I.

OBJECTIVES

i. General

The group aims to conduct and present this case in a systemic, analytical way and be
guided by the formulated specific objectives for the enhancement of our knowledge, skills and
attitudes towards nursing care.

ii. Specific

At the end of our case study, the group would be able to:

1. Choose a particular client/case for this study;

2. Ask permission to the patient about the study;

3. Obtain initial data about the client through his records along with a personal interview;

4. Gather, trace and collate the predisposing and precipitating factors that could have
contributed to the client’s illness;

5. Gather and review the results of the diagnostic exams done to the client;

6. Make a drug study on the discontinued and current prescribed medicines;

7. Identify nursing problems and come up with an appropriate and effective nursing care
plan;

8. Formulate prognosis based on the gathered information; and

9. Provide appropriate health teachings and recommendation for the client, family and
community

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 II. INTRODUCTION

Neonatal sepsis, sepsis neonaturom and neonatal septicemia are terms that have been used
to describe the systemic response to infection in the new born infant. There is a little agreement
on the proper use of terms i.e. whether it should be restricted to bacterial infections, positive
blood cultures, or severity of illness. Currently, there is considerable discussion of the
appropriate definition of sepsis in the critical care literature. This is a result of an explosion of
information on the pathogenesis of sepsis and the availability of new potentially therapeutic
agents e.g. monoclonal antibodies to endotoxin and tumor necrosis factor (TNF) which can alter
the lethal outcome of sepsis in animal experiments. To evaluate and utilize these new
therapeutic modalities appropriately “sepsis” requires a more rigorous definition. In adults, the
term “systemic inflammatory response syndrome (SIRS) is used to describe a clinical syndrome
characterized by two or more of the following: (1) fever or hyporthermia (2) tachycardia (3)
tachypnea and (4) abnormal white blood cells (WBC) or increase in immature forms. SIRS
maybe a result of trauma , hemorrhagic shock, other causes of ischemia, pancreatitis or
immunologic injury. When it is a result of infection, it is termed sepsic. These criteria have not
been established in infants and children and are unlikely to be applicable to the newborn infant.
Nevertheless, the concept of sepsis as a syndrome caused by a metabolic and hemodynamics
consequences of infection is logical and important. In the future, the definition of sepsis in the
new born infant and child will become more precise. At these time criteria for neonatal sepsis
should include documentation of infection in a new born infant with a serious systemic illness in
which noninfectious explanation for the abnormal pathophysiology state are excluded or unlikely.
Serious systemic illness in the new born infant may be caused by perinatal asphyxia, respiratory
tract, cardiac, metabolic, neurologic, hematologic disease. Sepsis occurs in a small proportion
of all neonatal infections. Bacteria and Candida are the usual etiologic agents, but viruses, and,
rarely protozoa may also caused sepsis. Blood cultures may be negative, increasing the difficulty
in establishing infection etiologically. Finally with or without sepsis may be present concurrently
with a non infectious illness in the new born infant, child or adult.

It has been explained that neonates are at the highest risk for bacterial sepsis, with the
prevalence at 1 to 10 per 1000 live births worldwide. Existing published data have suggested

2
that sepsis causes about 10% of all maternal, and 26% of all neonatal deaths. Mortality due to
sepsis has increased by approximately 13.7% each year over the past 2 decades.Furthermore,
the incidence of sepsis in the developing countries is much higher than in the developed world,
and in some of these countries, sepsis-related mortality rate was estimated as high as 50% for
those infants who are not treated.

Of the total 30,000 deaths of Filipino children less than one month old every year, nearly 8,000
is caused by neonatal sepsis, a serious blood bacterial infection. These estimates were compiled
for all countries, including the Philippines, by an expert body led by World Health Organization.

3
 III. DEFINITION OF DIAGNOSIS

I. Neonatal sepsis is a type of neonatal infection and specifically refers to the presence in
a newborn baby of a bacterial blood stream infection (BSI) (such
as meningitis, pneumonia, pyelonephritis, or gastroenteritis) in the setting of fever. Older
textbooks may refer to neonatal sepsis as "sepsis neonatorum".
Referrence: Mary T. Caserta, MD, Professor of Pediatrics, Division of Infectious Diseases
2016
II. Neonatal sepsis is invasive infection, usually bacterial, occurring during the neonatal
period. Signs are multiple, nonspecific, and include diminished spontaneous activity, less
vigorous sucking, apnea, bradycardia, temperature instability, respiratory distress,
vomiting, diarrhea, abdominal distention, jitteriness, seizures, and jaundice. Diagnosis is
clinical and based on culture results. Treatment is initially with ampicillin plus
either gentamicin or cefotaxime, narrowed to organism-specific drugs as soon as
possible.
Referrence: Arthur E. Kopelman, MD, Professor of Pediatrics and Neonatology
(Emeritus), The Brody School of Medicine at East Carolina University 2015
III. Neonatal sepsis is any infection involving an infant during the first 28 days of life.
Neonatal sepsis is also known as "sepsis neonatorum." The infection may involve the
infant globally or may be limited to just one organ (such as the lungs with pneumonia). It
may be acquired prior to birth (intrauterine sepsis) or after birth (extrauterine sepsis).
Viral (such as herpes, rubella [German measles]), bacterial (such as group B strep) and
more rarely fungal (such as Candida) causes may be implicated
Referrence: William C. Shiel Jr., MD, FACP, FACR, John Mersch, MD, FAAP, Medical
Surgical Nursing: Assessment of nursing 2013

4
 IV. PATIENTS PROFILE

Name: PATIENT X

Age: 1mos.

Sex:Male

Born: September 22, 2017

Nationality:Filipino

Religion:Catholic

Physician:Dr. Paragas

Diagnosis: Neonatal Sepsis

A.Present Medical History

The Baby was endorced, 2 days prior to admission when the baby had onset of
unproductive cough, no fever, vomiting, and diarrhea. Chest X-ray done.The baby diagnose
Neonatal Sepsis. Clarithromycin and Salbutamol nebulization given with an IVF of D5IMB 500
@15ml/hr. O2 given10LPM via face mask with resorvoir. NO KNOWN ALLERGY.

B.Past Medical History

The mother 35 yrs. Old with unremarkable prenatal history.She delivered the baby via
NSVD at Brokenshire hospital of the baby.She doesn’t have any severe complications during
pregnancy with good apgar. Patient was then discharge as well as the baby.

C.Family History

The mother stays only at home . The side of the mother has a trace High blood pressure
while the side of the father has Bronchial Asthma.

D.Immunization

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 As verbalized by the mother she is only immunized once with tetanus toxoid on her
pregnancy.For the baby, routine Newborn Care done,vaccinations given such as hepa B,BCG
and Vit.K.

E.Developmental Status

Sigmund Freud

The first stage is the oral stage. An infant is in this stage from birth to
eighteen months of age. The main focus in the oral stage is pleasure seeking through the
infant’s mouth. During this stage the need for tasting and sucking becomes prominent in
producing pleasure. Oral stimulation is crucial during this stage; if the infant’s needs are not
met during this time frame he or she will be fixated in the oral stage. Fixation in this stage can
lead to adult habits such as thumb-sucking, smoking, over-eating, and nail-biting. Personality
traits can also develop during adulthood that are linked to oral fixation; these traits can include
optimism and independence or pessimism and hostility.

In our client, Sucking is the primary source of pleasure for a newborn.

Everything goes in the mouth. Sucking = food. Dependency, A baby is very dependent and
can do little for itself. If babies needs properly fulfilled can move onto the next stage. But if not
fulfilled baby will be mistrustful or over-fulfilled baby will find it hard to cope with a world that
doesn�t meet all of his/her demands.

Erick Ericksons

Infant is entirely dependent upon his or her caregivers, the quality of

care that the child receives plays an important role in the shaping of the child’s personality.
During this stage, children learn whether or not they can trust the people around them. An infant's
ability to communicate his or her needs are limited, so crying carries an important message.
When a baby cries, there is some need that should be met with a response from caregivers,

6
whether it involves providing food, safety, a fresh diaper, or a comforting cuddle. By responding
quickly and appropriately to an infant's cries, a foundation of trust is established.

In our client, he is in the stage of trust vs mistrust if he feels hungry,

he cries for attention of the mother for feeding. The need for care and food must be met with
comforting regularity. The infant must first form a trusting relationship with the parent, otherwise
a sense of mistrust will develop.

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 V. REVIEW OF ANATOMY AND PHYSIOLOGY

ANATOMY OF IMMUNE SYSTEM

The immune system is an inherent self-defense system consisting of cells that helps the body
distinguish between self and non-self molecules. Different pathways regulate different immune
cells to help the body differentiate the bodies own healthy cells from disease-causing agents
including bacteria, viruses, fungi, parasites, cancerous cells, and many more.

All the components of the immune system have to continuously modify to keep the bodies
defense up against the ever-evolving organisms that constantly are on a quest to find a new way
to attack the host. This continuously evolving system sometimes reacts against the bodies own
cells, identifying it as foreign, which leads to healthy tissue destruction and causes autoimmune
diseases and cancers. Also, weakened defenses of the body by the immune system due to
genetic, acquired causes precipitate an inherent state of anergy (unresponsiveness) that can
lead to immunodeficiency diseases.

The immune system consists of multiple levels of defense against invading pathogens. It
consists of physical barriers, mechanisms of innate immunity as well as adaptive immunity. The

8
physical barrier can be mechanical, chemical, or biological and located at different sites in the
body including skin, secretions within the respiratory tract, and in the gastrointestinal or
genitourinary tract as flora. The cells that have the inherent property of innate and adaptive
immunity within the body are present at different sites including the blood, lymphatic system
(lymph, lymphoid nodules and lymphoid organs), epithelium, and connective tissues.

Antigen

Antigens are the molecules that are recognized and stimulate the cells of immune system. These
may be different molecules within the cells like proteins, polysaccharides, or nucleoproteins and
may also be the whole cell, like a tumor cell or organisms like bacteria, viruses, fungi, parasites,
or agents containing genetic material such as nucleic acids or lipids.

The body’s immune system can react adaptively against the antigen via 2 pathways: cellular or
humoral. The cellular response is mainly a lymphocyte-mediated reaction, whereas the humoral
response includes production of antibodies against the antigen by the plasma cells. Epitopes
are a component of the antigen that are recognized by the immune system and determine
whether the cellular or the humoral arm of the immune system shall be activated against that
particular antigen. An epitope may represent a linear amino acid sequence or antigenic tertiary
structure.

Immunoglobulin

Immunoglobulins (Igs), the term is sometimes used interchangeably with "antibodies," are
glycoprotein molecules produced by B lymphocytes and plasma cells in response to an
immunogen or after recognition of specific epitopes on the antigen. The antibodies then
specifically bind to only those particular antigens. Immunoglobulin (Ig) is the key component of
humoral immunity. The earliest cell in B-lymphocyte lineage that produces Ig is the pre-B
lymphocyte. An adult human produces approximately 2-3 grams of Ig every day.

Antibodies can be found on the surface of lymphocytes as an integral part of the cell membrane
protein or can be freely circulating in the blood or be part of one of the body’s gland secretion.
The Ig molecule is a polypeptide heterodimer that is composed of 2 identical light chains and 2
identical heavy chains connected by disulfide bonds. Antibodies belong to immunoglobulin family

9
of protein and have 5 isotypes (G, A, M, E, D) with further subclasses of G and A. The classes
are differentiated with the characteristics of the Ig heavy chain of the antibody. Each chain has
domains called the V (variable) region and C (constant) region. Variable region constitutes the
antibody binding region of the molecule to the different antigens as it consists of about 110 amino
acids that vary widely among the different antibody molecules. The constant region at the
carboxyl-terminal end of the heavy chain, called the Fc region, binds to the Fc receptors of
neutrophils, eosinophils, macrophages, dendritic cells, B cells, and the natural killer (NK) cells.
The Fc region is also involved in the activation of the complement system.

Antibodies can bind to the different antigens causing agglutination and precipitation of the
antigens leading to neutralization of the antigen effect. They can also stimulate the destruction
of antigen by cells like macrophages, neutrophils, and eosinophils by covering the surface of the
antigen by the Fc portion of the antibodies in a process known as "opsonization."

Cells of the immune system

Lymphocytes

Lymphocytes are further classified as T, B, and natural killer (NK) cells. T and B lymphocytes
can only identify an antigen. Functionally, they both differ in their production and maturation
history due to the receptors present on the surface of both the lymphocytes. All 3 are initially
formed in the bone marrow where the B-lymphocytes and the natural killer cells mature and
leave to seed lymphoid tissue and organs in different parts of the body. Whereas, the T
lymphocytes after leaving the bone marrow go to the thymus gland, where they further mature
by going through a selection process.

T and B Lymphocytes can also be differentiated from each other based upon the surface
receptors present on both of them. All these cells continuously circulate throughout the body and
also are present in the lymphoid tissue. The percentage of these different cells present in the
different lymphoid organs differ also, with T cells mainly present in the thymus and then blood,
lymph nodes, and spleen, whereas, the B lymphocytes are mainly present in the bone marrow
and then in the spleen, lymph nodes, and blood. No B lymphocytes are present in the thymus
gland.

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B lymphocytes on stimulation rapidly proliferate and produce antibodies against the antigen that
stimulated it initially. Sometimes, the antigen is presented to the T lymphocytes and then the
cytokines released from the helper T lymphocytes stimulate the B lymphocytes. leading to
production of antibodies against that antigen. In addition, some of the B lymphocytes are also
converted to memory cells that produce rapid response against the same antigen on repeated
exposure.

T lymphocytes are also stimulated by receptors present on their surface; however, T

lymphocytes only recognize antigens presented to them bound to the major histocompatibility
complex (MHC). T lymphocytes are divided into helper T cells and cytotoxic T cells. Helper T
cells have CD 4 marker on their surface, hence they are also known as CD4+ T cells and are
MHC class II restricted. On stimulation, they produce large amount of different cytokines, which
differentiate B cells into plasma cells leading to further antibody production.

Cytotoxic T lymphocytes and the macrophages play a significant role in the inflammatory
reaction against the presented antigen. The cytotoxic T cells have CD 8 marker on their surface
known as CD8+ T cells that are MHC Class I restricted. They destroy the cells via 2 mechanisms:
one by attaching to the cells and releasing proteins called perforins into the cells that create
holes in the cell membranes of the target cell with subsequent lysis of the cell. Second, they kill
the cells by inducing the programmed cell death by a term known as apoptosis.

Natural killer cells

Natural killer cells have the antigen recognizing receptors like the B and T lymphocytes on their
surface. They attack foreign cells or abnormal cells like cancer cells and virus infected cells
directly without any previous stimulation.

Antigen presenting cells

Antigen presenting cells include B lymphocytes, macrophages, and dendritic cells (also called
Langerhans cells in mucosa and epidermis). These cells have class II major histocompatibility
complex (MHC) present on their surface that forms the complex with the peptides to present it
to the helper T cells (CD4+).

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Immunity mechanisms: Physical barriers

Physical barriers include the following:

Skin

Nails

Mucosal barriers

Secretions of respiratory, gastrointestinal, and genitourinary flora and tracts

Nasal cilia

Innate immunity

Innate immunity consists of pattern recognition receptors, antimicrobial peptides, cells,

complement components and different cytokines. It is the fast, nonspecific response and does
not generate any memory against the attacking antigens.

Adaptive immunity

Adaptive immunity includes stimulation of both the cellular and humoral response to the
presented antigen with T lymphocytes mainly involved in the cellular response and B
lymphocytes involved in the humoral response. The T lymphocytes, after being stimulated,
release many cytokines, stimulating macrophages and other cells to destroy the presenting
antigen. Cytokines released by the T Lymphocytes also stimulate the B lymphocytes, eventually
leading to the production of antibodies against the antigen causing its destruction. In adaptive
immunity, the body’s immune system also forms memory T cells and memory B Cells after the
initial exposure, making the immune response much faster and specific on subsequent
exposures.

B lymphocytes: Humoral immunity pathway by producing immunoglobulin derived from and

maturing in bone marrow. They recognize linear epitopes, major ligands, markers, and
associations

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T lymphocytes: Cellular immunity pathway where precursors arise in bone marrow but then
mature in the thymus. They recognize conformational epitopes. They may subclassified into
helper T lymphocytes (CD4+), cytolytic T lymphocytes (CD8+), and T regulatory cells (Treg’s).
Once T lymphocytes are activated, they become either effector or memory T lymphocytes.
Activation requires a second signal or costimulation. The costimulatory molecules are on the
antigen presenting cells. Their ligands are on the T lymphocytes. No T lymphocyte response
exists without costimulation. The T lymphocyte that recognizes the antigen but is not
costimulated is said to be in a state of anergy (nonresponsiveness).

Costimulators may produce activation or induce negative regulation of the immune response.

ANATOMY OF RESPIRATORY SYSTEM

The cells of the human body require a constant stream of oxygen to stay alive. The respiratory
system provides oxygen to the body’s cells while removing carbon dioxide, a waste product that
can be lethal if allowed to accumulate. There are 3 major parts of the respiratory system: the
airway, the lungs, and the muscles of respiration. The airway, which includes the nose, mouth,
pharynx, larynx, trachea, bronchi, and bronchioles, carries air between the lungs and the body’s
exterior. The lungs act as the functional units of the respiratory system by passing oxygen into
the body and carbon dioxide out of the body. Finally, the muscles of respiration, including the

13
diaphragm and intercostal muscles, work together to act as a pump, pushing air into and out of
the lungs during breathing.

Nose and Nasal Cavity

The nose and nasal cavity form the main external opening for the respiratory system and are the
first section of the body’s airway—the respiratory tract through which air moves. The nose is a
structure of the face made of cartilage, bone, muscle, and skin that supports and protects the
anterior portion of the nasal cavity. The nasal cavity is a hollow space within the nose and skull
that is lined with hairs and mucus membrane. The function of the nasal cavity is to warm,
moisturize, and filter air entering the body before it reaches the lungs. Hairs and mucus lining
the nasal cavity help to trap dust, mold, pollen and other environmental contaminants before
they can reach the inner portions of the body. Air exiting the body through the nose returns
moisture and heat to the nasal cavity before being exhaled into the environment.

Mouth

The mouth, also known as the oral cavity, is the secondary external opening for the respiratory
tract. Most normal breathing takes place through the nasal cavity, but the oral cavity can be used
to supplement or replace the nasal cavity’s functions when needed. Because the pathway of air
entering the body from the mouth is shorter than the pathway for air entering from the nose, the
mouth does not warm and moisturize the air entering the lungs as well as the nose performs this
function. The mouth also lacks the hairs and sticky mucus that filter air passing through the nasal
cavity. The one advantage of breathing through the mouth is that its shorter distance and larger
diameter allows more air to quickly enter the body.

Pharynx

The pharynx, also known as the throat, is a muscular funnel that extends from the posterior end
of the nasal cavity to the superior end of the esophagus and larynx. The pharynx is divided into
3 regions: the nasopharynx, oropharynx, and laryngopharynx. The nasopharynx is the superior
region of the pharynx found in the posterior of the nasal cavity. Inhaled air from the nasal cavity
passes into the nasopharynx and descends through the oropharynx, located in the posterior of
the oral cavity. Air inhaled through the oral cavity enters the pharynx at the oropharynx. The

14
inhaled air then descends into the laryngopharynx, where it is diverted into the opening of the
larynx by the epiglottis. The epiglottis is a flap of elastic cartilage that acts as a switch between
the trachea and the esophagus. Because the pharynx is also used to swallow food, the epiglottis
ensures that air passes into the trachea by covering the opening to the esophagus. During the
process of swallowing, the epiglottis moves to cover the trachea to ensure that food enters the
esophagus and to prevent choking.

Larynx

The larynx, also known as the voice box, is a short section of the airway that connects the
laryngopharynx and the trachea. The larynx is located in the anterior portion of the neck, just
inferior to the hyoid bone and superior to the trachea. Several cartilage structures make up the
larynx and give it its structure. The epiglottis is one of the cartilage pieces of the larynx and
serves as the cover of the larynx during swallowing. Inferior to the epiglottis is the thyroid
cartilage, which is often referred to as the Adam’s apple as it is most commonly enlarged and
visible in adult males. The thyroid holds open the anterior end of the larynx and protects the
vocal folds. Inferior to the thyroid cartilage is the ring-shaped cricoid cartilage which holds the
larynx open and supports its posterior end. In addition to cartilage, the larynx contains special
structures known as vocal folds, which allow the body to produce the sounds of speech and
singing. The vocal folds are folds of mucous membrane that vibrate to produce vocal sounds.
The tension and vibration speed of the vocal folds can be changed to change the pitch that they
produce.

Trachea

The trachea, or windpipe, is a 5-inch long tube made of C-shaped hyaline cartilage rings lined
with pseudostratified ciliated columnar epithelium. The trachea connects the larynx to the
bronchi and allows air to pass through the neck and into the thorax. The rings of cartilage making
up the trachea allow it to remain open to air at all times. The open end of the cartilage rings faces
posteriorly toward the esophagus, allowing the esophagus to expand into the space occupied
by the trachea to accommodate masses of food moving through the esophagus.

The main function of the trachea is to provide a clear airway for air to enter and exit the lungs.
In addition, the epithelium lining the trachea produces mucus that traps dust and other

15
contaminants and prevents it from reaching the lungs. Cilia on the surface of the epithelial cells
move the mucus superiorly toward the pharynx where it can be swallowed and digested in the
gastrointestinal tract.

Bronchi and Bronchioles

At the inferior end of the trachea, the airway splits into left and right branches known as the
primary bronchi. The left and right bronchi run into each lung before branching off into smaller
secondary bronchi. The secondary bronchi carry air into the lobes of the lungs—2 in the left lung
and 3 in the right lung. The secondary bronchi in turn split into many smaller tertiary bronchi
within each lobe. The tertiary bronchi split into many smaller bronchioles that spread throughout
the lungs. Each bronchiole further splits into many smaller branches less than a millimeter in
diameter called terminal bronchioles. Finally, the millions of tiny terminal bronchioles conduct air
to the alveoli of the lungs.

As the airway splits into the tree-like branches of the bronchi and bronchioles, the structure of
the walls of the airway begins to change. The primary bronchi contain many C-shaped cartilage
rings that firmly hold the airway open and give the bronchi a cross-sectional shape like a flattened
circle or a letter D. As the bronchi branch into secondary and tertiary bronchi, the cartilage
becomes more widely spaced and more smooth muscle and elastin protein is found in the walls.
The bronchioles differ from the structure of the bronchi in that they do not contain any cartilage
at all. The presence of smooth muscles and elastin allow the smaller bronchi and bronchioles to
be more flexible and contractile.

The main function of the bronchi and bronchioles is to carry air from the trachea into the lungs.
Smooth muscle tissue in their walls helps to regulate airflow into the lungs. When greater
volumes of air are required by the body, such as during exercise, the smooth muscle relaxes to
dilate the bronchi and bronchioles. The dilated airway provides less resistance to airflow and
allows more air to pass into and out of the lungs. The smooth muscle fibers are able to contract
during rest to prevent hyperventilation. The bronchi and bronchioles also use the mucus and
cilia of their epithelial lining to trap and move dust and other contaminants away from the lungs.

Lungs

16
The lungs are a pair of large, spongy organs found in the thorax lateral to the heart and superior
to the diaphragm. Each lung is surrounded by a pleural membrane that provides the lung with
space to expand as well as a negative pressure space relative to the body’s exterior. The
negative pressure allows the lungs to passively fill with air as they relax. The left and right lungs
are slightly different in size and shape due to the heart pointing to the left side of the body. The
left lung is therefore slightly smaller than the right lung and is made up of 2 lobes while the right
lung has 3 lobes.

The interior of the lungs is made up of spongy tissues containing many capillaries and around
30 million tiny sacs known as alveoli. The alveoli are cup-shaped structures found at the end of
the terminal bronchioles and surrounded by capillaries. The alveoli are lined with thin simple
squamous epithelium that allows air entering the alveoli to exchange its gases with the blood
passing through the capillaries.

Muscles of Respiration

Sorrounding the lungs are sets of muscles that are able to cause air to be inhaled or exhaled
from the lungs. The principal muscle of respiration in the human body is the diaphragm, a thin
sheet of skeletal muscle that forms the floor of the thorax. When the diaphragm contracts, it
moves inferiorly a few inches into the abdominal cavity, expanding the space within the thoracic
cavity and pulling air into the lungs. Relaxation of the diaphragm allows air to flow back out the
lungs during exhalation.

Between the ribs are many small intercostal muscles that assist the diaphragm with expanding
and compressing the lungs. These muscles are divided into 2 groups: the internal intercostal
muscles and the external intercostal muscles. The internal intercostal muscles are the deeper
set of muscles and depress the ribs to compress the thoracic cavity and force air to be exhaled
from the lungs. The external intercostals are found superficial to the internal intercostals and
function to elevate the ribs, expanding the volume of the thoracic cavity and causing air to be
inhaled into the lungs.

17
Physiology of the Respiratory System

Pulmonary Ventilation

Pulmonary ventilation is the process of moving air into and out of the lungs to facilitate gas
exchange. The respiratory system uses both a negative pressure system and the contraction of
muscles to achieve pulmonary ventilation. The negative pressure system of the respiratory
system involves the establishment of a negative pressure gradient between the alveoli and the
external atmosphere. The pleural membrane seals the lungs and maintains the lungs at a
pressure slightly below that of the atmosphere when the lungs are at rest. This results in air
following the pressure gradient and passively filling the lungs at rest. As the lungs fill with air, the
pressure within the lungs rises until it matches the atmospheric pressure. At this point, more air
can be inhaled by the contraction of the diaphragm and the external intercostal muscles,
increasing the volume of the thorax and reducing the pressure of the lungs below that of the
atmosphere again.

To exhale air, the diaphragm and external intercostal muscles relax while the internal intercostal
muscles contract to reduce the volume of the thorax and increase the pressure within the
thoracic cavity. The pressure gradient is now reversed, resulting in the exhalation of air until the
pressures inside the lungs and outside of the body are equal. At this point, the elastic nature of
the lungs causes them to recoil back to their resting volume, restoring the negative pressure
gradient present during inhalation.

External Respiration

External respiration is the exchange of gases between the air filling the alveoli and the blood in
the capillaries surrounding the walls of the alveoli. Air entering the lungs from the atmosphere
has a higher partial pressure of oxygen and a lower partial pressure of carbon dioxide than does
the blood in the capillaries. The difference in partial pressures causes the gases to diffuse
passively along their pressure gradients from high to low pressure through the simple squamous
epithelium lining of the alveoli. The net result of external respiration is the movement of oxygen
from the air into the blood and the movement of carbon dioxide from the blood into the air. The
oxygen can then be transported to the body’s tissues while carbon dioxide is released into the
atmosphere during exhalation.

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Internal Respiration

Internal respiration is the exchange of gases between the blood in capillaries and the tissues of
the body. Capillary blood has a higher partial pressure of oxygen and a lower partial pressure of
carbon dioxide than the tissues through which it passes. The difference in partial pressures leads
to the diffusion of gases along their pressure gradients from high to low pressure through the
endothelium lining of the capillaries. The net result of internal respiration is the diffusion of
oxygen into the tissues and the diffusion of carbon dioxide into the blood.

Transportation of Gases

The 2 major respiratory gases, oxygen and carbon dioxide, are transported through the body in
the blood. Blood plasma has the ability to transport some dissolved oxygen and carbon dioxide,
but most of the gases transported in the blood are bonded to transport molecules. Hemoglobin
is an important transport molecule found in red blood cells that carries almost 99% of the oxygen
in the blood. Hemoglobin can also carry a small amount of carbon dioxide from the tissues back
to the lungs. However, the vast majority of carbon dioxide is carried in the plasma as bicarbonate
ion. When the partial pressure of carbon dioxide is high in the tissues, the enzyme carbonic
anhydrase catalyzes a reaction between carbon dioxide and water to form carbonic acid.
Carbonic acid then dissociates into hydrogen ion and bicarbonate ion. When the partial pressure
of carbon dioxide is low in the lungs, the reactions reverse and carbon dioxide is liberated into
the lungs to be exhaled.

Homeostatic Control of Respiration

Under normal resting conditions, the body maintains a quiet breathing rate and depth called
eupnea. Eupnea is maintained until the body’s demand for oxygen and production of carbon
dioxide rises due to greater exertion. Autonomic chemoreceptors in the body monitor the partial
pressures of oxygen and carbon dioxide in the blood and send signals to the respiratory center
of the brain stem. The respiratory center then adjusts the rate and depth of breathing to return
the blood to its normal levels of gas partial pressures.

19
 VI. PHYSICAL EXAMINATION

System Actual Findings Remarks

VITAL SIGNS  Temperature: 38.9°C Temperature results shown

that the baby has a fever.
 BP: not assessed Respiratory rate resulted
high.
 RR: 68cpm

 PR: 156 bpm

ANTHROPO-  Weight: The infants Body Mass Index

METRICMEASURE-MENT 5.3kilograms (BMI) was resulted that the
baby was with in normal BMI
 Height: 53cm with the result of 18.9. the
normal value was 17-24.

SKIN  Light brown and Child has a healthy skin and

uniform in color has no problem on this.
 No foul odor
 No masses, lesions
 No wounds,
Laceration

 Skin is moist
 Skin appeared flushed
because of heat
 No rashes
 Good skin turgor

20
HAIR  Even distribution Hair is jet black and
inflammation was not seen
 No scalp lesions upon assessment.

 No masses

 Fine to course

 Absence of
infestation

NAIL  Pinkish nail bed All of the findings for the

nails are found to be within
 Concave shape the normal range.

 Color of the nail

bed back to
original color in
less than three
seconds.

 Smooth to touch
HEAD  Asymmetrical with Normal findings .Posterior
frontal, parietal fontanel should close at two
and flatted months while anterior
occipital fontanel should close by12 -
prominences
18 months
 No palpable lymph
nodes

 No tenderness

 Symmetrical facial
expression such
as smiling,
frowning

 Posterior fontanel
is closed and
anterior fontanel is
still open

21
EYES  Symmetrical Eyelashes appeared to be
equally distributed and
curled slightly outward.
 Equal eyelashes
Eyelids was no presence of
distribution
discharges, no coloration
and lids close symmetrically
 Eyebrows are with involuntary blinks. The
symmetrically sclera appears white, there’s
aligned and evenly no edema or tearing of
distributed lacrimal glands. The pupils of
the eye are black and equal
 Equal movement in size.

 No discharge, no
discoloration of
eyelids

 When lids are

close, sclera is not
visible

 Sclera white

 Pink conjunctiva

 No edema or
tenderness over
the lacrimal gland
EARS  Symmetrical Auricles are symmetrically
 Color same as and has the same color with
facial skin his facial skin. The auricles
 Aligned to the are aligned with the outer
inner canthus canthus. The pinna recoils
 No lesions
when folded.
 Firm and not
tender

22
NOSE AND SINUSES  Symmetrical The nose appeared
symmetric, straight and
uniform in color. There was
 No discharge
no presence of discharges or
flaring. When lightly
 Absence of nasal palpated, there were no
flaring tenderness and lessions.

 Uniform in color

 Nose is non-tender

 No lesions

 Pink mucosa

 Nasal septum
intact and in the
midline

 Sinuses are not

tender
MOUTH  Tooth hasn't yet The lips of the patient are
erupted uniformly pink; moist,
 Soft, moist, symmetric and have a
smooth texture of smooth texture.
lips
 Uniform pink color
of gums, tongue
and tonsil
 Moist and slightly
rough tongue
 Smooth tongue
base
 Light pink, smooth
soft palate
 Light pink hard
palate
 Uvula is positioned
in the midline of
soft palate

23
THROAT AND  Uniform in color The neck muscle are equal
 No palpable lymph in size. The patient showed
NECK nodes coordinated, smooth head
movement with no
discomfort.
 Neck can move
freely

BREAST AND AXILLA  Skin is smooth and

uniform in color

 Symmetrical
breast

 Symmetrical axilla

 No tenderness

 No secretion

 No masses or
nodules
CHEST & RES-PIRATORY  Skin is intact The chest wall is intact with
 Irregular pattern of no tenderness and masses.
breathing The patient uses
 Absence of sternocleidomastoid muscle
tenderness, when breathing.
lesions and
palpable masses
 Symmetrical
shoulder height
 Absence of
dyspnea , but has
irregular depths of
respiration

24
ABDOMEN  Uniform in color The abdomen of the patient
has unblemished skin and is
 Symmetric contour uniform in color. The
abdomen has a symmentric
 Rounded or contour.
protuberant
abdomen

 Absence of lesions
and tenderness
MUSCULO-SKELETAL  Uniform in The extremities are
skin color symmetrical in size and
length. Both upper and lower
 Mobile extremities shows no scars.

 Equal size on both

sides of the body

 No deformities
noted

 No fractures and
dislocations noted

 No tenderness and
swelling

 Does not have

tremors and
palpable nodules

 10 fingers and
toes

25
VII. PATHOPHYSIOLOGY

26
NARRATIVE

Pneumonia is a serious infection or inflammation of your lungs. The air sacs in the lungs fill
with pus and other liquid. Oxygen has trouble reaching your blood. If there is too little oxygen
in your blood, your body cells can’t work properly. Because of this and spreading infection
through the body pneumonia can cause death. Pneumonia affects your lungs in two ways.
Lobar pneumonia affects a section (lobe) of a lung. Bronchial pneumonia (or
bronchopneumonia) affects patches throughout both lungs.
Bacteria are the most common cause of pneumonia. Of these, Streptococcus pneumoniae is
the most common. Other pathogens include anaerobic bacteria, Staphylococcus aureus,
Haemophilus influenzae, Chlamydia pneumoniae, C. psittaci, C. trachomatis, Moraxella
(Branhamella) catarrhalis, Legionella pneumophila, Klebsiella pneumoniae, and other gram-
negative bacilli. Major pulmonary pathogens in infants and children are viruses: respiratory
syncytial virus, parainfluenza virus, and influenza A and B viruses. Among other agents are
higher bacteria including Nocardia and Actinomyces sp; mycobacteria, including
Mycobacterium tuberculosis and atypical strains; fungi, including Histoplasma capsulatum,
Coccidioides immitis, Blastomyces dermatitidis, Cryptococcus neoformans, Aspergillus
fumigatus, and Pneumocystis carinii; and rickettsiae, primarily Coxiella burnetii (Q fever).
The usual mechanisms of spread are inhaling droplets small enough to reach the alveoli and
aspirating secretions from the upper airways. Other means include hematogenous or lymphatic
dissemination and direct spread from contiguous infections. Predisposing factors include upper
respiratory viral infections, alcoholism, institutionalization, cigarette smoking, heart failure,
chronic obstructive airway disease, age extremes, debility, immuno-compromise (as in
diabetes mellitus and chronic renal failure), compromised consciousness, dysphagia, and
exposure to transmissible agents.

Typical symptoms include cough, fever, and sputum production, usually developing over days
and sometimes accompanied by pleurisy. Physical examination may detect tachypnea and
signs of consolidation, such as crackles with bronchial breath sounds. This syndrome is
commonly caused by bacteria, such as S. pneumoniae and H. influenzae.

Bacterial organisms with increased antibiotic resistance have also emerged and have further
complicated the management of neonatal sepsis. The colonization patterns in nurseries and
personnel are reflected in the organisms currently associated with nosocomial infection. In
neonatal intensive care units (NICUs), infants with lower birth weight and infants who are less
mature have an increased susceptibility to these organisms.
S epidermidis, a coagulase-negative Staphylococcus, is increasingly seen as a cause of
nosocomial or late-onset sepsis, especially in the premature infant, in whom it is considered
the leading cause of late-onset infections. Its prevalence is likely related to several intrinsic

27
properties of the organism that allow it to readily adhere to the plastic mediums found in
intravascular catheters and intraventricular shunts.
The bacterial capsule polysaccharide adheres well to the plastic polymers of the catheters.
Also, proteins found in the organism (AtlE and SSP-1) enhance attachment to the surface of
the catheter. The adherence creates a capsule between microbe and catheter, preventing C3
deposition and phagocytosis.

In addition to being a cause of neonatal sepsis, coagulase-negative Staphylococcus is

ubiquitous as part of the normal skin flora. Consequently, it is a frequent contaminant of blood
and cerebrospinal fluid (CSF) cultures. When a culture grows this organism , the clinical
setting, colony counts, and the presence of polymorphonuclear neutrophils (PMNs) on Gram
staining of the submitted specimen often help differentiate true infection and positive culture
from a false-positive or contaminated specimen.

In addition to the specific microbial factors mentioned above, numerous host factors
predispose the newborn to sepsis.These factors are especially prominent in the premature
infant and involve all levels of host defense, including cellular immunity, humoral immunity, and
barrier function. Immature immune defenses, and environmental and maternal factors
contribute to the risk neonatal sepsis, morbidity, and mortality, particularly in preterm and/or
very low birthweight (VLBW) infants. There may also be a genetic association.

Cellular immunity
PMNs are vital for effective killing of bacteria. However, neonatal PMNs are deficient in
chemotaxis and killing capacity. Decreased adherence to the endothelial lining of blood
vessels reduces their ability to marginate and leave the intravascular space to migrate into the
tissues. Once in the tissues, they may fail to degranulate in response to chemotactic factors.
Furthermore, neonatal PMNs are less deformable and thus are less able to move through the
extracellular matrix of tissues to reach the site of inflammation and infection. The limited
capacity of neonatal PMNs for phagocytosis and killing of bacteria is further impaired when the
infant is clinically ill. Finally, neutrophil reserves are easily depleted because of the diminished
response of the bone marrow, especially in the premature infant.
Neonatal monocyte concentrations are at adult levels; however, macrophage chemotaxis is
impaired and continues to exhibit decreased function into early childhood. The absolute
numbers of macrophages are decreased in the lungs and are likely decreased in the liver and
spleen as well. The chemotactic and bactericidal activity and the antigen presentation by these
cells are also not fully competent at birth. Cytokine production by macrophages is decreased,
which may be associated with a corresponding decrease in T-cell production.
Although T cells are found in early gestation in fetal circulation and increase in number from
birth to about age 6 months, these cells represent an immature population. These naive cells

28
do not proliferate as readily as adult T cells do when activated, and they do not effectively
produce the cytokines that assist with B-cell stimulation and differentiation and
granulocyte/monocyte proliferation.
Formation of antigen-specific memory function after primary infection is delayed, and the
cytotoxic function of neonatal T cells is 50-100% as effective as that of adult T cells. At birth,
neonates are deficient in memory T cells. As the neonate is exposed to antigenic stimuli, the
number of these memory T cells increases.
Natural killer (NK) cells are found in small numbers in the peripheral blood of neonates. These
cells are also functionally immature in that they produce far lower levels of interferon gamma
(IFN-γ) upon primary stimulation than adult NK cells do. This combination of findings may
contribute to the severity of HSV infections in the neonatal period.

Humoral immunity
The fetus has some preformed immunoglobulin, which is primarily acquired through
nonspecific placental transfer from the mother. Most of this transfer occurs in late gestation, so
that lower levels are found with increasing prematurity. The neonate’s ability to generate
immunoglobulin in response to antigenic stimulation is intact; however, the magnitude of the
response is initially decreased, rapidly rising with increasing postnatal age.
The neonate is also capable of synthesizing immunoglobulin M (IgM) in utero at 10 weeks’
gestation; however, IgM levels are generally low at birth, unless the infant was exposed to an
infectious agent during the pregnancy, which would have stimulated increased IgM production.
Immunoglobulin G (IgG) and immunoglobulin E (IgE) may be synthesized in utero. Most of the
IgG is acquired from the mother during late gestation. The neonate may receive
immunoglobulin A (IgA) from breastfeeding but does not secrete IgA until 2-5 weeks after birth.
Response to bacterial polysaccharide antigen is diminished and remains so during the first 2
years of life.
Complement protein production can be detected as early as 6 weeks’ gestation; however, the
concentration of the various components of the complement system varies widely from one
neonate to another. Although some infants have had complement levels comparable to those
in adults, deficiencies appear to be greater in the alternative pathway than in the classic
pathway.
The terminal cytotoxic components of the complement cascade that lead to killing of
organisms, especially gram-negative bacteria, are deficient. This deficiency is more marked in
preterm infants. Mature complement activity is not reached until infants are aged 6-10 months.
Neonatal sera have reduced opsonic efficiency against GBS, E coli, and Streptococcus
pneumoniae because of decreased levels of fibronectin, a serum protein that assists with
neutrophil adherence and has opsonic properties.

Barrier function

29
The physical and chemical barriers to infection in the human body are present in the newborn
but are functionally deficient. Skin and mucous membranes are broken down easily in the
premature infant. Neonates who are ill, premature, or both are at additional risk because of the
invasive procedures that breach their physical barriers to infection.
Because of the interdependence of the immune response, these individual deficiencies of the
various components of immune activity in the neonate conspire to create a hazardous situation
for the neonate exposed to infectious threats.

Cardiopulmonary response to sepsis

In overwhelming sepsis, there may be an initial early phase characterized by pulmonary
hypertension, decreased cardiac output, and hypoxemia. These cardiopulmonary disturbances
may be due to the activity of granulocyte-derived biochemical mediators, such as hydroxyl
radicals and thromboxane B2 (an arachidonic acid metabolite).
These biochemical agents have vasoconstrictive actions that result in pulmonary hypertension
when they are released in pulmonary tissue. A toxin derived from the polysaccharide capsule
of type III Streptococcus has also been shown to cause pulmonary hypertension.

30
 VIII. COURSE IN THE WARD

1. DOCTOR’S PROGRESS NOTE

Patient’s Name: Tan, Juan Karlos Birthdate: 1month/M

Attending Physician: Dr. Grasparil

DOCTOR’S ORDER

11/14/17 12:15 am

 Please admit under the service of Dr. Grasparil

 Secure consent to care
 Breastfeeding: food c/o watcher
 VS every 2 hours and record
 Intake and Output q shift
 Insert heplock
 Labs: CBC,plt, UA, stool exam, CXR-APL – done as OPD, follow up result

Meds:

 Salbutamol (ventolin) ½ nebule + 2ml NSS every 4 hours. 1st dose at ER

 Ampicillin-Sulbacta, ( siligram) 135mg IVTT every 6 hours
 Amikacin (Amikacide) 80mg IVTT every 24 hours

 AP aware of admission

 Please inform Dr. Rustia once on floor

 For strict aspiration precaution

 Watch out for RR>60 CHEST RETRACTIONS, cyanosis, or other signs of respiratory
distress.

 Chest physiotherapy every after nebulization

31
11/15/17 1:00 pm

 Rounds with AP
 Continue present management
 Continue close monitoring
11/15/17 9:15 pm

 Rounds with AP
 Refer to Dr. Enreva for evaluation, secure consent
 Start prednisone 10mg/15ml PO BID
 Continue monitoring
 Watch out for unsualities
 Refer if RR> 50 cpm
 CPT very after neb
 P salb neb to every 2 hours will reassess in AM

11/16/17 2PM

 Rounds with AO
 Continue medication
 Follow up repeat CXR

11/17/17 2:50 P,

 Continue medications
 Increase salbutamol nebulization to every 4 hours

11/17/17 9:40 pm

 Revise schedule as follows

 Clarithromycin 8am-6pm
 Prednisone 10am-10 pm Q12

11/18/17 3:00 pm

 Rounds with AP
 Continue meds
 Please record vital signs especially when patient in at rest

32
  Prednisone to complete x5days only

11/18/17 6:35 PM

 Start omeprazole 5.5 mg IVTT now once daily

 Salbutamol nebulization to every 2 hours
 Strict aspiration precaution

11/18/17 8:40 PM

 Conferred with AP
 D/C prednisone

11/18/17 10:30 pm

 Conferred with AP
 Co- management with DR. Estrera, with secure consent
 Start o2 AT 2 CPM
11/19/17 9:00 AM

 Conferred with Dr. Estrera

 Shift ampicillin-Sulbactan to Cefepime 180mg IVTT every 8 hours
 For blood culture
11/19/17 2:30 pm

 Conferred with Dr. Gasparil

 For referral to Dr. Peli for evaluation
 Secure consent
11/19/17 3:30 pm

 Rounds with AP
 Please measure BP
 Maintain on NPO
 Continue meds
 Continue monitoring
 Check out for unsualities
 Refer
 Maintain on high back rest

33
  Shift cefepime to cepiran instead of axera

11/19/17 4:10 pm

 For 2D echo and ECG

 Please facilitate
11/20/17 12:40 pm

 Rounds with AP
 D/C Hgt monitoring
 Decrease O2 support to PRN
 Continue present management
 Refer
11/20/17 2:30 PM

 Conferred with AP
 For co-management with Dr. Paragas
 Increase O2 support at 10LPM via Face mask w/ reservoir

11/20/17 3:50 pm

 Rounds with AP
 Complete cefepime for 7days Clarithromycin 10 days and Amikacin at 10 days.

11/20/17 4:10 pm

 Conferred with Dr. Paragas

 Start sildenafil 25mg/ 1 tab 4mg?pptab, 1 pptab P.O every 6 hours
 Please use Viagra for sildenafil
 May resume feeding with strict aspiration precaution
11/21/17 4:00 pm

 Rounds with Dr. Paragas

 Repeat 2D echo on Nov. 23, 2017
 Refer

34
 2. LABORATORY/DIAGNOSTIC EXAMINATION

Diagnostic Test: COMPLETE BLOOD COUNT

Test Name Result/ Units Reference Interpretation
Values range
Hemoglobin (Hb or Hgb) is a protein in red
blood cells that carries oxygen throughout the
body. High hemoglobin count occurs most
commonly when your body requires an
increased oxygen-carrying capacity while if low
Hemoglobin 133.00 g/L 110-150 hemoglobin count can be associated with a
disease or condition that causes your body to
have too few red blood cells. This can occur if:
Your body produces fewer red blood cells than
usual and Your body destroys red blood cells
faster than they can be produced.
Ref:
https://www.mayoclinic.org/symptoms/low-
hemoglobin/basics/causes/sym-20050760
Hematocrit is a part of the total volume of the
blood of the body that composes the red blood
cells. A high hematocrit means the percentage
of red blood cells in a person's blood is above
the upper limits of normal for that person's
Hematocrit 0.38 10^12 0.37-0.45 age, sex, or pregnancy. Causes of a high
/L hematocrit can be dehydration, Low availability
of oxygen and etc. While when the result is low
hematocrit, this indicates the person may be
anemic.

35
 Ref:http://www.myhealthyfeeling.com/normal-
hematocrit-levels-low-high-hematocrit/
Erythrocytes are red and consist of a protein
called hemoglobin, which contains red iron.
High red blood cell count may be caused by
Erythrocytes 4.11 10^9/ 4.0-5.5 low oxygen levels, kidney disease or other
L problems while low red blood count can
indicate anemia, low hemoglobin and low
hematocrit levels.
Ref: http://study.com/academy/lesson/what-
are-erythrocytes-definition-function.html
Higher levels of leukocytes in the bloodstream
may indicate an infection while A low white
blood cell count usually is caused by Certain
disorders present at birth (congenital) that
involve diminished bone marrow function,
Leukocytes 11.20 10^9/ 4.5-13.5 Autoimmune disorders that destroy white blood
L cells or bone marrow cells and etc.
Ref:
https://www.mayoclinic.org/symptoms/low-
white-blood-cell-count/basics/causes/sym-
20050615

Platelets, also
called thrombocytes ("blood clot cell"),
are a component of blood whose
function (along with the coagulation

36
 factors) is to stop bleeding by clumping
Thrombocyte 414.00 150-400 and clotting blood vessel injuries. An
s H abnormally low level of platelets in the
bloodstream indicate as
Thrombocytopenia
Ref:https://www.emedicinehealth.com/th
rombocytopenia_low_platelet_count/arti
cle_em.htm
Neutrophils are a type of white blood cell that
your body uses to fight infections. High
*Neutrophil 0.21 L 0.55-0.65 neutrophil levels are often caused by an
infection while a low number
of neutrophils your immune system is weak.
Ref:https://www.cancer.org/treatment/treatmen
ts-and-side-effects/physical-side-
effects/infections/infections-in-people-with-
cancer/low-wbc-and-weak-immune-
system.html
Lymphocytes are one of several different types
of white blood cells. Low lymphocyte count
(Lymphocytopenia) could indicate that you are
at greater risk of developing infections while
Lymphocyte 0.51 H 0.29-0.49 High lymphocyte levels that persist may point
s to a more serious illness or disease, such as
hepatitis, influenza, tuberculosis and etc.
Ref:http://www.healthyandnaturalworld.com/lo
w-lymphocyte-count/
Monocytes are the biggest of all white blood
cells that play an important role in the defense
against germs and in inflammation. A high
*Monocytes 0.20 H 0.02-0.09 level of monocytes called monocytosis while

37
 low level of monocytes known as
monocytopenia.
Ref: https://selfhacked.com/blog/monocytes/
Eosinophils are a type of white blood cell that
play an important role in the body's response
to allergic reactions, asthma, and infection with
parasites. The most common causes of a high
number of eosinophils (called eosinophilia or
hypereosinophilia) are
Allergic disorders, infections by parasites and
Certain cancers while A low number of
*Eosinophil 0.06 H 0.02-0.04 eosinophils in the blood (eosinopenia) can
occur with Cushing syndrome, bloodstream
infections (sepsis), and treatment with
corticosteroids.
Ref:http://www.msdmanuals.com/home/blood-
disorders/white-blood-cell-
disorders/eosinophilic-disorders
Measurement of basophils in whole blood for
the evaluation and management of allergic,
hematologic, and neoplastic disorders, as well
as parasitic infections. When basophils levels
*Basophils 0.02 0-0.02 too high can cause hypothyroidism while
basophils levels too low can cause
hyperthyroidism.
Ref:https://www.healthline.com/health/basophil
s#what-happens-if-yourlevel-is-high
The ANC can be critical in assessing an
immunocompromised patient’s risk for
Absolute 2.35 10^9/ 1.8-7.8 developing opportunistic infections. And
Neutrophil L

38
 frequently used to assess neutropenic fever in
chemotherapy patients.
Ref:https://www.mdcalc.com/absolute-
neutrophil-count-anc
Assesses number of lymphocytes and predicts
CD4 count. Decrease in the number of
lymphocyte T-cells and natural killer (NK) cells
Absolute 5.71 H 10^9/ 1.0-4.8 will mean that it is harder to control certain
Lymphocyte L viral, fungal, and parasitic infections. While
s high levels it may represent something more
serious, such as a blood cancer or a chronic
infection.
Ref:https://www.mayoclinic.org/symptoms/lym
phocytosis/basics/causes/sym-20050660
An increased number of monocytes in the
blood (monocytosis) occurs in response to
Absolute 2.24 H 10^9/ 0.0-0.80 chronic infections, in autoimmune disorders, in
Monocytes L blood disorders, and in certain cancers while
A low number of monocytes in the blood
(monocytopenia) can be caused by anything
that decreases the overall white blood cell
count such as a bloodstream infection,
chemotherapy, or a bone marrow disorder.
Ref: http://www.msdmanuals.com/home/blood-
disorders/white-blood-cell-disorders/monocyte-
disorders
Absolute Basophil Count test is performed on
a sample of blood to measure the level of
Absolute 0.22 H 10^9/ 0.0-0.20 Absolute Basophil Count in the blood.It is
Basophils L performed to detect Allergy and
Hypothyroidism.

39
 Ref: https://www.practo.com/tests/absolute-
basophil-count-automated-blood/p
Mean corpuscular volume (MCV) is the
average volume of red cells in a
specimen. Microcytic anemia, also called
MCV 92.46 H fL 75-90 Microcytosis, occurs when the MCV blood test
number is lower than normal. A normal MCV
indicates normocytic (normal average RBC
size), and high MCV indicates macrocytic
(large average RBC size).
Ref: http://www.easy-immune-health.com/mcv-
blood-test.html
The Mean Corpuscular Hemoglobin (MCH) is
the most common reason for high MCH
is macrocytic anemia, which is a blood
disorder in which the body fails to produce
MCH 32.36 H pg 25-32 enough red blood cells. While Common
causes of Low MCH results include blood loss,
iron deficiency and microcytic anemia, which is
a condition in which red blood cells, are
abnormally small, carrying less hemoglobin.
Ref:
https://www.healthtestingcenters.com/what-
does-high-mch-blood-test-result-mean
The Mean Corpuscular Hemoglobin
Concentration (MCHC) is the most common
complication of living with low MCHC levels is
lack of energy and decreased stamina while A
high MCHC value is often present in conditions
MCHC 350 H g/L 320-362 where hemoglobin is more concentrated within
your red blood cells. Conditions that can cause

40
 high MCHC calculations are Autoimmune
hemolytic anemia, Hereditary spherocytosis
and Severe burns.
Ref: https://www.healthline.com/health/high-
mchc#takeaway
A high red blood cell distribution width (RDW)
means that the red
blood cells vary a lot in size. May be
associated with adverse outcomes in patients
with heart failure and risk of death, and
RDW 14.80 11.5-14.5 cardiovascular events in people with previous
myocardial infarction. While low RDW (below
10.2%) means that the red blood cells vary
very little in size. One reason for a low RDW
level is macrocytic anemia.
Ref:https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC2954027/
If the Mean platelet volume (MPV) is low or
high platelet count may hint that the individual
has developed abnormal levels that could have
MPV 7.90 H fL 2-20 resulted from a blood disorder or medical
condition associated with the bone marrow
where the cell fragments are produced.
Ref: http://www.thrombocyte.com/mean-
platelet

41
 Diagnostic test: Urinalysis
Test Name Result/ Unit Referenc Interpretation
Values s e range
PHYSICAL A light yellow urine color typically signifies very
EXAMINATI healthy urine.
ON LYTYLW http://www.urinecolors.com/urine-color/clear-urine
Color
Character CLEAR If your urine color is very clear, it is showing a high
concentration of water, and a lower concentration of
actual waste. Urine could mean you are very well
hydrated, but a low concentration of waste is not
necessarily a good thing.
Ref: http://www.urinecolors.com/urine-color/clear-
urine
Reaction 7.5 If your urine pH is consistently higher that 7.5 some
possible reasons. You could be at the opposite end
of the spectrum called alkalosis and your body is so
acidic that your kidneys are producing ammonia in
an effort to neutralize the toxic acids.
Ref:https://www.approachwellness.com/urine-
pH.html
Specific 1.015 A specific gravity greater than 1.035 is consistent
gravity with frank dehydration. In neonates; normal urine
specific gravity is 1.003.Hypovolemic patients usually
have a specific gravity >1.015.
Ref:https://en.wikipedia.org/wiki/Urine_specific_gravit
y
CHEMICAL
EXAMINATI A negative test result means that there is no
ON detectable amount of protein in the urine at the time

42
Albumin NEGATI of testing. Protein detected in a random urine
VE sample may be a transient elevation due to
an infection, medication, vigorous
exercise, pregnancy, diet, cold exposure, or
emotional or physical stress.
Ref:https://labtestsonline.org/understanding/analytes/
urine-protein/tab/test/
Sugar NEGATI A positive urine glucose test would indicate that the
VE blood glucose level is very high, and a negative urine
glucose test could mean that the level is low, normal,
or slightly elevated.
https://www.diabetesselfmanagement.com/diabetes-
resources/definitions/urine-glucose-test/
URINE
FLOW
CYTOMETR 11 /uL 0-17 White blood cells (leukocytes) may be a sign of an
Y infection.
Ref: http://www.mayoclinic.org/tests-
2 /HP 0-3 procedures/urinalysis/details/results/rsc-20255397
WBC F

7 /uL 0-11 Red blood cells (erythrocytes) may be a sign of

RBC 1 /HP 0-2 kidney disease, a blood disorder or another
F underlying medical condition, such as bladder cancer
6 /uL 0-17 The presence of a large number of epithelial cells in
Epithelial 1 /HP 0-3 a urinalysis test may indicate a bacterial infection,
cells F however, having many squamous epithelial cells
(SECs) in urine usually indicates that the urine
sample was contaminated.
Ref:http://www.healthyandnaturalworld.com/squamo
us-epithelial-cells/

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 1 /uL 0-1 Tube-shaped proteins — may form as a result of
3 /LPF 0-3 kidney disorders.
CAST Ref: http://www.mayoclinic.org/tests-
procedures/urinalysis/details/results/rsc-20255397
16 /uL 0-278 Bacteria may indicate an infection. An Asymptomatic
3 /HP 0-50 bacteriuria means you have bacteria in your urine but
Bacteria F you have no symptoms of infection.
Ref: http://www.mayoclinic.org/tests-
procedures/urinalysis/details/results/rsc-20255397

INTERPRETATION

CHEST AP LATERAL <PEDIA>

Heart size is within normal limits. Its configuration is unremarkable. Pulmonary vascularity is
normal. Linear infiltrates are noted in both lungs. The lateral costophrenic sinuses are sharp.
Hill are not enlarged. Visualized osseous structures are normal.
IMPRESSION:
- SUGGESTIVE OF AN INFLAMMATORY LUNG DISEASE COMPATIBLE WITH
PNEUMONIA OF INTESTITIAL PATTERN.

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 IX. DISCHARGE PLAN

M-E-T-H-O-D-S

To achieve the optimum wellness of the patient, the healthcare Providers and Family
caregivers all play roles in maintaining a patient’s health after discharge. An effective discharge
planning is needed to provide consistency in both the process and quality of care given.

M-medication:

1. The mother will be thought about:

 The dose of the drugs to take, the time, and the duration
 Expected action of the medication and possible side effects
 What to do if a dose is missed
 Special directions for mixing and administering the medications
 Proper storage and expiration and disposal.

2. Instruct the mother to avoid OTC drugs

3. Remind the patient to consult if any adverse effects occur

E-exercise:

1. Maintain a quiet, pleasant environment to promote relaxation

2. Advise the mother to schedule periods of uninterrupted rest for her baby

T-treatment:

1. Stress the importance of complying with the prescribed medications

H-health teaching:

1. Explain the underlying disorder and treatment plan

2. Follow the healthcare professional advice given to parents during hospitalization

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 3. Provide written and oral instructions about activity, diet recommendations, medications,
and follow up visits
4. Instruct the mother about the importance of adequate sleep of the newborn
5. Compliance with follow up examinations

O-outpatient:

1. Give the mother information about:

 Where to go for follow-up care
 When to seek help (for example, side effects to report)
 Where to get medical equipment or medications.
2. Remind the parents that frequent check-ups are important to improve their infant condition
and maintain optimum balance of wellness

D-diet:

1. Instruct the mother to give strict maternal breastfeeding during the first 6 months.
2. Instruct the mother to breastfeed the child as often as he manifests signs of hunger (e.g:
cry).

S-spiritual:

1. Encourage the patient to draw self-closure to God to impart the importance of spirituality.
2. Encourage the patient having a bond together with the family members like simply eating or
praying together to improve or enhance self-concept as well as a sense of hope that will help
in improving the wellness of the patient.

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