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
Previous
Damage Intra cerebral venous pressure
Smoking, Connective BP Relative Estrogen Blood
Sickle Cell Congenital
Alcohol, tissue with SAH Deficiency Transfusio Decreased BMI
disease AVM
HTN Disease n Direct Bleeding Venous blood leakage from Rupture and bleeding through
Increased stress
from AVM susceptible vessels adventitia layer
on intracerebral
vessel
Deceased
endothelium Mechanism Unknown
Abnormal
endothelial Blood Flow
integrity

Development of Saccular Aneurysm

Rupture of Saccular Aneurysm

Diagnostics: Hemorrhage LEGEND:

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

Puncture Coma and Death MANIFESTATIONS

Hydrocephalus

Manifestations: DIAGNOSTICS
Manifestations: Increased ICP
• Seizures
• Diplopia • Severe
Oculomotor
• Ptosis Headache
nerve • Nausea
• Visual Loss
compression
• Vomiting