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FRCS Part 2 > Vascular > Flashcards

Vascular Flashcards

1
Q

What is the investigation of choice to investigate pulsatile tinnitus without an audible skull bruit?

A

MRA is the initial diagnostic test.

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2
Q

What are the causes of pulsatile tinnitus?

A

Arterial lesions incl. AVDF, Caroticocavernous fistulas. FMD, ICA dissection, vascular anomaly of the ear and vascular compression of the CN8. Venous lesions incl. high riding jugular bulb / dehiscent jugular vein, dominant transverse sinus, BIH and mastoid emissary veins. Neoplasia incl. glomus jugulare tumours, facial nerve haemangiomas. Cavernous haemangioma and paget’s disease. Other systemic causes incl. high output cardiac failure, hyperthyroidism and otoscelrosis.

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3
Q

What is the investigation of choice to investigate pulsatile tinnitus with an audible skull bruit?

A

Digital subtraction angiography.

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4
Q

Which vessels may supply an anterior cranial fossa AVDF?

A

ICA – Opthalmic A / Ehtmoidal A; ECA – Maxillary A / Middle meningeal A.

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5
Q

Which veins may drain an anterior fossa AVDF?

A

Retrograde venous drainage to cortical vessels (orbitofrontal and olfactory veins) which drain to the basal vein of Rosenthal and anterograde drainage to the superior sagittal sinus.

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6
Q

What is the mobidity and mortality of the natural history of a DAVF with cortical venous reflux?

A

15% morbidity and 10% mortality.

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7
Q

Should anterior cranial fossa AVDF be treated?

A

These always have cortical venous reflux so should be treated aggressively.

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8
Q

What is the treatment of choice for anterior fossa AVDF?

A

Surgery.

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9
Q

Should AVDF with sigmoid sinus drainage but no cortical venous reflux be treated?

A

No, due to the very small risk (if any) of bleeding.

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10
Q

What is the goal of AVDF surgery?

A

To disrupt the draining veins at their dural origin.

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11
Q

What are the complications of AVDF surgery?

A

Haemorrhage, venous hypertension, venous infarction, cerebral oedema, seizure, death and stroke.

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12
Q

Should embolization be performed for AVDF?

A

Transarterial embolization can be performed to reduce intraoperative bleeding.

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13
Q

How are DAVFs classified?

A

Borden et al and Cognard et al classifications based on the pattern of venous drainage of the AVF.

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14
Q

What is the Borden classification?

A

1 – Dural AVF draining into a sinus directly; 2 – Dural AVF draining into a sinus and a cortical vein; 3 Dural AVF draining into a cortical vein only.

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15
Q

What is the Cognard classification?

A

1 – Dural AVF draining into a sinus directly; 2a - Dural AVF with sinus thrombosis draining into a contralateral sinus due to ipsilateral sinus occlusion (retrograde flow); 2b - Dural AVF with sinus thrombosis draining into a cortical vein and the ipsilateral sinus; 2a+b Dural AVF with sinus thrombosis causing contralateral sinus drainage (retrograde flow); and cortical venous drainage; 3 – Dural AVF draining into a cortical vein only; 4 – Dural AVF with venous telangiectasia and 5 – Spinal dural AVF. Subtype classification a – single and b – multiple.

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16
Q

What is anosognosia?

A

This is a deficit of self-awareness in which a patient is unaware of their disability. This is typically due to a parietal lobe lesion.

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17
Q

What is hemisomatognosia?

A

This is a lack of awareness of one half of the body (neglect).

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18
Q

What should you investigate for in a young patient with an intracerebral haemorrhage?

A

Underlying vascular malformation

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19
Q

What is the Spetzler-Martin Grade?

A

A surgical grading system for risk of resection of AVMs: Size - 6cm = 3 Eloquence = 1 Deep venous drainage = 1

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20
Q

What is the annual rupture risk of an AVM?

A

2-4% per year. Increases to double that if there is a nidal aneurysm.

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21
Q

How can lifetime risk of rupture be calculated?

A

Risk = 1 – (1-risk of annual haemorrhage) x years left to live

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22
Q

What are the treatment options for AVMs?

A

No intervention – if the risk of intervention is higher than lifetime rupture risk; Surgery Embolisation + Surgery Radiosurgery

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23
Q

What are the important steps in AVM surgery?

A

Mannitol prior to dural opening. Proximal temporary occlusion can be performed with aneurysm clips. Smaller vessels can be occluded with AVM clips. Large draining veins are clipped with large aneurysm clips. Do no occlude a vessel unless it is seen to enter the AVM.

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24
Q

What is the safety measure taken before taking a large draining vein?

A

An aneurysm clip is placed across it for 10-15 mins to make sure it is safe to take.

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25
Q

What is normal perfusion pressure breakthrough?

A

This is a disorder of autoregulation of the brain vasculature. It presents with sudden onset of brain swelling and bleeding. It may be due to taking a draining vein too soon.

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26
Q

How is normal perfusion pressure breakthrough treated?

A

Elevation of the patient’s head, administration of mannitol, barbiturate induced coma, hypotension and proximal vessel occlusion with temporary clips.

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27
Q

What are the MRI features suggestive of a cavernoma?

A

Pop-corn lesion with haemosiderin ring. Mixed signal intensity.

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28
Q

How are intracranial vascular malformations classified:

A

AVM / Venous malformations / Capillary malformations / Cavernous malformations (cavernomas)

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29
Q

What are the management options for cavernomas?

A

Conservative for asymptomatic or minimally symptomatic lesions that are surgically inaccessible and where risk of surgery exceeds the benefit and for multiple lesions with a family history. Radiosurgery for surgically inaccessible lesions with prior haemorrhage. Radiosurgery reduces the risk of haemorrhage to one third of the initial risk. Radiosurgery has fallen out of favour due to unclear natural history and inability to evaluation obliteration (angiographically occult). Surgery for lesions with recurrent symptomatic haemorrhage, progressive neurological deficit, intractable epilepsy, cortically based superficial lesions and those that do not respond to radiosurgery.

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30
Q

What is the annual bleeding risk of a cavernoma?

A

Rates vary widely in the literature. Kondziolkas prospective study of 122 cavernomas showed a bleeding risk of 4.5% pa.

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31
Q

How would you approach a basal ganglia cavernoma?

A

Syvian fissure dissection, image guided corticotomy along the insular gyrus to remove the cavernoma. Alternatively a parietal transcortical transventricular approach can be used.

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32
Q

What does the anterior choroidal artery supply?

A

GPi, Post. limb of internal capsule and choroid plexus

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33
Q

What demarcates A2 becoming A3?

A

Callosomarginal branch

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34
Q

What demarcates A3 becoming A4?

A

3 cm posterior to the genu

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35
Q

Branches of P1

A

Posterior thalamopeduncular perforators Long and short circumflex arteries

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36
Q

Branches of P2

A

Hippocampal Anterior temporal Inferior temporal Posterior medial choroidal artery Posterior lateral choroidal

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37
Q

Where is P3?

A

Quadrigeminal cistern

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38
Q

Branches of P4?

A

Parieto-occipital and calcarine

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39
Q

Branches of the ECA?

A

SALFOPSI: Superior thyroid Ascending pharyngeal Lingual Facial Occipital Posterior auricular Superficial temporal Internal maxillary

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40
Q

What are the segments of the ICA?

A

Based on the Cinicinnati system: Cervical, Petrous, Lacerum, Cavernous, Clinoid, Opthalmic, Communicating

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41
Q

Define the cervical segment of the ICA

A

Carotid bifurcation to Carotid canal (no branches!)

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42
Q

Define the petrous segment of ICA

A

Carotid canal to Fr. Lacerum

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43
Q

What are the 3 segments of the petrous carotid?

A

Verticle, posterior and horizontal segments

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44
Q

Define the lacerum segment of ICA

A

Above Fr. lacerum to petrolingual ligament

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45
Q

Define the cavernous segment of the ICA

A

Petrolingual lig to prox dural ring

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46
Q

Define the clinoidal segment of ICA

A

Prox to distal dural rings

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47
Q

How can you differential ACh from PCom on angio?

A

PCom is proximal, larger and runs straight back. Usually bifurcates.

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48
Q

What is the point of the angiogram called where the ACh enters the ventricle?

A

Plexal point

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49
Q

What does the Artery of Adamkiewicz supply?

A

Supplies T8 to conus (located on the left in 80%). Is a radiculomedullary branch of the segmental intercostal artery. Has a diameter of 1 mm.

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50
Q

Where is the thoracic watershed area?

A

T4/5

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51
Q

What is the arcade called where the anterior and posterior spinal arteries anastomose as the conus?

A

Arcade of Lazorthes

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52
Q

What is the blood supply to the thalamus?

A

Anterior thalamus by Tuberthalamic A (aka polar A) from the PCom

Lateral thalamus from P2 posterior thalamogeniculate A.

Medial thalamus from P1 paramedian A

Posterior thalamus from the posterior medial choroidal from the P2.

A of Percheron is a variant where both paramedian A arise from a single P1 perforator and infarction results in bilateral thalamic infarcts. Causes altered mental status, vertical gaze palsy and memory impairment.

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53
Q

What are the peaks in the ICP waveform?

A

1 = percussion (ejection of blood from the heart) 2 = tidal (brain compliance) 3 = dicrotic (closure of the aortic valve) In normal conditions the 1>2>3. With raised ICP and loss of cerebral compliance 1=2=3.

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54
Q

How does CBF change with PaO2 and PCO2?

A
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57
Q

How much cardiac output goes to the brain?

A

Brain weighs 1.4 kg.

It receives 15% of CO

It uses 20% of the oxygen

It uses 25% of the glucose

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58
Q

What is the metabolic requirement for oxygen of the brain?

A

50 ml 02/min (Based on oxygen content of 20ml per 100ml of blood and CBF of 50ml/100g/min the delivery is 150 ml O2/min so only 1/3 is extracted = oxygen extraction fraction)

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59
Q

At what CBF do EEG slowing occur?

A

<23 ml/100g/min.

When <10 ml/100g/min there is irreversible damage and this is the core. The surrounding area with CBF 10-17 ml/100g/min forms the penumbra.

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60
Q

What is the Bohr effect?

A

Shift of the oxygen dissociation curve to the right caused by increase in temperature, hypoxia and hypercapnia

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61
Q

What is the classification of haemorrhagic shock?

A
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62
Q

What is the evidence for hypothermia as cerebral protection in aneurysm surgery?

A

IHAST2 (Todd et al 2005 NEJM) compared WFNS1-3 aneurysm clipping with hypothermia 33 deg compared to normothermia 36.5 deg. No difference in outcome!

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63
Q

Summarise the eurotherm trial

A

TBI within 10 days that have ICP monitor and failure of tier 1 ICP management (I&V, sedated, head up etc)

Randomised to between 32-35 deg as per ICP via cold saline boluses

Odds of unfavourable outcome and death @ 6 months with cooling so trial discontinued

(Hypothermia for intracranial hypertension after traumatic brain injury. N Engl J Med 2015)

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64
Q

What is the equation for osmolality?

A

= 2x ([Na] + [K]) + urea + glucose in mmol/l

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65
Q

What is the [Na] in normal saline?

A

0.9% which means 9g per litre

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66
Q

Define SIADH

A

Hypotonic hyponatraemia with serum osmo <275 (dilute) and inappropriately concentrated urine with urine osmo >100.

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67
Q

What is the difference between CSW and SIADH?

A

CSW has extracellular fluid depletion due to renal sodium loss. Renal [Na] >20.

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68
Q

Why should you measure TSH in a patient with hypoNa?

A

To rule out hypothyroidism

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69
Q

What is the risk of rapid Na correction?

A

Central pontine myelinolysis

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70
Q

What is the classification of the severity of hypoNa?

A

Mild <135, Moderate <130 and Severe <125

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71
Q

What is the cause of a low Na in a dry patient i.e. Na <135 and serum osmo >295?

A

Hyperglycaemia or mannitol administration

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72
Q

What is the cause of a low Na in a hypotonic patient i.e Na <135 and serum osma <275?

A

If urine osmo dilute (urine osmo <100) then psychogenic polydipsia or low Na intake. If urine osmo conc (urine osmo >100) then check volume status. If dry and urine Na >20 then CSW / diuretics / Addison’s disease. If dry and urine Na <20 then extrarenal losses of Na such as GI tract or burns etc. If euvolemic then SIADH If hypervolaemic and urine Na >20 then renal failure or hypothyroidism. If hypervolaemic and urine Na <20 then CHF and cirrhosis.

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73
Q

What is the treatment for SIADH?

A

Fluid restriction > Vaptans (tolivaptan) = ADH-R antagonists > Demeclocycline induces nephrogenic DI

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74
Q

What is the treatment for CSW?

A

Volume replacement and Na replacement

Fludrocortisone can be used for low Na if refractory

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75
Q

What is the most common cause of hypoNa in Neurosurgery?

A

SIADH

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76
Q

What is the incidence of SIADH and CSW in SAH?

A

SIADH 35% and CSW 20%

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77
Q

What are the causes of isotonic hyponatraemia?

A

Osmo 275-295: pseudohyponatraemia due to hyperlipidaemia or hyperparaproteinaemia;

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78
Q

What are the causes of hypertonic hyponatraemia?

A

Osmo >295: Hyperglycaemia / mannitol administration

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79
Q

What are the causes of hypotonic hyponatraemia?

A

Osmo <275: Urine osmo <100 - psychogenic polydipsia Urine osmo >100 - depends on fluid status Hypervolaemic: Renal failure if urine Na >20 and CHF / cirrhosis if urine Na <10 Euvolaemic: SIADH Hypovolaemic: CSW / Addisons if urine Na >20 and GI tract or skin losses if urine Na <10

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80
Q

What are the causes of SIADH?

A

Malignancy Infection (meningitis / encephalitis / TB) Pulmonary disorders Endocrine disturbances (adrenal insufficiency / hypothyroidism) Drugs

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81
Q

What are the diagnostic criteria for SIADH?

A

Serum osmo <275 (hypotonic) Urine osmo >100 (inappropriately conc urine) Clinically euvolaemic Urinary Na >40 Normal thyroid and adrenal function No diuretic use

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82
Q

What is the most rapid recommended correction of Na?

A

8 mmol/24 hours

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83
Q

What is the solute ratio?

A

= Urine [Na] + Urine [K} / plasma [Na}

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84
Q

How does the solute ratio guide you?

A

A solute ratio >1 means fluid restriction of <500ml/day; if <1 then 1l/day

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85
Q

What urine osmo is suggestive of SIADH?

A

>100 mOsm/kg

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86
Q

What is the definitive test for SIADH?

A

Water load test: Give a water load of 20ml/Kg (max 1.5L). Urine output should be 2/3 of the water load at 4 hours, otherwise the patient has SIADH.

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87
Q

What is the contraindication to the water load test?

A

Na<125 or symptomatic hyponatraemia

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88
Q

How would you treat a patient with acute (<48 hours) and severe hypoNa (Na<125)?

A

ICU transfer 3% saline (1-2 ml/h/kg body weight) with 20mg Frusemide Check Na every 2 hours and adjust 3% saline infusion rate Replace K Max correction 8mEq/24 hours

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89
Q

How would you treat a patient with chronic (>48 hours) and severe hypoNa (Na<125)?

A

Fluid restriction based on the solute ratio For refractory cases consider demeclocycline (partial antagonist to ADH in the renal tubules) or conivaptan (vasopressin receptor antagonist)

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90
Q

How can CSW be differentiated from SIADH?

A

CVP, volume status and serum K (raised in CSW but not SIADH). Haematocrit is raised as patient is dry.

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91
Q

What is the treatment of CSW?

A

0.9% or 3% saline; salt can also be administered orally. Other treatments include fludrocortisone, hydrocortisone

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92
Q

What is a potential complication of saline administration for SIADH or CSW?

A

Hyperchloraemic acidosis (treat with sodium bicarbonate infusion instead)

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93
Q

What is the most common cause of hyperNa (Na >150)?

A

Diabetes insipidus

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94
Q

What is the mechanism behind DI?

A

Lack or insensitivity to ADH causing hypertonic serum osmo (patient is dry) with dilute urine (urine osmo <200 mOsmol/Kg OR urine SG <1.003). This leads to a high serum Na.

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95
Q

What is the difference between neurogenic and nephrogenic DI?

A

Neurogenic is a lack of ADH release; Nephrogenic is insensitivity to ADH in the kidneys

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96
Q

What are the causes of nephrogenic DI?

A

Lithium, demeclocycine, colchicine; also caused by chronic renal failure, sarcoidosis and sjorgren’s syndrome

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97
Q

What are the causes of neurogenic DI?

A

Iatrogenic following transsphenoidal surgery (most common after craniopharyngioma) Pituitary apoplexy Encephalitis / meningitis

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98
Q

What is the triphasic response?

A

1 - injury to posterior pituitary causes reduced ADH release (polyuria and polydipsia) 2 - cell death causes excess ADH release (SIADH symptoms) 3 - chronic reduction in ADH release due to loss of cells in post. pituitary

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99
Q

What are the diagnostic criteria for DI?

A

Polyuria with >250ml/h for 2 or more hours Dilute urine with urine osmo <200 or SG <1.003 High serum Na Normal adrenal function

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100
Q

What is the diagnosis in hypoNa if the serum and urine osmo are dilute?

A

Polydipsia because there is appropriately diluted urine

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101
Q

What is the water deprivation test?

A

In suspected cases of DI stop the patient from drinking / IV input. In a normal patient the urine output should decrease the urine osmo will rise to >600 mOsm/kg. In DI the urine will remain dilute.

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102
Q

What is the treatment for DI?

A

If mild - drink to thirst If severe - desmopressin

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103
Q

What is the action of ADH?

A

Water absorption from the collecting ducts through Aquaporin channels

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104
Q

Where does acetazolamide act in the kidneys?

A

Proximal convoluted tubule

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106
Q

Where do thiazides act?

A

DCT - increase Na and Cl absorption

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108
Q

Where do loop diuretics act?

A

Ascending loop of Henley

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110
Q

Where does Aldosterone and other K+ sparing diurects act?

A

DCT - inceases absorption of K+ and H+

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111
Q

What channel do loop diurectics (frusemide) act on?

A

NKCC2 - which increases absorption of Na / K and Cl

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112
Q

What is the action of Renin?

A

Released from the DCT and converts angiotensinogen to Angiotensin 1

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113
Q

What is the action of ACE?

A

Converts Angiotensin 1 to angiotensin 2 in the lungs

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114
Q

What is the most common cause of SAH?

A

Trauma

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115
Q

What is the peak age for SAH?

A

55-60 years

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116
Q

Which aneurysms cause subdural haemorrhages?

A

pCom and distal ACA (interhemispheric subdural)

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117
Q

What are the medical complications of SAH that cuase immediate mortality?

A

Neurogenic pulmonary oedema Myocardial stunning Arrhythmias (VF)

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118
Q

What is the rebleeding risk of an aneurysm?

A

14% by 2 weeks

50% by 6 months

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119
Q

What is the strongest prognostic indicator of outcome following SAH?

A

Severity of clinical presentation

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120
Q

Is SAH more common in men or women?

A

Women (1.24:1)

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121
Q

What are the risk factors for aneurysmal SAH?

A

Mnemonic: Genetic CASH Family history (1 first deg relative) Polycystic kidney disease (autosomal dominant) Ehlers-Danlos syndrome type 4 Cocaine Alcohol abuse Smoking Hypertension

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122
Q

What is the differential for a severe sudden onset headache?

A

SAH

Pituitary apoplexy

Benign thunderclap headache (a type of migraine)

Reversible cerebral vasoconstrictive syndrome (a string of beads appearance on angiography that resolves by 3 months). Associated with vasoconstrictive substances

Benign orgasmic cephlagia

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123
Q

What at Kernig’s and Brudzinski signs?

A

Kernig = flex thigh to 90 and straighten knee causing pain in Hamstring’s Brudzinzki = flex patients neck and the hip flexes

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124
Q

What are the causes of coma following SAH?

A

Seizure Hydrocephalus Raised ICP Brain damage Diffuse ischaemia

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125
Q

What ocular haemorrhages occur following SAH?

A

Subhyaloid (pre-retinal) - has a fluid level

Intraretinal - flame shaped

Vitreous humor (Terson’s syndrome) - usually bilateral and appears after a few days.

127
Q

What is the longterm prognosis for vision after Terson’s syndrome?

A

Most resolve spontaneously in 6-12 months Longterm visual prognosis is 80%

128
Q

What is the diagnostic sensitivity of CT for SAH?

A

95% @ 2 days

50% @ 7 days

129
Q

Which aneurysms cause blood in the sylvan fissure?

A

MCA and PCom

130
Q

Which aneurysms cause blood in the prepontine cistern?

A

Basilar tip and SCA

131
Q

Which aneurysms cause blood in the 4th ventricle?

A

PICA and vertebral A

132
Q

Which aneurysms cause blood in the 3rd ventricle?

A

Basilar tip

133
Q

What are the LP findings with SAH?

A

High opening pressure

No clotting bloody fluid that does not reduce with sequential tubes (take 3 samples)

Xanthochromia with spectrophotometry (sample should be shielded from light)

Cell count >100,000 rbc

Elevated protein

Normal or low glucose

134
Q

When does MRI become sensitive for SAH?

A

>4-7 days once enough met-Hb is present

135
Q

When should the LP be performed for CT negative SAH?

A

After 12 hours so xanthochromia can be formed (note: false positives with jaundice)

137
Q

Which MRI sequence is most sensitive for detecting SAH blood?

A

FLAIR

138
Q

How sensitive is MRA compared to DSA for aneurysm detection?

A

90%. Poor sensitivity for aneurysms <3 mm.

139
Q

What is the sensitivity of CTA compared to DSA?

A

97%

140
Q

What are the general principles of performing a DSA in SAH?

A

Study the vessel with greatest suspicion

4 vessel angio

Visualise both PICA origins

Visualise flow across the ACom - may need cross compression test

141
Q

What are the criteria for an infundibulum?

A

<3mm

Vessel at the apex

Triangular shape

142
Q

What factors should be considered when deciding clip v coil for an aneurysm?

A

Narrow (< 5mm) good for coiling

Broad (>5 mm) bad for coiling due to coil prolapse and recanalisation

Dome to neck ration >2 good for coiling

Presence of branches or perforators that may be occluded with coiling

143
Q

What is the Hunt and Hess grading scale for SAH?

A

Described in 1968:

1 - Asymptomatic

2 - Headache or CN palsy

3 - Confusion

4 - Stupor / decerebrate / hemiparesis

5 - Deep coma

Add one for severe comorbidities or severe vasospasm. Modified version has 0 for unruptured aneurysm.

144
Q

What are the mortality rates associated with H&H grade 1/2?

A

20%

145
Q

What is the WFNS SAH grade?

A

1 = GCS15

2 = GCS13/14 no deficit

3 = GCS13/14 with deficit

4 = GCS 7-12

5 = GCS 3-6

146
Q

What is the incidence of SAH during pregnancy?

A

1 in 10,000, but represents 10% of maternal deaths. Maternal mortality with SAH = 30%!

147
Q

How do you manage SAH in pregnancy?

A

Immediate surgical treatment reduced maternal mortality from 63% to 11 and fetal mortality from 27% to 5%. Fetal radiation exposure is a concern with coiling.

148
Q

What is the risk of hydrocephalus following SAH?

A

20-30%.

Increased risk in elderly, large ventricular blood volume and posterior circulation aneurysms

149
Q

What % of poor grade SAH patients and hydrocephalus improve with CSF diversion?

A

80%.

Keep the EVD at 15 to prevent rebleed

150
Q

What is the risk of vasospasm with modified Fisher grading system?

A

1 = Thin SAH no IVH = 24%

2 = Thin SAH with IVH = 33%

3 = Thick SAH no IVH = 33%

4 = Thick SAH with IVH = 40%

151
Q

What are the pathological changes the occur with vasospam?

A

Day 1-8 = increase in inflammatory cells in the adventitia and connective tissues, muscle necrosis and corrugation of elastin in tunica media and endothelial thickening with opening of tight junctions in the intima.

Day 9-60 - progressive smooth muscle proliferation in the intima causing intimal thickening

152
Q

Why does blood contact with vessels cause vasospasm?

A

OxyHb causing muscle contraction

Hb scavenges nitric oxide preventing wall dilation

PDGF induces proliferation and impairs dilation

Overproduction of Endothelin-1

153
Q

How do you diagnose vasospasm?

A

Delayed onset of neurological deficit

4-20 days post ictus

Deficit in the territory of the spastic arteries

Other causes of neurological decline (rebleed, hydrocephalus, cerebral oedema, seizure, hypoNa, hypoxia and sepsis) ruled out

TCD (Lindegaard ratio)

154
Q

What EEG feature predicts the onset of clinical vasospasm?

A

Reduction in the % alpha activity (relative alpha) falls.

155
Q

What tests can be done to confirm the presence of vasospasm?

A

TCDs

CTA and CT perfusion

DSA

156
Q

What is the Lindegaard ratio?

A

Insonate the ICA and MCA. If the ratio:

MCA:ICA < 3 = normal

MCA:ICA 3-6 = mild

MCA:ICA >6 = severe

**only 60% sensitive

Normal MCA velocity is 60 m/s whilst Spasm is 120 m/s

157
Q

How can you treat vasospasm?

A

Prophylactic Nimodipine

Hypertense (most important part of triple H) - need A-line and pressors

Angioplasty (mechanical or chemical with verapamil / nimodpine)

CSF drainage

158
Q

What are the risks associated with Triple-H therapy?

A

Pulmonary oedema

MI

Rebleed

159
Q

Which grading system is a predictor of vasospasm?

A

Modified Fisher (not Fisher) once you adjust for hypertension, neurological grade and high MAP which are independent predictors themselves.

Modified fisher:

1 = Focal or diffuse thin no IVH

2 = Focal or diffuse thin with IVH OR 1.6

3 = Focal or diffuse thick no IVH OR 1.6

4 = Focal or diffuse think with IVH OR 2.2

160
Q

What drug should moya moya patients be given lifelong?

A

Aspirin!

161
Q

What is the angiographic staging system for moya moya?

A

Suzuki staging

1- stenosis of ICP

2- development of moya moya vessels at base of brain

3- Increasing stenosis and prominance of vessels

4- Entire circle of willis occluded

5 - further progression

6 - Complete absence of major cerebral arteries and moya moya vessels

162
Q

What are the secondary causes of moya moya?

A

Atherosclerosis, autoimmune, meningitis, downs, NF-1, radiotherapy, sickle cell disease etc

163
Q

What imaging modality is needed to diagnose moya moya?

A

Unilateral - needs DSA

Bilateral - can be diagnosed on MRA

164
Q

What is the watershed shift phenomenon in moya moya?

A

Where the retrograde blood supply from the STA-MCA interferes with the antegrade supply from the MCA resulting in a decrease in CBF at the cortex in adjacent regions. More common in paediatrics than adults.

165
Q

What is cerebral hyperperfusion in moya moya?

A

After direct STA-MCA bypass at day 2-6, the increase in CBF causes a haemorrhage. Seen in 40% of adult moya moya cases.

166
Q

What is the optimal stroke management?

A

Thrombolysis and if unsuccessful within 30 mins proceed to mechanical thrombectomy (Trials = MRCLEAN, EXTEND 1A, ESCAPE, SWIFT PRIME and REVASCAT). Combined thrombolysis + thrombectomy doubles odds of favourable outcome compared to thrombolysis alone.

167
Q

What does the ASPECT score tell you?

A

Used to score how widespread strokes are. 1 point is reduced with every vascular territory involved. Scores <7 are associated with a worse functional outcome at 3 months.

168
Q

How would you treat a patient >70 years with a symptomatic carotid stenosis?

A

Endarterectomy safer than carotid stenting in older patients. Associated with higher risk of stroke and death but lower risk of MI.

169
Q

What is the evidence for Nimodipine in SAH?

A

British Aneurysm Trial 1989. Compared placebo with oral nimodipine 60mg 4 hourly and started within 4 days of SAH. Rate of cerebral infarction and mortality fell from 33% with placebo to 22% with nimodipine.

170
Q

What are risk factor for rebleeding?

A

Hypertension >175 mmHg systolic Female Large aneurysm

171
Q

What is the equation for cerebral O2 delivery (DO2)?

A

DO2 = CBF x arterial blood oxygen content

172
Q

What is the equation for arterial blood oxygen content?

A

= Sats x Hb x 1.34

173
Q

What is the equation for cerebral perfusion?

A

CPP = MAP - ICP

174
Q

What is the equation for cerebral blood flow?

A

CBF = CPP / CVR (cerebral vascular resistance)

175
Q

How can CBF be optimised following SAH?

A

Due to autoregulation increasing CPP does not improve CBF. Avoid hypotension using NorAd (if low HR) or Phenylephrine (if normal HR). Maintain euvolaemia Maintain normal ICP Sats 100% Hb 8-10

176
Q

What was the NEWTON-2 trial?

A

RCT comparison of sustained-release intrathecal Nimodipine vs oral nimodipine. No difference in outcomes.

177
Q

What is the SAHaRA trial?

A

Comparison of Hb >8 vs Hb>10 for SAH. Still on-going.

178
Q

How do you manage SAH?

A

Admit to ICU HOB 30 and bed rest Fluids 3L AEDs 7 days if aneurysm unsecured Laxative Analgesia Antiemetics BP control Nimodipine PPI

179
Q

What is the evidence for statins in SAH?

A

STASH trial 2014. No benefit with simvastatin 40 mg

180
Q

What increases the risk of DNID?

A

Hyponatraemia by 3x

181
Q

What is the cause of low Na in SAH?

A

Cerebral Salt Wasting

182
Q

Are seizures a predictor of outcome following SAH?

A

Yes, 65% with seizures compared to 23% without. Treat with AEDs for one week until aneurysm secure.

183
Q

What is the rebleed rate of an unsecured aneurysm?

A

20% @ 14 days and 50% @ 6 months

184
Q

What is the evidence for TXA in SAH?

A

Reduces the rebleed rate prior to definitive treatment from 10% to 2%. Hillman et al JNS 2002. Dose of TXA is 1 gram every 6 hours.

185
Q

What is the action of E-aminocaproic acid?

A

Reduces conversion of plasminogen to plasmin. Reduces the risk of rebleed but increases DNID rate.

186
Q

What is neurogenic stress cardiomyopathy?

A

AKA stunned myocardium due to catecholamine surge resulting in reduced cardiac contractility and output. 10% may progress to MI.

187
Q

What proportion of SAH patients have ECG changes?

A

50% - thought to be due to subendocardial ischaemia or coronary artery spasm from catecholamine surge

188
Q

What is the treatment for neurogenic pulmonary oedema?

A

Ventilation with low PEEP and normalisation of ICP

189
Q

What is the main time of risk for vasospasm?

A

3-17 days (peak incidence 6-8 days)

190
Q

What are the clinical features of vasospasm?

A

Non-localising = headache / reduced conciousness / confusion ACA syndrome = incontinence confusion leg weakness MCA syndrome = hemiparesis aphasia and parietal lobe syndromes

191
Q

What vessel wall changes are seen with aneurysms?

A

Less elastin and thin muscle in the tunica media

192
Q

What should be considered if a patient has a peripheral / distal aneurysm?

A

Mycotic aneurysm

193
Q

Where do fusiform aneurysms tend to occur?

A

Vertebrobasilar system

194
Q

What is the most common aneurysm location?

A

ACom 30% PCom 25% MCA 20% Basiar 10% Vertebral 5% *30% of patients has multiple aneurysms

195
Q

Through which structure do ACom aneurysms rupture through to cause IVH?

A

The lamina terminalis

196
Q

What visual field defect is normally seen with opthalmic artery aneurysms?

A

Nasal quadrantanopia

197
Q

What visual field defect is normally seen with Acom aneurysms?

A

Chiasmal syndrome (bitemporal hemianopia + optic atrophy)

198
Q

Why do intracavernous aneurysms cause facial pain>

A

Compression of V1 or V2 in the cavernous sinus

199
Q

Which conditions are associated with aneurysms?

A

Mnemonic - PF ME HEMAN Polycystic kidney disease Fibromuscular dysplasia Marfan’s Ehler’s Danlos type 4 HHT Endocarditis MEN type 1 AVMs NF1

200
Q

What % of patients with AD polycystic kidney disease develop intracerebral haemorrhages?

A

15% - mostly MCA. There is a 10 fold increase in SAH with these patients compared to the general population. Screening with MRA every 5 years may be beneficial.

201
Q

What is Hunterian ligation?

A

Ligation of the ICA or CCA for giant aneurysms. Usually needs bypass to prevent strokes.

202
Q

Which studies compare Clipping vs Coiling?

A

ISAT BRAT Finnish study Chinese study

203
Q

Summarise ISAT methodology

A

>2000 patients enrolled (from 10,000 eligible) Between 1997-2002 - mostly europe, canada and australia Stopped prematurely as there was a 7% absolute risk reduction with coiling (31% vs 24%) at 1 year of poor outcome

204
Q

What are the criticisms of ISAT?

A

Only 20% of eligible patients were enrolled - selection bias Expertise of surgeons vs interventionalists not reported 90% of aneurysms were <1 cm and 97% were anterior circulation. Probability of independent survival at 5 years was no different between groups.

205
Q

Summarise the BRAT trial

A

North American version of ISAT. Intention to treat - had high cross over from coil to clip. Difference 34% vs 20% poor outcome with clipping at one year but no difference at 3 years except posterior circulation aneuryms were better at all time time points with coiling.

206
Q

What are the results of the meta-analysis of clip vs coil trials?

A

Lanzino et al 2013 pooled data from Finnish/ISAT/BRAT at one year and showed that poor outcome at one year was less with coiled patients but mortality was unchanged. Rebleeding rates within the first month were higher with coiling.

207
Q

Which aneurysms favour clipping?

A

Treatment decisions should be MDT: MCA Wide neck Associated haematoma requiring evacuation Mass effect of aneurysm causing CN3 palsy Younger age

208
Q

What is the advantage of early aneurysm occlusion?

A

Removes early rebleed risk Facilitates treatment of complications e.g. vasospasm Overall mortality is reduced Allows clot removal decompressing the brain

209
Q

What is the risk of bleeding from a neck remnant after clipping?

A

4% over 10 years - occurs when the clip is no perpendicular across the neck leaving a dog ear

210
Q

How do you reduce the CMR02?

A

Barbiturates e.g. thiopentone titrated to isoelectric EEG. Also helps to redirect blood flow to ischaemic cortex.

211
Q

What is the maximum time for temporary clipping?

A

5 minutes

212
Q

When can aneurysm rupture occur during surgery?

A

Initial exposure - due to increased transmural pressure when opening the dura Aneurysm dissection - tearing with blunt dissection Clip application - inadequate exposure causing clip to penetrate aneurysm

213
Q

What is the rate of recurrence after clipping?

A

1% @ 5 years

214
Q

Which aneurysm may present with DI or hypothalamic dysfunction?

A

ACom

215
Q

What are the angiographic considerations with suspected ACom aneurysms?

A

If the ACom is not visualised on the DSA then cross compression is needed to visualise contrast flowing through the communicating segment.

216
Q

How do you approach ACom aneurysms?

A

Frontally biased pterional craniotomy

217
Q

How do you position for ACom aneurysms?

A

Shoulder roll Head turned 60 degrees

218
Q

What are the surgical steps in clipping an ACom aneurysm?

A

Subfrontal dissection > Olfactory > Optic > ICA > ACA. Drain CSF from optic and carotid cisterns and prox sylvian fissure split. Following A1>A2 ipsi. Identify contra A2 and A1. Proximal control Gyrus rectus resection may be needed. Circumferential neck dissection. **Watch out for Heubner!

219
Q

Where does Heubner arise?

A

A2 and runs backwards to the anterior perforated substance

220
Q

What approach is needed for distal ACA approaches?

A

Interhemispheric. Note prolonged retraction on the anterior cingulate may cause mutism or incontinence (persistent dribbling)

221
Q

Label the common carotid DSA

A
  1. Common carotid
  2. ICA
  3. Ascending pharyngeal
  4. Occipital
  5. Superficial temporal
  6. MCA
  7. ACA
  8. Middle meningeal
  9. Maxillary artery
  10. Facial artery
  11. Lingual
  12. ECA
  13. Superior thyroid

(Note: Posterior auricular artery not shown)

222
Q

What segment of the ICA is this?

A

Petrous segment

223
Q

What segment of the ICA is this?

A

Petrous segment

224
Q

Label the branches of the ICA

A

Petrous = Vidian / caroticotympanic / persistent stapedial

Cavernour = Inferior lateral trunk, Meningohypophysial trunk and McConnell’s capsular artery

Clinoidal = Opthalmic / PCom / Ant Choroidal

225
Q

Where is the A2 ACA?

A

From ACom to pericallosal / callosomarginal bifurcation

227
Q

What are the vascular territories of the ACA branches?

A
229
Q

What is the head position for PCom clipping?

A

Head turned 30 degrees to contralateral side

230
Q

How do you perform a PComm aneurysm clipping?

A

Pterional approach - head turned 30 deg

Subfrontal identification of olfactory nerve

Follow back to find Optic nerve

Look laterally to find ICA

Open arachnoid around optic and ICA to relax brain and gain prox. control

Proximal sylvian fissure split

PComs usually point lateral, posterior and inferion under the free edge of the tentorium

231
Q

How do you position the head for MCA clipping?

A

45 degree head turn to contralateral side

233
Q

What are the anatomical considerations for clipping of opthalmic artery aneurysms?

A

Opening of the falciform ligament to decompress the optic nerve. Removal of the anterior clinoid. Drilling down of the optic strut. Opening the distal dural ring to allow low exposure to the neck. Proximal control needed from the cervical cartoid.

235
Q

What is the dentate ligament?

A

Pial extensions from the spinal cord to the dura composed of 21 pairs of fibrous structures. These connect to the spinal cord between the ventral and dorsal roots.

237
Q

What approach is used to clip PICA aneurysms?

A

Far lateral. Clip placed below the CN9/10 complex but above the CN11.

Temporary lower CN palsies are common so may need to keep patient intubated after. Consent for the need for tracheostomy!

238
Q

What are the branches of the A2?

A

Orbitofrontal and Fronto-polar arteries (may arise from a common stem)

240
Q

What is the Drake approach for Basilar tip aneurysms?

A

Subtemporal transtentorial through Kawase’s triangle.

Alternative is through an OZ using the carotid-oculomotor triangle. Needs anterior and posterior clinoid processes to be drilled.

241
Q

What is a fetal PCom?

A

Where the PCA fills from the anterior circulation. The P1 is usually the same size as the PCom.

245
Q

What direction do opthalmic artery aneurysms project?

A

Medially and dorsally towards the optic nerve. 50% present with visual field defects (uniocular superior nasal quadrantiopia)

247
Q

What is Allcock’s test?

A

Vertebral DSA injection with carotid compression to allow patency of the flow from the posterior circulation to the anterior circulation through the PCom to be assessed.

249
Q

What is the cause of a fusiform aneurysm of the vertebral artery?

A

Dissection

251
Q

What is the most common posterior circulation aneurysm?

A

Basilar tip

252
Q

How are the heights of basilar tip aneurysms classified?

A

In relation to the posterior clinoid process (supraclinoidal, clinoidal and infraclinoidal)

254
Q

How do you decide which side to approach an ACom aneurysm from?

A

Based on the dominance of the A1, projection of the dome to allow direct access to the neck, dominant hemisphere and side of the cranial nerve palsy (if present)

255
Q

What are direct fistulas (aka dural AVM / dural AVF)?

A

Arteries connecting to veins without a nidus (tangle of abnormal vessels)

256
Q

Define an AVM?

A

A collection of dysplastic vessels where an artery feeds into a vein without any capillary bed.

257
Q

How do you classify AVMs?

A

Parenchymal, dural and mixed. Parenchymal are pial, subcortical, paraventricular or combined.

258
Q

Which hereditary syndrome is associated with AVMs?

A

HHT

259
Q

What age are AVMs diagnosed?

A

Most <40years. Present with haemorrhage, seizures, mass effect, ischaemia (steal phenomenon)

260
Q

What is the rupture rate for an AVM?

A

2-4% unless there are high-risk features such as flow aneurysms where the risk rises to 8%. Rupture risk is higher if purely deep drainage and prior haemorrhage.

261
Q

How do you calculate the culmulative risk of haemorrhage?

A

= 1 - annual risk bleed ^ expected years left to live or = 105 - age in years (assuming a 3% annual rupture rate)

262
Q

What is the Spetzler-Martin grade for AVMs?

A

Size (<3 = 1, 3-6 = 2 and >6 cm =3) Deep venous drainage (Yes =1) Eloquent (Yes =1)

263
Q

What is the Lawton-Young supplementary grade for AVMs? (ABC)

A

Age (<20y=1, 20-40y=2, >40y=3) Bleed (No =1) Compact/Diffuse nidus (Diffuse =1)

264
Q

What are the findings of the ARUBA (A Randomized trial of Unruptured Brain AVM) trial?

A

By 5 years the risk of any intervention is (surgery, SRS, embolization or a combination) greater than conservative management. Problem with ARUBA is that the follow up is too short.

265
Q

What is the role for SRS in AVM management?

A

Small <3 cm Deep Down-staging

266
Q

What is normal perfusion pressure breakthrough?

A

Swelling and haemorrhage after AVM resection due to loss of autoregulation.

267
Q

What are developmental venous anomalies associated with?

A

Cavernomas (so do a GRE or SWI)

268
Q

What is the characteristic finding of a cavernoma on MRI?

A

Popcorn lesion

269
Q

What do cavernomas look like histologically?

A

Sharp demarcation from neuropil. Large blood filled vascular spaces separated by connective tissue. Haemosiderin ring. May calcify.

Stains for vWF. No smooth muscle. Electron microscopy shows abnormal endothelial tight junctions.

271
Q

What is a risk factor for developing cavernomas?

A

Radiotherapy

272
Q

What is the inheritance of genetic cavernomas?

A

Dominant.

CCM1 = hispanics KRIT1 mutation

CCM2 = Malcavernin gene

CCM3 = PDCD10. For 3 new cavernomas per year.

273
Q

How do you define a haemorrhage from a cavernoma?

A

Angioma alliance definition:

Acute or subacute symptoms (headache, seizure, impaired conciousness or worsening neurological deficit) with radiological evidence of haemorrhage. An increase in size is not part of the defintion.

274
Q

What is the risk of cavernoma rupture?

A

0.1-2% annual rupture rate for incidental cavernomas

Risk of bleeding increased x5 if previous bleed and x4 if brainstem location.

5% annual risk in familial cases.

5% 5 year risk of seizures

275
Q

When should you operate on a brainstem cavernoma?

A

After a second bleed

276
Q

What is the evidence for SRS for cavernomas?

A

Can be considered for deep inaccessible lesions but on real evidence. Some suggestion that it reduces haemorrhage risk after 2-3 years.

277
Q

What are dural AV fistulas?

A

Where the vascular fistula is contained within the dura. Unlike AVMs these are considered to be acquired not congenital. Usually found adjacent to venous sinuses (most commonly the transverse/sigmoid). Thought to be secondary to venous thrombosis.

278
Q

What is the most common presenting feature of dural AVF?

A

Pulsatile tinnitus > occiptial bruit > headache > visual impairment / papilledema

279
Q

Why do dAVFs bleed?

A

Cortical venous reflux / hypertension

280
Q

What type of DSA is needed to evaluate a dAVF?

A

6 vessel

281
Q

What is the Borden classification?

A

1 - dAVF drains into sinus with normal antegrade flow

2 - dAVF drains into sinus but also has retrograde flow into cortical vein

3 - dAVF drains into cortical vein causing venous hypertension

282
Q

What is the Cognard classification?

A

Used more for transverse-sigmoid dAVFs:

1 - dAVF flows into sinus with normal antegrade flow

2a - dAVF flows into sinus with normal antegrade flow but also has retrograde flow within the sinus (20% haem risk)

2b - dAVF flows into sinus with normal antegrade flow but also has retrograde flow into cortical vein (10% haem risk)

2a+b - combination of above (66% haem risk)

3 - direct drainage into cortical vein only without venous ectasia (40% haem risk)

4 - direct drainage into cortical vein only with venous ectasia (65% haem risk)

5- drainage into spinal perimedullary veins (50% risk of venous congestive myelopathy)

283
Q

Which dAVF locations are through to have more aggressive behaviour?

A

Tentorial > Sylvian > Ethmoidal

284
Q

When should you treat a dAVF?

A

Cortical venous drainage

Neurological deficit

Bleed

Orbital venous congestion

Refractory headache / pulsatile tinnitus

285
Q

What are the treatment options for dAVFs?

A

Manual carotid compression (with the hand on the side of the compression). 10 minutes a day and then increase.

Endovascular embolization. Transarterial (onyx) or transvenous (coils).

Surgery by ligation of the fistula point with outflow vein. Surgery best for ethmoidal and tentorial dAVFs.

286
Q

When do vein of galen malformations form?

A

<3 months embyro.

These are fed from medial and lateral post. choroidal, anterior choroidal, pericallosal, mesencephalic and meningeal arteries.

287
Q

How do vein of galen malformations present?

A

Congestive heart failure in the first few weeks of life and a cranial bruit.

Hydrocephalus may be from aqueduct compression or increased venous pressures.

288
Q

How are vein of galen malformations treated?

A

Endovascular embolisation - arterial access is through the umbilical artery or femoral puncture. Cyanoacrylate glue is used to target the shunt in a staged fashion.

289
Q

What is the classical triad of presentation of a CCF?

A

Chemosis / pulsatle proptosis and ocular bruit

290
Q

What are the types of carotico-cavernous fisutal?

A

Type A = Direct (from ICA)

Type B = Indirect (from meningeal branches)

291
Q

How do you treat CCFs?

A

25-50% of low flow CCFs thrombose so observe if vision is not at risk. Try carotid compression.

High flow CCFs need embolisation - transarterial with coils deployed at the fistulas point through the ICA or transvenous through the superior ophthalmic vein (entered via the supraorbital vein through an eyebrow incision).

293
Q

What drain becomes engorged with CCFs?

A

Superior opthalmic vein

295
Q

What demographic are predominantly affected by FMD?

A

Middle-aged women (cervical ICA 75%) and bilateral 60%

Classic ‘string of beads’ appearance

296
Q

What investigation would you perform for a young patient with a spontaneous SDH?

A

CT angiogram to rule out PCom aneurysm

297
Q

What proportion of perimesencephalic haemorrhages are actually due to an aneurysm?

A

4%

298
Q

In which direction do superior hypophyseal arteries point?

A

Medially under the optic nerve toward the sella

299
Q

Where do ACom perforators supply?

A

Fornix, corpus callosum and septal region

300
Q

What can Heubner occlusion cause?

A

Hemiparesis or aphasia

301
Q

What is the management of a rupture during coiling?

A

Stop the bleeding by packing with coils if possible

Check pupillary reflexes and perform CT head

Insertion of external ventricular drain if required

Clinical reassessment regarding need for surgical intervention

302
Q

How does the basilar artery form embryologically?

A

From the union of paired longitudinal neural arteries that fuse at 5th week of gestation. Failed fusion may result in duplicate basilar arteries or a fenestration.

303
Q

What CN palsy is associated with large SCA aneurysms?

A

CN3

304
Q

Why do traumatic dissecting aneurysms form at the P2/3 junction?

A

As this is where the PCA crosses the tentorium resulting in trauma to the vessel and subsequent pseudoaneuryms formation

305
Q

What mutation is responsible for AD polycystic kidney disease?

A

PKD1 on Ch16

306
Q

Which gene is mutated in Marfan’s disease?

A

Fibrillin-1 (Ch15)

307
Q

Which gene is mutated in Ehlers-Danlos syndrome?

A

Multiple mutations including COL5A, COL3A and COL1A

308
Q

What is the NNT for malignant MCA decompressive hemicraniectomy?

A

4 to survive with a mRS of 3 or less

309
Q

What scleral vessels are seen with CCFs?

A

Corkscrew scleral vessels

310
Q

What are the features of Wallenberg’s syndrome?

A

Ipsilateral sensory loss to the face (spinal trigeminal nucleus damage)

Ipsilateral Horner’s (hypothalamo-spinal tract fibres)

Ipsilateral ataxia (Inf cerebellar peduncle / vestibular nuclei)

Contralateral fine touch loss (gracile / cuneate nuclei)

Loss of gag reflex (nuc ambiguus and solitary nucleus)

Contralateral hemibody loss of pain and temperature (spinothalamic tract)

311
Q

What is Dejerine Roussy syndrome?

A

Thalamic stroke resulting in contralateral body pain and hemisensory loss

312
Q

Label the skull base triangles

A
  1. Oculomotor triangle
  2. Opticocarotid triangle
  3. Supratrochlear triangle
  4. Infratrochlear triange (Parkinson’s triangle for access to the intracavernous ICA)
  5. Anteromedial triangle (Mullan’s triangle) between V1/V2
  6. Anterolateral triangle between V2/3
  7. Posterior lateral triangle (Glassock’s) Lateral to V3 - access to petrous cavernous ICA
  8. Posterior medial triange (Kawase) - access to anterolateral brainstem
  9. Inferior lateral - access to Meckel’s case
  10. Inferior medial - access to Dorello’s canal
313
Q

What is Balint syndrome?

A

Optic ataxia resulting in loss of voluntary but not reflex eye movements. Due to bilateral parieto-occipital injury (Bilateral P2 strokes)

314
Q

What is top of the basilar syndrome?

A

Opthalmoplegia

Behavioural abnormalities

Somnolence / hallucinations

No motor defect.

Due to Bilateral rostral midbrain and posterior thalamus damage

315
Q

What did the Japanese moya moya trial show?

A

Compared EC-IC bypass to conservative management for Moya Moya disease. Surgery reduces the risk of rebleed and stroke / haemorrhage at 5 years

317
Q

What are the STICH trials?

A

STICH1 randomized all ICHs >2cm with GCS>5 to surgery or conservative management where there was equipoise. No difference in outcomes but suggestion that superficial haematomas do better.

STICH2 randomised superficial ICHs <1cm from cortex with volume 10-100ml. No difference in outcomes. Suggestions that early surgery may be better if GCS9-12.

318
Q

How was the WFNS SAH grading scale derived?

A

From expert opinion based on the results of the Cooperative Aneurysm study in 1988.

The most important predictor of death of disability was the level of consciousness.

The most important predictor of disability was hemiparesis or aphasia.

WFNS grading is a good predictor of outcome with an unfavourable outcome at 3 months in 13% of Grade 1s and 66% of Grade 5s.

319
Q

What was the intention of the Hunt and Hess grading scale (1968)

A

To guide the timing of aneurysm clipping based on surgical risk. They found meningeal reaction alone (confusion) increases surgical risk.

1 = Minimal headache

2 = Severe headache, nuchal rigidity or cranial palsy

3 = confusion / drowsy

4 = Stupor / hemiparesis / decerebrate

5 = Deep coma / decorticate

*Add one point for severe comorbidity

320
Q

What factors determine the management of aneurysmal SAH?

A

WFNS grading (Good grade 1-3 vs low grade 4 &5) Rate of deterioration Age Haematoma Mass effect Hydrocephalus

321
Q

How do manage a patient with an MCA aneurysm and temporal lobe haematoma?

A

If low GCS and large ICH then priority is to treat raised ICP through medical management (raise HOB, I&V, pCO2, mannitol). Decompressive craniectomy and superficial clot evacuation. To prevent re-rupture - TXA, BP control Delayed aneurysm clipping / coiling.

322
Q

What factors do you consider when choosing the approach for an ACom aneurysm clipping?

A

Dominant hemisphere Projection of the dome Dominance of the parent vessel (for proximal control) Open / closed A2 complex

323
Q

What are the absorption spectra for metHb, oxyHb and bilirubin?

A

MetHb = 410 nm

OxyHb = 415 nm

Bilirubin= 450 nm

FRCS Part 2 (17 decks)

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