A CASE PRESENTATION HYPERTENSION THALAMIC HEMORRAGE WITH

INTRAVENTRICULAR EXTENSION AND OBSTRUCTIVE HYDROCEPHALUS, COPD

WITH BRONCHI-ECTASIS

Presented to the faculty of the School of Nursing

Adventist Medical Center College
Brgy. San Miguel, Iligan City

In Partial Fulfillment
Of the requirements for the Degree
BACHELOR OF SCIENCE IN NURSING

Cheryl C. Padura
Trisha C. Mangubat
Muhammmad Alnashry B. Sarip
Earl Juffeny M. Etulle
Kea R. Alinas
Amirah D. Amano
Marwah C. Najeeb
Omaima M. Mocsana
Omerah S. Mimbalawag

November 27, 2017

 TABLE OF CONTENTS

I. TITLE PAGE 1

II. TABLE OF CONTENTS 2

III. LIST OF TABLES 3

IV. LIST OF FIGURES

V. OBJECTIVES 4

General Objective
Specific Objectives
VI. DEFINITION OF TERMS 5

VII. INTRODUCTION 6-8

VIII. NURSING HEALTH HISTORY

Vital Information 9
History of Present Health Concern 10
Past Health History 10
Family Health History (genogram) 11
Physical Examination and Review of Systems 12-14
Gordon’s Functional Health Patterns Assessment 15-17
Diagnostic test 18-20
IX. NORMAL ANATOMY AND PHYSIOLOGY 21-22

X. CONCEPT MAPPING 23-24

XI. NURSING CARE PLAN 25-30

XII. DISCHARGE PLAN 31-37

XIII. REFERENCES 38
 LIST OF TABLES

TABLES PAGES

1 Physical Examination and Review of System (PEROS) 12-14

2 Gordon’s Assessment of Client Dauntless 15-17

3 Normal Anatomy and Physiology 21-22

4 Diagnostic tests

5 Drug study
 LIST OF FIGURES

FIGURES PAGE

1 Genogram Showing the Family History of Client Dauntless 11

2 Concept Mapping 23-24

 OBJECTIVES

General Objective:

At the end of one and a half hour case presentation, the listeners will be able to ask

questions, give suggestions and comments about the case presented in order to enhance their

critical thinking and skills in handling patients with such case in the clinical area.

Specific Objectives:

At the end of one and half hour case presentation

The presenters will be able to:

1. Present the case within the allotted time;

2. Discuss the case comprehensively;

3. Provide appropriate nursing interventions;

4. Answer the questions about the case presentation raised by the critique groups; and

5. Modify the presented case to uphold the criteria.

The students will be able to:

1. Use the nursing process as framework for care for patients with such case;

2. Gain knowledge about the disease process, risk factors, clinical manifestations and the

disease management;

3. Identify problems, develop a teaching plan and strategies appropriate for the goal

attainment for a client that manifests or is diagnosed with such disease;

4. Develop and establish interpersonal relationship with fellow audiences while the case

is ongoing; and
 5. Gain skills and appropriate attitudes needed to function as a student-nurse in the

community or in a clinical area.

DEFINITION OF TERMS

The following terms are operationally and conceptually defined for better understanding

of the study.

Aterial hypertension. It is an elevated blood pressure. According to Berkow and

Fletcher (2000) it is “
 INTRODUCTION

Hypertensive thalamic hemorrhage (HTH), also known as intraventricular bleeding, is

a bleeding into the brain's ventricular system, where the cerebrospinal fluid is produced and

circulates through towards the subarachnoid space. It can result from physical trauma or from

hemorrhaging in stroke. Hypertensive thalamic hemorrhage has remained a serious disease despite

recent improvements in medical treatment. This was designed to identify modifiable risk factors

for HT hemorrhage. Methods Health habits, previous diseases, and medication of 156 consecutive

patients with Hypertensive thalamic hemorrhage aged 16 to 60 years (96 men and 60 women) were

compared with those of 332 hospitalized control patients (192 men and 140 women) who did not

differ from case subjects in respect to age, day of onset of symptoms, or acuteness of disease onset.

Hypertensive thalamic hemorrhage most commonly results from hypertensive damage to blood

vessel walls (eg, hypertension, eclampsia, drug abuse), but it also may be due to autoregulatory

dysfunction with excessive cerebral blood flow (eg, reperfusion injury, hemorrhagic

transformation, cold exposure), rupture of an aneurysm or arteriovenous malformation (AVM),

arteriopathy (eg, cerebral amyloid angiopathy, moyamoya), altered hemostasis (eg, thrombolysis,

anticoagulation, bleeding diathesis), hemorrhagic necrosis (eg, tumor, infection), or venous

outflow obstruction (eg, cerebral venous thrombosis).

Nonpenetrating and penetrating cranial trauma are also common causes of hypertensive thalamic

hemorrhage. Patients who experience blunt head trauma and subsequently receive warfarin or

clopidogrel are considered at increased risk for traumatic hypertensive thalamic hemorrhage.

According to one study, patients receiving clopidogrel have a significantly higher prevalence of

immediate traumatic hypertensive thalamic hemorrhage compared with patients receiving

warfarin. Delayed traumatic hypertensive thalamic hemorrhage is rare and occurred only in

patients receiving warfarin.

Chronic hypertension produces a small vessel vasculopathy characterized by lipohyalinosis,

fibrinoid necrosis, and development of Charcot-Bouchard aneurysms, affecting penetrating

arteries throughout the brain including lenticulostriates, thalamoperforators, paramedian branches

of the basilar artery, superior cerebellar arteries, and anterior inferior cerebellar arteries.

Predilection sites for HT hemorrhage include the basal ganglia (40-50%), lobar regions (20-50%),

thalamus (10-15%), pons (5-12%), cerebellum (5-10%), and other brainstem sites (1-5%).

This is a life-threatening condition, and you should call 911 or go to an emergency room immediately.

The symptoms include, A sudden severe headache, Seizures with no previous history of seizures,

Weakness in an arm or leg, Nausea or vomiting, Decreased alertness; lethargy, Changes in vision,

Tingling or numbness, Difficulty speaking or understanding speech, Difficulty swallowing, Difficulty

writing or reading, Loss of fine motor skills, such as hand tremors, Loss of coordination, Loss of

balance, An abnormal sense of taste, Loss of consciousness. Complications of HTH include

hematoma expansion, perihaematomal edema with increased intracranial pressure, intraventricular

extension of haemorrhage with hydrocephalus, seizures, venous thrombotic events,

hyperglycaemia, increased blood pressure, fever, and infections. In view of the restricted number

of therapeutic options for patients with HTH, improved surveillance is needed for the prevention

of these complications, or, when this is not possible, early detection and optimum management,

which could be effective in the reduction of adverse effects early in the course of stroke and in the

improvement of prognosis. Further studies are needed to enhance the evidence-based

recommendations for the management of this important clinical problem. 30% of Hypertensive

thalamic hemorrhage (HTH) are primary, confined to the ventricular system and typically caused

by intraventricular trauma, aneurysm, vascular malformations, or tumors, particularly of the

choroid plexus. However 70% of HTH are secondary in nature, resulting from an expansion of an

existing intraparenchymal or subarachnoid hemorrhage. Hypertensive thalamic hemorrhage has

been found to occur in 35% of moderate to severe traumatic brain injuries. Thus the hemorrhage

usually does not occur without extensive associated damage, and so the outcome is rarely good.

Obstructive hydrocephalus (also called non-communicating hydrocephalus) is a form of

hydrocephalus which is caused by some visible blockage in the flow of cerebrospinal fluid.

Hydrocephalus is a condition caused by abnormal flow and/or re-absorption of the cerebrospinal

fluid, the water-like liquid that surrounds the brain and spinal cord and fills the open spaces within
the brain, the ventricles. This can lead to increased pressure inside the head which then can lead to

dysfunction and/or damage to the nervous system. In most forms of hydrocephalus, the ventricles

inside the brain enlarge as the pressure increases.

Hydrocephalus can be caused by a visible (on brain scans) obstruction of the normal flow this

fluid. This cause is called obstructive hydrocephalus because it is caused by obstruction of this

flow of fluid. Another name for this type of hydrocephalus is non-communicatinghydrocephalus.

Most commonly, obstructive hydrocephalus is caused either by a mass in the brain which blocks

the flow of fluid, such as a brain tumor, or some scarring or malformation which narrows or

completely blocks part of the flow of fluid. These are often termed rings or webs. They can occur

either due to some prior trauma, bleeding or infection, or can be congenital, present at birth. In

some cases they can be idiopathic, meaning that they have no known medical cause.

One of the most common sites in the brain for obstruction is the cerebral aqueduct. The symptoms

of obstructive hydrocephalus are generally indistinguishable from those of any form of

hydrocephalus, with a few exceptions. Generally, because of the increased pressure in the brain,

the ventricles enlarge and the brain gets compressed. Nervous system tissue does not function well

under pressure or compression. Some of the most common symptoms of hydrocephalus are

headache and progressive depression of the level of consciousness. If the pressure gets too severe

before treatment is administered, coma and even death can occur.

Normal CSF production is 0.20-0.35 mL/min; most CSF is produced by the choroid plexus, which

is located within the ventricular system, mainly the lateral and fourth ventricles. The capacity of

the lateral and third ventricles in a healthy person is 20 mL. Total volume of CSF in an adult is

120 mL.

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable slowly progressive

respiratory disease of airflow obstruction involving the airways, pulmonary parenchyma, or both.

The parenchyma includes any form of lung tissue, including bronchioles, brinchi, blood vessels,

interstitium, and alveoli. The airflow limitation limitation or obstruction in COPD is not fully

reversible. Most patient with overlapping signs and symptoms of emphysema and chronic

bronchitis, which are two distinct disease process. Risk factors of COPD include environment

exposures and both factors. The most important environmental risk factor for COPD wolrdwide is
cigarette smoking. A dose-response relationship exists between the intensity of smoking (pack-

year history) and the decline in pulmonary function. Host risk factors include a person’s genetic

make up. One well-documented genetic risk factor is a deficiency of alpha antitripsin, an enzyme

inhibitor that protects the lung parenchyma from injury. People with COPD commonly become

symptomatic during the middle adult years, and the incidence of the disease increases with age.

Although certain aspects of lung function normally decreases with age-for example, vital capacity

and forced expiratory volume in 1 second. COPD accentuates and accelerates these physiologic

changes. In COPD, the airflow limitation is both progressive and associated with the lungs

abnormal inflammatory response to noxious particles or gases. The inflammatory response occurs

throughout the proximal and peripheral airways, lung parenchyma and pulmonary vasculature.

Although the natural history of COPD is variable, it is generally a progressive disease

characterized by three primary symptoms: chronic cough, sputum production and dyspnea. These

symptoms often worsen over time. Chronic cough and sputum production often percede the

development of airflow limitation by many years. However, not all people with cough and sputum

production develop COPD. The cough may be intermettent and may be unproductive in some

patients. Dyspnea may be severe and interfere with the patient’s activities. It is usually progressive,

is worse with exercise, and is persistent. As COPD progresses, dyspnea may occur at rest. Weight

loss is common, because dyspnea interferes with eating and the work of breathing is energy

depleting. As the work of breathing increases over time, the accessory muscles are recruited in an

effort to breathe. Patients with COPD are at risk for respiratory insufficiency and respiratory

infections, which in turn increases the risk of acute and chronic respiratory failure.

Respiratory insufficiency and failure are major life-threatening complications of COPD. The

acuity of the onset and the severity of respiratory failure depend on baseline pulmonary function,

pulse oximetry or arterial blood gas values, comorbid conditions, and the severity of otheer

complications of COPD. Respiratory insufficiency and failure may be chronic (with severe COPD)

or acute (with severe brochospasm or pneumonia in a patient with severe COPD. Acute respiratory

insufficiency and failure may necessitate ventilatory support until other acute complications, such

as infection, can be treated. Other complications of COPD include pneumonia, chronic ateectasis,

pneumothorax, and pulmonary arterial hypertension (cor pulmonale).

According to the Mayo Clinic, hypertension is defined as a common condition in which the force

of the blood against a person’s artery walls is high enough that it may eventually cause severe

health issues. The more blood that the heart pumps and the narrower the arteries are, the higher

the blood pressure. How are COPD and hypertension connected then? As you may have guessed,

COPD takes a significant toll upon the body. Breathlessness, weight loss, sleeping and eating

problems, and a depletion in energy are just some of the effects that the disease can cause for a

person. COPD can also affect the workings of the heart. The nature of the disease forces the heart

to work overtime. Since the lungs are damaged, the amount of oxygen that goes to the blood is

reduced. This produces high blood pressure in the blood vessels from the heart to the lungs, and

makes it even more difficult for the heart to pump much-needed blood to the rest of the body. This

lung disease can also cause the body to produce more red blood cells, which can make the blood

thicker and harder to pump. The COPD and hypertension working together forces the person to

breathe faster in order to take in more oxygen.

 VITAL INFORMATION

Code name: X44

Age: 63 years old
Gender: Female
Civil Status: Married
Date of Birth: January 15, 1954
Place of Birth:
Race: Asian
Cultural or ethnic background: Maranao
Primary language (spoken and read): N/A
Secondary language (spoken and read): N/A
Religion: Islam
Highest Educational Attainment (Client): High School Graduate
Highest Educational Attainment (Partner/Spouse): High School Graduate
Occupation (Client): Housewife
Usual Health Care Provider/s: Doctor/Physician
Date of Admission: November 21, 2017; 1:20 PM
Date of Discharge:
Source/s of History:
50 % chart
50 % SO
Reason/s for Seeking Health Care: Generalized body weakness, altered mental status
Primary Attending Physician: Dr. Shydin Manticayan
Initial Impression/Diagnosis: Cardiovascular disease infarction left mid-cerebral artery,
Hypertensive cardiovascular disease, Community acquired pneumonia- Moderate risk
Final Diagnosis: HPN Thalamic Hemorrhage with intraventricular extension and obstructive
hydrocephalus, COPD with bronchi-ectasis, Advised for ventriculostomy
History of Present Health Concern
Five hours prior to admission, onset of body weakness was noted by the patient’s son.

Persistence of body weakness with numbness prompted consult, hence the patient was bought to

Adventist Medical Center Iligan (AMCI) in a comatose state. The patient was under the

supervision of Dr. Manticayan for observation because of the patient’s condition.

Past Health History

At the age of 20 she started smoking and consumed 1 pack/ day. Her grand-parents died

due to hypertension. They had a history of diabetes mellitus type 1 in their family. Her two elder

sisters died due to pneumonia and her elder brother died of stroke.

On April 2007, patient was diagnosed with pneumonia and was hospitalized in Global

City Hospital, Tamparan, Lanao Del Sur. Her blood pressure was elevated during her

hospitalization as verbalized by the patient hence she was given Lozartan for maintenance but

the patient was non compliant to it. She has no known allergies.
Figure 1

GENOGRAM DIAGRAM

Figure 1. Genogram showing the Family History of Client X44

 Table 1

Physical Examination and Review of System (PEROS)

AREA ASSESSED SUBJECTIVE OBJECTIVE FINDINGS PROBLEM IDENTIFIED

FINDINGS
General Health Patient is non-  Unconscious,  Ineffective
Survey responsive, incoherent, non- breathing
“nanghihina responsive, very pattern
siya” as weak, poorly  Imbalanced
verbalized by the nourished nutrition
significant other  Vital signs  Impaired gas
(ranged): exchange
T: 36.0 – 38.4  Activity
P: 110 - 180 intolerance
R: 20 - 50  Risk for infection
BP: 100/70 –
180/110
Integumentary “wala kaming  Senile, poor  Risk for impaired
System nakitang rashes turgor, warm to skin integrity
sa kanyang touch  Impaired tissue
balat, biglaan integrity
ang kanyang  Ineffective
pagbawas ng thermoregulation
timbang” as  Self-care deficit
verbalized by the
significant other
HEENT “hindi siya  Dry lips, dry  No problem
 Head nagsusuot ng conjunctivae fixed identified
and salamin, dilated pupil
Face nakakarinig din
 Eyes naman siya ng
 Ears maayos, bungi
 Nose siya kasi nawalan
 Oral siya ng mga
Cavity ngipin” as
verbalized by the
significant
others
Neck “ wala naman  Supple, negative  No problem
kaming nakita na for identified
namaga yung lymphadenopathy
leeg niya” as
verbalized by the
significant
others
Respiratory “naninigarilyo  Positive for  Impaired gas
System siya parati” as ronchi, positive exchange
verbalized by the for crackles both  Ineffective
significant upper and lower breathing
others lung fields pattern
 Cardiovascular “hindi naman  Tachycadic  Risk for cardiac
System siya arrest
nagrereklamo na
may sakit sya sa
dibdib” as
verbalized by the
significant other
Breast and Axilla  No lumps  No problem
palpated identified
Gastrointestinal  Flat, Hypoactive  Imbalanced
System and the bowel sounds, nutrition: less
abdomen soft than body
requirements
Genitourinary/  Patient is in  Risk for infection
Reproductive catheter
System (indwelling)
 No unusual odor
Musculoskeletal  Weakness on all  Risk for activity
System extremities intolerance
 Patient is  Impaired physical
unconscious mobility
 Fatigue
 Risk for injury
Neurologic System  Ate che, wala sa 
notes ni ate
bambs about diri
and di ko
kapataka input
diri og stuff kay
wa ko kita sa
result sa mga test
Lymphatic/  And also diri te 
Hematologic
System
Endocrine System  EPPP, Weakness  Impaired tissue
on both integrity
extremities, more  Risk for infection
profound on the
right side non-
cyanotic nail beds
 Table 2

Gordon’s assessment on patient X44

 Table 3

NORMAL ANATOMY AND PHYSIOLOGY

Normal Anatomical Structures with their Descriptions and Functions

Anatomical structure Description

Brain It contributes to homeostasis by receiving sensory input, integrating new and stored
information, making decisions and executing responses through motor activities. (Tortora
& Derrickson, 2011, p. 527)
Thalamus Measures about 3 cm in length and makes up 80% of the diencephalon. It is the major
relay stationfor most sensory impulses that reach the primary sensory areas of the
cerebral cortex from the spinal cord and brain stem. In addition, the thalamus contributes
to motor functions by transmitting information from the cerebellum and basal nuclei to
the primary motor area of the cerebral cortex. The thalamus also relays nerve impulses
between different areas of the cerebrum and plays a role in the maintenance of
consciousness. ( Tortora & Derrickson, 2011, p. 543)
Cerebrospinal fluid It is a clear, colorless liquid composed primarily of water that protects the brain and
(CSF) spinal cord from chemical and physical injuries. It has three basic functions; mechanical
protection, homeostatic function and circulation ( Tortora & Derrickson, 2011, p. 531 )
Arteries It carries air throughout the body. The wall of an artery has the three layers of a typical
blood vessel, but has a thick muscular-to-elastic tunica media. Due to their plentiful
elastic fibers, arteries normally have high compliance, which means that their walls
stretch easily or expand without tearing in response to a small increase in pressure. The
brain receives blood via internal carotid and vertebral arteries.
( Tortora & Derrickson, 2011, p. 805)
Lungs This are paired cone-shaped organs of the thoracic cavity.The lungs' main function is to
help oxygen from the air we breathe enter the red cells in the blood. Red blood cells then
carry oxygen around the body to be used in the cells found in our body. The lungs also
help the body to get rid of CO2 gas when we breathe out. (Tortora & Derrickson, 2011,
p. 929)
Alveoli It is a cup-shaped outpouching lined by simple squamous epithelium and supported by a
thin elastic basement membrane; an alveolar sac. It is where exchange of O2 and CO2
takes place. (Tortora & Derrickson, 2011, p. 932-934)
Bronchi Also called as the windpipe. This are the main passageway into the lungs. When someone
takes a breath through their nose or mouth, the air travels into the larynx. The next step is
through the trachea, which carries the air to the left and right bronchus. The bronchi
become smaller the closer they get to the lung tissue and are then considered
bronchioles.(Tortora & Derrickson, 2011, p. 928-929)
 Figure 2

Concept Map
 Table 4

Diagnostic test
 Table 5

Drug study
 Table 6

Nursing Care Plans

Health Education Plan