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Neuroscience > 10.2 Pathophysiology and management of raised intracranial pressure. > Flashcards

10.2 Pathophysiology and management of raised intracranial pressure. Flashcards

1
Q

What are the normal ranges of ICP for adults, children and infants?

A

Adults: 5-15 mmHg
Young Children: 3-7 mmHg
Term Infants: 1.5-6 mmHg

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2
Q

Describe the components that contribute to normal intracranial pressure

A 
Brain parenchyma (80%)
CSF volume (10%)
Blood volume (10%)
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3
Q

What is the normal volume of blood and CSF in the cranium?

A

150 ml of blood

150ml of CSF

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4
Q

How are the usual components of the cranium affected in a space occupying lesion?

A

CSF and blood volumes are depleated first, before the brain has to start reducing in volume. Done by herniating out between the different foramen of the skull

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5
Q

What is shown by the intracranial elastance curve?

A

Initially there is steady / stable pressure in the cranium as the volume increases. This is because of compensatory mechanisms. After compensatory mechanisms overcome/ exhausted then the pressure gradually increases

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6
Q

How much of the CO does the brain usually receive?

A

15-20%

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7
Q

What blood vessels supply the brain

A

Internal carotid arteries

Vertebral arteries

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8
Q

What is the equation for cerebral perfusion pressure?

A

CPP = mean arterial pressure - intracranial pressure.

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9
Q

What is the normal cerebral perfusion pressure?

A

Greater than 70mmHg

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10
Q

What is the normal mean arterial pressure?

A

90mmHg

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11
Q

What is the normal intracranial pressure?

A

10mmHg

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12
Q

How do we calculate mean arterial pressure?

A

DBP + 1/3 (SBP-DBP) = MAP

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13
Q

What systemic changes occur to maintain cerebral perfusion pressure when intracranial pressure increases?

A

Increase in blood pressure to increase the mean arterial pressure. This overcomes the increase in intracranial pressure.

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14
Q

Where is CSF produced?

A

choroid plexus

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15
Q

How much CSF is produced a day?

A

500ml

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16
Q

Name some of the main functions of CSF

A

Homeostasis, protection, buoyancy and waste clearance

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17
Q

What are the 3 types of brain herniation that occur during increased intracranial pressure?

A

Subfalcine herniation (most common)
Tonsillar herniation
Uncial herniation

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18
Q

What is subfalcine herniation?

A

Cingulate gyrus from one of the cerebral hemispheres shifting across the midline under the falx cerebri

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19
Q

What is a tonsillar herniation?

A

Cerebellar tonsils herniate through the foramen magnum, which can compress the medulla and the cardirespiratory centres so patients may present with problems with their breathing if this happens

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20
Q

What is uncal herniation?

A

Herniation of the uncus of the medial temporal lobe herniating through the tentorial notch which can compress important structures in the midbrain

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21
Q

What are the clinical features of raised intracranial pressure?

A 
Headaches - severe, wake at night, constant, worse on bending over
Nausea + vomiting 
Visual disturbances e.g. double vision/ diplopia
Confusion / changes in GCS 
Seizures 
Amnesia
Papilloedema 
Focal neurological signs E.g. CN3 palsy
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22
Q

What changes are seen on fundoscopy during papilloedema?

A

The optic disc appears larger, with a less well demarcated edge. Appears swollen

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23
Q

What is Cushing’s triad?

A

three primary signs that indicate raised intracranial pressure

  • hypertension
  • bradycardia
  • irregular breathing
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24
Q

Why are cushings triad not used to primarily indicate raised intracranial pressure

A

As they are late signs

25
Q

Describe the development of cushings triad

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
26
Q

What are the 2 main causes of too much blood within the cerebral vessels

A

Raised arterial pressure
- malignant hypertension
Raised venous pressure
- SVC obstruction

27
Q

What are the causes of too much blood outside of the cerebral vessels?

A

Extra dural, sub dural, subarachnoid haemorrhage

28
Q

What is malignant hypertension?

A

Systolic >180mmHg or Diastolic >120mmHg

29
Q

What are the systemic complications of malignant hypertension?

A 
Retinal haemorrhages
Encephalopathy 
Left ventricular hypertrophy 
Reduced renal function
Increased cardiovascular and cerebrovascular events risk due to hypertension being associated with a prothrombotic state.
30
Q

What is the treatment of malignant accelerated hypertension?

A

Urgent referral to hospital due to high mortality rate

Decrease BP gradually to avoid ischaemic events and hypoperfusion of organs.

31
Q

What are the common causes of superior vena cava obstruction

A

2 causes.
Extrinsic compression of the SVC. Most commonly caused by malignancy e.g lung cancers compressing the SVC or other cancers affecting the surronding lymph nodes e.g. lymphoma
Intraluminal obstruction of the SVC - clot formation around intraluminal devices.

32
Q

How is a superior vena cave obstruction treated?

A

Oncological emergency

Often receive dexomethosone if not contraindicated

33
Q

Briefly describe an extra dural haematoma

A 
Blood accumulation between skull and dura
Most common cause = trauma 
Unconscious Patient vs Patient
with a ‘Lucid Interval’ 
CT-Biconvex shape
34
Q

Briefly describe a subdural haematoma

A

Blood accumulation b etween Dura and Arachnoid mater
CT-Concave/Crescent
Can be Acute or Chronic. Acute: occurs suddenly, progresses quickly. Chronic: Slow progression
Usually caused by rupture of bridging veins

35
Q

Briefly describe a subarachnoid haemorrhage

A

Between arachnoid and pia mater
‘Thunderclap’ headache
85% rupture of intracranial aneurysm

36
Q

Give an example of congenital CSF accumulation

A

Congenital hydrocephalus

37
Q

What is congenital hydrocephalus?

A 
Present at birth 
Genetic and non-genetic factors
Eg. mutation in L1CAM gene linked to
aqueductal stenosis
Present with:
Enlargement of head circumference - sutures not fused 
Downward gaze 
Delay in neurological development
Irritable
Difficulty feeding
Seizures
38
Q

How does hydrocephalus appear on CT head?

A

Enlarged ventricles
Oedema in surrounding parenchyma- loss of markings
Small soul I

39
Q

What are the causes of obstructive hydrocephalus?

A

Blockage of flow of CSF

  1. Aqueduct stenosis (most common)
  2. Neural tube defects
  3. Dandy-walker syndrome
40
Q

What is aqueduct stenosis

A

Blockage or narrowing of the aqueduct of sylvius (between the third and fourth ventricles)
Can be congenital or acquired

41
Q

What is dandy-walker syndrome?

A

Congenital condition Enlargement of fourth ventricle
Outlets of ventricle partially blocked
Cerebellum not fully developed

42
Q

What is communicating hydrocephalus?

A

When there is no obstruction of the flow of CSF. Caused by:

  1. Overproduction of CSF e.g. choroid plexus papilloma
  2. Reduced absorption of CSF e.g. Infection and inflammation leading to scarring at subarachnoid space
43
Q

What are some causes of acquired CSF?

A

Intraventricular haematoma
Tumour
Infection (meningitis)
Trauma

44
Q

What are the 4 causes of cerebral oedema swelling of the brain

A

Vasogenic
Osmotic
Interstitial
Cytotoxic

45
Q

What is vasogenic cerebral oedema?

A

Disruption of blood brain barrier

Breakdown of tight junctions = increased permeability

46
Q

What is osmotic cerebral oedema?

A

Usually osmolarity of extracellular fluids is equal on both sides of BBB
If there is a change-osmotic gradient

47
Q

What is cytotoxic cerebral oedema?

A

Injury to cells of the brain (neurones, glial cells, axons)
Derangements in ATP-dependent transmembrane pumps - intracellular
accumulation of fluid

48
Q

What is interstitial cerebral oedema?

A

Increased pressure within the ventricles, eventual damage to their linings
CSF can now be found in brain parenchyma

49
Q

In hypoxic brain injury, how does a CT head scan appear?

A

Generalised cerebral oedema
Loss of differentiation of the grey and white matter
Sulci effaced
Small ventricles

50
Q

Why can a brain tumour and a cerebral abscess be hard to differentiate on a CT head?

A

Both appear as a small enhanced ring structure in the brain parenchyma

51
Q

Where do metastasis to the brain often come from?

A

Lung
Breast
Renal
Colon

52
Q

What is the difference between an intra axial and an extra axial brain tumour ?

A

Intra axial is within the brain tissue itself

Extra axial is when it is outside of the brain tissue such as derived from meninges

53
Q

What is a cerebral abscess?

A

Localised pus formation with capsulation within brain parenchyma.
Causes: Spread of infection (direct e.g. otomastoiditis vs distance), trauma, or unknown

54
Q

How does idiopathic intracranial hypertension present?

A

Present with headache and visual disturbances

Headaches are worse in the morning and at night and are relieved by standing.

55
Q

How is idiopathic intracranial hypertension treated?

A 
Weight loss (risk factor is increased BMI)
Blood pressure control
56
Q

How is raised intracranial pressure diagnosed?

A
  1. History and examination
    - look out for signs of raised intracranial pressure
  2. Investigations
    - bedside ( vital signs, ECG, fundoscopy)
    - Bloods ( FBC, U+E’s, CRP, Clotting, Group & Save, Cross- match, Blood culture)
    - Imaging (CT scan, MRI)
57
Q

How is raised intracranial pressure managed?

A

Primary survey and using ABCDE approach
Stabilise patient
Simple measures
- Elevate head of bed, Avoid pyrexia, Analgesia
Specific medical measures
Anticonvulsants, Sedation or neuromuscular blockade,
Mannitol or hypertonic saline
Surgical:
Ventriculostomy, Decompressive craniectomy

58
Q

What is the management of hydrocephalus?

A

Ventriculoperitoneum shunt

Ventriculoatrial shunt

59
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

Neuroscience (20 decks)

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