Paediadtrics & Paediatric Nursing.pdf

Kalupa Vincent (kalupavincent@gmail.com) Chipata College of Nursing & Midwifery -2009 Page 1
Kalupa Vincent
Chipata College of Nursing
& Midwifery -2009
PAEDIATRICS & PAEDITRIC NURSING

FETAL DEVELOPMENT
For the first 3 weeks following concept ion the term fertilized ovum or zygote is used, from 3.8 weeks after
conception it is known as the embryo and following this it is the fetus until birth, when it becomes a baby.
The development of fetus from conception up to birth is as follows:
1. 0-4 WEEKS AFTR CONCEPTION
 Rapid growth
 Formation of the embryonic plate
 Primitive central nervous system forms
 Heart develops and begins to beat
 Limb buds forms
2. 4-8 WEEKS AFTER CONCEPTION
 Very rapid cell division
 Head and facial features develop
 All major organs laid down in primitive form
 External genitalia present but sex not distinguishable
 Early movements
 Visible on ultrasound from 6 weeks
3. 8-12 WEEKS
 Rapid skeletal development – visible on x-ray
 Meconium present in gut
 Lanugos appears
 Nasal septum and palate fuse
4. 12-16 WEEKS

5. 16-20 WEEKS
 Quickening – mother feel fetal movements
 Fetal heart on auscultation
 Vernix caseosa appears
 Finger nails can be seen
 Skin cells begin to be renewed
6. 20-24 WEEKS
 Most organs become capable of functioning
 Periods of sleep and activity
 Responds to sound
 Skin red and wrinkled
7. 24-28 WEEKS
 Survival may be expected if born
 Eyelids reopen

 Respiratory movements
8. 28-32 WEEKS
 Begins to store fat and iron
 Testes descend into the scrotum
 Lanugos disappear from face
 Skin begins to paler and less wrinkled
9. 32-36 WEEKS
 Increased fats makes the body more round
 Lanugos disappear from body
 Head hair lengthens
 Nails reach tips of fingers
 Ear cartilage sot
 Planter crease visible
10. 36-40 WEEKS AFTER CONCEPTION ( 38-42 WEEKS AFTER LMP)
 Term is reached and birth is due
 Contours rounded
 Skull firm
FETAL ORGANS THEIR DEVELOPMENT AND PHYSIOLOGY
BLOOD
The origin of fetal blood is from the inner cell mass, along with all the other organs of its body.
 The fetus will inherit the genes that determines its blood group from both its parents; its ABO group
and Rhesus factor may therefore be the same or different from those of its mother
 The fetal hemoglobin is of different type from adult hemoglobin and is termed Hbf.
 It has a much greater affinity for oxygen and is found in greater concentration (18-20g/dl at term),
because O2 must be obtained from the mother’s blood in the placental site, where the oxygen tension is
lower than in the atmosphere.
 Towards the end of pregnancy the fetus begins to make adult type hemoglobin (HbA)
 In utero the red blood cells have a shorter life span this begins about 90 days by time the baby is
born
THE RENTAL TRACT
 The kidneys begin to function and the fetus passes urine from 10wks’ gestation.
 Urine is very dilute and does not constitute a route for excretion, since the mother eliminates
wastes products, which cross the placenta
 It is worth noting that superior vesicle arteries arise from the first few centimeters of the
hypogastric arteries which lead to the umbilical arteries so that if a single artery is found then abnormalities
of the rental tract are suspected
THE ADRENAL GLANDS
The fetal adrenal glands produce precursors for placenta formation of oestriols.

They are also thought to play a part in the initiation of labor.
THE LIVER
 The fetal liver is comparatively large in size, taking up much of the abdominal cavity, especially in
the early months
 From the 3rd
to the 6th
month of intrauterine life the liver is responsible for the formation of red
blood cells, after which the red bone marrow and the spleen mainly produces
 Towards the end of the pregnancy, iron stores are laid down in the liver
THE ALIMENTALLY TRACT
 The digestive tract is mainly non-functional before birth
 It forms from the yolk sac as a straight tube later growing out into the base of the umbilical code
and subsequently rotating back into the abdomen
 Sucking and swallowing of amniotic fluid containing shed skin cells and other debris begins about
12 wks after concept
 Most digestive juices are present before birth and they act on the swallowed substances and
discarded intestinal cells to form Meconium
 This is normally retained in a gut to until p with birth when it is passed as the first stool of the new
born.
THE LUNGS
 The lungs originate from a bad growing out of the pharynx which subdivides again to form the
branching structure of the bronchial trace
 The process continues after birth until 8 years when e full number of bronchial and alveoli will have
developed
 It is mainly the immaturity of the lungs that reduces the chance of bronchial and alveolar surface
area, the immaturity of the capillary system in the lungs and the lack of the capillary system in the lungs and
the lack of adequate surfactant.
 Surfactant is a lipoprotein that reduces the surface tension in the alveoli and assists gaseous
exchange
 It is first produced from about 20 weeks gestation and the amount increase until the lungs are
mature.
 At term the lungs contain about 1000mls of lung fluid. About one third of this is expelled during
birth and the rest is absorbed and carried away by the lymphatic and blood vessels as air take its place.
 There is thorax movement at the third month and more definite diaphragmatic movements from
the sixth month.
 Fetal breathing occurs in episodes of up to half an hour during rapid eye movement sleep.
THE CENTRAL NERVOUS SYSTEM
This derived from the ectoderm. It folds inwards by a complicated process to form the neural tube, which is
then covered over by the skin.
 This process is occasionally incomplete, leading to open neural tube defects.
 The fetus is able to perceive strong light and to hear external sounds.
 Periods of wakefulness and sleep occur, both in deep and rapid eye movement sleep.

THE SKIN
From 18weeks after conception the fetus is covered with a white, creamy substance called Vernix caseosa.
This protects the skin from the fluid and any friction against itself.
 At 20weeks the fetus will be covered with a fine downy hair called lanugo and at the time the head
hair and eyebrows begin to form.
 Lanugo is shed again from 36weeks and a full-term infant has little left.
 Fingernails develop from about 10weeks but the toenails do not form until about 18weeks.
 By term the nails usually extend beyond the finger tips, but length of the nails is an unreliable guide
to maturity.
PEDIATRIC HISTORY & PHYSICAL EXAM
(CHILDREN ARE NOT JUST LITTLE ADULTS)
GENERAL OBJECTIVE;
At the end the student should acquire knowledge on how to conduct a full physical examination of a child.
Specific objective
 At the end, the student must be able to;
 State the general principles for
 performing pediatrics physical examination
 Prepare the child for the examination
 List the requirements for physical examination
 Perform a physical examination in a sequence appropriate to the child’s age
GENERAL PRINCIPLES FOR PERFORMING PEDIATRIC EXAMINATION
1. perform the examination in an appropriate non threatening environment
2. provide time for play and becoming acquainted if signs of readiness are not seen
3. talk to parents while ignoring the child
4. focus on a favorite object such as a doll
5. tell a fun story or play a simple trick
6. try to involve the child and parents in the process
7. Avoid prolonged examination procedure
8. Perform an examination as quickly as possible
9. If several children are to be examined, start with the most cooperative child
10. Examine the child in a most comfortable and secure position e.g. sitting on the laps of the mother
11. Reassure the child through out the examination
12. Praise the child for being cooperative
13. Discuss findings with the family at the end of the procedure
HISTORY-
Learning Objectives:
1. To understand the content differences in obtaining a medical history on a pediatric patient compared to
an adult.
a. To understand how the age of the child has an impact on obtaining an appropriate medical history.
2. To understand all the ramifications of the parent as historian in obtaining a medical history in a pediatric
patient.

3. To understand the appropriate wording of open-ended and directed questions, and appropriate use of
each type of question.
4. To develop an awareness of which clinical settings it is appropriate to obtain a complete medical history
compared to a more limited, focused history.
Competencies:
1. To obtain an accurate and complete history of a pediatric patient in different age groups (<1 year; 1-5
years; > 5 years).
Differences of a Pediatric History Compared to an Adult History:
I. Content Differences
A. Prenatal and birth history
B. Developmental history
C. Social history of family - environmental risks
D. Immunization history
II. Parent as Historian
A. Parent’s interpretation of signs, symptoms
1. Children above the age of 4 may be able to provide some of their own history
2. Reliability of parents’ observations varies
3. Adjust wording of questions - “When did you first notice Johnny was limping”? instead of “When did
Johnny’s hip pain start”?
B. Observation of parent-child interactions
1. Distractions to parents may interfere with history taking
2. Quality of relationship
C. Parental behaviors/emotions are important
1. Parental guilt - nonjudgmental/reassurance
2. The irate parent: causes

Outline of the Pediatric History:
I. Chief Complaint
A. Brief statement of primary problem (including duration) that caused family to seek medical attention
II. History of Present Illness
A. Initial statement identifying the historian, that person’s relationship to patient and their reliability
B. Age, sex, race, and other important identifying information about patient
C. Concise chronological account of the illness, including any previous treatment with full description of
symptoms (pertinent positives) and pertinent negatives. It belongs here if it is relates to the differential
diagnosis for the chief complaint.
III. Past Medical History
A. Major medical illnesses
B. Major surgical illnesses-list operations and dates
C. Trauma-fractures, lacerations
D. Previous hospital admissions with dates and diagnoses
E. Current medications
F. Known allergies (not just drugs)
G. Immunization status - be specific, not just up to date
IV. Pregnancy and Birth History
A. Maternal health during pregnancy: bleeding, trauma, hypertension, fevers, infectious illnesses,
medications, drugs, alcohol, smoking, rupture of membranes
B. Gestational age at delivery
C. Labor and delivery - length of labor, fetal distress, type of delivery (vaginal, cesarean section), use of
forceps, anesthesia, breech delivery
D. Neonatal period - Apgar scores, breathing problems, use of oxygen, need for intensive care,
hyperbilirubinemia, birth injuries, feeding problems, length of stay, birth weight
V. Developmental History
A. Ages at which milestones were achieved and current developmental abilities - smiling, rolling, sitting
alone, crawling, walking, running, 1st word, toilet training, riding tricycle, etc (see developmental charts)
B. School-present grade, specific problems, interaction with peers
C. Behavior - enuresis, temper tantrums, thumb sucking, pica, nightmares etc.
VI. Feeding History
A. Breast or bottle fed, types of formula, frequency and amount, reasons for any changes in formula
B. Solids - when introduced, problems created by specific types
C. Fluoride use

VII. Review of Systems: (usually very abbreviated for infants and younger children)
A. Weight - recent changes, weight at birth
B. Skin and Lymph - rashes, adenopathy, lumps, bruising and bleeding, pigmentation changes
C. HEENT - headaches, concussions, unusual head shape, strabismus, conjunctivitis, visual problems,
hearing, ear infections, draining ears, cold and sore throats, tonsillitis, mouth breathing, snoring, apnea, oral
thrush, epistaxis, caries
D. Cardiac - cyanosis and dyspnea, heart murmurs, exercise tolerance, squatting, chest pain, palpitations
E. Respiratory - pneumonia, bronchiolitis, wheezing, chronic cough, sputum, hemoptysis, TB
F. GI - stool color and character, diarrhea, constipation, vomiting, hematemesis, jaundice, abdominal pain,
colic, appetite
G. GU - frequency, dysuria, hematuria, discharge, abdominal pains, quality of urinary stream, polyuria,
previous infections, facial edema
H. Musculoskeletal - joint pains or swelling, fevers, scoliosis, myalgia or weakness, injuries, gait changes
I. Pubertal - secondary sexual characteristics, menses and menstrual problems, pregnancies, sexual activity
J. Allergy - urticaria, hay fever, allergic rhinitis, asthma, eczema, drug reactions
VIII. Family History
A. Illnesses - cardiac disease, hypertension, stroke, diabetes, cancer, abnormal bleeding, allergy and asthma,
epilepsy
B. Mental retardation, congenital anomalies, chromosomal problems, growth problems, consanguinity,
ethnic background
IX. Social
A. Living situation and conditions - daycare, safety issues
B. Composition of family
C. Occupation of parents
PREPARING THE CHILD FOR PHYSICAL EXAMINATION
The child must be well prepared to promote cooperation. The physical examination should be as pleasant as
possible as well as educative. Use a doll to teach the child about the parts of the body being examined.
Allow the parents to remain with the child unless when examining an adolescent. Allow the child to undress
in privacy and give a gown.
PHYSICAL ASSESSMENT/EXAMINATION
The approach to and sequence of the physical assessment/examination differ according to the child’s age.
Initial assessment of an infant immediately following delivery is done using the apgar scoring system. The
score is based on the heart rate, respiratory effort, muscle tone, reflex, irritability and color. Each item is
given a score of zero, one or two.
Total scores ranges from zero to ten (0 – 10). The apgar score reflexes of the infant at one (1) and five (5)
minutes after birth.
-PHYSICAL EXAMINATION-
Objectives
1. To understand how the general approach to the physical examination of the child will be different
compared to that of an adult patient, and will vary according to the age of the patient.
2. To observe and demonstrate physical findings unique to the pediatric population, and to understand how
these findings may change depending upon the age of the child.
Competencies
1. To obtain accurate vital signs (Temperature, HR, RR, BP) in a pediatric patient in different age groups and
to be able to evaluate these vital signs compared to age-adjusted normals. To understand the normal
variation in temperature depending on the route of measurement.

2. To complete a thorough physical examination on a pediatric patients in different age groups.
Differences in Performing A Pediatric Physical Examination Compared to an Adult:
I. General Approach
A. Gather as much data as possible by observation first
B. Position of child: parent’s lap vs. exam table
C. Stay at the child’s level as much as possible. Do not tower!!
C. Order of exam: least distressing to most distressing
D. Rapport with child
1. Include child - explain to the child’s level
2. Distraction is a valuable tool
E. Examine painful area last-get general impression of overall attitude
F. Be honest. If something is going to hurt, tell them that in a calm fashion. Don’t lie or you lose credibility!
G. Understand developmental stages’ impact on child’s response. For example, stranger anxiety is a normal
stage of development, which tends to make examining a previously cooperative child more difficult.
II. Vital signs
A. Normals differ from adults, and vary according to age
1. See “code card” for charts of age-adjusted normals
B. Temperature
1. Tympanic vs. oral vs. axillary vs. rectal
C. Heart rate
1. Auscultate or palpate apical pulse or palpate femoral pulse in infant
2. Palpate antecubital or radial pulse in older child
D. Respiratory rate -Observe for a minute. Infants normally have periodic breathing so that observing for
only 15 seconds will result in a skewed number.
E. Blood pressure
1. Appropriate size cuff - 2/3 width of upper arm
2. Site
F. Growth parameters - must plot on appropriate growth curve
1. Weight
2. Height/length
3. OFC: Across frontal-occipital prominence so greatest diameter
(Occipital Frontal Circumference)
III. Unique findings in pediatric patients (See outline below)
Outline of a Pediatric Physical Examination
I. Vitals - see above
II. General
A. Statement about striking and/or important features. Nutritional status, level of consciousness, toxic or
distressed, cyanosis, cooperation, hydration, dysmorphology, mental state
B. Obtain accurate weight, height and OFC
C. assessment of Gestational age – this is important because prenatal morbidity and mortality are related to
gestational age and birth weight. The weight of the client collaret with the incidence of prenatal morbidity
and mortality.
III. Skin and Lymphatic

A. Birthmarks - nevi, hemangiomas, mongolian spots etc
B. Rashes, petechiae, desquamation, pigmentation, jaundice, texture, turgor
C. Lymph node enlargement, location, mobility, consistency
D. Scars or injuries, especially in patterns suggestive of abuse
IV. Head
A. Size and shape – observe the head for general shape and symmetry and flattening of the parts of the
head may indicate that the child lies on one side/position. Note head control in infants and head posture in
older infants. At the age of 4 months most infants should be able to hold the head erect.
B. Fontanel(s) – palpate the skull for patent sutures, fontanels, fractures and swelling. The posterior fontanel
closes by second to third month while the anterior fontanel closes at eighteen months of age.
1. Size
2. Tension - calm and in the sitting up position
C. Sutures - overriding
D. Scalp and hair
V. Eyes
A. General
1. Strabismus
2. Slant of palpebral fissures
3. Hypertelorism or telecanthus
B. EOM
C. Pupils – the pupil should be round, clear and equal, compose the size and movement, test their reaction
to light. Inspect the iris for color size and clarity. Any opacity can be a sign scaring or ulceration.
D. Conjunctiva, sclera, and cornea – normally the conjunctiva appears pink, the sclera should be clear and
the cornea should be clear and transparent.
E. Plugging of nasolacrimal ducts
F. Red reflex
G. Visual fields - gross exam
H. Eye lids – inspect the eye lids for proper placement on the eye. Infants normally keeps their eyes closed
so it is ideal to separate the eye lids to confirm the presence of the eye ball.
VI. Ears
A. Position of ears
1. Observe from front and draw line from inner canthi to occiput
B. Tympanic membranes
C. Hearing - Gross assessment only usually
V. Nose
A. Nasal septum – inspect the septum which should be in the midline. Note any diversions as they may
occlude the nostrils.
B. Mucosa (color, polyps)
C. Sinus tenderness
D. Discharge
E. Nostrils – note that the nostrils are present.
F. Smell – test for smell by letting the child identify odors such as coffee or alcohol from a swab.
VI. Mouth and Throat
A. Lips/ Cleft palette (colors, fissures) – check for the presence of the cleft palette or lip by placing a tongue
depressor along the sides of the tongue and use of light pen for visualizing.
B. Buccal mucosa (color, vesicles, moist or dry) – check the buccal mucosa, pharynx, cheeks, palette for
color, thrush, ulceration, bleeding, sensitivity and moisture.
C. Tongue (color, papillae, position, tremors) – note the size of the tongue and its mobility.
D. Teeth and gums (number, condition) – inspect the teeth for fracture, carries.
E. Palate (intact, arch)

F. Tonsils (size, color, exudates) – examine the oral pharynx and note the size and color of the palatine
tonsils. Report any white patches, swelling, or redness of the tonsils.
G. Posterior pharyngeal wall (color, lymph hyperplasia, bulging)
H. Gag reflex
V. Neck

A. Thyroid
B. Trachea position
C. Masses (cysts, nodes)
D. Presence or absence of nuchal rigidity
VI. Lungs/Thorax
A. Inspection
1. Pattern of breathing
a. Abdominal breathing is normal in infants
b. Period breathing is normal in infants (pause < 15 seconds)
2. Respiratory rate
3. Use of accessory muscles: retraction location, degree/flaring
4. Chest wall configuration
B. Auscultation
1. Equality of breath sounds
2. Rales, wheezes, rhochi
3. Upper airway noise
C. Percussion and palpation often not possible and rarely helpful
VII. Cardiovascular
A. Auscultation
1. Rhythm
2. Murmurs
3. Quality of heart sounds
B. Pulses
1. Quality in upper and lower extremities
VIII. Abdomen
A. Inspection
1. Shape – inspect the contor of the abdomen with child erect and supine. Diastasis rect may be seen if the
rectus abdominus muscle failed to join in the uterus. A tense board like abdomen is a sign of paralytic ilieus
and intestinal obstruction.
i. Infants usually have protuberant abdomens
ii. Becomes more scaphoid as child matures
2. Umbilicus (infection, hernias)
3. Muscular integrity (diasthasis recti)
B. Auscultation – auscultation for peristalsis and bowel sounds, or hyper peristalsis as they denote an
abdominal disorder.
C. Palpation – is done last because it can interfere with normal abdominal sounds.
1. Tenderness - avoid tender area until end of exam
2. Liver, spleen, kidneys -
a. May be palpable in normal newborn
3. Rebound, guarding
a. Have child blow up belly to touch your hand
IX. Musculoskeletal
A. Back
1. Sacral dimple
2. Kyphosis, lordosis or scoliosis
B. Joints (motion, stability, swelling, tenderness)
C. Muscles
D. Extremities

1. Deformity
2. Symmetry
3. Edema
4. Clubbing
E. Gait
1. In-toeing, out-toeing
2. Bow legs, knock knee
a. “Physiologic” bowing is frequently seen under 2 years of age and will spontaneously resolve
3. Limp
F. Hips
1. Ortolani’s and Barlow’s signs
X. Neurologic - most accomplished through observation alone
A. Cranial nerves
B. Sensation
C. Cerebellum
D. Muscle tone and strength
E. Reflexes
1. DTR
2. Superficial (abdominal and cremasteric)
3. Neonatal primitive
XI. GU
A. External genitalia - check the sex, note any sexual ambiquete.
MALES – palpate the scrotum to see if the tests have descended.
- examine the glands and shaft for signs of swelling, skin lesions and inflammation.
- note the presence of hyperspadiosis, urethral strictures.
FEMALES – the labia minora are prominent in the new born
- the urethra mitus is located approximately 2.5 cm below the clitoris.
- the clitoris is an erectile organ located at the anterior end of the labia minora.
- the vaginal orifice is located posterior to the urethra.
B. Hernias and Hydrocoeles
1. Almost all hernias are indirect
2. Can gently palpate; do not poke finger into the inguinal canal
C. Cryptorchidism
1. Distinguish from hyper-retractile testis
2. Most will spontaneously descend by several months of life
D. Tanner staging in adolescents - See Tanner Staging handouts
E. Rectal and pelvic exam not done routinely - special indications may exist
ANUS – assesses the tone of the anal sphincter, note the general firmness of the buttocks, patency of the
anus is noted by inserting a rectal thermometer.
BACK AND EXTREMITIES
Note the general curvature of the spine. The back of the new born has a ‘c’ shape from the thoracic and
pelvic curves. The older child has a typical ‘s’ curve due to development of cervical and lumber curves.
Inspect the back especially along the spine for any rifts of hair, dipiples or disc olouration. These are signs of
occult-spinal bifida.

EXTREMTIES
Inspect each extremity for length and size. Count fingers and toes to be contain of normal numbers. Note
the presence of extra digits, (polydactyl) or webbing of digits (syndactly). Note the presence of talips, knock
knee, or genu-valvum.
Test for congenital dislocation of the hip in infants.
SMALL FOR GESTATION AGE BABY (SGA)
DEFINION: Any baby whose birth weight is below the 10th
percentile for the gestation age standards.
These babies may or may not be preterm.
PREDISPOSING FACORS
1. MATERNAL FACTORS
 Pregnancy induced hypertension, pre-eclampsia
 Chronic hypertension
 Under nutrition
 Smoking, alcohol misuse
 Drugs- anticancer drugs and narcotics
 Renal diseases
 Anemia
 Irradiation
 Maternal age those below 16 and above 35 years
 Under weight mothers and those with small stature
2. FETAL FACTORS
 Multiple gestation
 Chromosomal/genetic abnormality, especially trisomy conditions, inborn errors of metabolism
 Intrauterine infections- toxoplasmosis, rubella, cytomegalovirus
3. PLACENTAL FACTORS
 Placenta Abruptio
 Placenta previa
 Chorioamnionitis
 Abnormal cord insertion
 Single umbilical artery
CHARACTERISTICS OF A SMALL FOR GESTATIONAL AGE (SGA) BABY
1. There is a lack of subcutaneous tissue
2. The infant appears to be thin, long and wasted
3. The skin is loose, peeling, has creases on the soles of the feet, is often dry and scaly
4. The baby has a wasted, dehydrated look

5. The features are; wizened, wide-eyed, alert and a worried expression.
6. There is meconium staining on the skin, nails, and the umbilical cord.
7. Some babies appear to be dwarfed, with a reduced weight
8. The hair is sparse, coarse and straight
9. The cord is usually thin and therefore dries more rapidly than in a normal baby.
10. The baby is active and hungry at birth.
11. The ear cartilage is well developed.
12. The skull bones are firm but small, and the head is hard.
13. The infant has a scaphoid (boat-shaped) abdomen.
14. The head is often large in comparison with the size of the body.
PROBLEMS ASSOCITED WITH LOW BIRTH BABIES
1. POOR THERMOREGULATION
Rapid heat loss due to large head-to-body ratio and large surface area and less subcutaneous fat, the infant
finds it difficult to conserve and regulate body temperature.
2. HYPOGLYCAEMIA
The babies have reduced glycogen stores in the liver.
Their greater brain-to-body mass and a tendency towards polycythaemia increases their energy glucose
requirements.
The babies usually feed within the first half hour of birth and demand for feeds every 2-3 hours.
Their susceptibility to hypoglycemia is short lived and is limited to the first 48 hours following birth.
3. INFECTION
Me conium stained skin is a good media for bacterial multiplication.
NURSING MANAGEMENT
The importance of providing an appropriate environment for small for dates cannot be over-stressed. The
ideal environment should resemble home, which provides a cycle of day and night, regular nourishment,
rest, stimulation and loving attention.
ENVIRONMENT
The room temperature should be above 22 degrees centigrade, in order to prevent heat loss by convection.
The baby should be wrapped in warm blankets and not in cold blankets, and should not be placed on cold
surface to prevent heat loss by conduction.
Close windows to prevent drought, if the temperature outside environment is colder than the environment
in which the baby is lying, heat will be lost by radiation to cold walls, windows, floors, ceilings, etc.
Nurse the baby in an incubator and control incubator temperature to suit the condition of the baby, either
by increasing or decreasing the incubator temperature.
Incubator temperature should range between 32- 36 degrees centigrade.
A Perspex heat shield can be placed over the baby and the baby can be dressed in woolen cap, gloves and
socks.
If no incubator is available, well insulated warm electric pads or well wrapped warm water bottles are
placed along side the baby.
Great care must be taken not to over heat the baby nor burn the baby’s tender skin.
The room temperature can be raised and overhead radiant heat sources can be utilized.

Bear in mind that hyperthermia can be as serious as hypothermia.
If no incubator available, kangaroo method can be used, where the baby is placed on mother’s chest and an
aluminum/silver swaddle placed over them both and covered with blankets.
This method is also very useful when transferring the infant to special baby care unit.
OBSERVATIONS
Frequent observation of color, respirations and are done half hourly at first, then hourly, two hourly as the
condition improves. Temperature is done 2 hourly.
Blood is tested by dextrostix for blood sugar levels.
Observe for normal movements and reflexes
NUTRITION
Hypoglycemia in small for date’s babies may be due to inadequate or depleted glycogen stores in the
placenta before delivery, or in the liver and skeletal muscles after delivery, or due to an increased demand
for glucose (respiratory distress, hypothermia, infection).
Early feeding is the best course. If the baby is very small and unable to suck, intravenous feeding is
commenced as soon as possible, or a nasogastric tube is inserted for feeds.
Keep the baby warm as hypothermia worsens hypoglycemia.
The baby is given a feed of 1-2mls 50% dextrose, added to 50ml of formulae, when blood sugar levels are
below minimum values.
10% dextrose water is given intravenously; it should be continuous and steady and is kept up until the baby
is able to tolerate milk feeds.
2 hourly feeds are maintained, the feeds are calculated at 90ml/kg on the first day with 30ml increments per
day.
Breast milk is the best for the baby because it contains long chain polyunsaturated omega-3 fatty acids,
which are thought to be essential for myelination of neural membranes and for retinal development.
Encourage the mother to express breast milk and give via a nasogastric tube or by cup as condition
improves.
Parents or caretakers should be encouraged to hold the bay during nasogastric tube feeding, and provide
support for the babies’ trunk and shoulders.
Monitor dextrostix levels every hour until the infant’s condition is stable.
Maintain dextrostix readings at 2.2mmol/L or above.
HYGIENE
Prevention of infection is particularly important because small for gestation age babies are vulnerable to
infections. Isolate the infant to prevent them from getting infections from other sick babies.
Meticulous hand washing before and after attending to the baby should be observed strictly.
Use individual thermometer for each baby if possible.
Maintain separate utensils for each baby and do not mix them.
Top and tail should be done three times a day to promote comfort. Change soiled linen and nappies
frequently.
Incubators should be cleaned every day with an antiseptic solution, thorough cleaning of incubators should
be done once a week.
Use of protective clothing when attending to the infant should be encouraged. (Gowns, masks, ect).
PROMOTION OF REST

Noise should be kept to a minimum. All extraneous noises should be eliminated from the clinical
environment, such as musical toys and mobiles, harsh clattering foot wear, telephones, radios and intercom
systems. Nurses should speak in low voices.
Quiet signs can be posted to remind visitors not to disrupt the peace.
Light should be dimmed to enhance the quality of sleep.
Do procedures collectively to give chance to the baby to rest.
POSITION
Nurse the baby in supine position to prevent asphyxia. Laying the baby in supine position is thought to be
effective in promoting engagement in self- regulatory behaviors such as exploration of the face, mouth,
hand and foot clasping, boundary searching, and flexion and extension of the limbs. Placing babies to sleep
in the prone position has been theoretically eradicated from neonatal practice.
DRUGS
The doctor may prescribe antibiotics for prophylaxis.
Oxygen is given by a head box.
Give any other drugs as prescribed by the doctor bearing in mind pediatric dosage and calculation of these
drugs must be done before administering them.
PSYCHOLOGICAL CARE
The mother is very worried about the baby and therefore should be reassured. Explain the condition to the
mother and involve her in the care of the baby. Allow her to handle and fondle the baby frequently to
promote baby –mother bondage. Teach her the kangaroo method of keeping the baby warm. The baby can
remain beneath the mother’s clothing for as long as it suits the mother.
Respiratory Distress Syndrome
DEF: Infant respiratory distress syndrome (IRDS), also called neonatal respiratory distress syndrom or
respiratory distress syndrome of newborn, previously called hyaline membrane disease, is a syndrome
(clinical disease process) in premature infants caused by developmental insufficiency of surfactant
production and structural immaturity in the lungs characterised by progressive respiratory distress.
 Is a disorder of lung immaturity caused by insufficient surfactant in the lungs. The infant looks normal at
birth with good Apgar score then they develop signs or respiratory distress such as tachypnea, grunting
respirations.
Causes
 The immediate cause is lack of surfactant a lipo-protein present in alveola and respiratory bronchioles.
Predisposing factors
- It can also result from a genetic problem with the production of surfactant associated proteins.
- Large for gestational age babies - The syndrome is more frequent in infants of diabetic mothers
- Prematurity – due to immature lungs
- Asphyxia – the greater the asphyxiation and shock, the more severe the respiratory distress.
- Hypoxia, Acidosis, Hypothermia and Hypoglycemia – inhibit the synthesis of surfactant

Pathophysiology
- The lungs of infants with respiratory distress syndrome are developmentally deficient in a material
called surfactant, which helps prevent collapse of the terminal air-spaces (the future site of alveolar
development) throughout the normal cycle of inhalation and exhalation.
- Surfactant is a complex system of lipids, proteins and glycoproteins which are produced in specialized
lung cells called Type II alveoli cells or Type II pneumocytes.
- The surfactant is packaged by the cell in structures called lamellar bodies, and extruded into the air-
spaces.
- The lamellar bodies then unfold into a complex lining of the air-space. This layer reduces the surface
tension of the fluid that lines the air-space.
- Surface tension is responsible for approximately 2/3 of the elastic recoil forces. In the same way that a
bubble will contract to give the smallest surface area for a given volume, so the air/water interface
means that the liquid surface will tend towards being as small as possible, thereby causing the air-space
to contract.
- By reducing surface tension, surfactant prevents the air-spaces from completely collapsing on
exhalation.
- In addition, the decreased surface tension allows re-opening of the air-space with a lower amount of
force.
- Therefore, without adequate amounts of surfactant, the air-spaces collapse and are very difficult to
expand.
- Microscopically, a surfactant deficient lung is characterized by collapsed air-spaces alternating with
hyper-expanded areas, vascular congestion and, in time, hyaline membranes.
- Hyaline membranes are composed of fibrin, cellular debris, red blood cells, rare neutrophils and
macrophages.
- They appear as an eosinophilic, amorphous material, lining or filling the air spaces and blocking gas
exchange.
- As a result, blood passing through the lungs is unable to pick up oxygen and unload carbon dioxide.
- Blood oxygen levels fall and carbon dioxide rises, resulting in rising blood acid levels and hypoxia.
- Structural immaturity, as manifest by decreased number of gas-exchange units and thicker walls, also
contributes to the disease process.
- Therapeutic oxygen and positive-pressure ventilation, while potentially life-saving, can also damage the
lung.
- The chest wall is very compliant and tends to collapse around the stiff lungs. Grunting respirations
results from attempt to expire against a partially closed larynx; as a result, alveolar ventilation is reduced
resulting in hypoxemia. Clinically, this presents as cyanosis with increased hypoxemia, there is retention
of carbon dioxide producing a respiratory and metabolic acidosis which impedes surfactant synthesis.
Clinical picture
 Respiratory distress syndrome begins shortly after birth and is manifest by;
- tachypnea

- tachycardia
- chest wall retractions (recession){intercoastal, subcoastal or sternal resection}
- audible expiratory grunting,
- flaring of the nostrils
- Hypotension
- Peripheral edema
- Oliguria
 In severe cases patient may present with;
- apnea,
- Bradicardia
- Cyanosis during breathing efforts.
- Pallor
- Frothy sputum
- Hypothermia due to immature nervous system and inadequate subcutaneous fat.
 Secondary signs and symptoms
- Infant is lethargic and usually maintains a frog’s position
- Bowel sounds are absent and passage of meconium is delayed for a few days
- Generalized edema is usually present within 24 hours
- Decreased urine out-put
 As the disease progresses, the baby may develop ventilatory failure (rising carbon dioxide
concentrations in the blood), and prolonged cessations of breathing ("apnea").
Diagnosis
- History - indicates preterm birth (before 28 weeks gestational), maternal history may include diabetes or
antepartum hemorrhage. Baby may be premature and born by caesarian section.
- Physical examination and Clinical picture – infant may present with nasal flaring, respiratory grunting,
cyanosis and chest in drawing.
- Aterial blood gas analysis - shows a diminished PaO2level, increased PaCO2 level and reduced pH. (a
combination of metabolic and respiratory acidosis).
- Chest x-ray - which demonstrates decreased lung volumes (bell-shaped chest), absence of the thymus
(after about 6 hours), a small (0.5–1 mm), discrete, uniform infiltrate (sometimes described as a "ground
glass" appearance) that involves all lobes of the lung. Fine reticulonodular pattern and dark strikes
indicating air fields may be evidenced, with diffused hyper distended bronchioles.
- Air-bronchograms (i.e. the infiltrate will outline the larger airways passages which remain air-filled). In
severe cases, this becomes exaggerated until the cardiac borders become inapparent (a 'white-out'
appearance).

 Before delivery of the infant
- Lecithin-sphingomyelin ratio ("L/S ratio") – helps to assess prenatal lung development and RDS risk. For
the L/S ratio, if the result is less than 2:1, the fetal lungs may be surfactant deficient.
- The presence of phosphatidol glycerol (PG) - The presence of PG usually indicates fetal lung maturity.
- Surfactant/albumin (S/A) ratio. For the S/A ratio, the result is given as mg of surfactant per gm of
protein. An S/A ratio <35 indicates immature lungs, between 35-55 is indeterminate, and >55 indicates
mature surfactant production (correlates with an L/S ratio of 2.2 or greater).
Treatment
 A radiant warmer or isollet for thermo regulation
 Oxygen is given with a small amount of continuous positive airway pressure ("CPAP") – to reduce
the concentration of carbon dioxide in the blood
 Intravenous fluids and sodium bicarbonate are administered to stabilize the blood sugar, blood salts,
and blood pressure, control acidosis and maintain fluid and electrolyte balance.
 If the baby's condition worsens, an endotracheal tube (breathing tube) is inserted into the trachea
and intermittent breaths are given by a mechanical device.
 An exogenous preparation of surfactant, either synthetic or extracted from animal lungs, is given
through the breathing tube into the lungs.
 One of the most commonly used surfactants is Survanta, derived from cow lungs, which can
decrease the risk of death in hospitalized very-low-birth-weight infants by 30%.
 Extracorporeal membrane oxygenation (ECMO) is a potential treatment, providing oxygenation
through an apparatus that imitates the gas exchange process of the lungs.
- However, newborns cannot be placed on ECMO if they are under 2 kg, because they have extremely
small vessels for cannulation, thus hindering adequate flow because of limitations from cannula size and
subsequent higher resistance to blood flow (compare with vascular resistance).
- Furthermore, in infants aged less than 34 weeks of gestation several physiologic systems are not well-
developed, especially the cerebral vasculature and germinal matrix, resulting in high sensitivity to slight
changes in pH, PaO2, and intracranial pressure.
- Subsequently, preterm infants are at unacceptably high risk for intraventricular hemorrhage (IVH) if
administered ECMO at a gestational age less than 32 weeks.
 Dextrose 5% or 10% to control hypoglycemia
 Tube feeding or total parenteral nutrition to maintain adequate nutrition since the neonate may
be too weak to eat.
 Drug therapy
 Pancuronium bromide (which paralyses muscles to prevent spontenous respirattions during
ventilation)
 Prophylactic antibiotics to prevent infection,
 Diuretics to reduce pulmonary edema
 Synthetic surfactant to prevent atelectasis.

 Vitamin K – to control bleeding tendencies
 Vitamin E to prevent complications associated with oxygen therapy,
 Before delivery of the infant, corticosteroids administered maternally to stimulation production
of surfactant in fetus at high risk of preterm birth.
Nursing management
Aims;
a. Promote ventilation/respirations
b. To maintain a clear and patent airway
c. To prevent hypoglycemia
d. To prevent hypothermia
e. To prevent infection
Environment
Psychological care
- Explain disease process to the parents
- Allow parents to participate in the care to promote bonding
- Explain the function of respiratory devices and equipment
- Inform parents that recovery may take long and reassure them without giving false hopes
- Arrange follow-up care with neonatal ophthalmologist to assess retinal damage
Rest, activity and exercises
Observations
- Monitor arterial blood gas levels
- Use pulse-oximeter to monitor SaO2 levels
- Assess skin color regularly
- Assess rate and depth of respirations
- Assess severity or retraction (chest in drawing), nasal flaring, frequency of expiratory respiratory
grunting and restlessness
- Watch for abnormal central nervous pressure
- Observe for infection, thrombosis and decreases circulation to the legs
- Regularly assess the effectiveness of oxygen therapy or ventilator therapy
- Watch for any complications that may result from oxygen administration
Position
Hygiene
- Promote infection prevention measures especially if using mechanical ventilation

- Provide mouth care every 2 hours
- Rubricate the infant’s nostrils and lips with water soluble ointments
- Do top and tailing
- Change soiled nappies
Elimination
Nutrition
Complications
- Metabolic disorders (acidosis, low blood sugar)
- Patent ductus arteriosus
- Low blood pressure
- Chronic lung changes/lung capacity damage
- Intracranial hemorrhage
- Respiratory insufficiency/respiratory failure
- Shock
- Retinopathy
- Congestive cardiac failure
- Necrotizing enterocolitis
- Neurological abnormalities
- Renal failure
Prevention
 Most cases of hyaline membrane disease can be prevented if mothers who are about to deliver
prematurely can be given glucocorticoids, one group of hormones.
- This speeds the production of surfactant. For very premature deliveries, a glucocorticoid is given without
testing the fetal lung maturity.
 In pregnancies of greater than 30 weeks, the fetal lung maturity may be tested by sampling the
amount of surfactant in the amniotic fluid, obtained by inserting a needle through the mother's
abdomen and uterus.
 Promote rest to prevent pre-term labour
 Prevent pre-term labour or delivery by good antenatal care
Neonatal conjunctivitis

DEF: Neonatal conjunctivitis, also known as ophthalmia neonatorum, is a form of bacterial conjunctivitis
contracted by newborns during delivery.
- The baby's eyes are contaminated during passage through the birth canal from a mother infected with
either Neisseria gonorrhoeae or Chlamydia trachomatis.
- Eyedrops containing erythromycin are typically used to prevent the condition. If left untreated it can
cause blindness.
Cause
Non infectious
- Chemical irritants such as silver nitrate can cause chemical conjunctivitis, usually lasting 2–4 days.
 Neomycin and chloramphenicol eye drops are used instead.
Infectious
- Many different bacteria and viruses can cause conjunctivitis in the neonate.
- The two most feared causes are;
- N. gonorrheae
- Chlamydia acquired from the birth canal during delivery.
Other causes
- Herpes simplex virus (HSV 2),
- Staphylococcus aureus,
- Streptococcus haemolyticus,
- Streptococcus pneumoniae.
 Ophthalmia neonatorum due to gonococci (Neisseria gonorrhoeae) typically manifests in the first
five days of life and is associated with:
- Marked bilateral purulent discharge and
- Local inflammation.
 In conjunctivitis secondary to infection with chlamydia (Chlamydia trachomatis) produces
conjunctivitis after day three of life, but may occur up to two weeks after delivery.
- The discharge is usually more watery in nature (mucopurulent) and less inflamed.
- Babies infected with chlamydia may develop pneumonitis (chest infection) at a later stage (range 2
weeks – 19 weeks after delivery).
- Infants with chlamydia pneumonitis should be treated with oral erythromycin for 10–14 days.
Signs & symptoms
1. Pain and tenderness in eyeball
2. Conjunctival discharge: purulent, mucoid or mucopurulent depending on the cause.
3. Conjunctiva shows hyperaemia and chemosis. Eyelids are usually swollen.
4. Corneal involvement (rare) may occur in herpes simplex opthalmia neonatorum.

Treatment
A. Prophylaxis needs antenatal, natal and post natal care.
1. Antenatal measures include thorough care of mother and treatment of genital infections when
suspected.
2. Natal measures are of utmost importance as mostly infection occurs during childbirth. Deliveries
should be conducted under hygienic conditions taking all asceptic measures. The newborn baby's
closed lids should be thoroughly cleansed and dried.
3. Postnatal measures include:
1. Use of 1% tetracycline ointment or 0.5% erythromycin ointment or 1% silver nitrate solution (crede's
method) into the eyes of babies immediately after birth 2. Single injection of ceftriaxone 50 mg/kg IM or IV
should be given to infants born to mothers with untreated gonococcal infection. B. Curative treatment as a
rule, conjunctival cytology samples and culture sensitivity swabs should be taken before starting treatment
 Chemical ophthalmia neonatorum is a self-limiting condition and does not require any treatment.
 Gonococcal ophthalmia neonatorum needs prompt treatment to prevent complications. Topical
therapy should include
1. Saline levarage hourly till the discharge is eliminated 2. Bacitracin eye ointment four times per day
(Because of resistant strains topical penicillin therapy is not reliable. However in cases with proved penicillin
susceptibility, penicillin drops 5000 to 10000 units per ml should be instilled every minute for half an hour,
every five minutes for next half an hour and then half-hourly till infection is controlled) 3. If the cornea is
involved then atropine sulphate ointment should be applied. Systemic therapy: Neonates with gonococcal
ophthalmia neonatorum should be treated for seven days with one of the following regimens
Ceftriaxone 75–100 mg/kg/day IV or IM, QID
Cefotaxime 100–150 mg/kg/day IV or IM, 12 hourly
Ciprofloxacin 10–20 mg/kg/day or Norfloxacin 10 mg/kg/day
Crystalline benzyl penicillin G 50,000 units (for full-term normal weight babies) or 20,000 units (for
premature or low weight babies) IM twice daily for three days (if the organism is penicillin susceptible)
 Other bacterial ophthalmia neonatorum should be treated by broad spectrum antibiotics drops and
ointment for two weeks.
 Neonatal inclusion conjunctivitis caused by Chlamydia trachomatis responds well to topical
tetracycline 1% or erythromycin 0.5% eye ointment QID for three weeks. However systemic
erythromycin should also be given since the presence of chlamydia agents in conjunctiva implies
colonization of upper respiratory tract as well. Both parents should also be treated with systemic
erythromycin.
 Herpes simplex conjunctivitis is usually a self-limiting disease. Topical antiviral drugs control the
infection more effectively and may prevent recurrence.

Complications
 Corneal ulceration, which may perforate resulting in corneal opacification and Staphyloma
formation.
Chickenpox
Chickenpox or chicken pox is an acute highly contagious airborne illness caused by primary infection with
varicella zoster virus (VZV) characterised by itchy skin rash.
- It usually starts with vesicular skin rash mainly on the body and head rather than at the periphery and
becomes itchy, raw pockmarks, which mostly heal without scarring.
Cause
- Varicella zoster herpes virus (the same virus that in its latent phase causes herpes zoster).
Transmission
- Chicken pox is an airborne disease spread easily through coughing or sneezing of ill individuals or
through direct contact with secretions from the rash.
- A person with chickenpox is infectious from one to five days before the rash appears.
- The contagious period continues for 4 to 5 days after the appearance of the rash, or until all lesions have
crusted over.
- Immunocompromised patients are probably contagious during the entire period new lesions keep
appearing.
- Crusted lesions are not contagious. It takes from 10 to 21 days after contact with an infected person for
someone to develop chickenpox.
 Incubation period is 13 to 17 days.
Signs and symptoms
During prodomal phase, patient may complain of;
- myalgia,
- nausea,
- fever,
- headache,
- sore throat,
- pain in both ears,
- pressure in head or swollen face,
- malaise in adolescents and adults
- Pruritis (rash begins as crops of small erythromatus macules on the trunk or sculp). Macules progress to
papules and then clear versicles on erythromatus base. The vescles becomes cloudy and break easly to
form scabs

- The rash spreads to the face and the extremities.
- Shallow ulcers may develop on the mucus membranes of the mouth conjunctival and genitalia.
 While in children the first symptom is usually the development of;
- a papular rash,
- followed by development of malaise,
- fever (a body temperature of 38 °C (100 °F), but may be as high as 42 °C
- Anorexia.
Diagnosis
 Clinical presentation with typical early "prodromal" symptoms, and then the characteristic rash.
 Confirmation of the diagnosis can be sought through either examination of the fluid within the
vesicles of the rash, or by testing blood for evidence of an acute immunologic response.
 Vesicular fluid can be examined with a Tsanck smear, or better with examination for direct
fluorescent antibody.
 Giemsa stain to distingish the varicella zoster virus from the vacinia-variola virus.
 The fluid can also be "cultured", whereby attempts are made to grow the virus from a fluid sample.
 Blood tests can be used to identify a response to acute infection (IgM) or previous infection and
subsequent immunity (IgG).
 Prenatal diagnosis of fetal varicella infection can be performed using ultrasound, though a delay of
5 weeks following primary maternal infection is advised.
 A PCR (DNA) test of the mother's amniotic fluid can also be performed, (though the risk of
spontaneous abortion due to the amniocentesis procedure is higher than the risk of the baby
developing foetal varicella syndrome).
Pathophysiology
o Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG),
immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies;
o IgG antibodies persist for life and confer immunity.
o Cell-mediated immune responses are also important in limiting the scope and the duration of
primary varicella infection.
o After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local
sensory nerves.
o VZV then remains latent in the dorsal ganglion cells of the sensory nerves.
o Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (i.e., shingles), and
sometimes Ramsay Hunt syndrome type II.
Infection in pregnancy and neonates
- For pregnant women, antibodies produced as a result of immunization or previous infection is
transferred via the placenta to the fetus.

- Women who are immune to chickenpox cannot become infected and do not need to be concerned
about it for themselves or their infant during pregnancy.
- Varicella infection in pregnant women could lead to viral transmission via the placenta and infection of
the fetus. If infection occurs during the first 28 weeks of gestation, this can lead to fetal varicella
syndrome (also known as congenital varicella syndrome).
- Effects on the fetus can range in severity from underdeveloped toes and fingers to severe anal and
bladder malformation.
 Possible problems include:
 Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain
 Damage to the eye: optic stalk, optic cup, and lens vesicles, microphthalmia, cataracts,
chorioretinitis, optic atrophy
 Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits,
absent deep tendon reflexes, anisocoria/Horner's syndrome
 Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction
 Skin disorders: (cicatricial) skin lesions, hypopigmentation
Prevention
 Hygiene measures
- The spread of chicken pox can be prevented by isolating affected individuals. Contagion is by
exposure to respiratory droplets, or direct contact with lesions, within a period lasting from three
days prior to the onset of the rash, to four days after the onset of the rash.
- Therefore, avoidance of close proximity or physical contact with affected individuals during that
period will prevent contagion.
- The chicken pox virus (VZV) is susceptible to disinfectants, notably chlorine bleach (i.e., sodium
hypochlorite). Also, like all enveloped viruses, VZV is sensitive to desiccation, heat and detergents.
Therefore these viruses are relatively easy to kill.
- It is important to maintain good hygiene and daily cleaning of skin with warm water to avoid
secondary bacterial infection. Scratching may also increase the risk of secondary infection.
 Vaccine
- Protection is not life long and further vaccination is necessary five years after the initial immunization.
- The chickenpox vaccine is not part of the routine childhood vaccination schedule
- Vaccine is currently only offered to people who are particularly vulnerable to chickenpox.
 Patients are frequently asked to cut their nails short or to wear gloves to prevent scratching and to
minimize the risk of secondary infections.
 As a protective measure, patients are usually required to stay at home while they are infectious to
avoid spreading the disease to others.
Treatment
- Strict isolation until all vesicles and most of the scabs disappear
- Varicella treatment mainly consists of easing the symptoms as there is no actual cure of the condition.

- Local or systemic antipruritics – e.g. Calamine lotion, diphenhyramine, cool sponge bath with baking
soda.
- Anlgesic – acetaminophen
- Antibiotics – can only be used in case of infection
- Vidarabin may slow versicle formation, spread skin healing and control systemic spreadof infection.
- Staying in a cold surrounding can help in easing the itching as heat and sweat makes it worse.
- a topical barrier preparation containing zinc oxide
- Natural chicken pox remedies include pea water, baking soda, vitamin E oil, honey, herbal tea or carrot
and coriander.
- A varicella vaccine is available for people who have been exposed to the virus, but have not experienced
symptoms. The vaccine is more effective if administered within three days and up to five days after
exposure. It has been shown that the chicken pox vaccine may prevent or reduce the symptoms in 90%
of cases, if given within three days after exposure.
- People who have been exposed to the virus but who are contraindicated to receive the vaccine, there is
a medication available, called varicella zoster immunoglobulin or VZIG which may prevent or reduce the
symptoms after exposure.
- Antiviral drugs (Acyclovir) and corticosteroids (Predinisolone) – these are contraindicated in immune
compromised patients.
Complications
- The most common late complication of chicken pox is shingles, caused by reactivation of the varicella
zoster virus decades after the initial episode of chickenpox.
- Infection, scaring, impertigo, furuncles and cellulitis resulting fro scratching due to severe prurtis
- Rerye’ssyndrome
- Pneumonia
- Myocarditis
- Bleeding disorders
- Arthritis
- Nephritis
- Hepatitis
- Acute myositis
 Congenital varicella causes hypoplastic deformity and limb scarring, retarded growth, CNS and eye
problens.
Information, education and communication
- Teach the patient and relatives on howto apply topical antipruritics
- Stress the importance of good hygiene and keeping short nails

- Tell the patient or care taker not to scratch the lessions since this may be overwelming.
- Educate the patient and relatives on the complications and inform them to report any complications.
- Addvise the patient or relatives not to use aspirin because of the risk of Reye’s syndrome.
**************************************************************************************
ASPHYXIA NEONATORUM
DEFINITION: Asphyxia neonatorum is a condition in which a new born fails to initiate or sustain respiration
after delivery.
 Asphyxia Neonatorum is a neonatal emergency as it may lead to hypoxia and possible brain damage or
death if not correctly managed.
CAUSES
DURING THE ANTENATAL PERIOD
1. MATERNAL CAUSES
1.1 Hypoxia - lack of oxygen in the maternal circulation and may be due to:
- Severe anemia
- Severe cardiac disease
- Respiratory disease: for example, tuberculosis, pneumonia, and asthma
1.2 A reduction in uterine blood flow due to vaso –constriction
 This may be due to:
 Aorto- caval compression and supine hypotensive syndrome.
 Severe hypertension.
 Ante partum hemorrhage: placenta abruption.
 Eclamptic convulsions.
 Infections: TORCH (Toxoplasmosis, other viral infections beside these, Rubella, Cytomegalic inclusion
disease, and Herpes infection and Hepatitis).
 Diabetes mellitus.
 Prolonged pregnancy.
 Multiple pregnancies.
 Chronic nephritis.
2. PLACENTAL CAUSES
 Placental infarcts.
 Placental separation (placenta previa, placenta abruption, trauma).

3. FETAL CAUSES
 Intra- uterine growth retardation.
 Rhesus iso- immunization.
 Prematurity
 Birth trauma
4. UMBILICAL CAUSES
 Knots in the cord.
 Cord compression.
 Cord prolapsed.
 A very short cord.
5. DURING LABOUR
 The following conditions occurring during labour can give rise to fetal and neonatal asphyxia:
 Excessive analgesia or anaesthesia.
 Mal-presentations; mal-positions.
 prolonged labor
 Hypertonic uterine contractions.
 Precipitate labour, with excessively strong expulsive contractions, causing cranial distortion and
modularly center damage
6. IN THE NEONATAL PERIOD
 Breathing may be impaired at delivery by:
 Blockage of air ways by, meconium, blood, mucus and or liquor.
 Congenital abnormalities, choanal atresia (nasal passage).
 Severe diseases such as, anemia, and septicemia.
 Lung immaturity
PATHOPHYSIOLOGY OF ASPHYXIA
In order to thrive, the fetus requires energy, which it obtains from its mother. This energy is transferred
from the mother to the fetus in form of glucose and oxygen which is carried in the maternal bloodstream
and is passed to the fetus via the placenta. Some of the glucose is used for the fetus’s immediate needs and
the remainder is converted into glycogen, which is stored in the liver, the cardiac and skeletal muscles. Some
is also converted into fat which is deposited behind the scapula and around the heart.
When there is insufficient oxygen reaching the fetus due to a number of reasons, the blood pressure will
increase, there will be bradycardia, and the cardiac out put will be concentrated in the placenta, the brain
and the myocardium.
As a result, the fetal partial-pressure of oxygen (PaO2) falls and the energy required is now produced by
anaerobic metabolism, converting glycogen to glucose and resulting in an accumulation of lactic acid. This
produces metabolic acidosis. If the episode of asphyxia persist, the fetus will become hypotensive and very
acidotic. This in turn will lead to circulatory collapse and increased bradycardia, which will damage many of
the organs of the body including the brain. Accumulation of lactic acid in the brain tissue leads to cerebral
oedema and brain damage.

CLASSIFICATION OF ASPHYXIA
Asphyxia can be classified as, mild to moderate or severe, using the apgar scoring method.
 An apgar score of 7 -9 indicates mild depression.
 An apgar score of 4 to 6 indicates moderate depression.
 An apgar score of 3 or less indicates severe depression.
DIFFERENTIAN BETWEEN MODERATE AND SEVERE ASPHYXIA
MODERATE SEVERE
COLOUR Deeply cyanotic Grayish-white, lips and gums blue
RESPIRATORY EFFORT Attempt to breath No attempt to breath
MUSCLE TONE Fair to good Poor pupils dilated
REFLEX IRRITABILITY Fair to good Poor or none
HEART RATE Fairly slow 60 to 80 bpm Slow, feeble heart rate less than
40bpm.
APGAR SCORE 4 to 6 Less than 3
MANAGEMENT
Aims of management are:
1. To establish and maintain respirations.
2. To maintain an effective circulation.
3. To correct acidosis.
4. To prevent hypothermia, hypoglycemia and hemorrhage.
The neonate can survive without brain or other tissue damage for up to 20minutes of complete oxygen
deprivation. This is because of the large glycogen stores in the brain, the liver and the myocardium, which
produce energy by anaerobic glycolysis.
Therefore, the nurse should bear in mind that resuscitating a neonate should not take longer than 20
minutes. Because of this, a timer should be started as soon as the baby is born.
The initial treatment is the same whatever the degree of asphyxia:
PREPARATION FOR RESUSCTATION
This will depend on the facilities available.
 Large hospitals have sophisticated resuscitation units available in the delivery room. These consist of:
 A mobile or fixed unit with a cleanable, working surface covered by an over head radiant heater, and
having good illumination, and a clock with a second hand.
 Piped oxygen is available, supplied through a water manometer.

 The unit has a built in suction. The suction apparatus which is available via a gauge pluged into a wall is
adjusted not to exceed 200mmHg.The gauge is be set at 100mmHg for routine use.
For health facilities without resuscitative units, adequate facilities can be provided which will work just as
effective.
 A table, trolley or shelf can be adapted to serve as a resuscitative surface.
 Warm hot water-bottles can be used to provide a warm working area.
 An oxygen cylinder and a suction apparatus (mucus extractor) must be provided.
RESUSCITATION ROOM/AREA
 Any area used for resuscitating an infant must be clean, with easily washable surfaces.
 A good light must be available.
 A clock with a second hand is necessary, and must be placed well so that it is easily read by the person
busy with resuscitation.
 Any area which is to be used for resuscitative procedures must be situated away from draughts, cold air-
conditioners and open doorways.
 During the resuscitation of an infant, all doors and windows nearby should be closed and fans and air
conditioners turned off, to prevent hypothermia from occurring during the procedure.
EQUIPMENT NEEDED FOR RESUSCITATION
 All equipment must be clean and in good working order at all times.
 This must be checked by the sister –in-charge of the unit at each hand over.
 In addition to the facilities mentioned above, the following equipment must be available:
 An infant laryngoscope with a straight blades, extra batteries and light bulbs .
 Disposable neonatal endotracheal tubes 2.0mm, 2.5mm, and 3.0mm.
 Neonatal airways sizes 0;00;000.
 Endotracheal tube introducer.
 Suction catherters sizes 6,8 and 10 FG.
 A Samson neonatal resuscitator, or bag and face masks of assorted sizes.
 Syringes in various sizes 2cc, 5cc, and 10cc.
 Needles of different sizes.
 Disposable sterile umbilical catheters size 3 and 5.
 Dextrostix.
 A pair of Magill’s forceps.
 A stethoscope.
 Sterile swabs and 0.5% chlohexidine in (70%) alcohol solution.
 Pre- warmed infant blankets and towels.
 Cord clamps.
 Adhesive tape
 Drugs-
 neonatal naloxone hydrochloride(narcan) 0.02mg/ml, ampoules
 Adrenaline ampules1:10 000.

 10% dextrose water 20ml ampoules
 50% dextrose water 20ml ampoules
 Bottles containing 4% human albumin solution.
As soon as the baby is born, the Apgar score is obtained and once it is apparent that the infant requires
resuscitation, the baby is quickly removed to the resuscitation area.
The timer should be set.
-Dry the baby quickly and transfer to the resuscitation table/area. If there is no overhead radiant heater,
make sure the infant is dry and wrapped up in pre-warmed- absorbent towel. The only areas to be left
uncovered are the face and a small potion of the chest.
- lie the baby on a flat surface, with the head extended into a ‘sniffing’ position, or elevate the baby’s
shoulders on a small towel, which causes slight extension of the head and straightens the trachea.
 REMEMBER HYPEREXTENSION OF THE INFANTS HEAD AND NECK CAN CAUSE SOFT TISSUE INJURY
AND OBSTRUCTION OF THE AIR WAY.
NB: Do not hold the baby upside down as this causes a sharp rise in cerebral venous pressure and abdominal
contents put pressure on the diaphragm, impeding respirations.
 The plan of action comprises of four steps, which should be followed in sequence.
STEP 1: CLEAR THE AIR WAY
 Make sure that the airways are clear of mucus and amniotic fluid.
 Suction under direct vision- using a laryngoscope.
 Insert the suction catheter gently into first, the mouth and then along the floor of each nostril.
 Suction is applied for 15 seconds only and the catheter withdrawn.
 Use end hole catheter to minimize trauma. Always remember that if the catheter touches the posterior
pharyngeal wall, it will stimulate the vagus nerve, causing a reflex bradcardia.
 The amount of suction exerted through the catheter should not exceed 100mmHg.
 If mechanical suction is used it should not exceed 10cm of water.
 A mucus extractor (old fashioned) is very useful for this purpose, because the user can not suck too hard
and therefore cannot damage any delicate infant tissues.
 Thick meconium should be aspirated out of the trachea with normal saline through an endotracheal
tube.
 A plastic infant airway can be inserted into the infant’s mouth to maintain a patent airway.
STEP 2: ESTABLISH AND MAINTAIN RESPIRATIONS
 Stimulate the baby to cry by flicking the soles on the feet, this will stimulate regular breathing.
 A administer oxygen via face mask at 2l/minute, to improve the breathing by increasing the PO2 level,
and causing the pale or cyanosed infant to become pink.
 If after 30seconds of oxygen administration by face mask, the breathing and color are still unsatisfactory
or the infant remains apnoiec, then,
 Place a close fitting mask, which is attached to a Samson neonatal resuscitator or paediatric ambu bag,
over the infant’s face.

 Keeping the jaw forward with a finger placed under the chin, gently pump oxygen into the infant’s
mouth and nose at a rate of 50 – 60 breaths per minute.
 Make sure the flow rate of oxygen administered is no higher than 5litres per minute.
 The oxygen must pass through a water manometer set at 30cm Hg
 Oxygen should be warmed and humidified if possible. If cold dry oxygen is blown across the infant’s
face, it may result in breath holding and bradcardia, as well as hypothermia.
 Reassess the condition of the infant to ascertain if regular respirations have been established.
 If mother received pethidine within 2 to 3 hours of delivery, give naloxone hydrochloride (Narcan)
0.01mg/kg.
 Inform the doctor if the baby is not responding to treatment.
 Give sodium bicarbonate 8.4% or 4.2% solution, 2-4ml/gk body weight, by slow intravenous injection at
a rate of 1ml/minute to avoid rapid elevation of serum osmolality leading to intracranial hemorrhage.
 Vitamin k(konakion) up to 1mg is administered to reduce the risk of hemorrhage.
 If severely asphyxiated, give dexamethasone 1 – 2mg intravenously to minimize the risk of cerebral
oedema.
 If the baby fails to respond by ambu bag and mask or if bradycardia is present, prepare to intubate.
A Skilled midwife should perform the procedure.
 INTUBATION
 INDICATION FORINTUBATION
1. Severe asphyxia and a low apgar rating: below 4.
2. A heart rate below 100.
3. No response to the routine care of the baby at delivery.
TECHNIQUE FOR INTUBATION
The person intubating the infant should stand or sit at the head of the infant and proceed as follows:
 Make sure the baby is lying flat on a flat surface, with the head extended into the ‘sniffing’ position.
 Using the left hand, pick up a straight-blade infant laryngoscope and gently insert the blade into the
right side of the mouth and along the surface of the tongue.
 Advance the blade a few millimeters, passing it beneath the epiglottis, then raise the blade slightly. The
vocal cords should be exposed as the tongue and the epiglottis are moved forward.
 Apply gentle pressure on the cricoids, to obtain a clear view of the vocal cords.
 Clear any mucus, blood or meconium obstructing the trachea by gentle suctioning.
 Select the correct size endotracheal tube, with the correctly fitting introducer and holding it in the right
hand, pass it gently through the vocal cords. A gentle twist is necessary to get the tip of the tube through the
cords.
 Insert the endotracheal tube 1.5 to 2 cm below the vocal cords. The broader shoulder of the tube will
rest on the cords.
 Remove the introducer from the tube.
 Hold the tube firmly against the right corner of the mouth, while with drawing the laryngoscope blade.
 Aspirate down the tube and remove any mucus.
 Connect oxygen to the tube, via the Samson Neonatal Resuscitator or the ambu bag.

 Observe for the rise and fall of the chest wall to indicate whether the tube is in the trachea. Confirm by
inflating the lungs, and at the same time listening to the chest using a stethoscope.
 Distention of the stomach indicates that the tube is in the esophagus, remove the tube and re- insert in
the trachea.
 If only one side of the chest wall rises, it means the tube has entered the right bronchus, withdraw up to
1cm.
 If endotrachea intubation is successful, connect to Intermittent Positive Pressure (IPPV) , giving 3 to 4
puffs of oxygen at a pressure of 25-30cm of water. Pressure can be reduced to 10 -15 cm of water and
ventilation maintained at about 40-50 puffs per minute.
If bradycadia persists or the heart rate is less than 40 bpm, external cardiac massage maybe applied. Two
people can do this (one continuing with ventilation the other doing cardiac massage).
 Place both hands around the infant’s chest, with the thumbs resting on the middle third of the sternum.
The fingers of both hands support the thoracic spine and the sternum is then depressed at a rate of 100 -120
times per minute.
 This technique is the best because there is little chance of breaking the ribs or rupturing the liver.
 The other technique is to place the tips of the index and middle fingers on the middle of the third of the
sternum, which is then pressed downward for 1- 1.5cm, at a rate of 100 beats per minute.
 Care must be taken because the ribs, the sternum and the liver can all be damaged if it is incorrectly or
over-enthusiastically performed.
COMPLICATIONS OF INTUBATION
1. Pneumothorax can occur if the endotracheal tube is inserted too far into the right bronchus, and if
inflation pressures are too high.
2. Tracheal perforation can occur but is very rare.
3. Esophageal perforation may occur when force is used to insert the tube.
4. Laryngeal edema may occur after extubation and this can cause respiratory distress.
After resuscitation, the baby is admitted to neonatal intensive care unit.
SUBSQUENT CARE OF THE INFANT
OBSERVATIONS
Through out the resuscitation, procedure, the baby’s response is monitored and recorded accurately.
Take note of the time when spontaneous respirations established.
Note color of the baby, muscle tone, and respiratory effort half hourly, hourly, 2hourly, 4hourly as condition
improves.
Observe for irritation, twitching and poor muscle tone, and convulsions. These must be reported
immediately.
NUTRITION
Insert a nasogastric tube for feeding, calculating the feeds according to the weight of the baby.
Maintain 2hourly feedings, and as condition improves, graduate to cup feeding.
HYGIENE
- Top and tail can be done twice daily

- Cord care must be done two to three times a day.
- Nurse as any sick infant.
- Emphasize the importance of follow up care, due to risk of mental retardation and epilepsy.
- Importance of avoiding infections- the caretaker should bring the infant back if they suspect infection.
- Encourage the mother to breastfeeding or feeding the child to prevent hypoglycemia.
- Encourage the caretaker to keep the baby warm at all times
*************************************************************************************
MEASLES
DEF: Measles is a highly contagious infection affecting the respiratory system which is caused by paramyxo
virus from the genus mobilli virus characterized by fever, cough, blotchy red spots (maculopapular rash),
coryza and conjunctivitis.
 This is an acute highly infectious disease caused by rubella virus and it is characterized by moderately
high temperature, inflammation of the mucus membranes of the respiratory tract and macular popular
rash.
CAUSE
 Paramyxo virus
MODE OF TRANSMISSION
 Through droplet
 Direct contact with infected secretions (contact)
INCUBATION PERIOD
 7 to 14 days
 It is highly contagious 2 to 3 days before the rush is seen and remains so until the rush disappears.
SIGNS AND SYMPTOMS
 Stage one (Catarrhal Stage)
 Harking cough (deep and horsy)
 Coryza
 Conjunctivitis (red irritated conjunctiva)
 Photophobia
 Fever (39 – 40o
c)
 Anorexia
 Malaise
 Koplik’s spots
 Periobital edema

 Stage two (Eruption stage)
 Occurs from 4th
to 5th
day of infection
 Mild itchy rush appears in front and below the ears
 Within 1 to 2 days it spreads to the trunk, arms and legs
 When it fades it leaves brown discoloration of the skin
 Stage three (Post eruption stage)
 In 3 to 5 days temperature reduces, child feels much better and the remaining rush quickly fades.
DIAGNOSIS
1. History taking and clinical presentation
2. Physical examination
3. Eye swab for microscopic examination, culture and sensitivity
4. blood for IgM
5. respiratory smear to isolate viral RNA
6. saliva for specific measles IgA test
TREATMENT
o Vitamin A (6 months to 11 months 100, 000iu, 12 months to …. 200, 000iu)
o Eye irrigation with normal saline
o Eye ointment (antibiotic) to eradicate any bacterial infections
o Oral/iv antibiotics to eradicate systemic bacterial infections e.g. X-pen, Chloramphenical
o Analgesics such as Brufen to relive pain
o Cough suppressants to reduce the cough
o Anti histamines to relive itchiness and coryza
o Calamine lotion/ steroid/ant inflammatory ointment
AGE IMMEDIATELY ON DIAGNOSIS NEXT DAY
0 – 5 MONTHS 50, 000iu 50, 000iu
6 – 11 MONTHS 100, 000iu 100, 000iu
>12 MONTHS 200, 000iu 200, 000iu
* For ocular manifestations, give a 3rd dose 2-4 weeks after the 2nd dose
COMPLICATIONS
o Otitis media
o Encephalitis
o Pneumonia

o Meningitis
o Corneal ulceration
o Blindness
o Malnutrition
o Bronchitis
o Laryngo-tracheal bronchitis
o Corneal perforation
o Acute diarrhea
PREVENTION
 Immunization of children under five years at the age of (9 months)
 Quarantine of children with confirmed measles
 Giving of vitamin A supplement to children above 6 months
 Early notification of the disease in case of un out break
 Community participation in national immunization campaigns
 Early diagnosis and treatment of upper respiratory tract infections
 Increase coverage of first dose measles vaccination provided through routine immunization services
 Provide a second opportunity for measles vaccination through campaign or routine strategies
 Improve surveillance for measles disease (case-based surveillance) and monitor measles vaccine
coverage (data management and epidemiological analysis)
 Improve case management, including vitamin A supplementation and treatment of complications
 Give vitamin A
 Control fever by giving antipyretics
 Tell mothers to return for further treatment if the patient’s general condition worsens
 Treat malnutrition and diarrhea with sufficient fluids and a high quality diet
 Treat pneumonia with antibiotics
 Respiratory isolation of hospitalized cases
NUSING CARE
Aims
 To prevent complication
 To determine and treat the cause
 To promote good nutrition
 To provide education
Environment
- Humidify the room using steam
- Isolate to prevent cross infection
- Barrier nursing as the child is susceptible to infection.
- Room should be warm with high humidity

- Room should be dimly light due to photophobia.
- Use of masks, gowns and gloves
- Decontaminate all equipment used
- Labeled all linen as infectious
- Restrict visitors to prevent the spread of infection
Observations
- Observe for convulsions which may result from meningeal irritation
- Fever which may result from infection
- Feeding paten which may be altered by mouth sores and anorexia
- Itchy rush on the body
- If patient is on oxygen therapy, observe for reterorental which may result from oxygen toxicity.
- Cyanosis which may result from impaired breathing
- General reaction of the child
- Do vital signs
- Observe signs and symptoms of complication such as
o Prolonged fever
o Respiratory difficulties
o Neck stiffness
o Increased lethargy
o Pulling at the ear
Reduction of fever
- Do tepid spongy bath to reduce temperature by evaporation
- Give extra fluid or IV therapy to reduce temperature by conduction and to prevent dehydration
- Open near by windows to promote loss of temperature by convection
- Give prescribed antipyretics.
Hygiene
- Bath the baby and apply calamine lotion
- Nail care to reduce transmission of the disease
- Mouth care to promote appetite and healing of mouth sores
- Eye care to remove eye discharge (Frequent rinse the eyes with normal saline)
Psychological care
 Allow the mother by bedside
 Provide toys for emotional therapy
Rest and activity
 Plan nursing care to allow adequate resting periods.
Nutrition
 Breast feeding adequate should be encouraged

 Encourage small frequent meals
 Encourage fluid intake e.g. juice and water to prevent dehydration.
Information, Education, and Communication
 Avoid over crowding
 Drug compliancy
 Hygiene (bathing the baby)
 Nutrition to facilitate healing (High proteins and energy diet to prevent malnutrition)
 Importance of immunization
 Explain the disease process, Signs and symptoms, drug side effects, treatment, and complications.
 Educate the patient on eye care - Severe conjunctivitis may lead to cornea ulcers, blindness and cataract
****************************************************************************************
JAUNDICE
THE BILIARY TRACT (BILE FLOW)
LIVER
SPLEEN
GENERAL CIRCULATION
Glucuronyl transfarase
conjugates (joins) bilirubin
to glucuronic acid
Bilirubin bond to
receptor protein
Y or Z
Conjugated H2O
soluble bilirubin
glucuronide
Protei
n
Iron & Globin
{re-used}
Hemoglobin
RBC
s
Unconjugated fat
soluble bilirubin
Free, unconjugated bilirubin attracted to
fatty tissue, to brain, high level causes
KENICTEREUS
PORTAL VEIN

Diag.: Schematic diagram showing the conjugation of bilirubin
 The right and left hepatic ducts join to form the common hepatic duct just out side the portal
fissure.
 The hepatic duct passes downwards about 3cm where it joins an acute angle by the cystic duct from
the gall bladder.
 The cystic duct and the hepatic duct together form the common bile duct which passes down wards
behind the head of the pancreas to join by the main pancreatic duct at the hepatopancreatic ampulla.
 Hepatopancreatic sphincter controls the opening of the combined ducts in to the duodenum.
 The common bile duct is about 7.5cm and has the diameter of about 6mm.
NEONATAL JAUNDICE
 DEF: It is the excessive accumulation of bilirubin in the blood above normal levels (3 – 13umol/L or
0.3 – 1.5mg/dL) resulting from excessive destruction of red blood cells characterized by yellowish
discoloration of the skin, sclera and mucus membranes.
Type of jaundice
i) Hemolytic Jaundice/ physiological Jaundice
o This results from an increase in the destruction of red blood cells in the spleen. The amount of
bilirubin is increased and if hypoxia develops, the efficiency hepatocyte activities are reduced.
- Appears after 24 hours of life and fades by 7th
day of life
- Duration may increase in pre-term babies
Causes
 Increased read blood cell destruction
 Reduced albumin binding capacity
 Deficiency of the enzyme Glucose 6 phosphate dehydrogenese
 Increased intero-hepatic re-absorption due to lack of normal enteric bacteria that breaks down
conjugated bilirubin to urobilinogene to be excreted in urine and stecobelin to be excreted in faeces
ii) Pathological Jaundice
o Can either be conjugated or unconjugated and appears within the first 24 hours of life.
GALL BLADDER
GUT
UROBILINOGEN
REABSORBED FROM
GUT EXCRETED BY
KIDNEY, COLOR URINE
Stecobilinogen
excreted in faeces,
make them brown
Urobilin
Bacteria
ERYTHROHEPATIC CIRCULATION
Beta glucuronidase
unconjugates

Causes
 AOB incompatibility and Rh incompatibility leading to hemolysis of red blood cells
 Hematoma (birth trauma) can result to excessive bilirubin
 Congenital disorders of conjugation
 Obstruction of the biliary tract (biliary atresia)
 Infections e.g. Septicemia
PATHOPHYSIOLOGY
o When red blood cells are destroyed, the broken down products are released into the circulation (Iron
[Haem] and protein [Globin]) which are used by the body. Globin is broken down into amino acids which
are re-used by the body to make proteins, Haem is broken down into Iron which is stored or used for new
red blood cells and is converted to biliverdin and then to unconjugated bilirubin.
o Normal bilirubin is raised from the break down of the red blood cells after the normal life span. When
red blood cells are broken down, bilirubin is raised into the blood stream in a fat soluble state which is also
known as indirect or unconjugated bilirubin. During the course of circulation the bilirubin combines with the
proteins in the blood vessels especially albumin. With the help of the protein (albumin) it is then transferred
to the liver where it is converted into conjugated or water soluble bilirubin by the action of the
glucornnyltransferase enzyme and becomes capable of being excreted in urine (urobilirubinogen) and in
stool (stecobilirubinogen). From the liver conjugated bilirubin is excreted to the gall bladder through the bile
duct where it is stored as bile.
o If conjugation does not take place, it accumulates in the circulation and since it is toxic and only fat
soluble, it will be deposited in the fatty tissues of the nervous tissue especially basal ganglia which contains
high proposition of fat leading to neurological disturbances and kernicuterus.
Signs and symptoms
i. Light to bright yellow discoloration of the skin, sclera and mucus membranes
ii. Dark and concentrated urine
iii. Irritability due to involvement of the central nervous system
iv. Lethargy due to involvement of the central nervous system
v. Pruritis due to excessive accumulation of bilirubin in the blood
vi. Dark or pale stools
vii. Skin excoriation due to excessive scratching
viii. Fever in cases of infection
Diagnosis
a. History –
b. Physical examination -
c. Blood studies –
- serum bilirubin levels will be increased (normal 0.2 – 1.4mg/dL)
- Hemoglobin/haematocrit levels will be low (anemia)
- Reticulocyte count will be raised due to hemolysis
- White blood cells may be raised in case of infection
d. Combs test – Rh and AOB incompatibility

Management
Aims
 Prevent kenicterus or brain encephalopathy
 Reverse the hemolytic process by administering oxygen, vitamin K and blood transfusion
 Prevent dehydration
Drugs
 Phenobabitone - 8mg/kg daily iv or po syrup
 Antibiotics to combat infection Gentamicin 2mg/kg bd, benzyl penicillin 50mg/kg bd
 Antipyretics in case of fever
 Exchange transfusion to prevent kenicterus in infants with rapid increase in bilirubin levels
- (80mls x body weight x 2). Give 10mls in and 10mls out until the total amount goes in. give fresh blood
especially rhesus negative blood.
 Calcium gluconate 10% 1 – 2mls after ½ the amount of blood is given to prevent hypokalemia.
Side effects of exchange transfusion
 Hypokalemia
 Thrombocytopenia
 Necrotizing enterocolitis
Phototherapy
 Put the neonate on phototherapy
 During phototherapy, the baby’s skin is exposed to the fluorescent light (blue light) which will help to
convent fatty soluble bilirubin to water soluble bilirubin to be excreted in urine and stool
 Keep the baby about 45cm – 60cm from light with entire skin exposed protecting the eyes and the male
genitals.
Indications for phototherapy
a. Jaundice occurring within 12 to 24 hours
b. Serum bilirubin levels raising rapidly especially in pre-term babies
c. Infants with serum bilirubin level of 8 – 10mg/dL
d. Severe jaundice (280 – 365umol/L)
Environment
 Admit the patient in the neonate unit
Observations
 Skin rashes indicating development of photo dermatitis
 Diarrhoea – observe frequency, color and quantity of stool
 Observe for dehydration which may result from diarrhea or fever

 Observe if irritability is reducing or increasing
 Monitor the eye shield to make sure they cover the eyes, not too tight and does not occlude the nose
 Ensure that the eye shield are not too tight or causing eye discharge or weeping
 Observe for signs or hypocalcaemia e.g. irritability, jitteriness, rash, loose stools, fever and convulsions
 Monitor the levels of serum bilirubin on daily basis; these tend to be high in the first 24 hours of
phototherapy.
 Any cyanosis, grayish or pallor is noted as this can indicate treatment failure or collapse
 Inspect the umbilicus for bleeding ½ hourly in the first 2 hours then 4 hourly.
 Careful monitoring is done during exchange transfusion; observe for color of the skin and extremities,
respirations, apex beat by using ECG machine.
 Document and report and changes observed.
Nutrition
 Feed the baby to prevent hypoglycemia and hypocalcaemia
 Give 2 hourly feeds according to body weight
 Encourage breast feeding and increase fluid in case of dehydration
Position
 Frequent change of position to expose all parts of the body during photo therapy
Complications
i. Kernicterus
ii. Anemia
iii. Seizures
iv. Mental retardation
v. Brain damage
vi. Blindness
vii. Hypocalcaemia
**************************************************************************************
Neonatal Tetanus / Tetanus neoneterum
 It is an acute preventable and often fatal disease caused by an exotoxin produced by anaerobic spore
forming gram positive bacillus clostridium tetanii characterized by painful muscle rigidity primarily
involving the masseter and neck muscles.
 It is an acute exotoxin mediated systemic (sometimes local) infection caused by spore forming gram
positive bacillus clostridium tetani characterised by lock jaw (trismus), difficult sucking.
Cause
 Anaerobic spore forming gram-positive bacillus clostridium tetani

 Incubation period 3 to 4 weeks
 Transmission occurs through a puncture wound/umbilicus that is contaminated by soil, dust or
animal excreta contaminated with clostridium tetani.
Predisposing factors
- Use of contaminated razor blades to cut the umbilical cord after delivery
- Use of contaminated instruments during delivery
- Application of dirty on the umbilical stump e.g. cow dung
- Women who are not fully protected for tetanus
Pathophysiology
The infection enters through a puncture or open wound (umbilicus) in to the body and it causes local
infection and tissue necrosis. It also produces toxins that enter the blood stream and lymphatic and
eventually spreads to the central nervous system and produce clinical manifestations of the disease. When
conditions are favorable such as in dirty wounds, the organism proliferate and release a potent exotoxin
that affects the central nervous system to produce clinical manifestation of the disease. The toxins become
fixed on the nerve cells of the anterior horn of the spinal cord and the brain stem. The toxins act on the
myoneural junction to produce muscular stiffness and lower threshold for reflex excitability.
Incubation period
Three (3) to ten (10) days after exposure and varies from 3 days to 3 weeks with an average of 8 days.
Signs & Symptoms
 Trismus (risus sardonicus smile) – due to spasms of facial muscles
 Neck stiffness
 Body rigidity
 Opisthotonus – due to contraction of the muscles
 Convulsions
 Painful muscle contraction
 High sensitivity to external stimuli (noise, touch, light)
 Irritability and restlessness
 Excessive crying
 Difficult sucking which may progress to total inability to suck.
 Respiratory muscle weakness resulting in death
Management
Nursing management
Environment
- The child is admitted to neonatal intensive care unit and isolated to a side ward
- Equipment for monitoring and respiratory support such as suction machine, oxygen machine will be
within reach and in good working condition
- The environment will be maintained quest by restricting visitors, doing procedures in blocks.

- The baby will be nursed in an incubator or a warm bed cot to prevent hypothermia and a constant
environmental temperature will be maintained.
- The baby will be nursed in a dim light room with light enough for observations to prevent irritation
- The baby will be handled as little as possible
Drugs
- Sedatives or muscle relaxants e.g. diazepam, phenobabitone to reduce muscle spasms and to prevent
convulsions
- Antibiotics e.g. benzyl penicillin, gentamycin to control proliferation of vegetative forms of the organism
at the site of infection
- Tetanus toxoid to neutralize the toxins
Nutrition
- Maintain adequate fluid intake to prevent dehydration and maintain electrolyte balance
- Monitor intake and out put and record
- Insert a nasogastric tube and maintain 2 hourly feeing
- In case of laryngospasms, restrict feeding to parenteral
Position
- Place in lateral position to facilitate drainage of secretions and prevent the tongue from falling back
leading to air way obstruction
- Frequent change of position to prevent pressure sores
- Pay particular attention when handling the baby especially if tracheostomy is made
Observations
- Monitor vital signs ¼ hourly, ½ hourly in acute stage, in acute stage and 2 hourly when the condition
stabilizes
- Monitor respirations for signs of respiratory distress
- Observe for drug side effects
- Observe decrease in the muscle rigidity, convulsions, hypersensitivity reactions
- Weigh the baby weekly
Psychological care
- Explain the condition to the or care taker and the reasons for isolating the baby
- Explain all procedures done on the baby to the mother/care taker to relieve anxiety
- Allow the parent to see and feed the child if possible
- Be calm, understanding and sympathetic to both mother and the child
- Give chance to mother to verbalize her fears and answer her questions honestly
Hygiene
- Top and tail, use a sponge to avoid spasms
- Change dirty linen frequently

- Do warm compresses to relieve muscle spasms
Elimination
- Ensure the baby passing urine frequently and opening bowels regularly
- Educate the parents on the disease process, causative agent and mode of transmission
- Educate the parents on the importance of hospital delivery
- Discourage the parents on the use/application of herbs or dirty such as cow dung on the umbilical stump
- Educate the parents on the importance of immunization for children and vaccination for women of the
child bearing age
How to Prevent Neonatal Tetanus
- Two complimentary strategies
1. Clean delivery - “3 C’s”= “3 CLEANS”
* Clean hands
* Clean delivery surface
* Clean umbilical cord and stump care
2. Immunization of pregnant women and women of child bearing age with tetanus toxoid
3. Give tetanus toxoid to all children with injuries/wound, burns to provide protection and activate immune
response
4. Advice traditional birth attendants to boil delivery equipment and to use new razor blades when cutting
the umbilical cord
5. Sensitize the community on early treatment of wounds and to avoid applying tradition herbbs on the
wounds.
Laryngotracheobronchitis [LTB] (Croup)
DEF: it is a severe inflammation and obstruction of the upper airway commonly affecting children between
the age of 3 months – 3 years usually resulting from viral infections characterized by a sharp barklike cough
and hoarseness of voice.
Causes
 LTB usually results from viral infection.
- Para-influenza virus
- Adeno virus
- Rhino virus
- Entero virus
- Coxsakie virus
- Respiratory syncytial virus
- Influenza viruses type A & B
- Measles viruses

 Bacteria infection
- B. pertusis
- Diphtheria
- Mycoplasma pneumonia
 Foreign bodies
 Trauma
 Inflammation causes obstruction of the airway in different stages
 Narrowing of the subglotic airway causing obstruction of the subglotic air way and the larynx
 Narrowing of the larynx causing hoarseness of voice
 Narrowing of the bronchioles causing obstruction of the bronchiole tubes thus preventing air from
entering or exiting the lung tissue
Signs and symptoms
 History of recurrent upper respiratory tract infections
 Nasal flaring and use of accessory muscles when breathing
 A sharp barklike cough and hoarseness or muffled vocal sound.
 Inspiratory stridor and reduced /diminished breath sounds, expiratory rhonchi and scattered
crackles (on auscultation)
 Dyspnea
 Fever
 Breathing problems (occurring mostly at night)
 Restlessness and exhaustion
 Cyanosis
Stage I
- Fever, harsh brassy cough (croup cough), respiratory stridor when disturbed
Stage II
- Continuous respiratory stridor, chest in drawing (lower rib retraction), retraction of soft tissue of the
neck, labored respirations
Stage III
- Signs of anoxia and carbon dioxide retention e.g. restlessness, anxiety, pallor, sweating, rapid
respirations
Stage IV
- Intermittent cyanosis, permanent cyanosis, cessation of breathing
 Symptoms are worse in the night especially the first two nights.
Diagnosis
 History and
 Physical examination – may reveal red and inflamed epiglottis

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