SUBARACHNOID HAEMORRAGE

1. Subarachnoid Haemorrhage
Dr. NITAY KUMAR GHOSH
Resident- Phase A
BSMMU

2. Subarachnoid Haemorrhage
Bleeding into the subarachnoid space (space
between the pia & arachnoid meningeal layers
where blood vessels lie & CSF flows.)

4. Epidemiology
• Incidence = 6/100000 people
• Immediate mortality : about 30%
• Recurrence: 40% in first 4 weeks, 3% annually
• Higher chance if:
• Female
• Middle-aged, usually before age of 65
• Abuse of stimulant drugs
• Connective tissue disorder
• Family history
• PCKD

5. Causes of SAH
• Rupture berry aneurysm 85-%
• Non aneurysmal or perimesencephalic haemorrhage-
10%
• Rupture AVM
• Vertebral Artery Dissection

6. SACCULAR (BERRY) ANEURYSM
• About 2% of adults harbor intracranial aneurysm.
• Size- 2mm to 3cm
• Average size- 7.5mm
• Those which rupture are usually 10mm or more but smaller ones can
also get ruptured.

7. What causes aneurysms to form?
• Defects in the media of the arteries
• Defects are thought to expand as a result of
hydrostatic pressure from pulsatile blood flow and
blood turbulence, which is greatest at the arterial
bifurcations
• Other theory says it is initiated by focal destruction of
internal elastic membrane caused by hemodynamic
forced acting at bifurcations & branching of arteries.
As a result of local weakness in vessel wall intima
bulges out covered only by adventetia.

8. Common Sites of Berry Aneurysm
•ACOM (30%)
•PCOM (25%)
•MCA (20%)

9. Common sites of aneurysm

10.  Most unruptured intracranial aneurysms are completely
asymptomatic
 Aneurysms can undergo small ruptures and leaks of blood into the
subarachnoid space, so called Sentinel bleeds.
 Symptoms are usually due to rupture .
 Although some present with mass effect on cranial nerves or brain
parenchyma.
Clinical Manifestations

11. With rupture, Subarachnoid hemorrhage cam
follow three patterns of presentations:
 Patient is stricken with severe headache & vomiting,
and falls unconscious immediately.
 Severe generalized headache occurs suddenly with
varying degrees of neck stiffness.
 Patient can become unconscious without any preceding
complaint. If bleeding is massive patient may die in
minutes to hours. So ruptured aneurysm should be
considered in the differential diagnosis of sudden death.

12. Headache
• A sudden, severe, ‘thunder-clap headache’
• Often in occipital region
• Lasts for hours or days
• Often accompanied by
Vomiting
Raised blood pressure
Neck stiffness
• Commonly occurs during physical exertion(45%
case), staining and sexual excitement.
• May loss consciousness at the onset.

13. What causes symptoms & signs?
• Blood leaking from the aneurysm
• Local pressure effects of the aneurysm
• Associated Intracranial Haemorrhage
• Emboli

14. What causes symptoms & signs?
• Blood leaking from the aneurysm
• Headache
• Meningism

15. What causes symptoms & signs?
 Local pressure effects of the aneurysm
Acom:
Visual symptoms due to optic chiasm
compression
Positive babinski.
Bilateral lower limb paresis
MCA
Contralateral hand & face paresis
Aphasia (dominant side)
ICA/Pcom
CNIII palsy.

16. What causes symptoms & signs?
 Associated ICH
The aneurysm usually lies within the subarachnoid
cisterns
It can become adherent to adjacent brain due to
adhesions (e.g. from a previous leak)
The bleed therefore can also extend into the brain
AVM is more likely to cause ICH as they usually
lie somewhat in brain parenchyma

17. What may I find on examination?
• Normal examination findings
• Patient usually distressed and irritable
• Photophobia
• Neck stiffness
• Confusion/memory loss
• Hemiparesis
• Aphasia
• CN abnormalities:
• CNII – papilloedema, usually mild initially &
retinal haemorrhages
• CNIII – palsy

18. DELAYED NEUROLOGICAL DEFECIT
• 1. RERUPTURE:
Incidence of re rupture in case of untreated aneurysm in the first
month following SAH 30% .
Peak in first 7 days .
Rerupture is associated with a 60% mortality rate and poor outcome .
Early treatment eliminate the risk .

19. • 2. HYDROCEPHALUS:
Acute hydrocephalus can cause stupor and coma .
Sub acute hydrocephalus may develop over a few days or weeks and
causes progressive drowsiness or slowed mentation with incontinence.
Chronic hydrocephalus may develop weeks to months after SAH &
manifest as gait difficulty , incontinence , or impaired mentation .

20. • 3. VASOSPASM :
The vasospasm usually occurs following subarachnoid hemorrhage and typically begins no
earlier than day three after hemorrhage and peak at days seven to eight. it is thought that the
blood clots release a spasmogenic substances following blot clots lysis which can result in
vasospasm. The vasospasm can lead to ischemia of the brain which is usually characterized as a
single cortical infarcts near the site of the ruptured aneurysm in most case. Ischemia of the
brain usually results in neurologic deterioration in level of consciousness or new focal
neurologic deficits.
Risk factors for developing vasospasm may include:
• Severe bleeding
• Bleeding the major intracerebral blood vessels
• Age less than 50 years
• Hyperglycemia

21. • 4. HYPONATREMIA:
Hyponatremia may be profound and can develop quickly in the first 2
weeks following SAH .
There is both natriuresis and volume depletion with SAH , so patient
become both hyponatremic and hypovolemic.
Both ANP & BNP have a role in this cerebral salt wasting syndrome .
Typically , it clears over the course of 1-2 weeks and, in the setting of
SAH , should not be treated with free water restriction .

22. Complications of SAH:
It can be acute, subacute, or chronic.
•Acute:
• Coma and brainstem herniation due to
increased intracranial pressure(ICP)
• Rebleeding
• Pulmonary edema ("neurogenic pulmonary
edema") as a result of the suddenly increased ICP
• Cardiac arrhythmiasand myocardial damage
• Hydrocephalus, which may also happen in the
subacute time frame
•Subacute:
• Vasospasm, leading to ischemia of the brain
• Hyponatremia (low sodium levels) - due
to SIADH or cerebral salt wasting syndrome
•Chronic:
• Long-term immobility
• Pneumonia and pulmonary embolism (due to
immobility)
• SAH recurrence (20% within two weeks if the
aneurysm is not secured by clipping or coiling)
• Persistent neurologic deficits