Raised intracranial pressure

Question 1

Describe the normal ICP for various age groups. (3)

Answer 1

Adults - 5-15 mmHg
Children - 5-7 mmHg
Term infant - 1.5-6 mmHg

Question 2

Explain why the ICP of a term infant is so low. (1)

Answer 2

Their cranium has fontanelles that expand.

Question 3

Describe the causes of raised ICP caused by “too much blood”. (10)

Answer 3

Rare causes:
Raised arterial pressure - only in malignant hypertension
Raised venous pressure - only in SVC obstruction

More common:
Haemorrhage (extradural, subdural, subarachnoid, intraventricular, haemorrhagic stroke).

Question 4

Describe the Monro-Kellie Doctrine. (3)

Answer 4

The idea that venous pressure, arterial pressure, brain matter and CSF are all balanced within the cranium, so as one increases, another must decrease.
This explains why CSF pulses out of a lumbar puncture in time with the heart.

Question 5

Describe the causes of raised ICP relating to “too much CSF”. (9)

Answer 5

Called hydrocephalus.
Acquired causes: meningitis, trauma, haemorrhage, tumour
Congenital causes: obstruction to outflow (neural tube defects, aqueductal stenosis)l communicating hydrocephalus (too much being made, not enough being absorbed).

Question 6

Explain the presentation of infants with raised ICP. (4)

Answer 6

Enlarged head - increased pressure pushed the bones of the cranium out at the fontanelles.
Sunset eyes - increased pressure compressed the midbrain containing the brainstem nuclei of cranial nerves III, and IV giving the eye a downwards gaze.

Question 7

Describe the treatment options for a child with raised ICP. (3)

Answer 7

Acute - drain with a needle through the fontanelles.
Moderate - external ventricular drain
Chronic - ventricular-perineal shunt

Question 8

Explain why a ventricular-atrial shunt would not be appropriate in a child with hydrocephalus. (1)

Answer 8

Children grow, and the shunt would need to be moved and replaced.

Question 9

Explain the disadvantage of all ventricular shunts. (1)

Answer 9

Can introduce infection to the brain.

Question 10

Describe the causes of raised ICP relating to “too much brain”. Explain each cause and give an example of when this might occur. (13)

Answer 10

Cerebral oedema
Interstitial - rupture of BBB, so CSF spreads - trauma, hydrocephalus
Osmotic - higher osmolarity in brain compared to serum - SIADH or excessive H2O intake.
Cytotoxic - intracellular retention of Na+ and H2O - toxins.
Vasogenic - breakdown of tight junctions in the BBB - vasoactive substances.

Question 11

Describe three other causes of raised intracranial pressure that are not “too much blood”, “too much CSF” or “too much brain”. (3)

Answer 11

Tumour
Abscesses
Iatrogenic

Question 12

Explain the normal cerebral perfusion pressure. (4)

Answer 12

Cerebral perfusion pressure = MAP - ICP
Normal MAP = 65-110 mmHg
Normal ICP = 5-15 mmHg
Normal CPP = > 70 mmHg

Question 13

Describe and explain the purpose of cerebral autoregulation. (4)

Answer 13

Abnormally high CPP leads to cerebral autoregulation.
Increased perfusion - vasoconstriction
Decreased perfusion - vasodilation
This is done to maintain the pressure within the cranium.

Question 14

Describe Cushing’s triad (4)

Answer 14

An indication of severely raised intracranial pressure.
1 - increased MAP
2 - Bradycardia
3 - irregular breathing

Question 15

Explain why the first stage of Cushing’s Triad occurs. (6)

Answer 15

The stage is Increased MAP
Low perfusion of the brain caused by increased intracranial pressure detected by brain baroreceptors 
Prompts sympathetic response
Increases BP and HR 
Better perfusion of the brain.

Question 16

Explain why the second stage of Cushing’s Triad occurs. (4)

Answer 16

Stage is bradycardia.
Aortic and carotid baroreceptors detect the higher BP
They reduce the HR to keep CO the same
Also vagus nerve squashed by a mass at the medulla to prompt bradycardia.

Question 17

Describe and explain one secondary symptom of the second stage of Cushing’s Triad (4)

Answer 17

A Cushing’s ulcer - caused by the parasympathetic release of excess gastric acid from the impulses that cause the bradycardia.

Question 18

Explain why the third stage of Cushing’s Triad occurs. (3)

Answer 18

Irregular breathing.

Cerebellar tonsils herniate through the foramen magnum and compress the respiratory centres in the brainstem.

Question 19

Describe tonsilar brain herniation and it’s consequences. (2)

Answer 19

Cerebellar tonsils herniate through the foramen magnum and compress the cerebellum and the brainstem leading to cerebellar signs (DANISH) and brainstem signs like Resp depression.

Question 20

Describe subfalcine brain herniation. (6)

Answer 20

Cingulate gyrus pushes under the free edge of the flax cerebri. Compresses the interventricular foramen and ACA leading to infarction and hydrocephalus.

Question 21

Describe uncial brain herniation. (10)

Answer 21

Uncus moves past the tentorium. Compresses the occulomotor nerve, PCA, corticospinal and corticobulbar spinal tracts. This leads to ipsilateral hemiparesis, “down and out” position, blown pupil, ptosis and a possible PCA infarct.

Question 22

Describe central downward brain herniation. (5)

Answer 22

Temporal lobes are pushed though the tentorial notch. Leads to a Duret Haemorrhage (basilar artery) which is most commonly fatal.

Question 23

Describe external brain herniation. (2)

Answer 23

Occurs through an open skull fracture. Structures damaged will depend on the location of the fracture.

Question 24

Describe initial symptoms of raised ICP. (7)

Answer 24

Acute trauma or bleed
Headache - present on waking, worse when bending.
Difficulty concentrating, drowsiness, confusion
Double vision, visual field defects, papilloedema
Nausea and vomiting
Seizures
Focal neurological signs.

Question 25

Describe tests you would undertake if someone presented with raised intracranial pressure. (6)

Answer 25

Full cranial and peripheral nerve study.
Fundoscopy, pupillary responses, eye movements, visual fields.
Blood tests - U+E, inflammatory markers, thyroid function, LFTs, Syphillis, Lyme’s Disease.
CT/MRI
Lumbar puncture.

Question 26

Explain the order you would do a lumbar puncture and CT/MRI in. (2)

Answer 26

Imaging first so if it is raised intracranial pressure you avoid reactive herniation.

Question 27

Describe idiopathic intracranial hypertension. (4)

Answer 27

Usually occurs in obese middle aged women, with no known aetiology. Improves with weight loss and bp control.
Diagnosed with lumbar puncture with opening pressure of >25 mmH20 - equal to > 18 mmHg

Question 28

Describe how you would monitor ICP in ITU. (1)

Answer 28

An ICP “bolt” that produces a continuous waveform.

Question 29

Describe brain protection methods if an adult presents with mild raised ICP or is at high risk of developing it.
Explain why each of them works.
(14)

Answer 29

Airways control and ventilitation - just the right amount of CO2 removed to avoid vasodilation or constriction (both bad)
Circulatory support - maintain MAP for good CPP.
Sedation paralysis and analgesia - reduces metabolic demand.
Head up position and removing of C spine collar - improves venous drainage.
Not hot temps - reduces metabolism demand
Anticonvulsants - reduces seizures and reduces metabolic demand.
Nutrition and PPIs long term - increased healing and reduces Cushing Ulcer risk.

Question 30

Describe how you would treat a patient presenting with severely raised intracranial pressure.
Explain why each treatment works.
(8)

Answer 30

Give either mannitol or 3% hypertonic saline - osmotic effect to reduce cerebral oedema.
External ventricular drain - drain CSF - can be hard to place if ventricles are flattened.
Decompressive craniotomy, leaving skull flap in a bone bank or the abdomen. Outcomes poor.