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N&SS - Neuro & Stroke > Neurological Emergencies > Flashcards

Neurological Emergencies Flashcards

To Do: Status Epilepticus Subarachnoid Haemorrhage Meningitis Other... Done:

1
Q

A patient presents to A and E with “the worst headache of ther life”. They have associated N and V.

What is the main differential diagnosis,
and what is the cause in 70% of these cases?

A

Subarachnoid haemorrhage

Berry auneurysms

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2
Q

A patient presents to A and E with “the worst headache of ther life”. They have associated N and V.

What is the main differential diagnosis,
and what is the cause in 15% of these cases?

A

Subarachnoid haemorrhage

AV malformations

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3
Q

A patient presents to A and E with “the worst headache of ther life”. They have associated N and V.

How might this condition have presented in a less fortunate patient?

A

Coma
Seizures
Sudden death

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4
Q

Why do some patients with a SAH get meningism?

A

Blood acts as an irritant -> chemical meningitis

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5
Q

A patient presents to A and E with “the worst headache of ther life”. They have associated N and V.

What signs might you elicit O/E?

A 
Kernig's sign
Signs of meningism
Impaired consciousness
Cranial nerve palsys
Hemiplegia
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6
Q

With a SAH, how quickly can CNS deficits become permenant?

A

Within minutes

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7
Q

What is the overall mortality for a patient with an SAH?

A

35-50%

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8
Q

Is prognosis with an SAH better or worse with an aneurysm than an AVM?

A

Worst with aneurysm, better with AVM, best with no lesion detected.

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9
Q

Why is blood in the subarachnoid space bad?

A

It acts as an irritant causing vasospasm -> ischaemia -> secondary brain damage.

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10
Q

How common is rebleeding following a SAH?

A

Very - usually ocurs within 7 days.

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11
Q

How do we investigate suspected SAH?

A

CT ASAP if within the first 12 hours.

LP 12 hours after the event.

Check clotting screen.

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12
Q

How good are CT scans for picking up subarachnoid haemorrhages?

A

95% can be picked up if done within 24 hours, but CT shows fresh blood up best so ideally do ASAP for clearest diagnosis.

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13
Q

What does a subarachnoid haemorrhage look like on CT?

A

No characteristic shape - just an area of hyperdensity.

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14
Q

Why do we do an LP 12 hours after a SAH, and what can it tell us?

A

To look for RBCs and xanthochromia in the CSF.

We do it after 12 hours so the SAH blood has time to break down and form the xanthochromia, so SAH isn’t confused with RBCs from the trauma of LP procedure.

It tells us if there has been a SAH.

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15
Q

What do we send off the CSF for when we do an LP for ?SAH?

A

Xanthochromia
MC&S
Glucose
Protein

Might as well screen for infection while we are in there!

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16
Q

A pt presents to A&E with a thunderclap headache. SAH has been confirmed.

How should we manage this patient?

A

Initially with ABCDE.

Stabilise
Prevent rebleed
Treat vasospasm
Correct any biochemical abnormalities e.g. hyponatraemia

Refer for neurosurgical intervention.

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17
Q

Why is it important to manage cerebral vasospasm in a SAH pt?

A

It causes focal cerebral ischaemia -> death.

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18
Q

How do we try and prevent cerebral vasospasm post-SAH?

A

Hydration with normal saline -> hypervolaemia and haemodilution

Nimodipine 60mg 4 hourly

Re-examine regularly for changes in function.

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19
Q

What is nimodipine?

A

A calcium antagonist used to prevent vasospasm post-SAH.

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20
Q

What neurosurgical interventions are possible for SAH?

A

Clipping or endovascular coiling of aneurysm depending on pt, site and size of aneurysm, and comorbidities.

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21
Q

A pt comes in with a thunderclap headache, and SAH is diagnosed.

After initial management, the pt appears stable, but after admission for observation, he suddenly becomes drowsy and his GCS drops.

What should we do?

A

Get an urgent CT head as he might have a re-bleed or hydrocephalus.

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22
Q

A pt comes in with a thunderclap headache, and SAH is diagnosed.

After initial management, the pt appears stable, but after admission for observation, he suddenly becomes drowsy and his GCS drops.

Other than drowsiness/drop in GCS, what other indications are there for urgent CT post SAH?

A

Seizures
Focal neurological deficit (new)
Coma
Cognitive decline (acute)

Need to check for a re-bleed or hydrocephalus!!

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23
Q

What are the common complications associated with SAH?

A 
Re-bleeding
Hydrocephalus
Cerebral ischaemia
Hyponatraemia
Headaches
Hypopituitarism

Death

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24
Q

A pt is brought to A&E by their partner, because they were complaining of a headache when they woke up this morning, and since then they have become drowsy and aren’t responding appropriately or at all to stimulus.

What are we most worried about here, and what could cause this?

A

RICP

Head injury
Intracranial tumour
Intracranial bleed
Infection (meningitis, encephalitis, abscess)
Hydrocephalus
Cerebral oedema
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25
Q

A pt is brought to A&E with a history of headache on waking then progressive cognitive decline. There was no history of trauma.

What signs might you see on assessment of this individual?

A 
Reduced GCS (drowsy, irritable, lethargic)
HR low but BP high (Cushing’s reflex)
Pupil changes
Reduced visual acuity
May have papilloedema
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26
Q

How should a patient with suspected RICP be investigated?

A

ABCDE

Identify the cause:

  • Focused hx and examination (e.g. may have purpuric rash, may have Hx of AF)
  • Bloods and urine for infection/metabolic disturbance/clotting/toxicology
  • CXR for ?infection source
  • CT head
  • LP if not contraindicated
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27
Q

What are the contraindications for lumbar puncture?

A
  • Bleeding diathesis
  • Infection at site of needle insertion
  • Cardiorespiratory compromise
  • RICP weirdly… unless treating known intracranial HTN. Get a CT first
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28
Q

How do we manage RICP?

A

Treat the cause, bring down ICP, and prevent secondary injury

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29
Q

What secondary injury can occur from RICP?

A
  • Herniation syndromes
  • Seizures
  • Stroke
  • Neurological damage
  • Death
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30
Q

What respiratory manoeuvre can we use to help reduce RICP? How does it work?

A

Hyperventilation if intubated.

Reduces pCO2 which causes cerebral vasoconstriction -> lowers ICP.

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31
Q

What agents can we give short term to reduce ICP?

A

Osmotic agents e.g. mannitol - 20% solution 0.25-0.5g/kg IV over 10-20 minutes.

Corticosteroids can be used only for oedema surrounding intracranial tumour.

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32
Q

What kinds of herniation syndromes are possible as a result of RICP?

A

Uncal herniation
Cerebellar tonsil herniation
Subfalcian (cingulate) herniation

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33
Q

A pt is being managed for RICP when he suddenly develops ataxia and a VIth nerve palsy.

What is likely to have happened?

A

Cerebellar tonsil herniation due to increased pressure in the posterior fossa -> cerebellar tonsils to herniate through the foramen magnum.

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34
Q

A woman presents to A&E with neck stiffness, photophobia, and a headache.

What other symptoms might she have considering the most likely diagnosis?

A

Fever
Cranial nerve palsy symptoms e.g. diplopia, facial drooping
Altered level of consciousness
Non-blanching rash

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35
Q

A woman presents to A&E with a headache, neck stiffness, and photophobia.

How should she be managed?

A

ABCDE

Septic screen -> sepsis 6

Try and find the source of infection

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36
Q

How is meningism different from RICP?

A

Meningism is signs of irritation to the meninges, but not necessarily with RICP.

Meningism - photophobia, stiff neck, Kernig’s sign.
Signs of RICP - altered level of consciousness, altered respiratory pattern, HTN, bradycardia.

They can occur together however.

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37
Q

How can we manage a pt who is meningitic but has no signs of shock?

A

Still ABCDE

Take blood cultures
Start IV abx
Give 10mg IV dexamethasone
Airway support and fluid resus

LP can wait until they are stable, and if they have no signs of RICP.

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38
Q

How can we manage a patient who is meningitic and in shock?

A

Get ICU involved

Basically the same, but start sepsis pathway and may also need intubation.

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39
Q

What antibiotics should be given for bacterial meningitis?

A

Depends on local policy, but generally:

Ceftriaxone, with amoxicillin if over 60 yo

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40
Q

Because Leicester is weird like tis, what organism can cause meningitis herethat you might not see elsewhere?

A

TB yayay that makes this so much fun!

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41
Q

How should encephalitis be managed?

A

Supportively

Give specific antivirals e.g. aciclovir for HSV, other treatments for CMV and toxoplasmosis.

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42
Q

How does encephalitis present differently to meningitis?

A 
Bizarre behaviour/confusion
Decreased GCS or coma
Focal neurological signs
Seizure
May have hx of recent travel or animal bite.

May be preceded by infectious prodrome.

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43
Q

Why is head trauma a neurological emergency?

A

It is a leading cause of death in adults under 45 years.

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44
Q

What is a factor in a significant number of head injuries?

A

Alcohol 🍻

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45
Q

What are the 2 types of head trauma?

A

Primary and secondary

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46
Q

What are the 2 types of primary head injury?

A

Focal and diffuse

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47
Q

What is status epilepticus?

A

Seizures lasting for 30 minutes or more, or multiple seizures with no complete regaining of consciousness in between.

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48
Q

What are the possible causes of status epilepticus?

A

Known epilepsy
Structural brain lesion (esp. if 1st seizure)
Eclampsia (any possibility of pregnancy?)
Infection
Metabolic/Toxins/Alcohol

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49
Q

How should ?status epilepticus be managed initially?

A

ABCDE

Including open/secure airway, O2, suction, metabolic screen, anticonvulsant levels.

IV bolus or lorazepam and repeat if required

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50
Q

How much lorazepam can be given to a pt in status, and how frequently?

A

4mg, repeat dose if no response after 10-20 minutes.

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51
Q

If lorazepam fails to get pt out of status, what other drugs can we give them?

A

IV Phenytoin 15-18 mg/kg at 50mg/min

If after 60-90 minutes no response to Phenytoin, escalate to general anaesthesia e.g. propofol

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52
Q

Who needs to be called if a pt has been treated for status epilepticus for more than 20 minutes?

A

An anaesthetist

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53
Q

Why might IV lorazepam be problematic for a pt in status epilepticus?

What can we do instead?

A

IV access may not be easy to establish in a seizing pt.

Can give buccal midazolam, or rectal diazepam instead

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54
Q

If you suspect alcohol withdrawal might be involved in status epilepticus, what can you give the pt?

A

Thiamine infusion

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55
Q

If we suspect metabolic disturbance causing status epilepticus, what can we di?

A

Treat the cause e.g. glucose for hypoglycaemia

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56
Q

If a pt who is in status epilepticus is already on phenytoin, what can we give instead?

A

IV Phenobarbital

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57
Q

Which neurological emergency are cancer pts at an increased risk of developing?

A

Spinal cord compression

Specifically metastatic SCC or secondary to direct tunour extension into vertebral column.

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58
Q

What % of cancer pts are affected by spinal cord compression?

A

Up to 5% of cancer pts

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59
Q

What are the features of spinal cord compression?

A

Back pain - earliest and most common symptom
Lower limb weakness
Sensory changes

Neurological changes depend on the level of the lesion

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60
Q

How should oncological spinal cord compression be managed?

A

Best rest
High dose oral steroids

May need radiotherapy or surgery

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61
Q

What is radicular pain?

A

Pain that radiates into the lower extremity along the course of a spinal nerve root.

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62
Q

What are the causes of spinal cord compression?

A 
Degenerative disc lesion
Degenerative vertebral lesions
TB
Epidural abscess
Vertebral neoplasm
Epidural haemorrhage
Paget’s disease
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63
Q

How can you tell where spinal cord compression has occurred?

A

By assessing the functional losses from hx and examination -the highest level of symptoms is the lowest possible level of spinal cord compression.

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64
Q

If there is autonomic involvement in SCC, what does that suggest?

A

A worse prognosis as it is a late stage sign.

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65
Q

Will spinal cord compression cause upper or lower motor neurone signs?

A

Upper motor neurone signs.

Although at the level of the compression, reflexes will be absent as the LMN within the ventral horn is compressed.

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66
Q

How should suspected spinal cord compression be investigated?

A

Full hx and examination
MRI of whole spine within a day (within a week if potentialy metastatic)
Routine bloods may be helpful, including a Group and Save, and a clotting screen.

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67
Q

How should spinal cord compression be managed?

A

High dose corticosteroids with a PPI for gastric protection

Imaging -> neurosurgical opinion for decompression

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68
Q

A woman presents to A&E with acute onset lower back pain and urinary incontinence.

What is your immediate worry?

A

Cauda equina syndrome

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69
Q

How should cauda equina be investigated?

A

PR examination
Post-void bladder scan

Whole spine MRI

70
Q

Why is cauda equina a neurosurgical emergency?

A

Pts can develop debilitating complications if it is left untreated

71
Q

What is the cauda equina formed from?

What does it therefore control?

A

The lower motor neurones of L1-S5

Motor and sensory impulses to lower limb, motor to anal sphincters, and parasympathetic fibres to the bladder.

72
Q

What can cause cauda equina syndrome?

A 
Disc herniation at L4/L5 or L5/S1 most commonly
Trauma
Neoplasm
Infection
Chronic inflammation e.g. Ank spond
Iatrogenic
73
Q

What are some possible iatrogenic causes of cauda equina syndrome?

A

Spinal anaesthesia -> haematoma

74
Q

A woman presents to A&E with acute onset lower back pain and urinary incontinence.

What other elements do you need to ask about in the history?

A

HPC - any bowel incontinence or loss of perianal sensation, sensation or motor changes in lower limbs, any trauma, any recent procedues involving the spine, any impotence.
PMH - Any known spinal disease or cancer.

75
Q

A woman presents to A&E with acute onset lower back pain and urinary incontinence.

What should we look for on examination?

A 
Lower limb loss of sensation, esp. saddle anaesthesia
Perianal loss of sensation
Loss of anal tone
Urinary retention
Lower motor neurone signs
76
Q

How can cauda equina syndrome be classified?

A
  1. Cauda equina syndrome with retention
  2. Incomplete cauda equina syndrome (only altered urinary sensation, not retention)
  3. Suspected cauda equina syndrome (variable neurological signs)
77
Q

How are cauda equina syndrome and spinal cord compression distinguished?

A

CE -> LMN signs

SCC -> UMN signs

78
Q

How should cauda equina syndrome be managed?

A

Early neurosurgical review
High dosesteroids
Possible surgical decompression

Chemo/radiotherapy if malignant

79
Q

What is a contusion and where do they occur?

A

A region of injured tissue in which capillaries have been ruptured.
The opposite side of the head to the injury.

80
Q

What is a primary brain injury?

A

Damage to the brain that occurs at the time of impact

81
Q

What is a secondary brain injury?

A

An injury that is the result of neurophysiological and anatomical changes that occur in the minutes to days following a primary head injury.

82
Q

Give some example of secondary brain injury mechanisms.

A

Cerebral oedema
Haematoma
RICP

83
Q

By which mechanisms might brain injury occur?

A

Falls (20-40%)
Assaults (30-50%)
Alcohol (involved in 65% of adult head injuries)
RTC (25%)

84
Q

What is the management of a head injury based on?

A

Immediate resus
Mechanism of injury
GCS at presentation

85
Q

How should a pt with normal/near-normal GCS be managed following a head injury?

A

ABCDE - resus as appropriate
Full Hx and Examination of neurological system
Check for other possible injuries

86
Q

How should a pt with reduced GCS be managed following a head injury?

A

GCS and assess pupils
ABCDE and resus
Get a CT head ASAP

87
Q

Following a head injury, what other injury is likely to have occurred, and what should be done about this?

A

C-spine injury

C-spine immobilisation pre-hospital i.e. by paramedics

88
Q

What indications are there for C-spine immobilisation?

A 
GCS lower than 15 at any time since injury
Neck pain or tenderness
Focal neurological deficit
Paraesthesia in extremities
Any other evidence of c spine injury
89
Q

What concerning parts of a pt hx would make them require hospitalisation following a head injury?

I.e. high risk pts

A

Age over 65
Previous cranial neurosurgical intervention
Hx of bleeding or clotting disorder
Anticoagulation

90
Q

What worrying signs might a pt exhibit following a head injury?

A 
Nausea/vomiting
Severe headaches
Amnesia
Seizures
Altered behaviour
91
Q

A pt is sent home following a minor head injury.

What safety-netting advice should we give to the patient on discharge?

A

Watch out for:

  • increasing drowsiness
  • worsening headache
  • confusion or strange behaviour
  • dizziness/loss of balance
  • seizures
  • visual problems
  • blood or clear fluid from nose or ear
  • unusual breathing patterns
92
Q

What is temporal arteritis aslo known as?

A

Giant cell arteritis

93
Q

Why is temporal arteritis an emergency?

A

It can cause sudden and sometimes bilateral vision loss

94
Q

What is giant cell arteritis?

A

Systemic immune-mediated vasculitis affecting medium and large arteries, especially the carotid and its extracranial branches.

95
Q

How common is giant cell arteritis?

A

Occurs in 2.2 per 10,000 pts in the UK.

96
Q

What is the M:F in giant cell arteritis?

A

1:2-3

97
Q

Which ethnic group is giant cell arteritis most common in?

A

European/Caucasian

98
Q

Is there a familial link to giant cell arteritis?

A

Yes - giant cell arteritis and polymyalgia rheumatica aggregate in families together.

99
Q

What are the classic symptoms for giant cell arteritis?

A 
Recent onset temporal headache
Myalgia/malaise/headache
Scalp tenderness
Transient visual symptoms
Jaw claudication
Unexplained facial pain
100
Q

How might a pt explain jaw claudication?

A

Pain that comes on gradually as they chew

101
Q

What bloods can indicate giant cell arteritis in a pt with a positive history?

A

Raised ESR

Anaemia

102
Q

What kind of headache do people experience with giant cell arteritis?

A

Recent onset, different to usual headaches.
Temporal or occipital region
Severe
May be worse at night

103
Q

How bad can the scalp tenderness be in a pt with giant cell arteritis?

A

Bad - they may find combing their hair or lying on a pillow to be too painful.

104
Q

Why do patient with giant cell arteritis get visual disturbances?

A

Inflammation of branches of the ophthalmic artery -> ischaemic optic neuritis.

Central retinal artery thrombosis can also occur.

105
Q

How common is thoracic aorta/aortic root involvement in giant cell arteritis?

A

Occurs in about 15%

106
Q

What signs might a pt have of giant cell arteritis?

A

There aren’t many:

  • Ocular/fundoscopic evidence of ischaemia
  • Temporal artery prominence
  • Bruis over carotid/axillary/brachial arteries.
  • Fever, muscle and joint tenderness.
107
Q

What are the criteria for diagnosing giant cell arteritis?

How many are needed for a diagnosis?

A

3 of these 5 criteria are needed:

  • age of onset 50+
  • New headache
  • Temporal artery abnromality (tender/decreased pulsation)
  • ESR >= 50mm/hour
  • Abnormal artery biopsy
108
Q

How should giant cell arteritis be investiagted once it is suspected?

A

Refer urgently for temporal artery biopsy.

109
Q

If ESR isn’t raised, what other blood test might indicate giant cell arteritis?

A

CRP can sometimes be raised.

110
Q

Tell me about the biopsy for temporal arteritis?

A

Take it from the symptomatic side. May not show area of giant cell arteritis as it affects the arteries in skip lesions.

111
Q

How should giant cell arteritis be manaed?

A

Start high-dose corticosteroids IMMEDIATELY to prevent sight loss.

112
Q

What dose of corticoteroids should be given to manage giant cell arteritis?

A

40mg prednisolone daily

60mg prednisolone daily for claudication symptoms.

113
Q

How is treatment different for giant cell arteritis with visual symtoms?

A

Admit for IV methylprednisolone

114
Q

What can be given alongside steroids to treat giant cell arteritis?

A

Daily dose of 75mg aspirin with PPI unless it’s contraindicated.

115
Q

What does aspirindo for giant cell arteritis?

A

Reduces rate of visual loss and strokes.

116
Q

What are the potential complications of giant cell arteritis?

A
  • Loss of vision
  • Aneurysms/dissections/stenotic lesions of aorta
  • CNS disease
  • Steroid side effects
117
Q

Does the visual loss associated with giant cell arteritis get better?

A

No - it is often irreversible. 15-20% of patients have partial or complete visual loss.

118
Q

What is bulbar palsy?

A

A syndrome of impairment of cranial nerves 9, 10, 11, and 12 which occurs due to LMN lesion in the medulla or outside the brainstem.

119
Q

How does acute bulbar palsy present?

A
  • Palsy of tongue/facial muscles/swallowing
  • Flaccid fasciculating tongue
  • Speech may be quiet, hoarse or nasal
  • Tremulous lips
120
Q

What can cause acute bulbar palsy?

A
  • Motor neurone disease
  • Guillian-Barre Syndrome
  • Polio
  • Brainstem tumours
  • Myasthenia gravis
  • Myotonic dystrophy
121
Q

What is pseudobulbar palsy?

A

Bilateral UMN lesions commonly in the corticobulbar tracts that presents like bulbar palsy.

122
Q

What causes pseudobulbar palsy?

A
  • MS
  • MND
  • Stroke
  • Vascular dementia
123
Q

How should bulbar palsy be managed?

A
  • Refer to neurology
  • Treat underlying cause
  • Supportive measures
  • SALT and dietician Ax
124
Q

What are the complications of acute bulbar palsy?

A
  • Poor dentition
  • Poor nutrition
  • Psychological dysfunction
  • Progression of underlying disease
125
Q

What is a cerebral contusion?

A

Bruising of brain whereby blood mixes with cortical tissue due to microhaemorrhages and small vessel leaks

126
Q

What is concussion?

A

Head injury with a temporary loss of brain function

127
Q

How does concussion occur?

A

Trauma -> stretching and injury to axons -> impaired neurotransmission -> temporary brain dysfunction

128
Q

What is diffuse axonal injury?

A

Shearing of interface between grey and white matter following traumatic acceleration/deceleration or rotational injuries to the brain damanging intra-cerebral axons and dendritic connections.

129
Q

What are racoon eyes a feature of?

A

Basilar skull fracture.

130
Q

What functions are affected in post-concussion syndrome?

A
  • Thinking and memory
  • Physical
  • Emotional/mood
  • Sleep
131
Q

Which bones are broken in a basilar skull fracture?

A

Any combination of temporal, occipital, sphenoid, and ethmoid bones.

132
Q

What kind of force is needed for a basilar skull fracture, and what does this mean clinically?

A

A huge amount of force is needed so you should ask about other possible injuries - tends to occur as part of poly-trauma.

133
Q

Other than raccoon eyes, what are the clinical signs of a basilar skull fracture?

A
  • CSF Rhinorrhoea
  • CSF ottorhoea
  • Battle sign
  • Haemotympanum
  • Bump
134
Q

What is Battle sign?

A

A bruise that appears at the base of the skull following a basilar skull fracture. It is typically seen posteriorly and inferiorly to the auricle.

135
Q

How should a basilar skull fracture be managed?

A

Follow traumatic brain injury management protocol inc. management of RICP.
Elevate any depressed skull fractures
Manage complications e.g. persistent CSF leakage may need surgery.

136
Q

What GCS indicates a head injury to be mild?

A

12-15

137
Q

What GCS indicates a head injury to be moderate?

A

9-12

138
Q

What GCS indicates a head injury to be severe?

A

3-8

139
Q

What is the NICE guidance for CT scanning a head based on GCS?

A

If GCS is less than 13 at any oint, or less then 14 2+ hours after injury, the CT them.

140
Q

What neurological abnormalities indicate a CT head after a head injury according to NICE?

A
  • Focal neurological deficit
  • Seizure
  • LoC with any of 1. age over 65, 2. coagulopathy, 3. dangerous mechanism of injury, 4. antegrade amnesia oer 30 minutes.
141
Q

Other than GCS and neurological abnormalities, what other NICE indications are there for a CT head following trauama to the head?

A
  • If a depressed or open skull fracture is suspected
  • Signs of basal skull fracture
  • 2 or more discrete episodes of vomiting.
142
Q

What are some acute intracranial events?

A
  • Extradural haemorrhage
  • Subdural haemorrhage
  • Subarachnoid haemorrhage
143
Q

What is an extradural haemorrhage?

A

A collection of blood between the inner surface of the skull and the periosteal dura mater.

144
Q

Why do extradural haemorrhages occur?

A

Nearly always secondary to head trauam or a skull fracture.

145
Q

Which artery is most commonly severed in extradural haemorrhage?

A

Middle meningeal artery

146
Q

How common is venous involvement in extradural haemorrhage?

A

Not very, but if it does occur it is usually involving a torn venous sinus.

147
Q

Are most extradural haemorrhages supratentorial or subtentorial?

A

Supratentorial (95% of cases)

148
Q

How does an extradural haemorrhage typically present?

A

Head injury with subsequent LoC, often followed by transient lucid interval with an ongoing headache.

149
Q

What causes the deterioration of consciousness following the lucid interval of an extradural haemorrhage?

A

The haematoma enlarges causing ICP to increase and compress the brain - this causes rapid deterioration of consciousness.

150
Q

Why might a pt with an extradural haemorrhage have cranial nerve palsies?

A

As ICP rises, brain structures herniate to cause compression of cranial nerves -> palsy.

151
Q

How does an extradural haemorrhage appear on a CT?

A

As a lemon shaped area of hyperdensity causing midline shift.

152
Q

Why do extradural haemorrhages become lemon shaped on CT?

A

The blood collects between the periosteal dura mater and the surface of the skull. Once it reaches a suture line on the skull it cannot extend further in the saggital plane, so it has to extend inwards.

153
Q

How should an extradural haemorrhage be managed?

A

ABCDE!!

  • Observe and manage conservatively if small.
  • Refer to neurosurgery if there is a large clot for craniotomy and clot evacuation.
154
Q

What is the prognosis like for extradural haemorrhages?

A

Good with early intervention.

155
Q

What complications can arise secondary to an extradural haemorrhage?

A
  • Permenant brain damage
  • Coma
  • Seizures
  • Weakness
  • Pseudoaneurysm
  • AV fistula
156
Q

What is a subdural haemorrhage?

A

A collection of blood between the meningeal dura mater and the arachnoid mater?

157
Q

Over what time scales can a subdural haemorrhage occur?

A

Time between injury and bleed progression to critical level can be:

  • Acute (under 3 days)
  • Subacute (3-21 days)
  • Chronic (over 3 weeks)
158
Q

Which vessels are sheared causing a subdural haemorrhage to form?

A

Cortical bridging veins

159
Q

What are the causes of subdural haemorrhages?

A

Usually traumatic but can be spontaneous.

160
Q

What process associated with aging can increase the risk of rupture -> subdural haemorrhage?

A

Cerebral atrophy as the cortical bridging veins are stretched.

161
Q

How does an acute sudbural haemorrhage present?

A

Head trauma with neurological deficits in about 80% of cases within 3 days of head injury.

162
Q

How do subacute and chronic subdural haemorrhages differ in presentation to acute?

A

Generally present in the elderly pts with vage or absent hx of head trauma. Insidious onset of confusion and cognitive decline similar to dementia is often seen.

163
Q

How does an acute brain bleed appear on CT?

A

Hyperdense i.e. brighter than other tissues.

164
Q

How do subacute and chronic subdural haemorrhages appear different to acute haemorrhages on CT scan?

A

The blood is older so the haematoma become less hyperdense over time i.e. it will get barker and become darker than the brain tissue i.e. hypodense the longer it is left.

165
Q

What shape does a subdural haemorrhage appear on CT?

A

Like a banana.

166
Q

How can chronic haematomas be evaluated?

A

With serial imaging by CT

167
Q

Why do acute subdural haemorrhages need immediate neurosurgical intervention?

A

The bleed causes RICP

168
Q

How are subacute and chronic subdural haemorrhages usually managed?

A

One or more burr holes to relieve the pressure and drain the haematoma.

169
Q

What is the prognosis like for subdural haemorrhages?

A

Relatively poor compared to extradural haemorrhages.

  • If an acute SDH needs surgery, mortality can exceed 50%.
  • If a pt is anticoagulated, there are worse outcomes.
  • Only 20% of pts fully recover.
170
Q

What is the proper name for the banana shape that a SDH becomes?

A

Crescent or sickle

171
Q

What is the proper name for the lemon shape that a EDH becomes?

A

Lentiform or biconvex

N&SS - Neuro & Stroke (10 decks)

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