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Neurology/Neurosurgery > Neurosurgery Passmedicine > Flashcards

Neurosurgery Passmedicine Flashcards

1
Q

What imaging is most sensitive for diagnosing diffuse axonal injury?

A

MRI

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2
Q

What are the two types of primary brain injury?

A

Focal - contusion/haematoma

Diffuse - diffuse axonal injury

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3
Q

What causes diffuse axonal injury?

A

Mechanical shearing following deceleration, causing disruption and tearing of axons

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4
Q

What are the two types of contusions?

A

Coup (adjacent to side of impact)

Contre-coup (contralateral to side of impact)

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5
Q

What are the different types of intra-cranial haematomas?

A

Extradural
Subdural
Intracerebral

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6
Q

What happens in secondary brain injury?

A

Cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury

The normal cerebral autoregulatory processes are disrupted following trauma so brain more susceptible to hypoxia

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7
Q

What is the cushing’s reflex?

A

HTN

Bradycardia (often a pre-terminal event, seen prior to coning)

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8
Q

Where do most extradural haemorrhages occur?

A

Temporal region (where skull fracture –> rupture of middle meningeal artery)

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9
Q

What are the features of an extradural haemorrhage?

A

Features of raised ICP

Lucid interval

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10
Q

Where is the bleeding in an extradural haematoma?

A

Between dura and skull

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11
Q

Where does subdural haematoma tend to occur?

A

Around the frontal and parietal lobes

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12
Q

What are risk factors for subdural haematoma?

A

Old age
Alcoholism
Anticoagulation

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13
Q

How does subdural haematoma tend to present?

A

Slower onset of symptoms

May be fluctuating confusion/consciousness

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14
Q

How does subarachnoid haemorrhage tend to present?

A

Sudden occipital headache

May occur spontaneously in context of rupture cerebral aneurysm or in assoc. with other brain injuries

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15
Q

Which patients with head injuries should be imaged immediately (within 1h)?

A

GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
suspected open or depressed skull fracture.
any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
post-traumatic seizure.
focal neurological deficit.
more than 1 episode of vomiting

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16
Q

Which patients should have a CT head 8h after a had injury?

A

Those with any of the following who have experienced LOC/amnesia:
age 65 years or older
any history of bleeding or clotting disorders
dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
more than 30 minutes’ retrograde amnesia of events immediately before the head injury

OR any patient on warfarin who has sustained a head injury

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17
Q

When should you do a CT c-spine after an injury?

A

Patient alert and stable, and clinically suspicion of cervical spine injury + any of:
age 65 years or older
dangerous mechanism of injury (fall from a height of greater than 1 metre or 5 stairs; axial load to the head, for example, diving; high-speed motor vehicle collision; rollover motor accident; ejection from a motor vehicle; accident involving motorised recreational vehicles; bicycle collision)
focal peripheral neurological deficit
paraesthesia in the upper or lower limbs

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18
Q

A patient with GCS of 8 or less needs what before they are imaged?

A

Urgent neurosurgical review

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19
Q

How should you manage lifethreatening rising ICP after a head injury?

A

Prepare for theatre/transfer

Use IV mannitol/furosemide

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20
Q

How is diffuse cerebral oedema managed in the context of head injury?

A

Decompressive surgery

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21
Q

When might exploratory burr holes be used?

A

Where imaging isn’t available

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22
Q

How should depressed skull fractures be managed?

A

Formal surgical reduction and debridement

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23
Q

Who might be appropriate for ICP monitoring in the context of head injury?

A

Those with GCS of 3-8 and normal CT scan

Definitely for those with GCS 3-8 and abnormal CT

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24
Q

Hyponatraemia in head injury is most likely due to what?

A

SIADH

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25
Q

What minimal cerebral perfusion pressure in adults?

A

70mmHg

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26
Q

What minimal cerebral perfusion pressure in kids?

A

40-70mmHg

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27
Q

Unilaterally dilated pupil with sluggish or fixed light response = ?

A

3rd nerve compression secondary to tentorial herniation

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28
Q

Bilaterally dilated pupil with sluggish or fixed light response = ?

A

Poor CNS perfusion

or Bilateral 3rd nerve palsy

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29
Q

Unilaterally dilated or equal pupil size with cross reactive (Marcus-Gunn) light response =

A

Optic nerve injury

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30
Q

Bilaterally constricted pupil =?

A

Opiates
Pontine lesions
Metabolic encephalopathy

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31
Q

Unilaterally constricted pupil + preserved light response = ?

A

Sympathetic pathway disruption

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32
Q

Binocular vision post-facial trauma is suggestive of what?

A

Depressed fracture of the zygoma

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33
Q

Where does the bleed occur in subarachnoid haemorrhage?

A

In between the arachnoid and pia mater

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34
Q

What is the most common cause of SAH?

A

Head injury

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35
Q

In the absence of trauma, what is SAH called?

A

Spontaneous SAH

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36
Q

What can cause spontaneous SAH?

A 
Intracranial aneurysm (most common)
AV malformation
Pituitary apoplexy
Arterial dissection
Mycotic (infective) aneurysms 
Perimesencephalic (idiopathic venous bleed)
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37
Q

What kind of aneurysms rupturing cause SAH?

A

Berry/sacular

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38
Q

What are berry aneurysms associated with?

A

Coarctation of the aorta
Adult polycystic kidney disease
Ehlers-Danlos syndrome

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39
Q

How does SAH present?

A 
Thunderclap headache - worst headache of life, occipital, very sudden onset
NV
Meningism (photophobia, neck stiffness)
Coma
Seizures
Sudden death
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40
Q

What ECG changes may be seen in SAH?

A

ST elevation may be seen

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41
Q

How do you confirm a SAH has occurred?

A

CT - +ve if acute blood (hyperdense) seen in basal cisterns, sulci + in severe cases in the ventricular system
If -ve carry out LP at least 12 hours after onset of symptoms to allow development of xanthochromia

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42
Q

What is xanthochromia?

A

Production from breakdown of red blood cells

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43
Q

What other CSF findings may you see with SAH?

A

Raised/normal opening pressure

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44
Q

How can you distinguish between traumatic tap and true SAH from LP?

A

Xanthochromia

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45
Q

What should you do as soon as a diagnosis of SAH is made?

A

Refer to neurosurgery

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46
Q

What investigations should be done after a diagnosis of SAH is made?

A

CT intracranial angiogram to identify AVM/aneurysm)

+/- digital subtraction angiogram (catheter angiogram)

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47
Q

Why should intracranial aneurysms be treated within the first 24h of a rupture?

A

They are at risk of a rebleed

48
Q

How are most intracranial aneurysms managed?

A

Coil insertion by interventional radiologist

Few req. craniotomy and clipping by neurosurgery

49
Q

How should a patient with a ruptured intracranial aneurysm be managed until they are coiled?

A

Bed rest, well controlled BP to avoid re-bleed

Vasospasm prevented using 21d course of nimodipine

50
Q

How should vasopasm following ruptured aneurysm be treated?

A

Hypervolaemia, induced HTN and haemodilution

51
Q

How is hydrocephalus treated in SAH?

A

Temporarily - external ventricular drain (CSF diverted into bag at bedside)
If long term may need ventriculo-peritoneal shunt

52
Q

What are complications of SAH?

A 
Re-bleed (30%)
Vasospasm (usually 7-14d after onset) 
Hyponatraemia (due to SIADH)
Seizures
Hydrocephalus
Death
53
Q

What are important predictive factors in SAH?

A

Conscious level on admission
Age
Amount of blood on CT

54
Q

What is xanthochromia?

A

Yellowish appearance of CSF due to breakdown of RBCs and bilirubin release

55
Q

What kind of bleed may cause neonatal deterioriation in premature babies?

A

Intraventricular haemorrhage

56
Q

Mass effect on the brain in extradural haematoma can lead to what?

A

Uncal herniation –> fixed, dilated pupil due to CNIII compression

57
Q

What do extradural haematomas appear like on CT?

A

Hyperdense (bright) biconvex collection around surface of brain

58
Q

What is the definitive management of an extradural haematoma?

A

Craniotomy and evacuation of the haematoma

59
Q

What do you see on CT in acute subdural haematoma?

A

Hyperdense crescentic collection surrounding the brain that is not limited by suture lines

60
Q

How is acute subdural haematoma definitively managed?

A

Decompressive craniectomy

61
Q

How do those with chronic subdural haematoma tend to present?

A

Several weeks after a mild head injury with progressive confusion, LOC, weakness or higher cortical function

62
Q

How is symptomatic chronic subdural haematoma managed?

A

Burr hole drainage

63
Q

What is a intracerebral haematoma?

A

Collection of blood within the substance of the brain

64
Q

What are risk factors for intracerebral haematoma?

A 
HTN
Vascular lesions (e.g. AVM, aneurysm)
Cerebral amyloid angiopathy
Brain tumour
Infarct (esp. in those undergoing thrombolysis)
65
Q

How do those with intracerebral infarct present?

A

Like they are having an ischaemic stroke

66
Q

What will CT show in intracerebral haematoma?

A

Hyperdensity within substance of brain

67
Q

How is intracerebral haematoma managed?

A

Usually under stroke physicians

Large clots may warrant surgical evacuation

68
Q

What is an intraventricular haemorrhage?

A

Bleed into ventricular system

69
Q

What tends to cause IVH in kids?

A

Prematurity of periventricular vascular structures

70
Q

What can cause IVH in adults?

A

May extend from SAH, vascular lesions (e.g. aneurysms/AVM) or tumours

71
Q

What does IVH look like on CT?

A

Hyperdensity within the dark CSF spaces within the ventricles

72
Q

What are patients with IVH at risk of?

A

Obstructive hydrocephalus

73
Q

In neonates when do most IVH occur?

A

In first 72h after birth (may be because of birth trauma + cellular hypoxia)

74
Q

What should be the first thing you do when a patient becomes unresponsive?

A

Assess and secure airway

75
Q

What are the three things that make up Cushings triad?

A

Widening of pulse pressure
Respiratory changes
Bradycardia

76
Q

How might rises in ICP be accommodated?

A

Shifts of CSF

77
Q

Does the brain autoregulate its blood supply?

A

Yes, so if the ICP rises the systemic circulation will display changes to try and need the perfusion needs of the brain
Usually –> HTN

78
Q

What occurs if ICP keeps rising?

A

Brain compressed
Cranial nerve palsies
Compression of essential centres in brainstem
Cardiac centre compression –> bradycardia

79
Q

Uncal herniation –> dilated pupil due to compression of what nerve?

A

CNIII

80
Q

What is uncal herniation?

A

When the uncus of the temporal lobe herniates under the free edge of the tentorium cerebelli and compresses CNIII –> ipsilateral fixed, dilated pupil and contralateral paralysis (due to compression of cerebral peduncle)

81
Q

What is brainstem compression called?

A

Coning

82
Q

How is coning managed?

A

Osmotherapy with hypertonic saline/mannitol or surgical decompression

83
Q

What is subfalcine herniation?

A

Displacement of cingulate gyrus under the falx cerebri

84
Q

What is central herniation?

A

Downwards displacement of the brain

85
Q

What is tonsillar herniation?

A

Displacement of the cerebellar tonsils through the foramen magnum, aka. coning

86
Q

What does tonsillar herniation lead to?

A

Compression of the cardiorespiratory centre

87
Q

In which condition is tonsillar herniation seen without raised ICP?

A

Chiari 1 malformation

88
Q

What is a transcalvarial herniation?

A

Brain displaced through a defect in the skull, e.g. fracture, craniotomy site

89
Q

Define hydrocephalus

A

Excessive volume of CSF within ventricular system of the brain

90
Q

What causes hydrocephalus?

A

Imbalance between CSF production and absorption

91
Q

What are the clinical features of hydrocephalus?

A 
Due to raised ICP - 
Headache (worse in morning, when lying down + during Valsalva)
NV
Papilloedema
Coma

In infants –> increased head circumference as sutures not fused yet (ant. fontanelle will bulge + become more tense) + failure of upward gaze

92
Q

Why do children with hydrocephalus get failure of upward gaze?

A

Due to compression of the superior colliculus in the midbrain

93
Q

What are the two types of hydrocephalus?

A

Obstructive - non-communicating

Non-obstructive - communicating

94
Q

What causes obstructive hydrocephalus?

A

Structural pathology blocking flow of CSF

95
Q

What do you see on imaging in obstructive hydrocephalus?

A

Dilatation of ventricular system superior to site of blockage

96
Q

What are causes of obstructive hydrocephalus?

A

Tumours
Acute haemorrhage (eg. IVH, SAH)
Developmental abnormalities, e.g. aqueduct stenosis

97
Q

What are causes of non-obstructive hydrocephalus?

A

Increased production of CSF –> choroid plexus tumour (v. rare)

Decreased resorption of CSF - e.g. meningitis or post-haemorrhagic

98
Q

What is normal pressure hydrocephalus?

A

Non-obstructive hydrocephalus where there is ventriculomegaly with normal ICP

99
Q

What are the classical symptoms of normal pressure hydrocephalus?

A

Dementia
Incontinence
Disturbed gait

100
Q

What investigation is first line for suspected hydrocephalus?

A

CT head

101
Q

What other investigation may be used for hydrocephalus?

A

MRI to check for underlying lesions

102
Q

What investigation is therapeutic and diagnostic in hydrocephalus?

A

LP - can sample CSF and measure opening pressure and drain CSF

103
Q

In what type of hydrocephalus would you avoid using LP and why?

A

Obstructive hydrocephalus since the difference of the cranial and spinal pressures induced by drainage –> brain herniation

104
Q

What is an external ventricular drain?

A

A drain inserted into the right lateral ventricle that drains into a bag at the bedside

105
Q

What is a ventriculoperitoneal shunt?

A

Long term CSF diversion that drains CSF from the ventricles to the peritoneum

106
Q

What drain is used in acute severe hydrocephalus?

A

EVD

107
Q

What is the management of obstructive hydrocephalus?

A

Surgically treating the obstructing pathology

108
Q

How does hydrocephalus present in children?

A 
Increasing head size
Bulging fontanelles
Impaired upward gaze
Dilated scalp veins
Bradycardias
Seizure
Coma
109
Q

How do you differentiate between cerebral salt wasting syndrome and SIADH?

A

Both can occur following SAH BUT
CSWS - sodium loss accompanied by water loss as kidneys are functioning normally so there is a relative fluid depletion

SIADH - kidneys hold on to too much water –> concentrated urine

110
Q

What are the criteria for testing for brainstem death?

A

Deep coma of known aetiology
Reversible causes excluded
No sedation
Normal electrolytes

111
Q

Who should test for brain death?

A

2 appropriately experienced doctors on two separate occasions

Both experienced in performing brainstem death + with at least 5 y post-grad experience
One must be a consultant
Neither can be a member of the transplant team

112
Q

What are the 6 tests to confirm brain death?

A 
Pupillary reflex
Corneal reflex
Oculo-vestibular reflex
Cough reflex (give bronchial stimulation or to gag response)
Absent response to supraorbital pressure
No spontaneous respiratory effort
113
Q

What is the oculo-vestibular reflex?

A

Eye movements following slow injection of at least 50ml ice cold water into each ear in turn

114
Q

Patients with intracranial bleeds who become unresponsive should have a CT urgently to rule out what?

A

Hydrocephalus

115
Q

What are the two components of diffuse axonal injury?

A
  1. Multiple haemorrhages

2. Diffuse axonal damage in the white matter

116
Q

What are the classical symptoms of basilar skull fracture?

A

Periorbital bruising (racoon eyes)
Post-auricular bruising (Battle’s sign)
CSF leaking from nose or ear
Haemotympanium

Neurology/Neurosurgery (2 decks)

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