Raised Intracranial Pressure Flashcards

1
Q

What pressure is raised in ICP?

A

Raising of the pressure inside the cranium above 15mmHg

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2
Q

What often causes raised intracranial pressure

A

Space occupying lesions
Bleeding
Blockage of CSF drainage, impaired absorption or excess production – choroid plexus papilloma
Venous outflow obstruction or venous sinus thrombosis
Cerebral oedema due to inflammation or stroke

Cytotoxic cellular oedema, further swelling and compression, reduction of blood supply to the brain cells e.g. compression by intracranial tumour and so more cytotoxic cellular oedema.

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3
Q

Describe the common presentation of raised ICP?

A

Headache: generalised ache, worst on waking in the morning as a result of hypoventilation (raised CO2 and so vasodilation) during the sleeping hours this may wake patient from sleep, aggravated by bending, stooping, coughing or sneezing and severity gradually progresses.

Papilloedema – transitions to exudate and haemorrhages
Sixth nerve palsy – false localising sign
Pupils – constricted at first then dilated (do not mask using pilocarpine to aid fundoscopy)
Blurring and transient blindness when bending over

Nausea and vomiting progresses to projectile vomiting due to compression of chemo centre in medulla.

Depression of conscious level due to compression of reticular centre.

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4
Q

What is Cushing’s reflex

A

If raised ICP is not treated and continues to rise this can lead to herniation through foramen magnum (conning). This results in cushing’s reflex which a poor prognostic sign and is a last effort to perfuse the brain.

Triad: High BP, Bradycardia and Low respiratory rate. Ischaemia at medulla (due to compression) –> causes sympathetic activation –> Rise in blood pressure + tachycardia. Compression of the vagus nerve –> bradycardia. Ischemia at pons/medulla at respiratory centres–> low respiratory rate. If untreated – death.

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5
Q

What’s the difference between compensated and uncompensated raised ICP

A

Compensated state is where the CSF and venous blood in the brain reduces to accommodate for a growing mass in the brain.
Uncompensated state is where the above has still happened, but you reach the maximum for the amount of CSF and venous blood which can be excluded.

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6
Q

What specific sign might you see in progressive raised ICP in infants?

A

In infants, slowly increasing intracranial pressure may present as a slowly increasing head size.

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7
Q

What is the investigation of choice for suspected raised ICP?

A

Urgent CT scan looking for lesion and midline shift and loss of ventricles

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8
Q

How should raised ICP be managed?

A

ABCDE
Correct hypotension maintaining MAP > 90mmHg and treat seizures
Elevate the head to 30-40 degrees
If intubated hyperventilate to 3.5-4kPa
Liaise with neurosurgeons and anaesthetists for decompressive craniotomy
IV dexamethasone (anti-inflammatory to reduce the swelling)

Cerebral Oedema – Treat the cause using Mannitol/furosemide or Hypertonic saline
Increased CSF – Shunt, tumour resection, use diuretics whilst awaiting intervention
Expanding mass – Surgical resection e.g. craniotomy

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9
Q

What are the risk factors for idiopathic intracranial hypertension?

A

Obese females in 3rd decade
Pregnancy
COCOP, Steroids, tetracycline, vitamin A and Lithium

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10
Q

What are the features of benign intracranial hypertension?

A
Narrowed visual fields
Blurred vision and diplopia
CNVI nerve palsy and enlarged blind spot
Consciousness and cognition preserved
Papilledema
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11
Q

How is benign/idiopathic intracranial hypertension managed?

A

Usually self-limiting but 10% get permanent visual loss
Weight loss
Treat with acetazolamide, topiramate (also causes weight loss)

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12
Q

Describe subfalcine/cingulate herniation

A

Herniation 1: Subfalcine/Cingulate – same side as mass. Cingulate gyrus pushed under the free edge of the falx cerebri. This causes compression of anterior cerebral artery by the cingulate gyrus resulting in Infarction and ischaemia of medial parts of the frontal lobe and corpus callosum causing gait problems and coma.

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13
Q

Describe tentorial herniation

A

Herniation 2: Tentorial – uncus/medial part of the temporal lobe herninates through the tentorial notch or tentorium cerebelli (structure separating cerebrum from cerebellum). Occlusion of blood flow in posterior cerebral and superior cerebellar arteries. This results in damage to the oculomotor nerve on the same side (clinical sign) and damage to the post ganglionic parasympathetic fibres as well as occipital infarction. Frequently fatal because of

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14
Q

Describe tonsilar herniation or coning?

A

Herniation 3: Tonsilar or Coning – cerebellar tonsils pushed into the foramen magnum compressing the medulla of the brainstem and potentially inhibiting the cardiorespiratory centres.

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15
Q

What causes Unilaterally dilated pupils with sluggish or fixed response to light after a head injury?

A

3rd nerve compression secondary to tentorial herniation

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16
Q

What causes Bilaterally dilated pupils with a sluggish or fixed response to light after a head injury?

A

Poor CNS perfusion and bilateral 3rd nerve palsy

17
Q

What causes Unilaterally dilated pupils or equal and cross reactive to light (Marcus Gunn) after a head injury?

A

Optic nerve injury

18
Q

What causes Bilaterally constricted pupils

A

Opiates, pontine lesions, or metabolic encephalopathy

19
Q

What causes Unilaterally constricted and preserved reaction to light after a head injury?

A

Sympathetic pathway disruption