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Medical Studies 2A > 2.3 CNS Complications: Intracranial Pressure > Flashcards

2.3 CNS Complications: Intracranial Pressure Flashcards

1
Q

The leading cause of death after TBI and stroke is…

A

Cerebral oedema

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2
Q

The mortality of malignant cerebral oedema is in excess of…

A

60-80%

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3
Q

Name the two mechanisms of cerebral oedema

A
  • Vasogenic oedema
  • Cytotoxic oedema
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4
Q

Explain the mechanism of vasogenic cerebral oedema

A
  • BBB increases permeability in response to damage
  • Proteins (e.g. albumin) enter brain
  • Water follows gradient, increase EXTRAcellular volume.
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5
Q

Describe the mechanism of cytotoxic cerebral oedema

A
  • Increased fluid inside brain cells
  • Often caused by failure of ion pumps
  • Increase in brain volume
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6
Q

True or false: the two main mechanisms of cerebral oedema usually occur in conjunction with one another

A

True

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7
Q

How do we calculate cerebral perfusion pressure?

A

CPP = Arterial pressure - ICP

If MABP = ICP, no perfusion to the brain

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8
Q

What is it called when the brain tries to regulate ICP in response to some kind of mass?

A

Spatial compensation

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9
Q

Describe the brain’s two mechanisms of spatial compensation

A
  1. Shunt off CSF (increase resorption, decrease production)
  2. Venous vasoconstriction
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10
Q

Describe the “desperate” arterial response in spatial compensation in the brain

A
  1. Arterial vasonstriction

(But then the brain runs out of breath)

  1. Arterial vasodilation; re-establishes blood flow, but increased ICP
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11
Q

Describe the fundamental positive feedback loop of ICP decompensation

A
  • Increased ICP
  • Decreased CPP
  • Decreased blood flow to cerebrum
  • Ischaemia > tissue injury
  • More oedema raises ICP
  • Hypercapnia (from low blood flow) causes further vasodilation andthus inc. ICP
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12
Q

List the three main kinds of brain herniation

A
  • Subfalcine (falx cerebri)
  • Transtentorial/uncal
  • Tonsillar (foramen magnum)
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13
Q

What is the most common kind of brain herniation?

A

Subfalcine

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14
Q

Symptoms of subfalcine hernation

A
  • Coma
  • Increased ICP (blocked blood vessel?)
  • Cerebral oedema
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15
Q

What is the characteristic symptom of uncal herniation?

A

Inability of pupil to dilate/respond to light

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16
Q

How do hyperosmotic agents reduce ICP?

A
  • Increased blood osmolarity
  • Draw water from brain into blood
  • Decreased cerebral oedema
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17
Q

How do barbituates lower ICP?

A
  • Suppress cerebral metabolism
  • Decreased blood flow to brain due to decreased demand
  • Decreased production of metabolic byproducts that lead to cerebral oedema
18
Q

How do steroids reduce ICP?

A

Inhibit inflammatory response (and therefore oedema)

19
Q

What kinds of drugs can be used to treat raised ICP?

A
  • Hyperosmotics
  • Barbituates
  • Steroids
20
Q

What surgical interventions are available for raised ICP?

A
  • Decompressive craniectomy
  • Ventricular drain
21
Q

At what ICP level should clinical intervention occur?

22
Q

Describe the three-tiered management of raised ICP

A

Tier 1: CSF drainage, slight hyperventilation

Tier 2: Mannitol/hypertonic saline, hyperventilation

Tier 3: Barbiturates, craniectomy/hypothermia

SMB = Super Mario Brothers = Surgery, Mannitol, Barbituates

23
Q

When trying to reduce intracranial pressure, the head should be tilted up by __ degrees.

24
Q

Why is an intact BBB required for mannitol therapy in ICP reduction?

A

If mannitol gains access to the brain, then water will flow into the brain, having the opposite effect.

25
List some basic side effects of mannitol
- Rebound ICP levels - Allergic reaction - Heart failure
26
List two obvious possible side effects of hypertonic saline administration
- Hypervolemia - Electrolyte imbalance
27
What are the purported mechanisms of action for steroids in ICP reduction?
- Reduce BBB permeability - Free radical scavenging
28
Does the onset of effects from corticosteroids happen immediately, or is it slower? Why?
- Slower - Effect is upstream of protein synthesis (steroid = enters nucleus and affects transcription)
29
What are some short term adverse effects of corticosteroids?
Glucocorticoid: inc. blood glucose, nervousness Mineralocorticoid: fluid retention, hypokalaemia, increased BP
30
Corticosteroids can be stopped suddenly as long as they've been taken for less than...
4 weeks
31
Can you start a patient on long-term corticosteroids straight away?
- No - Start on initial trial, wait for adverse effects, then consider long-term prescription
32
What are some long-term adverse effects of corticosteroids?
- Osteoporosis - Growth retardation - Poor wound healing
33
On imaging, what are the three most important causes of ventricular enlargement?
- Cerebral atrophy - Hydrocephalus - Encephalomalacia
34
How can subfalcine herniation cause cerebral infarct?
- ACAs run in longitudinal fissure - Get compressed by haemorrhage - Infarction
35
Describe the density of blood relative to brain tissue acutely, subacutely, and chronically
Acute: Hyperdense (bright) Subacute: Isodense (same) Chronic: Hypodense (darker)
36
Describe traumatic contusions as a class of intra-axial haemorrhage
Cortical haemorrhage in response to impact against skull
37
How does diffuse axonal haemorrhage present on CT?
Small haemorrhages at grey-white juncture -> often need MRI for further investigation as this is a severe injury
38
What does a haemorrhagic transformation look like on CT?
- Established, more hypodense region of infarct - Hyperdense region of haemorrhage within
39
What is the most common cause of lobar haemorrhage
Amyloid angiopathy
40
How does cerebral oedema show up on CT?
Loss of grey-white differentiation; regions of hypodensity.
41
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Medical Studies 2A (110 decks)

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