Haemorrhages Flashcards

1
Q

What are the meningeal layers of the brain?

A

Venous sinuses are found between endosteal and meningeal layers of the dura mater. Arachnoid granulations are arachnoid mater protrusions into the dural venous sinuses and facilitate movement of CSF into the blood.

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2
Q

What is an extradural haemorrhage?

A

Aka epidural haematoma. Is a collection of blood between the skull and dura mater, typically caused by a direct force.

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3
Q

What is the aetiology of an extradural haemorrhage? (x3)

A
  • Trauma
  • Blow to side of the head in pterion region which overlies the middle meningeal artery
  • Rarely, heat haematoma from severe burn causing contraction of the dura and exfoliate from the skill, causing exudation of blood from the venous sinuses
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4
Q

What is the pathophysiology of extradural haemorrhage?

A

Rapid onset because it is usually from arteries, though can come from veins in 10% of cases with less acute onset.

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5
Q

What are the symptoms of extradural haemorrhage? (x7)

A
  • Lucid period immediately after injury (regain consciousness is hallmark feature)
  • Severe headache
  • N&V
  • Contralateral hemiplegia
  • Confusion
  • Fixed and dilated ipsilateral pupil from CNIII impingement. The eye will also angle down and out due to unopposed innervation of the intact CNIV and CNVI, eyelid drooping, orbital pain and diplopia
  • Vision loss from compression of posterior cerebral artery
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6
Q

What are the complications of extradural haemorrhage?

A

Tonsillar herniation (causes Cushing’s triad in posterior cranial fossa: hypertension, bradycardia and irregular breathing) resulting in respiratory arrest.

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7
Q

What are the investigations for extradural haemorrhage?

A

CT/MRI: MRI has highest sensitivity and first choice. Important for differentiating from ischaemic attack or intracranial mass

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8
Q

How do extradural haemorrhages appear on MRI? (x3)

A
  • Convex in shape because dura adhesion to skull prevents easy expansion. Haemorrhages also stop at the skull’s sutures due to particularly tight adhesion of dura to these areas.
  • Will also be able to visualise skull fractures if this is the cause.
  • Penetration of haemorrhage can result in midline shift and ventricle compression
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9
Q

What is a subarachnoid haemorrhage?

A

Arterial bleeding into subarachnoid space (between arachnoid membrane and pia). Rapid onset.

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10
Q

What is the aetiology of subarachnoid haemorrhage? (x6)

A
  • Most common cause: rupture of intracranial saccular aneurysm in artery at base of the brain (usually at Circle of Willis)
  • Perimesencephalic haemorrhage – venous or capillary rupture characterised by haemorrhages at basal cisterns around the midbrain
  • Trauma – fracture or intracerebral contusion
  • Arteriovenous malformations
  • Carotid artery dissection with intracranial dissection
  • Blood diasthesis
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11
Q

What are the risk factors for subarachnoid haemorrhage? (x5)

A

Smoking, alcohol misuse, drug use (cocaine and amphetamines), hypertension, anticoagulants, connective tissue disorders.

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12
Q

What are the symptoms of SAH? (x5) !!! Note about consciousness?

A
  • Thunderclap headache and lasts more than an hour. Very sudden onset. Associated with agitation.
  • Depressed or loss of consciousness. NB: neurological examination needed for ALL patients with loss of consciousness
  • Meningism: neck stiffness and muscle aches
  • N&V
  • Photophobia due to irritation of meninges
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13
Q

What is a thunderclap headache?

A

Severe and sudden onset, defined as taking second to minutes to reach maximum intensity. SAH is most common cause.

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14
Q

What are the signs of SAH? (x5)

A
  • Diplopia with mydriasis, orbital pain and eyelid drooping from compression from CNIII, though not common
  • Meningism: neck stiffness. Associated with Kernig’s sign (resistance or pain on knee extension when hip is flexed) because of irritation of the meninges. Pyrexia may also occur.
  • Lowered GCS
  • Hypertension and bradycardia (brainstem herniation)
  • Fundoscopy: rarely subhyaloid haemorrhage (between retina and vitreous membrane)
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15
Q

What are the complications of SAH? (x3)

A
  • VASOSPASM: substances released from the haematoma may cause cerebral vessel vasospasm which can lead to ischaemia brain damage.
  • Obstructive hydrocephalus (CSF circulation blocked by blood clot in ventricles)
  • Communicating hydrocephalus (CSF circulation stopped by damaged arachnoid granulations)
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16
Q

!!! What are the investigations for SAH? (x5 (x4))

A
  • CT/MRI: standard is non-contrast CT. Shows hyperdense areas in cisterns - see photo
  • LUMBAR PUNCTURE: performed if CT negative or inconclusive but have high suspicion for SAH (NB: patient can have SAH with negative CT). LP will show blood and xanthochromia (straw-coloured CSF from broken down Hb).
  • ANGIOGRAPHY (CT or intra-arterial): detect source of bleeding
  • BLOODS: FBC may show leucocytosis and hyponatraemia which are risk factors for vasospasm. Troponin I and hyperglycaemia is also be elevated in some patients and both indicate poorer prognosis
  • ECG: half of SAH patients also have cardiac abnormality such as arrythmia, so should be offered an ECG on admission
17
Q

What are cisterns?

A

Anatomical space produced from openings in the subarachnoid space and are filled with CSF.

18
Q

What is the anatomy of the brain’s cisterns?

A

.

19
Q

What is a subdural haemorrhage?

A

Bleed between dura and arachnoid maters. More insidious clinical picture.

20
Q

How are subdural haemorrhages categorised? (x3)

A

Acute (within 72 hours), sub-acute (3-20 days), and chronic (after 3 weeks).

21
Q

What is the aetiology of SDH? (x3)

A
  • Trauma – rapidly changing velocities within the skull stretch the bridging veins
  • Less commonly associated with aneurysms or vascular malformations
  • Drop in CSF pressure
22
Q

What are risk factors for SDH?

A

Alcohol misuse, old age, anticoagulants,

23
Q

Why does old age and alcohol lead to SDH?

A

Both lead to cerebral atrophy which increases the length of bridging veins and increases likelihood of tear.

24
Q

How may drop in CSF pressure lead to SAH?

A

Leads to reduced pressure in the subarachnoid space, pulling the arachnoid away from the dura and leading to rupture of blood vessels.

25
Q

What is the pathophysiology of acute SDH? (x4 points)

A
  • Arachnoid mater and dura have bridging veins which drain into the venous sinuses. Tearing of these bridging veins leads to this haematoma.
  • As intracranial pressure rises, blood is squeezed into the dural venous sinuses, raising the dural venous pressure and resulting in more bleeding from the ruptured bridging veins
  • High pressure can lead to ischaemia brain damage
  • Substances released from haematoma also promote vasospasm which leads to ischaemia
26
Q

What is the pathophysiology of chronic SDH?

A

Blood accumulates in dural space from rupture of bridging veins linked to cerebral atrophy. Because there is atrophy, there is much more room for these haematomas to enlarge before they cause symptoms. As the haematoma develops, the dura undergoes inflammation which leads to fibrosis, angiogenesis and haemorrhagic exudate.

27
Q

What is the epidemiology of SDH: Relative to other haemorrhages?

A

More common that extradural.

28
Q

What are the symptoms of SDH: Acute? Sub-acute? Chronic?

A
  • ACUTE: low conscious level, headache, N&V
  • SUB-ACUTE: worsening headaches 7-14 days after injury, altered mental status
  • CHRONIC: can present with headache, confusion, psychiatric symptoms, gait deterioration, focal weakness, seizures
29
Q

What are the signs of SDH? (x3 and x4)

A
  • ACUTE: lowered GCS. In large haematomas: (i) diplopia with mydriasis, orbital pain and eyelid drooping from compression from CNIII, and (ii) decreased consciousness and bradycardia from herniation
  • CHRONIC: neurological examination may be normal. May be focal neurological signs such as CNIII dysfunction, papilledema, hemiparesis or reflex asymmetry.
30
Q

What are the investigations for subdural haemorrhage? (x2 (x3))

A
  • NON-CONTRAST CT: crescent or sickle-shaped mass, concave over brain surface. Acute subdurals are hyperdense, becoming isodense over 1-3 weeks. When haemorrhage becomes isodense, diagnosis can be inferred from disappearance of sulci, midline shift, ventricular compression and obliteration of basal cisterns). Chronic subdurals are hypodense – see photo
  • MRI: higher specificity especially for isodense or small SDHs
  • BLOODS: should have PT and APTT tested as many patients with severe head injury present in a state of disseminated intravascular coagulation and require normalisation of their coagulation profile
31
Q

How are subdural haemorrhages managed when acute? (x5)

A
  • ASSESS GCS: surgery not usually considered if 9 or above, and pupillary reflexes are intact, or if haemorrhage is less than 10mm and midline shift less than 5mm.
  • PROPHYLACTIC ANTIEPILEPTICS: as seizure is a common complication.
  • CORRECTION OF COAGULOPATHIES: suspend anticoagulants and antiplatelets
  • ICP LOWERING REGIME: head elevation, hyperosmolar therapy with hypertonic saline in concentrations between 3.0% and 23.4%, and osmotic diuretics such as mannitol can also be used
  • SURGICAL: prompt Burr hole or craniotomy and evacuation for symptomatic SDH, over 10mm, or at least 5mm midline shift.
32
Q

How are subdural haemorrhages managed when chronic? (x4)

A
  • ANTIEPILEPTICS
  • CORRECTION OF COAGULOPTHIES
  • SURGICAL: indicated if symptomatic.
  • MONITORING: if asymptomatic, monitor with serial imaging for spontaneous resorption
33
Q

What are the complications of subdural haemorrhage? (x3)

A

Raised ICP, cerebral oedema leading to ischaemic brain damage, mass effect (transtentorial or uncal herniation).

34
Q

What are the complications associated with surgical management of subdural haemorrhage? (x5)

A

Seizures, recurrence, intracerebral haemorrhage, subdural empyema, brain abscess/meningitis, tension pneumocephalus.

35
Q

What is subdural empyema?

A

Intracranial infection characterised by suppurative collection (pus) between dura and arachnoid mater.

36
Q

What is tension pneumocephalus?

A

Intracranial equivalent of tension pneumothorax.