Intracranial Haemorrhages Flashcards

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1
Q

First-line medication for preventing cerebral vasospasm in SAH patients.

A

Nimodipine

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2
Q

Two options for resolving SAH.

A

Coiling
Clipping

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3
Q

Typical age group for SAH occurrence.

A

35-65

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4
Q

Most common cause of SAH. Common sites.

A

Berry aneurysm rupture (80%). Common sites: junctions of posterior communicating artery with the internal carotid OR anterior communicating artery with the anterior cerebral OR bifurcation of the middle cerebral.

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5
Q

SAH differentials.

A

1) Meningitis
2) Migraine
3) Intracerebral bleed
4) Cortical vein thrombosis
5) Vertebral or carotid artery dissection
6) Benign thunderclap headache (triggered by Valsalva manoeuvre, cough, or coitus).

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6
Q

SAH management.

A

Refer all proven SAH to neurosurgery immediately.

> Re-examine CNS chart often; chart BP, pupils, and GCS. Repeat CT if deteriorating.

> Maintain cerebral perfusion by keeping the patient well hydrated, but aim for SBP <160 mm/Hg.

> Nimodipine (60mg/4h PO for 3 weeks, or 1mg/hr IVI).

> Surgery: coiling vs clipping— the decision depends on accessibility and size of aneurysm. Do catheter or CT angiography to identify single vs multiple aneurysms before intervening.

Note: Newer techniques, such as balloon remodelling and flow diversion, can be helpful in anatomically-challenging aneurysms.

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7
Q

Investigations for suspected SAH.

A

> Urgent CT (within first 24hrs).

> Consider LP if CT is negative but the history is very suggestive of SAH and there are no CI. This needs to be done >12hr after headache onset to allow breakdown of RBCs, so that a positive sample is xanthochromic (differentiates from ‘bloody tap’).

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8
Q

Complications of SAH.

A

1) Rebleeding (most common cause of death— occurs in 20%, often within first few days).

2) Cerebral ischaemia: due to vasospasm— may cause permanent CNS deficit, and is the most common cause of morbidity). If this happens, surgery is not helpful at the time but may be so later.

3) Hydrocephalus: due to blockage of arachnoid granulations— requires a ventricular or lumbar drain.

4)Hyponatraemiais common but should not be managed with fluid restriction (seek expert advice).

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9
Q

When does most mortality occur in SAH patients?

A

Within the 1st month.

Note: 90% of survivors of the 1st month survive >1yr.

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10
Q

Risk factors for SAH.

A

> Previous aneurysmal SAH (new aneurysms form, old ones get bigger).

> Smoking.

> Alcohol misuse.

> Hypertension.

> Bleeding disorders.

> Subacute bacterial endocarditis (mycotic aneurysm).

> Family history (3-5* increased risk in close relatives).

> Polycystic kidney disease, aortic coarctation, and EDS are all associated with berry aneurysms.

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11
Q

Symptoms of SAH.

A

Sudden excruciating headache (worst headache ever/thunderclap). This headache is typically occipital.

Vomiting, collapse, seizures, and coma often follow.

Coma/drowsiness may last for days.

Some patients report a preceding ‘sentinel’ headache (perhaps due to a small leak from the offending aneurysm).

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12
Q

Signs of SAH.

A

Meningism— Kernig’s sign may be present (may take 6hrs to develop).

Eye involvement: Retinal, subhyaloid, and vitreous bleeds (Terson syndrome).

Focal signs at presentation may suggest site of aneurysm (e.g. pupil changes indicating a 3rd CN nerve palsy due to posterior communicating artery aneurysm) or intracerebral haematoma. Later deficits suggest complications.

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13
Q

Subdural haematoma signs and symptoms.

A

Symptoms: Fluctuating level of consciousness (seen in 35% of patients) +/- insidious intellectual or physical slowing, sleepiness, headache, personality change, and unsteadiness.

Signs: increased ICP, seizures, localising neurological symptoms (e.g. unequal pupils, hemiparesis) occur late, often >1 month after injury.

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14
Q

Subdural haematoma imaging findings.

A

CT/MRI shows clot +/- midline shift (but beware bilateral isodense clots).

Crescent-shaped collection of blood over one hemisphere.

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15
Q

Management of subdural haematoma.

A

Reverse clotting abnormalities urgently.

Surgical management depends on the size of clot, its chronicity, and clinical picture (generally those >10mm or with midline shift of >5mm need evacuating— via craniotomy or burr hole washout).

Address cause of trauma (e.g. falls or abuse).

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16
Q

Extradural haematoma cause.

A

Suspect after any traumatic skull fracture. Often due to a fractured temporal or parietal bone causing laceration of the middle meningeal artery or vein (typically after trauma to a temple just lateral to the eye).

Any tear to a dural venous sinus will also produce an extradural bleed.

17
Q

Extradural haematoma differentials.

A

Epilepsy
Carotid artery dissection
CO poisoning

18
Q

Management of extradural haematoma.

A

Stabilise and transfer urgently to a neurosurgical unit for clot evacuation +/- ligation of bleeding vessel.

Maintain airway.

Reduce ICP.

Intubation and mechanical ventilation are often required.

Mannitol IVI.