PATHOPHYSIOLOGY (SUMMARY)

The precipitating factors that include stress and hypertension together

with the predisposing factors (age, gender, diabetes mellitus, family history,
history of stroke, hyperlipidemia, cigarette smoking, and race) would cause
an increase blood flow to the brain causing now the disruption and
compromise of the cerebral arterioles’ integrity thus resulting to the
deposition of lipid and hyaline materials in the arterial wall. This event would
eventually weaken the walls forming the Chalcot- Bouchard aneurysm. This
aneurysm is common to hypertensive clients. Through imaging using the MRI
and CT scan, the degree of bleeding caused by the rupture of aneurysm will
be seen and identified. The degree and severity of the bleed will also be
established. As of the case of our patient, the left frontal lobe was the
affected area so most probably; the artery that had ruptured was the
anterior cerebral artery. This artery supplies blood to the frontal lobe. Base
on the symptoms manifested by our client, the rupture of the artery had
caused inflammation, alteration in the brain component, hematoma
formation and presence of blood in the interstitial areas of the brain.

The inflammatory process had triggered the occurrence of fever, and

through the laboratory examination, a leukocytosis might develop. Alteration
in the brain component , hematoma formation and also inflammation would
cause an increase in the intracranial pressure of IC. An increase in the ICP
could be observed with the patient’s manifestation of the following;
restlessness, changes in LOC, sudden headache, confusion, and drowsiness.
Diagnostic examination such as cerebral angiography, PET scan, would verify
this finding. An the ICP increases, the body would initiate compensatory
mechanism to restore homeostasis and prevent complications. As a
compensatory mechanism, the body would initiate three regulatory
mechanisms. The first one is autoregulation in which continual cerebral
perfusion of brain tissue regardless of changes in systemic arterial pressure
happens. The second is CSF regulation. It will regulate the production and
reabsorption of the CSF with any changes in intra cerebral perfusion. The last
mechanism is the metabolic regulation in which a decrease in the oxygen
being fed to the brain and subsequent increase in the carbon dioxide would
cause vasodilation. Vasodilation occurs to permit increase blood to the brain.
But with the on going compensatory mechanisms, on going damage to the
brain will also accompany it. There will be decrease oxygen supply, further
swelling amd edema, and compression of the brain components will further
happen. Uf the compensatory mechanisms are not that effective, a decrease
in ocygen supply would eventually precede to ischemia causing an
irreversible damage and death of the neurons. Furthermore, the ischemia
causes scar formation that can be seen through x- rays, CT scan and MRI.
Ischemia would stimulate the vasomotor centers to increase the systemic
pressure to maintain cerebral blood flow and to prevent further damage.
These occurrences will be manifested through a slow bounding pulse, and
through respiratory irregularities. Another effect of ischemia is the alteration
in the function of the part of the brain affected. On our patient’s case, it is
the frontal lobe thus causing now the symptoms of Broca’s aphasia,
dysarthria, hemiparesis, and difficulty to or is incapable of abstract thinking.

Presence of free blood in the interstitial areas of the brain will stimulate
the formation of clots or thrombus and the destruction of the cell membrane.
This destruction would further cause cellular edema, vasospasm, electrolyte
imbalances and acidosis that through ABG and serum electrolyte test be
verified.

All of these complications if not treated at an early stage would further

lead to comatose, brain herniation, stupor and eventually death. But through
medical and surgical interventions, complications being discussed san be
prevented causing a FAIR OR GOOD PRONOSIS.