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

2.3 CNS Complications: Intracranial Pressure Flashcards

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USMLE® Step 1 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?

A

> 20mmHg

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.

A

30°

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
Q

List some basic side effects of mannitol

A
  • Rebound ICP levels
  • Allergic reaction
  • Heart failure
26
Q

List two obvious possible side effects of hypertonic saline administration

A
  • Hypervolemia
  • Electrolyte imbalance
27
Q

What are the purported mechanisms of action for steroids in ICP reduction?

A
  • Reduce BBB permeability
  • Free radical scavenging
28
Q

Does the onset of effects from corticosteroids happen immediately, or is it slower? Why?

A
  • Slower
  • Effect is upstream of protein synthesis (steroid = enters nucleus and affects transcription)
29
Q

What are some short term adverse effects of corticosteroids?

A

Glucocorticoid: inc. blood glucose, nervousness

Mineralocorticoid: fluid retention, hypokalaemia, increased BP

30
Q

Corticosteroids can be stopped suddenly as long as they’ve been taken for less than…

A

4 weeks

31
Q

Can you start a patient on long-term corticosteroids straight away?

A
  • No
  • Start on initial trial, wait for adverse effects, then consider long-term prescription
32
Q

What are some long-term adverse effects of corticosteroids?

A
  • Osteoporosis
  • Growth retardation
  • Poor wound healing
33
Q

On imaging, what are the three most important causes of ventricular enlargement?

A
  • Cerebral atrophy
  • Hydrocephalus
  • Encephalomalacia
34
Q

How can subfalcine herniation cause cerebral infarct?

A
  • ACAs run in longitudinal fissure
  • Get compressed by haemorrhage
  • Infarction
35
Q

Describe the density of blood relative to brain tissue acutely, subacutely, and chronically

A

Acute: Hyperdense (bright)
Subacute: Isodense (same)
Chronic: Hypodense (darker)

36
Q

Describe traumatic contusions as a class of intra-axial haemorrhage

A

Cortical haemorrhage in response to impact against skull

37
Q

How does diffuse axonal haemorrhage present on CT?

A

Small haemorrhages at grey-white juncture -> often need MRI for further investigation as this is a severe injury

38
Q

What does a haemorrhagic transformation look like on CT?

A
  • Established, more hypodense region of infarct
  • Hyperdense region of haemorrhage within
39
Q

What is the most common cause of lobar haemorrhage

A

Amyloid angiopathy

40
Q

How does cerebral oedema show up on CT?

A

Loss of grey-white differentiation; regions of hypodensity.

41
Q
A
42
Q
A

Medical Studies 2A (110 decks)

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