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Clinical Neuroscience (My own) > Raised Intracranial Pressure > Flashcards

Raised Intracranial Pressure Flashcards

1
Q

What makes up the contents of the skull?

A

CSF
Blood
Brain parenchyma

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2
Q

What proportion and volume makes up the CSF?

A

150ml (10%)

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3
Q

What proportion and volume make up the blood volume?

A

120ml (10%)

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4
Q

What proportion and volume make up the brain parenchyma>

A

1400ml (80%)

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5
Q

What is the normal CSF pressure within ICP in adults?

A

<10-15 mmHg

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6
Q

What is the normal CSF pressure within ICP in children?

A

3-7 mmHg

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7
Q

What are some methods of measuring ICP?

A 
Subarachnoid ICP monitor
Intraventricular ICP monitor
Transcranial doppler
Subdural ICP monitor
Intraparenchymal PBO2 monitor
Intraparenchymal ICP monitor
Epidural ICP monitor
NIRS sensors
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8
Q

WHat is NIRS?

A

A non-invasive method

Near Infrareed Spectroscopy

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9
Q

WHat is NIRS dependant on?

A

The relative transparency of tissue for light in the NIR range
The O2 dependant light absorbance of Hb

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10
Q

When is ICP measured?

A

Mainly in trauma
Continuous ICP monitoring
Goal directed treatment to reduce ICP

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11
Q

When is it ICP measurement used in acute cases?

A

In overall brain resuscitation

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12
Q

Describe the normal Time, ICP graph

A

Three waves:

P1-P3

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13
Q

What doe each of the ICP waveform changes represent?

A

P1- arterial pulsation
P2- brain tissue compliance
P3- dicrotic wave (aortic valve closure)

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14
Q

What happens to the graph in acute brain injury and why?

A

Acute brain injury compliance starts decreasing resulting in reversal of P1:P2 ratio and P2>P1

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15
Q

What are the Lundberg wave changes that occur in increased ICP?

A

A wave- Plateau
B wave- Rhythmic oscillation every 1-2 mins
C wave- oscillation every 4-8 months

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16
Q

What is the Monroe-Kellie Doctrine?

A

The brain has compensatory mechanisms for a mass in the brain

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17
Q

What are the immediate compensatory mechanisms of the brain?

A

Decrease in CSF volume by movement of fluid into lumbar area
Reduced CSF production
Decrease in the blood volume by squeezing the blood out of the sinuses

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18
Q

What are the delayed compensatory mechanisms of the brain?

A

Decrease in extracellular fluid

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19
Q

How does anoxic changes occur in the brain?

A

Pressures exceed arterial supply –> increased blood supply –> Anoxic changes

20
Q

What are the volume pressure relations of Monro-Kellie doctrine?

A

The sum of the intracranial volumes within blood brain and CSF and other components is constant
Non-linear association between volumes and pressure

21
Q

Describe the graph of Monro-Kellie doctrine?

A

Sudden acceleration of intracranial volume, there is a point at which there’s acceleration of pressure therefore brains pushed through foraman magnum

22
Q

Why is ICP important?

A

Leads to death or disability most acute cerebral conditions and there major consequences are:
Brain shifts
Brain ischaemia

23
Q

What is cerebral perfusion pressure?

A

The calculated difference between the mean arterial pressure and the ICP

24
Q

What are the symptoms of raised ICP?

A

Headache
Nausea and vomiting
Double vision
Other neurological symtpoms

25
Q

What are the signs of raised ICP?

A 
Bradycardia
Systolic hypertension
Irregular respirations
Cheyne Stokes respirations
Decreased mental abilities
Confusion
Non-reactive pupils
Loss of consciousness
Papilloedema
26
Q

What are the features of Cushing Reflex?

A

Bradycardia
Sytolic hypertension
Irregular breathing

27
Q

Describe the Cushing Reflex?

A

Increased ICP
Decreased cerebral blood flow
Increase in CO2, stimulating the vasomotor centre of the brain
Sympathetic response leads to vasoconstriction= Inc. MAP to inc. CPP
Baroreceptors in aortic arch and carotid arteries
Reflex bradycardia
HIGH BP LOW HR

28
Q

What can the causes of ICP be split into?

A

Stuff from blood e.g. haemotoma, injury and haemorrhage
CSF- hydrocephalus
Brain- tumult pr acute brain oedema

29
Q

What is Craniosynostosis?

A

Sutures that are fused and so no space for the expanding brain in babies

30
Q

What is the sequelae of extradural haemorrhage?

A

Loss of consciousness on initial injury
Transient recovery with headache known as lexus interval in many
As haemotoma enlarges, ICP will increase causing compression of the brain and rapidly deteriorating consciousness
Cranial nerve palsies can be found

31
Q

When should an urgent head CT be ordered?

A 
GCS below 13
Focal neuro deficit
Seizure
Loss of consciousness within older people, coagulopathy, dangerous mechanism of injury, amnesia
Skull fracture
32
Q

What is the image on a CT of an extradural haemorrhage?

A

Like a lemon
No lateral ventricles
Midline shift
No sulci

33
Q

Where is an extradural haemorrhage found? Thus which artery is severed?

A

Collection of blood between inner surface of skull and periosteal dura mater
Middle meningeal artery

34
Q

What are 4 sites of brain herniation?

A

Subfalcine
Transtentorial
Uncal
Tonsillar (coning, involving midbrain)

35
Q

What does an acute subdural haemorrhage look like on a CT?

A

Banana

36
Q

Who is most affected by subdural haemorrhage and why?

A

Older people because it is usually a haemorrhage of the bridging veins that are stretched due to shrinking of the brain

37
Q

WHat is the difference in CT scan between acute and chronic subdural haemorrhages?

A

Chronic is more dark than acute

There is also less midline shift which means neurological abnormalities may not be present immediately

38
Q

WHat are the treatments of subdural haemorrhages?

A

Burr hole

Craniotomy

39
Q

What is tier 0 in the treatment of rICP

A 
Airway
Ventilation
Blood pressure
Fluids
Sedation
Fever
Glucocorticoids
Facilitate cerebral venous drainage
Bed elevation
Nursing care
40
Q

What is tier 1 in treatment of rICP?

A

General physiological homeostasis
CSF drainage
Osmotic therapy works by reducing brain water
Mannitol, hyperosmolar therapy as cells swell
Diuretics
Neuromuscular blockade
Hyperventilation

41
Q

What is tier 3 in treatment of rICP?

A

Barbiturate coma
Optimised hyperventilation
Hypothermia
Decompressive craniotomy

42
Q

Describe communicating hydrocephalus?

A

Impaired CSF reabsorption in the absence of any obstruction

Functional impairment of the arachnoid granulations

43
Q

Describe non-communicating hydrocephalus?

A

Foramen of Monro- blockage of lateral ventricles
Aqueduct of sylvia’s
4th ventricle obstruction –> dilation of the aqueduct and the other ventricles (chiari)
Congenitral malformation leading to blockage of Lusaka and Magendie

44
Q

Describe cerebral oedema?

A

Grey matter blends imperceptibly into white matter
Loss of grey-white discrimination
Lateral borders of both ventricles displaced medially
Sign of central herniation begins to funnel through central opening in tentorium

45
Q

Describe the pathophysiology of anoxic brain injury?

A 
Decreased cerebral blood flow
Decreased O2
Failure of ATP driven ion pump in brain cell
Efflux of K from cell
Influx of Na into cell
Depolarisation of neurones
Water follows Na into cell and causes Odrma
Activated NOS--> NO
Toxic O2 radicals produced
46
Q

What is given for brain resuscitation?

A 
Barbiturates
SO dismutase
calcium channel antagonist
glutamate antagonist
NO syntheses inhibitors
Hypothermia

Clinical Neuroscience (My own) (9 decks)

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