ANEURYSMAL SUBARACHNOID HEMORRHAGE NON-ANEURYSMAL SUBARACHNOID HEMORRHAGE

MODIFIABLE FACTORS: NON-MODIFIABLE FACTORS:

1. Excessive alcohol intake 1. Sickle Cell disease
2. Congenital AVM NON-MODIFIABLE FACTORS:
2. Smoking
3. Relative with SAH 1. Congenital AVM
3. Sympathomimetic drugs MODIFIABLE FACTORS:
4. Estrogen deficiency 2. Cervical or Head Trauma
(eg. Caffeine, 1. Physical Exertion
5. Previous blood 3. Hypertension
amphetamines, cocaine)
4. Acute anger transfusion
5. Physical Exertion 6. Decreased BMI
7. Connective Tissue
Disease

Physical Exertion Cervical or Head Trauma HTN

Sympathomimetic AVM
Physical Exertion Drugs (Caffeine, Acute Anger/
Amphetamine, Startling Intra-thoracic Pressure Injure and tear intima layer of
Abnormal Blood
Cocaine Basilar artery
Flow
Jugular Venous return
Dissection of
Endothelial
Acute increased Media Layer
Damage Intra cerebral venous pressure
BP Previous
Smoking, Connective Relative Estrogen
Sickle Cell Congenital Blood Decreased BMI
Alcohol, tissue with SAH Deficiency
HTN Disease
disease AVM Transfusion Direct Bleeding Venous blood leakage from Rupture and bleeding through
Increased stress from AVM susceptible vessels adventitia layer
on intracerebral
vessel
Deceased Abnormal
endothelium Mechanism Unknown
endothelial Blood Flow
integrity

Development of Saccular Aneurysm

Rupture of Saccular Aneurysm

Hemorrhage LEGEND:
Diagnostics:

1. MRI MODIFIABLE FACTORS

Blood Obstruction on Arachnid Decreased Cerebral Blood Flow
Meningeal
2. Non Conrast Irritation
Villi
NON MODIFIABLE FACTORS
CT scan Transient Intacranial circulatory
arrest
3. Lumbar Nucchal
Disrupted
Reabsorption of CSF
DISEASE PROCESS
Puncture Rigidity

Hydrocephalus
Coma and Death MANIFESTATIONS
Manifestations: DIAGNOSTICS
Manifestations: Increased ICP
 Seizures
 Diplopia  Severe
Oculomotor Headache
 Ptosis
nerve  Nausea
 Visual Loss
compression  Vomiting