Extradural Haemorrhage Flashcards

1
Q

What is an extradural haematoma?

A

collection of blood in the extradural space (between skull + dura mater)

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2
Q

Describe the aetiology of extradural haemorrhage

A

Almost always TRAUMA
typically LOW IMPACT e.g. fall/ blow to head
Collection often in temporal region as thin skull at pterion overlies the middle meningeal artery where parieto-temporal fractures cause damage (+ thus is vulnerable to injury)

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3
Q

What is the pterion?

A

Anatomical landmark where the parietal, frontal, sphenoid + temporal bones fuse.
MMA lies underneath

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4
Q

Describe the epidemiology of extradural haemorrhage

A

~2% of all head injuries
M>F
Most commonly seen in YOUNG ADULTS (20-30s)

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5
Q

Describe the time frame of symptoms of extradural haemorrhage

A
  1. Immediate brief LOC
  2. Temporary recovery “lucid interval”
  3. Progressive deterioration in conscious level

This pattern is not always seen

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6
Q

List 3 symptoms of extradural haemorrhage

A

Headache
N+V
Progressive drowsiness

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7
Q

List 6 signs of extradural haemorrhage

A

Reduced consciousness (GCS)
Focal neurological deficit e.g. weakness
Tenderness of the skull (in context of injury)
Hyperreflexia + spasticity
Upgoing plantars (Babinski’s sign)
Cushing’s triad

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8
Q

What is Cushing’s triad?

A

Physiological response to raised ICP
Bradycardia
HTN
Irregular breathing.

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9
Q

What sign is indicative of herniation?

A

Fixed + dilated pupil
Uncus of temporal lobe herniates around tentorium cerebelli
Causes compression of parasympathetic fibres of CN3

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10
Q

What may cause ipsilateral weakness in EDH? What is this known as?

A

Compression of the contralateral cerebral peduncle
Kernohan’s phenomenon

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11
Q

What bedside investigations are required in EDH?

A

Monitoring GCS
Blood glucose (r/o hypoglycaemia as cause of reduced consciousness)
ECG (r/o heart block as cause of bradycardia)

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12
Q

What bloods are required in EDH?

A

FBC: detect anaemia + thrombocytopenia
U+Es: r/o electrolyte abnormalities which may contribute to low GCS
Coagulation: r/o underlying coagulopathy
G+S: if going to theatre
Cross match: for blood products

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13
Q

What is the gold standard investigation to be performed for EDH?

A

Urgent CT Head

(non-contrast)

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14
Q

Describe the appearance of extradural haemorrhage on CT

A

“Lemon shaped haematoma”

Hyperdense bi-convex mass: haematoma expands medially due to being unable to expand past the points at which the dura is tightly bound to the suture lines of the skull.

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15
Q

Name 2 possible secondary features on a CT head in EDH

A

Midline shift
Brainstem herniation

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16
Q

Give a risk factor for extradural haemorrhage

A

Bleeding tendency
E.g. haemophilia, anticoagulant therapy

17
Q

What features may allow for conservative management of EDH?

A

<30cm3 with
low thickness,
minimal midline shift +
GCS >8 w/o any focal neurological deficits

18
Q

Which feature indicates a patient should be managed surgically regardless of other factors?

A

> 30cm3

19
Q

Describe medical management of EDH

A

Neuroprotective measures
ICP Mx
Seizure Mx

20
Q

Describe conservative management of EDH

A

Serial CT imaging + close observation

21
Q

What neuroprotective measures can be employed in EDH?

A

Normoxia (maintain normal O2 sats)
Normocarbia (CO2 can be altered it ventilated)
Normothermia (maintain normal temp)
Adequate sedation + paralysis
ICP monitoring: < 22 mmHg

22
Q

What can be used for ICP management in EDH?

A

Hypertonic saline 2.7%
(Mannitol not commonly used but may still be in guidelines)

23
Q

What can be used for seizure management in EDH?

A

Levetiracetam (Keppra)

24
Q

What is definitive treatment of EDH?

A

Craniotomy + evacuation of the haematoma
(Trauma or Burr hole craniotomy)

25
Q

Describe post-op management of EDH

A

Observation on neuro-critical care or HDU with close neuro-obs + routine post-op CT scans

26
Q

What is the prognosis of EDH?

A

Good if treated rapidly
Poor if surgical Mx delayed

27
Q

List 5 complications of EDH

A

Infection
Cerebral Ischaemia
Seizures
Hemiparesis
Cognitive impairment