A comprehensive presentation on subarachinoid hemorrhage.

1. Spontaneous Subarachnoid
Haemorrhage:
Dr Idowu A. O

2. Outline
• Aim
• Introduction
• Epidemiology
• Pathophysiology
• Aetiology
• Risk factors
• Clinical manifestations

3. Introduction
• Subarachnoid hemorrhage (SAH) is the extravasation of blood into the
subarachnoid space between the pia and arachnoid membranes
• Stroke caused by subarachnoid hemorrhage is defined as rapidly
developing signs of neurological dysfunction and/or headache
because of bleeding into the subarachnoid space (the space between
the arachnoid membrane and the pia mater of the brain or spinal
cord) not caused by trauma. (AHA/ASA)

4. Epidemiology
• A study done by Imarhiagbe FA et al to profile all first-ever strokes
using cranial computed tomography (CT) scan among 334 patients at
UBTH in 2015. Totally, 251 had cerebral infarct (75.15%), 81 (24.25%)
had ICH, 2 (0.60%) had subarachnoid hemorrhage.
• The autopsy prevalence of unruptured aneurysm ranges from 0.2 t0
7.9% (Vlak et al)

5. Epidemiology
• Annual incidence of aneurysmal SAH in the United States is 6-16 cases
per 100,000 population, with approximately 30,000 episodes
occurring each year.
• The risk is higher in blacks than in whites
• The incidence of SAH in women is higher than in men (ratio of 3 to 2)
• Incidence increases with age and peaks around age 50 years.

6. Epidemiology
• Approximately 80% of cases of SAH occur in people aged 40-65 years,
with 15% occurring in people aged 20-40 years.
• Only 5% of cases of SAH occur in people younger than 20 years. SAH is
rare in children younger than 10 years, accounting for only 0.5% of all
cases.
• A multicenter study done in Kenya by Waweru et al in 2017. Of the 158
patients sampled, 38 (24.1%) died in hospital and 42 (26.6%) died within
1 month. In total, 87 patients were discharged home and followed-up in
this study, of which 72(45.6%) reported favourable functional outcomes

7. Risk factors
Modifiable Risk Factors
◆ Hypertension
◆ Smoking
◆ Heavy alcohol use
◆ Sympathomimetic drug use (e.g, cocaine, Amphetamine)

8. Risk factors
Nonmodifiable Risk Factors
◆ Increasing age (peak in fifth
and sixth decade)
◆ Female sex
◆ African American ethnicity
◆ Hispanic ethnicity
◆ Japanese or Finnish ethnicity
◆ Prior history of subarachnoid
hemorrhage
◆ Family history of
subarachnoid hemorrhage
◆ History of aneurysm in two
or more first-degree relatives
◆ Autosomal dominant
polycystic kidney disease
◆ Type IV Ehlers-Danlos
syndrome

9. Aetiology
• Ruptured Saccular aneurysm
• Rupture of arteriovenous malformations (AVMs)
• Ruptures from Mycotic aneurysm, Angioma, Neoplasm, Cortical
thrombosis

10. Aneurysms

11. Aetiology

12. Pathogenesis

13. Pathogenesis
• Saccular aneurysms occur at the bifurcations of the large- to medium-
sized intracranial arteries; rupture is into the subarachnoid space in
the basal cisterns and sometimes into the parenchyma of the
adjacent brain.
• As an aneurysm develops, it typically forms a neck with a dome. The
arterial internal elastic lamina disappears at the base of the neck. The
media thins, and connective tissue replaces smooth-muscle cells

14. Pathogenesis
• At the site of rupture (most often the dome), the wall thins, and the
tear that allows bleeding is often ≤0.5 mm long.
• Aneurysm size and site are important in predicting risk of rupture.
Those >7 mm in diameter and those at the top of the basilar artery
and at the origin of the posterior communicating artery are at greater
risk of rupture.

15. CLINICAL FEATURES
• Headache
• Severe, sudden onset "thunderclap headache“ (often occipital ) and usually described as
the worst headache ever.
•
• Sentinel headache:
• Occurs days to weeks (about 2-8wks) before an aneurysmal SAH which is perhaps due to a small
warning leak from an offending aneurysm.
• Nausea / Vomiting: ICP
• Photophobia
• Neck pain
• Loss of consciousness
• From sudden rise in ICP
• Transient/persistent – 50% at onset.
*Atypical presentation-Seizures,acute confusional state, intermittent loss of consciousness.

16. SIGNS (Focal physical findings)
SIGNS (Focal neurological deficits)
Findings Likely Cause
Third nerve palsy Usually PCoA
Sixth nerve palsy Elevated ICP(False localizing sign)
Hemiparesis and aphasia or visuospacial
neglect
MCA aneurysm,thick subarachnoid
clots,parenchymal hematomas
Bilateral leg weakness ACoA aneurysm
Opthalmoplegia ICA aneurysm impinging upon the cavernous
sinus
Unilateral visual loss or bitemporal
hemianopia
ICA aneurysmcompressing optic nerve or
optic chiasm
Neck stiffness,Kernig’s sign Meningeal irritation by the presence of
subarachnoid blood.
Impaired level of consciousness and impaired
upward gaze
Pressure on the dorsal midbrain due to
hydrocephalus
Retinal and subhyaloid hemorrhages,
Preretinal hemorrahages (Terson syndrome)
Sudden increase in ICP
Vitreous hemorrhage due to severe
elevations of ICP

17. Evaluation and Management

18. Clinical Evaluation
• The emergency evaluation and management of patients with SAH
should focus on the airway, breathing, and circulation (the ABCs).
• Patients unable to protect their airway should be intubated
immediately, which include patients in coma or stupor from
hydrocephalus or those with seizures.

19. Clinical Evaluation – take a brief and focused history
Before the LOC During the LOC – (ask a witness) After the LOC
Are there any warning signs
(aura/ pre-syncope)
Ask how the event unfolds Is the patient confused or sleepy
In what circumstances do the LOC
occur
Does the patient twitch or are
they stiff or floppy
Does the patient remember the
event and how much
Any preceding Fever, headache,
neck pain, neck stiffness,
photophobia, irrational behaviour
(Meningitis, Encephalitis)
Is there incontinence
Does the patient bite his tongue
Muscle ache /transient memory
loss - Seizure
Any preceding sudden severe or
thunderclap headache (SAH, ICH,
Carotid Artery Dissection)
How long does the LOC last
Any associated symptoms (Chest
pain , Palpitation, dyspnea)
Any comorbid medical condition

20. Diagnosis
• After resuscitation, brief history and physical examination, the next
step in diagnosis of SAH is with a non-contrast Cranial Computed
Tomography scan
Non-contrast CT
• Most sensitive imaging study in SAH
• Approximately 100% sensitivity if performed within 12hrs of
headache onset
 sensitivity of head CT changes over the first 7 days from
close to 100% - first 12 hours
93% - first day
60–85% - at 5 days
< 60% - at 7 days

21. Images
CT Features of SAH:
SA Hyperdensity
Clot around aneurysm, basal cistern, major fissures and within the ventricles
IVH, ICH, CI, Hydrocephalus
Other clue to the cause of the subarachnoid hemorrhage

22. Diagnosis
Falsely negative CT:
• Anemia ≤ 30% (blood is isodense with brain)
• Small-volume SAH
• Old SAH
• Interpretation skill
• Technical limitations (poor CT quality)
Lumbar puncture
• In cases of +ve or high suspicious history but –ve or equivocal CT, a lumbar
puncture is the immediate next recommended step
• R/o “Traumatic tap” (20% of all LPs)
• Xanthochromia
• most reliable
• Sensitivity = 100% b/w 12hrs & 2wks
• Spectrophotometry > visual inspection.
• High CSF pressure

23. Diagnosis
MRI – Head CT and MRI are considered to be equally sensitive in detecting
SAH in the first 2 days, however, due to greater availability, lower cost,
more rapid acquisition, and greater experience with CT interpretation,
Cranial CT remains the recommended first imaging modality.
 Superior to CT in detecting subacute or chronic SAH
• If MRI is used as the initial imaging test, an LP is still necessary if the MRI
is negative

24. Images

25. Diagnosis - identification of bleeding source
• Once SAH is confirmed by any means (CT, LP or MRI), Vessel imaging should
be the next step
• The gold standard of vessel imaging remains cerebral digital subtraction
catheter angiography (DSA) however CT angiography (CTA) has become
widely available and is now commonly performed as the first-line vascular
imaging in many institutions especially for unstable pts, in emergency settings.
• The sensitivity and specificity of CTA can range from 90% to 97% and 93% to 100%,
respectively, when compared to DSA.
• However, CTA may miss aneurysms as small as 4 mm or less.

26. Diagnosis - identification of bleeding source
• MR Angiography
• MRA may be useful for evaluating aneurysms and other vascular lesions
that cause SAH
• Less sensitivity for aneurysms smaller than 5mm
• Inability to evaluate small aneurysm contour irregularities

27. MRA, CTA and DSA Images

28. Investigations - others
• Serum E & U, Cr
• FBC + ESR
• Clotting profile (PT, PTTK, INR)
• Cardiac enzymes
• Lipid profile
• RBG
• Serology
• ECG: non specific ST and T wave changes, widespread giant T-wave inversion, Decreased
PR intervals, Presence of U waves, Prolonged QTc, Dysrhythmia (PVCs, SVT,
bradyarrhythmia)

29. Disease Severity scores
• The severity of neurological impairment and the amount of subarachnoid
bleeding on admission are the strongest predictors of neurologic
complications and outcome.
• There are several scoring systems available:
• World Federation of Neurological Surgeons scale(WFNSS)
• Modified Fisher scale – depicts risk of vasospasm
• Comprehensive grading scale - Ogilvy & Carter
• Hunt & Hess scale - surgical risk

30. Disease Severity scores
Periop Mortality
•0-5%
•2-10%
•10-15%
•60-70%
•70-100%

31. The World Federation of Neurological Surgeons
SAH Scale
WFNS Grade GCS Score Motor deficit
I 15 Absent
II 14-13 Absent
III 14-13 Present
IV 12-7 Present or absent
V 6-3 Present or absent

32. Treatment
• Admit in the ICU or Neurocritical care unit of high volume centers
• Early referral from low volume centers (<10 cases per year) to high
volume centers (>35 cases per year)
• Multidisciplinary management: Neurologist, Cerebrovascular
neurosurgeons, endovascular specialists and Specialist nurses.

33. Treatment
• Most are for prevention of rebleed
• Bed rest – reduces rebleed
• Nurse 300
head up
• Antihypertensives – titratable, short acting agent such as labetalol or
Nicardipine to balance the risk of stroke and hypertension-related rebleeding.
• Avoid nitroprusside or nitroglycerin
• Nimodipine 60mg 4hrly for 21days
• Prevents vasospasm, reduces cerebral ischemia, neurologic deficit, & mortality
• Target BP – SBP <160mmHg

34. Treatment
• IVF – Maintenance of euvolemia and normal circulating blood volume to
prevent delayed cerebral ischemia and maintain cerebral perfusion
• Cerebral decompression
• Mannitol, Furosemide
• Antifibrinolytic agents: For patients with an unavoidable delay in obliteration
of aneurysm, short-term (less than 72 hours) therapy with tranexamic acid or
aminocaproic acid can be used to reduce the risk of early aneurysm rebleeding
• 40-60% rebleed reduction
• Inhibit CSF fibrinolytic activity, stabilize aneurysmal clot.

35. Treatment
• Seizure prophylaxis – Phenytoin
• A very short course of prophylactic antiseizure medications should be used in the
immediate posthemorrhagic period because of a concern for seizure-related
aneurysm re-rupture
• Intermittent pneumatic pressure stockings
• Liberal use of anti-emetics is justified especially if vomiting occurs with
stool softeners
• Antipyretic - aggressive control of fever to a target of normothermia
• Glucose control - strict avoidance of hypoglycemia
Target 80 – 200mg/dl (4.4 – 11.1mmol/L)ncs

36.  A catheter guided by a wire is inserted
through the femoral artery and threaded all
the way to the affected brain artery
 The guide wire is removed
 A microcatheter carrying a soft platinum coil
is introduced inside the initial catheter and is
navigated into the aneurysm opening
 The coil is then deployed into the aneurysm
sac and a small electrical current is passed to
detach the coil from the catheter

37. Surgical Clipping

38. Preference for Treatment of Unsecured Aneurysms
Endovascular coiling Surgical clipping
Older age Aneurysm with wide neck-to-body ratio
poor clinical grade crucial arteries arising from aneurysm
dome
multiple comorbidities middle cerebral artery aneurysm
top of the basilar aneurysm aneurysm with large parenchymal
hematoma
aneurysm suitable for coiling or clipping

39. Complications
Neurologic:-
- Rebleeding
- Hydrocephalus (acute obstructive versus delayed communicating)
- Delayed cerebral ischemia
- Seizures
Medical:-
• Cardiopulmonary (ECG changes, Takotsubo Cardiomyopathy ,
Cardiogenic shock, Pulmonary edema)
• Thromboembolism(DVT) - 2% and 20%
• Glucose abnormalities
• Hyponatraemia (Cerebral Salt wasting > SIADH)

40. Rebleeding
• Most immediate life-threatening neurologic complication (first few minutes to
hours)
• mortality rate - 20% to 60%
- 50% to 90% occurring within the first 6 hours
• Clinical feature – sudden deterioration
• Best measure to reduce the risk of rebleeding
- early and rapid treatment of the unsecured, ruptured aneurysm
- aggressive blood pressure control
- seizure control
- treat pain and prevent Valsalva

41. Delayed Cerebral Ischemia
• Average 3 to 14 days after SAH.
• Pathophysiology
• Current evidence indicates that the pathophysiology of delayed cerebral
ischemia includes:
• an interaction of early brain injury, neuronal swelling & depolarization,
glutamate release
• Microthrombosis
• cortical spreading depolarizations and related ischemia, and
• cerebral vasospasm

42. Delayed Cerebral Ischemia
• Clinical feature : sudden decline in consciousness, focal neurological
deficits (may fluctuate, exacerbated by hypotension & hypovolemia).
• Conventional Angiography (DSA): definitive imaging study, reveals
vasoconstriction, delayed forward flow, evidence of collateral flow
• Transcranial Doppler USS: Abnormal absolute linear blood flow
velocity (LBFV) - Mild>120cm/s, mod. >160cm/s, sev. > 200cm/s

43. Delayed Cerebral Ischemia
• Prevention and Treatment
• Maintenance of euvolemia and normal circulating blood volume
• The standard treatment is maintain relative hypertension and mild
hypervolemic therapy (HHT)
• An IV fluid bolus (1 L to 2 L of 0.9% saline) and maintain fluids can
be instituted for euvolemia or mild hypervolemia.
• α1 receptor agonists (norepinephrine or phenylephrine) is the
preferred vasopressors of choice in SAH.

44. Differentials
• Meningitis / Meningoencephalitis
• Intracerebral Haemorrhage
• Cortical vein thrombosis
• Intracranial hypotension
• Intracranial arterial dissection
• Call-Fleming syndrome (RCVS)

45. Prognosis
• Age
• Neurologic deficit / impairment
• Amount of subarachnoid bleeding
• Hunt and Hess grade
• Hypertension
• History of Smoking
• Presence of complications
• Presence of comorbid conditions
• Location of aneurysm: Anterior circulation aneurysms better prognosis.
• Multiple aneurysms

46. Conclusion
• SAH is a devastating disease and the main area of emphasis when
caring for patients with SAH should include prompt diagnosis and
treatment, immediate transfer to appropriate centres, expeditious
diagnosis and treatment and overall good neurocritical care .

47. References
• Continuum Journal of American Academy of Neurology.
• AHA/ASA Guideline for the management of aneurysmal SAH
• Emergency Neurocritical Life Support
• Medscape Subarachnoid Haemorrhage

48. THANK YOU