TABLE OF CONTENTS

 Dedication i
 Acknowledgement ii
 Introduction 4-5

 Review of Related Literature 6-15

 Nursing Health History 16

 Client Health History 17

 Treatments/ Medications 17
 Past Illness/Hospitalization 17
 Allergies 17
 Family Health History 17
 Developmental History 17-18
 Nutritional Metabolic Pattern 18
 Elimination Pattern 18
 Activity Exercise Pattern 19
 Sexuality Reproduction Pattern 19
 Sleep-Rest Pattern 19
 Sensory-Perceptual Pattern 19
 Cognitive Pattern 20
 Role Relationship Pattern 20

 Self-Perception-Self-Concept Pattern 20

 Coping Stress Tolerance 20

 Value Belief Pattern 20
 Health History 21
 History of Present Illness 21
 Past History 21

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 Physical Examination 22
 General Physical Survey 22
 Mental Status Examination 22
 Skin 22
 Head and Face 22
 Eyes 22
 Ears and Nose 23
 Mouth and Throat 23
 Neck 23
 Arms, Hands and Fingers 23
 Posterior and Lateral Chest 23
 Anterior Chest 23
 Breasts (Male) 23
 Heart 24
 Abdomen 24
 Legs, Feet and Toes 24

 Genitalia (Male) 24
 Musculoskeletal and Neurologic Examination 24
 Cranial Nerve Assessment 25
 Review of System 26
 General Survey 26
 Integumentary System 26
 EENT 26
 Gastrointestinal System 26
 Musculoskeletal System 26
 Neurologic System 27
 Urinary System 27
 Reproductive System 27
 Hematologic 27
 Endocrine 27

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  Psychiatric 27
 Laboratory Results 28
 Hematology 28-29
 Bilirubin 30
 Anatomy and Physiology 31-43
 Pathophysiology 44-45
 Drug Study 46-84
 Nursing Care Plan 56-75
 Discharge Plan 76
 Appendices 77
 IVF Chart 77
 Daily Weight 77
 Vital Signs 78
 I and O Sheet 78
 CFAC 79
 Genogram 80
 References 81

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 INTRODUCTION

The term “sepsis” has been around since ancient times; modern definitions of “sepsis” were
described in detail in the early 1990s, at a consensus conference convened by the American College
of Chest Physicians and the Society of Critical Care Medicine. At that time, “sepsis” was described
as a systemic response to a physiologic insult – including infectious and other etiologies – that lead
to the development of further organ injury, ultimately culminating in multiple organ dysfunction
syndromes. Neonatal sepsis, also termed Sepsis neonatorum, refers to a group of physical and
laboratory findings that occur in response to invasive infection within the first 30 days of life. As
will be discussed below, there are various infectious causes of neonatal sepsis; however, the pattern
of presentation is quite similar in all cases, as is the approach to treatment. The importance of
neonatal sepsis as a diagnosis is found in the fact that this diagnosis occurs in between 1 to 8
children per 1000 live births in the United States, and may be associated with a fatality rate of up
to 30%. As such, it is essential that caregivers that are involved with the management of neonates
have a reliable approach to the diagnosis and treatment of infants with sepsis, and that appropriate
intervention be instituted in a timely manner.

Neonatal Sepsis is an infection in the blood that spreads throughout the body and occurs in
a neonate. Neonatal Sepsis is also termed as Neonatal Septicemia and Sepsis Neonatorum.
Neonatal Sepsis has 2 types: The one that is seen in the first week of life is termed as Early- onset
sepsis and most often appears in the first 24 hours of life. The infection is often acquired from the
mother. This can be cause by a bacteria or infection acquired by the mother during her pregnancy,
a Preterm delivery, Rupture of membranes (placenta tissue) that lasts longer than 24 hours,
Infection of the placenta tissues and amniotic fluid (chorioamnionitis) and frequent vaginal
examinations during labor. The second type or the Late-onset Sepsis is acquired after delivery.
This can be cause by contaminated hospital equipment, exposure to medicines that lead to
antibiotic resistance, having a catheter in a blood vessel for a long time, staying in the hospital for
an extended period of time.

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 Signs and symptoms of Neonatal Sepsis includes but is not limited to: body temperature
changes, breathing problems, diarrhea, low blood sugar, reduced movements, reduced sucking,
seizures, slow heart rate, swollen belly area, vomiting, yellow skin and whites of the eyes
(jaundice). Possible complications are disability and worst is death of the neonate. (Greene, 2007)

Patient A. a two days old child residing in Barangay Rizal, Surigao City, Surigao del Norte was
admitted at Surigao Medical Center last September 24, 2019 at exactly 11:31 pm with chief
complain of jaundice for further management. Patient A was diagnosed Neonatal Sepsis.

I, a third year student chose the case of Patient A to gain more knowledge and experience
in the field of nursing to establish holistic approach to the S.O and to the patient promoting for
optimal health of the patient’s condition. Enhance critical thinking and skills that can be useful in
the future as to provide appropriate nursing care to our clients. Also this output will be useful for
future purposes related to the case of Neonatal Sepsis.

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 Review of Related Literature

According to World Health Organization as of 2009, Newborns are susceptible to infection

because of their underdeveloped immune system. Neonatal sepsis also known as Neonatal
Septicemia or Sepsis Neonatorum is an infection in the blood that spreads throughout the body and
occurs of a neonate that kills 8,000 newly born babies each year based on Philippine experience.

Neonatal sepsis, sepsis neonatorum 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 hypothermia (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 sepsis. 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 hemodynamic 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 explanations 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.

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Blood cultures may be negative, increasing the difficulty in establishing infection etiologically.
Finally infections with or without sepsis may be present concurrently with a non infectious illness
in the new born infant, child or adult.

Neonatal Sepsis has 2 types:

The one that is seen in the first week of life is termed as Early- onset sepsis and most often
appears in the first 24 hours of life. The infection is often acquired from the mother. This can be
cause by a bacteria or infection acquired by the mother during her pregnancy, a Preterm delivery,
Rupture of membranes (placenta tissue) that lasts longer than 24 hours, Infection of the placenta
tissues and amniotic fluid (chorioamnionitis) and frequent vaginal examinations during labor.

The second type or the Late-onset Sepsis is acquired after delivery. This can be cause by
contaminated hospital equipment, exposure to medicines that lead to antibiotic resistance, having
a catheter in a blood vessel for a long time, staying in the hospital for an extended period of time.

The disease can be classified as: congenital, early-onset and late-onset. Congenital neonatal
sepsis is when the child is infected during pregnancy before birth. The baby can be infected by
virus through placenta or birth canal. HIV (Human Immunodeficiency Virus), syphilis is some of
the viruses that can infect the child before delivery. Early-onset neonatal sepsis is when the infant
is infected, while taking birth or soon after the delivery. Group B streptococcus (GBS) and
Escherichia coli (E. coli) are considered as chief viruses that infect the baby, while birth. Early-
onset neonatal sepsis is a result of asymptomatic colonization in the intestinal or genital tract of
the mother. Colonization is existence of bacteria’s/viruses in a body part. An infant is said to be
affected by late-onset neonatal sepsis, when it is infected a few days after delivery. This infection
can be due to the organisms present in the environment of the hospital. After getting discharged
from hospital, babies can get infected due to the bacteria’s present in the environment at home.
GBS and E. coli are also responsible for late-onset neonatal sepsis. Symptoms of early-onset
neonatal sepsis are observed mostly within 24 hours of delivery, while that of late-onset neonatal
sepsis can be observed between 8th-89th days of delivery.

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Signs and Symptoms
Signs and Symptoms observed in infants suffering from neonatal sepsis are unstable body
temperature, unable to suck breast milk properly, apnea, fever in rare cases, vomiting and diarrhea,
respiratory distress, reduced heart rate, jaundice, belly area may be swollen, breathing problems,
low blood sugar, reduced movements, reduced sucking, seizures, slow heart rate, and whites of the
eyes.
WHO as of 2009, an estimated 82,000 children die every year before their fifth birthday in
the Philippines. Half of these deaths are related to common infectious diseases such as diarrhea,
pneumonia, neonatal sepsis and measles. In fact, half of neonatal deaths occur during the first two
days of life. Progress to curtail neonatal deaths is miserable, with death rates among this age group
showing only the barest decline over the past 20 years.

Risk Factors

Risk factors identified in different studies for the development of neonatal jaundice in
healthy term babies include Asian race, instrumental delivery, babies born via C-section, normal
vaginal delivery, infant bruising, induction of labour with oxytocin and exclusive breastfeeding,
while moderate smoking of the mother and black race may be protective. Including contaminated
hospital equipment, exposure to medicines that lead to antibiotic resistance, having a catheter in a
blood vessel for a long time, staying in the hospital for an extended period of time. Bacteria or
infection acquired by the mother during her pregnancy, a Preterm delivery, Rupture of membranes
(placenta tissue) that lasts longer than 24 hours, Infection of the placenta tissues and amniotic fluid
(chorioamnionitis) and frequent vaginal examinations during labor.

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Complications

 Sepsis - Sepsis occurs when your body has a strong immune response to the infection. This
leads to widespread inflammation throughout the body. It’s called severe sepsis if it leads
to organ failure. People with chronic diseases are at a higher risk of sepsis. This is because
they have a weakened immune system and can’t fight off the infection on their own.

 Septic shock - One complication of septicemia is a serious drop in blood pressure. This is
called septic shock. Toxins released by the bacteria in the bloodstream can cause extremely
low blood flow, which may result in organ or tissue damage.Septic shock is a medical
emergency. People with septic shock are usually cared for in a hospital’s intensive care
unit. You may need to be put on a ventilator, or breathing machine, if you’re in septic shock.

 Acute respiratory distress syndrome (ARDS) - A third complication of septicemia is acute

respiratory distress syndrome (ARDS). This is a life-threatening condition that prevents
enough oxygen from reaching your lungs and blood. It often results in some level of
permanent lung damage. It can also damage your brain, leading to memory problems.

 Seizure: neonates without an underlying seizure disorder, brain pathology, or significant

metabolic disturbance who had a repeated seizure attack or an abnormal epileptiform
discharges on the electroencephalography after bacteremia that required regular
anticonvulsants medications.

 Post-infectious encephalopathy: Neonates who had consciousness change after

stabilization of vital signs that lasted >24 hours after the onset of bacteremia.

 Hydrocephalus and/or ventriculomegaly: documented by transcranial ultrasound after the

onset of bacteremia, and in neonates without previous brain pathology.

 The presence of any newly focal infections, including subdural empyema, arachnoiditis,
ventriculitis, and spinal abscess or brain abscess.

 Other neurologic complications: included neonates with encephalomalacia or cerebral

infarction due to hypotension.

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  Disability

 Death

Causes

Neonatal sepsis can be caused by bacteria such as Escherichia coli (E coli), Listeria, and
some strains of streptococcus. Group B streptococcus (GBS) has been a major cause of neonatal
sepsis. However, this problem has become less common because women are screened during
pregnancy. The herpes simplex virus (HSV) can also cause a severe infection in a newborn baby.
This happens most often when the mother is newly infected.

Prognosis
Many babies with bacterial infections will recover completely and have no other problems.
However, neonatal sepsis is a leading cause of infant death. The more quickly an infant gets
treatment, the better the outcome.

Prevention
Women may need preventive antibiotics if they have: Chorioamnionitis, Group B strep
colonization, Given birth in the past to a baby with sepsis caused by bacteria, Other things that can
help prevent sepsis include: Preventing and treating infections in mothers, including HSV,
Providing a clean place for birth, Delivering the baby within 12 to 24 hours of when the membranes
break (Cesarean delivery should be done in women within 4 to 6 hours or sooner of membranes
breaking.)

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Test and Diagnosis:

Lab tests can help diagnose neonatal sepsis and identify the cause of the infection. Blood tests may
include:

 Blood culture - helps your doctor figure out if you have a kind of infection that is in your
bloodstream and can affect your entire body. Doctors call this a systemic infection. The
test checks a sample of your blood for bacteria or yeast that might be causing the infection.
 C-reactive protein - A c-reactive protein test measures the level of c-reactive protein (CRP)
in your blood. CRP is a protein made by your liver. It's sent into your bloodstream in
response to inflammation. Inflammation is your body's way of protecting your tissues if
you've been injured or have an infection. It can cause pain, redness, and swelling in the
injured or affected area. Some autoimmune disorders and chronic diseases can also cause
inflammation.

 Complete blood count (CBC) - A complete blood count (CBC) is a blood test used to
evaluate your overall health and detect a wide range of disorders, including anemia,
infection and leukemia.

A complete blood count test measures several components and features of your blood, including:

 Red blood cells, which carry oxygen

 White blood cells, which fight infection

 Hemoglobin, the oxygen-carrying protein in red blood cells

 Hematocrit, the proportion of red blood cells to the fluid component, or plasma, in your blood

 Platelets, which help with blood clotting

If a baby has symptoms of sepsis, a lumbar puncture (spinal tap) will be done to look at the spinal
fluid for bacteria. Skin, stool, and urine cultures may be done for herpes virus, especially if the
mother has a history of infection.

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A chest x-ray will be done if the baby has a cough or problems breathing. Urine culture tests are
done in babies older than a few days.

Medication/Treatment

They are frequently treated with antibiotics empirically until cultures are sufficiently proven
to be negative. In addition to fluid resuscitation and supportive care, a common antibiotic regimen
in infants with suspected sepsis is a beta-lactam antibiotic (usually ampicillin) in combination with
an aminoglycoside (usually gentamicin) or a thirdgeneration cephalosporin (usually cefotaxime—
ceftriaxone is generally avoided in neonates due to the theoretical risk of kernicterus.) The
organisms which are targeted are species that predominate in the female genitourinary tract and to
which neonates are especially vulnerable to, specifically Group B Streptococcus, Escherichia coli,
and Listeria monocytogenes (This is the main rationale for using ampicillin versus other beta-
lactams.) Of course, neonates are also vulnerable to other common pathogens that can
cause meningitis and bacteremia such as Streptococcus pneumoniae and Neisseria meningitidis.
Although uncommon, if anaerobic species are suspected (such as in cases where necrotizing
enterocolitis or intestinal perforation is a concern, clindamycin is often added.

Granulocyte-macrophage colony stimulating factor (GM-CSF) is sometimes used in neonatal

sepsis. However, a 2009 study found that GM-CSF corrects neutropenia if present but it has no
effect on reducing sepsis or improving survival.

Prevalence
According to the Global Sepsis Alliance, infections leading to sepsis are responsible for
about one-fifth of the world’s annual 2.7 million neonatal deaths, and in South Asia and sub-
Saharan Africa, it was about 25% of all neonatal deaths. Incidence of neonatal sepsis is around 40
times higher and mortality rates are two times higher in middle-income countries than in high-
income countries. Neonatal sepsis poses a massive public health burden for sub-Saharan Africa,
with significant associated economic consequences. On the other hand, the survivors of neonatal
sepsis are vulnerable to short- and long-term neurodevelopment morbidity.

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Epidemiology

Neonatal sepsis is uncommon (2-4 per 1000 live births in developed countries), but the rate
increases dramatically in premature newborns and those born to mothers with infections or
prolonged rupture of the fetal membranes. While infections caused by organisms contracted from
the mother at birth have decreased in the past two decades, there has been an increase in
nosocomial infections. Today, most infants with sepsis have been hospitalized in neonatal intensive
care units for weeks or months because of extreme prematurity, or because of a congenital
malformation or surgical condition. Antimicrobial therapy is usually begun prior to the isolation
of a pathogen and is based upon knowledge of the likely microbes in the particular clinical
situation. The number of antimicrobial agents that can be safely used in neonates is relatively
small, and dose administration usually needs to be adjusted based upon birth weight and post-
gestational age. The decision whether to treat with antimicrobials should be made with
consideration of the history, physical examination, and laboratory data. One should also consider
the effects of the use of antimicrobials on the flora of the care unit. Bacterial resistance in the
resident flora of the unit has become a major problem where there has been indiscriminate use of
broad-spectrum agents.

Etiology

Neonatal Sepsis has 2 types: The one that is seen in the first week of life is termed as
Early- onset sepsis and most often appears in the first 24 hours of life. The infection is often
acquired from the mother. This can be cause by a bacteria or infection acquired by the mother
during her pregnancy, a Preterm delivery, Rupture of membranes (placenta tissue) that lasts longer
than 24 hours, Infection of the placenta tissues and amniotic fluid (chorioamnionitis) and frequent
vaginal examinations during labor. The second type or the Late-onset Sepsis is acquired after
delivery. This can be cause by contaminated hospital equipment, exposure to medicines that lead
to antibiotic resistance, having a catheter in a blood vessel for a long time, staying in the hospital
for an extended period of time.

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Current Issues and Trends in Neonatal Sepsis

Milk Protein Supplement May Help Prevent Sepsis In Very Low Birth-Weight Infants
ScienceDaily (Oct. 8, 2009) — Very low birth-weight newborns who received the milk protein
lactoferrin alone or in combination with a probiotic had a reduced incidence of late-onset sepsis,
according to a study in the October 7 issue of JAMA.

Infections are the most common cause of death in premature infants and a major threat for poor
outcomes," the authors write. Late-onset sepsis, i.e., infections arising after the perinatal period
(immediately before and after birth), mainly occur in the hospital and affect 21 percent of very low
birth-weight (VLBW; less than 3.3 lbs) neonates according to background information in the
article. Bovine lactoferrin (BLF; a milk glycoprotein) inhibits the growth of a wide variety of
bacteria, fungi, and viruses and has been shown to exhibit even higher in vitro antimicrobial
activity than human lactoferrin. Whether lactoferrin can reduce the incidence of sepsis is unknown.
In animal tests, the probiotic Lactobacillus rhamnosus GG (LGG) improved the activity of
lactoferrin but has not been studied in infants.

The researchers examined whether oral supplementation with BLF alone or in combination with
LGG reduces late-onset sepsis in VLBW neonates. The randomized trial was conducted in 11
Italian neonatal intensive care units and included 472 VLBW infants who were assessed until
discharge for development of sepsis. Infants were randomly assigned to receive orally
administered BLF alone (n = 153), BLF plus LGG (n = 151), or placebo (n = 168) from birth until
day 30 of life (day 45 for neonates less than 2.2 lbs. at birth). Demographic, clinical and
management characteristics of the 3 groups were similar, including type of feeding and intake of
maternal milk.

Forty-five infants had a first episode of late-onset sepsis. The researchers found that overall, late-
onset sepsis occurred less frequently in the BLF and BLF plus LGG groups (9/153 [5.9 percent]
and 7/151 [4.6 percent], respectively) than in the control group (29/168 [17.3percent]). The
decrease occurred for bacterial as well as fungal episodes. The sepsis-attributable risk of death was

14
significantly lower in the two treatment groups. No adverse effects to treatment occurred. The
researchers recommend this study confirming the safety and efficacy of lactoferrin in VLBW
infants, including more extremely preterm infants, because they potentially will benefit the most
from lactoferrin. Combination strategies, such as the use of BLF plus LGG in the study should be
pursued, and substances that might affect lactoferrin activity, such as iron supplementation, should
be investigated. The effect of lactoferrin on hematocrit [the proportion of blood that consists of
packed red blood cells should be monitored, and the effects of lactoferrin on neurodevelopmental
outcome, hospital length of stay, and costs should be studied.

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 NURSING HEALTH HISTORY

Biographic Data:
Hospital : Surigao Medical Center
Case No. : 89244
Ward : Private Room
Name of Patient : Patient A
Age : 2 days old
Sex : Male
Civil Status : Child
Address : BRGY RIZAL, SURIGAO CITY, SURIGAO
DEL NORTE
Occupation : NONE
Date of Birth : September 22, 2019
Religion : ROMAN CATHOLIC
Height : 48cm
Weight : 2.4kg

Admission Data:
Mode of Transmission : Wheelchair
Date and Time of Admission : September 24, 2019 11:31PM

Vital Signs upon admission

 Heart Rate : 163bpm
 Respiratory Rate : 54cpm
 Body Temperature : 39 degree celsius
Admitting Physician : Stephanie Grace D. Edrial, MD
Attending Physician : Linda C. Chua, MD
Chief Compliant : Jaundice
Impression : Neonatal Sepsis
Final Diagnosis : Neonatal Sepsis

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 CLIENT HEALTH HISTORY

Client Profile
Patient A is a 2 days old boy, catholic, Filipino child, born on September 22, 2019. An only
child and currently living with his family at Barangay Rizal, Surigao City, Surigao del Norte,.
Major reason for seeking health care is due to jaundice on the morning of September 24, 2019.
Treatments/Medications:
Prescribed: No prescribed medications
OTC: No over the counter drugs
Past Illness/Hospitalization
No known past illness
Allergies
No known food allergies and drug allergies
Family Health History
Patient’s grandfather on his mother’s side had history of hypertension at the age of 40. Also
his grandmother on his mother’s side had history of pneumonia at the age of 35. He is the only son
of the family

DEVELOPMENTAL HISTORY
A. Erik Erikson’s Psychosocial Development Theory: Trust vs. Mistrust
Developmental task is to form a sense of trust versus mistrust. Child learns to love and be loved.
This was exhibited by Baby Sepsis when the student nurse was holding him, he kept fidgeting and
started to cry, while whenever his mother touches him, he keeps calm. This proves that he can
differentiate between his mother’s touch and a stranger’s touch, he cries because he is unfamiliar
with the student nurse and so has not yet established trust. It would be important for the student
nurse to provide a primary care giver, provide experiences that add to security, such as soft sound
and touch, provide visual stimulation for active child involvement.

B. Sigmund Freud’s Psychosexual Stage: Oral Stage

The child explores the world by using his mouth especially the tongue. Baby Sepsis manifested
this through his eagerness to suck on his pacifier and his instant reaction of calming down once he

17
begins sucking on a pacifier. It would do good to provide oral stimulation by giving pacifiers, not
discouraging thumb sucking.

C. Jean Piaget’s Theory of Cognitive Development: Sensorimotor Stage

Babies relate to the world through their senses, using only reflex behaviour. Stimuli are assimilated
into beginning mental images. This was evident from Baby Sepsis when his reflexes were tested
such as rooting reflex, sucking reflex, swallowing reflex, plantar grasp reflex, babinski reflex, and
magnet reflex.

NUTRITIONAL METABOLIC PATTERN

Before hospitalization: The mother eats nutritional foods such as fruits and vegetables with no
tea, coffe or softdrink during pregnancy but drinks water. After pregnancy the mother does not
drink enough water due to busy taking care of the baby and household chores, While the baby is
breastfed with less production of breast milk and aspiration precaution. The baby is with diaper
and has less soft stool due to breastfeeding.
During Hospitalization: The mother eats nutritional foods such as fruits and vegetables with no
tea, coffe or softdrink after pregnancy but does not drink enough water she drinks 2-3 glasses a
day. While the baby is breastfed with less production of breast milk and aspiration precaution. The
baby is with diaper and has less soft stool due to breastfeeding.

ELIMINATION PATTERN
Before Hospitalization:
Bowel habits: The mother defecates everyday and her stool is soft, formed and its color is brown
and has a foul odor. She has no discomfort in defecating
Bladder habits: She urinates 5-6 times per day and is yellowish in color. Doesn’t have current
problems like dysuria, hematuria, incontinence and he has no discomfort in urinating.

During Hospitalization:
Bowel habits: The mother defecates 3 times a day. Her stool is soft, formed and brownish in color.
Bladder Habits: She urinates 4 times a day and it is yellowish in color.

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ACTIVITY EXERCISE PATTERN
Before Hospitalization: The mother usually do household chores and walks early in the morning
as a form of exercise during pregnancy. After delivery while both mother and child is in the
hospital, the mother usually gives the child sun bathing to eliminate the yellowish discoloration of
the skin. The primitive reflexes of the child are present and strong.
Occupational activities: Housewife
During Hospitalization: The mother wakes up when the baby is crying, she takes a nap when the
baby is sleeping. Sometimes she takes stretching.

SEXUALITY-REPRODUCTION PATTERN
Before and during Hospitalization: The patient is married and has a normal sex life. She cannot
remember her LMP and did not undergo any reproductive examination due to knowledge deficit
and financial instability.

SLEEP-REST PATTERN
Before and During Hospitalization: The baby sleeps most of the time and the mother wakes up
when the baby urinates, pass out stool or when hungry.

SENSORY-PERCEPTUAL PATTERN
Before and during Hospitalization:
Vision: Doesn’t have any difficulty in vision
Hearing: Doesn’t have any difficulty in hearing
Smell: Doesn’t have difficulty with smell, pain, postnasal drip, sneezing and nosebleed
Touch: no difficulty in touching
Taste: no difficulty tasting foods

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COGNITIVE PATTERN
Before Hospitalization: The mother does not have difficulty in hearing and has no hearing aid.
According to the significant others, If ever the mother get sick, they immediately go to Barangay
health center
During Hospitalization: The mother consult first a health care provider when takes the prescribed
medications for recovery.

ROLE-RELATIONSHIP PATTERN
Before and During Hospitalization: The members in the patient’s family are very close. They
have a healthy relationship with one another and supports each other during trying moments in
their lives.

SELF-PERCEPTION-SELF-CONCEPT PATTERN
Before and during Hospitalization: Mother has a positive outlook for her child’s future if God
would lengthen the child’s life. She has also a good relationship with her husband and their in
laws. The mother carry out her roles positively with enthusiasm and happiness in her heart as a
mother, wife, in law, sister and relative.

COPING-STRESS TOLERANCE
The mother shares that praying and reading the Bible gives her strength and helps her face the
stresses in life although she does not go to church regularly. Her family and her relatives show
support by visiting her in the hospital and through texting or calling her to ask how she and the
baby is doing.

VALUE-BELIEF PATTERN
A Roman Catholic child and the mother does not attended mass every sunday with his family but
reading bible gives her strength and helps her face the stresses in life.

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 HEALTH HISTORY

A. History of Present Illness

Prior to admission, when baby Sepsis was only 2 days old, he began to had jaundice and
had a fever of 39oC and case of sudden onset of pale and cyanotic, the baby is also anorexia . So,
the family decided to rush the client at Surigao Medical Center September 24, 2019.

B. Past History

No past history. He had completed all vaccinations including BCG, DPT, Oral Polio
Vaccine, MMR and Hepatitis B vaccine. The patient had never been any of the childhood disease
such as measles, mumps and chicken pox. The patient had no history of accident or any injury. He
does not have allergy in any food

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 PHYSICAL EXAMINATION
General Physical Survey

The client is properly groomed. Lying comfortably on bed sleeping, appears fatigue, thin
and has dry skin and poor skin turgor. There is also a yellowish discoloration in the skin. With an
ongoing IVF of D10 water 500cc @ 8-9gtt/h hooked at right cephalic vein infusing well . Ht: 1’6’’
Wt: 5.29lbs, Apical pulse: 163, Resp: 54, Temp: 39 degree celcius, BMI: 10.4

Mental Status Examination

The client is sleeping; unconscious and does not alert

Skin
Extreme pallor, bluish(cyanosis) noted. Skin is yellow, very warm and dry to touch. Poor skin
turgor noted. No edema. No scalp lesions or flaking.

Head and Face

No scalp lesions or flaking. Head symmetrically rounded upon palpation. Function of CN V, pt.
identifies light touch and sharp touch to forehead, cheek and chin. Bilateral corneal reflex intact.
Masseter muscles contract equally and bilaterally. Function of CN VII pt. smiles, frowns, shows
teeth, blow cheeks, and raises eyebrows as instructed.

Eyes
Eyeballs are not sunken. Eyebrows sparse with equal distribution. No scaliness. Lids brown,
without edema, nor lesions. Sclera without increased vascularity nor lesions. Palpebral and bulbar
conjunctiva pale without lesions. Irises uniformly black. Pupils are round and react to light and
accommodation.

22
Ears and Nose
Auricle without deformity, lumps nor lesions. Auricles and mastoid processes non-tender. Auricle
aligned with outer canthus of eye about 10 degree from vertical. Pinna recoils after it is folded.
Whisper test: Client hears words . Nose is symmetrical and straight upon palpation. Nares patent.
No tenderness, masses, and displacement of bone cartilages. No redness, swelling, and abnormal
discharge on the nasal mucosa.

Mouth and Throat

Lips are pale and dry to touch. Tonsils appear to be normal. No swelling on uvula.

Neck
Neck symmetrical without masses and scars. Lymph nodes are non-palpable. Trachea is in center
placement in midline of neck.

Arms, Hands, and Fingers

Arms are equal in size and symmetry bilaterally; yellow; warm and dry to touch without edema.
No lesions and bruising on hands. Three flexion creases present in palm. Fingernails are finely cut
and clean. Pale or cyanotic nails are seen. Clubbing 180 degrees is noted. Capillary refill of <3sec

Posterior and Lateral Chest

Posterior lateral diameter is 1:2 ratio. Respiration rate is 30 cpm. Symmetrical expansion on
posterior thorax.

Anterior Chest
Chest symmetry is equal. Anterior lateral diameter is 1:2 ratio. Shape and position of sternum is
level with ribs. Position of trachea is in midline. No pain nor tenderness in the anterior thorax.
Symmetrical expansion on anterior thorax.

Breasts (Male)
Skin is yellow. No swelling, ulcerations, or nodules noted. Flat disk of undeveloped breast tissue
under nipple noted.

23
Heart
Apical pulse rate is 130 bpm. No gallops nor murmurs, nor rubs.

Abdomen
Visceral pain in the umbilical region . Abdomen is yellow in color upon inspection. No rashes or
lesions. No evidence of enlargement of liver and spleen upon inspection and palpation. Navel is
protruding. High-pitched, irregular gurgles 5-35 times/min; present equally in all four quadrants.

Legs, Feet and Toes

Legs has no abrasion and wound. Skin intact, yellow, warm and dry to touch without edema.
Lymph nodes are non-palpable. No edema palpated. Toenails are not finely cut, not clean and clear.
No clubbing.

Genitalia (Male)
No bulging or masses in inguinal area. No discharge. No pubic hair. Not yet circumcised

Musculoskeletal and Neurologic examination

Muscle strength 4/5. No edema noted at both lower extremities. Active resistive range of motion
against some resistance noted. No deviations, inflammations, nor bony deformities. Moves upper
and lower extremities freely against gravity and against resistance. Patient is unconscious.

24
 Cranial Nerve Assessment
Cranial Nerve Name Result

I Olfactory Identifies scent correctly with

each nostril

II Optic Light falls symmetrically within

each pupil

III Occulomotor Pupils are round and react to light

and accommodation.

IV Trochlear Both eyes are well coordinated

and moves in unison without
tenderness felt when left and right
eyes moves. Patient lids close
symmetrically.

V Trigeminal Eyelids blink bilaterally

VI Abducens Can move left and right eyeballs

in a moderate manner.

VII Facial Raises his left and right eyebrows

whenever you say something to
him. Can close his both eyes.

VIII Acoustic Can clearly hear normal voice

tone.

IX Glossopharyngeal Positive gag reflex

X Vagus Positive swallowing reflex

XI Spinal Accessory Patient can move his neck

XII Hypoglossal Can protrude tongue

25
 REVIEW OF SYSTEMS

General Survey
The usual weight of the client is 2kg upon hospitalization. Extreme pallor and bluish,
yellowish in color of skin, appears fatigue, thin and warm skin noted upon assessment.

Integumentary System
Patient has history of jaundice and cyanosis, no history of edema, no skin allergies, no burns, No
history of scalp lesions or flaking, pigmented lesions, cellulitis, adenopathy.

Head, Eyes, Ears, Nose, and Throat (EENT)

Head: Patient has no history of head injuries, lightheadedness, vertigo

Eyes: Patient has no history of conjunctivitis, visual problems, edema, lesions, scaliness, sore eyes.
No history of double vision ( Diplopia )

Ears: Patient has no history of ear infection, draining ears, lumps or lesions. No discharged
( Otorrhea ). No history of ear pain ( Otalgia ) .Ear Ringing ( Tinnitus )

Nose: Patient has no history of Nasal Bleeding (epistaxis), nasal stuffiness. No nasal discharge
( Rhinorrhea ), laryngitis

Throat: Patient has no history in swelling on uvula, tonsillitis, sore throats bleeding gums
( Gingival Hemorrhage )

Gastrointestinal System
Patient has no history of nausea, diarrhea and constipation. No history of bright red stools
( Hematochezia ). No history of black tarry stools ( melena ), stool incontinence ( Encopresis )

26
Musculoskeletal System
No history of edema at both lower extremities. No deviations, inflammations, or bony
deformities. No joint pain . No muscle pain.

Neurologic System
Patient has no history of memory loss, seizure, dizziness, sensation changes such as numbness and
coldness.

Urinary Systems
Patient has no history of any urinary tract infection. No pain in urination. No discharge.

Reproductive System (Male)

No history of bulging or masses in inguinal area. No discharge. No pubic hair. Not yet circumcised.

Hematologic or Lymphatic
Patient has no history of lymph node enlargement. No history of easy bleeding or bruising.

Endocrine
No history of Diaphoresis . No polyuria.

Psychiatric
No history of depression, memory change, or suicide attempts.

27
 HEMATOLOGY
COMPLETE BLOOD COUNT
September 24, 2019
TEST RESULT NORMAL UNIT SIGNIFICANT Rationale
VALUES
RED BLOOD 5.67 4-6 10^12/L Normal
CELL
HEMOGLOBIN 18.5 12-17 g/dL Increased Polycythemia
HEMATOCRIT 56.6 37-54 % Increased Polycythemia
MCV 99.8 87 ± 5 Fl Increased Macrocytic
anemia
MCH 32.6 29 ± 2 Pg Normal
PLATELET 248 150-450 10^9/L Normal
COUNT
RDW 18.6 11.6-14.6 % Increased Macrocytic
anemia
WHITE 12.3 4.5-10 10^9/L Increased Infection
BLOOD CELLS
LYMPHOCYTE 30.1 20-40 % Normal
SEGMENTERS 54.7 50-70 % Normal
MID CELL 15.2 1.0-7.0 % Increased Infection

ANALYSIS:
Hemoglobin and hematocrit are increased may indicate polycythemia vera, MCV and RDW
are increased may indicate macrocytic anemia. WBC and mid cell are also increased respond to a
bacterial infection.

28
 LABORATORY RESULTS
HEMATOLOGY
COMPLETE BLOOD COUNT
September 25, 2019
TEST RESULT NORMAL UNIT SIGNIFICANT RATIONALE
VALUES
RED BLOOD 4.71 4-6 x10^12/L Normal
CELL
HEMOGLOBIN 15 12-17 g/Dl Normal
HEMATOCRIT 46.3 37-54 % Normal
MCV 98.3 87 ± 5 Fl Increased Macrocytic
anemia
MCH 31.8 29 ± 2 Pg Normal
PLATELET 224 150-450 x10^9/L Normal
COUNT
RDW 17.7 11.6-14.6 % Increased Macrocytic
anemia
WHITE BLOOD 9.5 4.5-10 10^9/L Normal
CELLS
SEGMENTERS 52.4 50-70 % Normal
LYMPHOCYTE 33.3 20-40 % Normal
MID CELL 14.3 1.0-7.0 % Increased Infection

ANALYSIS:
MCV and RDW increased that may indicate macrocytic anemia, mid cell also increased it
respond to a bacterial infection.

29
 LABORATORY RESULTS
BILIRUBIN

September 24, 2019

TEST RESULT NORMAL UNIT SIGNIFICANT RATIONALE
VALUES
BILIRUBIN 2.77 0.2-1.2 mg/dl Increased Jaundice

September 25, 2019

TEST RESULT NORMAL UNIT SIGNIFICANT RATIONALE
VALUES
BILIRUBIN 2.58 0.2-1.2 mg/dl Increased Jaundice

ANALYSIS:
Bilirubin increased that may indicate neonatal jaundice, newborn jaundice occurs when a
baby has a high level of bilirubin in the blood.

30
 Anatomy and Physiology

Fetal Circulation

During pregnancy, the fetal circulatory system works differently than after birth:

 The fetus is connected by the umbilical cord to the placenta, the organ that develops and
implants in the mother's uterus during pregnancy.
 Through the blood vessels in the umbilical cord, the fetus receives all the necessary
nutrition, oxygen, and life support from the mother through the placenta.
 Waste products and carbon dioxide from the fetus are sent back through the umbilical cord
and placenta to the mother's circulation to be eliminated.

Blood from the mother enters the fetus through the vein in the umbilical cord. It goes to the liver
and splits into three branches. The blood then reaches the inferior vena cava, a major vein
connected to the heart.

31
Inside the fetal heart:

 Blood enters the right atrium, the chamber on the upper right side of the heart. Most of the
blood flows to the left side through a special fetal opening between the left and right atria,
called the foramen ovale.
 Blood then passes into the left ventricle (lower chamber of the heart) and then to the aorta,
(the large artery coming from the heart).
 From the aorta, blood is sent to the head and upper extremities. After circulating there, the
blood returns to the right atrium of the heart through the superior vena cava.
 About one-third of the blood entering the right atrium does not flow through the foramen
ovale, but, instead, stays in the right side of the heart, eventually flowing into the
pulmonary artery.

Because the placenta does the work of exchanging oxygen (O2) and carbon dioxide (CO2) through
the mother's circulation, the fetal lungs are not used for breathing. Instead of blood flowing to the
lungs to pick up oxygen and then flowing to the rest of the body, the fetal circulation shunts
(bypasses) most of the blood away from the lungs. In the fetus, blood is shunted from the
pulmonary artery to the aorta through a connecting blood vessel called the ductus arteriosus.

Blood circulation after birth:

With the first breaths of air the baby takes at birth, the fetal circulation changes. A larger amount
of blood is sent to the lungs to pick up oxygen.

 Because the ductus arteriosus (the normal connection between the aorta and the pulmonary
valve) is no longer needed, it begins to wither and close off.
 The circulation in the lungs increases and more blood flows into the left atrium of the heart.
This increased pressure causes the foramen ovale to close and blood circulates normally.

32
IMMUNE SYSTEM DEVELOPMENT

The immune system begins very early in fetal development with the origin of blood
formation in the third week of gestation. In the fourth week of gestation the thymus forms. The
thymus helps to mature and develop white blood cells so that they can play a key role in fighting
infections. By the eighth week of gestation, T cells, B cells, and natural killer cells can all be found
in the thymus.

T cells, which make an important component in cell-mediated immunity, are formed solely
in the thymus. B cells, which are the precursors of antibody producing cells, are first produced in
the liver but by 12 weeks gestation move into the bone marrow where it remains. Natural killer
cells, which are cytotoxic cells that have the ability to attack viruses, mature in the thymus.
Interestingly, greater concentrations of natural killer cells are found in the peripheral blood of
newborns and the newborn usually has adult levels of these cells at birth, but they diminish rapidly.
Orlando Regional Healthcare, Education & Development © Copyright 2004 Page 4

Neutrophils are relatively numerous in both the term and pre-term infant. A neutrophil is a
type of white blood cell that defends the body from organisms that cause infection. The stages of
neutrophil development, from immature to mature, are myeloblast, promyelocyte, myelocyte,
metamyelocte, band, and segmented neutrophil. When an infection is present, the neutrophils
migrate out of the capillaries and into the infected site, where they ingest and destroy the pathogens
causing the infection. The amount of circulating neutrophils in the newborn peaks around 12 hours
after birth and then starts to decline to normal levels. Even though a large number of circulating
neutrophils can be found in the newborn, the bone marrow storage pool of neutrophils at birth is
only 20% to 30% of the circulating pool in adults.

33
Differences in Immune Responses in Full and Preterm Infants

Immune System Full Term Infant Preterm Infant

Component

Immunoglobulin G Complete placental transfer, Incomplete placental transfer,

concentrations comparable to concentrations decreased
mother

Lymphocytes Concentrations of T and B cells Concentrations of T and B cells

comparable to those in adults with comparable to those in adults with
normal response to antigens normal response to antigens

Complement 50%-75% of concentration in adult Decreased concentration

Neutrophils Elevated numbers at birth, with Elevated numbers at birth, with

impaired functional ability impaired functional ability

Monocytes Normal number at birth but have Normal number at birth but have
impaired chemotaxis impaired chemotaxis

Macrophages Normal number at birth but Normal number at birth but

decreased function decreased function

Natural Killer Cells Concentration similar to adult level, Concentration similar to adult level,
but have diminished cytotoxic but have diminished cytotoxic
effects effects

34
Immune System Physiology

Despite the immune system and immune system components, early development during
gestation the newborn still remains vulnerable to infections after they are born because of the
immaturity of their immune system.

A newborn has a poor response to invading pathogens. This immune response will
gradually improve with age. During the initial postpartum phase, the infant relies on maternal
antibodies and the mother’s breast milk, which is rich with immunoglobulins. When a pathogenic
organism overcomes the infant’s defenses, infection and sepsis result. Sepsis is defined as the
presence of microorganisms or their toxins in blood or other tissues. Newborn sepsis is still one of
the most significant causes of neonatal disability and death today.

Reviewing the functions of the infant’s immune system will help provide a better
understanding of the interaction between the pathogenic organisms and the newborn’s
susceptibility to infection. Infections occur when the infant comes in contact with a pathogenic
organism. The organism, whether it is a virus, fungus, or bacteria, enters into the infant’s body
system and begins to multiply.

The infant’s immune system response to an organism is divided into three phases. The first
phase is the primary or nonspecific phase, which occurs immediately following the infant’s
inoculation with a pathogenic organism. During this phase, there is a migration of the neutrophils
to the primary site of the infection. The neutrophils enter into the cells through membrane filters
and adhere to the pathogen. Ingestion and destruction of the invading organism then takes place.

The next phase in the immune response is called the secondary phase or the specific
response phase. During this phase, there is interaction of T and B cells to help develop
immunoglobulins or antibodies to protect the infant from the infection. There are three major types
of immunoglobulins: Immunoglobulin G (IgG), Immunoglobulin M (IgM), and Immunoglobulin
A (IgA).

Immunoglobulin G is the major immunoglobulin of the serum and interstitial fluid. It

provides immunity against both bacterial and viral pathogens. It starts to cross the placenta and
th
enter into fetal circulation around 30 weeks’ gestation and continues until the 40 week. Term

35
infants have IgG levels that are equal to or exceed maternal levels. Since IgG is not transferred
th
until around the 30 week of gestation, the preterm infant does not have this protective barrier.
Preterm infants are thus at higher risk for infections. Research has shown that there are also
decreased levels of IgG in post-term and small for gestation age infants, which suggest that there
may be some inhibition of transfer with placental damage.

Immunoglobulin M does not cross the placenta thus, little or no IgM is transferred to the
fetus. This lack of IgM increases the infant’s susceptibility to gram negative infections. The infant
does however begin synthesis of this immunoglobulin very early in their fetal life. Levels of IgM
have been detected around 30 weeks’ gestation with higher levels detected when there is an
intrauterine infection present.

Immunoglobulin A is the most common immunoglobulin found in the gastrointestinal tract,

respiratory tract, human colostrum, and breast milk. IgA does not cross the placenta, and
intrauterine synthesis is minimal. Levels of IgA are usually not detected until the infant is around
2 to 3 weeks old.

The last immune response is the tertiary phase. This phase provides long-term immunity
against the organism. During the second phase, the B cells produce memory cells that recognize
the invading pathogen on subsequent exposures. These memory cells recognize the invading
organism and cause them to be neutralized, preventing the infant from becoming sick again.
Although adequate numbers of B cells are present at birth, antibody production is diminished in
the neonate due to a lack of uterine exposure to foreign pathogens.

NON-SPECIFIC IMMUNITY

The elements of the non-specific (innate) immune system (Table 2) include anatomical
barriers, secretory molecules and cellular components. Among the mechanical anatomical barriers
are the skin and internal epithelial layers, the movement of the intestines and the oscillation of
broncho-pulmonary cilia. Associated with these protective surfaces are chemical and biological
agents.

36
A. Anatomical barriers to infections

1. Mechanical factors

The epithelial surfaces form a physical barrier that is very impermeable to most infectious
agents. Thus, the skin acts as our first line of defense against invading organisms. The
desquamation of skin epithelium also helps remove bacteria and other infectious agents that have
adhered to the epithelial surfaces. Movement due to cilia or peristalsis helps to keep air passages
and the gastrointestinal tract free from microorganisms. The flushing action of tears and saliva
helps prevent infection of the eyes and mouth. The trapping effect of mucus that lines the
respiratory and gastrointestinal tract helps protect the lungs and digestive systems from infection.

2. Chemical factors

Fatty acids in sweat inhibit the growth of bacteria. Lysozyme and phospholipase found in
tears, saliva and nasal secretions can breakdown the cell wall of bacteria and destabilize bacterial
membranes. The low pH of sweat and gastric secretions prevents growth of bacteria. Defensins
(low molecular weight proteins) found in the lung and gastrointestinal tract have antimicrobial
activity. Surfactants in the lung act as opsonins(substances that promote phagocytosis of particles
by phagocytic cells).

3. Biological factors

The normal flora of the skin and in the gastrointestinal tract can prevent the colonization
of pathogenic bacteria by secreting toxic substances or by competing with pathogenic bacteria
for nutrients or attachment to cell surfaces.

37
B. Humoral barriers to infection

The anatomical barriers are very effective in preventing colonization of tissues by

microorganisms. However, when there is damage to tissues the anatomical barriers are breached
and infection may occur. Once infectious agents have penetrated tissues, another innate defense
mechanism comes into play, namely acute inflammation. Humoral factors play an important role
in inflammation, which is characterized by edema and the recruitment of phagocytic cells. These
humoral factors are found in serum or they are formed at the site of infection.

1. Complement system – The complement system is the major humoral non-specific defense
mechanism (see complement chapter). Once activated complement can lead to increased vascular
permeability, recruitment of phagocytic cells, and lysis and opsonization of bacteria.

2. Coagulation system – Depending on the severity of the tissue injury, the coagulation system
may or may not be activated. Some products of the coagulation system can contribute to the non-
specific defenses because of their ability to increase vascular permeability and act as chemotactic
agents for phagocytic cells. In addition, some of the products of the coagulation system are directly
antimicrobial. For example, beta-lysin, a protein produced by platelets during coagulation can lyse
many Gram positive bacteria by acting as a cationic detergent.

3. Lactoferrin and transferrin – By binding iron, an essential nutrient for bacteria, these proteins
limit bacterial growth.

4. Interferons – Interferons are proteins that can limit virus replication in cells.

5. Lysozyme – Lysozyme breaks down the cell wall of bacteria.

6. Interleukin-1 – Il-1 induces fever and the production of acute phase proteins, some of which are
antimicrobial because they can opsonize bacteria.

38
Cellular barriers to infection

Part of the inflammatory response is the recruitment of polymorphonuclear eosinophiles and

macrophages to sites of infection. These cells are the main line of defense in the non-specific
immune system.

1. Neutrophils – Polymorphonuclear cells (PMNs, figure 4) are recruited to the site of infection
where they phagocytose invading organisms and kill them intracellularly. In addition, PMNs
contribute to collateral tissue damage that occurs during inflammation.

2. Macrophages – Tissue macrophages (figure 5, 6, 7) and newly recruited monocytes (figure 4

and 8), which differentiate into macrophages, also function in phagocytosis and intracellular
killing of microorganisms. In addition, macrophages are capable of extracellular killing of infected
or altered self target cells. Furthermore, macrophages contribute to tissue repair and act as antigen-
presenting cells, which are required for the induction of specific immune responses.

3. Natural killer (NK) and lymphokine activated killer (LAK) cells – NK and LAK cells can
nonspecifically kill virus infected and tumor cells. These cells are not part of the inflammatory
response but they are important in nonspecific immunity to viral infections and tumor surveillance.

4. Eosinophils – Eosinophils (figure 6a and b) have proteins in granules that are effective in killing
certain parasites.

39
PHAGOCYTOSIS AND INTRACELLULAR KILLING

A. Phagocytic cells

1. Neutrophiles/Polymorphonuclear cells

PMNs are motile phagocytic cells that have lobed nuclei. They can be identified by their
characteristic nucleus or by an antigen present on the cell surface called CD66. They contain two
kinds of granules the contents of which are involved in the antimicrobial properties of these cells.
The primary or azurophilic granules, which are abundant in young newly formed PMNs, contain
cationic proteins and defensins that can kill bacteria, proteolytic enzymes like elastase, and
cathepsin G to breakdown proteins, lysozyme to break down bacterial cell walls, and
characteristically, myeloperoxidase, which is involved in the generation of bacteriocidal
compounds. The second type of granule found in more mature PMNs is the secondary or specific
granule. These contain lysozyme, NADPH oxidase components, which are involved in the
generation of toxic oxygen products, and characteristically lactoferrin, an iron chelating protein
and B12-binding protein.

2. Monocytes/Macrophages

Macrophages are phagocytic cells that have a characteristic kidney-shaped nucleus. They
can be identified morphologically or by the presence of the CD14 cell surface marker. Unlike
PMNs they do not contain granules but they have numerous lysosomes which have contents similar
to the PNM granules.

40
B. Response of phagocytes to infection

Circulating PMNs and monocytes respond to danger (SOS) signals generated at the site of
an infection. SOS signals include N-formyl-methionine containing peptides released by bacteria,
clotting system peptides, complement products and cytokines released from tissue macrophages
that have encountered bacteria in tissue. Some of the SOS signals stimulate endothelial cells near
the site of the infection to express cell adhesion molecules such as ICAM-1 and selectins which
bind to components on the surface of phagocytic cells and cause the phagocytes to adhere to the
endothelium. Vasodilators produced at the site of infection cause the junctions between endothelial
cells to loosen and the phagocytes then cross the endothelial barrier by “squeezing” between the
endothelial cells in a process called diapedesis.

Once in the tissue spaces some of the SOS signals attract phagocytes to the infection site by
chemotaxis (movement toward an increasing chemical gradient). The SOS signals also activate the
phagocytes, which results in increased phagocytosis and intracellular killing of the invading
organisms.

41
Initiation of Phagocytosis

Phagocytic cells have a variety of receptors on their cell membranes through which infectious
agents bind to the cells. These include:

1. Fc receptors – Bacteria with IgG antibody on their surface have the Fc region exposed and
this part of the Ig molecule can bind to the receptor on phagocytes. Binding to the Fc
receptor requires prior interaction of the antibody with an antigen. Binding of IgG-coated
bacteria to Fc receptors results in enhanced phagocytosis and activation of the metabolic
activity of phagocytes (respiratory burst).
2. Complement receptors – Phagocytic cells have a receptor for the 3rd component of
complement, C3b. Binding of C3b-coated bacteria to this receptor also results in enhanced
phagocytosis and stimulation of the respiratory burst.
3. Scavenger receptors – Scavenger receptors bind a wide variety of polyanions on bacterial
surfaces resulting in phagocytosis of bacteria.

4. Toll-like receptors – Phagocytes have a variety of Toll-like receptors (Pattern Recognition

Receptors or PRRs) which recognize broad molecular patterns called PAMPs (pathogen

42
 associated molecular patterns) on infectious agents. Binding of infectious agents via Toll-
like receptors results in phagocytosis and the release of inflammatory cytokines (IL-1,
TNF-alpha and IL-6) by the phagocytes.

D. Phagocytosis

After attachment of a bacterium, the phagocyte begins to extend pseudopods around the
bacterium. The pseudopods eventually surround the bacterium and engulf it, and the bacterium is
enclosed in a phagosome. During phagocytosis the granules or lysosomes of the phagocyte fuse
with the phagosome and empty their contents. The result is a bacterium engulfed in a
phagolysosome which contains the contents of the granules or lysosomes.

43
 PATHOPHYSIOLOGY

Predisposing factors: Precipitating factors:

Age: 2 days old
Late Onset:
Impaired immune system
Malnourished Presence of foreign body
BMI : 2.4kgs Cross infection
Poor environmental sanitation
Low Birth weight
Poor breastfeeding

Invasion of bacteria Production of

inflammatory mediators
and initiation of an
inflammatory response

Bacteria goes to circulation Cellular activation of

the mononuclear
phagocyte

Fever Increased mid cell Infection

Paracetamol

Cyanosis Increase oxygen demand Hypoxia

Oxygen therapy

Jaundice, Fatigue, Systemic Reaction Anti-Inflammatory

Pale, Extreme pallor, response, Pro-
Poor skin turgor, Inflammatory
Dehydration, Response, Sepsis
abdominal pain
(Cytokines)
Amikacin, Ceftazidime, TNF
Ranitidine, D10 water

44
If Left Untreated

If infection is severe

Hypovolemic shock

Septic shock

Multiorgan dysfunction
syndrome

Death

LEGEND:

= Disease Process

= Client Manifestation

= Clinical Manifestation

= Treatment/management

= If Left Untreated

= Death

45
 Drug Study No. 1

Generic:
ranitidine

Brand:
ZANTAC

Classification:
Anti-ulcer

Dosage:
5mg/ampoule

Route:
IVTT

Frequency:
q 12 hours

Mechanism of Action:
Inhibits the action of histamine at the H2 receptor site located primarily in gastric parietal cells,
resulting in inhibition of gastric acid secretion has some antibacterial action against H. pylori

Indications
Treatment and prevention of heartburn, acid indigestion, and sour stomach
Prophylaxis of GI hemorrhage from stress ulceration

Contraindications
Hypersensitivity, Cross-sensitivity may occur; some oral liquids contain alcohol and should be
avoided in patients with known intolerance

46
Nursing Considerations

 Instruct patient not to take new medication w/o consulting physician

 Instruct patient to take as directed and do not increase dose
 Allow 1 hour between any other antacid and ranitidine
 Avoid excessive alcohol
 Assess patient for epigastric or abdominal pain and frank or occult blood in the stool,
emesis, or gastric aspirate
 Nurse should know that it may cause false-positive results for urine protein; test with
sulfosalicylic acid
 Inform patient that it may cause drowsiness or dizziness
 Inform patient that increased fluid and fiber intake may minimize constipation
 Advise patient to report onset of black, tarry stools; fever, sore throat; diarrhea; dizziness;
rash; confusion; or hallucinations to health care professional promptly
 Inform patient that medication may temporarily cause stools and tongue to appear gray
black
 Instruct patients to monitor for and report occurrence of drug-induced adverse reaction

47
 Drug Study No. 2

Generic name:
ceftazidime

Brand name:
Fortaz, Tazicef

Dosage:
140mg

Route:
IVTT

Frequency:
q 12hr

Classification
Antibiotics

Mechanism of action
Inhibits cell-wall synthesis, promoting osmotic instability; usually bactericidal.

Indications
Prevention of serious UTI and lower respiratory tract infection; skin, gynecologic, intra-
abdominal, bone and joint, and CNS infection; bacteremia; and septicemia caused by susceptible
microorganisms, such as streptococci (including Streptococcus pneumonia and S. pyogenes),
penicillinase and non-penicillinase producing Staphylococcus aureus, Escherichia coli, Klebsiella,
Proteus, Enterobacter, Haemophilus influenzae, Pseudomonas, and some strains of Bacteroides

48
Contraindications
 Contraindicated in patients hypersensitive to drug or other cephalosporins
 Use cautiously in patients hypersensitive to penicillin because of possibility of cross –
sensitivity with other beta-lactam antibiotics
 Prolonged use can result in superinfection, including Clostridium difficile- associated
diarrhea and pseudomembranous colitis
 Use cautiously in breastfeeding women and in patients with history of colitis, renal
insufficiency or seizures

Adverse effect
CNS:
Seizures

CV:
Phlebitis, thrombophlebitis

GI:
Pseudomembranous colitis, nausea, vomiting, diarrhea, abdominal cramps

Hematologic:
Agranulocytosis, leukopenia, thrombocytopenia, eosinophilia, thrombocytosis, hemolytic anemia.

Skin:
Maculopapular and erythematous rashes, urticaria, pain, induration, sterile abscesses, tissue
sloughing at injection site

Nursing Considerations

 If large doses are given, therapy is prolonged, or patient is at high risk, monitor patient for
signs and symptoms of superinfection.
 Look alike-sound alike: Don’t confuse drug with other cephalosporins that sound alike.

49
 Drug Study No. 3

Generic name:
amikacin sulfate

Brand name:
Amikin, Amikin Pediatric

Dosage:
42mg

Route:
IVTT

Frequency:
OD

Classification
Antibiotics

Mechanism of action
Inhibits protein synthesis by binding directly to the ribosomal subunit; bactericidal

Indications
Prevention of serious infections caused by sensitive strains of Pseudomonas aeruginosa,
Escherichia coli, Proteus, Klebsiella, or Staphylococcus. Prevention of uncomplicated UTI caused
by organisms not susceptible to less toxic drugs. Prevention of active tuberculosis, with other
antituberculotics.

50
Contraindications
 Contraindicated in patients hypersensitive to drug or other aminoglycosides
 Use cautiously in patients with sulfite sensitivity
 Use cautiously in patients with impaired renal function or neuromuscular
disorders(myasthenia gravis, parkinsonism), in neonates and infants, and in elderly
patients.

Adverse effect
CNS:
Neuromuscular blockade

EENT:
Ototoxicity

GU:
Azotemia, nephrotoxicity, increase in urinary excretion of casts.

Respiratory:
Apnea.

Nursing Considerations

 Weigh patient and review renal function studies before therapy begins
 Correction dehydration before therapy because of increased risk of toxicity
 Monitor serum amikacin peak and through concentrations periodically during therapy.
Peak drug levels greater than 35mcg/mL and through levels greater than 10mcg/mL may
be linked to a higher risk of toxicity.
 Watch for signs and symptoms of superinfection(especially of upper respiratory tract), such
as continued fever, chills, and increased pulse rate.

51
 Therapy usually continues for 7 to 10 days. If no response occurs after 3 to 5 days, stop
therapy and obtain new specimens for culture and sensitivity testing.
 Look alike-sound alike: Don’t confuse amikacin with anakinra.

52
 Drug Study No. 4

Generic name:
paracetamol

Brand name:
Acetaminophen

Dosage:
30mg

Route:
IVTT

Frequency:
q4

Classification
Anti-pyretic

Mechanism of action
Thought to produce analgesia by inhibiting prostaglandin and other substances that sensitize pain
receptors. Drug may relieve fever through central action in the hypothalamic heat-regulating
center.

Indications
Treatment for fever, mild pain, prevention for adverse reactions with diphtheria, tetanus toxoids,
and pertussis vaccination.

53
Nursing Contraindications
 Contraindicated in patients hypersensitive to drug. I.V. form is contraindicated in patients
with severe hepatic impairment or severe active liver disease
 Use cautiously in patients with any type of liver disease, chronic malnutrition, severe
hypovolemia(dehydration, blood loss), or severe renal impairment (CrCl of 30mL/minute
or less), and in pregnant and breast-feeding women.
 Use cautiously in patients with long-term alcohol use because therapeutic doses cause
hepatotoxicity in these patients. Chronic alcoholics shouldn’t take more than 2g of
acetaminophen every 24 hours.

Adverse effect
CNS:
Anxiety, fatigue, headache, insomnia, pyrexia

CV:
Hypertension, hypotension, peripheral edema, periorbital edema, tachycardia (I.V.)

GI:
Nausea, vomiting, abdominal pain, diarrhea, constipation (I.V.)

GU:
Oliguria (I.V.)

Hematologic:
Hemolytic anemia, leukopenia, neutropenia, pancytopenia, anemia(I.V.)

Hepatic:
Jaundice

54
Metabolic:
Hypoglycemia, hypokalemia, hypervolemia, hypomagnesemia, hypophosphatemia(I.V.)

Musculoskeletal:
Muscle spasms, extremity pain (I.V.)

Respiratory:
Abnormal breath sounds, dyspnea, hypoxia, atelectasis, pleural effusion, pulmonary edema,
stridor, wheezing (I.V.)

Skin:
Rash, urticaria; infusion site pain, pruritus

Nursing Considerations
 In children, don’t exceed five doses in 24 hours.
 Consider reducing total daily dose and increasing dosing intervals in patients with hepatic
or renal impairment.

55
 NURSING CARE PLAN #1

Assessment

Subjective: “ Sige sija hilak’’ as verbalized by the SO

Objective:

Facial expression of pain ( e.g., grimace, eyes lack luster)

Wong Baker’s face rating scale is 5

Cries more than usual

Irritable

Nursing Diagnosis: Acute pain related to biological injury agent ( e.g., Infection )

Planning: Within 2 hours of nursing intervention the patient will be able to manifest pain is relieve

or control.

Nursing Intervention Rationale

INDEPENDENT To fully understand client’s pain symptoms.

Obtained client’s or significant others or SO
assessment of pain to include location,
characteristics, onset, duration, frequency, quality,
intensity. Identify precipitating or aggravating and
relieving factors.
Evaluated pain characteristics and intensity Use pain rating scale appropriately for age and
cognition(e.g 0-10 scale)

56
 Performed pain assessment each time pain occurs. To demonstrate improvement in status or to
Documented and investigate from previous reports identify worsening of underlying
and evaluate results of pain interventions. condition/developing complications.
Established collaborative approach for pain To assist client to explore methods for
management based on clients understanding about alleviation/control of pain.
and acceptance of available treatment options.
Acknowledged the pain experience and convey Reduces defensive responses, promotes trust, and
acceptance of clients response to pain enhances cooperation with regimen
Encouraged adequate rest periods To prevent fatigue that can impair ability to manage
or cope with the pain.
Identified specific signs/symptoms and changes in Provides opportunity to modify pain management
pain characteristics requiring medical follow-up. regimen and allows for timely intervention for
developing complications.
DEPENDENT
Administered medications as prescribed To eliminate the pain
( Ranitidine 5mg ampule q 12h IVTT)

Evaluation: Goal met within after 2 hours of nursing intervention, the patient was able to manifest

pain is relieved and controlled.

57
 NURSING CARE PLAN #2

Assessment

Subjective: “ Init kaayo ako bata maam ’’ as verbalized by the SO

Objective:

Temperature above normal level (39 oC)

Skin warm to touch
Appears weak
Flushed skin

Nursing Diagnosis: Hyperthermia related to sepsis

Planning: After 1-2 hrs of nursing intervention the patient will be able to maintain normal core
temperature as evidenced by vital signs within normal limits

Nursing Intervention Rationale

INDEPENDENT
Monitor neonate’s condition. To determine the need for intervention and the
effectiveness of therapy.

Monitor Vital signs

To have a baseline data

Provide TSB Helps in lowering down the temperature

Ensure that all equipment used for infant is sterile, This would prevent the spread of pathogens to the
scrupulously clean. Do not share equipment with infant from equipment

Monitor use of hypothermia blanket and wrap To minimize shivering

extremities with bath towels

58
 Promote client safety To prevent injury
Maintain bed rest To reduce metabolic demands and oxygen
consumption
DEPENDENT
Administer antipyretics as ordered (paracetamol Aids in lowering down temperature
30mg q 4 hours IVTT)

Evaluation: Goal met within 1-2 hrs of nursing intervention the patient was able to maintained

normal core temperature as evidenced by vital signs within normal limits

59
 NURSING CARE PLAN #3

Assessment

Subjective: “luja ako bata maam’’ as verbalized by the SO

Objective:

Weakness
Poor Skin turgor
Malnourished (weight : 2.4kg)
Less fluid intake due to less production of breast milk from the mother
Decreased urine output

Nursing Diagnosis: Deficient Fluid Volume related to Hypotonic dehydration

Planning: After 8 hours of thorough nursing intervention, the client will be able to maintain
fluid volume at a functional level, as evidenced by individually adequate urinary output, stable
vital signs, moist mucous membranes , good skin turgor

Nursing Intervention Rationale

INDEPENDENT
Maintained accurate intake and output, calculate It serves as a baseline for doing such interventions
24-hour fluid balance and weigh daily

Monitor vital signs

To have a baseline data

Obtain history of usual pattern of fluid intake and Intake may be reduced because of current physical
recent alterations. or environmental issues or a behavior pattern

Ensure that all equipment used for infant is sterile, This would prevent the spread of pathogens to the
scrupulously clean. Do not share equipment with infant from equipment

60
 Note change in usual mentation, behavior, or These signs indicate sufficient dehydration to cause
functional abilities poor cerebral perfusion or electrolyte imbalance
Maintain accurate intake and output (I&O). In order to monitor and document trends.
calculate 24 hour fluid balance, and weigh
regularly
Offer fluids on a regular basis to infants, young Who may not sense or be able to report thirst.
children, and the elderly
DEPENDENT
Administer fluids and electrolytes( D10 water 500 To gradually correct the deficient in fluid
cc), as ordered (hypertonic)

Establish 24 hour replacement needs and routes to Steady rehydration over time prevents peaks and
be used( IV, PO, enteral feedings) valleys in fluid level

Evaluation: Goal met after 8 hours of thorough nursing intervention the client was able to
maintained fluid volume at a functional level, as evidenced by individually adequate urinary
output, stable vital signs, moist mucous membranes , good skin turgor

61
 NURSING CARE PLAN #4

Assessment

Subjective: “gamay ra ija madidi na gatas sa ako maam’’ as verbalized by the SO

Objective:

Body weakness
Malnourished (weight : 2.4kg)
Poor muscle tone

Nursing Diagnosis: Imbalanced nutrition: less than body requirements related to inability to ingest
or digest food; inability to absorb nutrients

Planning: After 3 hours of nursing interventions, the SO will be able to verbalize understanding
of causative factors when known and necessary interventions.

Nursing Intervention Rationale

INDEPENDENT
Monitor and record vital signs To provide comparative baseline

Monitor weight To monitor progression of condition

Assist in developing individualized regimen To correct or control underlying factors

Evaluate total daily food intake. Obtain dairy of To reveal possible cause of malnutrition and
calorie intake, patterns, and times of eating changes that could be made in client’s intake
Note change in usual mentation, behavior, or These signs indicate sufficient dehydration to
functional abilities cause poor cerebral perfusion or electrolyte
imbalance
Provided diet modifications To gradually correct the deficient in fluid ( ex.
milk formula with strict aspiration precaution
Note age, body build, strength, activity level, and Helps determine nutritional needs
current condition or treatment needs
DEPENDENT
Collaborate with interdisciplinary team To set nutritional goals when client has specific
dietary needs, malnutrition is profound, or long
term feeding problems exist

62
 Consult with dietitian or nutritional support team, For long term needs
as necessary.

Evaluation: Goal met after 3 hours of nursing interventions, the SO was able to verbalize
understanding of causative factors when known and necessary interventions.

63
 NURSING CARE PLAN #5

Assessment

Subjective: “nag yellow ako bata” as verbalized by the SO

Objective:

Yellowish skin color

Abnormal blood profile

Nursing Diagnosis: Neonatal jaundice related to deficient feeding pattern

Planning: After 4 hours of nursing interventions, the client will be able to display decreasing
bilirubin levels with resolution of jaundice

Nursing Intervention Rationale

INDEPENDENT
Determine successful initiation and adequacy of Poor caloric intake and dehydration associated
breastfeeding with ineffective breastfeeding increase the risk of
developing hyperbilirubinemia.

Assess the infant for signs of hypoglycemia such as Hypoglycemia necessitates the use of fat stores for
jitteriness, irritability, and lethargy. Obtain heel energy-releasing fatty acids, which compete with
stick glucose levels as indicated bilirubin for binding sites on albumin

Evaluate the infant for pallor, edema, or These signs may be associated with hydrops
hepatosplenomegaly fetalis, Rh incompatibility, and in-utero hemolysis
of fetal red blood cells (RBCs)

Note the infant’s age at onset of jaundice This aids in differentiating the type of
jaundice(i.e., physiological, breast milk induced,
or pathological)

64
Assess the infant for progression of signs and Early stage toxicity involves neuro-depression-
behavioral changes associated with bilirubin lethargy, poor feeding, high-pitched cry,
toxicity diminished or absent reflexes; late stage toxicity
signs may include hypotonia, neuro-hyperreflexia-
twitching, convulsions, opisthotonos, and fever
Encourage frequent breastfeeding 8-12 times per To maintain milk production
day. Assist the mother with pumping of breasts as
needed
Initiate early oral feedings within 4 to 6 hr This establishes proper intestinal flora necessary
following birth, especially if infant is to be for reduction of bilirubin to urobilinogen and
breastfed. decreases reabsorption of bilirubin from bowel.
Keep the infant warm and dry; monitor skin and This prevents cold stress and the release of fatty
core temperature frequently acids that compete for binding sites on albumin,
thus increasing the level of freely circulating
bilirubin.
Apply eye patches, ensuring correct fit during To provide visual stimulation and interaction with
periods of phototherapy, to prevent retinal injury. caregivers/parents
Remove eye covering during feedings or other care
activities as appropriate
Evaluate the appearance of skin and urine, noting An uncommon side effect of phototherapy involves
brownish black color. exaggerated pigment changes (bronze baby
syndrome) that may last for 2 to 4 months but are
not associated with harmful sequelae
Avoid application of lotion or oils to skin of infant To prevent dermal irritation or injury.
receiving phototherapy
Cover male groin with small pad To protect from heat related injury to testes
Reposition the infant every 2 hour To ensure that all areas of skin are exposed to bili
light when fiberoptic pad or blanket is not used
Monitor the infant’s weight loss, urine output and To determine adequacy of fluid intake
specific gravity, and fecal water loss from loose
stools associated with phototherapy

65
 Review proper formula preparation/storage and To enhance or reestablish breastfeeding process
demonstrate feeding techniques, as indicated
Provide a written explanation of home Home phototherapy is recommended only for full-
phototherapy, safety precautions, and potential term infants after the first 48 hour of life, if serum
problems bilirubin levels are between 14 and 18mg/dL, with
no increase in direct reacting bilirubin
concentration
DEPENDENT
Administer small amounts of breast milk The use of feeding additives is under investigation
substitute (L-aspartic acid or enzymatically for inhibition of beta-glucuronidase leading to
hydrolyzed casein [EHC]) for 24 to 48 hr if increased fecal excretion of bilirubin; results have
indicated been mixed.

Initiate phototherapy per protocol, using This is the primary therapy for neonates with
fluorescent bulbs placed above the infant or unconjugated hyperbilirubinemia.
fiberoptic pad or blanket.

Evaluation: Goal met after 3 hours of nursing interventions, the client was able to display
decreasing bilirubin levels with resolution of jaundice

66
 NURSING CARE PLAN #6

Assessment

Subjective: “nan luspad ako bata ug may pagka bluish ija skin” as verbalized by the SO

Objective:

Cyanosis
Pale

Nursing Diagnosis: Impaired Gas Exchange related to Altered oxygen-carrying capacity of blood
Planning: After 3 hours of nursing interventions, the SO will be able to verbalize understanding
of causative factors and appropriate interventions

Nursing Intervention Rationale

INDEPENDENT
Monitor vital signs and cardiac rhythm All vital signs are impacted by changes in
oxygenation

Maintain adequate input and output For mobilization of secretions

Encourage adequate rest and limit activities to This helps limit oxygen needs and consumption
within client tolerance. Promote a calm, restful
environment.
Keep environment allergen and pollutant free To reduce irritant effect of dust and chemicals on
airways
Emphasize the importance of nutrition In improving stamina and reducing the work of
breathing

67
 DEPENDENT
Provide supplemental oxygen at lowest Which may occur in a client receiving long-term
concentration indicated by laboratory results and oxygen therapy
client symptoms or situation.

Assist with procedures as individually indicated To improve respiratory function/oxygen-carrying

capacity.

Evaluation: Goal met after 3 hours of nursing interventions, the SO was able to verbalize
understanding of causative factors and appropriate interventions

68
 NURSING CARE PLAN #7

Assessment

Subjective: “dili sija halos maka didi kay gamay ra ang gatas” as verbalized by the SO

Objective:

Nonexclusive breastfeeding
The mother unable to provide breast milk to newborn continuously

Nursing Diagnosis: Interrupted breastfeeding related to insufficient breast milk production

Planning: After 1 hour of nursing interventions, the mother will be able to identify and
demonstrate techniques to sustain lactation until breastfeeding is initiated

Nursing Intervention Rationale

INDEPENDENT

Assess mother’s perception and knowledge about To know what the mother already knows and
breastfeeding and extent of instruction that has needed to know.

been given.

Give emotional support to mother and accept To assist mother to maintain breastfeeding as
decision regarding cessation/ continuation of desired.
breast feeding.

Demonstrate use of manual piston-type breast Aid in feeding the neonate with breast milk
pump. without the mother breastfeeding the infant.

Review techniques for storage/use of expressed To provide optimal nutrition and promote
breast milk continuation of breastfeeding process

69
 Determine if a routine visiting schedule or So that infant will be hungry/ ready to feed
advance warning can be provided

Provide privacy, calm surroundings when mother To promote successful infant feeding
breast feeds.

Recommend for infant sucking on a regular basis Reinforces that feeding time is pleasurable and
enhances digestion.

Encourage mother to obtain adequate rest, To sustain adequate milk production and breast
maintain fluid and nutritional intake, and schedule feeding process
breast pumping every 3 hours while awake
DEPENDENT
Refer to support groups and community resources For further information

Evaluation: Goal met after 1 hour of nursing interventions, The mother was able to identify and
demonstrate techniques to sustain lactation and identify techniques on how to provide the
newborn with breast milk.

70
 NURSING CAREPLAN #8

Assessment

Subjective: “Kaluja tawon sa ako bata” as verbalized by the SO

Objective:

Lack of energy

Decrease activity performance

Weakness

Nursing diagnosis: Fatigue related to Physiological condition

Planning: After 5 hours of nursing interventions, the SO will be able to report improve sense of

energy of the infant.

Nursing intervention Rationale

INDEPENDENT

Monitor vital signs. To evaluate fluid status and cardiopulmonary

response to activity

Planned interventions to allow patient adequate rest To maximize patient participation

periods, schedule activities for periods when client

has the most energy

Instructed methods to conserve energy such as To conserve and maximize patient’s energy

sitting when doing daily care or other activities,

71
 combining and simplifying activities and taking

frequent short rest periods during activities

Assessed patient in self-care needs and with To protect client from injury

ambulation as needed

DEPENDENT

Provided supplement fluids as indicated D10 water To gradually correct the deficient in fluid

500cc @ 8-9gtts/h

Evaluation:

Goal met after 5 hours of nursing interventions, the SO was able to report improved sense of energy

of the infant.

72
 NURSING CAREPLAN #9

Assessment

Subjective: “gamay ra ang mogawas na gatas sa ako totoy” as verbalized by the SO

Objective:

Expresses breast milk less than prescribed volume

Delay in milk production

Suckling time at breast appears unsatisfactory; frequent crying

Malnourished (2.4kg)

Nursing diagnosis: Insufficient Breast Milk related to insufficient fluid volume

Planning: After 2 hours of nursing interventions, the mother will be able to demonstrate
techniques to enhance milk production and achieve mutually satisfactory breastfeeding pattern
with infant content after feedings and gaining weight appropriately

Nursing intervention Rationale

INDEPENDENT

Perform a physical examination, noting the Inadequate mammary gland tissue, breast surgery
appearance of breasts and nipples, and minimal or that has damaged the nipple, and areola enervation
no breasts, obvious inverted or flat nipples, and result in irremediable primary lactation failure
minimal or no breast enlargement during
pregnancy
Monitor vital signs. To evaluate fluid status and cardiopulmonary

response to activity

Evaluate the signs of inadequate infant intake Infant arching and crying at the breast with
resistance to latching on, decreased urinary

73
 output/frequency of stools, and inadequate weight
gain indicate the need for further evaluation and
intervention.
Provide emotional support to the mother. Use one- To assist with induced lactation techniques
to-one instruction with each feeding during the
hospital stay and clinic or home visits. Refer
adoptive mothers choosing to breastfeed to a
lactation consultant
Monitor increased filling of breasts in response to To help evaluate the effectiveness of interventions
nursing and/or pumping
Demonstrate the breast massage technique to Gently massaging the breast while the infant feeds
increase milk supply naturally from it can improve the release of higher-calorie
hindmilk from the milk glands
Use the breast pump 8-12 times a day Expressing with a hospital-grade, double
(automatic) pump is ideal for
stimulation/reestablishing milk supply
Suggest using a breast pump or hand expression Continued breast stimulation cues the mother’s
after the infant finishes breastfeeding
body that more milk is needed, increasing supply

Discuss appropriate /safe use of herbal May have a negative affect on milk supply if taken
supplements in large quantities. A number of herbs have been
used for centuries to stimulate milk production,
such as fenugreek(Trigonella foenum-graecum),
the most commonly recommended herbal
galactogogue to facilitate lactation
Discuss the possible use of prescribed Domperidone (Motilium) is approved by the
medications(galactogogues) to increase milk American Academy of Pediatrics for use in
production breastfeeding mothers and has fewer side effects.
Metoclopramide(Reglan) has been shown to
increase milk supply anywhere from 72% to 110%,

74
 depending on how many weeks the mother is
postpartum.
Encourage frequent rest periods, sharing household Having assistance can limit fatigue(known to
and childcare tasks impact milk production) and facilitate relaxation at
feeding time.
Discuss with the spouse/SO the mother’s This enhances understanding of mother’s needs,
requirement for rest, relaxation, and time together and family members feel included and are therefore
with family members more willing to support breastfeeding
activity/treatment plan
DEPENDENT
During lactation, there is an increased need for
Arrange a dietary consult to review nutritional
energy requiring supplementation of protein,
needs and vitamin/mineral supplements, such as
vitamins, and minerals to provide nourishment for
vitamin C, as indicated
the infant.

Refer to support groups For further information

Evaluation:

Goal met after 2 hours of nursing interventions, the mother was able to demonstrate techniques to
enhance milk production and achieved mutually satisfactory breastfeeding pattern with infant
content after feedings and gaining weight appropriately

75
 DISCHARGE PLAN

M - Medication

- Ceftazidime 140mg/IV every 12 hours (7am- 7pm)

- Amikacin 42mg, IV once a day (10 am)

E - Exercise

- Stressed that the baby sleeps most often times

T - Treatment

- Stressed importance of complying with the medications

H - Health Teachings

- Instructed Mother to bring back the baby in the hospital for his medication
- Instructed Mother on the time the medication will be given

- Instructed Mother for the drug’s side effect which includes constipation; diarrhea;
dizziness; headache; indigestion; nausea; pain, swelling, or redness at the injection
site; sleeplessness; vomiting.
- Instructed Mother of the importance of breastfeeding
- Instructed Mother on Proper Breastfeeding
- Instructed Mother to expose the baby to sunlight at 6:00 am to 10:00 am
- Instructed Mother that formula milk is only good for 4 hours
- Instructed Mother on strict aspiration precaution
- Instructed Mother to burped the baby after each feedings
- Instructed Mother to bathe daily their baby

D - Diet

- Instructed Mother to feed the baby as tolerated with strict aspiration precaution

76
 APPENDICES

IVF CHART

Date # of Bottle Solution Additive Rate of Drop Time

Volume

9/24/19 1 500 cc D10 water 8-9 gtts 11:55 am

9/25/19 2 500 cc D10 water 8-9 gtts 1:00 pm

DAILY WEIGHT

Date Weight

9/24/19 2.4kg

9/25/19 2.5kg

Usual weight 2.4kg

77
 Vital Signs

Date Time BP HR RR Temp

1/24/19 12 nn - 163 54 39

4 pm - 155 54 37.6

8 pm - 156 55 37

1/25/19 12 am - 153 54 36.5

4 am - 158 54 37

8 am - 138 38 37

12 nn - 138 38 37

4pm - 142 40 37

I AND O SHEET

Date IVF Oral Total Urine Total Output

Credit Consumed fluid Taken Output Vomitus Bm

taken

9/24/19 - - BF BF 50ml - 1x 50+1xBM

9/25/19 - - BF BF 60ml - 1x 60+1xBM

78
 CFAC

COLOR FREQUENCY AMOUNT CHARACTERISTICS

1/24/19 YELLOWISH 1X SMALL SOFT

(12PM)

1/25/19 YELLOWISH 1X SMALL SOFT

(12PM)

79
 GENOGRAM

60 y/o 65 y/o 68 y/o

Pneumonia 70 y/o
HTN 80&y/o
A W
A&W

27 y/o 29 y/o
A&W A&W

3 days old
Neonatal Sepsis

LEGENDS:

Patient, Neonatal Sepsis

Mother, alive and well Father, alive and well

Grandfather, HTN Grandfather, alive and well

Grandmother, Pneumonia Grandmother, alive and well

80
References:
1. World Health Organization 2005( A manual for Physicians and other Senior Health Workers by
Ellis D. Avner, MD page 40-41 Chapter 3 Vol. 1 15th edition)
2. Centers for Disease Control and Prevention or CDC(Gastroenteritis outbreaks in Health Care
Settings by Kurt B. Stevenson, MD page 55-58 Chapter 22 volume 1 7th Edition)
3. Baby and Child Health Care by Dr. Miriam Stoppard page 140 volume 1 3rd edition

4. https://medlineplus.gov/ency/article/007303.htm
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5913776/
6. The 5-Minute Pediatric Consult by Pramod Kerkar,MD,FFARCSI page 60-64 Chapter 50
Volume 1 8th Edition
7. Nelson Textbook of Pediatrics by Richard E. Behrman, MD page 1272 Chapter 321 volume 2
17th Edition
8. Atlas of Infectious Diseases by Robert M. Kliegman, MD page 1900 Chapter 300 volume 2 16th
edition

81