SAH TOSCE

A 46 year old gentleman was brought to the Emergency Department by ambulance

following a witnessed fall to the ground with loss of conscious. Minutes previously he
had reported the onset of a severe occipital headache. He had presented to the Emergency
Department one week previously with a headache and was discharged home with a
diagnosis of tension headache.

What is the most likely diagnosis?

Subarachnoid Headache

List 3 differential diagnoses:

Seizure
Infectious meningo-encephalitis
Space-Occupying Lesion

Outline your immediate management:

ABC
Cardiac Monitoring
Collateral History
Urgent Non-contrast CT Head
Finger-Stick Glucose
Laboratory Tests: FBC, Electrolyes, Glucose, Electrolytes, Toxicology Screen, Cardiac
Enzymes, ABG
12- Lead ECG
LP-send for cell count, microscopy, cultures, sensitivity, protein, glucose, xanthochromia
(not usually detectable until at least 8 hours post bleed onset)
4-Vessel Cerebral Angiography: CT/MR

Later that evening a lumbar puncture is performed.

CSF analysis the revealed the follwing:

Sample 1 2 3

RCC (/mm3) 18,600 19,300 17,900

WCC (/mm3) 19 21 18

CSF Protein (mg/dL) 55 {15-45}

CSF Glucose (mmol/L) 5.2
Serum Gucose (mmol/L) 3.4

G stain No organisms seen

Opening pressure (cm H2O) 30 {6-20}
Comment on the results above:

High RCC in 3 serial samples-consistent with SAH

Mild elevation in WCC as a result of presence of blood in CSF (if Peripheral Blood WCC
is normal, allow for approx. 1 white cell per 500-1500 red cells in CSF)
Protein elevated as a result of presence of blood in CSF (allow apprx. 1mg/dL rise in
CSF protein per 1000 red cells in CSF)
Normal CSF glucose (at least 2/3 blood glucose)

Outline your management following confirmation of the diagnosis:

Surgical Clipping/Endovascular Coiling

Admit to ICU-continuous haemodynamic monitoring

Reduce haemodynamic fluctuations with analgesia/stool softeners
Stop anticoagulants/antiplatelets & reverse anticoagulation

Reduce ICP: Ventriculostomy-monitor ICP (high in SAH due to hydrocephalus).

Prevent Rebleeding: Placement of ventriculostomy reduces systemic HTN and reduces

risk of rebleeding. MAP-ICP=CPP, therefore CPP often reduced in SAH.

Management if no ICP monitoring available:If alert, CPP is ok, therefore can give
labetolol to lower SBP<140 to prevent rebleeding. If reduced level of consciuosness, this
may be due to reduced CPP therefore do not lower BP as if MAP falls, CPP also falls by
above equation.
Do not give vasodilators (GTN/nitroprusside) to lower BP-increase intracerebral bld
vol.)

Prevent Vasospasm: Nimodipine 60mg q4hr, within 4 days (shown to improve outcome in
SAH).
Use Trans Cranial Doppler to monitor for vasospasm-may see changes on TCD several
days before clinical deterioration. Vasospasm occurs w/in several days and may cause
cerebral ischaemia/infarction (acute neuro change). Acute neuro change could also
represent a rebleed.
Triple H therapy-haemodilution, induced HTN with pressors, hypervolaemia- may be of
some benefit(inconclusive).
Intrathecal urokinase-reduces vasospasm.
Intra-arterial/intrathecal vasodilators
Intra-arterial angioplasty
Statin - start within 2/7-continue until discharged from ICU-may reduce vasospasm.

Treat hypoxaemia, hyperglycaemia(>10mmol/L), metabolic acidosis(HCO3<20), CVS

instability (MAP<70,>130)- these factors are associated with increased mortality and
disability at 3/12.
Antiepileptics - not routine. May be associated with a worse outcome.
Antifibrinolytics-do not improve outcome.

Screening for recurrence (RR of recurrence is 22 compared to normal cohort).

If aneurysm is treated with surgical clipping , CTA should be performed at 3/12 and 6/12.

If endovascular coil-Plain Film of skull to look for evidence of aneurysm recanalisation,

eg coil displacement-Digital Subtraction Angiography if suspect same.
Routine DSA at 3/12.

Screen 1st degree relatives: 3-5x increased risk.

What complications are associated with this condition?

Rebleed
Vasospasm-cerebral infarction
Hydrocephalus-obstruction to CSF outflow by blood products/adhesions. Impaired CSF
reabsorption at arachnoid granulations-place ventricular drain
ICP increase-multifactorial
Hyponatraemia-due to SIADH(normovolaemic) or cerebral salt wasting(volume deplete)
Seizures
CVS complx due to autonomic dysfxn (?posterior hypothalamic hypoperfusion with
increased myocardial catecholamine release), increased myocardial O2 demand.
LV subendocardial ischaemia- ST depression, QT prolongation, deep symmetric T wave
inversions, and prominent U waves. torsade de pointes, AF, A flutter,LV RWMAs,
Takotsubo CM
Hypothalamic/pituitary dysfunction