Neuro - SAH

Question 1

Why is subarachnoid haemorrhage important?

Answer 1

• 5% of all strokes- high level of mortality and morbidity- 1/3 of survivors are dependent on carers1/2 have life-changing cognitive deficits

Question 2

What are the causes of subarachnoid haemorrhage?

Answer 2

1. Aneurysmal (ACOM, MCA bifurcation, PCOM)
2. AVMs
3. Trauma
4. Moyamoya disease

Question 3

What are the risk factors for SAH?

Answer 3

1. age 40-60 years
2. Hypertension
3. Atherosclerosis
4. Smoking
5. Alcohol abuse
6. Cocaine use
7. Inherited conditions: Autosomal dominant polycystic kidney disease, collagen vascular disease.

Question 4

How does SAH present?

Answer 4

• Classical thunderclap headache - possible sentinel bleed headache- Nausea and vomiting- Altered consciousness- Neck stiffness- Photophobia- Coma- Seizures

Question 5

How is SAH diagnosed?

Answer 5

1. Unenhanced CT
2. Lumbar puncture (after 12 hours symptom onset) for xanthochromia
3. Digital subtraction CT angiography
4. Cerebral angiography

Question 6

How is SAH graded?

Answer 6

Clinically or radiologically

Clinically - WFNS:
1 - GCS 15 and no motor defect
2 - GCS 13-14 and no motor deficit
3 - GCS 13-14 with motor deficit
4 - GCS 7-12
5 - GCS <7

Radiologically - Fisher CT criteria
1 - no blood seen
2 - blood layers <1mm thick
3 - Localised clots or blood layers >1mm
4 - Non-subarachnoid blood or intraventricular involvement

Question 7

What is the immediate management of SAH?

Answer 7

ABCDE approach to prevent secondary brain injury and focuses on neuroprotection.
A&B - control of airway in reduced consciousness and control of ventilation aiming pCO2 4.5-5.0 and pO2 >10C - Optimise BP to prevent ischaemia from raised ICP or worsen bleed - target BP 80110. Nimodipine to prevent delayed cerebral ischaemia/vasospasmD - seizure control and prevention of raised ICP, frequent pupil monitoring. Prompt CT scan. E - Normothermia, normoglycemia. D/W neurosurgical centre.

Question 8

What definitive management options are there for aneurysmal SAH?

Answer 8

• Protective measures against secondary brain injury and delayed cerebral ischaemia.- Clipping or coiling of an aneurysm (ISAT trial 2002 - coiling had lower death and dependence but higher re-bleed risk).- prevention and treatment of other non-neurological conditions/complications

Question 9

What is delayed cerebral ischaemia?

Answer 9

Vasospasm and delayed cerebral ischaemia (DCI) occurs in ≥60% of patients with
SAH.
The Neurocritical Care Society defines DCI as neurological deterioration related
to ischaemia (unrelated to treatment of the aneurysm) that persists for one hour
and has no other cause.
Vasospasm can be diagnosed when a patient exhibits symptoms and signs of
DND following SAH secondary to arterial narrowing that is demonstrable angiographically or with TCD. Incidence peaks at 4–10 days post-SAH, persists for
several days and is associated with a worse outcome. It is more common in
smokers and patients with high grade SAH or large clot size.
Transcranial Doppler is non-invasive and images flow velocity in the basal cerebral arteries. It is highly specific and moderately sensitive. Vasospasm is diagnosed if:
1 Flow velocities are >120 cm/s
2 Velocities increase >50 cm/s/day from baseline
3 Lindegaard ratio >3 (ratio of flow velocity in ipsilateral MCA and internal carotid artery

CT angiography is highly specific but may overestimate the degree of vasospasm. Digital subtraction angiograp

Question 10

What are the complications following SAH and how are they managed?

Answer 10

Neurological:
1. Obstructive hydrocephalus -> EVD
2. Re-bleeding ->Re-coiling/clipping
3. Seizures -> Exclude non-convulsive status, manage with AEDs.

Non-neurological:
- Respiratory: VAP/aspiration/ARDS/neurogenic pulmonary oedema
- CVS: Neurogenic stunned myocardium due NA release/Takotsubo cardiomyopathy/VTE
- Metabolic: fever, hyperglycaemia/hypoglycaemia/SIADH/CSWS/DI

Question 11

How is vasospasm prevented or treated?

Answer 11

Prevention and treatment of vasospasm includes:
1 Nimodipine
L-type CCBs relax arterial smooth muscle, and nimodipine appears to have
a particularly cerebro-selective effect. Nimodipine is administered routinely
(60 mg PO 4 hourly) for 21 days following SAH.
In 2006, the Cochrane collaboration performed a meta-analysis collecting
data from 12 randomised trials of the use of calcium antagonists including
nimodipine in patients following acute SAH. Administration of CCBs reduced
the risk of death or severe dependency (ARR 5.1%, NNT 20).
2 Triple H therapy
Triple therapy has been advocated traditionally and consists of:
i Hypertension – with vasopressor support if required to maintain cerebral
perfusion pressure
ii Haemodilution – to a haemoatocrit of 30–35%
iii Hypervolaemia – using crystalloid infusion targeting a CVP of 12 mmHg
The use of triple H therapy is controversial, with some small trials supporting
benefit with hypertension alone. However, it is important to avoid
hypovolaemia and hypotension.
3 Magnesium sulphate
The MASH-2 trial (Lancet, 2012) showed no improvement in outcome with IV
magnesium after aneurysmal SAH. Its routine use is not recommended (see
page 283).
4 Statins
Statins are HMG-CoA (3-hydroxy-3-methyl-glutaryl-CoA) reductase inhibitors
and have been shown to have anti-inflammatory effects. However, the STASH
trial (Lancet, 2014) did not detect any difference in long-term or short-term
outcome when compared with placebo. Patients with SAH should not be
treated routinely with simvastatin during the acute stages.
5 Antiplatelet therapy
Due to an increased risk of haemorrhagic complications, antiplatelets are only
recommended in situations in which stenting has been performed.
6 Endovascular intervention
Aggressive endovascular treatment (angioplasty and/or intra-arterial
vasodilator therapy) may improve neurological outcome. Suggested criteria
for the use of endovascular treatment include a new neurological deficit
without other cause, absence of cerebral infarction on CT, failure of medical
therapy, and vasospasm on angiography. There is no substantial evidence for
optimal timing or technique at present, although prophylactic use is thought
to involve greater risk than benefit and is not recommended.

Question 12

What is cerebral salt-wasting syndrome? Describe the
pathophysiology

Answer 12

Cerebral salt-wasting syndrome may occur following brain injury (typically SAH
or TBI) and is characterised by renal loss of sodium. There is polyuria, hyponatraemia and hypovolaemia. The precise pathogenesis is unknown but is likely to
be mediated by increased levels of ANP and BNP in combination with increased
sympathetic tone, contributing to increased renal perfusion pressure and subsequent natriuresis.

Question 13

How is CSWS diagnosed and what is the management?

Answer 13

The biochemical criteria for a diagnosis of CSWS are:
1 Low or normal serum Na+
2 High or normal serum osmolality
3 High or normal urine osmolality
4 Urinary sodium >40 mEq/l
5 Biochemical evidence of hypovolaemia (increased haematocrit, urea, bicarbonate and albumin)

Importantly, the daily sodium excretion exceeds intake resulting in low total
body sodium, and the patient will exhibit symptoms and signs of hypovolaemia.
In addition to treatment of the underlying cause, specific management of CSWS
involves correction of fluid and sodium depletion (see page 239 for detailed
management of hyponatraemia).
1 Fluid resuscitation with 0.9% saline is the mainstay
2 In acute symptomatic hyponatraemia, hypertonic (1.8% or 3%) saline is
recommended
– Furosemide may be used to minimise the risk of fluid overload
3 Once the patient is normovolaemic and normonatraemic, ongoing losses
should be matched with IV crystalloid and sodium tablets until CSWS resolves
(usually 2–4 weeks)
4 Refractory CSWS may necessitate fludrocortisone therapy (0.1–0.4 mg/
day)
– Limits natriuresis by increasing sodium reabsorption from the renal tubule
(aldosterone agonist)
– Monitor for hyperkalaemia