NURSING SERVICE DIVISION

NURSING EDUCATION AND TRAINING BRANCH

V. Luna Avenue, Quezon City

A Case Study On

Severe Leptospirosis; Weils Syndrome

In Partial Fulfilment of the Requirements for the

Nurse Corps Mentoring Program
Class 05-2016

Submitted By:

P2LT LEA MARI T MACADANGDANG NC

AFPNCMP CL 05-2016

May 2017
 DISCLAIMER

This is an official document of the Nursing Education and Training Branch,

Nursing Service Division, Victoriano Luna General Hospital, Armed Forces of the
Philippines Medical Center. Quotations from, contractions from, or reproduction of all or
any part of this document is not authorized without specific permission from the Chief
Nurse of Victoriano Luna General Hospital Armed Forces of The Philippines Medical
center

The opinions, ideas and proposals expressed herein are those of the nurse
authors and do not necessarily represent the official views of the Nursing Service
Division or any government agency. Reference of this work should include in the
foregoing statement.

Nursing Education and Training Branch

Nursing Service Division
AFP Medical Center
V. Luna Avenue Quezon City

i
 APPROVAL SHEET

This case study entitled Severe Leptospirosis; Weils Disease, prepared and
submitted by P2LT LEA MARI T MACADANGDANG NC in partial fulfilment of the
requirements for the Armed Forces of the Philippines Nurse Corps Mentoring Program
Class 05-2016 is hereby endorsed.

PANEL OF REACTORS

Approved by the Committee on the Panel of Evaluators with a grade of PASSED ( )

_______________________________ ______________________________
CPT JOHN JOTHAM G. REPOLLO NC 1LT KAREN JOY N.AYON-AYON NC
Panelist Panelist

________________________________ ___________________________
1LT CHERRY LYNNE IMEE DAMOYAN NC MS. FLORDELIZA M. GAGAN RN
Panelist Panelist

Accepted and approved in partial fulfilment of the requirements for the course
Armed Forces of the Philippines Nurse Corps Mentoring Program Class 05-2016.

ii
ACKNOWLEDGEMENTS

iv
 TABLE OF CONTENTS

I. INTRODUCTION
A. Background of the Study
B. Objectives of the Study
C. Significance of the Study
D. Scope and Limitation
II. PROFILE, HISTORY AND PHYSICAL EXAMINATION
A. Patients Profile
B. Socio-Demographic Characteristics
C. History of Present Illness
D. Past Medical History
E. Family History and Genogram
F. Nursing History (Gordons Eleven Functional Health Patterns)
G. Physical Examination (Review of Systems)
III. CLINICAL DISCUSSION
A. Anatomy and Physiology
B. Pathophysiology / Schematic Diagram
C. Course in the Ward
D. Laboratory and Diagnostic Procedures
E. Drug Profile
IV. NURSING MANAGEMENT
A. Problem List
B. Long Term Objective
C. Nursing Care Plans
D. Discharge Plan
V. CONCLUSION
VI. BIBLIOGRAPHY
VII. APPENDICES
I. INTRODUCTION

A. Objectives of the Study

General Objective

The general objective of this study is to present a case study in order to expand
the groups knowledge, enhance the technical skills, and develop the appropriate
attitude of nurses in managing and caring of patients with Leptospirosis, Weils Disease.

Specific Objectives

To become updated of the growing number of cases of leptospirosis in the

world, especially in the Philippines
To gather detailed history from the patient necessary for the case
To acquire vital information regarding the clinical manifestations and identify
the disease process
To recognize and prioritize nursing problems and be able to construct
appropriate nursing diagnoses in accordance with the patients status
To generate and implement pertinent plan of care and to establish goals
towards the patients welfare
To determine the possible management necessary for clients with
leptospirosis
To evaluate the outcome of the care rendered

B. Significance of the Study

The case study will impart additional knowledge to the readers, particularly
healthcare providers,regarding the disease process and possible management
necessary for the promotion of health and prevention of illness. Further, this study
would empower them to help reduce the prevalence of leptospirosis in the country
by simply disseminating basic but essential information about its prevention.

The study would also help patients to become familiar with their condition and
learn the feasible plan of care that could help them return to their optimal level of
functioning.

In addition, the study will educate and at the same time encourage the patients
significant others to participate in the plan of care and help the patient adhere to the
treatment course.

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 The study also intends to aid nurses to refine their nursing skills in the
recognition of symptoms and prevention of complications.

Finally, this study will benefit future studies by providing updated information
regarding the nursing management of patients suffering from leptospirosis.
C. Scope and Limitation

The study is conducted in the Nephrology Ward (6A) of the Armed Forces of the
Philippines Medical Center. This study began on 04 March 2017, when the client was
admitted until 24 March 2017. The clients data was gathered from the date of
admission until 20th day of confinement.

The information needed for working on the study was obtained directly from the
client and significant others; details from clientschart were also utilized. The identity and
data gathered were kept with utmost confidentiality.

This study focuses on the main diagnosis of the client, which is Severe
Leptospiros, Weils Disease.

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I. NURSING HISTORY

A. Patients Profile

Patients Name : EL
Rank : SGT
Age : 33
Sex : Male
Weight : 60kg
Address : Brgy. Silangan, Infanta, Quezon
Civil Status : Married
Religion : Roman Catholic
Educational Attainment : College Graduate
Chief Complaint : decreased urine output, epigastric pain, painful urination
Date Admitted : 04 March 2017
Admitting Diagnosis : Leptospira Infection T/C Weils Disease

Revised Diagnosis : Severe Leptospirosis, Weils Syndrome

B. Sociodemographic Characteristic

SGT EL was born in Cotabato City and settled in Infanta, Quezon when he
married his wife, ML. EL and ML were blessed with two children. He is not a smoker but
an occasional drinker. SGT EL knows two languages, English and Filipino, and can also
speak a dialect, which is Bisaya. He graduated Criminology and had a course in
Advance ROTC which made him decide to enter the military, right after graduating,
specifically in the Candidate Soldier in the Naval Force. He now lives in his barracks at
Fort Bonifacio and occasionaly visits his wife, 2 children, and family at Infanta, Quezon
during vacations.

C. Concept of Health Illness and Hospitalisation

EL knows that health is essential and important, specially in his line of duty,
because he can not function as a military personnel if he has poor health. In addition to
that, he thinks that illness is a part of life and a result of an abusive lifestyle, such as
having vices and overworking.

Being in a hospital is not new to EL because he was previously admitted as a

battle casualty due to his gunshot wound on his right feet. He believes that staying in a
hospital is only for the sick, and as long as he can tolerate his illness, he stays away
from being admitted or consulting a doctor in a hospital.

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 D. Common Health Practice at Home

When EL was young, he was healthy and does not acquire any illness easily.
Drinking plenty of water when he had diarrhea and cough, and taking over-the-counter
medications such as Paracetamol for fever was their way of treatment. During his
military career, he was open about the idea of consulting a doctor; however, RP
admitted that he seldom followed medical instructions especially when he already felt
better. In 2009, he was admitted at AFP Medical Center due to gunshot wound on his
right feet. He was operated on and was able to survive the injury and operation.

E. Immediate Factor that Brought About Illness

One of the factors that brought about ELs illness was his negligence. On 20
February 2017, he was cleaning the canal, that was already causing flood in their area,
on bare foot. He knows that his feet were previously bitten by large ants near their
house, but thought that his wounds are already healed. He neglected his symptoms
such as intermittent fever, body malaise and chills for days, and self-medicated. This
contributed to the worsening of his case and brought about the severity of his
illness.Another factor was his lack of knowledge when it comes to the risks of acquiring

F. Comprehensive History

History of Present Illness

One month prior to admission, EL cleaned the canal near their house that was
causing flood in their area. He said that he saw some rats pestering around but still
cleaned it on bare foot knowing that he has wounds on his feet caused by ant bites. He
went back to work a day after to work overtime 2 days in a row. He then complained of
body malaise and chills but didnt seem to be worried about it because he thought it was
due to his lack of sleep. He experienced intermittent fever and drank 3 tabs of Bioflu
then rested after.

One day prior to admission, EL vomited 4 times and experienced loose bowel
movement , epigastric pain, decreased urine output and shortness of breath. He
decided to seek consult at the hospital near his work, which is Manila Naval Hospital.
Upon consulting, the doctors found out that his creatinine level were elevated so they
decided to retro-evac him at AFP Medical Center for further evaluation and
management.

Past Medical history

SGT EL has no known illness and was not diagnosed of any disease. He has no
known allergies to food nor drugs. He had a previous surgery when he was admitted at
AFP Medical Center last April 2009 due to gunshot wound on his right foot.

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7
 Family and Social History

ELs grandmother from his mother side was diagnosed with hypertension and
died when she was 65 years old. He doesnt recall his grandfathers sickness when he
died but he thinks it was due to old age at 87 years old. His grandparents had 3 children
and his mother was the middle child. His mother was diagnosed with myoma and is now
55 years old.

EL doesnt recall any illness from her father sides grandparents but both are
already dead, his grandfather at age 75 and grandmother at age 85. His grandparents
had 2 children, his father was the eldest among them. His father was diagnosed with
arthritis and died of brain stroke when he was 58 years old.

EL is the second child among 6 children. He verbalized that his siblings doesnt
have any illness that he knows of.

Family Genogram

MOTHER SIDE FATHER SIDE

Grandmother: Grandfather
Grandfather Grandmother
Hypertension

ELs Mother: RPs Father:

Myoma Arthritis
Cerebrovascular accidet

Eldest brother EL: 3rd sibling

4th sibling 5th sibling Youngest
35yo Weils Disease 31yo
30yo 21yo 14yo

Legend:
- Female / - Alive

- Male / - Deceased

- Client

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9
Nursing History (Gordons 11 Functional Health Patterns)

1. Health Perception/ Health Management

Before hospitalisation
SGT EL refers to health as a requirement for his work as a soldier because in
order to become a militray personnel, he must be physically fit and healthy. He barely
catch any illness and when he does, its just common colds or cough that he treats by
himself with over-the-counter medications. EL is a non-smoker, and an occasional
drinker who usually drinks 2 gins or a glass of lambanog during special occasions. EL
doesnt let himself get intoxicated and had never tried nor abused any illegal drugs.

During hospitalisation

EL values health more in such a way that he participates in any plan of care
necessary for his fast recovery, including adhering to the drug regimen specifically
needed for his case. EL appreciated the help of the healthcare team because since he
was admitted he thought that he was already going to die but he was thankful that we
were able to provide him the appropriate care that he needs and he is now hopeful that
he will be able to go back to his normal state of health. EL thinks that the reason for his
sickness was his carelessness when it comes to protecting himself against infections.
EL said that this is a lesson learned for him to be more careful of his well being and
therefore values his health more.

2. Nutritional Metabolic Process

Before hospitalisation

According to EL, he usually eats meat before and his favorite dish was adobo.
He was not picky when it comes to food, has no known allergies and was not taking any
vitamins.His weight was 76kg before, he eats three times a day with snacks in between
and can consume about 2 liters of fluid a day.

During hospitalisation

EL claims to have developed loss of appetite during the first few weeks of
admission, but is compliant when it comes to his uremic diet. He is able to avoid fruits
and fruit juices and eats the meal being given to him from the dietary department. He
lost 6 kg when he got sick and is currently weighing 70kg. He noticed that during
hospitalisation, his skin became dry but he is still taking care of his body hygiene,
bathing daily and brushing his teeth 3 times a day.

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 3. Elimination Pattern

Before hospitalisation

Prior to his illness, EL was able to urinate approximately 800ml light yellow urine
within two to four times per day. Also, he was able to defecate, soft in consistency and
brown in colour, at least once a day.

During hospitalisation

ELs urination pattern became oliguric during his first few weeks and he was only
able to urinate approximately 110-400 cc per day then became diuretic urinating about
4000-6000cc per day. Also, when it comes to his defecation, during his first day of
admission, he experienced loose bowel movement about 12 times characterized as
loose, slimy, and greenish in color.

4. Activity/ Exercise Pattern

Before hospitalisation

Before, SGT EL jogs every morning and goes to the gym to lift weights every
afternoon. He was an athlete and a runner before he had his injury on his right foot,
although hes no longer competing, hes still active in running and maintaining his
physical fitness.

During hospitalisation

Walking from his bed to the comfort room and walking around the ward and
hospital is his only means of exercise now. He spends most of his time lying and resting
in bed or watching TV, chatting with patients and playing games on his mobile phone.

5. Sleep and Rest pattern

Before hospitalisation

Prior to hospitalisation, EL sleeps eight hours every night and naps in the
afternoon for about 2-3 hours a day. He had no trouble sleeping, but is easily awaken.
He has no specific ways of relaxation but he usually sleeps or pray before sleeping in
order to relax. Before sleeping, he usually brushes his teeth first, takes a bath and pray.

During hospitalisation

During his first few weeks of being hospitalised, he had difficulty in sleeping
because of the pain and discomfort he was feeling. He was also easily awaken by the
noise made by other patients in the ward and could only sleep intermittently for 30mins

11
to an hour during the night. In the morning he sleeps for around 3-4 hours. He still
practices his ritual of brushing his teeth first, taking a bath, and praying before sleeping.

6. Cognitive-Perceptual Pattern

Before hospitalisation

After EL was injured in a battle that caused him the operation on his right foot, EL
had some difficulty hearing on both of his ears. EL said that he could still hear people
but has a hard time controlling the volume of his voice since he couldnt hear himself
well. Despite this hearing problem, he is not wearing any hearing devices and has not
consulted a specialist because he could still tolerate it. When it comes to his vision, EL
has clear eye sight of 20/20. He is a quick decision maker and has no problems in
making difficult decisions.

During hospitalisation

During the interview, it is evident that EL had a hard time hearing well, and he
still have the same problem as before though he still has no intentions of having it
checked and is still not using any kind of hearing aid. He still have a clear vision of
20/20, and had no changes in his memory nor concentration. During the first few weeks
of admission, he experienced epigastric pain characterized as sharp, stabbing, non-
radiating, and continous, specifically on right lower quadrant, rated as 9/10 aggravated
by movement.

7. Self-Perception/Self-Cognitive Pattern

Before hospitalisation

EL descibes himself as a quiet, strict, and friendly person. He feels good about
himself most of the time, and has always been optimistic when it comes to problems he
encounter in life. He considers himself as a family person who is the main decision
maker in his household. EL said that he is usually patient and doesnt get angry
immediately, however, when it comes to his family, if others are disrespectful to them, it
trigers him to be annoyed and furious.

During hospitalisation

When EL was admitted, he noticed sudden change in his weight. Although he

can still do his routine activities of daily living, he felt like he was going to die during his
first days in the ward. He feels that this was a lesson learned for him. He felt a bit
depress when he found out that his father died after he was admitted at the ward, but
his wife helped him in coping and supported him all throughout his stay.

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 8. Role-Relationship Pattern

Before hospitalisation

EL is the 2nd among 6 children. He is currently living in his barracks at Fort

Bonifacio but frequently visits his wife and children, a 6 years old and a one month old
baby. EL said that he hasnt encountered a problem that was difficult to handle. When it
comes to his family, besides his wife and children, he is also giving financial assistance
to his mother. EL had no problems when it comes to his children and that things are
generally going well when in comes to his work and that his income is sufficient to their
needs.

During hospitalisation

EL said that he is managing his condition well right now. EL verbalized that his
admission to the hospital greatly affected his family and hat they became worried and
lonely specially because it happened during the death of his father. Despite this, he
never lost hope, although there was a time when he felt lonely due to his condition, his
family were his support system through everything that happened to him.

9. Sexuality-Reproductive Pattern

Before hospitalisation

EL was circumcised when he was 10 years old. He said that he was sexually
active with his wife before being hospitalised and is generally satisfied with this sex life
and relationship. Due to his line of work, problems that occur in their relationship usually
happen due to his wifes jealousy. Despite this, he thinks that this is just a normal
phenomenon as husband and wife. They are using withdrawal method as a
contraceptive measure.

During hospitalisation

During ELs stay in the hospital, eventhough his wife is with him, they express
their love in other ways rather than having intercourse; he understands that he is
ongoing treatment and that his wife just gave birth to their youngest child.

10. Coping/Stress Tolerance Pattern

Before and during hospitalisation

In the past year or two, the biggest change that happened to his life was when
his eldest child started to go to school. When a crisis arrives, the one that he usually
consults is his wife. Although right now, the most accesssible person that he calls for
help is his brother because hes the one closest to his place. He is mostly relaxed and
doesnt smoke, use drugs nor drink when stressed. In order to cope with stress he

13
usually share his problems with his wife and pray. He said tht most of the time this
method is helpful to him.

11. Values-Belief Pattern

Before hospitalisation

EL said that he generally gets things he wants in life, but not all. Before he
married his wife, he was a Protestant, but is now a baptized Roman Catholic. He thinks
that the religion itself is not important, but the faith you have with Him. He seldom goes
to church but prays every night usually before he sleeps and mostly when he has
problems.

During hospitalisation

In the future, EL plans on providing a new house for his wife and children and to
be able to help his children graduate from college. He became closer to God after this
great trial in his life. EL said that he doesnt have any sperstitious belief before and he
still doesnt have any now. He is unable to go to church during his stay in the hospital
but still prays every night before he goes to sleep. He believes that going to church is
not the only means to prove that he has faith in God.

G. Physical Assessment

Physical Examination (Date of Exam: 04 March 2017)

GENERAL SURVEY: Conscious, and coherent, ambulatory

Vital Signs: Blood Pressure: 100/70mmHg

Cardiac rate: 99 beats per minute
Respiratory rate: 26 breaths per minute
Temperature: 37.1 Celsius via axilla
Oxygen saturation: 97%

Anthropometric Measurement:
Height: 167 cm
Weight: 70 Kg

APPEARANCE

(-) gross deformities

Generalized body weakness
With good hygiene and well-groomed

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 Well-dressed wearing the patients gown
SKIN
Warm to touch
with grade 2 edema noted on both feet and arms
Generalized yellowish discoloration of the skin
HEAD
Normocephalic
(-) lesions and deformities
NAILS
(-) clubbing or deformity of hands
With good capillary refill of less than 3 seconds
EYES
PERRLA: Pupils equally round and reactive to light accommodation
With periorbital edema
icteric sclera
EARS
(-) pain, inflammation, drainage and hearing loss
NOSE
(-) congestion, lesions, nasal flaring

MOUTH/THROAT/ORAL CAVITY
With soft lips; pinkish buccal mucosa
pinkish gums; no dentures
No inflammation of tonsils
NECK
no neck vein distention

CHEST
Symmetrical chest expansion,
Normal rate and regular rhythm
LUNGS
No retractions
With clear breath sounds upon auscultation
ABDOMEN
Soft and flabby; not distended, no ascites
(+) tenderness upon palpation on epigastric area
Epigastric pain of 9/10
With 12 episodes of watery stools amounting to 1 cup per bout non-
bloody, slimy, greennish in color
GENITO-URINARY
(-) urinary frequency,
With pain and burning sensation upon urination
Oliguric with urine output of 110-400 cc per day
EXTREMITIES
With good grips on both upper and lower extremities

15
 No gross deformities
No cyanosis
With atrophic right leg with scars noted

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CLINICAL DISCUSSION

A. Anatomy and Physiology

The Lymphatic System

The lymphatic system sometimes is considered to be a part of the circulatory

system because it transports a fluid through vessels and empties it into venous blood.
Because it consists of organs that work together to perform certain functions, it may be
treated as a separate system. The lymphatic system has a major role in the bodys
defense against disease.

Function

The lymphatic system has three primary functions. First, it returns excess
interstitial fluid to the blood. Capillary microcirculation happends when fluid leaves the
capillary at the arteriole end and returns at the venous end of the fluid that leaves the
capillary, about 90% is returned. The 10% that does not return becomes part of the
interstitial fluid that surrounds the tissue cells. Small protein molecules may leak
through the capillary wall and increase the osmotic pressure of the interstitial fluid. This
further inhibits the return of fluid into the capillary, and fluid tends to accumulate in the
tissue spaces. If this continues, blood volume and blood pressure decrease significantly
and the volume of tissue fluid increases, which results in edema. Lymph capillaries pick
up the excess interstitial fluid and proteins and return them to the venous blood. The
second function of the lymphatic system is the absorption of fats and fat-soluble
vitamins from the digestive system and the subsequent transport of these substances to
the venous circulation. The mucosa that lines the small intestine is covered with
fingerlike projections called villi. There are blood capillaries and special lymph
capillaries, called lacteals, in the center of each villus. Most nutrients are absorbed by
the blood capillaries, but the fats and fat-soluble vitamins are absorbed by the lacteals.
The lymph in the lacteals has a milky appearance because of its high fat content and is
called chyle. The third function of the lymphatic system is defense against invading
microorganisms and disease. Lymph nodes and other lymphatic organs filter the lymph

17
to remove microorganisms and other foreign particles. Lymphatic organs contain
lymphocytes that destroy invading organisms.

Components of Lymphatic System

The lymphatic system consists of a fluid (lymph), vessels that transport the
lymph, and organs that contain lymphoid tissue. Lymph is a fluid similar in composition
to blood plasma. It is derived from blood plasma as fluids pass through capillary walls at
the arterial end. About 90% of the fluid reenters the capillary at the venule end. The
remaining 10% is added to the interstitial fluid. As the interstitial fluid begins to
accumulate, it is picked up and removed by tiny lymphatic vessels which eventually
return it to the blood. As soon as the interstitial fluid enters the lymph capillaries, it is
called lymph. Returning the fluid to the blood prevents edema and helps to maintain
normal blood volume, plasma protein concentration, and blood pressure.

Lymphatic vessels, unlike blood vessels, only carry fluid away from the tissues.
The smallest lymphatic vessels are the lymph capillaries, which begin in the tissue
spaces as blind-ended sacs. Lymph capillaries are found in all regions of the body
except the bone marrow, central nervous system, and tissues that lack blood vessels,
such as the epidermis. The wall of the lymph capillary is composed of endothelium in
which the simple squamous cells overlap to form a simple oneway valve. This
arrangement permits fluid to enter the capillary but prevents lymph from leaving the
vessel. The microscopic lymph capillaries merge to form lymphatic vessels. These
vessels are similar to veins in structure, but they have thinner walls and more valves
than veins. Small lymphatic vessels join to form larger tributaries, called lymphatic
trunks, which drain large regions. Lymphatic trunks merge until the lymph enters the two
lymphatic ducts. The right lymphatic duct receives lymph from the vessels in the upper
right quadrant of the body. This includes the right side of the head and neck, the right
upper extremity, and the right side of the thorax. The right lymphatic duct empties into
the right subclavian vein. The thoracic duct collects the lymph from the remaining
regions of the body. The thoracic duct begins in the upper abdomen and ascends
through the thorax to empty into the left subclavian vein. The beginning of the thoracic
duct is called the cisterna chyli. The cisterna chyli collects lymph from two lumbar trunks
that drain the lower limbs and from the intestinal trunk that drains the digestive organs.
Lymph nodes that filter the lymph are located along the various routes of the lymphatic
system.

Like veins, the lymphatic tributaries have thin walls and have valves to prevent
backflow of blood. There is no pump in the lymphatic system like the heart in the
cardiovascular system. The pressure gradients to move lymph through the vessels have
to come from external sources. These pressure gradients come from skeletal muscle
contraction, from respiratory movements, and from contraction of the smooth muscle
within the wall of the vessel. Because there is no rhythmic heart to pump it along, lymph
transport is sporadic and much slower than the transport of blood in the veins. Anything
that interferes with the flow of lymph, such as an obstruction or surgical ligation, may
cause tissue fluid to accumulate, resulting in edema.

18
 Lymphatic organs are characterized by clusters of lymphocytes and other cells,
such as macrophages, enmeshed in a framework of short, branching connective tissue
fibers. The lymphocytes originate in the red bone marrow with other types of blood cells
and are carried in the blood from the bone marrow to the lymphatic organs. When the
body is exposed to microorganisms and other foreign substances, the lymphocytes
proliferate within the lymphatic organs and then travel in the blood to the site of the
invasion. This is part of the immune response that attempts to destroy the invading
agent. The lymph nodes, tonsils, spleen, and thymus are examples of lymphatic organs.

Lymph nodes are small, bean-shaped structures that are usually less than 2.5
centimeters (cm) in length. They are widely distributed throughout the body along the
lymphatic pathways, where they filter the lymph before it is returned to the blood. Lymph
nodes are not present in the central nervous system. There are three superficial regions
on each side of the body where lymph nodes tend to cluster. These areas are the
inguinal nodes in the groin, the axillary nodes in the armpit, and the cervical nodes in
the neck.

The Spleen

The spleen is located in the upper left abdominal cavity, just beneath the
diaphragm, and posterior to the stomach. It is similar to a lymph node in shape and
structure but it is much larger. The spleen is the largest lymphatic organ in the body.
Surrounded by a connective tissue capsule, which extends inward to divide the organ
into lobules, the spleen consists of two types of tissue called white pulp and red pulp.
The white pulp is lymphatic tissue consisting mainly of lymphocytes around arteries.
The red pulp consists of venous sinuses filled with blood and cords of lymphatic cells,
such as lymphocytes and macrophages. Blood enters the spleen through the splenic
artery, moves through the sinuses where it is filtered, and then leaves through the
splenic vein. The spleen filters blood in much the same way that the lymph nodes filter
lymph. Lymphocytes in the spleen react to pathogens in the blood and attempt to
destroy them. Macrophages then engulf the resulting debris, the damaged cells, and the
other large particles. The spleen, along with the liver, removes old and damaged
erythrocytes from the circulating blood. Like other lymphatic tissue, it produces
lymphocytes, especially in response to invading pathogens. The sinuses in the spleen
are a reservoir for blood. In emergencies such as hemorrhage, smooth muscle in the
vessel walls and in the capsule of the spleen contracts. This squeezes the blood out of
the spleen into the general circulation. If the spleen must be removed (splenectomy), its
functions will be performed by other lymphatic tissue and the liver.

19
The Liver

Structure

The liver is a large reddish brown organ that is located primarily in the right
hypochondriac and epigastric regions of the abdomen, just beneath the diaphragm. It is
the largest gland in the body, weighs about 1.5 kilograms, and has numerous functions.

On the surface, the liver is divided into two major lobes and two minor lobes. On
the anterior surface, the falciform ligament, a double fold of peritoneum that attaches
the liver to the abdominal wall, separates the right lobe from the left lobe. Two additional
small lobes are evident on the visceral surface. The caudate lobe is between the
ligamentum venosum and the inferior vena cava. The quadrate lobe is between the
ligamentum teres and the gallbladder. The porta is also on the visceral surface. The
porta is where the hepatic artery and hepatic portal vein enter the liver and where the
hepatic ducts exit. The substance of the liver is divided into functional units called liver
lobules. A liver lobule consists of hepatocytes (liver cells) that radiate outward from the
central vein like spokes of a wheel. The central veins of adjacent lobules unite to form
larger vessels, until they form the hepatic veins, which drain into the inferior vena cava.
Tiny channels, called bile canaliculi, are interwoven with the liver cells and carry the bile
that is produced by the hepatocytes toward the periphery of the lobule. Bile canaliculi
merge to form larger right and left hepatic ducts. These two ducts combine to form the
common hepatic duct, which transports bile out of the liver. The plates of hepatocytes
are separated from each other by venous channels, called sinusoids, which carry blood
from the periphery of the lobule toward the central vein. The sinusoids are lined with
special phagocytic cells, called Kupffer cells, that remove foreign particles from the
blood as it flows through the sinusoids. Portal triads, which consist of a branch of the
hepatic portal vein, a branch of the hepatic artery, and a branch of a hepatic duct, are
located around the periphery of the lobule.

The liver receives blood from two sources. Freshly oxygenated blood is brought
to the liver by the common hepatic artery, a branch of the celiac trunk from the
abdominal aorta. The common hepatic artery branches into smaller and smaller vessels
until it forms the small hepatic arteries in the portal triads at the periphery of the liver
lobules. Blood that is rich in nutrients from the digestive tract is carried to the liver by the
hepatic portal vein. The portal vein divides until it forms the small portal vein branches in
the portal triads at the periphery of the liver lobules. Venous blood from the hepatic
portal vein and arterial blood from the hepatic arteries mix together as the blood flows
20
through the sinusoids toward the central vein. The central veins of the liver lobules
merge to form larger hepatic veins that drain into the inferior vena cava.

Function

The liver has a wide variety of functions and many of these are vital to life.
Hepatocytes perform most of the functions attributed to the liver, but the phagocytic
Kupffer cells that line the sinusoids are responsible for cleansing the blood. Liver
functions include the following:
SecretionThe liver produces and secretes bile.
Synthesis of bile saltsBile salts are cholesterol derivatives that are produced in
the liver and facilitate fat digestion and the absorption of fats and
fat-soluble vitamins.
Synthesis of plasma protein The liver synthesizes albumin, fibrinogen,
globulins (except immunoglobulins), and clotting factors.
StorageThe liver stores glucose in the form of glycogen and also stores iron
and vitamins A, B12, D, E, and K.
DetoxificationThe liver alters the chemical composition of toxic compounds,
such as ammonia, to make them less harmful. It also
changes the configuration of certain drugs, such as penicillin, and
excretes them in the bile to remove them from the body.
ExcretionHormones, drugs, cholesterol, and bile pigments from the breakdown
of hemoglobin are excreted in the bile.
Carbohydrate metabolismThe liver has a major role in maintaining blood
glucose levels. It removes excess glucose from the blood and
converts it to glycogen for storage; it breaks down glycogen into
glucose when more is needed; it converts
noncarbohydrate molecules into glucose.
Lipid metabolismThe liver functions in the breakdown of fatty acids, in the
synthesis of cholesterol and phospholipids, and in the conversion
of excess carbohydrates and proteins into fats.
Protein metabolismThe liver converts certain amino acids into different amino
acids as needed for protein synthesis. It also converts
ammonia, produced in the breakdown of proteins, into urea,
which is less toxic and can be excreted in the bile.
FilteringThe phagocytic Kupffer cells that line the sinusoids remove bacteria,
damaged red blood cells, and other particles from the blood.

The Urinary System

21
Structure

The urinary system consists of the kidneys, ureters, urinary bladder, and urethra.
The kidneys produce the urine and account for the other functions attributed to the
urinary system. The ureters convey the urine away from the kidneys to the urinary
bladder, which is a temporary reservoir for the urine. The urethra is a tubular structure
that carries the urine from the urinary bladder to outside of the body.

Function

The overall function of the urinary system is to maintain the volume and
composition of body fluids within normal limits. One aspect of this function is to rid the
body of waste products that accumulate as a result of cellular metabolism, and because
of this the urinary system is sometimes referred to as the excretory system. Although
the urinary system has a major role in excretion, other organs contribute to the
excretory function. Some waste products, such as carbon dioxide and water, are
excreted by the lungs in the respiratory system. The skin is another excretory organ that
rids the body of wastes through the sweat glands. The liver and intestines excrete bile
pigments that result from the destruction of hemoglobin. The major task of excretion still
belongs to the urinary system, and if the system fails the other organs cannot
adequately compensate and toxic levels of waste products accumulate rapidly. In
addition to ridding the body of waste materials, the urinary system maintains an
appropriate fluid volume by regulating the amount of water that is excreted in the urine.
Other aspects of its function include regulating the concentrations of various electrolytes
in the body fluids and maintaining normal pH of the blood. In addition to maintaining
fluid homeostasis in the body, the urinary system controls red blood cell production by
secreting the hormone erythropoietin. The urinary system also plays a role in
maintaining normal blood pressure by secreting the enzyme renin, which activates
angiotensin II to increase blood pressure.

Components of Urinary System

22
 The kidneys are a pair of bean-shaped organs found along the posterior wall of
the abdominal cavity. The left kidney is located slightly higher than the right kidney
because the right side of the liver is much larger than the left side. The kidneys, unlike
the other organs of the abdominal cavity, are located posterior to the peritoneum and
touch the muscles of the back. The kidneys are surrounded by a layer of adipose that
holds them in place and protects them from physical damage. The kidneys filter
metabolic wastes, excess ions, and chemicals from the blood to form urine.

The ureters are a pair of tubes that carry urine from the kidneys to the urinary
bladder. The ureters are about 10 to 12 inches long and run on the left and right sides of
the body parallel to the vertebral column. Gravity and peristalsis of smooth muscle
tissue in the walls of the ureters move urine toward the urinary bladder. The ends of the
ureters extend slightly into the urinary bladder and are sealed at the point of entry to the
bladder by the ureterovesical valves. These valves prevent urine from flowing back
towards the kidneys.

The urinary bladder is a sac-like hollow organ used for the storage of urine. The
urinary bladder is located along the bodys midline at the inferior end of the pelvis. Urine
entering the urinary bladder from the ureters slowly fills the hollow space of the bladder
and stretches its elastic walls. The walls of the bladder allow it to stretch to hold
anywhere from 600 to 800 milliliters of urine.

The urethra is the tube through which urine passes from the bladder to the
exterior of the body. The female urethra is around 2 inches long and ends inferior to the
clitoris and superior to the vaginal opening. In males, the urethra is around 8 to 10
inches long and ends at the tip of the penis. The urethra is also an organ of the male
reproductive system as it carries sperm out of the body through the penis. The flow of
urine through the urethra is controlled by the internal and external urethral sphincter
muscles. The internal urethral sphincter is made of smooth muscle and opens
involuntarily when the bladder reaches a certain set level of distention. The opening of
the internal sphincter results in the sensation of needing to urinate. The external urethral
sphincter is made of skeletal muscle and may be opened to allow urine to pass through
the urethra or may be held closed to delay.

23
 B. Pathophysiology

Leptospirosis is caused by a microorganism of the genus Leptospira. Leptospires

may enter the host thorugh abbrasions in the skin or through intact mucous
membranes, especially the conjunctiva and the lining of the oro- and nasopharynx.
Drinking of contaminated water may introduce eptospires through the mouth, throat, or
esophagus. After entry of the organisms, leptospiremia develops, with subsequent
spread to all organs. Multiplication takes place in blood and in tissues. The organism
then enters the bloodstream, multiplies, and spreads to all organs, particularly the liver
and kidneys. In humans, leptospires rarely persist in the kidneys for longer than 60 days
and leptospires can be isolated from the blood and cerebrospinal fluid (CSF) during the
first 4 to 10 days of illness. It is not clear why the presence of leptospires in the CSF
does not cause damage. All forms of leptospires can damage the wall of small blood
vessels; this damage leads to vasculitis with leakage and extravasation of cells,
including hemorrhages. The most important known pathogenic properties of leptospires
are adhesion to cell surfaces and cellular toxicity.

Vasculitis is responsible for the most important manfestations of the disease.

Although leptospires mainly infect the kidneys and liver, any organ may be affected. In
the kidney, leptospires migrate into the interstitium, renal tubules, and tubular lumen,
causing intertitial nephritis and tubular necrosis. Hypovolemia due to dehydration or
altered capillary permeability may contribute to the development of renal failure. Acute
renal failure has three distinct phases: oliguric, diuretic, and recovery. In oliguric phase,
there is a decreased urine output of less than 400ml/24hours (oliguria), decreased
blood flow to the kidneys (pre-renal oliguria), impairment of kidneys ability to conserve
sodium, acute tubular necrosis possibly resulting from pre-renal oliguria, increased
blood urea nitrogen (BUN) to creatinine levels and decreased ration of BUN to ceatinine
(from normal levels of 20:1 to abnormal decrease of 10:1). That would result to
hypovolemia and causes edema, weight gain, and elevated blood pressure. In the
Diuretic phase, there is a slow increase in BUN and creatinine levels that would result to
hypovolemiaand weight loss. Decreased potassium, sodium, and water levels if not
treated will lead to death. In Recovery Phase, there is a normal BUN and creatinine
levels with urine output between 1 and 2 L/day. In the liver, centrilobular necrosis with
proliferation of Kupffer cells may be found, with hepatocellular dysfunction. However,
severe hepatocellular necrosis is not a feature of leptospirosis. Pulmonary involvement
is the result of hemorrhage and not of inflammation. Invasion of skeletal muscle by
leptospires results in swelling, vacuolation of the myofibrils, and focal necrosis. In
severe leptospirosis, vasculitis may ultimately impar the microcirculation and increase
capillary permeability, resulting in fuid leakage and hypovolemia.

When antibodies are formed, leptospires are eliminated from all sites in the host
except the eye, the proximal renal tubules, and perhaps the brain, where they may
persist for weeks or months. The persistence of leptospires in the aqueous humor
occasionally causes chronic or recurrent uveitis. The systemic immune response is
effective in eliminating the organism but may also produce symptomatic inflammatory

24
reactions. A rise in the antibody titer coincides with the development of meningitis; this
association suggests that an immunologic mechanism is responsible. After the start of
antimicrobial treatment for leptospirosis, a Jarisch-Herxheimer reaction similar to that
seen in other spirochetal diseases may develop. Although frequently described in older
publications, this reaction seems to be rare event in leptospirosis and is certainly less
frequent in this infection than in other spirochetal diseases.

If with no management, there will be decreased urine output; increased BUN and
creatinine, hypervolemia, edema, weight gain and increased BP. Probably would result
to multiple organ failure that may lead to death.

25
 C. Schematic Diagram
Predisposing Factor
-walking barefoot with
wounds on both feet
(10 February 2017)

Etiologic Agent: Leptospires via

rodents urine

Anicteric/Leptospiremic Abrasions in the skin or through

Phase: intact mucous membranes
-Fever with chills
-Nausea and vomiting
-Body malaise Multiplication: blood and tissues Diagnostics:
-Nausea and vomiting -increased
BUN and
Vasculitis with leakage and
Crea
extravasation
-hypokalemia
Immune Phase:
-afebrile -decreased
Hgb, Hct, RBC
-increased
Icteric/Weils Disease:
WBC
-jaundice
-oliguria
-generalized edema KIDNEY LIVER
-pulmonary
complications like
dyspnea, chest pain
Adhesion to cell surfaces Centrilobular necrosis with
and cellular toxicity proliferation of Kupffer cells

Invasion interstitium of the kidney, renal With hepatocellular dysfunction

tubules, and tubular lumen

Hepatomegaly
Altered Capillary Permiability

Diagnostics:
Acute Tubular Necrosis -Increased ALT, AST, Total
BIlirubin, Total Direct
Bilirubin, Total indirect
Acute Renal Failure bilirubin
-Decreased albumin

Oliguric Phase:
-decreased urine output (110-400cc/day)
-increased BUN and Crea
-hypervolemia
-edema, weight gain 26
 No Management With Management

Surgical Management: Medical Management:

Multiple Organ Failure -Medication
-Blood Transfusion
-Renal Replacement
Therapy
-Rhabdomyolosis (Hemodialysis)
-Hemolysis
-Myocarditis
-Pericarditis
-Congestive heart failure Diuretic Phase:
-Cardiogenic shock -slow decrease in BUN
-Adult Respiratory distress and Crea
syndrome -hypovolemia and
-Necrotizing pancreatitis weight loss
-increased K, Na, and
water levels
Death -increased output

Recovery Phase:
-Normal BUN and Crea levels with
urine output ay 1-2L/day
-Removal of IJ cath
-Continous monitoring of renal
function

Good Prognosis

27
 D. Course in the Ward

DAY 1 (Admission)

A 33 years old male clent was admitted at exactly 1300H last 04 March 2017 at
ER Medicine with chief complaints of decreased urine output, epigastric pain, and
painful urination. He underwent certain diagnostic procedures, primarily KUB Ultrasound
to include cortical thickness, Chest X-ray PA view, Leptocheck, Leptomat Test, ABG, 12
lead ECG, urinalysis, ABG and blood chemistry including CBC with QPC with toxic
granulation, BUN, Crea, AST, ALT, Na, K, Ca, LDH, Mg, Random Albumin, TB B1, B2,
PT, INR, PTT, ESR, CRP and ASO.

Lab results from ER medicine revealed increased WBC count of 12.5x10^9/L,

increased PT of 14.9secs and increased APTT of 32.6secs. Creatine revealed high
results of 704.10 umol/L, increased BUN of 17.20mmol/L, decreased potassium of
3.49mmol/L, decreased calcium of 2.08mmol/L, high SGOT of 45U/L, and low albumin
of 29g/L. Total bilirubin was also high at 107.90umol/L, high direct bilirubin of
86.90umol/L, and high indirect bilirubin of 21umol/L. Patient was negative for toxic
granulation. Serology for ASO came in postive with 800iu/ml. Urinalysis came in with
pus cells in the urine of 25-30/hpf, 10-12/hpf, proteinuria of +3, sugar of +1.

He was placed on a uremic diet at 1800kcal/day in 3 regular meals and 2 light

snacks to include protein of high biologic value. IV access was placed on his right arm
with ongoing line of PNSS 1L x 4 hours. He was then transferred to the Nephrology
Ward for continuity of management.

1630H at Nephrology ward (6A):

Patient was accompanied by ward man and his wife via wheel chair, with
ongoing IVF of PNSS 1 L x 4hours and IFC attached to urine bag. He was ushered to
bed at cubicle A, safely and comfortably by the nurse on duty. Initial nursing history
assessment was done and vital signs were taken and recorded as follows: BP: 90/60
mmHg, PR: 70 bpm, RR: 19 cpm, T: 36C. Patient was oriented on ward policies and
evacuation plan. Patient was for bood cs of 2 sites, fbs, and lipid profile. Proper
instructions for fasting instructed to patient.

1800H at Nephrology ward

Patient experienced loose bowel movement with episodes of watery stool 6 times
accompanied by epigastric pain rated as 9/10 with facial grimacing noted. Referred
patient to resident on duty, with orders made and carried out. Instructed patient
regarding fecalysis and stool collection. Omeprazole 40mg TIV given now as ordered
then every 24hours.

Patient had a total of 12 episodes of LBM for the whole day.

28
 Fecalysis result came in with rare yeast found in stool, color is greenish, mucoid
in consistency, no RBC nor pus cells found, no ova nor parasite seen.

DAY 2 (05 March 2017)

0700H at Nephrology ward

Patient experienced loose bowel movement with episodes of greenish watery
stool 3 times accompanied by epigastric pain rated as 9/10 with facial grimacing and
sunken eyeballs noted.

0740H at Nephrology ward

Patients IVF rate was increased and 20 meqs KCL was incorporated to PNSS1L
x 6hours. Loperamide was started to be given at 2mg/tab, 2 tabs now then 1 tab after
each stool, not to exceed 16mg/day.

1000H at Nephrology Ward

Patients total urine output yesterday was 110cc drained from urine bag of IFC
with 100cc tea-colored urine output noted during rounds. Patient was seen and
examined by Dr. Soriano. Furosemide 80mg TIV was given stat as ordered with urine
output of 30cc noted after an hour. Another dose of furosemide 110mg TIV was given
stat as ordered with urine output of 50cc after an hour.

Leptocheck(ICT) revealed patient was positive. Patients diagnosis was reversed

to Severe Leptospirosis; Weils Syndrome.

1330H
Patient was seen by TCVS and underwent emergency IJ catheterization at right
neck under local anesthesia at bedside. Chest x-ray revealed correct placement of IJ
catheter. Vitamin K 1 amp every 8 hours x 3 doses was given as ordered.
Patients IV rate was decreased to KVO. Furosemide 200mg TIV was given stat
as ordered wth urine output of 150cc noted after an hour.
Patients total urine output for the whole 7am-3pm shift was 1430cc.

1630H
Patient urine output was 50cc. Furosemide drip was started at 80mg + 80cc
PNSS to run at 12mg/kg/hr as ordered. Strict monitoring of intake and output hourly was
done. Loperamide was shifted to be given at 2mg/tab, 2 tabs q 6 hours as ordered.

Patient had a total of 6 bowel movement for the whole day. Loperamide was
discontinued.

DAY 3 (06 March 2017)

0800H
Laboratory results revealed low potassium level of 3.49mmol/L.Patient was seen
and examined by Cpt Arellano and team. IVF was shifted to D5LR 1L + 40meqs KCL to

29
run at 6 hours. Serum creatinine was also high at 1,046.6 umol/L. Patient was advised
to adhere to dietary and fluid restrictions.
At the end of 7-3 shift patient had a total urine output of 1,405cc.

DAY 4 (07 March 2017)

Laboratory result revealed latest potassium of 3.32umol/L with episodes of

generalized muscle weakness noted. Patient was seen and examined by Capt Arellano
and team. IVF of D5LRS 1L + 40meqs KCL was maintained at 6 hours rate.
Domperidone 10mg/tab 1 tab was given stat.

1700H
IVF of D5LR 1L + 40meqs KCL was consumed and shifted to PNSS1L + 40meqs
KCL to run at 8 hours.

Total urine output from 11pm-7am shift was 1,300cc with dark yellowish urine
draining from urine bag.

DAY 5 (08 March 2017)

1000H
Patient was seen and examined by Cpt Arellano and team. Furosemide 80mg
TIV was given stat as ordered with urine output of 600cc after an hour.

Patient had total urine output of 3,280cc during the 7-3 shift with yellowish urine
draining from urine bag.

Patient was dropped from SIL status with same diagnosis.

1530H
IVF was shifted to PNSS1L x 10 hours.

DAY 6 (09 March 2017)

0950H
Laboratory results revealed still high crea but decreased to 338.40 umol/L with
normal potassium at 4.01mmol/L.Patients labs also revealed high but decreased
SGOT/AST of 85U/l, SGPT/ALT of 85U/L, Total Bilirubin of 35.30 umol/L, Direct
Bilirubin of 26.10umol/L and normal range of Indirect Bilirubin at 9.2umol/L.

Patients on day 6 of Ceftriaxone 2g TIV every 24 hours given as ordered for

completion of dosage treatment.

1600H

30
 IVF rate increased to PNSS1L x 12 hours. Monitored intake and output every 4
hours and record.

1800H
Patients IFC was removed aseptically by duty nurse as ordered.

DAY 7 (10 March 2017)

0800H
Maintained patient on IVF at PNSS1L x 12 hours. Latest urinalysis results
revealed negative sugar and negative protein, with RBC at 6-8/hpf and pus cells at 0-
2/hpf.

Patients lates intake for the whole day was 4,930cc and output of 3,360cc.
Patient had 2 episodes of bowel movement with brownish colored stool, semi-formed in
consistency. No pain upon urination or any discomfort verbalized.

DAY 8 (11 March 2017)

Maintained patient on IVF at PNSS1L x 12 hours. Still for funding of Leptomat

Test. On continuity of care and management.

DAY 9 (12 March 2017)

Patient seen by Infectious Department Service, discontinued Ceftriaxone as

ordered.

DAY 10 (13 March 2017)

IVF of PNSS x 12 hours consumed and terminated as ordered. Leptomat Test

deferred.

DAY 11 (14 March 2017)

Omeprazole IV shifted to Lanzoprazole FDT 30mg/tab 1 tab ODBB.

DAY 12 (15 March 2017)

DAY 13 (16 March 2017)

DAY 14 (17 March 2017)

Patient was seen and examined by Dental Service for oral prophylaxis and
treatment.

31
DAY 15 (17 March 2017)

Patient was referred to TCVS for removal of IJ catheter with latest Creatinine at
127.90umol/L and normal BUN a 5.20mmol/L. Patients sodium was 140.2mmol/L and
potassium was 4.17mmol/L, all are also at normal levels.

DAY 16 (18 March 2017)

Patient had no complaints. On conitnuity of care and management.

DAY 17 (19 March 2017)

Patient had no complaints. On conitnuity of care and management.

DAY 18 (20 March 2017)

For EDRD effective 24 March 2017 with final diagnosis of Severe Leptospirosis,
Weils Syndrome, resolving. Patient has no home medications ordered, with stable
status and P3T profile. Patient is for REprofiling after 3 months on July 2017.

DAY 19 (21 March 2017)

With latest creatinine decreased but slightly high at 111.20umol/L and BUN at
5.60mmol/L. For EDRD effective 24 March 2017 with complete discharge requirement.

E. Medical Management

Laboratory / Diagnostic Procedures

SPUTUM MICROSCOPY

DATE: 12 NOVEMBER 2013

Specimen 1 2
Visual Appearance Salivary Salivary
Reading 0 0
Laboratory Diagnosis Negative Negative

RADIOLOGIC REPORT

DATE: 25 OCTOBER 2013

32
Chest PA result:
Nodulohazed densities are seen diffusely scattered on both lungs.
Heart is slightly enlarged by CT ratio (0.55).
Aorta is not dilated.
Diaphragm and sulci are intact.
The rest of the visualized chest structures are unremarkable.

Impression: EXTENSIVE PTB, BILATERAL

CANNOT TOTALLY RULED OUT PULMONARY NODULES
MILD CARDIOMEGALY

Implication: Chest X-ray was done to make images of the heart, lungs, airways, and the
bones of the spine. It is also done to localize and visualize the extent of
lesions in the lung fields.

33
 HEMATOLOGY

DATE: 23 SEPTEMBER 2013

Blood component Results Normal Values Units

Hemoglobin 125 135 180 gms/L
Hematocrit 0.38 0.35 0.51
RBC Count 4.31 3.93 5.22 x10^12/L
WBC Count 7.00 5.0 10.0 x10^9/L
Neutrophils 0.75 0.55 0.65
Lymphocytes 0.17 0.25 0.35
Eosinophils 0.03 0.02 0.04
Monocytes 0.04 0.02 0.10
Basophils 0.01 0.00 0.01
MCV 87.4 80 100 fl
MCH 28.9 27 31 pg
MCHC 33 31 36 g/dL
RDW 12.3 11.0 15.0
Platelets 203 130 500 x10^9/L

BLUE = Below Normal RED = Above Normal

Interpretation:
Based on the obtained values of the hematology result, the hemoglobin shows a
decrease in normal value which indicates that, as the disease condition progresses,
accumulation of exudates in alveoli increment that may lead to diminished oxygen
supply due to less lung expansion. And as a primary defense against infection,
neutrophils increased in amount to ingest and digest the bacteria that invaded the body
system. On the other hand, as an integral part of immune system, lymphocytes declined
as it destroy the tubercle bacilli that cause the disease.

ABG (ARTERIAL BLOOD GAS)

DATE: 23 SEPTEMBER 2013

Results Normal Values

Blood pH 7.48 7.35 - 7.45
PaCO2 47 35 - 45 mmHg
PaO2 99.7 80 - 100 mmHg
Bicarbonate (HCO3) 35.2 22 - 26 mEq/L
TCO2 36.8 15 20 ml/dl
O2 saturation 97% 95 - 100%

BLUE = Acidosis RED = Alkalosis

34
Interpretation:
The ABG findings resulted to Metabolic Alkalosis due to diuretic therapy that
promotes excretion of potassium (K+) such as thiazide, and excessive adrenocorticoid
hormones.

URINALYSIS

DATE: 24 SEPTEMBER 2013

Results Normal Values

Color Light Yellow Amber Yellow
Transparency Slightly Turbid Clear
pH 5.0 4.8 - 7.6
Specific gravity 1.010 1.015 - 1.025
Glucose Negative Negative
Protein Negative Negative
RBC 3-5 0.1/HPF
Pus cells 2-4 0.2/HPG

BLUE = Below Normal RED = Above Normal

Interpretation:
The result showed a decline of specific gravity within normal range, this is
due to frequent urination of the patient as he is taking diuretics to control his
hypertension. Presence of red blood cells and pus cells in the urine may indicate that
the body is fighting an infection in the lower or upper urinary tract.

35
 BLOOD CHEMISTRY

TEST 23 SEPT 24 SEPT 26 SEPT 13 OCT 14 NOV Normal Values

Creatinine 108.4 82.3 95.5 103.4 62.0106.0 umol/L
Urea/BUN 5.10 2.787.64mmol/L
AST 25.4 10.0 34.0 U/L
ALT 61.2 10.0 44.0 U/L
Uric Acid Ver 2 374 202406
Cholesterol Gen 2 3.74 0.00 5.20
Glucose HK Gen 3 5.16 3.90 5.80
HDL-C plus 3rd Gen 1.09 > 1.40
LDLCALC 2.4 >3.36
Triglycerides Liquid 0.64 0.45 1.82
Albumin 45.8 35.0 50.0
Sodium (Na) 141 144 141 136145 mmol/L
Chloride (Cl) 103 97111 mmol/L
Calcium (Ca) 2.30 2.202.75 mmol/L
Magnesium (Mg) 1.028 0.601.10 mmol/L

BLUE = Below Normal RED = Above Normal

Interpretation:
The blood chemistry result shows slight elevation of creatinine from the
beginning, which indicates that the patient has an ongoing renal impairment, but is
resolving as seen on succeeding results. The Alanine Aminotransferase resulted high
interpreting slight liver impairment.
With regards to High Density Lipoprotein and Low Density Lipoprotein results,
both shows lower than normal level. It is good that the LDL is lower in normal value as it
increases the deposition of these substances in the wall of arterial vessels when it is
elevated, that could lead to incidence of CAD. On the other hand, HDL should be high
as it lowers the risk of CAD by transporting cholesterol away from the tissues and cells
of the arterial wall to the liver for excretion.

24 HOURS URINE TEST

DATE: 18 OCTOBER 2013
SI CONVENTIONAL
TEST RESULT NORMAL VALUES RESULT NORMAL VALUES
Potassium, Urine 55 25 125 55 25 125
mmol/24 mmol/24hrs mEq/24hrs mEq/24hrs
hrs
Total Volume 2520
ml/24hrs
Total Volume (ml/min) 1.8 ml/min

Interpretation:
The test showed a normal result of potassium in the urine collected within 24hrs.

36
 SERUM POTASSIUM TESTS

DATE RESULTS NORMAL VALUES

23 SEPTEMBER 2013 2.1 3.5 - 5.1 mEq/L
26 SEPTEMBER 2013 2.40 3.5 - 5.1 mEq/L
28 SEPTEMBER 2013 2.1 3.5 - 5.1 mEq/L
30 SEPTEMBER 2013 2.3 3.5 - 5.1 mEq/L
1 OCTOBER 2013 2.8 3.5 - 5.1 mEq/L
4 OCTOBER 2013 3.0 3.5 - 5.1 mEq/L
7 OCTOBER 2013 2.7 3.5 - 5.1 mEq/L
9 OCTOBER 2013 3.0 3.5 - 5.1 mEq/L
13 OCTOBER 2013 3.1 3.5 - 5.1 mEq/L
17 OCTOBER 2013 2.8 3.5 - 5.1 mEq/L
21 OCTOBER 2013 3.2 3.5 - 5.1 mEq/L
24 OCTOBER 2013 3.3 3.5 - 5.1 mEq/L
25 OCTOBER 2013 2.9 3.5 - 5.1 mEq/L
26 OCTOBER 2013 3.0 3.5 - 5.1 mEq/L
31 OCTOBER 2013 3.4 3.5 - 5.1 mEq/L
4 NOVEMBER 2013 3.6 3.5 - 5.1 mEq/L
8 NOVEMBER 2013 3.5 3.5 - 5.1 mEq/L
11 NOVEMBER 2013 3.5 3.5 - 5.1 mEq/L

BLUE = Below Normal RED = Above Normal

Interpretation:
The test shows that the patient is hypokalemicat the time of admission and
several days which may be due to excessive adrenocorticoid hormone that lowers
potassium level, and as a way to control hypertension, the patient is taking
Hydrochlorothiazide, a diuretic that promotes excretion of potassium. Also, the result
showed an improvement as viewed of back to normal potassium level on 42nd day of
confinement.

37
Drug Study
Mechanism of Action and
Drug Name
Indication
Cefriaxone MOA: Works by inhibiting the
Dose: 2g every 24 mucopeptide synthesis in the
hours bacterial cell wall. The beta-
Route: Intravenous lactam moiety of Ceftriaxone
Drug Classification: binds to
Antibiotic/ carboxypeptidases,endopepti
Cephalosporin- 3rd dases,and transpeptidases in
generation the bacterial cytoplasmic
membrane. These enzymes
are involved in cell-wall
synthesis and cell division.By
binding to these enzymes,
Ceftriaxone results in the
formation of defective cell
walls and cell death
I: Neurologic complications,
carditis and arthritis, gram
negative infections,
Side Effects and Adverse Effects
Body Whole:Pruritus, fever,
chills, pain, induration at IM
injection site; phlebitis (IV site)
GI: Diarrhea, abdominal
cramps, pseudomembranous
colitis, biliary sludge
Urogenital:Genital pruritus;
moniliasis
38
Nursing Responsibilities
Observe 10 Rights on
giving medication
Instruct to take drug with
meals to avoid side effect
of GI upset
Instruct patient to report
any discomforts like
bleeding or pain
Instruct patient to complete
course of treatment to
prevent antibiotic
resistance
Skin testing must be done
before administration of
medication
 meningitis, gonorrhea. Also
for bone and joint infections,
lower respiratory tract
infection, middle ear
infection, septicemia, and
urinary tract infection.
Sodium MOA: Increases plasma
Bicarbonate bicarbonate, neutralizes
Dose: 650mg per gastric acid which forms
tab, one tab p.o. TID water, sodium
Route: Oral chloride,carbon dioxide, and
Drug Classification: raises blood pH
Gastro-intestinal
agent; antacid; fluid I: Treatment of metabolic
and electrolyte acidosis,promotion of
balance agent gastric,systemic and urine
alkalinization in the case of
intoxication with weak
organic acids
GI:Belching, gastric distention,
flatulence
Metabolic:Metabolic alkalosis;
electrolyte imbalance: sodium
overload (pulmonary edema),
hypocalcemia (tetany),
hypokalemia, milk-alkali
syndrome, dehydration
Urogenital:Renal calculi or
crystals, impaired kidney
function
39
Observe 10 Rights on
giving medication
Assess the clients fluid
balance throughout the
therapy. Includes intake
and output, daily weight,
edema and lung sounds
Symptoms of fluid overload
should be reported such as
hypertension, edema, and
difficulty breathing
Signs of acidosis should be
assessed such as
disorientation, headache,
and hyperventilation
Assess for alkalosis by

Furosemide MOA: Thought to inhibit
Dose: 100mg sodium and chloride
Route: Intravenous reabsorption from ascending
drip loop of Henle and proximal
Drug Classification: and distal renal tubules.
Sulfonamide Loop Increases potassium
Diuretic excretion and plasma
volume, promoting renal
excretion of water, sodium,
CV:Postural hypotension,
dizziness with excessive
diuresis, acute hypotensive
episodes, circulatory collapse
Metabolic:Hypovolemia,
dehydration, hyponatremia,
hypokalemia, hypochloremia
metabolic alkalosis,
hypomagnesemia,
40
monitoring the client for
confusion, irritability, and
paresthesia
Tablets must be taken with
a full glass of water
Monitor the clients serum
calcium, sodium,
potassium, bicarbonate
concentrations, serum
osmolarity, acid-base
balance and renal function
before and throughout the
therapy
Observe 10 Rights on
giving medication
Monitor vital signs before
and after giving of medicine
Do not administer if BP is
below 90/60mmHg
Monitor intake and output
Instruct patient to move
slowly when rising to avoid
chloride, magnesium, and
calcium
I: Acute pulmonary edema,
edema secondary to heart
failure, hypertension, ascites
hypocalcemia (tetany), light-headedness or
hyperglycemia, glycosuria, dizziness from sudden
elevated BUN, hyperuricemia decrease of BP
GI:Nausea, vomiting, oral and Watch for signs of allergic
gastric burning, anorexia, or adverse reactions
diarrhea, constipation,
abdominal cramping, acute
pancreatitis, jaundice
Urogenital:Allergic interstitial
nephritis, irreversible renal
failure, urinary frequency
Hematologic:Anemia,
leukopenia, thrombocytopenic
purpura; aplastic anemia
pecSenses:Tinnitus, vertigo,
feeling of fullness in ears,
hearing loss (rarely
permanent), blurred vision
BodyWhole:Increased
perspiration; paresthesias;
activation of SLE, muscle
spasms, weakness
41
Vitamin K MOA: Phytomenadione
Dose: 10mg or 1 promotes hepatic synthesis
ampule every 8 hours of clotting factors. It is a
Route: Intravenous naturally occurring compound
Drug Classification: that is used to prevent and
Haemostatic agent treat haemorrhages related to
vitamin K deficiency
I:Hypoprothrombinemia
secondary to vitamin K
malabsorption, drug therapy,
or excessive vitamin A
dosage;
hypoprothrombinemia
secondary to effect of oral
anticoagulants; prevention of
hemorrhagic disease of
newborn
Domperidone MOA:
Dose: 10mg tab now I: Symptomatic management
Route: Oral of upper gastrointestinal
Dyspnea, Cyanosis,
Erythematous skin eruptions,
Pruritus , Scleroderma-like
lesions, Flushing,
Hyperbilirubinemia (in
premature neonates),
Hypotension, Injection site
reactions, Taste alterations
CNS: dry mouth,
headache/migraine, insomnia,
nervousness,dizziness, thirst,
42
Monitor PT to determine
dosage effectiveness as
ordered
Watch for signs of flushing,
weakness, tachycardia and
hypotension; may progress
to shock
Assess for bleeding or
bruising: hematuria, black
tarry stools, hematemesis
If severe bleeding occurs,
dont delay other
measures, such as fresh
frozen plasma or whole
blood
Advise patient to avoid IM
inj., hard toothbrush,
flossing until treatment is
terminated
Assess for nausea,
vomiting, abdominal
distention, and bowel
Drug Classification: motility disorders associated
Ant-idopaminergic; with chronic and subacute
Anti-emetic gastritis and diabetic
gastroparesis.May also be
used to prevent
gastrointestinal symptoms
associated with the use of
dopamine agonist
antiparkinsonian agents
Omeprazole MOA: An antisecretory
Dose: 40mg every compound that is a gastric
24 hours acid pump inhibitor.
lethargy,irritability
Gastrointestinal:abdominal
cramps, diarrhea,regurgitation,
changes inappetite, nausea,
heartburn,constipation
Endocrinological:hot flushes,
gynecomastia
Mucocutaneous:rash,
pruritus, urticaria,stomatitis,
conjunctivitis
Urinary: urinaryfrequency,
dysuria
Cardiovascular: edema,
palpitations
Musculoskeletal: leg cramps
Miscellaneous: drug
intolerance
CNS:Headache, dizziness,
fatigue
GI:Diarrhea, abdominal pain,
43
sounds before and after
administration
Monitor BP (sitting,
standing, lying down) and
pulse before and
periodically during therapy.
May cause prolonged QT
interval, tachycardia, and
orthostatic hypotension,
especially in patients older
than 60 yrs or taking >30 m
g/day
Monitor serum prolactin
prior to and periodically
during therapy. May cause
serum prolactin levels
Advise patient to avoid
grapefruit juice during
therapy
Give before meals,
preferably in the morning
Drug can interfere with
Route: Intravenous Suppresses gastric acid nausea, mild transient absorption of vit b12,
Drug Classification: secretion by inhibiting the H+, increases in liver function tests monitor patient for
Proton-pump inhibitor K+-ATPase enzyme system Urogenital:Hematuria, amacrolytic anemia
[the acid (proton H+) pump] proteinuria Encourage to avoid
in the parietal cells. Skin:Rash alcohol, aspirin products,
I: Duodenal and gastric ulcer. ibuprofen, and foods that
Gastroesophageal reflux may increase secretions
disease including severe during therapy
erosive esophagitis (4 to 8 wk
treatment). Long-term
treatment of pathologic
hypersecretory conditions
such as Zollinger-Ellison
syndrome, multiple endocrine
adenomas, and systemic
mastocytosis. In combination
with clarithromycin to treat
duodenal ulcers associated
with Helicobacter pylori.
Loperamide MOA: Inhibits GI peristaltic Body Whole:Hypersensitivity Monitor fluid and electrolyte
Dose: 2mg/tab 2 activity by direct action on (skin rash); fever balance
tabs every 8 hours circular and longitudinal CNS:Drowsiness, fatigue, Notify physician promptly if

44
Route: Oral intestinal muscles. Prolongs
Drug Classification: transit time of intestinal
Gastrointestinal contents, increases
agent; Anti-diarrheal consistency of stools, and
reduces fluid and electrolyte
loss.
I: Acute nonspecific diarrhea,
chronic diarrhea associated
with inflammatory bowel
disease, and to reduce fecal
volume from ileostomies.
Potassium Chloride MOA: Potassium acts as the
Dose: 20mEqs major cation in intracellular
Route: Intravenous fluid, activating many
incorporation enzymatic reactions essential
Drug Classification: for physiologic processes,
dizziness, CNS depression
(overdosage)
GI:Abdominal discomfort or
pain, abdominal distention,
bloating, constipation, nausea,
vomiting, anorexia, dry mouth;
toxic megacolon (patients with
ulcerative colitis)
CNS: Confusion, paralysis,
paresthesia, weakness
CV: Arrhythmias
GI: Abdominal pain, GI
bleeding, perforation or
45
the patient develops
abdominal distention or
other GI symptoms
(possible signs of
potentially fatal toxic
megacolon)
Notify physician if diarrhea
does not stop in a few days
or if abdominal pain,
distension, or fever
develops
Record number and
consistency of stools
Learn measures to relieve
dry mouth; rinse mouth
frequently with water, suck
hard candy
Observe 12 Rights of Drug
Administration
Dilute potassium
concentrate for injection
with adequate volume of
Electrolyte including nerve impulse
replacement transmission and cardiac and
skeletal muscle contraction.
Potassium also helps
maintain electro-neutrality in
cells by controlling exchange
of intracellular and
extracellular ions. It also
helps maintain normal renal
function and acid-base
balance.
I: Hypokalemia
ulceration, nausea, vomiting
Respiratory: Dyspnea
Skin: Rash
Other: Hyperkalemia
46
solution before IV use
Infuse potassium slowly to
avoid phlebitis and
decrease risk of adverse
cardiac reactions
Monitor serum potassium
levels
Regularly assess for signs
of hypokalemia or
hyperkalemia
Advise patient to watch
stools for change in color
and consistency
II. NURSING MANAGEMENT
A. Problem List

Date of Date Problem Active Inactive Date

Onset Identified Resolved
23 Aug 13 23 Sept 13 Cough 23 Nov 13
20 Sep 13 23 Sep 13 Lightheadedness 25 Sep 13 26 Sep 13
23 Aug 13 23 Sept 13 Imbalanced 23 Oct 13 23 Oct 13
Nutrition less than
body requirements

B. Long Term Objective

RP with the help of significant others will be able to regain optimum level of
functioning and wellness, and will resume normal activities of daily living.

47
 C. Nursing Care Plan

1. Diarrhea related to infectious process secondary to leptospirosis

Date: 05 March 2017

NURSING NURSING
INTERVENTIONS E
DIAGNOSIS OBJECTIVES

Subjective Cues: After an hour of Goal w

nursing care, the
Objective Cues: patient

D. Discharge Plan

Upon discharge, client and significant others will adhere to the following
instructions:

MEDICATION

EXERCISE AND ACTIVITY

Encouraged to perform light activities such as simple range of motion as

tolerated
Instructed client to avoid stressful activities
Advised to get plenty of rest to maintain progress towards full recovery and to
avoid relapse

TREATMENT

Instructed client to strictly comply with the treatment regimen

HEALTH EDUCATION

Provided information regarding the diseases nature, manifestations, and

complications
Instructed to properly discard used tissue and place in infectious waste bin
Advised
Encouraged to

48
OUT PATIENT FOLLOW-UP

Instructed to keep all of follow-up clinic appointments and laboratory examination

results
Instructed client to consult the physician immediately if any complications
occurred

DIET

Encouraged to
Instructed client to
Advised to avoid smoking and alcohol intake

SPIRITUALITY/SEXUALITY

Reminded client that intercourse is safe after 2 weeks of continuous treatment

Advised to attend support counseling together with the significant others
Encouraged to join organizations/ church activities.
Encouraged to strengthen faith in God through attending the mass on Sundays

49
III. CONCLUSION

Pulmonary Tuberculosis is a communicable disease affecting the lungs.

Everyone could be at risk since it is easily transmitted through droplet nuclei. With a
simple cough or sneeze by an infected person, anybody within close contact can
acquire the bacteria. In relation to the case, the client must have come in contact with
an infected person without him knowing it. Unaware, he had the bacteria dormant in his
body for years; since there were no signs and symptoms present, he did not seek
medical attention, hencedid not consider himself infectious. The bacteria were
reactivated when his immune system went down thus progressing into the disease.

Nursing management is all about the promotion of health and prevention of

illness. With the growing number of cases of tuberculosis worldwide, it is part of the
responsibility of nurses to inform the people of the nature of the disease and its possible
management. Through thorough assessment and history taking, nurses are able to
formulate an appropriate nursing diagnosis and create a plan of care. Intervention would
act tobe the crucial part and since patients are highly infectious, meticulous actions
should be applied. Reassessment of the patient is likewise necessary to determine
whether or not the patient was treated from the disease; this is also one way to prevent
further complications.

This study was undertaken to provide information regarding tuberculosis infection

and the different ways to which it can be treated. The patient, together with the family,
and the healthcare providers act hand-in-hand in order to free the patient from its
suffering condition. The findings of this study suggest that PTB is a treatable disease;
though not thoroughly, people who have been infected are still able to return to their
optimal health and wellness with enough effort and proper care.

50
IV. BIBLIOGRAPHY

BOOKS

NEWSPAPER

ONLINE SOURCES

World Health Organization.(2013).

http://www.wpro.who.int/mediacentre/factsheets/fs_13082012_leptospirosis/en/

51
 APPENDIX A

MALE FEMALE
MALE:
YEAR 0-14 15-24 25-34 35-44 45-54 55-64 65+ 0-14 15-24 25-34 35-44 45-54 55-64 65+ FEMALE
RATIO
1995 2 43 56 61 46 47 26 1 20 32 26 20 19 11 2.2
Philippines

2000

2005 482 7358 11275 13253 12531 7646 4279 374 3710 5268 5565 4603 3274 2029 2.3

2010 511 9320 12224 13716 13651 8923 4742 454 4825 5489 5301 4643 3329 2070 2.4

2011 573 9725 12804 14474 14002 9568 4845 448 5155 5848 5521 4880 3501 2236 2.4

2012 583 9754 12576 14140 13996 9676 5097 466 5104 5954 5584 5068 3605 2380 2.3

aEmptyrows indicate an absence of high-quality survey or surveillance data. In the

absence of high-quality national data, high-quality sub-national data are used.

Source: WHO Global Tuberculosis Report 2013

52
 APPENDIX B
PTB Cases in AFPMC

As of Dec 2013, AFPMC has catered to the following number of Pulmonary

Tuberculosis cases from CY 2010-2013:

*This data was obtained from the Registrar Department of AFPMC

*It was not determined in the data the number of cases for male and female patients.
*Mortality cases for PTB were not provided

53