Analysis of Cerebral Hemorrhage and Hypertension: A Nursing Case Study
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Case Study
AI Summary
This case study presents the case of Mr. X, a 60-year-old male diagnosed with cerebral hemorrhage and hypertension. The assignment details his medical history, including a history of hypertension, smoking, and alcohol use, and his presenting symptoms such as severe headache, nausea, and weakness. The case study outlines the diagnostic tests performed, including a non-contrast head CT scan, and the patient's vital signs. The pathophysiology of cerebral hemorrhage is discussed, including the causes and types of hemorrhage (extra-axial and intra-axial). The case study further examines the impact of atherosclerosis and hypertension on the development of cerebral hemorrhage. Nursing interventions are proposed, focusing on monitoring neurological status, assessing blood pressure, and providing interventions to improve cerebral perfusion. The case study includes SMART goals for the patient's care and rationale for the nursing interventions. The patient's non-compliance with prescribed diets and medications is highlighted as a contributing factor to his condition.
Running header: CEREBRAL HEMORRHAGE AND HYPERTENSION 1
Cerebral hemorrhage and hypertension
Student’s name
Institutional
Cerebral hemorrhage and hypertension
Student’s name
Institutional
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A. Background
Case presentation
Mr. X a 60 year old male driver from Australia, married and having six children the youngest
being twenty years old, retired driver (was a driver) and cigarette smoker was admitted to the
nursing unit from his physician’s office. He was diagnosed with cerebral hemorrhage and
hypertension. He complained of a severe headache, nausea and vomiting, weakness on the arm
and the leg, trouble with vision and swallowing. Three months ago he was treated with
hypertension, with a blood pressure of 170/100 and a reduced urine creatinine removal. He
complained of headache and blurred vision. He was recommended three months therapy which
included diet restriction such as avoidance of food with high cholesterol did not show a response
to the blood pressure elevation. His medical history showed that he had not been complying with
reduced sodium, cholesterol diet and medication that were prescribed to him. His social history
showed that he has been an alcohol addict and smoked five cigarette per day. An emergent non-
contrast head computed tomography showed a left frontal cerebral hemorrhage.
Signs and symptoms
Mr. X was admitted to the hospital complaining of the following sign and symptoms
- Severe headache
- Nausea and vomiting
- Weakness on the arm and leg
- Trouble with vision and swallowing
A. Background
Case presentation
Mr. X a 60 year old male driver from Australia, married and having six children the youngest
being twenty years old, retired driver (was a driver) and cigarette smoker was admitted to the
nursing unit from his physician’s office. He was diagnosed with cerebral hemorrhage and
hypertension. He complained of a severe headache, nausea and vomiting, weakness on the arm
and the leg, trouble with vision and swallowing. Three months ago he was treated with
hypertension, with a blood pressure of 170/100 and a reduced urine creatinine removal. He
complained of headache and blurred vision. He was recommended three months therapy which
included diet restriction such as avoidance of food with high cholesterol did not show a response
to the blood pressure elevation. His medical history showed that he had not been complying with
reduced sodium, cholesterol diet and medication that were prescribed to him. His social history
showed that he has been an alcohol addict and smoked five cigarette per day. An emergent non-
contrast head computed tomography showed a left frontal cerebral hemorrhage.
Signs and symptoms
Mr. X was admitted to the hospital complaining of the following sign and symptoms
- Severe headache
- Nausea and vomiting
- Weakness on the arm and leg
- Trouble with vision and swallowing
Running header: CEREBRAL HEMORRHAGE AND HYPERTENSION 3
Physical exam
The client was examined and his vital signs were as follows. Temperature of 36.9, blood pressure
of 155/133 mmHg, pulse 69, respiratory rate of 20 and oxygen saturation of 94 %. Both lungs
were clear during bilateral auscultation. The client had a normal heart rate with a regular S1 and
S2. There was no murmurs and the abdomen was soft with normal bowel sounds. In the
peripheral areas there was no sign of edema. Glasgow coma scale was done and the result was a
fifteen. He had a best eye response (E4), he was oriented to date and place (V5). He had a fluent
speech, his eye were reactive to light bilaterally.
Medical history
Mr. X was diagnosed with hypertension three months ago and he was given the following drugs.
Diuretics example hydrochlorothiazide so as to reduce the blood volume and cardiac output.
Adrenergic agents’ example clonidine hydrochloride which affects the central nervous system
leading to a reduction in blood pressure. Vasodilator example hydralazine hydrochloride which
reduces resistance in the periphery.
Diagnostic test results
Patient Control
White blood cell 9.7 4-11
Hemoglobin 10.4 11.5-15.5
Platelets 231 150-450
Creatinine 2.34 0.5-1.2mg/dl
Blood urea nitrogen 54 6-20 mg/dl
Potassium 4.4 3.5-5.5 mmol/l
Physical exam
The client was examined and his vital signs were as follows. Temperature of 36.9, blood pressure
of 155/133 mmHg, pulse 69, respiratory rate of 20 and oxygen saturation of 94 %. Both lungs
were clear during bilateral auscultation. The client had a normal heart rate with a regular S1 and
S2. There was no murmurs and the abdomen was soft with normal bowel sounds. In the
peripheral areas there was no sign of edema. Glasgow coma scale was done and the result was a
fifteen. He had a best eye response (E4), he was oriented to date and place (V5). He had a fluent
speech, his eye were reactive to light bilaterally.
Medical history
Mr. X was diagnosed with hypertension three months ago and he was given the following drugs.
Diuretics example hydrochlorothiazide so as to reduce the blood volume and cardiac output.
Adrenergic agents’ example clonidine hydrochloride which affects the central nervous system
leading to a reduction in blood pressure. Vasodilator example hydralazine hydrochloride which
reduces resistance in the periphery.
Diagnostic test results
Patient Control
White blood cell 9.7 4-11
Hemoglobin 10.4 11.5-15.5
Platelets 231 150-450
Creatinine 2.34 0.5-1.2mg/dl
Blood urea nitrogen 54 6-20 mg/dl
Potassium 4.4 3.5-5.5 mmol/l
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Albumin 3.4/7.2
Alanine aminotransferase/
Asparate aminotransferase
19/34 Up to 33U/L
Bilirubin 0.39 Up to 1.1 mg/dl
blood glucose 199
pH 7.46
partial pressure of carbon
dioxide
30-4
Bicarbonate 19.5
Medication
- Albumin, IV dose: 100u
- Hydrocortisone, IV dose: 50mg
- Cloxascillin, IV dose: 19m
- Phenytoin, IV dose: 100mg
- Levophed IV dose
Pathophysiology
Brain hemorrhage is defined as bleeding around the brain, it is either caused by raptured
aneurysm also known as hemorrhagic stroke or head trauma. Brain hemorrhage is divided into
two types, extra-axial hemorrhage meaning outside the brain tissue and intra-axial hemorrhage
Albumin 3.4/7.2
Alanine aminotransferase/
Asparate aminotransferase
19/34 Up to 33U/L
Bilirubin 0.39 Up to 1.1 mg/dl
blood glucose 199
pH 7.46
partial pressure of carbon
dioxide
30-4
Bicarbonate 19.5
Medication
- Albumin, IV dose: 100u
- Hydrocortisone, IV dose: 50mg
- Cloxascillin, IV dose: 19m
- Phenytoin, IV dose: 100mg
- Levophed IV dose
Pathophysiology
Brain hemorrhage is defined as bleeding around the brain, it is either caused by raptured
aneurysm also known as hemorrhagic stroke or head trauma. Brain hemorrhage is divided into
two types, extra-axial hemorrhage meaning outside the brain tissue and intra-axial hemorrhage
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which is within the brain tissue. Extra-axial bleeding is also known as intracranial bleeding, this
is the bleeding within the skull. Examples of the extra-axial bleeding include the epidural,
subdural and subarachnoid. Intra-axial hemorrhage include the intracerebral hemorrhage and
intraventricular hemorrhage.
Extra-axial hemorrhage is bleeding that occurs within the skull but outside the brain tissue. An
epidural hemorrhage is a hemorrhage that occurs between the skull and the dura membrane. It’s
often as a result of trauma to the head. The bleeding that occurs between the dura and the skull is
often from the middle meningeal artery. Clinical manifestation include altered consciousness,
headache, vomiting, confusion and aphagia. Subdural hemorrhage is the hemorrhage that occurs
below the dura matter. The hemorrhage occurs between the dura matter and the sub-arachnoid
membrane. The source of blood is often from the bridging veins. Clinical manifestation of
subdural hemorrhage are the same are those occurring in epidural hemorrhage. The final type of
extra-axial hemorrhage is the subarachnoid. The bleeding occurs mostly in the subarachnoid
space. It is often as a result of the cerebral artery specifically an aneurism within the artery. The
most common cause, is a rapture of a saculam type of an aneurism which leads to subarachnoid
hemorrhage. The clinical manifestation are the same as those mentioned above except that in
subarachnoid hemorrhage there is a sudden severe headache, loss of consciousness and
meningismus. Causes of epidural hematoma include head trauma such motor vehicle accident,
falls and assault.
Intracerebral hemorrhage is divided into two, lobam hemorrhage which is the hemorrhage that
occurs on specific lobes in the brain, thalamic hemorrhage which is the hemorrhage that occurs
in the thalamus pontine hemorrhage which is the hemorrhage that occurs in the pons and lastly
which is within the brain tissue. Extra-axial bleeding is also known as intracranial bleeding, this
is the bleeding within the skull. Examples of the extra-axial bleeding include the epidural,
subdural and subarachnoid. Intra-axial hemorrhage include the intracerebral hemorrhage and
intraventricular hemorrhage.
Extra-axial hemorrhage is bleeding that occurs within the skull but outside the brain tissue. An
epidural hemorrhage is a hemorrhage that occurs between the skull and the dura membrane. It’s
often as a result of trauma to the head. The bleeding that occurs between the dura and the skull is
often from the middle meningeal artery. Clinical manifestation include altered consciousness,
headache, vomiting, confusion and aphagia. Subdural hemorrhage is the hemorrhage that occurs
below the dura matter. The hemorrhage occurs between the dura matter and the sub-arachnoid
membrane. The source of blood is often from the bridging veins. Clinical manifestation of
subdural hemorrhage are the same are those occurring in epidural hemorrhage. The final type of
extra-axial hemorrhage is the subarachnoid. The bleeding occurs mostly in the subarachnoid
space. It is often as a result of the cerebral artery specifically an aneurism within the artery. The
most common cause, is a rapture of a saculam type of an aneurism which leads to subarachnoid
hemorrhage. The clinical manifestation are the same as those mentioned above except that in
subarachnoid hemorrhage there is a sudden severe headache, loss of consciousness and
meningismus. Causes of epidural hematoma include head trauma such motor vehicle accident,
falls and assault.
Intracerebral hemorrhage is divided into two, lobam hemorrhage which is the hemorrhage that
occurs on specific lobes in the brain, thalamic hemorrhage which is the hemorrhage that occurs
in the thalamus pontine hemorrhage which is the hemorrhage that occurs in the pons and lastly
Running header: CEREBRAL HEMORRHAGE AND HYPERTENSION 6
cerebellar hemorrhage which occurs in the cerebellar. Intracerebral hemorrhage is the most
common cause of stroke.
Cerebral atherosclerosis leads to a condition known as hypertension which is defined as a
systolic blood pressure of more than 140mmHg and a diastolic pressure of more than 90mmHg
over a long period of time. Cerebral atherosclerosis is caused by several factors. First, high levels
of triglycerides and cholesterol in the blood which destroys the endothelium. Second, high blood
pressure which is caused by two forces the first is the pressure created by the heart as it pumps
blood and the other is resistance in the arteries during blood flow. The harder it is for the blood
to flow, the higher the blood pressure. This rapid increase of blood pressure damages the arteries.
The third and the last is cigarette smoking. Tobacco particles exacerbate atherosclerosis in the
following ways, the tobacco smoke contains toxins which reduce high density lipoprotein while
increasing the levels of low density lipoproteins. Carbon monoxide and nicotine found in
cigarette smoke destroys the endothelium increasing the risk of plaque formation. Lastly is high
blood pressure, smoking by a hypertensive person may increase the risk for malignant
hypertension which is a life threatening form of high blood pressure. Atherosclerosis is
characterized by fat deposit known as atheroma that infringe on the lumen of the large arteries in
the brain. Macrophages which develop from T lymphocytes and monocytes infiltrate the area and
eat away the lipids and then die. This causes the proliferation of the smooth muscle cell forming
a dead fatty core. This plaque causes an obstruction in the blood flow due to narrowing.
Tiny arteries take blood to deep areas in the brain. High blood pressure causes the rapture of the
thin walled arteries releasing blood into the tissues. The clotted blood which is enclosed in the
rigid skull causes the buildup of fluid which leads to an increase in pressure (Demchuk and
cerebellar hemorrhage which occurs in the cerebellar. Intracerebral hemorrhage is the most
common cause of stroke.
Cerebral atherosclerosis leads to a condition known as hypertension which is defined as a
systolic blood pressure of more than 140mmHg and a diastolic pressure of more than 90mmHg
over a long period of time. Cerebral atherosclerosis is caused by several factors. First, high levels
of triglycerides and cholesterol in the blood which destroys the endothelium. Second, high blood
pressure which is caused by two forces the first is the pressure created by the heart as it pumps
blood and the other is resistance in the arteries during blood flow. The harder it is for the blood
to flow, the higher the blood pressure. This rapid increase of blood pressure damages the arteries.
The third and the last is cigarette smoking. Tobacco particles exacerbate atherosclerosis in the
following ways, the tobacco smoke contains toxins which reduce high density lipoprotein while
increasing the levels of low density lipoproteins. Carbon monoxide and nicotine found in
cigarette smoke destroys the endothelium increasing the risk of plaque formation. Lastly is high
blood pressure, smoking by a hypertensive person may increase the risk for malignant
hypertension which is a life threatening form of high blood pressure. Atherosclerosis is
characterized by fat deposit known as atheroma that infringe on the lumen of the large arteries in
the brain. Macrophages which develop from T lymphocytes and monocytes infiltrate the area and
eat away the lipids and then die. This causes the proliferation of the smooth muscle cell forming
a dead fatty core. This plaque causes an obstruction in the blood flow due to narrowing.
Tiny arteries take blood to deep areas in the brain. High blood pressure causes the rapture of the
thin walled arteries releasing blood into the tissues. The clotted blood which is enclosed in the
rigid skull causes the buildup of fluid which leads to an increase in pressure (Demchuk and
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Buchan, 2014). The created pressure can compress the brain against the bone or cause a
herniation. The distributed blood in the tissue causes a decrease in blood supply in the arteries
called a stroke (Alberts, Hademenos and latchaw, 2013). Blood cells contained within the clot die
releasing toxins which cause further damage to the brain cells around the hematoma.
A swelling occurs leading to a buildup pressure in the affected area. It’s caused by blood pools in
the brain due to blood vessel break. The blood pressure formed cannot be released out through
the bone, it pushes and compresses the brain causing damage. The damaged area of the brain
affects the body system. Individuals may go through loss of memory, lingering impairments, a
delay in reaction time and also death.
Discussion of the pathophysiology
Mr. X lived a sedentary lifestyle which included, cigarette smoking and unhealthy diet which
included food with high cholesterol intake and sodium intake. This caused abnormal
accumulation of fats in the blood vessels leading to cerebral atherosclerosis (Fredman and
Rosenman, 2015) hence leading to intracerebral hemorrhage. Fat deposition causes narrowing of
the blood vessels which leads to a condition known as hypertension. Hypertension signs and
symptoms include severe headache and blurred vision as witnessed in Mr. X. The client never
complied with the doctors instructions on high cholesterol restriction and treatment therapy. His
main reason for not complying was that he had been busy with work all day. Since the
hypertension was left untreated for a long time it resulted to the collapsing of the thin arteries in
the brain leading to a release of blood into the brain tissues, leading to a condition known as
cerebral hemorrhage which was evidenced by severe headache, nausea and vomiting, weakness
Buchan, 2014). The created pressure can compress the brain against the bone or cause a
herniation. The distributed blood in the tissue causes a decrease in blood supply in the arteries
called a stroke (Alberts, Hademenos and latchaw, 2013). Blood cells contained within the clot die
releasing toxins which cause further damage to the brain cells around the hematoma.
A swelling occurs leading to a buildup pressure in the affected area. It’s caused by blood pools in
the brain due to blood vessel break. The blood pressure formed cannot be released out through
the bone, it pushes and compresses the brain causing damage. The damaged area of the brain
affects the body system. Individuals may go through loss of memory, lingering impairments, a
delay in reaction time and also death.
Discussion of the pathophysiology
Mr. X lived a sedentary lifestyle which included, cigarette smoking and unhealthy diet which
included food with high cholesterol intake and sodium intake. This caused abnormal
accumulation of fats in the blood vessels leading to cerebral atherosclerosis (Fredman and
Rosenman, 2015) hence leading to intracerebral hemorrhage. Fat deposition causes narrowing of
the blood vessels which leads to a condition known as hypertension. Hypertension signs and
symptoms include severe headache and blurred vision as witnessed in Mr. X. The client never
complied with the doctors instructions on high cholesterol restriction and treatment therapy. His
main reason for not complying was that he had been busy with work all day. Since the
hypertension was left untreated for a long time it resulted to the collapsing of the thin arteries in
the brain leading to a release of blood into the brain tissues, leading to a condition known as
cerebral hemorrhage which was evidenced by severe headache, nausea and vomiting, weakness
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on the arm and leg, trouble with vision and swallowing and lastly an emergent non-contrast head
computed tomography which showed a left cerebral hemorrhage (Pfohman and Criddle, 2015).
Brain hemorrhage is the leading cause of the severe headache due to the leaking cerebral
aneurism. The small arteries around the brain which deliver oxygen around the brain bulge and
form an aneurysm. The aneurism causes outflow blood to tissue which causes tissue irritation
hence the severe headache. Weakness in the arm and the leg is due to loss of voluntary motor
movements. Damage of motor neurons located in the opposite side of the brain is the leading
cause of weakness of the arm and the leg. Mr. X visual disturbance is due to damage of the
sensory pathways located between the eye and visual cortex. The high blood pressure of 155/133
is due narrowed arteries caused by accumulation of fat lipids in the blood vessel.
on the arm and leg, trouble with vision and swallowing and lastly an emergent non-contrast head
computed tomography which showed a left cerebral hemorrhage (Pfohman and Criddle, 2015).
Brain hemorrhage is the leading cause of the severe headache due to the leaking cerebral
aneurism. The small arteries around the brain which deliver oxygen around the brain bulge and
form an aneurysm. The aneurism causes outflow blood to tissue which causes tissue irritation
hence the severe headache. Weakness in the arm and the leg is due to loss of voluntary motor
movements. Damage of motor neurons located in the opposite side of the brain is the leading
cause of weakness of the arm and the leg. Mr. X visual disturbance is due to damage of the
sensory pathways located between the eye and visual cortex. The high blood pressure of 155/133
is due narrowed arteries caused by accumulation of fat lipids in the blood vessel.
Running header: CEREBRAL HEMORRHAGE AND HYPERTENSION 9
Actual or Potential problem
1. Ineffective cerebral perfusion related to bleeding evidenced by changes in vital signs
SMART nursing
goal(s)
a) The client
will show
Improvemen
t cerebral
perfusion
within two
months
evidenced
by strong
peripheral
pulses and
vitals within
the normal
range.
Nursing interventions Rationale Strategies to determine
effectiveness of actions
Actual or Potential problem
1. Ineffective cerebral perfusion related to bleeding evidenced by changes in vital signs
SMART nursing
goal(s)
a) The client
will show
Improvemen
t cerebral
perfusion
within two
months
evidenced
by strong
peripheral
pulses and
vitals within
the normal
range.
Nursing interventions Rationale Strategies to determine
effectiveness of actions
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1. Check for alteration in
blood pressure by
comparing both readings
in both arms
Make sure the left
arm is has rested
at the heart level
The patient
should avoid
taking caffeine or
tobacco at least
one hour before
taking the
measurement
(Papakonstaninou
, 2016).
1. A variation in blood
pressure may happen
when the vasomotor area
is injured. Blockage of
blood due to clot formation
may result to an increase in
intracranial pressure. If the
results show that there is
in readings of both arms
this will signify the
presence of a blockage in
subclavian artery (Qureshi,
Tuhrim and Broderick,
2015).
Placing the clients arm at
the arms rest instead of
the right atrial level may
result to high blood
pressure values. This may
be important during the
diagnosis and later
treatment actions for
clients with hypertension.
Caffeine intake results to a
striking increase in blood
pressure since caffeine
blocks a hormone that
assists in the widening of
the arteries and it also
enhances the adrenaline
glands to release more
adrenaline which cause a
1. Attains an
optimum cerebral
tissue perfusion
The patients
understands
the effects
caffeine and
tobacco in his
body
The client
attains a
normal blood
pressure
The clients
shows no sign
of standing
hypotension
1. Check for alteration in
blood pressure by
comparing both readings
in both arms
Make sure the left
arm is has rested
at the heart level
The patient
should avoid
taking caffeine or
tobacco at least
one hour before
taking the
measurement
(Papakonstaninou
, 2016).
1. A variation in blood
pressure may happen
when the vasomotor area
is injured. Blockage of
blood due to clot formation
may result to an increase in
intracranial pressure. If the
results show that there is
in readings of both arms
this will signify the
presence of a blockage in
subclavian artery (Qureshi,
Tuhrim and Broderick,
2015).
Placing the clients arm at
the arms rest instead of
the right atrial level may
result to high blood
pressure values. This may
be important during the
diagnosis and later
treatment actions for
clients with hypertension.
Caffeine intake results to a
striking increase in blood
pressure since caffeine
blocks a hormone that
assists in the widening of
the arteries and it also
enhances the adrenaline
glands to release more
adrenaline which cause a
1. Attains an
optimum cerebral
tissue perfusion
The patients
understands
the effects
caffeine and
tobacco in his
body
The client
attains a
normal blood
pressure
The clients
shows no sign
of standing
hypotension
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sudden increase in blood
pressure
(Papakonstaninou, 2016).
2. The client attains a
normal
neurological status
The client
open his
eyes on
request
He follows
command
with
appropriat
e motor
response
The client
show no
evidence if
increased
intracrania
l pressure
The client
speaks
eloquently
The client
pupils
reacts
normally
to light
2. Asses and check the
neurological status
Monitor pupils’ size,
reaction to light, and
equality.
Assess and document the
changes in vision and give
an account for blurred
vision and any change in
depth perception or visual
field.
Monitor the higher
functions which include
speech and if the patient
is alert
Check for factors that are
associated with the
client’s condition for
reduces cerebral
perfusion and risk for
increased intracranial
pressure.
2. It monitors the courses in the
degree of consciousness and a
possible raise in intracranial
pressure. It is useful in finding the
position, extension and the
progress of damage (Marmarou
and Butcher, 2012).
Any alteration in the
client’s pupil’s reaction is
an indication of an
increased intracranial
pressure and the
compaction of the optic
nerve. The oculomotor
cranial nerve controls pupil
reaction and it is important
in finding out whether the
brain stem is damaged. The
pupil’s size assessment is
important in ascertaining
the equilibrium between
the sympathetic and
parasympathetic
innervation. Reaction to
light is shows a joined
function of the oculomotor
and optic cranial nerve.
Pupil’s reaction to light
sudden increase in blood
pressure
(Papakonstaninou, 2016).
2. The client attains a
normal
neurological status
The client
open his
eyes on
request
He follows
command
with
appropriat
e motor
response
The client
show no
evidence if
increased
intracrania
l pressure
The client
speaks
eloquently
The client
pupils
reacts
normally
to light
2. Asses and check the
neurological status
Monitor pupils’ size,
reaction to light, and
equality.
Assess and document the
changes in vision and give
an account for blurred
vision and any change in
depth perception or visual
field.
Monitor the higher
functions which include
speech and if the patient
is alert
Check for factors that are
associated with the
client’s condition for
reduces cerebral
perfusion and risk for
increased intracranial
pressure.
2. It monitors the courses in the
degree of consciousness and a
possible raise in intracranial
pressure. It is useful in finding the
position, extension and the
progress of damage (Marmarou
and Butcher, 2012).
Any alteration in the
client’s pupil’s reaction is
an indication of an
increased intracranial
pressure and the
compaction of the optic
nerve. The oculomotor
cranial nerve controls pupil
reaction and it is important
in finding out whether the
brain stem is damaged. The
pupil’s size assessment is
important in ascertaining
the equilibrium between
the sympathetic and
parasympathetic
innervation. Reaction to
light is shows a joined
function of the oculomotor
and optic cranial nerve.
Pupil’s reaction to light
Running header: CEREBRAL HEMORRHAGE AND HYPERTENSION 12
should be quick and after
the light source is removed
the pupil should go back to
its original size. Lack of
reaction to light maybe
induced by a developing
mass, which can include a
blood clot which causes
pressure on the optic nerve
the third cranial nerve; the
unchanging pupil may be
due herniation of the
medial temporal lobe.
Any change in visual
alteration shows the areas
of the brain involved.
Stroke causes blurred
vision and headache.
Any alteration in speech
content and cognition is a
signal cerebral involvement
and the location of
damage. It may also
indicate and increased
intracranial pressure.
The assessment will
influence and establish the
alternative of intervention.
Failure of the neurological
signs may show a reduced
intracranial adaptive
capacity which may force
should be quick and after
the light source is removed
the pupil should go back to
its original size. Lack of
reaction to light maybe
induced by a developing
mass, which can include a
blood clot which causes
pressure on the optic nerve
the third cranial nerve; the
unchanging pupil may be
due herniation of the
medial temporal lobe.
Any change in visual
alteration shows the areas
of the brain involved.
Stroke causes blurred
vision and headache.
Any alteration in speech
content and cognition is a
signal cerebral involvement
and the location of
damage. It may also
indicate and increased
intracranial pressure.
The assessment will
influence and establish the
alternative of intervention.
Failure of the neurological
signs may show a reduced
intracranial adaptive
capacity which may force
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