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Head and Neck > Elective Neurosurgery > Flashcards

Elective Neurosurgery Flashcards

(51 cards)

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1
Q

Typical site of primary intracerebral haemorrhage

A

Basal ganglia

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2
Q

Cause of primary intracerebral haemorrhage

A

Rupture of microaneurysms of Charcot-Bouchard of the perforating arteries supplying the basal ganglia

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3
Q

List the risk factors associated with subarachnoid aneurysms

A
  • HTN
  • Smoking
  • Cocaine
  • Polycystic kidney disease
  • Marfans
  • Ehlers-Danlos
  • Neurofibromatosis type 1
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4
Q

What is associated with mycotic subarachnoid aneurysms

A

Infective endocarditis

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5
Q

List the complications of SAH

A
  • Rebleeding - 3% in first 24 hours
  • Hyponatraemia
  • Vasospasm
  • Hydrocephalus
  • Seizures
  • Cardiac abnormalities
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6
Q

What is the aim of surgery in SAH

A

Prevent rebleeding

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7
Q

How is hyponatraemia secondary to SAH managed

A

Triple ‘H’ therapy:

  • Hypervolaemia (3L saline per day)
  • Hypertension
  • Haemodilution
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8
Q

List the risk factors for chronic subdural haematoma

A
  • Age
  • Alcohol
  • Dementia
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9
Q

How are chronic subdural haematomas managed

A

Burr hole drainage (posterior frontal and posterior parietal)

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10
Q

What is the most common brain tumour

A

Cerebral metastases

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11
Q

What is the most common primary brain tumour

A

Glioblastoma multiforme (Glioma)

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12
Q

What is the most common childhood brain tumour

A

Astrocytoma (Glioma)

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13
Q

Where do cerebral metastases typically seed

A

At the interface between grey and white matter

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14
Q

List the common origins of cerebral metastases

A
  • Lung
  • Bowel
  • Breast
  • Renal
  • Melanoma
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15
Q

If no primary tumour is identified by non-invasive means, how should you proceed

A
  • Stereotactic brain biopsy

- Excision biopsy

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16
Q

List the brain tumours of glial cell origin (gliomas)

A
  • Astrocytoma
  • Oligodendroglioma
  • Ependymoma
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17
Q

Describe the macroscopic appearance of Glioblastoma multiforme

A
  • Grey-ish ill-defined mass

- Areas of necrosis and haemorrhage

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18
Q

List the diagnostic histological features of Glioblastoma multiforme

A
  • Vascular proliferation and thrombosis

- Necrosis

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19
Q

What WHO grade is Glioblastoma multiforme

A

4

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20
Q

What WHO grade is anaplastic astrocytoma

A

3

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21
Q

Why are both glioblastoma multiforme and anaplastic astrocytoma non-resectable

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A

Due to tumour cell migration to some distance from the original lesion

22
Q

Describe the macroscopic appearance of anaplastic astrocytoma

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A

White ill-defined mass, sometimes expanding into the gyrus

23
Q

From where do meningiomas arise

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A

Arachnoid cap cells

24
Q

With regards to position relative to the tentorium cerebelli, what is the difference between paediatric and adult CNS tumours

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A
  • Paediatric = most infratentorial

- Adult = most supratentorial

25
What WHO grade are meningiomas
1
26
Describe the macroscopic appearance of meningiomas
- Rubbery, round, lobulated mass | - Firmly attached to the dura
27
What are the indications for stereotactic radiotherapy in CNS lesions
- AVM - Vestibular schwannoma - Metastasis
28
When is de-bulking surgery indicated in CNS tumours
For young patients <65 with GBM and AA: - Decrease mass effect for symptom relief - Reduce ICP - Remove lesion causing motor symptoms
29
How are pituitary tumours divided
1. Functional (secrete hormones) 2. Non-functional OR 1. Microadenomas <10mm 2. Macroadenomas >10mm
30
List the indications for surgery in pituitary tumours
- Non-functional tumours with mass effect - Cushing's disease - Acromegaly - Acute visual deterioration - Pituitary apoplexy (infarction/haemorrhage of the gland)
31
How are prolactinomas managed
Most shrink with dopamine agonists
32
What is the typical surgical approach to pituitary tumours
Trans-sphenoidal
33
How does pituitary apoplexy present (bleeding/infarction)
- Sudden-onset headache - Sometimes visual disturbance - Deteriorating conscious level - Panhypopituitarism with addisonian crisis
34
How is SIADH managed
- Fluid restriction <1L/day | - Monitor sodium
35
How is hydrocephalus categorised
1. Communicating | 2. Non-communicating (obstructive)
36
Describe communicating hydrocephalus
- CSF resorption at the arachnoid granulations is arrested or slowed e.g. secondary to SAH - All CSF spaces are increased in volume
37
Describe non-communicating hydrocephalus
Block to CSF flow proximal to the arachnoid granulations
38
How do you determine the difference between communicating and non-communicating hydrocephalus
CT/MRI
39
Why is it important to distinguish the difference between communicating and non-communicating hydrocephalus
- LP is life-saving in communicating hydrocephalus | - LP can cause coning in non-communicating hydrocephalus
40
Describe normal-pressure hydrocephalus
Clinical triad of: 1. Dementia 2. Gait dyspraxia 3. Incontinence
41
How is normal-pressure hydrocephalus managed
Ventriculo-peritoneal shunt
42
Describe ventriculo-peritoneal shunts
- Ventricular catheter inserted into occipital horn of the lateral ventricle via burr hole - Peritoneal catheter is tunnelled under the skin to insert into the peritoneal cavity at the costal margin
43
What bacteria complicate ventriculo-peritoneal shunts
Staphylococcus epidermiidis and staphylococcus aureus
44
How may non-communicating hydrocephalus be managed
Third ventriculostomy
45
What is the main pathogen in cerebral abscesses
Streptococci mainly
46
How may cerebral abscesses present
- Symptoms of raised ICP - Seizure - Focal neurology
47
From what sites does haematogenous spread cause cerebral abscesses
- Bronchiectasis - Bacterial endocarditis - Dental abscess and caries
48
From where does local spread cause cerebral abscesses
- Middle-ear (esp. cholesteatoma) - Frontal and sphenoid sinusitis - Skull base bone erosion
49
How are cerebral abscesses managed
- Needle drainage | - Antibiotics
50
From where does subdural empyema develop from
Spread from paranasal sinuses
51
How is subdural empyema managed
Surgical drainage via burr hole or craniotomy

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