Case Pres.

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: Significant Others: Matute(daughter)

College Graduate(BS Commerce) Mary Ann Gollayan(sister) and Marites

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: BP:

36.7 150/100

36.5 160/110

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 BLOOD COUNT

NORMAL VALUES

HEMOGLOBI N

M: 130-180 g/L F: 110-160 g/ L M: 40-54 F: 37-47 5-10X10⁹/1

HEMATOCRIT WHITE CELL COUNT DIFFERENTIA L COUNT SEGMENTER S

RESUL TS

8.3

85.3

LYMPHOCYT ES

25-35%

10.4

EOSINOPHIL S

1-3 %

MONOCYTES BASOPHILS STABS JUVENILE PLATELET COUNT

NORMAL VALUES

ESR

M:0-10 mm/hr F: 0-20 mm/hr 5-15X10⁶/1 0.5-1.5% 1.3 min

145

50-65%

3-7%

TEST

4.3

PETIC COUNT BLEEDING TIME CLOTTING TIME BLOOD TYPING

3-6 min

TOXIC GRANULES BSMP

RESUL TS

INTERPRETATIO N Within normal range. Within normal range Within normal range Within normal range Increase in number signals for presence of inflammation. A patient was given dexamethasone(c orticosteroids) which may decrease lymphocytes level as an effect on lab. Test results. Within normal range

0-1 % 5-10 % 150-450 X 10⁹/1

256

Within normal range

BLOOD PRESSURE 11-7

6am- 190/130 7am- 170/90 8am -170/120 9am - 160/100

8pm- 180/120 9pm- 180/120 10pm- 150/100 11pm- 150/100

10am11am- 150/110 12pm-150/110 1pm- 160/100 2pm- 160/10 4pm- 160/110 6pm- 170/120 7pm- 170/120

TEST GLUCOSE FASTING RANDOM 2hr PPRS

NORMAL VALUES 70-115 mg/dl 90-160 mg/dl 75-125 mg/dl

RES ULTS

Triglycerid es HDL

KIDNEY FXN TEST BLOOD URIC ACID BUN

155-428 µmol/L 7-18 mg/dl

CREATININE

F ( 53-97) µmol/L M (80-115) µmol/L

TE ST LIPID PROFILE: Cholesterol

SERUM ELECTROLYTE S: K+ Na+ Cl

TEST GLUCOSE FASTING RANDOM 2 hr PPRS

S 3.6-55 mmol/L 135-155 mmol/L 98-106 mmol/L

NORMAL VALUES 70-115 MG/dL 90-180 MG/dL 75-125

3.90-6.20 mmol/L .70-1.70 mmol/L M: 0.781.55 mmol/L F: 1.03-1.81 mmol/L 3.88-4.91 mmol/L

1

LDL

6

LIVER PROFILE: SGOT/AST

0-40 IU

SGPT/ALT

M: 13-61 IU

4.2 6.4

NORMAL VALUES

INTERPRETATI ON

Within normal range Within normal range

F:3-42 IU

RESUL TS 152

ALK PO4

10-35 IU

TOTAL PROTEIN ALBUMIN A/G RATIO

S 65-85 g/l

TEST LIPID PROFILE: Cholesterol Triglycerid

30-50 g/l 2:1-3:1

NORMAL VALUES 3.906.20mmol/L .70-

INTERPRETATIO N Within normal range. Within normal range

mg/Dl KIDNEY FXN TEST BLOOD URIC ACID BUN CREATININE

SERUM ELECTROLY TE K+ Na+ Cl

es HDL L

155428µmol/L 7-18 mg/dl F(53.97) µmol/L M(80-115) µmol/L

S 3.6-55 mmol/L 135-155 mmol/L 98-106 mmol/L

LDL

1.70mmol/L M: 0.78-1.55 mmol/L F: 1.03-1.81 mmol/L 3.88-4.91 mmol/L

LIVER PROFILE: SGOT/AST

0-40 IU

SGPT/ALT

M:13-61 IU

3.9

F: 3-42 IU ALK PO4

10.35 IU

TOTAL PROTEIN ALBUMIN A/G RATIO

s 65-85 g/l 30-50 g/l 2:1-3:1

Within normal range

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 HYPERTENSION

Vasoconstriction of cerebral 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. Narrowing of blood vessels Restriction of blood flow Rapture of the arterioles

Constant pressure on walls of blood vessels.

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 ➢ Oliguria and dysuria

Cerebral ➢ decrease Cerebral tissue perfusion • 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 lipidladen 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 longstanding 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

INTERPRETATION -provide valuable information about the patients condition(hypertensive bleeding),

HYDRALAZINE 50mg IV stat then PRN for BP: 160 D5NSS 1L x 20gtts/min O₂ Inhalation q 1-2 hour

Dexamerhasone stat

-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.

Citicholine 50mg q 8 hours

-it is a brain enhancer. It stimulates the brain to function.

ECG

-provides graphic recording of the heart’s electrical activity of Mrs. Matute.

Ranitidine

CT scan

-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. -from the time of confinement, Mrs. Matute never defecate. So, dulcolax is given to increase perystalsic.

Dulcolax

DISCHARGE PLANNING Medication CONZACE Vitamin A, C, E and Zinc before hour of bed CATAPRES Antihypertensive 150mg hour of bed

10 10

0-0-1 taken 0-0-1 taken before

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.