I.

Introduction

Spontaneous/Hypertensive Bleed, left basal ganglia

Spontaneous intracranial hemorrhage is a bleeding in the brain caused by

the breaking(rapture) of a blood vessel in the head. It may be cause by
trauma or abnormalities of the blood vessel. hypertension is the etiology.

Mortality/Morbidity

Spontaneous intracranial hemorrhage causes 10-20% of strokes and 15-20%

of stroke related deaths.

Race

The incidence of spontaneous intracranial hemorrhage may be higher than

white persons, since a higher incidence of hypertension is seen in black
persons younger than 45 years old.

Sex

Men have a 5-20% higher incidence of ICH than women.

Age

Of spontaneous intracerebral hemorrhage patients, 90% are older than 45

years old.

Risk Factors

• Hypertension
• Diabetes
• Current cigarette smoking
• Alcoholic drinks
• Caffeine

Significant of the Study

The goal of our case study is to explore areas of information regarding

spontaneous hypertensive bleeding. It aims to study about the following:
overview of the disease, signs and symptoms, causes, treatments,
complications, prognosis of patient experiencing hypertensive hemorrhage.

This research can assist student nurse, nurses and other health care member
in revealing and educating individuals and family members about
Intracranial hemorrhage treatment and intracranial recovery. This would
permit the development of appropriate strategies to target high risk group.

This study would aid us to understand how patient will live through and
expand to the experience of intracranial hemorrhage. This will help us in
providing proper approach and improve standard in providing proper
approach and improve standard of nursing care that wound maintain and
promote wellness of the patient with hypertensive bleeding(ICH).

I. A. Patients Data

Demographic Data:

Name: Mrs. Marlyn Matute

Address: #14 Looban Batal, Santiago City

Gender: female

Age: 45 years old

Date of Birth: June 17, 1964

Religion: Roman Catholic

Nationality: Filipino

Civil Status: Widow

Educational Attainment: College Graduate(BS Commerce)

Significant Others: Mary Ann Gollayan(sister) and Marites

Matute(daughter)

Admission Data:

Chief Complain: Dizziness accompanied with inability to speak

Date of Admission: June 24,2009

Time of Admission: 4:15 AM

Mode of Arrival: Received via wheelchair

Attending Physician on ER: Dra. Cabanilla

Attending Physician on Ward: Dra. Costales

Latest Vital Signs of the Patient as of July 06, 2009:

8:00 AM 12:00 NN

PR: 77 bpm 85 bpm

RR: 17 cpm 14 cpm

Temp: 36.7 36.5

BP: 150/100 160/110

 B. Nursing History

1) History of Present Illness

According to patient relatives, the patient is self medicating with

nifedipine 10 mg daily intake for 2 years to control her high blood
pressure. She did not seek medical advice from physician. Patient take
medication(nifedipine) as advice by her cousin who is a med tech by
profession.

On the night of June 23,2009 the patient is happily celebrating her

nephew’s birthday together with their other relatives but around
midnight, the patient suddenly loss her consciousness, she was carried
home and allow to rest, no medication was given. Around 3 to 4 in the
morning her partner noticed that Mrs. Matute was moaning and had SOB,
vomited 4 times and feels dizzy and nauseated. She’s also complaining of
chest pain, later on accompanied with inability/difficulty to speak. Her
blood pressure(BP) was taken by a medtech cousin and had a reading of
220/160 mmHg.

Noticing that the symptoms did not subside, her sister and daughter
decided to rush Mrs. Matute at Southern Isabela General Hospital(SIGH)
located at Santiago City. She was received via wheelchair at emergency
room(ER) and admitted for confinement at 4:15 AM of June 24, 2009. The
patient was attended by Dra. Cabanilla. The doctor ordered her to be on
NPO and Intravenous(IV) Therapy given. She had received Initial
Medications: Hydralazene 500 mg, Dexamethasone and citicolene.
Oxygen inhslstion is ordered every `1-2 hours.

2) Past Medical History

According to her sister, Mrs. Matute doesn’t haze any allergy to food
and drugs. She never experienced any serious medical condition during
her childhood except for common sickness like colds, fever and cough. No
known immunization received. Previous hospitalization was 6 years ago
for prolong menstrual bleeding. She had dilatation and curettage and
release from hospital after a day.

The patient is self medicating with nifedipine for control of high

blood pressure. She did not seek/consult medical advice from physician.

3) Family Medical History

According to her sister, their father side have history of

hypertension. Patient elder siblings(except the youngest) also have
hypertension and taking oral medication(nifedipine). No history of cancer
and diabetes.
4) Socio economic History

Patient is a college graduate. Works as saleslady at Washington

Construction Supply. She is the sole bread winner. She had raise her 3
children alone when she was widowed. To augment their family income,
she raised and sells pig.
C. Gordon’s Functional Pattern

1. Nutritional and Metabolic Pattern

The patient eating habit is regular meals a day, 3 times with

additional snack in the afternoon. She is fond of eating vegetables like
inabraw and adobong sitaw. Her food content usually contain protein like
fish, egg and meat; carbohydrates like rice and bread. During her
confinement, the patient usual dietary pattern and her nutritional needs
was disturbed since she wasn’t able to ingest food. Her doctor ordered
she was inserted with Nasogastric tube(NGT) and assisted during feeding.
Six(6) divided feedings of 1500 k cal osterized food via NGT was
prescribed.

2. Elimination

Prior to admission, patient’s urination and defecation are in regular

duration and quantity. She defecates 1-2 times a day and voids within
normal quantity without difficulty initiating. During hospitalization the
patient elimination pattern is affected, she hadn’t defecated for 4 days,
on the fifth day of confinement the doctor ordered to give
suppository(laxative) and defecated once. Hence, no change in quantity
of voiding, 3-4 adult diaper consume per day, patient felt pain upon
voiding(dysuria).

3. Activity-Exercise Pattern

According to her daughter, the patient has no daily exercises

activity but she considers walking to the market and her daily household
activities as her exercise. But during confinement there is a limited
physical movement, dressing and grooming. She looks lethargic, unable
to grasp firmly, can move extremities(abduct and adduct) slightly but
weak.

4. Sleep-Rest Pattern

According to her daughter, the patient had a normal sleep pattern,

she sleep 8 hours a night before hospitalization. She usually sleep at
around 8-9 o’clock in the evening and wakes up at around 4-5 o’clock in
the morning. During confinement, the patient always sleep even day time
but can be awaken from sleep when called. She is drowsy during first 4
days of hospitalization.

5. Cognitive Perceptual Pattern

During confinement the patient is still oriented with the significant

person and her location. She has no hearing and visual problems. She
seldomes communicate but when asked questions she reply in a clear
language but low voice volume.

6. Role Relationship Pattern

She is a very much concern with the future of her family, she is very
supportive to her 3 children since the death of her husband. She is a
strong willed woman performing both the roles and responsibilities as a
mother and father to her children prior to confinement, she is in charge to
all decisions regarding family matters. Hence, upon her hospitalization it
is her sister and daughter that taking care of her and her other children.
She will be brought home to her sister residence upon discharge for
recovery.

7. Sexual-Reproductive Pattern

She is living with a partner for two(2) years and has active sexual
life, uses oral contraceptive as birth control measure. She menstruate
regularly.

8. Coping-Stress Tolerance Pattern

According to her sister, the patient can easily decide on simple

problems but for complicated ones, she always consults her elder siblings
and her parents when they are still alive.

9. Value-Belief Pattern

The patient is a Roman Catholic, goes to church every Sunday, and

is an active participant of church activities. She also believes in Quack
Doctor.
 LABORATORY TEST
COMPLETE NORMAL RESUL TEST NORMAL RESUL INTERPRETATIO
BLOOD VALUES TS VALUES TS N
COUNT
HEMOGLOBI M: 130-180 ESR M:0-10 Within normal
N g/L 145 mm/hr range.
F: 110-160 g/ F: 0-20
L mm/hr
HEMATOCRIT M: 40-54 PETIC 5-15X10⁶/1 Within normal
F: 37-47 COUNT 0.5-1.5% range
WHITE CELL 5-10X10⁹/1 8.3 BLEEDING 1.3 min Within normal
COUNT TIME range
DIFFERENTIA CLOTTING 3-6 min Within normal
L COUNT TIME range
SEGMENTER 50-65% 85.3 BLOOD Increase in
S TYPING number signals
for presence of
inflammation.
LYMPHOCYT 25-35% 10.4 A patient was
ES given
dexamethasone(c
orticosteroids)
which may
decrease
lymphocytes level
as an effect on
lab. Test results.
EOSINOPHIL 1-3 % TOXIC Within normal
S 4.3 GRANULES range
3-7% BSMP
MONOCYTES
BASOPHILS 0-1 %
STABS 5-10 %
JUVENILE
PLATELET 150-450 X 256 Within normal
COUNT 10⁹/1 range

BLOOD PRESSURE

11-7 6am- 190/130 8pm- 180/120

7am- 170/90 9pm- 180/120
8am -170/120 10pm- 150/100
9am - 160/100 11pm- 150/100
 10am-
11am- 150/110
12pm-150/110
1pm- 160/100
2pm- 160/10
4pm- 160/110
6pm- 170/120
7pm- 170/120

TEST NORMAL RES TE NORMAL INTERPRETATI

VALUES ULTS ST VALUES ON
GLUCOSE 70-115 LIPID
FASTING mg/dl PROFILE:
RANDOM 90-160 Cholesterol 3.90-6.20
mg/dl mmol/L
2hr PPRS 75-125 Triglycerid .70-1.70
mg/dl es mmol/L
KIDNEY FXN HDL M: 0.78-
TEST 1.55
mmol/L
BLOOD URIC 155-428 F: 1.03-1.81
ACID µmol/L mmol/L
BUN 7-18 mg/dl 1 LDL 3.88-4.91 Within normal
4.2 mmol/L range
CREATININE F ( 53-97) 6 LIVER Within normal
µmol/L 6.4 PROFILE: range
M (80-115) SGOT/AST 0-40 IU
µmol/L
SERUM SGPT/ALT M: 13-61 IU
ELECTROLYTE
S:
K+ S 3.6-55 F:3-42 IU
mmol/L
Na+ 135-155 ALK PO4 10-35 IU
mmol/L
Cl 98-106 TOTAL S 65-85 g/l
mmol/L PROTEIN
ALBUMIN 30-50 g/l
A/G RATIO 2:1-3:1

TEST NORMAL RESUL TEST NORMAL INTERPRETATIO

VALUES TS VALUES N
GLUCOSE 70-115 LIPID Within normal
FASTING MG/dL PROFILE: range.
RANDOM 90-180 152 Cholesterol 3.90- Within normal
MG/dL 6.20mmol/L range
2 hr PPRS 75-125 Triglycerid .70-
 mg/Dl es 1.70mmol/L
HDL M: 0.78-1.55
mmol/L
KIDNEY FXN L F: 1.03-1.81
TEST mmol/L
BLOOD URIC 155- LDL 3.88-4.91
ACID 428µmol/L mmol/L
BUN 7-18 mg/dl
CREATININE F(53.97) LIVER
µmol/L PROFILE:
M(80-115) SGOT/AST 0-40 IU
µmol/L
SERUM SGPT/ALT M:13-61 IU
ELECTROLY
TE
K+ S 3.6-55 3.9 F: 3-42 IU Within normal
mmol/L range
Na+ 135-155 ALK PO4 10.35 IU
mmol/L
Cl 98-106 TOTAL s 65-85 g/l
mmol/L PROTEIN
ALBUMIN 30-50 g/l
A/G RATIO 2:1-3:1
PHATOPHYSIOLOGY

Overview of the Disease

Spontaneous/Hypertensive Bleed, left basal ganglia

Alternative names: Intracerebral Hemorrhage(ICH), Hypertensive Hemorrhage,

Spontaneous Intracranial Hemorrhage, Hemorrhagic
Cerebrovascular Disease.

What Is It?

Hypertensive hemorrhage is one of the most common causes of

spontaneous bleeding into the brain. Hypertension, high blood pressure, can
lead to several forms of injury to blood vessels over time. It is a significant
risk factor for blood vessel disease throughout the body, including coronary
artery disease, peripheral vascular disease and stroke. With high blood
pressure, some of the small arteries within the brain become injured and
diseased. This can lead to a spontaneous rupture of these arteries, leading to
a brain hemorrhage.

This type of bleed into the brain, intracerebral hemorrhage, can be

considered one form of hemorrhage stroke because it happens suddenly,
often without any warning sign other than long-standing high blood pressure.
Additionally, some of the presenting symptoms can be similar to those of
ischemic stroke which is due to a blood clot blocking blood flow to a part of
the brain, not bleeding into the brain.

The bleeding can occur in any part of the brain. Blood may build up in
the brain tissues, or in the space between the brain and the membranes that
covers it. Bleeding may only be in one hemisphere, or it may occur in other
brain structures such as thalamus, basal ganglia, Pons or cerebellum.

Causes: An Intracerebral hemorrhage can be caused by:

• Abnormalities of the blood vessels(aneurysm or vascular

malformation)
 • High blood pressure(hypertensive intracerebral
hemorrhage)
• Protein deposit along blood vessels(anyloid angiopathy)
• Traumatic rain injury

What Type of Symptoms are Typical?

Patients with a hypertensive brain hemorrhage typically patient with

the sudden onset of new neurological symptoms. The specific symptoms
depend on the size of the hemorrhage and its location in the brain.

The most common site for these hemorrhage are the deep grey matter
of the brain, including areas called BASAL GANGLIA and the THALAMUS. They
occur deep in the brain. In this type of hemorrhage, common symptoms
include hemiparesis or hemiplagia(weakness or paralysis of the opposite side
of the body) because the fibers of the motor system(called the internal
capsule) run right alongside this location in the brain. Hemorrhage in the
dominant hemisphere(usually the left side in most patients) can result in
aphesia(abnormalities in the comprehension or production of normal
language). If the hematoma is large enough it can increase the pressure on
the brain in general and lead to a deterioration in the level of consciousness
including coma and death if severe enough.

Another area where hypertensive hemorrhage can occur is the Pons,

part of the brain stem. Hemorrhage in this area can often lead to coma or
death because of the importance of the brain stem in the normal functions
that support life(alertness, breathing, etc.)

Finally, hemorrhage can occur in the cerebellum, a part of the brain

important for motor coordination and gait. Symptoms associated of these
hematomas can include unbalanced gait, poor coordination and instability. If
large enough they can obstruct the fourth ventricle, a fluid-filled space within
the brain, and lead to acute hydrocephalus.

Symptoms vary depending on the location of the bleed and the amount
of brain tissue affected. The symptoms usually develop suddenly, without
warning, often during activity. They may occasionally develop in a stepwise
patter, or they may worse over time.

Symptoms include:
• Abnormal sense of taste
• Change in alertness(level of consciousness)
✔ Apathetic, withdrawn
✔ Sleepy, lethargic, stuporous
✔ Unconscious, comatose
• Difficulty speaking or understanding speech
• Difficulty swallowing
• Difficulty writing or reading
• Headache
✔ May occur when lying flat
✔ May awaken patient from sleep
✔ May increase with change in position
✔ May increase with bending, straining and
coughing
• Loss of coordination
 • Loss of balance
• Movement change
✔ Difficulty moving any body part
✔ Hand tremor
✔ Loss of fine motor skills
✔ Weakness of any body part
• Nausea and vomiting
• Seizure
• Sensation changes
✔ Abnormal sensations
✔ Decreased sensations
✔ Facial paralysis
✔ Numbness or tingling
• Vision changes
✔ Any change in vision
✔ Decreased vision, loss of all or part of vision
✔ Double vision
✔ Eyelid drooping
✔ Pupils different size
✔ Uncontrolled eye movement

When to Contact a Medical Professional?

Go to emergency room if there is symptoms of ICH. This is a life
threatening condition.

Emergency symptoms include:

• Difficulty breathing
• Inability to speak and swallow
• Loss of consciousness
• Paralysis of an arm, leg, or half of the body only and
seizure

How is the Diagnosis Typically Made?

If a patient with high blood pressure presents with the sudden onset of
new neurological symptoms, the diagnosis of intracerebral hemorrhage is
generally made on an imaging study such as a CT scan or MRI scan which
demonstrate a hemorrhage within the brain in one of the usual locations.
Because some of the symptoms may be similar to ischemic stroke(weakness
of half the body, difficulty with speech and language, etc.) this must be ruled
out. Generally the CT scan is adequate to demonstrate the hemorrhage.

Other tests may include:

• Bleeding time
• Complete blood count(CBC)
• Kidney function tests
• Liver function tests
• Platelet count
• Prothrombin time(PT) in partial thromboplastin time(PTT)

What are Some Common Treatments?

 Treatment varies depending on the specifics of each case and cannot
be generalized to all patients. However, most patients are admitted to the
intensive care unit and undergo general supportive measure and
observation. Aggressive surgery to remove the hematoma has been show to
not be beneficial in most patients. However, for very large hemorrhage
surgery is sometimes considered. This can be performed through a long
craniotomy or sometimes through a small opening with an endoscope.

In some centers a catheter is placed into the hematomas and a drug

called tPA is injected to attempt to break up and drain the clotted blood. In
patients of hemorrhage into cerebellum surgery is more frequently
recommended to prevent brain stem compression and hydrocephalus. If
hydrocephalus is present, a ventriculostomy catheter is sometimes placed to
decreased the pressure inside the head.

Medicines used may include:

• Anticonvulsants to control seizure
• Corticosteroid or diuretics to reduce swelling
• Painkillers

You may need blood, blood products in fluids given through a vain(IV)
to make up for loss of blood and fluids.

Prognosis:
How will a patient does depends on the size of the hematomas and the
amount of swelling. These may be a complete recovery, or some permanent
loss of brain function. Death is possible and may occur quickly despite
prompt medical treatment. Recovery depends in the area where the bleeding
occur. Medications, surgery, or other treatment may have severe side
effects.

Prevention:
Treating and controlling underlying disorders may reduce the risk of
dwelling ICH. Get high blood pressure treated. Do not stop taking
medications unless told to do so by your doctor.

PROLONGED Vasoconstriction of cerebral

HYPERTENSION arterioles

Inflammation and necrosis of

arterioles (saclike out
pouching) (blood flow exerts
pressure against arterial wall,
stretching it like an over blow
balloon and making it likely to
rupture.
Constant pressure on
Narrowing of blood
walls of blood vessels.
vessels

Restriction of blood
flow
Rapture of the
arterioles
 Subarachnoid
haemorrhage/bleeding
 Blood spills into the space normally occupied by
cerebrospinal fluid or in brain tissue.

SIGNS AND SYMPTOMS:

-severe headache

-nausea and projectile vomiting related to inc. Pressure

Organ damage
-decrease oxygen

Renal
Cerebral
➢ Oliguria and
➢ decrease Cerebral tissue perfusion
dysuria • drowsy
• lose of consciousness
➢ impaired mobility
• Weakened muscles
• General body weakness
➢ Altered motor function
• Bradykinesia ( slow movement,
difficulty initiating voluntary
movement)
 INEFFECTIVE CEREBRAL TISSUE
PERFUSION

IMPAIRED PHYSICAL MOBILITY

Decrease in oxygen
Disruption of blood supply in the rain area

Tissue and cell neurons

Decrease cardiac output

Destruction of neuromuscular
junctions

Failure to nourish tissue at the

capillary level

Interruption in transportation of electrical impulses to neuromuscular receptors

Decrease tissue perfusion

Objectives:

•Changes in motor
response
Muscle weakness (myalgia)
• Extremity weakness
 SELF CARE DEFICIT

Altered motor function of

frontal lobe

Bradykinesia

Inability to perform ADL

Self care deficit

PATHOPHYSIOLOGY
Increased blood pressure damages the cerebral vessels primarily in 2 ways:

• Chronic hypertension stimulates the brain's blood vessels to make

gradual, adaptive changes in an attempt to preserve the blood-brain
barrier. One gradual change that may develop is lipohyalinosis.
Subintimal fibroblast proliferation occurs, with an accumulation of lipid-
laden macrophages and cholesterol deposits; this results in
hyalinization and lipidosis of the blood vessels. This process
segmentally affects the smaller penetrating arteries (<200 mm in
diameter) and may account for many lacunar infarcts of the basal
ganglia and thalamus, which seem to occur without known symptoms.
Lipohyalinosis may be an intermediate stage between fibrinoid
necrosis from severe hypertension and microatheromas from long-
standing hypertension.1,2
Plasma leakage from persistently elevated blood pressures also can result in
hyaline degeneration of the cerebral blood vessels. Serum protein
accumulates in the basement membranes of the arterioles and results in
collagen formation. Arterial sclerosis and fibrinoid necrosis may occur, as
well as focal aneurysmal dilatation

Figure 1. An intracerebral hemorrhage (ICH) is usually caused by rupture of tiny arteries

within the brain tissue (left). As blood collects, a hematoma or blood clot forms causing
increased pressure on the brain. Arteriovenous malformations (AVMs) and tumors can
also cause bleeding into brain tissue (right).
 Figure 2. CT scan showing a large ICH
COURSE IN THE WARD
PHYSICIAN’S ORDER
CBC
HYDRALAZINE 50mg IV stat then
PRN for BP: 160
D5NSS 1L x 20gtts/min
O₂ Inhalation q 1-2 hour
Dexamerhasone stat
Citicholine 50mg q 8 hours
ECG
Ranitidine
CT scan
INTERPRETATION
-provide valuable information about the
patients condition(hypertensive bleeding),
-antihypertensive. Given to lowers Mrs.
Matute’s blood pressure from 190/130 to
normal value.
-IV fluids are given to maintain fluid balance,
using isotonic solution.
-she needs oxygen because when the time
of confinement she has difficulty of
breathing.
-decreases inflammation, mainly by
stabilizing leukocyte lysosomal membranes;
suppresses immune response.
-it is a brain enhancer. It stimulates the brain
to function.
-provides graphic recording of the heart’s
electrical activity of Mrs. Matute.
-since Mrs. Matute take different
medications/drugs, ranitidine is given to
prevent gastric irritation.
-she undergone this procedure because
these has the unique capability of
distinguishing minor differences in the
density of tissue.
 Catapres 75mg ½ tab -the patient’s BP is monitored q 2 hours and
it is constantly changing from 150/120 to
170/110. This drug is prescribed to lower or
normalized the BP of the patient.

NGT -These is inserted so that feeing and

medications can be administered.
Senokot -indicated for functional constipation of
hospitalized patient due to intake of certain
drugs.
Dulcolax -from the time of confinement, Mrs. Matute
never defecate. So, dulcolax is given to
increase perystalsic.

DISCHARGE PLANNING

Medication
CONZACE Vitamin A, C, E and Zinc 10 0-0-1 taken
before hour of bed

CATAPRES Antihypertensive 150mg 10 0-0-1 taken before

hour of bed

Enhance the client and caregiver in understanding the value of continuing

home medication by providing them information.

Emphasize to the client and caregiver the need and importance for
medication/treatment by providing them information that would enhance
their knowledge and understanding of the said regimen.

Exercise
Refer to Physical therapist to regain physical mobility. Provide teaching
about strengthening exercises and assistive devices such as walker, if
indicated.
Treatment
Prescribed medicine was given for continuous oral medication. Teaching plan
for medication and care of NGT is implemented. The caregiver is instructed
on how to properly feed in NGT.

Hygiene
Instruct caregiver on how to properly groom Mrs. Matute for her to maintain
proper grooming.

OPD follow up
Appointment for first visit to there attending Physicians is scheduled on July
16, 2009.

Diet
Reinforce Physician’s advised of weaning the patient from NGT by
introducing oral soft diet slowly until patient is able to ingest food by her self.