process when an expanding mass eg tumour causes a rising ICP

A
  1. compensation of extrusion of CSF and venous blood
  2. iCP still starts to rise, causing CPP to reduce, reducing arterial blood flow
  3. in order to stop the CPP reducing, vasodilation increases as does blood pressure
  4. ICP still continues to rise, CPP can’t compete and brain becomes hypoxic
  5. cerebral hypoxia causes cerebral oedema, rising intracranial vol and pressure
  6. eventually compression of brain and brainstem
52
Q

what does a midline shift of a Brain X-ray suggest? and what are some other radiographic signs of raised ICP

A

subfalcine herniation → under edge of falcs cerebri

  1. evidence of other brain herniation
  2. effacement (obliteration) of ventricle
  3. loss of grey-white matter differentiation
53
Q

what are the four major pathophysiologies that play a role In stroke to trauma

A
  • 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)
54
Q

what is Idiopathic intracranial hypertension

A
  • benign intracranial hypertension
  • May present with headache and visualdisturbance
  • Usually obese middle aged females
  • Poorly understood aetiology
  • Diagnosis can be confirmed by raised
  • opening pressure on an LP

• 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!

 Treat with weight loss and blood pressure control

55
Q

what are some management options

A
  1. airway and breathing
  2. circulatory support (maintain MAP→ CPP)
  3. sedation, analgesia and paralysis (reduce metabolic demand and shivering that can increase ICP)
  4. head up tilt = improve venous drainage
  5. temp (prevent hyperthermia)
  6. anti-convulsants (prevent seizures, reduced metabolic demand
  7. nutrition and PPI (improve injury healing and stomach ulcers from increased vagal activity)
56
Q

what are some other management options

A

→ mannitol or hypotonic saline (osmotic diuresis)

→ ventricular drainage

→ decompressive craniectomy → LAST RESORT

SA Clinical Neuroscience (23 decks)

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