Republic of the Philippines

UNIVERSITY OF NORTHERN PHILIPPINES

Tamag, Vigan City
2700 Ilocos Sur
College of Nursing
Website: www.unp.edu.ph Mail: [email protected]
CP# 09177148749, 09175785986

NCM 109 PEDIA

ACTIVITY 1
Case Situation
By: Catherine A. Prado BSN II – B

Medical Diagnosis
Neonatal Sepsis. Maternal history reveals exposure to pathogens during gestation like shingles and a case
of Urinary Tract Infection, unsterile delivery and far flung community manifesting socioeconomic status
may also serve as precipitating factors. And there are factors that qualify the disease of the infant: “unable
to feed and has the inability to gain weight” as verbalized by the mother, they were living in the far flung
community, the mother had NSVD by “komadrona” at home, 3 days PTA, infant weight 2100 g with
intermittent fever. During pregnancy the mother was not visiting the RHU religiously, had UTI on 2’nd
Trimester and given antibiotics, at her HPPI she had contact with relatives with shingles, she was also
smoker during pregnancy. The laboratory result also shows that the infant’s RBC decreased, WBC-
400,000, ABG Analysis shows low pH and low Bicarb (Metabolic Acidosis), and the vital signs:
temperature:

 8 am: 37.8 deg. Celsius

 12 nn: 35.6 deg. Celsius
 4 pm: 38.2 deg. Celsius per axilla

Pathophysiology

Neonatal sepsis is defined as generalized systematic features of infection, associated with pure
growth of bacteria from one or more sites, in new born. When pathogenic bacteria gain access into blood
stream, they may cause overwhelming infection without much localization, may get predominantly to the
lungs, or the meninges. Certain maternal perinatal and obstetric factors increase risk, particularly of
early-onset neonatal sepsis, such as the following: premature rupture of membranes (PROM)
occurring ≥ 18 h before birth, untreated bacteria during pregnancy, Maternal chorioamnionitis (most
commonly manifesting as maternal fever shortly before or during delivery with maternal leukocytosis,
tachycardia, uterine tenderness, and/or foul-smelling amniotic fluid), colonization with GBS, ,
intrapartum infection, birth asphyxia, congenital anomaly that disrupts the skin. Hematogenous and
transplacental dissemination of maternal infection occurs in the transmission of certain viral

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 (eg, rubella, cytomegalovirus), protozoal (eg, Toxoplasma gondii), and treponemal (eg, Treponema
pallidum) pathogens. A few bacterial pathogens (eg, L. monocytogenes, Mycobacterium tuberculosis)
may reach the fetus transplacentally, but most are acquired by the ascending route in utero or as the
fetus passes through the colonized birth canal. Though the intensity of maternal colonization is directly
related to risk of invasive disease in the neonate, many mothers with low-density colonization give
birth to infants with high-density colonization who are therefore at risk. Amniotic fluid contaminated
with meconium or vernix caseosa promotes growth of group B streptococcus and  E. coli. Hence, the
few organisms in the vaginal vault are able to proliferate rapidly after PROM, possibly contributing to
this paradox. Organisms usually reach the bloodstream by fetal aspiration or swallowing of
contaminated amniotic fluid, leading to bacteremia. While the risk factor in late-onset sepsis is preterm
delivery. Others include: prolonged use of intravascular catheters, low birth weight, invasive procedure,
prolonged hospitalization, contaminated equipment or IV or enteral solutions. Gram-positive organisms
(eg, coagulase-negative staphylococci and Staphylococcus aureus) may be introduced from the
environment or the patient’s skin. Gram-negative enteric bacteria are usually derived from the patient’s
endogenous flora, which may have been altered by antecedent antibiotic therapy or populated by
resistant organisms transferred from the hands of personnel (the major means of spread) or
contaminated equipment. Therefore, situations that increase exposure to these bacteria (eg, crowding,
inadequate nurse staffing, inconsistent provider handwashing) result in higher rates of hospital-acquired
infection.

Algorithm of Neonatal Sepsis

Early On-set Late On-set

Premature
rupture of
membranes (
PROM)
occurring ≥  2
18 h before
birth
 untreated colonization intrapartum birth Conge- Prematurity Invasive
bacteria with GBS infection asphyxia nital or low birth Procedures
during anomaly weight
pregnancy

Direct transmission of Disruption in neonatal host Underdeveloped Direct

bacteria from maternal birth defenses immune system introduction of
canal to fetal blood during bacteria to the
Increased likelihood of deliver neonate’s
introducing bacteria to the blood
fetus

Predisposed to infection
vertical transmission of
maternal bacteria from lower
genital tract to uterus

Contamination of
Neonatal Sepsis
amniotic fluid

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 Fetal bacteremia

Gastrointestinal Urological CVS/Resp Metabolic CNS General

Poor Feeding Decreased Urine Apnea/Tachypnea Jaundice Lethargy Low APGAR

Output
Vomiting Labored breathing Hypo/hyperglycemia Irritability Temperature
instability
Diarrhea, Pallor or Cyanosis Metabolic Acidosis Focal Neurological
constipation, or signs Bulging or sunken
bloody stool fontanels
Legend: Brady/tachycardia

Hypotension

Pathophysiology Mechanism Sign/Symptoms Complication

Nursing Care Plan

Assessment Nursing Planning Intervention Rationale Evaluation
Diagnosis
Subjective: Impaired gas Short term: 1. Assess 1. Rapid, 1. Patient is free
exchange respirations: shallow of signs of
• Unable to related to • Patient will quality, rate, breathing and distress.
feed and difficulty of maintain pattern, depth hypoventilation
inability to gain breathing as normal ABG and breathing affect gas 2. ABGs show
weight as manifested by • Patient will effort. exchange by respirations are
verbalized by low pH level be alert. affecting of a normal rate
the mother and low HCO3 CO2 levels. 
• Patient will 2. Assess for and depth.
in ABG Flaring of the
• Weighs 2100 demonstrate life-threatening
analysis. nostrils,
g, with normal depth, problems. (i.e. 3. Patient’s lungs
intermittent rate, and resp arrest, flail dyspnea, use of
accessory sounds are clear
fever that told pattern of chest, sucking to auscultate
by the mother respirations. chest wound). muscles,
tachypnea and throughout all
/or apnea are all lobes
Objective: Long Term: 3. Auscultate signs of severe
lung sounds.  distress that 4. Patient is free
• Difficulty of • Patient will Also assess for require of signs of
breathing and maintain the presence of immediate hypoxia
increased in optimal gas jugular vein intervention.
heart rate exchange. distention
•Temperature: (JVD) or 5. ABGs show
37.8 Degree tracheal 2. Absence of normal results.
celsius at 8am, deviation. ventilation,
35.6 at 12 noon, asymmetric 6. Patient is free
and 38.2 degree breath sounds, of cyanosis.
4. Assess for dyspnea with
celsius at 4pm signs of accessory
• Decreased hypoxemia. muscle use,
CBC
dullness on chest

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• 400,000 5. Monitor percussion and
WBC ABGs. gross chest wall
• ABG instability (i.e.
Analysis – low 6. Assess skin flail chest or
pH level and color for sucking chest
low HCO3 development of wound) all
level cyanosis, require
especially immediate
circumoral attention.
cyanosis.
3. Absence of
lung sounds,
JVD and / or
tracheal
deviation could
signify a
Pneumotho-rax
or Hemothorax.

4.Tachycar-dia,
restlessness,
diaphoresis,
headache,
lethargy and
confusion are all
signs of
hypoxemia.

5. Increasing
PaCO2 and
decreasing
PaO2 are signs
of respiratory
failure.

6. Lack of
oxygen delivery
to the tissues
will result in
cyanosis. 
Cyanosis needs
treated
immediately as
it is a late
development in
hypoxia.
Hyperthermia Short Term: 1. Monitor 1. To determine 1. Neonates
related to neonate’s the need for condition is well.
infection as • Patient will condition. intervention and
evidence by maintain the effectiveness 2. Neonate’s
evidenced by an normal core 2. Monitor vital of therapy. vital signs are
increase in body temperature as signs normal.
temperature, evidenced by 2. To have a
and tachycardia vital signs baseline data 3. Body
within normal Helps in temperature of

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 limits and 3. Provide TSB lowering down the infant
normal WBC the temperature lowered.
level 4. Ensure that
all equipment 3. Prevents the 4. Ensured that
Long Term: used for infant spread of all equipment
• Patient will is sterile, pathogens to the used for infant is
still maintain scrupulously infant from sterile,
normal core clean. Do not equipment scrupulously
temperature as share equipment 4. Aids in clean.
evidenced by with other lowering down 5. Infants body
normal vital infants temperature temperature gets
signs and Administer back to normal.
normal antipyretics as
laboratory ordered
results.

Imbalanced • Patient 1. Get the body 1. To get the • After 2 weeks

Nutrition: Less shows no signs weight using the actual weight of nursing
Than Body of weight loss. standard and to determine intervention,
Requirements weighing scale if the patient’s goal met. Patient
related to • Patient weight meets the was able to eat
unable to eat as shows no signs 2. Provide normal body that helps in
manifested by of small, frequent mass index. achieving
weight loss. malnutrition. feedings cessation of
2. To reduce weight loss; and
3. For infants fatigue and gained at least 10
• Patient takes
older than age 6 improve intake percent of ideal
adequate
months, offer to facilitate body weight.
amount of food
solid foods swallowing.
with the
before formula
appropriate
or breast milk. 3. Older infants
calories
Place solid and young
foods in the toddlers may
center of the resist solid
tongue, using a foods, preferring
small spoon to milk or formula.
press downward
slightly 4. To accurately
monitor the
4. Obtain and response to
record the therapy.
child’s weight
each morning
before the first
feeding.