Pathophysiology and Management of Raised Intracranial Pressure Flashcards

1
Q

What is the normal ICP?

A

7-20 cmH2O

(5 - 15 mmHg)

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2
Q

What is autoregulation in the brian?

A

the maintainance of adequate blood flow to the brain thorough vasoconstriction and vasodilation of small arterioes

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3
Q

What is chemoregulation in the brain, and therefore what would be the effect of breath holding?

A

altering blood flow in response to pH/CO2 levels

breath holding > elevates CO2 (dropping pH) > vasodilation to increase blood flow

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4
Q

If a patient were to develop an intracranial mass, how would the volume contribution of each of the components of the cranial cavity change?

A

reduce venous blood volume

reduce CSF volume

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5
Q

How can decreased blood flow in the brain lead to cerebral oedema?

A

decreased blood flow > neuronal cell hypoxia > failure of Na+/K+ATPase > intracelular Na+ rises > water moves into cells > neuronal swelling > further compression of blood vessels and increase in ICP > decreased blood flow cycle continues

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6
Q

Why do patients report an increase in headache due to raised ICP first thing in the morning?

A

intracranial venous pressure is increased when lying flat (normally around -10mmHg when standing)

hypoventilation during sleep > elevated CO2 > cerebral arteriole vasodilation > increased blood flow > increaed pressure

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7
Q

Why does coughing, bending and sneezing increase headaches due to raised ICP?

A

increase in thoracic pressure causes SVC inflow obstruction, limiting venous drainage from head

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8
Q

What may be seen on fundoscopy if a rise in ICP has been very sudden?

A

Retinal Haemorrhages

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9
Q

Why may a patient with raised ICP present with vision loss?

A

compression of the optic nerve
(surrounded by dura mater)

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10
Q

What is belived to cause vomiting in patinet with raised ICP?

A

hypoxia stimulates the vomiting centre in the brainstem

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11
Q

How may a slowly increasing ICP manifest in an infant?

A

increasing head circumference size

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12
Q

Summary of raised ICP

A

Summary of raised ICP

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13
Q

Why may a CN6 palsy present as a false lateralising lesion in a patinets with riased ICP?

A

CN6 origniates from posterior pons

runs ventrally over petrous part of temporal bone

raised ICP can compress CN6 against cranial floor

riased ICP may be due to a mass anywhere in cranial value but CN6 palsy would suggest it was around that region

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14
Q

What is a subfalcine herniation and why may some patinets present with contralateral leg weakness, whereas others could be asymptomatic?

A

herniation of the cingulate gyrus under the falx cerebri

hernation can lead to compression of anterior cerebral artery > supplies medial aspect of pre-central gyrus (primary motor cortex) with humuncular correlation to the lower limb

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15
Q

What are the possible effects of uncal herniation over the tentorium cereblli?

A

ipsilateral occulomotor nerve palsy
(dilated pupil due to loss of parasympathetics)

compression of cerebral peduncle
(contralateral leg weakness)

decreased level of consciousness
(compression of RAS in brainstem)

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16
Q

What is the greatest threat to life following a tonsilar herniation?

A

compression of the respiratory and cardiovascular centres in the medulla

17
Q

What are the three features of Cushing’s Reflex?

A

Hypertension

Bradycardia

(medulla ischaemia activates SNS > hypertension detected by baroreceptors and slows HR)

Bradypnoea
(± irregular)

18
Q

How can the causes of rasied ICP be characterised into 4 groups?

A

CSF

Brain Tissue

Blood

Other

19
Q

Give 3 examples of causes of raised ICP

A

Hydrocephalus

Intracranial Haemorrhage

Intracerebral Abscess

(CSF Outflow Obstruction)

20
Q

What is the most common cause of raised ICP?

A

Traumatic Brain Injury

21
Q

How does the osmolarity of plasma differ from the cerebrospinal fluid?

A

CSF is HYPEROSMOLAR compared to plasma

(143 mEq/L vs. 138mEq/L)

22
Q

Outline the flow of CSF throughout the brain?

A

lateral ventricles > interventricular foramen > third ventricle > cerebral aqueduct > fourth ventricle > median & lateral appertures, central canal

23
Q

Which artery provides the blood supply for the lateral ventricle choroid plexus?

A

internal carotid artery

24
Q

How does the CSF get reabsorbed from the subarachnoid space?

A

arachnoid villi extend into the dural venous sinuses

CSF moves across villi and is reabsorbed back into the venous circulation

25
Q

What is the difference between a communicating and non-communicating hydrocephalus?

A

Non-Commnicating

obstruction of CSF flow within or between the ventricles

Communicating
due to excess CSF production or obstructed venous drainage

(no obstruction of CSF flow within or between ventricles - there IS communication between ventricles)

26
Q

What is the most common cause of brain malignancy in adults?

A

metastatic disease

27
Q

What is idiopathic intracranial hypertension and which population of people is commonly affected?

A

raised ICP with no identifiable abnormality
(e.g. no mass or hydrocephalus)

obese young women commonly affected

28
Q

How can raised ICP caused by the following be rectified:

Hydrocephalus

Abscess

Tumour

A

Hydrocephalus
(ventriculoperitoneal shunt)

Abscess
(antibiotics / inscision & drainage)

Tumour
(resection)

29
Q

What are common steps in the management of raised ICP?

A

ABCDE approach

30 degree head up

IV mannitol / hypertonic saline

intubate and ventilate
(target CO2 between 4 - 4.5 kPa)