Cerebral;Oedema and Increased Intracranial Pressure Flashcards

1
Q

What are the INTRACRANIAL contents?

A

Brain Tissue (70%)

CSF (15%)

Blood (15%)

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2
Q

Intracranial Pressure (ICP)

A

Normally 5-15 mm Hg

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3
Q

Cerebral Perfusion Pressue (CPP)

A

CPP = MABP - ICP

When ICP > MABP, CPP is ZERO

  • no blood flow and death
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4
Q

What causes increased ICP?

A
  • Space (volume occupying lesions)
  • non-neoplastic lesions (haemorrhage, abscess, swollen infarct)
  • generalised swelling (oedema)
  • malignant tumors of brain (primary and secondary)
  • benign tumors (of menigies, nerves)
  • increased vascular volume
  • increased CSF volume
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5
Q

Oedema

A
  • common to any injury
  • represents an increase in the fluid content of the brain tissue and hence and increase in the volume of the brain itself
  • PROBLEM - when it occurs in the brain it is going to cause a risk of increase to INTRACRANIAL PRESSURE
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6
Q

Cerebral Oedema (generally what happens)

A

With cerebral oedema there may be an ACCUMULATION of fluid in either the intracellular or extra cellular spaces

  • compromises blood vessels
  • reduces perfusion
  • displaces brain tissue
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7
Q

Vasogenic Oedema (detail)

A

= accumularion of extracellular vasogenic fluid is due to increased blood pressure and/or increased permeability of vasculature

The blood/brain barrier is disrupted allowing plasma proteins to enter the extracellular space

Plasma proteins INCREASE the osmotic concentration oft he brain tissue, thus causing WATER TO LEAVE CIRCULATION AND ENTER THE BRAIN

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8
Q

Vasogenic Oedema - does fluid move AROUND the cells or INTO the cells??

A

Fluid moves and accumulates AROUNF THE CELLS therefore there is an INCREASE in PRESSURE

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9
Q

Cytotoxic Oedema (detail)

A
  • an accumulation of intracellular fluid (cytotoxic oedema) is associated with cellular energy failure

As a result there is REDUCED activity of the Na+/K+ pumps and Na accumulates in the cell

WATER THEREFORE ENTERS THE CELL DUE TO THE OSMOTIC GRADIENT

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10
Q

Cytotoxic Oedema - Does the fluid more AROUND the cells or INTO the cells?

A

WITHIN THE CELLS

The actual cell becomes bugger in side. Therefore NO DIFFERENCE IN PRESSURE

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11
Q

What does the body do to compensate the increased ICP?

A

Generally, incrased ICP means that perfusion of blood and oxygenation becomes difficult

* Arterial vasodilation occurs in order to increase perfusion - intracranial hypertension - increases ICP (i.e. brings more blood but more blood = more pressure)

Followed by spacial compensation - shunt CSF, venous vasoconstriction, arterial vasoconstriction (i.e. removes CSF)

If it CONTINUES TO INCREASE – the brain begins to experiance HYPERCAPNIA (slowly increasing ICP)

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12
Q

What are the CONSEQUENCES of increased ICP?

A

The individual rapidly deteriorates with decreasing levels of consciousness, bradycardia, hyperventilation, dilated and sluggish pupils

  • herniation, loss of autoregulation (when ICP below 40 mm Hg)
  • volume increases cause futher ICP increases and the brain experiences HYPOXIA and lactic acid build up = FURTHER vasodilation and volume increases
  • Once ICP = systolic arterial pressure BLOOD FLOW CEASES

ICP = BP this means NO BLOOD FLOW AT ALL

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13
Q

What is it called when the brain moves to one side?

A

MID LINE SHIFT

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14
Q

THREE DIFFERENT TYPES OF HERNIATION (a consequence of raised ICP)

A
  • SUB - FALCINE HERNIATION
  • TRANSENTORIAL HERNIATION
  • TONSILLAR HERNIATION
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15
Q

HERNIATION (A COMPLICATION OF RAISED ICP)

  1. UNCAL
A

Herniation of innermost part of temporal lobe (uncus) towards tentorium

Puts pressure on the brain stem (mainly midbrain)

Can affect the eye due to compression of the third cranial nerve (why we look when car accident etc)

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16
Q

HERNIATION (A COMPLICATION OF RAISED ICP)

  1. Central Herniation
A

Parts of cerebellar hemispheres and temporal lobes squeezed through a notch in tentorium cerebelli
Downward herniation

17
Q

HERNIATION (A COMPLICATION OF INCREASED ICP)

  1. Sub-Facline Herniation
A

Most common
Innermost part of the frontal lobe pushed under part of the falx cerebri
Caused by swelling of one hemisphere, pushing cingulate gyrus under the falx cerebri
Can interfere with blood vessels –> potential effects on ICP
Can progress to central herniation

Symptoms not well defined
abnormal posturing, coma, increased ICP, cerebral oedema, altered LOC, change in neuro exam

18
Q

HERNIATION

4. Transcalvarial Herniation

A

Brain squeezes through a fracture or surgical site in skull
Eg: through craniectomy
= external herniation

19
Q

5. Upward Herniation

A

Increased pressure within the posterior fossa causes the cerebellum to move up through the tentorial opening
Midbrain pushed up through tentorial notch
= upward cerebellar herniation

20
Q

6. Tonsillar Herniation

A

= downward cerebellar herniation; “coning”
Cerebellar tonsils move downward through foramen magnum
Compression of lower brain stem and upper cervical spinal cord (these structures pass through foramen magnum)
Increased pressure within brain stem –>dysfunction of centres within the brain responsible for controlling respiration and cardiac function –>intermittent respirations/cessation of breathing; cardiac dysfunction
Life threatening

21
Q

Management of Increased ICP

A
  • Treatments have not changed for many years
  • Osmotic agents
  • steroids
  • CSF drainage
  • Decompressive craiectomy
  • hypothermia
  • barbituates
  • hyperventilation
22
Q

Treatment of raised ICP

“Decompressive Crainectomy”

A

= Removal of some skull

Increased the area that tissue can expand so not compressing on itself and therefore less dammage.

23
Q

Substance P Immunoreactivity in the Cortex

A

This peptide is released in the brain and it causes vasodilation and inflammatory cells.

It is thought that this can REDUCE OEDEMA

This substance regulates the BBB permeability and reduces ICP

Tested on sheep