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ENT, neuro, eyes > Intracranial bleed > Flashcards

Intracranial bleed Flashcards

1
Q

First line for subarrach

A

CT head

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2
Q

Presentation of subarrachnoid haemorrhage

A

Sudden explosive headache 10/10 pain in back of head - thunderclap
Nausea and vomitting
Photophobia

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3
Q

What is seen on lumbar puncture in a subarrachnoid haemorrhage?

A

Xanthachromia

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4
Q

What is a subarrahcnoid haemorrhage?

A

Bleed into subarachnoid space between arachnoid and pia mater meningeal layers

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5
Q

Complications of SAH

A

Brain damage - hypoxia, raised ICP, direct cranial injury
Neurological disabilities
Coma
Death

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6
Q

Causes of SAH

A

Traumatic injury or spontaneous
Intracranial aneurysms
Arteriovenous malformation
Unknown
Rare disorders

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7
Q

Risk factors for spontaneous SAH

A

HPTN
Smoking
FH
Autosomal dominant PCKD
Over 50
Female

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8
Q

Clinical findings in SAH

A

reduced LOC due to raised ICP
Neck stiff - meningeal irritation
Kerniges sign

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9
Q

What is kerniges sign caused by?

A

Irritiation of motor nerve roots pass through innflamed meninges as under tension
Non specific

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10
Q

Lab investigations for SAH

A

FBC and U+Es to obtain a baseline
Coag studies - before LP/surgery

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11
Q

Imaging investiations SAH

A

Plain CT head - blood in SA space, hydrocephalus
CT angiogram - arterial vessel highlights - aneurysm

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12
Q

When is an LP necessary in SAH?

A

When SAH suspected but CT scan does not show evidence of bleeding or raised ICP

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13
Q

How quickly does an LP need to be performed after onset?

A

12 hours

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14
Q

What is xanthochromia?

A

CSF stained yellow - infiltration of blood
jbilirubin, oxyhaemoglobin from haemolysis RNCs

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15
Q

Management SAG

A

A to E
Airway - reduced LOC
B - hypoxia - oxygen
C - BP - IV fluids, electrolyte replacement - Na
CCBs MUST be given
D - intracranial pressure monitoring. Pupils dilated = blown = brainstem damage

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16
Q

Why are CCBs given in SAH?

A

eg nimodipine
To reduce cerebral artery spasm and secondary cerebral ischaemia

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17
Q

General cpmplications ICH

A

Obstructive hydrocephalus - ventricular drain
Arterial vasospasm
Re-bleeding of aneurysms
Neurological deficits
Cerebral ischaemia

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18
Q

What is an epidural haemotoma?

A

Haemorrhage between dura mater and inner surface of skull

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19
Q

Subarrach on CT

A

white in ventricles

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20
Q

Epidural on CT

A

Lemon on CT
Midline shift
Tentorial/brainstem herniation

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21
Q

Subdural on CT

A

Moon

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22
Q

How can an Epidural haemotoma cause brainstem death?

A

Raised ICP can cause cerebellar herniation -> brainstem death

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23
Q

Causes of epidural haemotoma

A

Skull traum and temporparietal region
eg fall, assault, sporting injury
Rupture of a vein - MMV or dural sinus
Arteriovenous abnormalities, bleeding disorders

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24
Q

Which part of the sull is espicially vulnerable to fracture?

A

Pterion = pariteal, sphenoid and temporal bones fuse

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25
Q

What artery does a fracture to the pterion dmaage?

A

Middle meningeal artery

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26
Q

Symptoms of epidural haemotoma

A

Headache
N+V
Confusion
LOC followed by period of lucidity, progressively decreasing LOC after several

27
Q

Clinical findings in EDH

A

Tender skull
Confusion
Reduced GCS
Cranial nerve deficits
Motor or sensory deficits of upper and lower limbs
Hyperreflexia and spasticity
Upgoing plantar reflex - babainskis sign
Cushings triad

28
Q

What is cushings triad?

A

Raised ICP to attmept to improve perfusion
-HPTN
-Bradycardia
Irrefular breathing pattern

29
Q

Bedside investigationsEDH

A

Cap blood glucose - rule out hypoglycaemia
ECG - heart block - bradycardia cause

30
Q

Lab investigationsEDH

A

FBC
U+Es
GCS
CRP
Coagulation
Group and save

31
Q

Imaging investigations for intracranial bleed gold standard

A

CT head

32
Q

When do you do a skull x ray?

A

When skull fracture to assess for evidence of EDH

33
Q

Management of EDH

A

Conservative - bleed is small with miinimal mass effect
Medical - Reversal of anitcoagulation, Prophylatctic antibiotics - in context of open skull fracture, mannitol, barbituates
Surgical - Burr hole craniotomy, trauma craniotomy, hemicranectomy

34
Q

Coagulopathy

A

Thrombocytopenia
Porlonged PT

35
Q

Agents to reduce ICP

A

Mannitol - IV - osmotic effect prior to surgery
Barbituates - reduce ICP and protect brain from anoxia

36
Q

Burr hole craniotomy

A

evacuation of the haematoma.

37
Q

When is trauma craniotomy used?

A

Significant mass effect - evacuate blood, treat cause of bleeding (litigation) + reduced ICP

38
Q

When do hemicraniectomy?

A

Prevent brain stem herniation + death due to raising ICP in SDH

39
Q

Post surgical management EDH

A

ICP monitoring and repeat CT scans

40
Q

Complications of EDH

A

Infection
Cerebral ischaemia (adjacent to haemotoma)
Seizures
Cognitive impairment
Hemiparesis
Hydrocephalus (ventricle obstruction)
Brainstem injury (raised ICP)

41
Q

Types of subdural haematoma

A

Acute < 3 dyas
Subacute 3 - 21 days
Chronic > 21 days
sIMPLE OR COMPLICATED - PARENCHYMAL injury or not

41
Q

Types of subdural haematoma

A

Acute < 3 dyas
Subacute 3 - 21 days
Chronic > 21 days

42
Q

Cause of subdural haematoma

A

Trauma
Rupture of cerebral aneurysm
Cerebral hypotension
Malignancy - rare
Spontaneous

43
Q

Risk factors for developing subdural haemotama

A

History of trauma
Co-morbidities that make patient vulnerable to falls
Age over 65
Anticoagulant
History of coagulopathy
History of LOC
Fctors that stretch bridging veins eg cerebral atrophy, low CSF pressure after shunt
Alcoholism

44
Q

Symptoms of subdural haematoma

A

Headache
Nausea and vomitting
Fluctuating consciousness level:
Confusion, drowsiness, personality change, memory loss
Intervening lucid periods
Poor balance
Weakness
Paraesthesia or numbness
Aphasia if on L side

45
Q

Findings on exam for subdural haematoma

A

Neurological exam of CNs, upper limb and lower limb
Limb weakness or sensory disturbance
Cranial nerve abnormalities
Ataxia
Seizures
Reduced LOC

46
Q

Lab investgiations

A

FBC
U+Es
LFTs
Coag studies
Group and save - crossmatch

47
Q

What do you need FBC, U+Es, LFTs and coag studies for in subdural haematoma?

A

FBC - identify anaemia - raised WCC
U+Es - assess pre-op renal function and electrolyte abnormalities
LFTs = baseline + synthetic function of liver (vit K dependent clotting factors)
Coag studies - identify coagulopathy needing correction to reduce haematoma extension and allow for surgical intervention

48
Q

Imaging investigations

A

Non contrast CT head - required for all intracranial bleeding sus
Crescent shaped collection blood overlying one of cerebral hemispheres

49
Q

CT appearances of SDH acute

A

Crescent - banana shaped
Acute - hyperdense
Chronic - hypodense - dissolution of liquified blood
Not limited by suture lines

50
Q

Management of subdural haematoma - medical

A

Correct coagulation studies - reversal agents, haematology
Anticonvulsants - eg levetiracetam, phenytoin

51
Q

Complications of SDH

A

Seizures
Neurological deficits
Recurrent haemorrhage
Infection

52
Q

ECG subarrach

A

Peaked P and T waves
Short PR interval
Prolonged QT interval
tall U waves

53
Q

When do you not perform an LP?

A

Sus raised ICP

54
Q

When are CT/MRI angiographyies done in bleed?

A

TO find sourve of bleed in those fit for surgery

55
Q

Classification for SAH

A

Hunt and HEss
1-5

56
Q

Grades in Hunt and HEss classification for SAH

A

1 - asymptomatic
2 - moderate - severe headache, nuchal rigidity, CN palsy
3 - drowsy, confused, mild neurological deficit
4 - stupor, moderate to severe hemiparesis
5 - Coma, decerebrate posturing

57
Q

Risk factors SAH

A

HPTN
Smoking
Cocaine
Alcohol exceess
Genetic disorders - marfans, ehlers dhanlos, NF type I, polycystuc disease
1st degree relatives

58
Q

How does trauma cause a SDH

A

Teearing of bridging veins from tortex to one drainging venous sinuses - rapid acceleration decelration of head
Damaged cortical artery
Blunt head trauma

59
Q

Investgiations SDH

A

Bloods - FBCs, U+Es, LFTs, coag screen, grouo and save/crossmatch
CT head = 1st line
Skull X ray
MRI head

60
Q

Chronic subdural haematoma on CT head

A

hypodense (dark), crescentic collection around the convexity of the brain

60
Q

Acute to chronic subdural haematoma

A

Acute: Symptoms usually develop within 48 hours of injury, characterised by rapid neurological deterioration
Subacute: Symptoms manifest within days to weeks post-injury, with a more gradual progression.
Chronic: Common in the elderly, developing over weeks to months. Patients may not recall a specific head injury.

61
Q

Neuro symptoms of subdural haematoma

A

Altered Mental Status: Ranging from mild confusion to deep coma. Fluctuations in the level of consciousness are common.
Focal Neurological Deficits: Weakness on one side of the body, aphasia, or visual field defects, depending on the haematoma’s location.
Headache: Often localised to one side, worsening over time.
Seizures: May occur, particularly in acute or expanding hematomas.
ESP memory loss in elderly

61
Q

Cushings triad raised ICP

A

Bradycardia
HPTN
resp irregularities

ENT, neuro, eyes (34 decks)

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