Essentials of Pediatric Nursing: Mr. Ramadan Ali Hassan BSN, MPH

Essentials of
Pediatric Nursing
Prepared by:
Mr. Ramadan Ali Hassan

BSN, MPH
2018
Dedication
I dedicate this work to the soul of my father who generously dedicated his life for us.
To my dear mother that the secret of my success is her du'aa.
To the soul of Dr. Ibrahim Shamia who inspire me and spent his life to learn others
To the Palestinian people especially for martyrs who sacrificed their lives for
Palestine and Al-Aqsa.
To the nurses who spend their times in serving patients and alleviation of their
suffering.
Essentials of Pediatric Nursing 2018 1

Table of Contents
Topic Page
Chapter (1) Introduction to child health and Pediatric Nursing
Definition of pediatric nursing 6
Roles of the Pediatric Nurse 6
Health during infancy and childhood 7
Growth and development 8
Factors affecting growth and development 10
Assessment of growth 11
Growth chart 12
Vital signs measurement in pediatric 14
Development and developmental assessment 15
The hospitalized child 19
Safety Measures 20
Chapter (2) Overview of Neonatal Nursing
Adjustment to extra-uterine life 26
Methods of heat loss 28
Assessment of the newborn 32
Care of the Well Newborn 44
Chapter (3) Health problems of newborn infants
Pre-term Infant 51
Post-mature infant 55
Infant of diabetic mother 57
Septicemia Neonatorum 58
Neonatal jaundice 60
Transient Tachypnea of Newborn 66
Meconium Aspiration Syndrome 67
Congenital Diaphragmatic Hernia 68
Respiratory distress syndrome 69
Apnea in the newborn 71
Chapter (4) Child With a Respiratory Disorder
Bronchiolitis 77
Cystic fibrosis 79

Chapter (5( Child With a Cardiovascular Disorder
Fetal circulation 84
Congenital Heart Diseases 86
Dextrocardia 89
Aortic Stenosis 89
Pulmonary Stenosis 91
Coarctation of the Aorta 91
Patent Ductus Arteriosus 92
Atrial Septal Defect 93
Ventricular Septal Defect 95
Teratology of Fallot 96
Transposition of the Great Arteries 97
Tricuspid Atresia 99
Acute Rheumatic Fever 100
Chapter (6) Child With a hematological health problem
Iron deficiency anemia 106
Sickle Cell Disease 108
(G-6-P D) Deficiency Anemia 109
Thalassemia 111
Hemophilia 114
Idiopathic thrombocytopenic purpura 116
Chapter (7) Child with a Gastrointestinal health problem
Acute Gastroenteritis 120
Cleft Lip and Cleft palate 125
Gastro-esophageal Reflux 129
Esophageal Atresia and Tracheoesophageal Fistula 131
Hirschsprung Disease 133
Celiac Disease Gluten-induced Enteropathy 135
Chapter (8) Child with a genitourinary health problem
Acute Glomerulonephritis 141
Nephrotic Syndrome 143
Abnormalities Of The Genitourinary Tract 146
Chapter (9) Child with a neurologic health problem

Meningitis 149
Spina Bifida 155
Hydrocephalus 158
Cerebral Palsy (CP) 160
Seizure Disorders 163
Chapter (10) Child with genetic and nutritional health problem
Rickets 170
Down Syndrome 172
Phenylketonuria 174
Chapter (11) Child with an emergency health problem
Poisoning 178
References 187

Chapter (1)
Introduction to child health and Pediatric Nursing
Learning objectives
On completion of this chapter, the student should be able to:
 Define health, mortality, morbidity, infant mortality rate,

pediatric, pediatric nursing, growth, development
 List the major roles of pediatric nurse
 Differentiate between growth and development and gives
examples
 Describe factors that affect growth and development
 Rank the leading causes of death among children in Palestine
 Describe the normal anthropometric measurements for
newborn baby (weight, height, head circumference)
 Explain the developmental age periods
 Explain the developmental milestones for different ages
 Discuss the appropriate use of growth charts.
 Describe the methods used for assessing body temperature for

infants and children
 Explain the normal ranges for vital signs and the specific
consideration that should be taken when measuring vital signs
 Explain the child reaction for hospitalization
 Describe the safety measures that should be taken for

hospitalized children

Pediatric Nursing
Introduction:
Children are the future of our society and special gifts to the world. The overall mortality and
morbidity have decreased locally and globally but we still must focus on the children's health.
Habits and practices established in the childhood have profound effects on the health and illness
throughout life.
As a society, creating a solid health care system which promote the health of the children is
important. Pediatric nurses play a major role in this task. They are often advocating on various
issues, drawing attention to the importance of health care for children, and dealing with lack of
resources, lack of access to health care, and the focus on acute care rather than education and
disease prevention.
Pediatrics is the branch of medicine that deals specifically with children, their development,
childhood diseases, and the treatment of such diseases.
Pediatric nursing is the practice of nursing involved in the health care of children from infancy
through adolescence. In developed countries child health extended up to adolescence but in
developing countries including Palestine child care extended up to 10-12 years of age.
Roles of the Pediatric Nurse
1) Family advocacy
 The advocate nurse has the goal of ensuring that families are aware of all available health
services, informed adequately of treatments and procedures, involved in the child’s care
when possible, and encouraged to change or support existing health care practices.
2) Health teaching
 Health teaching may be a direct goal of the nurse, such as during parenting classes, or may be
indirect, such as informing parents and children of a diagnosis or medical treatment,
encouraging children to ask questions about their bodies, referring families to health-related
professional or play groups, and supplying patients with a appropriate literature.
3) Support /Counseling
 Counseling involve a mutual exchange of ideas and opinions that provides the basis for
mutual problem solving.
4) Therapeutic role
 Nurses are involved with meeting the physical and emotional needs of children, including
feeding, bathing, toileting, dressing, security, and socialization.
5) Coordination/Collaboration

 The nurse, as a member of the health team, collaborates and coordinates nursing services
with the activities of other professionals in order to provide high quality health services.
For example: coordinate with the dietitian, physiotherapist, the physician, psychologist etc.
6) Health care planning
 The nurse must involve herself in policy and decision making on the community and
national level to enhance health care delivery to benefit all children.
7) Disease prevention/health promotion:
 The emerging trends toward health care have been prevention of disease and maintenance
of health rather than treatment of disease or disability.
 The best approach to prevention is education and anticipatory guidance.
8) Research:
 Nurses need to be more involved in research and in applying research findings to their
practice (evidence based practice).
Measurement of Children's Health Status
 Health as defined by the world health organization (WHO) is a state of complete physical,
mental and social well-being and not merely the absence of disease or deformity.
 One method of assessing the health of children within a country is to observe the rates of
mortality (deaths) and morbidity (illness) over a period of time.
 Mortality is the number of individuals who have died over a specific period.
 Infant Mortality Rate:
Is a number of deaths per 1000 live births during the first year of life.
Infant mortality rate (IMR) = No. of infant deaths during a specific year X1000
No. of live births in same year
 Neonatal mortality rate: number of deaths per 1000 live births during neonatal period
(the first 28 days of life).
Neonatal mortality rate = No. of death infants younger than 28days of age in a year X1000
 Post-neonatal mortality rate: number of deaths per 1000 live births during Post-
neonatal period (29 day to 1 year).
Post neonatal mortality rate = No. of death infants at age (29 days – 1 year) in a year X1000
In Palestine
 The infant mortality rate is used as an index of the general health of a country. Generally,
this statistic is one of the most significant measures of children's health.

 Infant mortality rates in Palestine have decreased slowly over the last two decades.
 Reported infant mortality rate in Palestine in 2017 was 10.7 per 1,000 live births. In
2016, the infant mortality rate was 10.5 per 1,000 live births and in 2015 were 10.9 per
1000 live births.
According to MOH 2016, Major causes of infant mortality in Palestine were ranked as:
1. Congenital anomalies (22.3%)
2. Respiratory problems (18.1%) Preterm birth is the
3. Prematurity and low birth weight (16.8%) leading cause of
newborn deaths
4. Heart diseases (10.4%)
worldwide
5. Sudden infant death syndrome (7.5%)
6. Septicemia (7%)
7. Malnutrition and metabolic diseases (1.3%)
8. Cerebral Palsy (1.2%)
9. Other accidents (1%)
10. Malignant neoplasm (0.5%)
Childhood Mortality:
After 1 year of age there is a dramatic change in causes of death with injuries (accidents) being
the leading cause during childhood "injuries is the leading killer". They include:
1. Motor vehicle 2. Drowning 3. Fire and burns
4. Ingestion of food/object 5. Mechanical suffocation 6. Falls
7. Poisoning
Morbidity:
 Is the prevalence of specific illness in the population at a particular time.
 Unlike mortality statistics, morbidity is often difficult to define and record because the
definitions used vary widely. For example, morbidity may be defined as visits to the
physician or diagnosis for hospital admission. Also, data may be difficult to obtain.
Growth and development

Growth:

 The natural increase in body size as well as sizes of different body organs. It is quantitative
change and can be measured in cm. or kg.
Development:
 Maturation of organs and systems, gaining of skills and ability of adaptation and assuming
responsibilities.
 It is qualitative change that cannot be weighed or measured in cm, or kg.
 It can be observed.
 Development is a continuous process from conception to maturity, Examples are:
o Child sits before standing.
o Stand before walking.
o Learn alphabet before wards.
o Rate of development, varies with each child.
Developmental Age Period
1. Prenatal period: From conception to birth, divided into:

a) Germinal: conception to approximately 2-3 weeks .
b) Embryonic: From 3 - 8 weeks.
c) Fetal: From 8 - 40 weeks (birth).
2. Infancy period: From birth to 12 months.
a) Neonatal: From birth to 28 days. The most critical period in the whole life.
۞ The main problems: prematurity, birth injuries, congenital anomalies and
infections.
b) Post-neonatal (Infancy): From 29 days to 12 months. The period of most rapid
physical growth and mental development.
۞ The main problems: infectious diseases and nutritional disorders.
3. Early childhood: From 1 to 6 years.
a) Toddler: 1 to 3 years.
b) Preschooler: 3 to 6 years.
۞ The main problems: accidents, nutritional disorders and infections.
4. Middle childhood: 6 to 12 years. (School age).
۞ The main problems: Accidents, Infections, Rheumatic fever , Malignancies as
leukemia and lymphoma, Psychological and emotional problems
5. Later childhood: 12 to 18 years. The period of passage from childhood to adulthood.
a) Pre-pubertal period: 11 to 13 years.

b) Adolescence: From13 to approximately 18 years.
۞ The main problems: Psychological, Rheumatic fever, Malignancies Diabetes
mellitus, Accidents, and Sex hormone related problems.
Factors affecting growth and development
1) Genetic factors:
 Parental size has a direct influence on a child’s growth potential and their predicted
adult height; more so for height than weight.
 Some genetic disorders affects growth and development e.g. achondroplasia (an
inherited skeletal disorder characterized by impairment in the formation of cartilage
at the epiphyses of long bone and cartilage is converted to bone resulting in
dwarfism)
2) Endocrinal factors: the growth hormone, thyroid hormone and sex hormones are
essential for normal growth and development. Congenital hypothyroidism is a good
example for delayed growth and development.
3) Environmental factors: as health of the mother during pregnancy and socioeconomic
status of the family.
4) Nutritional factors : poor feeding, lack of vitamins and trace elements and so on affect
the growth and development.
5) Congenital anomalies : as congenital heart disease.
6) Chronic diseases as tuberculosis.
7) Activities : a bed ridden child will not grow normally.

Assessment of Growth
Anthropometric measurements (Weight, Height, Head circumference, Chest circumference)

1: Weight:
 The average weight at birth = 3.5 Kg (2.7-4.2 kg)
 There is an initial period of loss of weight in the first 3-4 days due to redistribution of
body fluids with loss of extra-fluid in the extracellular fluid compartment.
 Most of the full term infants regain their birth weight by the age of 10 days.
 Then, during the first year of life the body weight increases as follows:
۞ 3/4 kg every month in the first 4 months (i.e. 3 kg in 4 months).
۞ 1/2 kg every month in the second 4 months (i.e. 2 kg in 4 months).
۞ 1/4 kg every month in the third 4 months (i.e. 1 kg in 4 months).
 After the first year, the average weight of a child can be calculated by the following
formula:
 Between 3-12 months:  Weight is doubled at 4
months and tripled at 12
Weight in kg = (Age in months) + 9
2 months.
 Between 1-6 years: 2 kg/y  Height is doubled at 4 years
Weight in kg = (Age in years x 2) + 8 and tripled at 12 years.
 Between 7-12 years: 2.5 kg/y
Weight in kg = (Age in years x 7) – 5

2
2. Length or height:
The length is measured in the recumbent position below the age of 2 years while the height is
measured in the standing position usually after the age of 2 years.
 The average length at birth = 50 cm (45-55 cm).
 During the first year of life, the length increases as follows :
۞ 3 cm every month in the first 3 months.
۞ 2 cm every month between the 3rd and 6th month.
۞ 1.5 cm every month from the 6th -12th months of age.
 In the second year of life, the average length increases 1 cm/month.
 After 2 years, the average length is calculated by the following formula
Length in cm = Age in years x 5 + 80

3. Head circumference:
The size of the skull depends on the growth of the brain. If the brain does not grow adequately,
the skull will be small (microcephaly).
۞ At birth the average HC = 35 cm (32.5-37.5)
۞ During the 1st year, the average increase in HC = 2 cm/month in 1st 3 months then
0.5 cm/month in next 9 months.
Average head circumference (cm)
Age HC Age HC
Birth 35 3 years 49
3 months 41 5 years 50
1 year 47 Adult 55
NB: Head circumference increases 12 cm during the first year and only 6 cm during the next 11
years. This demonstrates the importance of brain growth in the first year.
4. Chest circumference
It is usually measured in mid-respiration at the level of the xiphoid. It is usually related to head.
۞ At birth: The head is larger by 2 cm.
۞ Between 1-2 years: both are equal
۞ After 2 years: the chest is larger than the head.
Anthropometric Measurements at Birth
Average Range
Weight 3.5 kg 2.7-4.2 kg
Length 50 cm 45-55 cm
H.C. 35 cm 32.5-37.5
Growth Charts
 A growth chart is used to follow a child's growth over time.

 Growth charts are different for boys and girls because they grow in different patterns and at
different rates specially in puberty so it is important to select the growth chart to use based on
the age and gender of the child
 The anthropometric measurements (weight, length, head and chest circumferences) are plotted
on the charts and by follow up a line can be drawn which represents the rate or velocity of
increase in the anthropometric measurement.
 Any deviation of this curve is used for early detection of abnormal growth, thus growth charts
can help in early diagnosis of conditions as short stature, over/underweight or hydrocephalus

 There are wide range of normal variations among infants and children of the same
chronological age. These normal differences are described in term of percentile
 These percentiles are (5th, 10th, 25th, 50th, 75th, 90th, and 95th percentile) where 50th percentile
represents the average and indicates that 50% of the normal children are below this value.
25th, 10th, and 5th percentiles are low normal values while 75th, 90th and 95th are high normal
values.
 Values below 5th and above 95th are abnormal.
 A child falls on the 25th percentile means that this child weighs more than 25% of other
children of the same age but less than 75% of them.
Abnormalities in physical growth:
Below 5th percentile Above 95th percentile
Weight Underweight Overweight
Length or height Short stature Tall stature
Head circumference Small head Large head

Assessment of Vital Signs in Pediatric
Temperature:
 Never leave the child alone when taking his temperature.
 For security, safety and accuracy, keep one hand on the thermometer when it is in place.
 Oral and rectal routes should not be routinely used to measure the body temperature in
children aged from birth to five years.
Respiration:
 Count respiration on an infant for one full minute.
 Respiration may be counted for 30 seconds and multiply by 2 in the older children.
 Observe chest movements as well as abdominal movements.
 Obtain respiratory rate prior to taking temperature and pulse, since the child may cry
during these procedures.
 Determine if respiration is predominantly costal or abdominal.
 Dyspnea should be suspected in a school-age child who is breathing primarily with
abdomen.
 Listen for unusual noises such as expiratory grunting, wheezing or inspiratory stridor.
Pulse:
 Take apical rate of an infant, place stethoscope between left nipple and sternum, and take
heart rate for one full minute.
 With an older child, the pulse rate may be obtained easily at the radial, temporal or
carotid locations. Pulse may be taken for 30 seconds and multiplied by 2.
 Take pulse prior to taking temperature because child may cry when temperature is taken
and elevates pulse rate and makes it more difficult to hear the apical rate.
 Record accurately the following: rate, rhythm (regular or irregular); strength of beat and
activity of child at time pulse is taken (sleepy, crying).
Blood pressure:
 The cuff should be of sufficient size to ensure overlap to cover 100% of the
circumference of the arm and no less than half and no more than 2/3 of length of upper
arm or lower leg .
 The bladder within the cuff must cover 80% of the arm’s circumference and should be
positioned over the artery from which the blood pressure will be taken.
 Cuff that is too narrow will produce an apparent increase in BP.
 Cuff that is too wide will produce an apparent decrease in BP.
 If the child is excited or uncomfortable or if he distrusts the person taking the BP, systolic
pressure may rise significantly.

o Mean diastolic = 55+ age in years
o Mean systolic = 90 + age in years
Normal heart and respiratory rates and blood pressure by age
Age Respiratory Rate Heart Rate Blood pressure

Newborns 40 (35-45) 120 (90-150) 80/50
Infants 30 (25-35) 110 (80-140) 80/50
Young children 25 (20-30) 100 (80-120) 85/55
Old children 20 (15-25) 80 (70-100) 90/60
NB: Each degree rise in body temperature increases the respiratory rate about 5 breath/minute
and heart rate about 10 beats/minute.
Pulse oximetry
 A pulse oximeter machine measures the amount of oxygen saturation in the blood using
infrared light giving the percentage of the hemoglobin that is oxygenated.
 Normal children should have a saturation of at least 96% . Levels of less than 94% imply
significant illness. Levels below 90% are alarming.
 Be cautious with monitoring as movement, skin temperature and probe placement can be
factors affecting accuracy.

Development and developmental assessment
 Development is intimately related to the maturation of the nervous system.

 It is an important indicator of a child’s wellbeing, and delay or abnormal development
may indicate serious limitations for later life. Advanced development of language and
fine motor skills may be a sign of intelligence.
 Parents are always interested in their child’s developmental progress and are usually
concerned if any aspect is delayed.
Milestones that are essential to remember
Age Milestone
4–6 weeks Smiles responsively
6–7 months Sits unsupported
9 months Gets to a sitting position
10 months Pincer grasp
12 months Walks unsupported
Two or three words
18 months Tower of three or four cubes
24 months Two to three word sentences
Gross motor development: 1. Prone position 2. Pull to sit 3. Sitting 4. Standing & walking

Standing and walking
Fine motor development: 1. Grasping and reaching 2. Building bricks 3. Manipulation 4. Pencil skills

The hospitalized child
 Hospitalization is often confusing, complex and overwhelming for children and their
families.
Children’s Reactions to Hospitalization
1) Anxiety and fear: which may resulted from: hospital situation, fear of injury, or
bodily mutilation, separation from family or friends, changes in routines, painful
procedures and treatment and unfamiliar events and surrounding.
2) Separation anxiety: which resulted from removal from family and familiar
surroundings.
3) Feeling of anger and guilt
4) Regression: return to previous stage of development
5) Resistance and violence
The nurse’s role in caring for hospitalized child :

The nurse is probably the first one to see the child and family and will spend more time with
them than other health care personnel.
Essential Nursing Roles in Caring with Hospitalized Children:
1. Enhance the child self-dependence, thus helping him develop confidence and trust
2. Incorporate aspects of child's routine at home such as toilets habits, dietary habits,
friends and peers and use terms similar to those used at home
3. Attempt to maintain home ties to meet psychological needs of the child by:
 Have family photograph at the child bedsides.
 Encourage use of telephone.
 Talk about the people at home.
 For the adolescent, assign roommate of same age.
4. Explanations of treatment plan and preparation for tests, procedure and surgery is
essential.
 Listen to him carefully.
 Correct misinformation.
 Avoid use of terminology (may increase stress).
 Include parents in preparation process.
5. Orient child and family to the unit and the child’s room to familiarize them with the
facility.

6. Explain all events, treatments, procedures, and activities to the parents and child (at a
level the child can understand) in a calm, relaxed manner to help the child prepare for
what is to come and decrease fear of the unknown.
7. Encourage parents to room-in if possible to provide the child with support; if parents
cannot stay, encourage them to call to reduce child’s fear of being alone.
8. Urge parents to inform the child when they will be leaving and when they are expected to
return to help child cope with their absence and promote trust.
9. Offer comfort measures such as holding, stroking, and rocking to relieve distress.
10. Encourage the child to play (unstructured and therapeutic play as necessary) to allow for
expression of feelings and fears and promote energy expenditure.
11. Suggest that parents bring in a special toy or object from home to promote feelings of
security.
12. Provide positive reinforcement for participation in care activities to foster self-esteem.
13. Allow the child to project his fears to help him cope with an unpleasant experience
Safety Measures for hospitalized child
Accidents are a leading cause of death among infants and small children. Great emphasis should
be placed on the prevention of accidents in the hospital. The following discussion is concerned
briefly with accidents in the hospital, but certain of these also occur at home. Many safety
measures deal with construction of the building or unit and are beyond the control of the
nurse, among these are the following:
1. Fire proof, wide good-lighted stairways.
2. Windows protected by locked screens and window guards.
3. Gates at the entrance to rooms where small children play so constructed that a child can
not open it, or catch his fingers between the door and its frame.
Other measure for children safety which are directly under the nurse's control are as
follows:
1. Bedside rails should be in good condition, when giving care with side rail down, the nurse
should keep one hand on the infant or small child to prevent his falling specially on looking
away from him.
2. Restraints if used should be applied correctly to prevent constriction of any part of the
child's body.
3. Medicine cabinets should be locked when not in use and medications should never be left
standing on bed side table.

4. Instruments and solutions should be kept in cabinets or on shelves where children can not
reach it.
5. Toys should have rounded rather than sharp edges, they should never be painted with
lead paint and should not have small parts, which a child can remove and swallow or
aspirate.
6. Wet areas on the floor should be dried immediately.
7. Electronic outlets and fans should be covered when not in use and fans should be placed
out reach of children.
8. Facilities should be provided to perform isolation techniques for all children with infectious
illness.
9. Nursing bottles should never be propped, nor should feedings be forced upon a little child,
there is a danger of aspiration which may cause pulmonary disease or even sudden death.
10. In giving medication to an infant or a little child who will not cooperate, a second nurse is
required to assist in gentle restrain, oral medication should not be given to a child who is
crying because of the danger of aspiration.
11. Hot water bottles must always be tightly stoppered and covered before being placed near a
child's body or even in the bed with him. The water temperature should not be over 46 oC.
12. The bulb of thermometer should be checked not to be cracked.

Review question
Answer the following questions

1. ……………………. Is branch of medicine that deals specifically with children, their
development, childhood diseases, and the treatment of such diseases.
2. ……………………. is the practice of nursing involved in the health care of children from
infancy through adolescence.
3. Roles of the Pediatric Nurse:
1. …………………………………. 2. ………………………..3. …………………..................
4. ………………………………… 5. ………………………..6. ………………………………
7 ………………………………………… 8. ………………………………………………….
4. ………………………….. a state of complete physical, mental and social well-being and not
merely the absence of disease or deformity.
5………………………… Is a number of deaths per 1000 live births during the first year of life.
6. ………………………… number of deaths per 1000 live births during neonatal period (the
first 28 days of life).
7. ……………………….. number of deaths per 1000 live births during Post-neonatal period
(29 day to 1 year).
8. …………………………. The natural increase in body size as well as sizes of different
organs.
9. …………………………. Maturation of organs and systems, gaining of skills and ability of
adaptation and assuming responsibilities.
10. Factors affecting growth and development:
11. During the first year of life the body weight increases as follows:
…………. kg every month in the first 4 months
………… kg every month in the second 4 months
………... kg every month in the third 4 months
12. An infant's age is 5 month, you expect that his weight will be ………………kg and
length ……………….cm. At 5 years, his weight will be approximately …………….kg and
length ……………..cm.
13. During the 1st year, the average increase in HC = ……….. cm/month in 1st 3 months then
……….. cm/month in next 9 months.
14. ………………….. is used to follow a child's growth over time.

15. A child's weight below the 5th percentile is considered …………………. While above
90th percentile is ………………………
16. Each degree rise in body temperature increases the respiratory rate about…………
breath/minute and heart rate about …………… beats/minute.
17.
Newborn measurement Average Range
Weight
Length
Head circumference
Chest circumference
18.
Age Milestone
4-6 weeks
6-7 months
9 months
10 months
12 months
18 months
24 months

Chapter (2)
Overview of Neonatal Nursing
Learning objectives
 Explain the neonatal adjustment to extrauterine life

 Identify the principal cardiorespiratory changes that occur during
transition to extrauterine life.
 Describe the stimuli that help the newborn to initiate the first
breathing
 Differentiate between fetal and adult circulation
 Explain methods of heat loss and the appropriate ways to prevent
heat loss
 Identify the immature physiologic functioning of each body system
and its significance to nursing care of the newborn.
 Perform an initial and transitional assessment of the newborn
including the Apgar score and gestational age assessment.
 Perform a newborn physical assessment based on recognition of
expected normal findings.
 Classify the newborn according to gestational age, birth weight,
and according to gestational age and birth weight.
 Differentiate between normal and pathological findings during
newborn assessment
 Describe Immediate care of the newborn at delivery room
 Describe the routine care of the newborn

Neonatal Adaptation to Extra-uterine Life
o The neonatal period (the first 28 days of life) is a highly vulnerable period during which many
of physiologic adjustments required for extra-uterine existence are completed.
o An infant’s transition from intrauterine to extra-uterine life requires many biochemical and
physiologic changes (Table 1).
Table (1): Comparison between fetal and neonatal physiological adjustments
Comparison Fetus Newborn
Respiratory system o Fluid-filled o Air-filled
o High-pressure system causes o Low-pressure system encourages blood
blood to be shunted from the flow through the lungs for gas exchange
lungs through the ductus o Increased oxygen content of blood in the
arteriosus to aorta lungs contributes to the closing of the
ductus arteriosus (becomes a ligament).
Site of gas exchange Placenta Lung
Circulation through Pressure in the right atrium is Pressures in the left atrium are greater than
the heart greater than in the left, encouraging in the right, causing the foreman ovale to
blood flow through the foreman close.
ovale.
Hepatic portal Ductus venosus bypasses; maternal Ductus venosus closes (becomes a
circulation liver performs filtering functions ligament); hepatic portal circulation begins.
Thermoregulation Body temp. is maintained by Body temperature is maintained through a
maternal body temp. & the warmth flexed posture and SC.fat.
of intrauterine environment.
Physiologic Adaptations
The mechanics of birth require a change in the newborn for survival outside the uterus.
Immediately, respiratory gas exchange, along with circulatory modifications, must occur to
sustain extra-uterine life. During this time, as newborns strive to attain homeostasis, they also
experience complex changes in major organ systems. Although the transition usually takes place
within the first 6 to 10 hours of life, many adaptations take weeks to attain full maturity.
Cardiovascular System Adaptations
 Successful transition from fetal to postnatal circulation requires removal of the placenta,
increased pulmonary blood flow, and closure of the intra-cardiac (foramen ovale) and
extra-cardiac shunts (ductus venosus and ductus arteriosus).
 Once the lungs are expanded, the inspired air dilates the pulmonary vessel leads to
increase pulmonary blood flow.
 The most important factor controlling ductal closure is the increased oxygen
concentration of the blood, secondary factors are the fall in endogenous
prostaglandin's and acidosis.

Respiratory System Adaptation:
Stimuli that help initiate the first respiration:
1. Chemical factors: ↓02, ↑C02, ↓ pH → stimulate respiration by stimulating the aortic and
carotid chemoreceptors initiating impulses that trigger the medulla's respiratory center.
2. Thermal stimuli: There is a significant decrease in environmental temperature after birth
from 37oC to 21oC -24oC. The cold stimulates skin nerve endings that are initiating impulses
that trigger the respiratory center and the newborn responds with rhythmic respirations.
3. Mechanical factor: After passage of fetus in birth canal and squeezing the fetal lung fluid,
the newborn's chest wall recoils creating a negative intra-thoracic pressure which is thought
to produce a small passive inspiration of air that replaces that fluid that is squeezed out.
4. Sensory stimuli: Tactile, auditory, visual stimuli (Intrauterine Life....dark, sound-
dampened, fluid-filled environment that is nearly weightless. After birth.....light, sounds,
and the effects of gravity for the first time.
5. Re-absorptive changes: Most of the lung fluid is reabsorbed within 2 hours after birth and
is completely absorbed within 12 to 24 hours after birth.

Thermoregulation:
o Neonates and, in particular, premature neonates are at high risk of heat loss and subsequent
hypothermia due to the following factors:
1. Large body surface area relative to body weight. Newborns compensate the large surface
area by flexion position
2. Lack of subcutaneous fat, which provides insulation
3. Immature heat regulation center in the hypothalamus.
4. Inability of neonates to generate heat by shivering until 3 months of age.
5. Thin skin with blood vessels close to the surface
o Hypothermic preterm babies have a poor outcome in the intensive care setting and therefore
body temperature must be aggressively regulated.
Methods of Heat Loss
1. Evaporation
When wet surfaces are exposed to the air evaporation occurs. Heat is lost when the surface dries.
At birth the neonate is bathed with amniotic fluid. As the amniotic fluid dries up on the infant’s
skin (evaporation), the infant loses heat. The same occurs in bathing an infant.
Ways to prevent heat loss by evaporation:
1. Drying the infant as quickly as possible after birth.
2. Drying the infant immediately after bathing.
2. Conduction
When heat is transferred to cooler objects that are in direct contact with infant, heat loss by
conduction occurs. For example when an infant is placed on a cooler surface or touching them
with a cool object or hands.
Ways to prevent heat loss by conduction:
1. Warming the objects that will touch an infant.
2. Placing an infant against the mother’s skin helps prevent conductive heat loss.
3. Radiation
When heat is transferred to cooler objects that are not in direct contact with the neonate , heat
loss by radiation occurs. When infants are placed near cold windows or walls heat is lost by
radiation. Even neonates placed in incubators losses heat to the walls of the incubator if it is cold
even if the surrounding air temperature is warm.
Ways to prevent heat loss by radiation:
1. Incubators must have double walls.
2. Cribs and incubators should be placed away from the walls and windows.
4. Convection
When heat is transferred to the air surrounding the infant heat loss by convection takes place. If
an air conditioner is kept on or when people move around near the infant increase loss of heat
occurs.
Ways to prevent heat loss by convection:
1. Keeping the newborn out of drafts.
2. Maintaining warm environmental temperature.
3. Keeping a preterm neonate in an incubator.

Hepatic System Function
At birth, the newborn’s liver assumes the functions that the placenta handled during fetal life.
The liver is the most immature of the GI organs, which affect the followings:
1. Conjugation of bilirubin with glucourinic acid leading to physiological jaundice.

2. The liver is deficient in forming plasma protein which leading to edema.
3. Deficiency of Prothrombin, and other coagulation factors especially the vitamin K-
dependent clotting factors (II, VII, IX, X) leading to bleeding.
4. Store less glycogen at birth leading to hypoglycemia, which can be relieved by
feeding.
Breast milk is a relatively poor source of vitamin K

and endogenous synthesis by the GI flora is not Liver immaturity
established for the first few weeks after birth. leads to:
Therefore, vitamin K prophylaxis is administered to 1) Jaundice
2) Edema
all newborn babies to protect against hemorrhagic
3) Bleeding
disease of the newborn until normal levels of vitamin 4) Hypoglycemia
K are synthesized.
Gastrointestinal System Adaptations

o The full-term newborn has the capacity to swallow, digest, metabolize, and absorb food
taken in soon after birth.
o Stomach capacity: at birth is 30 -60 ml, 90 - 130 ml at one month of age with a variable
emptying time of 2 to 4 hours.
Bowel Elimination
o The frequency, consistency, and type of stool passed by newborns vary widely.
o The evolution of a stool pattern begins with a newborn’s first stool, which is meconium.
Hematology.
o Neonatal blood contains both adult (HbA) and fetal hemoglobin (HbF). Fetal hemoglobin
(HbF) makes 80% of the total Hb at birth.
o (HbF) has a greater affinity for oxygen but has lower life span than HbA.
o A combination of low levels of erythropoietin due to improved tissue oxygenation after
birth, decreased lifespan of (Hb F) leading to the physiological anemia of infancy which
usually occurs at around 8-10 weeks of age.
o Hematopoiesis occurs in the liver in uterus but is restricted to bone marrow from 6 weeks
post-delivery, thus limiting potential sites for hemoglobin synthesis.

o White cells: higher at birth, fall over 2-3 weeks then rise again.
Renal system
 The majority of term newborns void immediately after birth, indicating adequate renal
function. The first voiding should occur within the first 24 hour
o Although the newborn’s kidneys can produce urine, they are limited in their ability to
concentrate it until about 3 months of age, when the kidneys mature.
o About six to eight voidings daily is average for most newborns; this indicates adequate
fluid intake
Musculoskeletal system:
 At birth the skeletal system contain larger amount of cartilage than have ossified bone
 The muscular system is almost completely formed at birth.
Immunology:
 The first line of defense against infections is the skin and mucus membrane.
 The second line is the cellular elements, which produce several type of cells capable of
attacking a pathogen e.g. neutrophils, monocytes and lymphocytes.
 The third line is the formation of specific antibodies to an antigen, this process requires
exposure to foreign agent. Newborn receive antibodies from mother (IgG) and not
capable to produce antibodies till the age of 2 months.
 Placenta can pass Ig G only, mainly in last trimester of pregnancy. IgM are synthesized
in fetal blood in response to infection.
Endocrine system
 Limited quantities of ADH, so the infant is susceptible to dehydration.
 The effect of maternal sex hormones leading to breast engorgement and production of
milk from the first few days until 2 months of age.
 The female newborn may has pseudo-menorrhea.
Neurologic System Adaptations
The newborn’s sensory capabilities include:
o Hearing—well developed at birth, responds to noise by turning to sound
o Taste—ability to distinguish between sweet and sour by 72 hours old
o Smell—ability to distinguish between mother’s breast milk and breast milk from others
o Touch—sensitivity to pain, responds to tactile stimuli
o Vision—ability to focus on objects only in close proximity (7–12 inches away); tracks
objects in midline or beyond (90 inches); this is the least mature sense at birth.

Assessment of the newborn
(1) Initial assessment: Examination at Birth

۞ Examination in the delivery room should not be extensive and consist largely of:
o Observation & inspection for congenital anomalies and birth trauma
o Auscultation of the chest
۞ During the initial newborn assessment, look for signs that might indicate a problem in
which medical intervention may be necessary. These signs include:
• Nasal flaring • Chest retractions • Grunting on exhalation
• Labored breathing • Generalized cyanosis
• Abnormal breath sounds: crackles, wheezing, stridor
• Abnormal respiratory rates (tachypnea (↑60 breaths/minute) bradypnea↓25 /minute)
• Flaccid body posture • Abnormal newborn size: small or large for gestational age
• Abnormal heart rates (tachycardia (↑160 bpm); bradycardia (↓100 bpm)
۞ The number of umbilical cord vessels should be determined. Normally, there are two
arteries and one vein.
۞ The APGAR score should be recorded at 1 and 5 minutes of age.
APGAR Score
o The Apgar score, introduced in 1952 by Dr. Virginia Apgar, is used to evaluate
newborns at 1 minute and 5 minutes after birth. An additional Apgar assessment is done
at 10 minutes if the 5-minute score is less than 7 points.
o Assessment of the newborn at 1 minute provides data about the newborn’s initial
adaptation to extrauterine life.
o Assessment at 5 minutes provides a clearer indication of the newborn’s overall central
nervous system status.
o Five parameters are assessed with Apgar scoring. A quick way to remember the
parameters of Apgar scoring is as follows: Dr. Virginia APGAR
• A = appearance (color)
• P = pulse (heart rate)
• G = grimace (reflex irritability)
• A = activity (muscle tone)
• R = respiratory (respiratory effort)

Score
Sign (APGAR) 0 1 2
Appearance (color) Blue or pale Pink body with blue Completely pink
Extremities
Pulse (heart rate) Absent Slow (<100 bpm) >100 beats/min
Grimace (Reflex No response Grimace Cough or sneeze
irritability)
Activity (muscle tone) Limp Some flexion Active movement
Respirations Absent Slow, irregular Good, crying
NB: Reflex irritability is examined by making stimuli, such as suctioning or rubbing the soles of
the feet.
 A total score of 7 to 10 indicates that the neonate is in good condition
 A total score of 4 to 6 indicates fair condition (the neonate may have moderate CNS
depression, muscle flaccidity, cyanosis, and poor respirations)
 A total score of 0 to 3 indicates danger (the neonate needs immediate resuscitation, as
ordered).
 Resuscitation efforts such as oxygen, endotracheal intubation, chest compressions,
positive pressure ventilation or nasal continuous positive airway pressure, and
epinephrine administration should also be documented.
Classification of newborn
1. According to gestational age:

Classification Gestation
Premature < 37 weeks
Full-term 37 to 42 weeks
Post-term > 42 weeks
2. According to the birth weight independent of gestational age

Classification Birth Weight
Normal birth weight 2500 to 4000 grams
Low birth weight < 2500 g
Very low birth weight < 1500 g
Extremely low birth weight < 1000 g
3. According to gestational age and birth weight

Classification Percentile
Small for gestational age (SGA) < 10th percentile
Appropriate for gestational age (AGA) 10th to 90th percentile
Large for gestational age (LGA) > 90th percentile

(2) Systematic physical examination
General look and posture
 Active or not (crying, movements and suckling)
 Pale, cyanotic, or in respiratory distress (grunting, acting alae nasi)
 Convulsions
Normally, the newborn takes the position of the intrauterine life with flexed extremities, which
are somewhat hypertonic and clinched fits.
Position of comfort in a 20-hour-old infant. When placed in this position, the infant, who had been crying, was quiet.

Anthropometric measurements:
o Weight: average: 3.5 Kg (range: 2.7- 4.2 Kg)
 Weight the newborn without diaper.
 If the diaper in place, subtract the weight of the diaper from the total weight.
 Use the same scale each time the patient is weighed
 A further consideration in weighing the critically ill newborn is lifting the intravenous
infusion lines, as well as other pieces of equipment, such as ventilator tubing, so they
do not cause an inaccurately high measurement.
 Newborn typically loses up to 10% of birth weight in the first week of life due to
elimination of extracellular fluids (edema) and meconium.
 The baby should regain normal birth weight by 2 weeks.
o Length: average: 50 cm (range: 45-55 cm)
 Fully extend the newborn's leg and record the length from the crown of the head to the
heel.
 One person should hold the infant in place while another person completes the
measurements.
o Head circumference: average: 35 cm (range: 32.5-37.5 cm)
 Measuring the circumference of the skull from the frontal to occipital area by placing
the tape measure above the ears.
 Because of edema and molding due to the birth process, the subsequent occipital-
frontal circumference measurements may increase or decrease as much as 2 cm during
the first week of life.
o Chest circumference: 30.5 to 33 cm
 Chest circumference is obtained by measuring around the infant's chest at nipple line
midway between inspiration and expiration.

Skin Assessment:
1. Non-pathological conditions:
 Color: pink ,often mottled (due to vasomotor instability).
 Vernix caseosa: Whitish greasy material covered the newborn skin at birth. It has a
protective value as it contains antibodies absorbed by the skin.
 Lanugo hair: fine hair characteristic of the newborn best seen on the forehead, cheeks,
shoulder and back. It gradually lost during the first month.
 Mongolian spots: irregular areas of blue pigmentation usually present in the sacral and
gluteal regions due to increased melanin. They disappear after a few years and have no
pathological significance.
 Acrocyanosis: means peripheral cyanosis of the hands and feet. It's probably caused by
venous stasis and not hypoxia.
 Edema of subcutaneous tissues: is commonly present and is more evident in the eyelids,
face, dorsum of the hands, feet and legs. It disappears after several days.
 Milia: distended sebaceous glands seen as minute white papules on the cheeks, nose, and
chin. They disappear spontaneously in 2-3 weeks
2. Pathological conditions:
 Jaundice: may be seen in the 60% of the normal full term infant on the 2nd or 3rd day of
life and disappear by the 7th day. Jaundice in the first 24 hours is abnormal and should be
evaluated.
 Seborrhea of the scalp (Cradle cap): is a yellowish, patchy, greasy, scaly and crusty skin
rash that occurs on the scalp of newborn babies.
Warning signs of the skin assessment that would warrant further investigation and/or
immediate intervention include:
 Long nails and desquamation, indicating postmaturity

 Thin translucent skin with abundant vernix and lanugo, indicating prematurity
 Pallor, possibly caused by hypothermia, anemia, sepsis, or shock
 Cyanosis, possibly caused by cardiorespiratory disease, hypoglycemia, polycythemia,
sepsis, or hypothermia
 Meconium staining, possibly caused by intrauterine asphyxia
 Pustules, possibly caused by staphylococcal infection
Head Assessment:
The newborn has two fontanels at the juncture of the cranial bones (anterior and posterior)
o Anterior fontanel:
 Diamond-shaped. It can be palpated midline, above the forehead.
 Its antero-posterior measurement is approximately 4–5 cm
 Normally closes by 18 months of age (range from 4 months to 26 months).
 The fontanel is best palpated with the second or third finger pad when the infant is
quiet and in an upright position.
o Posterior fontanel:
 Its postero-lateral measurement is approximately 0.5–2 cm
 Normally closes by 2 months of age or at birth.
 Can be palpated midline, toward the back of the head, above the occiput.
 Delayed closure of posterior fontanel is associated with congenital hypothyroidism
Abnormality of head shape and size:
o Molding: overriding of cranial bones due to compression during birth. The bones return
to their normal positions in a few days.
o Craniosynostosis: premature closure of cranial sutures causing problems with normal
brain and skull growth and skull and facial deformities.
o Caput succedaneum: edema of the newborn’s scalp that is present at birth and caused by
head compression against the cervix.
o Cephalhematoma: is a collection of blood between the periosteum and the skull
Characteristic Caput Succedaneum Cephalhematoma

Fluid Edema Blood
Layer involved Scalp Between periosteum & skull
Relationship to suture line May cross the suture lines Does not cross suture lines
Appears Present at birth First or second day
Disappears 2 to 3 days 3 to 6 weeks

Face Assessment:
The face should have full cheeks and should be symmetric when the baby is resting and crying.
The newborn's face often gives the first clue to the presence of a dysmorphic syndrome such as:
 Cleft lip
 Characteristics of the Pierre Robin syndrome with a small mandible (micrognathia)
 Microcephaly
 Facial palsy
 Forceps marks: Forceps often leave bruises on the face, usually in the shape of the
forceps blade.
 Eyes Assessment:
o The eye lids appear puffy, the iris is grey in color, tears are absent. The infant looks
toward the light source.
Abnormal findings:
 Subconjunctival, sclera, and retinal hemorrhage
 Congenital lid ptosis (a drooping of the eyelid)
 Failure to close the eye fully can occur with facial paralysis
 Purulent eye discharge (Opthalmia neonatorum)
 Ear Assessment:
 At term, the ears are well formed and contain sufficient cartilage to retain a normal shape
and resist deformation.
 Malformed auricles or low-set-ears are found in many
dysmorphic syndromes and are associated with urogenital malformations.
 Nose Assessment:
 The nose should be assessed for placement, shape, patency, and the presence of drainage.

 Copious or discolored nasal discharge may be a sign of congenital syphilis or respiratory
problems .
 Obstructed nasal passages are an important finding as newborns are obligatory nose
breathers and usually cannot breathe orally even when compromised.
 Coughing in the newborn period is abnormal and usually accompanies interstitial lung
disease such as viral pneumonia.
 Mouth Assessment:
 Large tongue (macroglossia) appears in such cases like dawn syndrome & congenital
hypothyroidism.
 Excessive oral secretions suggest esophageal atresia or a swallowing disorder.
 Natal teeth: If teeth are present, they should be noted and reported. Natal teeth are
generally removed to prevent a choking hazard, especially if they are loose.
 Neck Assessment:
 Infants are generally not capable of supporting their heads at birth and will experience
head lag when they are moved to a sitting position from a lying one.
 Chest Assessment:
 Neonatal Gynecomastia is common in either gender and may be noted as late as the
second or third day of life. It is caused by high levels of maternal estrogen that have
passed through the placenta and should resolve spontaneously.
Breasts should not be squeezed to avoid mastitis, and abscess formation.
 The most frequent birth injury to the thoracic region is fracture of the clavicles,
identified by crepitation when the clavicle is palpated.
 Heart Assessment:
 The heart rate may be 160 to 180 bpm during the first few hours after birth.
 In aortic coarctation , pulses are diminished in the lower extremities.
 In hypoplastic left heart and critical aortic stenosis, pulses are diminished at all sites.
 Abdomen Assessment:
 Meconium (first passed stool which is odorless, very dark olive green-colored,
viscous and sticky like tar) should be passed within 24 hours . By the second or third
day, the infant should begin to have transitional stool, which is green or yellowish and
may have a seedy appearance.
 The shape of abdomen should be domed or cylindrical because of immature
musculature.
 Single umbilical artery, associated with congenital anomalies, especially renal
anomalies.

 Examine the abdominal wall for hernias like umbilical and inguinal hernia.
 Omphalitis (infection of the umbilicus) is a serious infection requiring intravenous
antibiotic therapy because of possible spread along the umbilical vein into the portal
venous sinus of the liver.
 The anus should be inspected for patency and absence of fissures.
 Spine Assessment:
 The spine of the newborn is quite flexible in both the dorsoventral and lateral axes;
restricted movement suggests vertebral anomalies.
 Check for obvious congenital anomalies such as neural tubal defects like:
o Meningomyelocele: A severe form of spina bifida in which the spinal cord and
nerves develop outside of the spine and are contained in a fluid-filled sac
o Meningocele: an opening in the spine in which a sac-like cyst of meninges, filled
with spinal fluid, but involves no nerves or neurological defects and covered by skin
 Genitourinary:
 Failure to void with in the first 24 hours is considered a warning sign and needs
further evaluation.
 The normal urine output for an infant is at least 1–2 cc/kg/hr. Output may be as high
as 4 cc/kg/hr. in the first few days of life.
 Exstrophy of the bladder: is a congenital anomaly in which part of the urinary
bladder is present outside the body.
 Hypospadias: is malposition of the urethral opening. The urethra open on the lower
surface of the penis.
 Epispadias: is malposition of the urethral opening. The urethra open on the upper
surface of the penis
 Cryptorchidism: ( undescended testis): is the absence of one or both testes from the
scrotum. The testes may be located in the abdominal cavity or inguinal canal.
 Pseudo-menstruation Mucous and possible blood-tinged vaginal discharge may be
present for several days.
 Neurological examinations:
Assess the newborn’s reflexes to evaluate neurologic function and development. Absent or
abnormal reflexes in a newborn, persistence of a reflex past the age when the reflex is normally
lost, or return of an infantile reflex in an older child or adult may indicate neurologic pathology.
Root reflex
 Trigger: A gentle stroke on the newborn’s cheek
 Response: Baby turns mouth toward the touch, with mouth open

 Appears: At birth
 Disappear: Until baby is three to four months old (sometimes, babies continue doing this
in their sleep past four months old)
 Reason: Helps baby find food
Suck reflex
 Trigger: Something, such as a nipple (breast or bottle) or parent’s finger, touching roof
of baby’s mouth
 Response: Baby sucks on nipple
 Appears: ≥28 weeks gestation
 Disappears: Three to four months
 Reason: Helps baby eat
Moro reflex (also called Startle reflex)
 Trigger: Loud noise (even baby’s own cry!), sudden movement, or sensation of falling
 Response: baby quickly abducts extremities and forms the index finger and thumb into a
“c” shape.
 Appears: As early as 32 weeks gestation
 Disappears: Until baby is four to six months old
 Reason: Baby’s first attempts to protect himself from harm
 Absence or poor Moro response: it indicates either marked prematurity <28 weeks or
depression of CNS (sedation ,or anesthesia given to the mother during delivery).
 Asymmetrical or unilateral Moro response: indicates fracture clavicle or Erb's palsy.
 Persistence of the reflex beyond 6months: indicates cerebral palsy or mental retardation
Palmar grasp reflex
 Trigger: Pressing a finger or other object, such as a rattle, into baby’s palm
 Response: Baby makes a fist and tries to grab finger
 Appears: As early as 28 weeks gestation
 Disappears: Three to four months
 Reason: May prepare baby developmentally for voluntary grasping later
 Fun fact: Baby’s grip can be strong enough to support his entire body weight
Planter grasp reflex
 Trigger: Pressing a finger or other object, such as a pencil , into baby’s base of toes
 Response: Baby Curls toes downward
 Appears: At birth
 Disappears: 8 months of age

Tonic neck (Fencing) reflex
 Trigger: Lying on his back and rapidly head turned to one side
 Response: The arm on that side extends, while the opposite arm bends at the elbow (a
“fencing” position)
 Appears: Between birth and 2 months of age
 Disappears: About 4-6 months
 Absence: spinal cord lesion
 Persistence or abnormal response: cerebral damage.
Walking (or stepping) reflex
 Trigger: Holding baby upright with his feet on a flat surface
 Response: Baby lifts one foot, then the other, as if walking
 Appears: at birth
 Disappear: About two months
 Reason: May prepare baby developmentally for walking several months from now
Babinski’s reflex
 Trigger: A gentle stroke on lateral aspect of the sole of the foot (from heel to toe)
 Response: Negative Babinski’s sign: flexion of all toes
Positive Babinski’s sign: The great toe dorsiflexes and the other toes fan out
 Disappears: 2 years of age
 Reason: Perhaps an attempt to protect against falling
The crawling reflex
 Trigger: placing the baby on his abdomen
 Response: baby will pull her legs under her body and kick them out in a crawling motion
 Disappears: after just a few weeks

Care of the Well Newborn
Immediate care of the newborn includes:

1. Obtaining the APGAR score: at 1 and 5 minutes after birth
2. Provide resuscitation (if needed)
3. Providing a neutral thermal environment
 Receive the newborn in warm blanket/towel
 Dry the infant thoroughly and gently; the wet towels should be promptly removed.
 Place the infant skin to skin with the mother, once he is stable.
 Provide warmth by placing the infant under a radiant warmer or incubator.
 Avoid heat loss by the 4 different methods (conduction, convection, radiation and
evaporation)
4. Immediate umbilical cord care
 Fix the cord clamp 3-5 cm away from the umbilicus, and cut the cord using a sterile
scalpel.
 Examine for any abnormality (single umbilical artery).
 Wipe the umbilical stump with ethyl alcohol 70%.
5. Proper identification of the infant
 Place 2 bracelets with identical hospital numbers (one on the wrist and the other
on the ankle).
 Take footprints or fingerprints and record in the medical record
6. Perform a brief physical examination
7. Parent/infant bonding: assists parents in holding their baby
8. Prophylactic care.
 Give vitamin K1 (0.5-1 mg IM) within 2 hrs. of life. to prevent .
 Apply antibiotic eye drops (e.g. erythromycin) within 1 hr. of delivery to prevent
ophthalmia neonatorum
Routine Care of newborn:
 Keep newborn with mother all the time (rooming-in).
 Bathing:
 Do not bathe immediately after birth; vernix caseosa
does not need to be removed.
 The first bath can be given with non-medicated soap
and warm tap water once infant's temperature has stabilized (4-6 hrs after delivery).
 Do not bathe the infant in a basin until after the umbilical stump has fallen off.

 Routine umbilical cord care
 Keep the cord dry and loosely covered with clean sterile gauze.
 Fold the diaper below the umbilicus.
 If soiled, wash with soap and clean water and dry it well.
 Apply alcohol after each diaper change.
 Place the newborn infant supine (on the back) to sleep and not prone (on the stomach).
 Feedings
 Support immediate and exclusive breastfeeding during the first hour postpartum
preferably in the DR.
 Offer standard term formula to infants for whom breast-feeding is contraindicated at least
every 3-4 hrs.
 Instructions to the Mothers or Other Care-Givers
 Observe baby’s temperature, respiration & effort at feeding.
 Observe for passage of urine and stools.
 Newborn Male Circumcision:
 Tests to exclude a bleeding disorder should be done.
 Contraindications: sick or unstable infant, congenital bleeding disorder (except
after giving the specific therapy to the infant), and anomalies (e.g., hypospadias,
ambiguity, or micropenis)
 After circumcision: apply a gauze dressing with petroleum jelly or an antibiotic cream,
remove at the first diaper change, and apply a new dressing. Keep the penis clean with
soap and water.
 Screening:
 Bilirubin screening is recommended before discharge.
 Congenital hypothyroidism screening (3rd to 7th day of life)
 Phenylketonuria (PKU) (the baby must be full milk feeds for 3 days).
 Galactosemia
 Vaccination
 Educate parents about vaccination schedule.
 Administer HBIG (0.5 ml/kg IM) to all newborns of HBs Ag-positive mothers as soon as
possible after birth (within 12 hrs.), followed by HBV vaccine (0.5 ml IM).
 Discharge Process:
 Instruction by the nurse on feeding and infant care.

 Distribution of books and pamphlets on care of newborn Observe for jaundice, skin
infection, signs of illness (fever, lethargy and change in feeding behavior), and
adequacy of breast milk intake.
 Give follow-up date, 2-3 days after discharge.

An important definitions
Term Definition
Full-term An infant born between 37 and 42 weeks of gestation
Preterm An infant born before 37 completed weeks of gestation regardless
of birth weight
Post-term (post-mature) An infant born after 42 completed weeks of gestation regardless
of birth weight
Low birth weight An infants born with weight of 2500 g or less regardless of
gestational age
Very low birth weight A baby born with a birth weight of 1500 g or less regardless of
gestational age
Extremely low birth weight A baby born with a birth weight of 1000 g or less regardless of
gestational age
Appropriate for A baby of birth weight lies between the 10th and 90th percentile of
gestational age (AGA) the expected for his gestational age
Small for gestational age A baby of birth weight lies below the 10th percentile of the
(SGA) expected for his gestational age
Large for gestational age A baby of birth weight lies above the 90th percentile of the
(LGA) expected for his gestational age
Stilborn infant A baby who shows no signs of life (including no heart beat) after
delivery. ‘Stillbirth’ is a term used only if the infant is of 24
weeks of gestation or above

Review questions
1. Explain stimuli that initiate the first respiration of newborn.
2.
Term Definition
An infant born between 37 and 42 weeks of gestation
An infant born before 37 completed weeks of gestation regardless of
birth weight
An infant born after 42 completed weeks of gestation regardless of
birth weight
An infants born with weight of 2500 g or less regardless of gestational
age
A baby born with a birth weight of 1500 g or less regardless of
gestational age
A baby born with a birth weight of 1000 g or less regardless of
gestational age
A baby of birth weight lies between the 10th and 90th percentile of the
expected for his gestational age
A baby of birth weight lies below the 10th percentile of the expected
for his gestational age
A baby of birth weight lies above the 90th percentile of the expected
for his gestational age
A baby who shows no signs of life (including no heart beat) after
delivery. ‘Stillbirth’ is a term used only if the infant is of 24 weeks of
gestation or above
3. Discuss the stimuli that help initiate the first respiration:

1. …………………………………………………………………………………
2. ……………………………………………………………………………………..
3. …………………………………………………………………………………………
4. ……………………………………………………………………………………………
5. …………………………………………………………………………………………….
4. Successful transition from fetal to postnatal circulation requires:
1. ………………………………………………………………………….
2. …………………………………………………………………………..
3. ……………………………………………………………………………
5. Why newborn infant is at risk to develop hypothermia?
1. ………………………………………… 2. ……………………………………
3. ………………………………………… 4. ……………………………………….

6. Methods of Heat Loss are:
1. …………………………2 …………………… 3. …………………….. 4. ………….……...
7. Ways to prevent heat loss by evaporation:
1. …………………………………….. 2. ………………………………………………
8. Ways to prevent heat loss by conduction:
1. …………………………………………………….. 2. …………………………………
9. Ways to prevent heat loss by convection:
1. …………………………………………. 2. ……………………………………………….
10. Ways to prevent heat loss by radiation:
1. ………………………………………. 2. ……………………………………………….
11. Stomach capacity at birth is …………….. ml and…………………ml at one month of age.
12. Explain the effects of liver immaturity on the body of the neonate:
1. …………………………………… 2. ………………………………………
3. ………………………………………4. ………………………………………
13. The Apgar scores grade the infant's response to extrauterine life according to five parameters:
1. ……………………………………….. 2. ………………………3. …………………………
4. ……………………………………… 5. ………………………………….
14. If Lower limbs systolic pressure < upper limbs systolic pressure by 6-9 mmHg, this condition
may indicate ……………………………
15. ………………………………… whitish greasy material covered the newborn skin at birth.
16. ……………………………….. fine hair characteristic of the newborn best seen on the
forehead, cheeks, shoulder and back.
17. ………………………………….. irregular areas of blue pigmentation usually present in the
sacral and gluteal regions, but may be present also at any area of the body as the extremities.
18. ………………………… peripheral cyanosis of the hands and feet.
19. ………………………Sebaceous glands seen as minute white papules on the cheeks, nose,
and chin.
20. …………………………… are tumors made-up of dilated blood vessels that are a common
vascular birthmark.
21. ……………………………….. is a yellowish, patchy, greasy, scaly and crusty skin rash that
occurs on the scalp of newborn babies.
22. There are numerous causes for bulging anterior fontanel such as:
1. ……………………….2 ……………….. 3. ………………………. 4. …………………..
23. ………………………….. overriding of cranial bones due to compression during birth.

24. …………………………. premature closure of cranial sutures causing problems with normal
brain and skull growth.
25. ……………………… is the formation of edema of the scalp at the presenting part of the
head.
26. ………………………..is a collection of blood beneath the periosteum.
27. A small mandible is called …………………………..
28. …………..…………………….. is Purulent eye discharge.
29. ……………………………… is a blockage in the posterior nasal passage.
30. Large tongue is called ……………………………………
31. A tongue tie is called ……………………………………
32. …………………………. Is infection of the umbilicus
33. The normal urine output for an infant is at least …….. cc/kg/hr. Output may be as high as
………. cc/kg/hr in the first few days of life.
34. ……………………………… is the collection of fluid around the testes in the scrotum and a
relatively common finding.

Chapter (3)
Health problems of newborn infants
Learning objectives
 Define the key terms including preterm, post-term, infant of

diabetic mother, jaundice, apnea, ..etc.
 Describe the clinical manifestations, diagnostic evaluation,
complications, nursing care for common health problems of
newborn including preterm, post term, infant of diabetic
mother, neonatal jaundice, neonatal sepsis, respiratory distress
syndrome, transient tachypnea of newborn, diaphragmatic
hernia, gastroesophageal reflux, esophageal atresia,
imperforated anus.
 Differentiate between physiological and pathological jaundice
 Differentiate between RDS and TTN
 Explain types of TEF and the surgical preparation for correction
surgery.

Pre-term Infant
 Preterm birth, also known as premature birth, is the birth of a baby at less than 37 weeks
gestational age
 The preterm infant is a viable infant born before the 37 weeks’ gestation, regardless of birth
weight.
Etiology:
1. Idiopathic (Unknown)
2. Maternal factors:
■ Poor nutrition ■ Diabetes ■ Multiple pregnancy (twins, triplets, etc) ■ Drug abuse
■ IUD in gravid uterus ■ Chronic disease (heart disease, kidney disease, infection)
■ Complications of pregnancy (PIH, bleeding, placenta Previa, abruptio placenta, incompetent
cervix, polyhydramnios or oligohydramnios, preterm rupture of membrane).
3. Fetal factors:
■ Chromosomal abnormalities ■ Feto-placental dysfunction.
Clinical features:
 Low anthropometric measurements (Weight, length, Head circumference).
 Hypoactive with weak cry and poor suckling.
 The head and abdomen appears large as compared with the limbs.
 Skin: thin, red, shiny, wrinkled and translucent with
excess lanugo hair and vernix caseosa.
 Subcutaneous fat is decreased or absent.
 Respiration is irregular with attacks of apnea.
 Slight edema is often present.
 Frog leg position due to hypotonicity
(thighs are widely abducted, ankles and knees flexed) with head looking to one side .
Pathophysiology:
The preterm infant has altered physiology due to immature and often poorly developed systems.
The severity of any problem that occurs depends upon the gestational age of the infant:
Respiratory system:
Respiratory distress is a common problem due to:
1) Alveoli begins to form at 26-28 weeks’ gestation so lungs is poorly developed.
2) Respiratory center and muscles are poorly developed.
3) Production of surfactant is reduced.
4) Gag and cough reflexes are poor (aspiration is a problem).

Digestive system:
 Weak suckling and swallowing reflexes .
 Tolerance is decreased related to decreased enzymes.
 Lack of bile salts that aid digestion of fats and absorption of vitamin D and other fat-
soluble vitamins.
 Limited ability to convert glucose to glycogen and break down of glycogen to glucose.
 Limited and immature ability to release insulin in response to glucose.
 Weak cardiac sphincter with active pyloric sphincter and small capacity of stomach
lead to gastro-esophageal reflux (GER) and vomiting.
 Hypotonia of muscle coat of colon leading to abdominal distention and constipation.
Temperature regulation mechanisms:
Preterm baby is liable to hypothermia because preterm baby:
 Has very little subcutaneous fat
 Has Limited ability to shiver
 Has large body surface area in comparison to body weight
 Has Decreased sweating mechanisms, infant cannot perspire under 32 weeks’ gestation.
 Usually has poor muscle activity.
 Has flaccid posture (increased surface area exposed).
Renal function:
 Sodium excretion is probably increased which may lead to hyponatremia. There is
difficulty in excreting potassium.
 Decreased ability to concentrate urine, which may result in dehydration.
 Decreased ability to acidify urine.
Nervous system:
 Suck, swallow and gag reflexes are poor (aspiration).
 Cough reflex is weak or absent.
 Centers that control respiration, temperature and other vital functions are poorly
developed.
Immune system:
 The immune response is compromised so there is weak active immunity
Liver function: immature liver leads to edema, jaundice, hemorrhage, and hypoglycemia
Eyes:
 If preterm baby is receiving oxygen at high concentration, retinopathy of prematurity
or retrolental fibroplasia will develop which to lead eventually blindness

 The exact amount and level of oxygen needed to produce retrolental fibroplasia are
unknown.
Complication of prematurity:
1. Respiratory system: such as Asphyxia, Apnea, Aspiration pneumonia, Atelectasis & RDS
2. Cold injury secondary to hypothermia
3. Hypoglycemia 4. Brain damage 5. Jaundice
6. Malnutrition, rickets, and anemia 7. Liability to hemorrhage 8. Liability to infection
9. Retinopathy of prematurity 10. Necrotizing Enterocolitis (NEC)
11. Congenital malformation 12. Intra-ventricular hemorrhage (IVH)
13. Complication of therapeutic measures: pneumothorax, bronchopulmonary dysplasia due
to mechanical ventilation.
Nursing care for preterm infants:
1. Improving respiratory functions
 Observe for changes in respiratory effort, rate, depth, breath sounds, and regularity of
respirations or apnea
 Note any expiratory grunting or chest retractions (substernal, suprasternal, intercostal,
subcostal) including severity, and nasal flaring to determine the newborn’s ability to
maintain respirations.
 Ensure that oxygen support or ventilator settings and placement of an endotracheal (ET)
tube, if ordered, is as prescribed to ensure adequacy of ventilation and respiration
assistance.
 Repositioning the newborn every 2 hours helps to reduce the risk for pneumonia and
atelectasis.
 Frequent suctioning may be necessary to prevent airway obstruction, hypoxia, and
asphyxiation.
 If not contraindicated, elevate the head of the bed as needed to maintain a patent airway.
2. Maintaining Body Temperature
 The delivery room temperature at a minimum of 25º C; drying of the infant immediately
after birth; removing any wet blankets and wrapping the infant in a pre-warmed blanket;
pre-warming any contact surfaces; avoiding draughts; and use of radiant warmers or
incubators
 Placement of preterm/low birth weight infants inside a plastic bag at birth
 The preterm newborn’s body temperature must be monitored closely and continuously.
 Be sure to expose as little of the newborn’s skin as possible during procedures to
minimize heat loss.
 Observe for signs of cold stress, such as low temperature, body cold to touch, pallor, and
lethargy
3. Preventing Infection
 The primary means of preventing infection is hand-washing.
 All persons who come in contact with the newborn must practice good hand-washing
immediately before touching the newborn and when moving from one newborn to another
 Regular cleaning or changing of humidifier water, IV tubing, and suction, respiratory, and
monitoring equipment.
 Personnel from other departments (radiology, respiratory therapy, or laboratory) put a
cover gown over their uniforms while working with these newborns.
 Routine laboratory tests used to diagnose and treat infections include blood cultures,
cerebral spinal fluid analysis, urine tests, tracheal aspirate culture, and superficial cultures.
 Expect antibiotics to be ordered to treat suspected or confirmed bacterial infections.
4. Maintaining Adequate Nutrition
 NG tube feeding is essential before age of 32 weeks of gestation because gag &
swallowing reflexes are not developed before this time.
 Mothers can pump their breast milk and freeze it to use for bottle or gavage feedings until
the preterm newborn is strong enough to breast-feed.
 IV fluids or TPN with high calories
 Weigh the preterm newborn daily.
5. Maintaining Skin Integrity
 Pay special attention to areas in which equipment is attached or inserted.
 Reposition the preterm newborn every 2 to 4 hours and PRN as necessary.
 Changing the diaper as soon as possible after soiling will maintain clean and dry skin.
 Keep the skin clean and dry but avoid excessive bathing, which furthers dries the skin.
 Pad pressure prone areas by using waterbeds, pillows to help prevent skin ulcer.
 Apply creams and ointments and medication as prescribed for relief of itching, infections,
and to prevent breakdown.

Post-term infant
Post term infant is a viable infant born after completed 42 weeks of gestation regardless of birth
weight
Incidence: 12% of all births.
Predisposing factors:
 Primigravida (first pregnancies between the ages of 15 and 19 years)
 Woman older than 35 years with multiple pregnancies
 History of prolonged gestation in the previous pregnancies
Altered physiology:
 The postmature infant appear to have suffered from intrauterine malnutrition and hypoxia,
before termination of pregnancy but at the point when birth should have occurred the
placental function begins to diminish resulting in impaired oxygen exchange and
inadequate nutrient transfer to the fetus.
 The severity of the associated problems is determined by length of gestation “ the longer
the gestation, the more severe the problems”.
Clinical manifestations:
 Wasted physical appearance, little subcutaneous fat ( long, thin appearance).
 Long fingernails and toenails. ■ Reduced amount of vernix caseosa.
 Absence of lanugo hair. ■ Abundant scalp hair.
 Skin is dry, cracked, peeling, loose and wrinkled.
 Hypoglycemia
 Meconium staining of skin, nails and umbilical cord (it explained by intrauterine hypoxia
which opens the rectal sphincter).
Diagnostic evaluation:
 Evaluate general appearance.
 Determine gestational age, APGAR scoring and blood gas analysis and blood sugar.
 Measure wt., length, & HC and compare percentiles.
Complications:
 Meconium aspiration.
 Hypoglycemia: in the last weeks of gestation, the infant relies on glycogen for nutrition.
This depletes the liver glycogen stores and may result in hypoglycemia.
 Polycythemia due to intrauterine hypoxia. Polycythemia puts the infant at risk for
cerebral ischemia, thrombus formation, and respiratory distress as a result of hyper-
viscosity of the blood.

 Pulmonary hemorrhage, pneumonia and pneumothorax.
Nursing care for post-term baby:
o Administer supplemental oxygen therapy as ordered for respiratory distress.
o Monitoring of blood glucose level is essential because the post-term newborn is at risk
for hypoglycemia.
o Intravenous glucose infusions may be ordered to stabilize the newborn’s glucose level.
o Provide a thermo-regulated environment, such as a radiant heat warmer or isolette
o Monitor Hematocrit levels to evaluate for Polycythemia.
Infant of diabetic mother (IDM)
Is the infant born to a mother with diabetes. The mother may be an chronic diabetic or
gestational diabetic. The severity of infant problems depends on the severity of maternal
diabetes.
Altered physiology:
 Maternal diabetes leads to trans-placental passage of high amount of glucose. Insulin
does not cross placenta. So, Maternal hyperglycemia fetal hyperglycemia
fetal hyperinsulinemia (increased insulin).
 Since insulin is an anabolic hormone, increased glycogen synthesis and storage in
the liver, increased fat synthesis, and increased protein synthesis, this results in increased
size and weight of the infant organs (except the brain) Macrosomia & myocardial
hypertrophy
 After birth, ligation of the cord suddenly interrupt glucose infusion to the neonate without
a similar effect on the hyperinsulinemia hypoglycemia during the first hours after
birth.
 Macrosomia and obesity → increased incidence of birth injury due to obstructed labor.

 Plump with plethoric face resembling that of patients who receive cortisone.
 Cardiomegaly, hepatomegaly.
 Abundant fat, hair and vernix caseosa.
 Tendency to be large for gestational age, some may be AGA or SGA.
 Intrauterine growth retardation when mother has had long standing insulin dependency.
 Hypoglycemia (first 6-12 hrs. after birth)
 Blood glucose level
 Serum calcium & magnesium level
 Hematocrit
 Serum bilirubin levels
 Other tests: blood gas analysis, CBC and cultures, as clinically indicated.
 Echocardiography, if cardiomyopathy or cardiac anomalies are suspected.
Complications:
 Hypoglycemia: the onset is frequently within 1-2 hrs. of age.
 Hypocalcemia (due to functional hypo-parathyroidism and hypomagnesaemia): it
becomes apparent 48-72 hrs. after birth.
 Macrosomia and organomegaly
 Prematurity ■ Perinatal asphyxia
 Infection
 Birth injuries: fracture clavicle, Erb's palsy
 Respiratory distress syndrome (due to delayed lung maturation, because
hyperinsulinemia may block cortisol induction which affect lung maturation and
surfactant synthesis).
 Congenital anomalies (most common skeletal and cardiac)
 Hyperbilirubinemia due to:
 Polycythaemia (increased RBC mass).
 Increased extravascular haemolysis (bruising, Cephalhematoma).
 Delayed oral feeding (increased enterohepatic circulation).
 Liver immaturity.
 Polycythemia (HCT ↑65% or HB: ↑20g/ dl) and hyper-viscosity
Management:
 Observe closely for hypoglycemia.
 Check by dextrostix at delivery and at 1, 2, 3, 6, 12, 24, 36, and 48 hrs. of age; readings
<45 mg/dl should be verified by serum glucose measurements.
o If the infant is normo-glycemic: give milk feeding every 2 hours.
o If infant is hypoglycemic: give IV 1-2 ml/ kg of glucose 10% followed by
maintenance dose of 4-8 mg/kg/min of glucose 10%.
 Monitor infant closely for changes in acid-base status, respiratory distress temperature,
hypocalcaemia, sepsis, cardiac anomalies and hyperbilirubinemia.
 Correction of hypoglycemia, hypocalcaemia, hypomagnesaemia.
 Oxygen therapy.
 Support the mother who may have feeling of sever guilt.
Neonatal Sepsis
Neonatal sepsis or septicemia neonatorum is the systemic invasion and proliferation of

pathogenic bacteria into the blood stream and frequently involves the meninges.
Incidence:
 1 in 1000 live full term births.
 I in 250 live premature births.
Etiology:
The etiologic bacterial agents varies from year to year and from institution to another.
Predisposing factors:
1. Perinatal factors:
 Maternal complications e.g. prolonged rupture of membranes, prolonged and difficult
labor, UTI, maternal illness, and abruption placenta
 Infant complications e.g. prematurity, LBW, congenital heart disease, RDS, IDM,
babes with congenital anomalies leading to exposure of internal organs as meningocele
and omphalocele
2. Iatrogenic or environmental factors e.g. unclean equipment, surgical procedures, obstetric
and nursery practice
1. Early manifestations:
 The early signs of sepsis usually vague and subtle
 Poor suckling ▪ Lethargy, hypotonic
 Hypothermia or hyperthermia.
2. Manifestation in an established case:
 GIT: vomiting, constipation, diarrhea, abdominal distension, hepatomegaly, jaundice
 Lungs: tachypnea, respiratory distress, apnea, cough
 CVS: tachycardia, bradycardia, heart failure, hypotension, pallor or cyanosis or shock
 CNS: tremors, convulsions, apnea, bulging anterior fontanel, hypotension, weak cry,
absent Moro reflex
 Blood: jaundice, anemia, thrombocytopenia, purpura, ecchymosis, splenomegaly.
3. late manifestation:
- Organomegaly - Direct hyperbilirubinemia - DIC - Purpura - Convulsions
Investigations:
 Septic work-up including: Culture and sensitivity for blood, urine, umbilical stump,
skin lesions, nose, throat, rectum, CSF, external auditory canal or/and gastric fluid.
 CBC, Blood chemistry, bilirubin and blood gas analysis.
 CXR
 Seroassays for TORCH infections (Toxoplasmosis, Other infections e.g. HIV,
Syphilis,...etc., Rubella, Cytomegalovirus, Herpes simplex virus)
 CSF analysis and culture: if meningitis is present, the CSF will contains ˃ 100 cells/ ml
with neutrophil predominance, protein concentration of ˃ 150 mg/dl and very low
glucose concentration. (normal CSF value in newborn: Cells ˂ 20 /ml (˂ 10%
neutrophil), Protein ˂ 150 mg/dl, glucose > 60% of simultaneous Serum Glucose)
Complications:
● Meningitis and neurological damage ● Shock ● Pneumonia ● Congestive heart failure
● DIC (Disseminated intravascular coagulation) ● High mortality rate.
Medical management:
 Antibacterial: Ampicillin and aminoglycoside or according to culture and sensitivity.
 Supportive therapy: - Observation. - Isolation if indicated. - Oxygen therapy.
- Fluid and caloric maintenance - Regulation of thermal environment.
Nursing interventions:
■ Review maternal history, identify infant at risk for infections.
■ Practice measures, which will prevent the transmission of infection in the nursery.
■ Observe infants for the vague symptoms that appear early in the course of sepsis.
■ Observe for episodes of apnea and initiate measures to stimulate respiration.
■ Maintain isolation as prescribed to minimize exposure to infectious organisms.
■ Observe the infant for convulsions which may occur with sepsis:
■ Ensure that diagnostic tests be initiated to avoid altered results from contamination " Tests
should be completed prior to starting antibiotics".
■ Provide for the nutritional needs of the infant to provide his caloric needs.
■ Provide measures to maintain the infant temperature within normal range.

■ Administer the prescribed antibiotic therapy to control infection.
Neonatal jaundice
Definition of jaundice:
 Yellow discoloration of skin, mucous membranes and sclera due to excess bilirubin in the
blood (hyperbilirubinemia).
 Jaundice appears clinically when serum bilirubin reaches 5-7 mg/dl in newborn and more
than 2 mg/dl in adult.
Incidence: Occurs in 50% of term infants, 80% of preterm.
Altered physiology:
Types of jaundice:
1) Un-conjugated hyperbilirubinemia (golden yellow in color)
2) Conjugated hyperbilirubinemia. (greenish color).

Unconjugated bilirubin Conjugated bilirubin
Fat soluble Water soluble
Not excreted by kidneys Excreted by kidneys
Pass through BBB to CNS Doesn’t pass through BBB to CNS
Causes kernicterus Does not cause kernicterus
Reduced by phototherapy Not reduced by phototherapy
Causes of jaundice:
1. Bilirubin overproduction
2. Decreased bilirubin conjugation
3. Impaired bilirubin excretion
Physiological Jaundice in the Newborn

It occurs in about 60% of normal full term infants during the first week of life.
Why newborn infant is more likely to develop physiologic jaundice?
1) Polycythemia so the destruction of RBCs is more
2) Short life span of neonatal hemoglobin which is mainly fetal hemoglobin with life span
of 90 days instead of 120 day (adult hemoglobin).
3) Immature hepatic uptake and conjugation processes
4) Increased enterohepatic circulation which result in return back of unconjugated
bilirubin circulation.
Physiological Jaundice Pathological jaundice
nd rd
The onset is in the 2 or 3 days, never in the The onset is before 1st day (24 hours of age).
first day.
Jaundice disappears by the end of 1 week in full  Clinical jaundice persisting beyond 2 weeks of life
term infant and by 2 weeks in the preterm infant.
The total serum bilirubin is not more than 12 Serum bilirubin exceeds that levels
mg/dl in full term and 15 mg/dl in preterm and
the direct bilirubin is less than 1mg/dl.
The daily rise of serum bilirubin never exceeds 5 Rise in serum bilirubin by more than 5 mg/ dl/ day
mg/dl.
No kernicterus Causes kernicterus in indirect hyperbilirubinemia
The newborn is good sucker, no anemia, not sick, The newborn looks sick, poor sucking, pale,
normal stool and urine color Clay/white colored stool and/or dark urine staining
the clothes yellow
Requires no treatment Treatment is important as soon as possible
Pathological un-conjugated jaundice

1. Rh incompatibility
 The mother is Rh negative and the infant is Rh positive.
 It usually does not occur in the first infant (except if there is history of previous abortion
or blood transfusions).
 Jaundice is not present at the time of delivery (because bilirubin is metabolized by
maternal liver while in utero).
 Jaundice starts to appear few hours after birth. Rh incompatibility is one of the major
causes of jaundice in the first day.
 The infant is pale and anemic.
The laboratory investigations reveal the following
 Increased unconjugated bilirubin
 Anemia.
 Positive direct Coomb's test.
 Elevated reticulocyte count
2. ABO Incompatibility
o The mother blood group is (O) while the infant has blood group A or B.
o All other information resembling Rh incompatibility

3. Breast Milk Jaundice
o It occurs in about 1 out of 200 breast fed babies.
o It starts 5-7 days after birth.
o It reaches a maximum in 2nd or 3rd week.
o If left without treatment, the serum bilirubin reaches normal by the end of 3rd month.
o The condition is usually benign i.e. no kernicterus.
o If breast feeding is stopped for 3-4 days, the serum bilirubin decreases markedly.
o Returning back to breast is not associated with further rise.
o The cause is supposed to be due to certain substances in the milk of these mothers
(progesterone metabolite or free fatty acids) that inhibit the glucuronyl transfers enzyme and
thus inhibits bilirubin conjugation.
4. Breast- feeding jaundice

o Also called "lack-of-breast-milk jaundice.
o The pathogenesis is probably poor enteral intake and increased enterohepatic circulation.
Because of poor intake the baby become dehydrated and lack of calories which cause
jaundice.
o The infant should receive supplemental formula and the mother should be instructed to nurse
more frequently to decrease jaundice.
Transcutaneous bilirubin- meter
Evaluation of un-conjugated jaundice:
1. Initial evaluation:
• Transcutaneous bilirubinometer
• Total serum and direct bilirubin
• Blood type and Rh (infant & mother)
• Hematocrit • Direct (Coombs) test on infant
2. Later evaluation (as indicated):

• RBC smear, reticulocyte count (if evidence or suspicion of hemolytic disease).
• Blood culture, urinalysis, urine culture
• Thyroid function tests, G6PD assay, Hb electrophoresis.

Complication of un-conjugated hyperbilirubinemia:
 Kernicterus or Bilirubin encephalopathy is the deposits of bilirubin in the brain tissues
causing brain damage. Kernicterus is the most dangerous complication of jaundice
 Kernicterus usually occurs if the level of unconjugated bilirubin exceeds 20 mg/dl in full-term
babies and 15 mg/dl in premature.
 Essentials of Diagnosis & Typical Features:
 Lethargy, poor feeding.
 Irritability, high-pitched cry.
 Arching of the neck (retrocollis) and trunk (opisthotonos).
 Apnea, seizures, coma (late).
Management of Un-conjugated Hyperbilirubinemia
1. Phototherapy:
 By exposing the naked jaundiced baby with unconjugated hyperbilirubinemia to certain
wave lengths of florescent light (blue or white) with wave length 425-475 nanometer,
unconjugated bilirubin in the skin is converted to a water-soluble stereoisomer that can be
easily excreted in bile and urine.
 This method of treatment is of moderate effect and is not sufficient alone in severe cases.
 Phototherapy is used alone if serum bilirubin is:
 5-9 mg/dl in the first day of life.
 9-15 mg/dl in the second day of life.
 15-20 mg/dl in the third day of life.
 Serum bilirubin of higher values is an indication of exchange transfusion in addition to
phototherapy.
 Nursing care for infant under phototherapy:
1) The infant should be undressed except for eye patches (eye patches must be in place but
should not be too tight or occlude the nares).
2) The lamp should be 5-8 cm over the incubator and 45 cm above the infant.
3) Give phototherapy continuously and turn the infant every 2 hrs.
4) Infant’s temperature should be carefully monitored every 4 hours and incubator
temperature should be adjusted.
5) Weigh the infants daily (twice daily in small infants).
6) Carefully monitor infant’s fluid balance to avoid dehydration (↑fluid therapy by 20%).

Side effects of phototherapy:
1. Retinal damage by light (the eyes must be covered during phototherapy).
2. Temporary weight loss due to water loss caused by the exposure to light. This should be
corrected by increasing the fluid intake.
3. Looseness of stools (watery diarrhea).
4. Skin rash
2. Exchange Transfusion:
 A catheter is introduced into the umbilical vein after cutting the cord. Through a special
valve, the umbilical catheter is connected with the donor blood.
 Exchange is carried out over 45-60 minutes periods by alternating aspirations of 20 ml of
infant's blood and infusions of 20 of donor blood.
 The aim should be an exchange of double the blood volume of the infant (2 x 85 ml x
body weight in kg).
 The donor blood in Rh incompatibility should be of the same group of the infant but
Rh negative, while in ABO incompatibility it should be group (O).
 The procedure decreases serum bilirubin acutely by approximately 50% and removes
about 80% of sensitized or abnormal red blood cells and offending antibody so that
ongoing hemolysis is decreased.
 Exchange transfusion is also indicated in any infant with TSB above 30 mg/dL, in infants
with signs of encephalopathy, or when intensive phototherapy has not lowered TSB by at
least 0.5 mg/dl/h after 4 hours.
Side effects of exchange transfusion:
● Cardiac arrhythmias ● Electrolyte disturbances (hypocalcemia)
● Infection (septicemia). ● Embolism (blood clots or air)
● Portal and splenic vein thrombosis ● Hypo/hyperthermia
3. Pharmacologic agents
 Intravenous immunoglobulin (IVIG 500-1,000 mg/kg IV over 2-4 hrs.) is recommended
in immune hemolytic type, if TSB is rising despite intensive phototherapy. Dose may be
repeated in 12 hrs., if necessary.
 Enzyme induction agent: by inducing hepatic enzyme system involved in bilirubin
clearance e.g. Phenobarbital

Transient Tachypnea of Newborn (TTN)
o Transient tachypnea of the newborn (TTN) involves the development of mild respiratory
distress in a newborn as a result of a delay in absorption of fetal lung fluid after birth.
o TTN typically occurs after birth, with the greatest degree of distress occurring approximately
36 hours after birth. TTN commonly disappears spontaneously around the 3rd day.
o TTN is also called wet lung syndrome.
Contributing Factors:
 TTN is commonly seen in newborns born by cesarean delivery.
 Newborns who are preterm or SGA
 Infant of diabetic mother
Clinical Manifestations:
 Mild respiratory distress, with a respiratory rate greater than 60 breaths per minute.
 Mild retractions, nasal flaring, and some expiratory grunting may be noted.
 However, cyanosis usually does not occur. Although some infants will require oxygen to
remain pink
 Often the newborn has difficulty feeding because he or she is breathing at such a rapid rate
and is unable to suck and breathe at the same time.
Diagnostic tools:
 ABG: may reveal hypoxemia and decreased carbon dioxide levels.
 CXR: Fluid in the transverse fissure or pleural space

Treatment:
 Supplemental oxygen often is ordered, and oxygen saturation levels are monitored via pulse
oximetry.
 IV fluids and gavage feedings may be used to meet the newborn’s fluid and nutritional
requirements
Meconium Aspiration Syndrome (MAS)
o Meconium aspiration syndrome (MAS) refers to a condition in which the fetus or newborn
develops respiratory distress after inhaling meconium mixed with amniotic fluid.
o Meconium staining of amniotic fluid usually occurs as a reflex response to hypoxia that
allows the rectal sphincter to relax. Subsequently, meconium is released into the amniotic
fluid. The fetus may aspirate meconium while in utero or with his or her first breath after
birth.
o The meconium can block the airway partially or completely and can irritate the newborn’s
airway, causing respiratory distress.
Risk Factors:
Post-term pregnancy, pre-eclampsia, eclampsia, maternal hypertension, maternal diabetes
mellitus, IUGR, and evidences of fetal distress.
 Low Apgar score at delivery
 Meconium staining
 Tachypnea, intercostal and subcostal retractions, cyanosis, hyper-inflated lung, diminished
air entry, wheezes or crepitation.
X- ray chest:
 Flattened diaphragm, hyper-inflated lungs, areas of collapse or consolidation may be seen
 Air leak (pneumo-mediastinum, pneumothorax) may be evident.
Management:
1. Prevention: by suction and clearing of airway immediately after delivery of the head and
before taking the first breath.
2. Treatment:
 Oxygen administration, endotracheal suction and antibiotics.
 Mechanical ventilation may be needed
 Antibiotics

Scaphoid abdomen
Congenital Diaphragmatic Hernia
 Herniation of abdominal contents into the thorax with collapse of lung and shifting of
mediastinum. The infant fails to establish spontaneous respiration.
 The baby will have poor chest movements, intercostal retractions, and cyanosis.
 Scaphoid abdomen (anterior abdominal wall is sunken and presents a concave rather than a
convex contour) and hearing of intestinal peristalsis in the chest help the diagnosis.
Diagnosis is proved by X-ray chest
Management: ventilate by endotracheal tube. Mask should not be used as air enters stomach
increasing the distress. Surgery is mandatory.

Respiratory distress syndrome (RDS)
 Also called Hyaline Membrane Disease (HMD)

 Is the commonest cause of respiratory distress among immature infants.
 The incidence increases from 5% of infants born at 35–36 weeks' gestation to more than
50% of infants born at 26–28 weeks' gestation.
Altered physiology:
 This condition is caused by a deficiency of surfactant which typically begins in
production at 24–28 weeks of gestation and but mature levels of pulmonary surfactant are
present usually after 35 wk.
 Surfactant is a lipoprotein produced by Type II cells or Type II pneumocytes.
 Surfactant decreases surface tension in the alveolus during expiration, allowing the
alveolus to remain partly expanded after expiration & thus requiring less negative
pressure and exertion to take next breath.
 Microscopically, a surfactant deficient lung is characterized by collapsed air-spaces and,
in time, hyaline (a glass-like appearance) membranes which are lining or filling the
alveoli and blocking gas exchange.
Risk factors for RDS:
Synthesis of surfactant depends in part on normal pH, temperature, and perfusion.
Conditions with high risk for RDS:
● Prematurity ● Maternal diabetes ● Cold stress ● Acidosis
● Hypothermia ● Hypovolemia ● Multiple births ● Elective CS without labor
● Genetic disorders of surfactant production (e.g., surfactant protein B mutation)
Clinical manifestation: Symptoms are usually observed soon after birth.
o Expiratory grunting (When infant is not crying).
o Sub-sternal and inter-costal retractions.
o Inspiratory nasal flaring.
o Tachypnea (up to 80-120 breaths/minute).
o Hypothermia.
o Cyanosis when child is in room air (in severe cases may be cyanotic even with oxygen
given).
o Decrease breath sound and dry sandpaper breath sound

Complications:
1. Complications related to respiratory therapy:
- Pneumothorax - Pneumo-mediastinum - Pneumonia - Pulmonary emphysema
2. Patent ductus arteriosus.
3. DIC "due to consumption of clotting factors".
4. Tracheal stenosis.
5. Retrolental fibroplasia
6. Necrotizing enterocolitis.
7. Broncho-pulmonary dysplasia (BPD): chronic lung disease that occurs in infants treated
for prolonged periods by O2 and mechanical ventilator.
1. laboratory test:
 Arterial blood gases (ABG): ● ↓ PH ● ↑ PC02 ● ↓P02 (Respiratory acidosis)
2. Chest x-ray: congested lung field with ground-glass appearance.
Management:
1. Prevention:
 Prevention of prematurity and other risk factors
 Antenatal corticosteroid therapy (betamethasone 12 mg/dose IM for 2 doses, 24 hrs apart,
or dexamethasone 6 mg/dose IM for 4 doses, 12 hrs apart) for pregnant women 24-34
wks' gestation at high risk of preterm delivery within the next 7 days.
 Early CPAP administration in the delivery room.
 Delaying premature birth. Tocolytics may delay delivery by 48 hours and therefore
enable time for antenatal corticosteroids to be given.
 Prophylactic administration of a 1st dose of surfactant into the trachea of symptomatic
premature infants immediately after birth reduces air leak and mortality from RDS.
Treatment:
1. Supportive care in neonatal intensive care unit (NICU)
 Care appropriates for small premature infant.
 Maintenance of oxygenation PaO2 at 60-80 mmHg to prevent hypoxia.
 Maintenance of respiration with ventilatory support if necessary.
 Maintenance of thermo-neutral state (to prevent hypothermia).
 Maintenance of fluid, electrolyte and acid-base balance.
 Maintenance of nutrition.
 Antibiotic is indicated only when hyaline membrane disease can not be differentiated
from early onset of sepsis.

 Constant observation and treatment of complication.
2. Specific treatment: Surfactant replacement therapy by intra-tracheal installation.
NB: Artificial surfactant may be synthetic or animal derived surfactant e.g. cow, pig and calf
lungs.
Apnea in the newborn
Definition: cessation of breathing more than 20 seconds accompanied by bradycardia (HR less
than 100 beats/minute) and cyanosis.
Etiology:
● Prematurity ● Septicemia ● Intracranial hemorrhage ● Hypoglycemia
● Hypocalcemia ● Pharyngeal suction ● Over-flexion or extension of the neck
Pathophysiology:
Mechanisms of apnea of
1) Central Apnea: there is no signal to breathe being transmitted from the CNS to the
respiratory muscles. This is due to immaturity of brainstem control of central respiratory
drive.
2) Obstructive Apnea: A pause in alveolar ventilation due to obstruction of airflow within
the upper airway, particularly at the level of the pharynx e.g. neck flexion & excessive
secretions
3) Mixed Apnea: A combination of both types of apnea
Management:
1) Treat the underlying causes is essential.
2) Tactile stimulation: Gentle rubbing of soles of feet or chest wall is usually all that is
required for episodes that are mild and intermittent.
3) Positioning: Ensure the neonate's head and neck are positioned correctly (head and neck
in neutral position) to maintain a patent airway.
4) Clear airway: Suction mouth and nostrils.
5) Provision of positive pressure ventilation (CPAP or Intermittent Mandatory
Ventilation): May be required until spontaneous respirations resume.
6) Stop oral feeding.
7) Pulse oximeter / cardio-respiratory monitor: Detect changes in the heart rate,
respiratory rate and oxygen saturation due to apneic episodes.
8) Apnea monitor: This detects abdominal wall movement and may alarm falsely with
normal periodic breathing.

9) IV Aminophylline may help in premature babies.

Review questions
1. Maternal factors associated with pre-term baby include:

1. …………………………… 2. …………………………… 3 . …………………………..
4. …………………………… 5. …………………………….6. …………………………..
2. Complication of prematurity:
1. ............................................ 2. ............................................... 3. ..........................................
4. ................................................. 5. ................................................ 6. ........................................
3. Compare between preterm and post-term infants:
Criteria Preterm Post-term
Gestational age
Skin
SC fatty tissue
Vernix caseosa
Lanugo hair
4. Why oxygen therapy should be given cautiously in preterm baby:
...........................................................................................................................................................
...........................................................................................................................................................
5. Complication for post-maturity:
6. Complications for IDM:
7. Early manifestations of neonatal septicemia:

1. ................................................ 2. ..................................... 3. ................................................
8. Nursing interventions for patient with septicemia:
9 ...................................... is yellow discoloration of skin, mucous membranes and sclera due to

excess bilirubin in the blood.

10. Jaundice appears clinically when serum bilirubin reaches ........... mg/dl in newborn and
more than ........... mg/dl in adult.
11. In the liver unconjugated bilirubin binds with ...................................................
12. The unconjugated Bilirubin is bound to ........................ in the blood and transferred to the
liver.
13. Types of jaundice are:
1. ............................................................................ 2. ....................................................................
14. Causes of physiologic jaundice in neonate:
1. ....................................................................................................................................
2. .....................................................................................................................................
3. .....................................................................................................................................
4. .....................................................................................................................................
15. ........................................ jaundice is due to certain substances in the milk of the mother
(progesterone metabolite or free fatty acids) that inhibit the glucuronyl transfers enzyme and thus
inhibits bilirubin conjugation.
16. ............................................. jaundice is due to probably poor enteral intake of breast
feeding and increased enterohepatic circulation.
17. Conjugated Hyperbilirubinemia is caused by:
1. ....................................................................................................................................
2. .....................................................................................................................................
3. .....................................................................................................................................
18. Criteria for physiologic jaundice:
1. ....................................................................................................................................
2. .....................................................................................................................................
3. .....................................................................................................................................
4. .....................................................................................................................................
5. ......................................................................................................................................
6. .......................................................................................................................................
19. ..................................................... is Yellow coloration of the basal nuclei of the brain.
20. Nursing care for infant under phototherapy:
1. ....................................................................................................................................
2. .....................................................................................................................................
3. .....................................................................................................................................
4. .....................................................................................................................................
5. ......................................................................................................................................

21. Side effects for phototherapy:
1. ....................................................................................................................................
2. .....................................................................................................................................
3. .....................................................................................................................................
22. ................................ is the formation of edema of the scalp at the presenting part of the head.
23. ................................. Is a collection of blood beneath the periosteum of the skull bone
24. ............................... Lateral traction during delivery may damage the upper root of the
brachial plexus involving the 5th and 6th cervical roots.
25. .................................................. is a sterile , thick , black-green odorless material that results
from accumulation of debris in the fetal intestine during the third month of gestation.
26. .................................................. is Herniation of abdominal contents into the thorax with
collapse of lung and shifting of mediastinum.
27. ................................................. Is the commonest cause of respiratory distress among
immature infants.
28. Surfactant typically begins in production at ..................... weeks of gestation and but mature
levels of pulmonary surfactant are present usually after ................ wk.
29. ......................................... is a complex system of lipids, proteins and glycoproteins which
decreases surface tension in the alveolus during expiration and thus preventing alveolar collapse.
30. Predisposing factors for RDS:
1........................................................ 2................................................. 3........................................
4........................................................ 5................................................. 6......................................
31. .................................................... cessation of breathing more than 20 seconds accompanied
by bradycardia (HR less than 100beats/minute) and cyanosis.
32. Causes of apnea:
1.............................................. 2................................................. 3................................................
4................................................... 5................................................. 6...............................................
7........................................................ 8...............................................

Chapter (4)
Child With a Respiratory Disorder
Learning objectives
 List the major signs of respiratory distress in infants and

children.
 Identify various factors associated with respiratory illness in
infants and children.
 Distinguish different respiratory disorders based on their signs
and symptoms.
 Discuss nursing interventions commonly used for respiratory
illnesses.
 Devise an individualized nursing care plan for the child with a
respiratory disorder
 Describe the physiologic effects of cystic fibrosis on the
gastrointestinal and pulmonary systems.
 Outline a plan of care for the child with cystic fibrosis.

Bronchiolitis
o Bronchiolitis is inflammation of the bronchioles, the smallest air passages of the lungs.
o Bronchiolitis is the most common serious acute respiratory illness in infants and young
children especially infant from 1 to 6 months.
o One to 3% of infants with bronchiolitis will require hospitalization, especially during the
winter months.
The causative agents:
 The most common organism is respiratory syncytial virus.
 Para-influenza virus.
 Influenza virus.
 Mycoplasma pneumonia.
Pathophysiology:
Inflammatory obstruction of the bronchioles lead to decrease the ventilation of the alveoli,
which result in hypoxemia early, and hypercapnea later on in severe cases.
 Onset is often gradual and associated with exposure to respiratory infection, nasal
discharge, sneezing with or without fever and coryza of 1-3 days.
 Tachypnea with a respiratory rate of 60-80\minute.
 Dyspnea, irritability.
 Dry cough, paroxysmal cough.
 Central cyanosis, dehydration and fever.
 Intercostal and substernal retraction.
 Expiratory wheezes or rhonchi.
 X-ray chest (hyperinflation of the lungs).
 Serologic studies to isolate virus on throat swab.
 ABG analysis (decreased PaO2, increased PaCO2 finding).
Course:
 The most critical is the first 2-3 days during which the patient may develop apneic spells
and respiratory acidosis.
 It has a good prognosis.
 Death may occur from prolonged apneic spell or attack, uncompensated acidosis and
heart failure.

Treatment and nursing management:
1. Antibiotic therapy given to severely ill child until laboratory confirmation is established.
2 Humidified oxygen to relief arterial hypoxemia.
3. Inhalation of adrenaline is commonly used.
4. Monitor ABG and correction acidosis.
5. Possible ventilatory assistant.
6. Maintain fluid, electrolyte and acid base and nutritional balance.
7. Keep nasal air way open and clear of mucus.
8. Position (semi-sitting position).
9. Be alert for signs of impending respiratory acidosis, dehydration and cardiac involvement.
10. Feeding: Infants with bronchiolitis frequently have poor feeding, are at risk of aspiration
and may be dehydrated. Small frequent feeds as tolerated can be allowed in children with
moderate respiratory distress. Nasogastric feeding, although not universally practiced, may
be useful in these children who refuse to feed and also to empty the dilated stomach.
11. Intravenous fluids for children with severe respiratory distress, cyanosis, apnea.
Fluid therapy should be restricted to maintenance requirement of 100 ml/kg/day
for infants, in the absence of dehydration.

Cystic fibrosis (CF)
o CF is a genetic multisystem disorder that primarily affects the exocrine (mucus producing)
glands.
o It is the most common serious pulmonary and gastric disease of children and accounts for a
large percentage of lung disease of children..
Etiology:
 CF is inherited as an autosomal-recessive trait and has an equal sex distribution.
Pathophysiology:
o In CF, the mutant gene results in epithelial ion transport on mucosal surfaces resulting in
generalized dysfunction of exocrine glands.
 Respiratory system:
 Decreased ciliary action and thus decrease expelling of secretion
 Bronchi and bronchioles become plugged, resulting in bronchiectasis and
bronchiolitis
 Increased production of thick secretion (increased risk of infection)
 Atelectasis and hyperinflation of lungs
 Irreversible fibrotic changes occur in lungs.
 Gastrointestinal and Pancreatic:
 Pancreatic enzyme activity is lost and mal-absorption of fats, proteins, and carbohydrates
occurs, resulting in poor growth
 Localized Biliary obstruction and fibrosis are common in the liver and become more
extensive with time leading to biliary cirrhosis.
 The majority of children show evidence before 1 year of age.
 The earliest manifestation of CF is meconium ileus in the newborn, in which the small
intestine is blocked with thick, tenacious meconium (in about 10% of cases).
 Gastrointestinal manifestations:
o Large, bulky, loose, frothy, and extremely foul smelling stools.
o Voracious appetite (early m disease). Loss of appetite (later in disease).
o Weight loss with marked tissue wasting.
o Distended abdomen and thin extremities.
o Anemia and pale skin .
o Evidence of deficiency of fat-soluble vitamins ( A,D,E, and K).
 Pulmonary manifestations:

Initial Signs: Wheezy respirations, dry non-productive cough.
Eventually: Increased dyspnea, paroxysmal cough, emphysema and atelectasis.
Progressive Involvement: Cyanosis, clubbing of fingers and toes, overinflated barrel-
shaped chest, repeated episodes of bronchitis and bronchopneumonia.
Complication:
 Pulmonary infections most frequently caused Pseudomonas, staphylococcus and
hemophilus influenza.
 Emphysema, atelectasis, hemoptysis and pneumothorax.
 Growth retardation.
 Biliary cirrhosis with portal hypertension, splenomegaly and esophageal varices.

 Cor pulmonale (failure of the right side of the heart)
 Chronic sinusitis, nasal polyps
 Pancreatitis, diabetes and hyperglycemia (after 10 years).
 Fibrosis of epididymis and vas deferens (aspermia) in males and amenorrhea and
decreased fertility in females (cervical mucus plug).
Diagnostic Evaluation:
 Measurement of sodium and chloride in sweat (Sweat test).

 Normally, the sweat chloride content is less than 40 mEq/L
 40- 60 mEq/L is borderline and should be repeated.
 Chloride concentration greater than 60 mEq/ L is diagnostic of CF.
NB: Two reliable positive results on two separate days is diagnostic for CF.
 Measurement of trypsin concentration in duodenal secretions. Absence of normal
concentration is diagnostic.
 Analysis of digestive enzymes in stool.
 Chest X-Ray
 Analysis of stool for steatorrhea.
The diagnosis of CF is established on the basis of:
1. A history of the disease in family.
2. Absence of pancreatic enzymes.
3. Increase in electrolyte concentration in sweat.
4. Chronic pulmonary involvement.
Therapeutic Management:

The goals of care are aimed at promoting a normal life for the child.
1. Pulmonary Therapy:
The most important aspect of treatment is to improve pulmonary function and loosen and
eliminate bronchial secretions.
 Antimicrobial therapy as indicated.
 Bronchodilators to relief bronchospasm.
 Aerosol expectorants and mucolytic agents to decrease viscosity of secretions.
 Postural drainage and chest physiotherapy.
o Usually follows aerosol therapy 3-4 times per day ideally done before eating to
prevent vomiting.
o Clapping "with cupped hands and vibrating for 1 or 2 minutes in each area
loosens mucus plugs.
o Coughing should be encouraged after postural drainage, otherwise suctioning will
be necessary.
 Oxygen therapy is usually recommended for children with acute episodes. For those with
chronic CO2 retention, the unsupervised use of oxygen can be harmful.
2. Gastrointestinal Therapy:
 Pancreatic enzyme supplements with each feeding (Creon).
 Increased caloric (carbohydrate) and protein intake.
 Decrease fat intake.
 Daily intake of water-soluble and fat-soluble vitamins.
 Adequate fluid and salt intake.
3. Promote Normal Growth and Development:
 Treat the child as a normal person.
 Encourage normal relationships with peers and family.
 Promote positive self-image.
Prognosis:
No exact figures are available regarding the life expectancy of a child with CF. Many still die
in infancy and early childhood, but increasing number are living into the third and fourth
decades and even beyond. More than 50% of the patients now live into adulthood.

Review questions
1. Inability to pass meconium is indicative for ................................. or ...............................

2. Complications of cystic fibrosis on respiratory system include:
1. ............................................ 2. ............................................. 3. ................................................
3. Complication of cystic fibrosis on GIT include:
1. .................................................. 2. ........................................ 3. ...............................................
4. The diagnosis of CF is established on the basis of:
1. ...................................................................... 2. ..................................................................
3. ....................................................................... 4. ..................................................................
5. ................................... is a diagnostic test for CF.
6. Normally, the sweat chloride content is ...................................
7. Chloride concentration greater than 60 mEq/ L is diagnostic of CF.
8. ................... mEq/L is borderline and should be repeated.
9. ………………………… is the most common causative agent for bronchiolitis
10. Bronchiolitis is the most common serious acute respiratory illness in infants and young
children especially infant from age …………….. to ……………….
11. Treatment and nursing management of acute bronchiolitis:
12. CF is a genetic multisystem disorder that primarily affects the ………………..glands.
13. CF is inherited as ………………………….. trait

Chapter (5)
Child With a Cardiovascular Disorder
Learning objectives
 Compare anatomic and physiologic differences of the

cardiovascular system in infants and children versus adults.
 Distinguish cardiovascular disorders common in infants, children,
and adolescents.
 Identify appropriate nursing assessments and interventions related
to medications and treatments for pediatric cardiovascular
disorders.
 Develop an individualized nursing care plan for the child with a
cardiovascular disorder.
 Describe the psychosocial impact of chronic cardiovascular
disorders on children.
 Classify the congenital heart diseases
 Describe in details the definition, pathophysiology, clinical
manifestations , diagnostic measures, treatment and nursing care
of child with congenital heart diseases, acquired heart diseases e.g.
rheumatic fever .
 List the major and minor criteria for rheumatic fever

Cardiovascular Diseases in pediatric
 Cardiovascular disease is a significant cause of chronic illness and death in children.
 Typically cardiovascular disorders in children are divided into two major categories:
1) Congenital heart disease is defined as structural anomalies that are present at birth.
2) Acquired heart disease includes disorders that occur after birth. These disorders
develop from a wide range of causes, or they can occur as a complication of CHD such
as: myocarditis, heart failure and rheumatic heart disease.
Fetal Circulation
 Oxygenated blood comes from the placenta and enters the fetus, at the umbilicus, through
the umbilical vein.
 Umbilical vein divides at the liver with a small branch going to the liver and the other
branch, the ductus venosus, entering the inferior vena cava.
 The blood is now partially deoxygenated by the blood coming from the lower part of the
fetus’s body. This blood enters the right atrium and moves through the foramen ovale (a
flap opening in the atrial septum that allows only right-to-left movement of blood) to the
left atrium and then to the left ventricle.
 A small portion of this blood passes into the right ventricle. The left ventricle pumps the
blood out through the aorta. Blood entering the right atrium from the superior vena cava
flows to the right ventricle. It is pumped out through the pulmonary arteries.
 Most of this blood goes into the aorta through the ductus arteriosus , a fetal vessel
connecting the pulmonary trunk to the aorta. Normally this closes at birth. A small
amount of blood goes to the lungs to nourish the lung tissue
 The aorta and its branches supply blood to the rest of the body. The two umbilical arteries
branch from the internal iliac arteries and return blood to the placenta to be oxygenated.
 The circulatory system of the fetus functions much differently from that of a newborn.
The most significant difference is that oxygen is received from the placenta during fetal

life and via the lungs after birth. In addition, the fetal liver does not perform the
metabolic functions that it will after birth because the mother’s body performs these
functions.
 Three shunts also are present during fetal life:
o Ductus venosus: connects the umbilical vein to the inferior vena cava.
o Ductus arteriosus: connects the main pulmonary artery to the aorta.
o Foramen ovale: anatomic opening between the right and left atrium.
Soon after birth:

When the infant breathes for the first time, there is a decrease in the resistance in the pulmonary
vasculature, which causes the pressure in the left atrium to increase relative to the pressure in the
right atrium. This leads to the closure of the foramen ovale functionally.
Additionally, the increase in the concentration of oxygen in the blood leads to a decrease in
prostaglandins, causing closure of the ductus arteriosus.
These closures prevent blood from bypassing pulmonary circulation, and therefore allow the
neonate's blood to become oxygenated in the newly operational lungs.
Later after birth:
o Ductus arteriosus becomes Ligamentum arteriosum
o Foramen ovale becomes Fossa ovalis
o Ductus venosus becomes Ligamentum venosum
o Umbilical vein becomes Ligamentum teres
o Umbilical arteries become Medial umbilical ligaments

Congenital Heart Diseases (CHD)
o Congenital heart disease (CHD), Also called congenital heart defects or congenital heart
anomaly, is a structural malformation of the heart or; great vessels presents at birth.
o CHD is frequently associated with other congenital defects.
Incidence: It is the most common congenital malformation. Eight in 1000 infants are born with
a congenital heart defect
Etiology
o The exact cause is unknown, results from abnormal embryonic development or the
persistence of fetal structure beyond the time of normal involution.
o It is known that certain environmental factors operating in early pregnancy can result in
malformation as:
1. Maternal infection as rubella 2. Poor nutrition of mother.
3. Diabetic mothers 4. Maternal alcoholism.
5. Maternal exposure to radiation 6. Genetic defect e.g. down syndrome

Classification:
1. Acyanotic (without cyanosis):
A. Without shut
 Dextrocardia
 Obstructive lesion e.g. aortic stenosis, pulmonary stenosis and coarctation of the aorta.
B. Left - to - Right shunts
 Patent ductus arteriosus (PDA)
 Atrial septal defect (ASD)
 Ventricular septal defect (VSD)
2. Cyanotic: (Right - to - Left shunt)
 Tetralogy of Fallot (TOF)
 Tricuspid atresia.
 Transposition of great arteries (TGA)
 Pulmonary atresia
 Hypoplastic left heart syndrome

Clinical Manifestations: Children who have not been diagnosed before birth may present with:
o Murmurs on routine screening.
o Tachycardia.
o Heart failure.
o Difficulty feeding, and failure to thrive.
o Shortness of breath.
o Cyanotic episodes (especially during feeding).
o Sudden collapse.
Diagnostic tools:
 Echocardiography is the initial investigation of choice. It is non-invasive. It can clarify
both anatomy and flow and will give some indication of the underlying abnormality.
 Cardiac catheterization may be required in more severe cases to assess the extent of the
problem, and prepare for correction of the problem.
 Electrocardiography
 Chest x ray
 ABG, CBC, Chemistry
Treatment:
o Sometimes CHD improves without treatment.
o Medical management: such as diuretics, digoxin, antihypertensive, antiarrhythmic,
prostaglandin, indomethacin, heparin, Spironolactone, inotropic agents
o Surgical procedures to restore circulation back to normal and in some cases, multiple
surgeries are needed

Dextrocardia
o Dextrocardia is congenital defect in which the apex of the heart is located on the right
hemithorax.
o It may be either Isolated Dextrocardia (only the heart is located on the right hemi-thorax)
or Dextrocardia situs inversus (abdominal and thoracic organs transposed to opposite side
of the body).
Diagnosis:
1. Clinically: apex beat on the right side, stomach {percussion} on right side, the liver on
the left side.
2. X-ray: situs inversus.
3. Electrocardiograph {ECG}: lead I is the mirror image of the normal tracing with
inverted P and T waves.
Aortic Stenosis
Occurs when there is obstruction to the left ventricular outflow usually at the level of the aortic
valve.
Pathophysiology:
o As a consequence of aortic stenosis, the left ventricle must generate a higher pressure with
each contraction to effectively move blood forward into the aorta left ventricular
hypertrophy.
o Myocardial ischemia may occur as a result of an imbalance between the increased O2
requirements and the amount of O2 supplied.
 Rarely symptomatic during infancy, in severe cases infant may demonstrate evidence of
decreased cardiac output such as faint peripheral pulses or exercise intolerance.

 Older children may experience anginal chest pain, dyspnea and fatigue with exertion.
 Narrow pulse pressure.
 Weak peripheral pulses.
 X-ray: normal heart to varying degrees of left ventricular hypertrophy.
 A harsh ejection systolic murmur is best heard in the aortic area.
 E.C.G.: left ventricular hypertrophy {T. wave inversion).
Diagnosis: Echocardiography, Cardiac Catheterization
Complications: C.H.F, M.I., bacterial endocarditis, and death.
Treatment:
 Mostly live well to middle age.
 Surgery: Valvotomy (incision into a stenosed cardiac valve to relieve the obstruction) or
prosthetic valve replacement.

Pulmonary Stenosis
Occurs when there is obstruction to the right ventricular outflow usually at the level of the
pulmonary valve.
Pathophysiology:
Blood flow from the right ventricle through the obstructed pulmonary valve into the pulmonary
artery increased Rt. ventricular pressure Rt. ventricular hypertrophy Rt. sided
heart failure Rt. Atrial pressure persistent opening of the foramen ovale
shunting of un-oxygenated blood from the Rt. atrium into the left atrium cyanosis.
Clinical Manifestation:
 Generally asymptomatic, the child may have decreased exercise tolerance, no cyanosis.
 With sever obstruction, the child may have dyspnea and cyanosis.
 May complain precordial pain.
 Systolic ejection murmur over the pulmonic area.
 X- ray and ECG: right ventricular hypertrophy.
Diagnosis: Echocardiography, Cardiac Catheterization
Complication: anoxic spells, bacterial endocarditis, death. ''Heart Failure"
Treatment:
Asymptomatic children should be evaluated at regular intervals.
Surgical: Valvotomy or prosthetic valve replacement
Coarctation of the Aorta
Is a narrowing or constriction of the aorta at any point. Most common, the constriction is located
just distal to the origin of the left subclavian artery in the vicinity of the ductus arteriosus.
Altered Physiology:
The narrowing of the aorta obstructs the blood flow through the constricted segment of the aorta
increasing the left ventricular pressure collateral vessels develop from the subclavian
arteries bypassing the coarcted aorta and supplying circulation to the lower extremities
 Usually asymptomatic in childhood.
 May demonstrate: occasional fatigue, headache, nose bleed and leg cramps,
 Absent or greatly reduced femoral pulses.
 Hypertension in upper extremities, hypotension in lower one.
 Sever anomalies growth retardation, dyspnea, peripheral edema and C.H.F.

 Non-specific systolic murmur heard along the left sternal border.
 E.C.G-normal to left ventricular hypertrophy.
Diagnosis: Echocardiography, Cardiac Catheterization, Angiography
Complication: Cerebral Hemorrhage, Rupture Aorta, and C.H.F.
Treatment:
 Management of C.H.F.
 Surgical: resection of the anastomosed part and anastomosis or graft at 2-7 years.
Patent Ductus Arteriosus (PDA)
Is the persistence of a fetal connection between the pulmonary artery and the aorta through
which blood leaving the right heart bypasses the lungs.
Altered physiology:
 During fetal life, the ductus arteriosus allows most of the right ventricular blood to
bypass the nonfunctioning lungs by directing blood from the pulmonary artery to the
aorta.
 After birth, with initiation of respiration, it is no longer necessary, functionally close
within hours and anatomically close within weeks, by degenerative changes and become
a cord of fibrous connective tissue "ligamentum arteriosum".
 When this duct remains patent, oxygenated, blood from the higher pressure {aorta} flows
to the lower pressure of the pulmonary circulation.
 The volume of blood that the heart must pump in order to meet the demands of the
peripheral tissue is increased.
 A greater volume is placed on the lungs and the left heart
1) Small PDA: usually asymptomatic.
2) Large PDA: may develops symptoms during early infancy, slow weight gain, feeding
difficulties, frequent respiratory infection, C.H.F —► Physical retardation.
 Systolic murmur in the second left intercostal space is heard.
Diagnostic evaluation :
1- E.C.G: normal or left ventricular hypertrophy.
2- Echocardiogram.
3- Angiocardiography.
4- Cardiac Catheterization.
Complication: C.H.F, infective endocarditis.
Treatment:
 Controlling of C.H.F.
 Device closure of PDA in which a device such as a coil, very small rings of wire is
placed over the PDA causing the blood to clot and thus closing the open ductus.
 Surgical by ligation or division and ligation of the duct "electively by 1 -2 years".
 Indomethacin may trigger the natural closing of the duct.
Atrial Septal Defect
Is an abnormal opening in the septum between the left atrium and right atrium.
Types:
1) Ostium Secundum (most common): at the center of atrial septum.
2) Ostium Primum: large gap at the base of the atrial septum, usually Associated with
deformities of the mitral or/and tricuspid valves and ventricular septal defect.
Altered Physiology:
 The pressure in the left atrium is greatening than that in the right one, which promotes the
flow of oxygenated blood from the left to the right atrium.
 The blood flow through the shunt circulates through the lung, thus increasing the total
blood flow through the lung.
 The major hemodynamic abnormality is volume overload of the right ventricle.
 If the pulmonary resistances is great increase right atrial pressure reversal the
shunt with un-oxygenated blood flowing from 'the right to left atrium cyanosis.
o Ostium Secundum: asymptomatic {underdeveloped due to decrease left output}.
o Ostium Prirnum: asymptomatic, slow weight gain, easy fatigability, dyspnea with
exertion frequent respiratory infections, C.H.F.

1. Auscultation: systolic murmur at the second left intercostal space.
2. X-ray: increased vascularity of the lungs.
3. E.C.G.: right ventricular hypertrophy, prolonged P - R interval.
4. Echocardiogram.
5. Cardiac catheterization.
6. Angiocardiography.
Complication: C.H.F., Pulmonary Hypertension.
Treatment:
 ASD device closure
 Surgical closure with cardiopulmonary bypass.

Ventricular Septal Defect
 Is an abnormal opening in the septal between the right and left ventricles. It may vary in
size from very small defect to very large defect {1-15 mm in diameter}, most commonly
found in the fibrous portion of the septum.
 Most common cardiac anomaly.
Altered Physiology:
 The pressure in the left ventricle is greater than that of the right one promotes the
flow of oxygenated blood from the left to the right ventricle increasing the total
blood flow through the lungs.
 The major hemodynamic abnormality is increased right ventricular and pulmonary
arterial pressure.
 If the pulmonary resistance is great, increase right ventricular pressure, thus causing
reversal of the shunt with un-oxygenated blood flowing from the right ventricle to the left
one "Eisenmenger's complex" cyanosis.
 Small VSD: usually asymptomatic
and may close spontaneously.
 Large VSD: may develop symptoms
at 1-2 months of age.
 Slow weight gain, feeding difficulties,
frequent respiratory infections.
 Tachypnea, C.H.F.
 Systolic murmur at the fourth interspace to the left of the sternum. .
 X- ray: biventricular hypertrophy.
 E.C.G: normal to biventricular hypertrophy.
 Echocardiogram.
 Cardiac Catheterization.
 Angiocardiography.
Complication: C.H.F
Treatment:
 Medical management of C.H.F.
 Surgical closure.

Cyanotic Congenital Heart Disease
Teratology of Fallot
The most common type of cyanotic {C.H.D.} in children over the age of one year, it consists of
4 abnormalities:
1. Pulmonary stenosis.
2. Ventricular septal defect {VSD}={left to right shunt}.
3. Overriding of the aorta,
4. Right ventricular hypertrophy.
Altered Physiology:
 Pulmonary stenosis: un-oxygenated is shunted from the right ventricle from the VSD
directly into the aorta.
 The right ventricle is hypertrophied because of high right ventricular pressure.
 Cyanosis: not cyanotic at birth {left to right shunt} may starts later, may be at 1 -2 years, first
observed with exertion or crying, then cyanotic even at rest.
 Clubbing of fingers.
 Squatting posture
 Slow weight gain.
 Hypoxia spells.
 Insignificant murmur.
 E.C.G: right ventricular hypertrophy.
 Cardiac Catheterization.
 Angiocardiography.
 Laboratory data: polycythemia, increasing of H.C.T.
Complication: C.H.F (rare), infective endocarditis, C.V.A. {cerebral hypoxia)
Treatment:
 Improve oxygenation.
 The infant is put in knee chest position to decrease the venous return from the legs (as
squatting position).
 Phlebotomy and adequate hydration to prevent cerebral thrombosis.

 Palliative: anastomosis between the right or left subclavian artery and the right
pulmonary artery or between the aorta and pulmonary arteries to increase the pulmonary
blood flow (Blalock-Taussig operation).
 Total correction: removing the previous shunt, pulmonary Valvotomy and VSD is
repaired, with cardiopulmonary bypass later on at age of 6 years.
A: original: subclavian artery is directly connected to the

pulmonary artery
B: Modified: a tube connects between aortic arch and
pulmonary artery
Clubbing of fingers Squatting position: increases

pressure on the left side of the heart,
decreasing the right to left shunt thus
decreasing the amount of
deoxygenated blood entering the
systemic circulation

Transposition of the Great Arteries
(TGA)
 TGA occurs when the aorta arises from the-right ventricle and the pulmonary artery from
the left.
 Other anomalies are usually present e.g. VSD {this if present is of good prognostic value},
ASD, PDA.
o Marked cyanosis since birth.
o Failure to thrive, Fatigability.
o Dyspnea with subcostal retractions
at rest and during feeding.
o Cardiomegaly.
o Early clubbing of fingers.
o CH F
1) Auscultation: insignificant murmur.
2) Chest x -ray (cardiomegaly).
3) Laboratory tests: polycythemia.
4) E.C.G: biventricular hypertrophy.
5) Echocardiogram.
6) Cardiac Catheterization.
7) Angiocardiography.
Prognosis: Without surgical treatment, 85 % die in the first 6 months of age.
Complication:
C.H.F., infective endocarditis, brain abscess, C.V.A {thrombotic}.
Treatment:
 Management of C.H.F.
 Palliative procedures: creation of A.S.D. with a balloon catheter during catheterization or
surgical creation of A.S.D.
 Complete correction: by cardiopulmonary bypass

Tricuspid Atresia
Is a condition in which there is:

1. Atresia of the tricuspid valve so that there is no communication between the right atrium
and right ventricle.
2. Atrial septal defect.
3. Hypoplastic right ventricle.
 There is usually a V.S.D. allowing some blood to enter the underdeveloped right ventricle.
Pathophysiology:
 Blood from the systemic circulation is shunted from this right atrium through an inter-atrial
communication to the left atrium, to the left ventricle.
 Pulmonary blood flow is established either through PDA or VSD.
 Cyanosis {marked since birth}.
 Dyspnea on feeding.
 Early clubbing of fingers.
 Hypoxia spells.
 Failure to thrive.
 Right heart failure may occur.
 No murmur or murmur of associated defects.
 E.C.G.: left sided hypertrophy of the heart.
 Echocardiogram.
 Cardiac catheterization.
 Angiocardiography.
Complication: C.V.A, brain abscess, and bacterial endocarditis.
Treatment:
 Palliative procedures: to increase the pulmonary blood flow
 Anastomosis between the ascending aorta and right pulmonary artery.
 Subclavian to pulmonary artery anastomosis.
 Complete correction:
Fontan Procedure: placement of a tubular condition with a valve between the right atrium and
the main pulmonary artery. The atrial defect is closed and the main pulmonary artery is ligated
just above the pulmonary valve.

Acquired Cardiovascular Disorders
Acute Rheumatic Fever
Is a systemic disease characterized by inflammatory lesions of connective and endothelial tissue

which involving mainly the joints and the heart and less frequently the CNS, skin, and the
subcutaneous tissue. It remains the most common form of acquired heart disease worldwide..
Etiology:
 The exact pathogenesis is unknown:
 It is thought to be an autoimmune response to group A beta hemolytic streptococci.
 Most first attacks of rheumatic fever are preceded by streptococcal infection of the throat
or upper respiratory tract at an interval of several days to several weeks.
The diagnosis is based on a combination of manifestations ch.ch. of this disease .
The presence of 2 major criteria or 1 major and 2 minor criteria, plus evidence of preceding
streptococcal infection are required to establish the diagnosis.
1. Major manifestations:
1) Carditis:
 All layers of the heart are involved i.e. pancarditis (pericarditis, myocarditis,
endocarditis) with resultant of significant murmurs, signs of cardiomegaly or
congestive heart failure.
2) Polyarthritis:
 It affects mainly the big joints e.g. knee, wrist, ankles, elbow.
 The affected joint shows signs acute inflammation swollen, tender and red, hot,
limitation of movement associated with severe pain).
3) Subcutaneous nodules:
 Firm, painless bodies seen or felt over the extensor surface, of certain joints
particularly the elbow, knees and wrists.
 Disappear mostly after 4 months.
 Presence of nodules is an indicator that the heart is involved.
4) Erythema Marginatum:
 It appears in rings, crescents, ovals, or irregular forms ch.ch. by a thin red margin
outlining a patch of normal skin.
 It distributed mainly on the trunk and proximal parts of the limbs.
 The rash does not appear on the face and there is no itching or discomfort.
5) Chorea:

 Purposeless involuntary movement often associated with muscle weakness,
incoordination of voluntary movements and emotional instability.
 It often to appear to occur alone rather than in the company of other manifestation.
2. Minor manifestations:
1. Fever
2. Arthralgia {must not be included with polyarthritis in diagnosis}
3. Prolonged P-R interval in the E.C.G.
4. Increased E.S.R., leukocytosis, Positive C-reactive protein
5. A history of streptococcal infection, scarlet fever,
previous history of the rheumatic fever.
3. Evidence of preceding Streptococcal infection:
 History of scarlet fever.
 Increase A.S.O.T. —► more than 250 at 2-6 weeks
 Positive; throat cultures for group A streptococci.
Treatment:
1) Bed rest: To decrease cardiac demands for 2 weeks then gradual ambulation.
2) N.B.: With significant signs of carditis, bed rest until heart murmur has diminished,
normal sleeping pulse, C.R.P. is normal and E.S.R. is decreasing → this entails 2-3
months, then gradual ambulation for 3 months.
3) Prevention of rheumatic fever through control of streptococcal infection: Procaine
penicillin to eradicate any microorganisms for 10 days. Then benzathine penicillin G
1.200.000 units once a month. Erythromycin is substitute for penicillin in case of allergy.
4) Anti-inflammatory:
A. cases of arthritis without cardiac involvement:
 Aspirin 100 mg/kg/day orally in 4-5 divided doses for 2 weeks after ESR return to
normal.
B. cases of arthritis with cardiac involvement
 Prednisone 2mg/kg/day in 2-3 divided doses until ESR return to normal. It is
gradually withdrawn.
 Aspirin 100 mg/kg/day orally in 4-5 divided doses for 2 weeks after ESR return to
normal.
5) For rheumatic chorea: Haloperidol or barbiturate or chlorpromazine is useful to
control involuntary movements and agitation.
6) Treatment of CHF: complete bed rest, oxygen therapy, fluid restriction, diuretics,
digoxin

Red borders of erythema
Nursing diagnosis: marinatum
1. Pain related to polyarthritis.
2. Potential for infection related to steroid therapy.
3. High risk for injury related to chorea.
4. Altered body image related to chorea or\and steroid therapy.
5. Activity intolerance related to muscle weakness.
6. Knowledge deficit about rheumatic fever and its treatment.
7. High risk for injury related to presence of streptococcal
8. organism and recurrence of rheumatic fever and bacterial
endocarditis.
Nursing intervention:
1. Initiate specific preventive teaching in order to prevent recurrence or an additional case of
rheumatic fever within the family.
 Screen all family members for streptococcal infection.
 Institute measures to encourage compliance with therapeutic regimen.
 Explain to the child and family importance of ongoing long- term health supervision,
since the child is susceptible to recurrent' rheumatic fever.
 Explain to the child and family the need for antibiotic prophylactic for dental work,
infection and any invasion procedures.
2. Encourage adequate rest and nutrition to support body defense.
3. Administer salicylate as ordered.
4. Explain that chorea is a manifestation of the disease because the child and family may
misinterpret it
5. Give the family and child the opportunity to verbalize feeling.
6. Stress that chorea is involuntary, transient and will disappear.
7. Give the child information about rheumatic fever in terms can be understood.
8. Give and provide safe, supportive care for the child with chorea:
- Padded side rails. - Feed slowly. - Administer sedation.
9. Prepare this child and his family for the expected side effects of steroid therapy:
 Body appearance.
 Excessive hair and acne.
 Weight daily.
 Don't place the child with other children with infection disease in the same room.

Review questions
1.................................................. structural anomalies that are present at birth
2. Environmental risk factors operating in early pregnancy can result in CHD:
1. .......................................................2. ............................................. 3. ........................................
4. ......................................................5. ................................................ 6 ........................................
3. Cyanotic heart defects include:
1. ......................................................2. .............................................
3. ..................................................... 4. ...................................................
4. Acyanotic heart defects include:
1. .......................................................2. ............................................. 3. ........................................
4. ......................................................5. ................................................ 6 .........................................
5. Teratology of Fallot consists of 4 abnormalities:
1. ................................................... 2. .................................................
3. .....................................................4. ..................................................
6 .................................. and ........................................ are manifested by cyanosis since birth.
7. Most first attacks of rheumatic fever are preceded by infection with

..................................................................... of the throat or upper respiratory tract
8. Major manifestations of rheumatic fever are:
1. .................................... 2. ................................... 3. ....................................4. ..............................
9. ................................................ is Purposeless involuntary movement often associated with
muscle weakness, incoordination of voluntary movements and emotional instability.
10. Minor manifestations of rheumatic fever are:
1. ......................................... 2. ................................... 3. ....................................
4. ..................................... 5. ..........................................................
True or false
( ) 1. Bronchiolitis commonly affects infants between 1to 6 months.

( ) 2. The most common organism is respiratory syncytial virus
( ) 3. Cystic fibrosis is a genetic disorder that primarily affects the endocrine glands.
( ) 4. Cystic fibrosis causes FTT.
( ) 5. Steatorrhea is evident in cystic fibrosis

( ) 6. Sweat test is diagnostic for celiac disease.
( ) 7. The normal value of chloride in sweat is more than 40 mEq/l
( ) 8. Clubbing of fingers is a progressive manifestation of cystic fibrosis
( ) 9. Absent or greatly reduced femoral pulses is evident in tetralogy of fallot
( ) 10. Hypertension in upper extremities, hypotension in lower one is evident in
coarctation of aorta
( ) 11. Indomethacin may trigger the natural closing of the ductus arteriousus.
( ) 12. Prostaglandin maintains ductus arteriousus patent
( ) 13. Ostium Secundum is an opening at the center of atrial septum
( ) 14. Ostium Primum is a large gap at the base of the atrial septum, usually associated
with deformities of the mitral or/and tricuspid valves and ventricular septal defect
( ) 15. TGA is the most common type of cyanotic CHD in children over the age of one year
( ) 16. Cyanosis associated with TOF appears immediately after birth
( ) 17. Squatting is a posture assumed by children with tricuspid atresia
( ) 18. To decrease cyanosis associated with TOF, immediately put the child in knee chest
position.
( ) 19. Fontan Procedure is done for tricuspid atresia
( ) 20. Group A beta hemolytic streptococci excrete a toxic substance called streptolysin O
( ) 21. Presence of erythema marginatum is an indicator that the heart is involved
( ) 22. The presence of 3 major criteria or 2 major and 1 minor criteria, plus evidence of
preceding streptococcal infection are required to establish the diagnosis of rheumatic
fever.
( ) 23. VSD is the most common cardiac anomaly.

Chapter (6)
Child With a hematological Disorder
Learning objectives
 Distinguish between the various categories of anemia
 Describe the prevention of and care of the child with iron-
deficiency anemia
 Compare sickle cell anemia and β-thalassemia major in relation to
pathophysiology and nursing care.
 Describe the mechanisms of inheritance and nursing care of the
child with hemophilia
manifestations , diagnostic measures, treatment and nursing care of
child with thalassemia, iron deficiency anemia, sickle cell anemia,
G6PD deficiency anemia, hemophilia and ITP.

Iron deficiency anemia
 Iron-deficiency anemia is a common anemia caused by insufficient dietary intake and

absorption of iron, and/or iron loss from intestinal bleeding.
 Hypochromic, microcytic (small red blood cells) anemia.
 Occur most commonly between the ages of 6 months 2years.
 Initially the neonates iron requirement are usually met by reserves acquired during fetal life,
but after 3-4 month of age additional iron must be derived from the diet
 Iron is necessary for formation of RBCs. When the body has sufficient iron to meet its needs
(functional iron), the remainder is stored for later use in all cells, but mostly in the bone
marrow, liver, and spleen.
Hypochromic means that the
 Daily requirements (8-15 mg) 16-20% is absorbed . red blood cells have less color
than normal when examined
Causes:
under a microscope.
1) Inadequate stores of iron at birth : This usually occurs when
there is not enough of the
 Prematurity, or multiple births. pigment that carries oxygen
 Severe maternal iron deficiency during pregnancy. (hemoglobin) in the red blood
cells
 Fetal blood loss at or before delivery
2) Inadequate intake:
 Breast milk cannot supply the infant with all his needs of iron especially after 6
months of life.
 Also, Cow's milk is poor in iron. Iron should be supplied to the infant when he
doubles his birth weight.
3) Impaired absorption of iron : as in chronic diarrhea, celiac disease & malabsorption.
4) Excessive demands of iron :
 Blood loss : particularly from the GIT as in parasite infestation, polyps,...etc.
 Rapid growth : in prematures and adolescence.
Clinical manifestation:
 Pallor is the most important finding.
 Other signs and symptoms include: anorexia, dysphagia, glossitis, decreased attention,
irritability, low school performance, easy fatigability, tachycardia, enlarged spleen.
Investigations:
 Decreased HB level, decreased hematocrit but RBCs count is slightly below normal (as
iron deficiency anemia affects Hb synthesis much more than RBCs formation)
 Decreased MCV, MCH, MCHC and increased RDW
 Serum iron less them 40 microgram (80-120 normal)

 Iron binding capacity (IBC) more than 400 mg/dl (normal 100-400 mg/dl)
Treatment:
 Oral iron: 6mg/kg/day of elemental iron in 3 divided oral dose for 4-6 weeks.
 IM. Iron dextran: 50 mg -100 mg for 3-5 days in case of intolerance or mal-absorption
of iron.
 Correction of the diet and treatment of the causes as parasite infection.
 The simultaneous addition of Vit. C enhances the absorption of iron. not with eggs or
milk or tea
 Ensure that iron-deficient infants are fed only formulas fortified with iron.
 Interventions for breastfed infants include beginning iron supplementation around the
age of 4 or 5 months (iron-fortified cereals) or giving iron drops.
 Encourage breastfeeding mothers to increase their dietary intake of iron or take iron
supplements when breast feeding, so that the iron may be passed on to the infant.
 Limit fast-food consumption and encourage intake of iron-rich foods such as red meats,
tuna, salmon, eggs, tofu, enriched grains, dried beans and peas, dried fruits, leafy green
vegetables (iron from red meat is the easiest for the body to absorb).
 Teach the parents about dietary intake, and encourage them to provide a variety of
foods for iron support and vitamins and other minerals necessary for growth.

Sickle Cell Disease
Sickle cell disease is an inherited disorder in an autosomal recessive pattern. This means that a
child will not inherit the disease unless both parents pass down a defective copy of the gene. It
mostly affect the black children.
Pathophysiology:
 In sickle cell anemia, an abnormal gene results in production of an irregular red blood
cell called hemoglobin (Hgb) S that replaces some of the normal hemoglobin A.
 Hemoglobin S differs from normal adult hemoglobin (hemoglobin A) only by a single
amino acid substitution (There is substitution of the amino acid valine for the amino acid
glutamine in the 6th position of the beta chain of globins).
 The red blood cells collapse into a crescent shape (sickling) when stressed such as during
dehydration, hypoxemia, or acidosis.
 These irregularly shaped cells get stuck in the blood vessels and are unable to transport
oxygen effectively, causing pain and damage to the organs.
 Sickle cells are fragile and rapidly destroyed in the circulation results in anemia.
 Sickle cells are rigid, inflexible and thus unable pass through very small blood vessels,
instead they become elongated and obstruct the blood vessels result in interference with
blood supply to various tissue and thus causing infarctions.
Precipitating factors for sickle crisis include:
1. Dehydration 2. Infections 3. Trauma 4. Exertion 5. Cold exposure 6. Hypoxia.
7. Acidosis
 These are related to the hemolytic anemia and to
tissue ischemia and organ dysfunction caused by vaso-occlusion.
Symptoms includes:
o Painful swelling of hands and feel in infancy.
o Painful swelling of large joints in children.
o Abdominal pain (spleen affection).
o Cerebral occlusion —strokes, hemiplegia blindness
o Pulmonary infarction: decreased gas exchange,
producing hypoxia, which leads to further sickling.
o Impaired liver function.
o Spleen and liver becomes massively enlarged due to pooling
of blood within these organs

 Hb: 6-8 gm%
 Blood smear: sickle cell are observed under the microscope
 Hemoglobin electrophoresis: Hb is subjected to an electric current which separate the
various types of Hb and determine the amount presents (90% Hb-s).
Treatment and nursing interventions:-
1. Dilute the blood and reverse the agglutination
of sickle cells within the small blood vessels
2. Increase fluid intake
3. Maintain I.V fluid if indicated
4. Record intake and output.
5. Reduce fever to prevent dehydration
6. Alleviate the child pain during crisis.
7. Give analgesic as prescribed
8. Maintain bed rest.
9. Treat associated or precipitating condition e.g. infection.
10. Administer blood transfusion in case of severe anemia
11. Provide emotional support to child and parents.
Prognosis
 Most patients now live well into adulthood, but eventually dead from complications
Glucose-6-Phosphate Dehydrogenase (G-6-P D)

Deficiency Anemia
 Glucose-6-phosphate dehydrogenase deficiency is an X-linked recessive hereditary disease

characterized by abnormally low levels of glucose-6-phosphate dehydrogenase enzyme.
 Globally, around 400 million people are affected by G6PD deficiency and occurs with high
frequency among persons of African, Mediterranean, and Asian.
Pathophysiology:
 G6PD is one of many enzymes that help the body process carbohydrates and turn them into
energy. G6PD also protects red blood cells from potentially harmful byproducts that can
accumulate in the RBCs cell membrane make it unstable and thus hemolysis of RBCs.
 Hemolysis occurs 2-4 days after exposure to oxidants as:
1. Drugs: synthetic vitamin K, some sulfonamides, Para-aminosalicylic acid,…etc.
2. Fava Bean: Anemia following intake of Fava Bean is called Favism.
3. Infections: bacterial or viral and may occur in typhoid fever.
NB: The name favism is sometimes used to refer to the enzyme deficiency as a whole, although
this is misleading as not all people with G6PD deficiency will manifest a physically observable
reaction to consumption of broad beans.
 G6PD deficiency can produce hemolysis in the neonatal period & hyperbilirubinemia
and even kernicterus may occur.
 When a pregnant woman ingests oxidant drugs, they may be transmitted to her
G6PD-deficient fetus, and hemolytic anemia and jaundice may be apparent at birth.
 Acute onset of anemia ch.ch. history of exposure to oxidizing agent followed by pallor,
jaundice, dyspnea, irritability, vomiting, hematuria dark urine and stool and in severe
cases anemic heart failure.
Investigation:
 Normochromic, normocytic anemia
 Reticulocytosis: reticulocyte may reach 10-20% denoting hyperactivity of bone marrow
(normally 0.5-1.5%)
 Decreased Hb and increased unconjugated serum bilirubin
 Increased urobilinogen in urine.
 Measuring the activity of G-6-PD
Treatment:
 Avoid the causative agents (fava beans ingestion or drugs) and treat the infection
promptly.
 PRBCs transfusion 10-15 ml/kg. mild cases may be compensated within few days by
hyperactivity of bone marrow.

Thalassemia
 Thalassemia is a general name for a group hereditary hemolytic anemia in which there is
decreased synthesis of one or more hemoglobin polypeptide chains.
 Thalassemia come from the Greek thalassa ("sea") and -emia ("blood"). It indicates the
epidemiology of the disorder in that it commonly occurs in patients of Mediterranean
descent. The term was first used in 1932.
 Normal hemoglobin is composed of four protein chains, two α and two β globin chains.
 Thalassemia patients produce a deficiency of either α or β globin, unlike sickle-cell disease,
which produces a specific mutant form of β globin.
 The thalassemia is classified according to which chain of the hemoglobin molecule is
affected.
 In α thalassemia, production of the α globin chain is affected, while in β thalassemia
production of the β globin chain is affected.
 Beta thalassemia occur more often, and can be divided into three subcategories based on
severity:
1. Thalassemia minor (also called beta-thalassemia trait): leads to mild microcytic
anemia often no treatment is required.
2. Thalassemia intermedia: child requires blood transfusions to maintain adequate
quality of life.
3. Thalassemia major: to survive the child requires ongoing medical attention, blood
transfusions, and iron removal (chelating therapy).
Thalassemia major "Cooley's anemia"
Thalassemia major is the most severe of the β thalassemia and is also known as Cooley's
anemia.
Pathophysiology:
 In β-thalassemia major, the β-globulin chain in hemoglobin synthesis is reduced or
entirely absent. A large number of unstable globulin chains accumulate, causing the
RBCs to be rigid and hemolyzed easily. The result is severe hemolytic anemia and
chronic hypoxia.
 In response to the increased rate of RBC destruction, bone marrow is activated
results in bone marrow expansion and thinning of the bony cortex. Growth

retardation, pathologic fractures, and skeletal deformities (frontal and maxillary
Thalassemia face
bossing) result.
Etiology:
 Genetically determined inherited disease.
 Autosomal recessive pattern of inheritance.
Prognosis:
 No known cure.
 Often fatal in late childhood or early adolescent.
Preventive measures:-
 Parents of a child with thalassemia should be tested for the trait and referred for genetic
counseling.
 Prenatal diagnosis → terminates pregnancy.
Clinical Manifestations: The patient usually becomes symptomatic from 6-12 months of age.
 Manifestations of anemia: Pallor, anorexia, easy fatigability, dyspnea, dizziness and
may be cardiac enlargement
 Manifestations of Hemolysis: jaundice (often mild), dark urine and dark stools
Manifestations of increased erythropoiesis inside bone marrow (Thalassemia face):
prominence of the frontal and parietal bones, enlargement of the head, protrusion of
maxillae and teeth, depression of the nasal bridge, and may be exposure of upper central
teeth
 Manifestations of increased erythropoiesis outside the bone marrow: Hepato-
splenomegaly occurs leading to abdominal enlargement.
Complications:
1. Hemosiderosis: increase in tissue iron stores caused by the iron overload which may lead to
tissue damage (Hemochromatosis). The organs affected by Hemosiderosis and thus
Hemochromatosis include:
1) Heart: Arrhythmias, pericarditis, congestive heart failure "the usual cause of death
of thalassemia.
2) Liver: which leads to liver cirrhosis, liver failure and coagulation abnormality.
3) Spleen: enlarged spleen
4) Lungs: hemoptysis
4. Skin: greenish brown pigmentation due to the presence of pallor + jaundice+
hemosiderosis.
5) Endocrinal glands:
 Growth retardation.
 Delayed development of secondary sex Ch.Ch.
 Diabetes in older children due to iron deposition in pancreas.
 Adrenal and pituitary dysfunction.
6) Kidney: interstitial nephritis
2. Complications from repeated blood transfusion: Allergy, mismatched blood,
infections, circulatory overload.
3. Pathological fractures: expansion of bone marrow due to hyperactivity leads to thinning
of bones.
 Hb electrophoresis: performed after 6–12 months of age is usually diagnostic when
levels of hemoglobin A2, hemoglobin F, or both are elevated.
 Reticulocytes level: elevated
 Severe hypochromic, microcytic anemia
 Hb level: usually falls to 5–6 g/dL or less
Medical treatment:
 Transfusions of RBCs as needed to keep Hb > 9.5 g/dl.
 Deferoxamine (Desferal), an iron chelating agent
 Splenectomy may be done to decrease destruction of blood cells and to decrease
abdominal pressure.
 Bone marrow transplantation may be done in some children.
 After splenectomy, patient is at risk for infection and should receive vaccines to prevent
influenza, meningitis, and pneumonia in addition to regular immunizations.
Nursing Interventions:
 Promote adherence to treatment regimen.
 Support child during illness and distressing treatments.
 Promote child and family coping.
 Anticipate adolescent concerns related to appearance.
 Monitor closely for complications of the condition and treatment:
 Multiple transfusions and iron buildup.
 Infection post splenectomy.
 Genetic counseling:
 Encourage testing of siblings to allow for childbearing planning.
 Explain that each pregnancy when both parents are carriers presents a 25% chance
a child will be born with the disease and a 50% chance the child will have the
thalassemia trait.
Hemophilia
 Hemophilia is a group of X-linked recessive disorders that result in deficiency in one of the
coagulation factors in the blood. X-linked recessive disorders are transmitted by carrier
mothers to their sons, so usually only males are affected by hemophilia.
 The coagulation factors in the blood are essential for clot formation either spontaneously or
from an injury, and when factors are absent bleeding will be difficult to stop.
 There are several types of hemophilia, including:
1. Hemophilia A: Factor VIII deficiency
2. Hemophilia B: Factor IX deficiency or Christmas factor
3. Hemophilia C: Factor XI deficiency.
 The most common type is hemophilia A, occurs when there is a deficiency of factor VIII in
an individual. Factor VIII is essential in the activation of factor X, which is required for the
conversion of Prothrombin into thrombin and thus fibrinogen into fibrin (clot).
 Hemophilia is classified according to the severity of the disease, ranging from mild to
severe. The more severe the disease, the more likely there will be bleeding episodes.
Clinical manifestations:-

1. Seldom diagnosed in infancy unless excessive bleeding is observed from the umbilical cord
or after circumcision, hematoma after injection or tooth extraction.
2. Usually diagnosed after the child become active.
 Easily bruised
 Prolonged bleeding after laceration.
 Spontaneous soft tissue hematomas.
 Hemarthrosis "elbow, knee and ankle".
 Spontaneous hematomas.
 GIT bleeding.
 Prolonged clotting time
 Prolonged PTT
 Normal PT
 Decreased level of factor VIII
Complications:
1. Airway obstruction caused by hemorrhage into neck and pharynx.
2. Intestinal obstruction
3. Compression of nerves by hemorrhage in deep tissue which leads to paralysis .
4. Intracranial bleeding
5. Joint deformity secondary to hemoarthrosis
Prognosis
 Normal life span due to advances in treatment.
 Death may occur due to intracranial hemorrhage.
Treatment and nursing intervention:-
1. Prevention of trauma and maintain safe environment
 Adolescent have shaving problem, use of electrical shaving machine instead of blades
 Safe environment at home as crib or bed.
 Dental care as soft toothbrush with water irrigation for mouth care to prevent oral
bleeding.
 Avoidance of hard sports is important.
2. Provide emergency care for bleeding wounds.
 Cleanse the wound.
 Immobilize the affected part and elevate above the level of the heart.
 Administer cryoprecipitate, fresh plasma or fresh frozen plasma as prescribed.
 Apply local measures to control bleeding pressure 10-15 minutes.
 Keep the child calms or quit during cares giving.
 Suturing and cauterization should be avoided
3. Provide supportive care for the child hemoarthrosis
 Control bleeding.
 Ice packs may be applied.
 Elevate the affected part.
 Immobilize the affected part .
 Alleviate pain.
 Weight reduction is important to decrease the load on joints.
 Avoid excessive manipulation.
 Maintain the child on bed rest.
4. Prevent hemorrhage during nursing procedure.
 Insert thermometer gently to measure temperature.
 Administer medications orally whenever possible.
 Choose injection site carefully and rotate them.
 Use small needle for SC or IM injections. Apply pressure for 5 minutes.
 Aspirins and NSAID should be avoided. Paracetamol may be used instead.
5. Provide emotional support to the child and his family.
Idiopathic thrombocytopenic purpura (ITP)
 ITP is the most common type of bleeding disorder in which the immune system destroys
platelets, which are necessary for normal blood clotting.
 It is also called immune thrombocytopenic purpura.
Etiology and pathogenesis:
 ITP occurs when certain immune system cells produce antibodies against platelets. The
antibodies attach to the platelets. The spleen destroys the platelets that carry the antibodies.
 In children, the disease sometimes follows a viral infection.
 ITP may be acute, chronic, or recurrent. In children the acute form is most usual.
1. In the acute form, the platelet count returns to normal within 6 months after diagnosis
and relapse does not occur.
2. In the chronic form, platelet count does not return to normal within 6 months.
3. In the recurrent form, the platelet count decreases after having return to normal.
 Purpuric rash: multiple petechiae occur in groups on leg,

o arm, neck and upper chest.
o Character: pin head not raised above the skin,
o don't blanch on pressing fade within 14 days.
 Bruises, ecchymosis , hemorrhage in mucous membranes.
 Epistaxis, intracranial hemorrhage, retinal hemorrhage, subconjuctival hemorrhage.
 Decreased platelet count, always ↓ 100,000/ml
 In mild to moderate cases: ↓ 50,000/ml
 In severe cases: ↓20,000/ml
 Blood clotting tests (PTT and PT) are normal.
 Bleeding time is prolonged.
 Platelet associated antibodies may be detected.
 A bone marrow aspiration or biopsy appears normal
or may show a greater than normal number of cells
called megakaryocytes. These cells are an early form of platelets.
Treatment:
 No treatment is required in mild cases with mild bruising with no evidence of mucous
membrane bleeding. Avoid use of aspirin and avoid violent sports
 In severe cases with severe bleeding from mucous membranes and if platelet ↓50,000/ml:
 Prednisone 2 mg/kg/day for 2-3 weeks or
 IV immunoglobulin 0.8-1g/kg/day for 1-2 days induces a rapid rise in platelet count
(usually >20,000/ml) in 95% of patients within 48 hr.
 In case of dangerous bleeding like intracranial hemorrhage: Massive dose of platelets+
high dose of IV Methylprednisone + IV immunoglobulin + emergency splenectomy should
be carried.
Brusies
 Splenectomy is indicated in:
 Emergency condition of intracranial hemorrhage
 Chronic ITP not responding to medical treatment.
Nursing Considerations:
 Protective environment with padding to prevent injury.
 Patient and family teaching. Teach to avoid all contact sports.
 Medical examination with any abdominal or head trauma to rule out internal bleeding.
 Teach client and family to avoid using aspirin or NSAIDs for pain management due to effect
on platelets.


Review questions
1. Explain the dietary management of iron deficiency anemia
2. Clinical manifestations of iron deficiency anemia include:

1. …………………………. 2. ………………………….. 3. …………………………….
4. ………………………….5. ………………………….. 6 ………………………………
3. Precipitating factors for sickle cell anemia are:
1. ……………………….. 2. ………………………… 3 …………………………….
4. ………………………. 5. ………………………….
4. What are characteristics of sickle cell?
5. Explain the 5 As of the management of sickle cell anemia.
6. Explain the type of inheritance for the following hematological disorders.

 Sickle cell disease
 G6PD deficiency anemia
 Thalassemia
 Hemophilia
7. Explain the medical treatment for Thalassemia
8. What are the nursing intervention for a patient with hemophilia to manage bleeding
9. ......................................... ch.ch by platelet count returns to normal within 6 months after

diagnosis and relapse does not occur.
10. ...................................... ch.ch. by platelet count does not return to normal within 6 months.
11. ...................................... ch.ch. by the platelet count decreases after having return to normal
Chapter (7)
Child With a gastrointestinal Disorder
Learning objectives
child with AGE, pyloric stenosis, cleft lip and palate, Hirschsprung
disease, celiac disease, GER, GEF
 Formulate a plan of care for the infant with acute diarrhea.
 Formulate a plan for teaching parents preoperative and

postoperative care of the child with a cleft lip or palate
 Discuss common medical treatments for infants and children with

gastrointestinal disorders.
 Discuss common laboratory and diagnostic tests used to identify

disorders of the gastrointestinal tract.
 Discuss medication therapy used in infants and children with

gastrointestinal disorders.
 Recognize risk factors associated with various gastrointestinal

illnesses.

Acute Gastroenteritis
 Gastroenteritis is a medical condition characterized by inflammation of the GI tract that

involves both the stomach ("gastro"-) and the small intestine ("entero"-), resulting in some
combination of diarrhea, vomiting, and abdominal pain and cramping.
 Acute gastroenteritis is a leading cause of childhood morbidity and mortality and is also an
important cause of malnutrition. Many diarrheal deaths are caused by dehydration from fluid
and electrolytes loss.
 Diarrhea: Increase frequency, fluidity and volume of feces relative to the usual habit of each
individual.
 As why diarrheal disorders are serious during infancy? This is because dehydration is much
more quickly occur than adults.
Etiology:
Acute and infectious factors:
 Bacterial such as E. coli, salmonella, shigella and vibrio cholera,
 Viral such as rotavirus, Enterovirus and adeovirus.
 Fungal such as Candida enteritis.
 Parasitic such as Giardia Lamblia.
 Normal flora after ingestion of antibiotics.
NB: Globally, most cases in children are caused by rotavirus
Non-infectious factors:
 Allergy to certain foods. Sunken
 Metabolic disorders ( celiac disease). Eyes
 Overfeeding.
 Unsuitable formula for age.
Environmental factors:
 Rise of atmospheric temperature
 Poor sanitation
 Exposure to cold drafts
 Low socio-economic status.
۞ Stool:
 Greenish to yellow-green in color.
 Loose and fluid in consistency.

 May contain pus, mucus or blood. Frequency varies from 2 to 20 times.
۞ Fever, anorexia, vomiting, rapid respiration, irritability and general weakness
۞ Dehydration:
 Poor skin turgor, dry mucus membrane.
 Decreased urinary output. (NB: urinary output= 1-3 ml/kg/hr.)
 Sunken eyes and anterior fontanel. Lost (decreased) skin
 Rapid pulse, low blood pressure. turgor
 Few or no tears when crying
 Dry mouth, thirst
 Loss of weight.
 Deep, rapid breathing indicate acidosis.
Types of dehydration:
1) Isotonic (Isonatremic): equal loss of water and electrolytes
2) Hypertonic (Hypernatremic): primarily a loss of water
3) Hypotonic (hyponatremic): primarily a loss of electrolytes, particularly sodium
۞ In humans, the most commonly seen type of dehydration by far is isotonic (isonatraemic)
dehydration which effectively equates with hypovolemia, but the distinction of isotonic from
hypotonic or hypertonic dehydration may be important when treating children who become
dehydrated.
Three types of dehydration based on severity:
1) Mild: when the body has lost (< 5% in an infant; < 3% in an older child or adult) of total
fluid

2) Moderate: when the body has lost (5-10% in an infant; 3-6% in an older child or adult)
of total fluid
3) Severe: when the body has lost (>10% in an infant; > 6% in an older child or adult) of
total fluid , severe dehydration is considered an emergency
Mild Moderate Sever
Mouth and lips Dry Dry Dry
Urine output Normal Reduced None for 12 hr.
Mental status Normal Lethargic Irritable or coma
Pulse rate Normal Tachycardia Tachycardia
Blood pressure Normal Normal Low
Capillary refill time Normal Delayed Very delayed
fontanel Normal Sunken Very sunken
Skin and eye turgor Normal Reduced Very reduced
Complications of acute gastroenteritis:
 Dehydration  Metabolic Acidosis (↓PH, ↓HCO3)
 Electrolyte imbalance (Hypokalemia & hypocalcaemia)
 Hypovolemic shock  Pre-renal failure due to poor kidney perfusion.
 Septicemia  DIC: Disseminated intravascular coagulation.
 Health history  General physical appearance
 Laboratory studies:
 Serum electrolytes (Na, K) and renal function tests (urea).
 Arterial blood gases analysis.  CBC ( high HCT).
 PT, PTT to exclude DIC  Urine and stool analysis and culture.
Treatment:
Sunken anterior fontanel
 Prevention
 Breastfeeding
 Health education (mothers).
 Enteric isolation precautions to prevent spread of infection.
 Maintain hydration (IV fluid therapy).
 Electrolyte and sodium bicarbonate replacement.
 Supportive care.
Oral Rehydration Solution (ORS)
Indication: for ill Cases of dehydration as long as the child strong to drink.

Advantages:
1. Effective in all age groups.
2. For diarrhea of any etiology.
3. Correct severe acidosis.
4. Control fever.
5. Correct mild and moderate dehydration.
6. Little chance for over hydration.
7. Available everywhere.
8. Non-expensive.
Limitations: coma, shock, severe dehydration, abdominal distention and persistence vomiting.
Dosage: Mild dehydration ( 50 ml/kg over 4-6 hours)
Moderate dehydration (100 ml/kg over 4 hours).
Drug treatment:
 Symptomatic anti-diarrheal drugs are usually not recommended
 Anti-emetic drugs are not indicated.
 Antibiotic in treatment of diarrhea:
 Shigella ( Ampicillin or Resprim).
 E. Coli (Resprim).
 Cholera ( Tetracycline).
 Giardia and Entameba histolytica ( Metronidazole)
Nursing Care:
1. Fluid volume deficit R/T excessive loss through diarrhea or vomiting
Goal: pt. will exhibit sign of Rehydration.
Interventions:
1. Administer ORS for rehydration and maintain adequate hydration.
2. Give ORS in small amounts to avoid vomiting.
3. Administer and monitor IV fluids as prescribed.
4. Administer antibiotics as prescribed.
5. After rehydration, offer child regular diet as tolerated.
6. Maintain strict record of intake and output.
7. Weigh the child daily to assess for dehydration,
8. Assess vital signs, skin turgor, mucus membranes and mental status every 4 hours
or as indicated.
9. Encourage family participation in caring for their child.
Expected outcome: child exhibits signs of adequate hydration.

2. Altered nutritional status less than body requirement R/T inadequate intake.
Goal: Pt. will consume nourishment adequate to maintain appropriate weight for age.
Interventions:
1. Encourage breastfeeding.
2. Observe and record response to feeding to assess tolerance.
3. Instruct family in providing appropriate diet to gain compliance with therapeutic
regimen.
4. Avoid giving types of diet such as banana, apples and toast or tea.
Expected outcome: child takes prescribed diet and exhibit a satisfactory weight.
3. Risk for infection R/T microorganisms invading GIT.
Goal: others will not exhibit signs of GI infections.
Interventions:
1. Implement body substance isolation or other hospital infection-control practice as
appropriate handling of specimens and disposal of stool.
2. Maintain careful hand washing.
3. Use super absorbent disposable diapers.
4. Attempt to keep infant from placing hands and objects in contaminated areas.
5. Instruct family members and visitors in isolation practices.
Expected outcome: infection does not spread to others.

4. Impaired skin integrity R/T irritation caused by frequent loose stools.
Goal: skin will remain intact.
Interventions:
1. Change diaper frequently to keep skin clean and dry.
2. Cleans buttocks gently.
3. Apply ointment to protect skin from irritation.
4. Expose slightly reddened intact skin to air whenever possible.
5. Observe buttocks and perineum for infection.
6. Apply antifungal medication to treat fungal skin infection.
Expected outcome: child has no evidence of skin breakdown.

Cleft Lip and Cleft palate
 The most common facial malformations, cleft lip and cleft palate, occur either alone or in
combination.
 Cleft lip occurs in about 1 in 1,000 live births and is more common in males. Cleft palate
occurs in 1 newborn in 2,500, more often in females.
 A cleft is a fissure or opening or a gap. It is the non-fusion of the body's natural structures
that form before birth.
Cleft lip
 Is malformation resulting from failure of the maxillary and median nasal processes to fuse
during embryonic development.
 Partial or incomplete cleft
 Complete cleft: it continues into the nose
 Unilateral: One sided
 Bilateral: Two sided
Unilateral Unilateral Bilateral

incomplete complete complete
Incomplete cleft Unilateral complete lip Bilateral complete lip

palate and and
palate palate

Cleft Palate
 Cleft palate: Is a malformation in which the two plates of the skull that form the hard palate
(roof of the mouth) are not completely joined. The soft palate is in these cases cleft as well.
 Complete cleft: involved both soft and hard palate
 Incomplete cleft: a 'hole' in the roof of the mouth, usually as a cleft soft palate
NB: When cleft palate occurs, the uvula is usually split.
Etiology:
 Causes not known.
 Hereditary factor may be due to mutant genes chromosomal abnormalities
 Exposure to teratogens: anti-seizure/anticonvulsant drugs, acne drugs containing Accutane,
and methotrexate, a drug commonly used for treating cancer, arthritis, and psoriasis
Associated Problems and Complications:
 Trouble feeding: Due to lack of suction and food returns through the nose.
 Nasal speech  Lack of dental appearance .  Aspiration
 Otitis media and hearing loss.  Psycho-social problems
Treatment:
 Cheiloplasty to surgically repair the cleft lip within the first 3 months after birth to
provide adequate sucking.
 Palatoplasty to surgically repair the cleft palate between 12 months and18 months of age
before the child begins speaking
Complete Cleft lip 1 month after surgery the same girl at age 8
Nursing Care Plan:

1. Altered nutrition (less than body requirements) R/T physical defect.
Goal: will consume adequate nourishment.
Interventions:
 Soft nipple with large hole can be used or dropper.
 Feed baby in an upright or sitting position to minimize aspiration.
 Feed slowly, bubble frequently during feeding.

 Avoid removing of nipple frequently to avoid choking.
 Smaller but more frequent feedings may be necessary.
 Advance diets as appropriate for age. "Eating often improves when solids are introduced."
 Monitor weight to monitor adequacy of intake.
 Encourage mother to begin feeding infant as early as possible so that she becomes adept in
feeding technique before discharge.
Expected Outcome: infant exhibits appropriate weight gain.
2. High risk for altered parenting R/T the child's appearance.
Goal: will demonstrate acceptance of infant
 Allow Expression of feeling to encourage family's coping.
 Convey attitude of acceptance of infant and family because parents are sensitive to
affective attitudes of others.
 Indicate by behavior that child is a valuable human being to encourage acceptance of
infant.
 Describe results of surgical correction of defect.
 Use photographs of satisfactory results to encourage feeling of hope.
Expected Outcome: family exhibits an attitude of acceptance of infant.
3. High risk for trauma of the surgical site R/T surgical procedure, dysfunctional
swallowing
Goal: will experience no trauma to operative site.
Intervention:
 Position on back or side or in infant seat (cleft lip) to prevent trauma to operative site.
 Maintain lip protective device (Logan bow) to protect the suture line.
 Use non-traumatic feeding techniques (dropper or syringe) to avoid sucking and trauma
to suture line.
 Restrains elbows to prevent access to operative site..
 Avoid placing objects in the mouth following cleft palate repair (suction catheter, tongue
depressor, straw, pacifier or small spoon).
 Prevent vigorous crying that can cause tension on sutures.
 Cleanse sutures line gently after feeding as necessary,
 Teach cleansing at restraining procedures to family before discharge with sutures not
removed.
Expected Outcome: operative site remains undamaged.
4. Altered nutrition (less than body req.) R/T difficulty eating following surgical
procedures.
Goal: will consume adequate nourishment.
Intervention:
 Monitor IV fluids.
 Administer diet appropriate for age and as prescribed, clear liquids —► full
liquids —► soft foods.
Logan bow
 Feed in sitting position.
 Bubble frequently.
 Assist in breast-feeding.
 Teach family to ensure optimum home care.
Expected Outcomes: infant exhibits appropriate weight gain
5. Pain R/T surgical procedure.
Goal: will experience optimum comfort level.
Intervention:
 Assess behavior and vital signs.
 Adm. analgesics as ordered.
 Remove restraints periodically while supervised.
 Provide cuddling and tactile stimulation as need for growth and development.
 Involve parents in infant's care.
Expected Outcomes: infant appears comfortable and rests quietly.
7. Infection and aspiration R/T cleft palate

Gastro-esophageal Reflux (GER)
 Is a malfunction of the distal end of the esophagus permitting return of stomach content in to
esophagus. Reflux means to flow backward.
 Gastro-esophageal (GE) reflux is common in young infants.
Etiology: not known.
Possible Causes: neuromuscular imbalance, immaturity.
Altered Physiology:
• GER is a malfunction of the lower segment of the esophagus so allowing gastric contents to
return back to the esophagus and vomiting
NB: An important differential point in evaluating infants with GE reflux is whether the vomited
material contains bile. Bile-stained emesis in an infant requires immediate evaluation as it may
be a symptom of intestinal obstruction (volvulus or intussusception).
Infants:
 Vomiting (unexplained) immediately after feeding, especially when infant is placed in
prone position, regurgitation not projectile, Onset: soon after birth ch.ch.: non-bile stained
 Weight loss
 Dehydration ■ Recurrent pulmonary symptoms.
Older Children:
 Substernal burning. ■ Upper abdominal discomfort ■ Dysphagia.
Complications:
■ Aspiration pneumonia ■ Chronic esophagitis ■ FTT ■ Anemia due hematemesis
■ Esophageal stricture ■ Cyanotic episodes.
• Upper GI barium x-Ray with fluoroscope.
• Monitor PH of esophagus.
• Serum studies (electrolytes)
Management:
1) Prevent and treatment of dehydration
2) Maintain adequate nutrition and prevent vomiting.
 Thickened formula (cereal).
 Large nipple hole.
 60 degree supine position.

 Handle gently.
 Propping in upright position 60 degree angle (supine), 30 degree (prone)
 Small and frequent feedings
 Support family especially the month and encourage them to participate in care and
feeding of the infant
3) Antacids and antiemetic
4) Surgical treatment (fundoplication)

Esophageal Atresia and Tracheoesophageal Fistula
 Atresia is the absence of a normal body opening or the abnormal closure of a body passage.
Esophageal Atresia (EA): It causes the esophagus to end in a blind-ended pouch rather than
connecting normally to the stomach.
 Esophageal atresia with or without fistula into the trachea is a serious congenital anomaly and
is among the most common anomalies causing respiratory distress. This condition occurs in
about 1 in 2,500 live births.
 Tracheoesophageal fistula: is an abnormal connection (fistula) between the esophagus and
the trachea.
Types:
1. Type (A): 80-90%, proximal esophagus segment terminates in a blind pouch, and the distal
segment is connected to the trachea or primary bronchus by a short fistula at or near the
bifurcation.
2. Type (B): 8%, blind at each end of the esophagus, widely separated with no connection to
the trachea.
3. Type (C): 5%, fistula without atresia.
2. Type (D): Rare, proximal segment of esophagus opens into trachea, distal end is blind.
4. Type (E): Rare, both upper and lower esophagus segments connected to the trachea.
 Appear soon after birth, excessive amount of secretions, constant drooling, intermittent
cyanosis, abdominal distention, choking, fluids return through nose and mouth through
feeding process.
 Inability to pass catheter through nose or mouth. "Be aware of coiling of the catheter".
o Recognize infants at risk "premature + polyhydramnios".
o Observe symptoms
o Inability to pass 10-12 F stiff catheter.
o X-Ray (chest + abdomen) Gas in stomach, tip of the catheter in blind pouch.
Complication and associated Problems:
 Pneumonitis (salivary or gastric acid reflux)
 Congenital heart disease
 Imperforated anus
 Prematurity

 Post-Op Complications:
 Leak at anastomosis site.
 Recurrent fistula, Stricture.
 Gastroesophageal reflux.
 Feeding problems
Treatment:
1. Immediate Treatment:
 Propping infant at 30 degree angle to prevent reflux
of gastric content
 Suctioning
 Supportive: I .V. fluids, antibiotic, respiratory support
2. Surgery:
 One stage: surgical repair to close the fistula/s and reconnect the two ends of the
esophagus to each other (end to end anastomosis)
 Two stage: for sick infants with gastrostomy tube placement until final re-anastomosis
at 1 2 - 2 4 months (Intestinal segment may be used).
Hirschsprung Disease

Hirschsprung Disease
 Is congenital anomaly that results in mechanical obstruction from inadequate motility of part
of the intestine because the nerves are missing from this part of the bowel.
 Hirschsprung is also sometimes called congenital aganglionic megacolon.
 This disease is named after Harald Hirschsprung, the Danish physician who first described
two infants who died of this disorder in 1888.
Etiology:
 Arrest in embryological development affecting the migration of parasympathetic nerves of the
intestine (prior to the 12th week of gestation).
 Of unknown cause or may be familial.
Incidence:
 1:5000 of all intestinal obstructions in the newborn
 More common in males.
Altered Physiology:
 Absence or reduced number of the parasympathetic nerves (ganglion cells) in the
intestinal wall (usually in the distal end of the colon-recto-sigmoid) no peristalsis
of the intestine (the section usually narrow) no fecal mass through it
(accumulation of fecal material above this segment).
 Proximal to the narrow affected section, the colon is dilated, filled with fecal material
and gas with hypertrophy of muscular coating.
 The rectal sphincter (internal) fails to relax and evacuation of fecal material and gas is
prevented abdominal distention and constipation.
Clinical Manifestations: {vary depending on degree of involved bowel}
 Failure to pass meconium within 24-48 hours after birth Step 1: The doctor removes the
diseased section.
 Vomiting (bile-stained or fecal)
 Abdominal distention.
 Reluctance to ingest fluids.
 Overflow -type diarrhea
Older children:
 History may reveal constipation at birth
 Abdominal distention.
 Constipation (relieved temporary with enema)
 Ribbon-like, foul -smelling stool.

Step 2: The healthy section is
 Inadequate weight again, attached to the rectum or
 Fecal masses may be palpable.

 Rectal examination: no fecal material
 Barium enema: narrow intestine proximal to anus, dilated
intestine proximal to narrow segment.
 Rectal biopsy: absence or reduced number of ganglion nerve cells.
Complications:
 Prior to Surgery: Enterocolitis (major cause of death), anus.
water intoxication (enemas), Perforation.

 Post op.: Enterocolitis, leak of anastomosis, pelvic abscess
 Colostomy: hemorrhage, shock, and infection.
Treatment:
 Initially: colostomy or ileostomy to decompress the intestine rest normal bowel.
 Definitive Surgery: abdominal Pull-through. A surgeon removes the segment of the large
intestine lacking nerve cells and connects the healthy segment to the anus. The pull-
through procedure is usually done soon after diagnosis.
 Administer saline enemas as prescribed to empty bowel.
 Administer systemic antibiotics as prescribed to reduce bacterial flora in bowel.
 Administer fluid and electrolytes as prescribed.
 Measure and record abdominal circumference.
 Closely monitor vital signs for signs of shock (Enterocolitis)
 Observe for symptoms of perforation (fever, abdominal distention, vomiting, tenderness,
dyspnea with cyanosis)
 Clarify any misconceptions about colostomy.
 Stress to child and family that the colostomy is temporary.
 Prevent infection: {dressing change, diaper below dressing,
hand-washing, change position frequently}
 Mouth care.

Celiac Disease
o Celiac disease, also called Gluten-induced Enteropathy, is an autoimmune disorder

characterized by a mal-absorption of the proximal small intestine, that is characterized by
abnormal mucosa with permanent intolerance to gluten.
o Gluten is a protein that is found in many grains including wheat, rye, barley, oats and
spelt. Gluten is the composite of a gliadin and a glutenin.
o Celiac disease results from intestinal sensitivity to the gliadin fraction of glutens.
o Most children present during the second year of life, but the age at onset and the severity
are variable.
Etiology:
■ Unknown. ■ Genetics. ■ Toxic. ■ Allergic.
Altered physiology:
Characteristics of the disease include:
 Impaired intestinal absorption.
 Histological abnormalities of small intestine.
 Clinical and histological improvement with gluten-free diet.
 Recurrence of clinical manifestations and histological changes after re-introduction of
dietary gluten.
Histological changes:
 Loss of normal villous pattern
 Obliteration of inter-villous spaces
 Loss of epithelial cell brush border
These changes result in:
o Mal-absorption result from decreased area of absorption.
o Inability to absorb fats, fat-soluble vitamins, minerals and some proteins and
carbohydrates.
 Diagnosis is most commonly made at 6-24 months of age (it can be made in adult),
breast-feeding delays the appearance of symptoms.
 Chronic or recurrent diarrhea ( foul, bulky, and greasy stool),
 Anorexia, vomiting, abdominal distention, muscle wasting and hypotonia.
 Steatorrhea.
 Malnutrition.

 Weight loss and dehydration.
 Mood changes (irritability and nervousness),
 Secondary deficiencies such as anemia, hypocalcaemia and hypoproteinemia.
 History and general status,
 Small bowel biopsy (diagnostic)
 D-Xylose test: a laboratory test to determine how well the intestines absorb a simple
sugar (D-xylose). 25 gram of D-xylose is given orally then blood level measured after 1
hour (if less than 20-25 mg/ dl at 60 minutes, the pt have celiac).
 Hb level.
 Stool test (fecal fat excretion)
 Sweat test (to rule out cystic fibrosis),
 X-ray.
Treatment:
 Lifelong strict adherence to a gluten free diet
 Adequate caloric intake
 Supplemental vitamins
 Decreased fat intake.
 Treatment of celiac crisis:
 Restore fluid and electrolyte balance.
 TPN
 Steroids.
Nursing care:
1. Altered nutritional status (less than body requirement) R/T mal-absorption.
1
Goal: will consume adequate nourishment. Interventions:
1. Provide gluten free diet.
2. Avoid lactose containing milk products.
3. Administer corticosteroids as prescribed.
4. Monitor characteristics of stools.
5. Arrange conference with dietitian to help select food compatible with diet and child
preferences.
6. Monitor weight and height at regular basis.
7. Assess the child and family understanding of the disorder and treatment
8. Give a list of common food sources of wheat and rye.
9. Emphasize suitable substitutes especially com and rice.
10. Stress importance of reading labels of prepared food for hidden sources of gluten.
11. Give instructions concerning vitamins and minerals supplements.
12. Encourage child and family express their feelings and concerns.
13. Make referral to community health nurse for continued care and support.
14. Refer to organizations that provide support and guidance for children with celiac disease.
Expected outcomes:
1. Child and family comply with prescribed diet.
2. Child and family utilize appropriate resources.
2. High risk for injury R/T celiac crisis.
Goal: will not experience complications from celiac crisis.
Interventions:
1. Monitor I.V. fluids closely to prevent dehydration or over hydration.
2. Give mouth care during period when nothing is given by mouth.
3. monitor naso-gastric suctioning and record drainage.
4. Observe for signs of shock to initiate treatment early.
5. Administer steroids as ordered.
6. make all precautions to prevent infections.
Expected Outcome: child recovers from crisis, complications are recognized care is instituted.
3. Altered family processes R/T a child with chronic illness.
4. Risk for infection R/T malnourishment and anemia.

Review questions
1. ....................................... Is malformation resulting from failure of the maxillary and median

nasal processes to fuse during embryonic development.
2. ............................................ is a malformation in which the two plates of the skull that form
the hard palate are not completely joined.
3. Teratogens associated with cleft lip and palate include:
1. ................................................... 2. ...................................................3.
..........................................
4. Associated Problems and Complications of cleft lip and palate:
1. .......................................................2. ............................................. 3. ........................................
4. ......................................................5. ................................................ 6 .........................................
5. The role of 10s in corrective surgery for cleft lip and palate is:
1. .......................................................2. ............................................. 3. ........................................
6. .......................................... Is a malfunction of the distal end of the esophagus permitting return
of stomach content in to esophagus.
7. .............................................is a congenital malformation which affects the GI tract. It causes
the esophagus to end in a blind-ended pouch rather than connecting normally to the stomach.
8. ....................................................is an abnormal connection (fistula) between the esophagus
and the trachea.
9. ................................... Is a congenital malformation in which the rectum has no outside
opening.
10. ..................................................... Is congenital anomaly that results in mechanical
obstruction from inadequate motility of part of the intestine because the nerves are missing from
this part of the bowel.
11. .................................................. Is a mal-absorption disease of the proximal small intestine,
that is characterized by abnormal mucosa with permanent intolerance to gluten.
12. Intestinal histological changes associated with celiac disease are:
1. .......................................................2. ............................................. 3. ........................................
4. ......................................................5. ................................................ 6 .........................................
13. ................................................ Increase frequency, fluidity and volume of feces relative to the
usual habit of each individual.
14. Clinical manifestations of dehydration are:
1. .......................................................2. ............................................. 3. ........................................

4. ......................................................5. ................................................ 6 .........................................
7. .......................................................8. ............................................. 9. ........................................

15. Types of dehydration are:
1. ....................................... equal loss of water and electrolytes
2. ........................................primarily a loss of water
3. .......................................... primarily a loss of electrolytes, particularly sodium
16. Complications of acute gastroenteritis:
1. .......................................................2. ............................................. 3. ........................................
4. ......................................................5. ................................................ 6 .........................................
17. Advantages of ORS:
1. .......................................................2. ............................................. 3. ........................................
4. ......................................................5. ................................................ 6 .........................................
18. Limitations of ORS:
1. .......................................................2. ............................................. 3. ........................................
4. ......................................................5. ................................................ 6 .........................................
True or false
( ) 1. ITP is a bleeding disorder in which the immune system destroys platelets.
( ) 2. In ITP Blood clotting tests are prolonged, bleeding time is decreased, and bone marrow
aspiration sample shows abnormal decrease in megakaryocytes.
( ) 3. Complete cleft lip occurs when the cleft continues to the nose
( ) 4. Complete cleft palate involved both soft and hard palate
( ) 5. Incomplete cleft palate is usually as a cleft hard palate
( ) 6. The major complication of cleft lip and palate is aspiration
( ) 7. The vomiting associated with GER is projectile and bile stained.
( ) 8. Thickened formula, propping in upright position and small frequent meals are
therapeutic measures used for GER
( ) 9. In Esophageal Atresia with Tracheoesophageal Fistula, excessive amount of
secretions, constant drooling appear soon after birth,
( ) 10. In assessing the baby with imperforated anus, the nurse should inspect the urine for
mucus
( ) 11. The vomiting associated with Hirschsprung Disease is projectile and bile stained.
( ) 12. Barium enema shows dilated intestine proximal to anus, narrow intestine proximal
to narrow segment in Hirschsprung disease.
( ) 13. Diagnosis of celiac disease is established at birth
( ) 14. Patient with celiac disease should be on gluten free diet for 6 months after diagnosis.
( ) 15. Rotavirus is the common causative agent for gastroenteritis.
( ) 16. Normal urine output is 4-6 ml/kg/hr.
( ) 17. In humans, the most commonly seen type of dehydration by far is isotonic

Chapter (8)
Child With a genitourinary Disorder
Learning objectives
 Describe the various factors that contribute to urinary tract
infections in infants and children.
 Differentiate between nephrotic syndrome and acute

glomerulonephritis
 Demonstrate an understanding of the causes and mechanisms of

edema formation in nephrotic syndrome.
 Outline a nursing care plan for a child with nephrotic syndrome.

child with acute glomerulonephritis, and nephrotic syndrome
 Define the various types of genitourinary malformations

Acute Glomerulonephritis (AGN)
 Refers to a disease of the kidney in which there is an inflammation of the glomerular

capillaries caused by an antigen-antibody reaction following an infection of group A beta-
hemolytic streptococcal infection in some part of the body.
 It is a predominantly a disease of childhood and is the most common type of nephritis in
children.
Incidence: Most common in preschool and early school age groups 5-10 years, rare in children
under 3 years of age.
Altered physiology:
 The organism responsible for nephritis contain antigens similar to those of the basement
membrane of the renal glomeruli (small blood vessels in the kidneys).
 Antibodies produced to fight the invading organism also react against the glomerular
tissue forming immune complex.
 The immune complex become trapped in the glomerular loop and cause an inflammatory
reaction in the affected glomeruli.
 Onset usually 1-3 weeks after the initial streptococcal infection
 Urinary changes: hematuria, smoky or brown in color, oliguria.
 Edema: usually mild, often manifested by periorbital edema in the morning. Edema may
appear only as rapid weight gain,
 Hypertension: present in 60-70% of patients. Severe hypertension may develop rapidly
over a period of few hours, therefore frequent measurement of the blood pressure must
be made in the first few days of the disease,
 Malaise, headache, low grade fever, anorexia and vomiting.
1. Urinalysis:
 Specific Gravity usually high, gross hematuria.
 Mild to moderate proteinuria.
 Decreased urinary output.
2. Blood:
 Urea and creatinine often mildly to moderately elevated
 ESR is elevated.
 ASOT is usually elevated.

 Renal function is normal in 50 % of patients.
Prognosis:
 95% of affected children recover completely
 Small percentage of children develop chronic nephritis
 Death may occur due to the effect of hypertensive encephalopathy or heart failure.
Complications: Periorbita
1. Hypertensive encephalopathy. edema
2. Congestive heart failure.

3. Uremia.
4. Anemia.
Treatment: .
1. Hospitalization and daily weight, urine output, urinalysis and more frequent measuring of
blood pressure.
2. Bed rest during the acute phase.
3. Dietary restriction: fluid amount should be equal to 24 hours urinary output, salt
restriction, low potassium diet, low protein diet.
4. Drug therapy: 10 days penicillin - Hydralazine to treat hypertension.
Nursing diagnosis:
1. Risk for life threatening complications R/T disease process.
2. Reduced urinary output R/T glomerular dysfunction.
3. Fluid volume excess R/T decreased urinary output,
4. Knowledge deficit regarding AGN and its management.
5. Activity intolerance R/T fatigue.
6. Anxiety R/T uncertain course of disease and hospitalization.
 Maintain bed rest during the acute phase of illness.
 Protect the child from infection, avoid placing the child in a room with patients who have
fever, URTI or other infectious diseases, administer antibiotics as prescribed and provide
daily hygiene.
 Provide diet appropriate for age, without added salt and restricted in protein and
potassium
 Fluid must be restricted in children with edema, CHF, hypertension or renal failure.
 Administer antihypertensive drugs as prescribed.
 Measure total intake and output.

 Weigh the child daily on the same scale and at the same time each day.
 Record blood pressure at frequent intervals.
 Observe for signs of complications.
 Provide emotional support to the child and his family during hospitalization.
Nephrotic Syndrome (NS)
 Is a clinical state characterized by an increased permeability of the glomerular membrane to

protein, which result in massive urinary protein loss.
 Characteristic of nephrotic syndrome:
1. Proteinuria 2. Hypoproteinemia.
3. Hyperlipidemia 4. Generalized edema.
Etiology: The syndrome may be classified as
1. Primary: Idiopathic nephrotic syndrome.
2. Secondary: Resulting from D.M., syphilis, AGN, or other conditions.
3. Congenital (usually inherited): rare
Altered Physiology:
 Increased glomerular permeability results in the passage of larger plasma proteins
through the glomerular basement membrane. This results in excess loss of protein
(albumin) in the urine (proteinuria) and decreased protein and albumin
(hypoalbuminemia) in the bloodstream.
 Protein loss in nephrotic syndrome causing hypoalbuminemia results in a change in
oncotic pressure, and fluid shifts from the bloodstream into the interstitial tissue (causing
edema).
 This decrease in blood volume triggers the kidneys to respond by conserving sodium and
water, leading to further edema.
 Lipid catabolism is decreased due to lower levels of lipoprotein lipase, the main enzyme
involved in lipoprotein breakdown. Hyperlipidemia then develops as the excess lipids
cannot be excreted in the urine.
 Edema, weight gain, puffiness of face, abdominal swelling
 Respiratory difficulty (pleural effusion)
 Diarrhea, anorexia, malabsorption
 Extreme skin pallor, muscle wasting

 Irritability, easily fatigued, lethargic
 Decreased urinary output
 Normal or decreased blood pressure
 Susceptibility to infection.
1. Urinalysis: Oliguria, proteinuria.
2. Kidney function test: usually normal
3. Blood:
 Reduced total serum protein. Normal ( 6.5-8 g/dl)
 Reduced serum albumin. Normal ( 3.5-4.5 g/dl)
 High serum cholesterol. Normal ( 180-250 mg/dl)
Complications:
1) Infections due to use of corticosteroids
2) Hypercoagulopathy: due to hyper-viscosity of blood, elevation of fibrinogen and other
clotting factors, decrease fibrinolysis, increased platelet aggregation.
3) Hypovolemic shock: may follow rapid use of diuretics.
4) Renal failure
5) Hyperlipidemia may lead to ischemic heart disease.
Management:
1. Rest: should be kept in bed during periods of severe edema.
2. Prevention and treatment of infection.
3. Diet:
 Appropriate for child age.
 Moderate protein intake can definitely preserve renal functions.
 Increase intake of calcium and vitamin D.
 Restriction of fluid intake if edema is progressive.
3. Drugs:
 Diuretics.
 Corticosteroids: Prednisone
 Human albumin
Nursing Care:
1. Fluid volume excess R/T fluid accumulation in tissues and glomerular dysfunction.
Goal: to reduce edema.
Interventions:

 Assess intake relative to output, measure and record intake and output
 Weigh daily or more often to assess fluid retention
 Assess changes in edema, measure abdominal girth, monitor edema around the eyes.
 Test urine for specific gravity and albumin
 Administer corticosteroids as prescribed
 Administer diuretics if ordered,
 Limit fluids as indicated during massive edema.
Expected Outcome: child exhibits no or minimal evidence of edema.
2. Risk for infection R/T lowered body defenses.
Goal: to prevent infection.
Interventions:
 Protect child from contact with infected persons
 Teach visitors appropriate preventive behaviors e.g. hand washing
 Use hand washing technique
 No live vaccination or immunization
 Observe medical asepsis
 Keep child warm and dry
 Monitor temperature for early evidence of infection.
 Monitor the child’s vital signs
Expected Outcome: child exhibits no evidence of infection.
3. Risk for impaired skin integrity R/T edema.
Goal: will maintain skin integrity.
Interventions:
 Provide meticulous skin care
 Avoid tight clothing that may cause pressure areas
 Cleans and powder opposing skin surfaces several times a day
 Change position frequently.
Expected Outcome: no evidence of skin redness or irritation.
4. Altered nutrition less than body requirement R/T loss of appetite.

Goal: will receive optimum nutrition.
Interventions:
 Restrict sodium during edema and steroid therapy
 Administer supplementary vitamins and iron as ordered
 Provide cheerful, clean, relaxed atmosphere during meals

 Serve small quantities initially to stimulate appetite
 Provide special and preferred food
 Offer moderate protein diet, high caloric diet
Expected Outcome: child consume adequate amount of nutritious diet,
5. Activity intolerance R/T fatigue.
Goal: Will receive adequate rest.
Interventions:
 Maintain bed rest initially if severely edematous,
 Balance rest and activity when ambulatory,
 Plan and provide quit activities,
 Instruct child to rest when begins to feel tired,
 Allow for periods of uninterrupted sleep.
Expected Outcome: child engages in activities appropriate to capabilities.
5. Altered family process R/T a child with a serious disease.
6. Knowledge deficit about nephrotic syndrome.
Abnormalities Of The Genitourinary Tract
o Exstrophy of the bladder: is a congenital anomaly in which part of the urinary bladder is
present outside the body.
o Hypospadias: is malposition of the urethral opening. The urethra open on the lower
surface of the penis.
o Epispadias: is malposition of the urethral opening. The urethra open on the upper surface
of the penis.
o Cryptorchidism ( undescended testis): is the absence of one or both testes from the
scrotum. The testes may be located in the abdominal cavity or inguinal canal.
Treatment: Orchiopexy,( should be done by the time the child is 5 years of age to
prevent damage to the tissues)
Exstrophy of the bladder

Review questions
1. Clinical manifestations of acute glomerulonephritis are:

1. .......................................................2. ............................................. 3. ........................................
4. ......................................................5. ................................................
2. Complications of acute glomerulonephritis are:
1. .......................................................2. ............................................. 3. ........................................
4. ......................................................
3. Nursing interventions for patient diagnosed with acute glomerulonephritis:
1. ..................................................................................................................
2. ..................................................................................................................
3. ..................................................................................................................
4. ..................................................................................................................
5. ..................................................................................................................
6. ..................................................................................................................
4. Nephrotic Syndrome is characterized by:
1. .......................................... 2. ................................ 3. ...............................4. .....................................
5. .................................................... is a congenital anomaly in which part of the urinary bladder
is present outside the body.
6. .......................................... : is malposition of the urethral opening. The urethra open on the
lower surface of the penis or into vagina.
7. ............................................: is the absence of one or both testes from the scrotum.
8. ................................................... is an operation to fix testes in the scrotum.

Chapter (9)
Child With a neurological Disorder
Learning objectives
 Differentiate between septic and aseptic meningitis
 Describe types of hydrocephalus
 Differentiate between the various types of seizure disorders
 Describe the preoperative and postoperative care of a child with

hydrocephalus

child with meningitis, encephalitis, hydrocephalus, spina bifida,
cerebral palsy, seizure disorders

Meningitis
 Is inflammation of the protective membranes covering the brain and spinal cord, known
collectively as the meninges.
 Inflammation may be caused by infection with viruses, bacteria, or other microorganisms.
 Meningitis can be life-threatening because of the inflammation's proximity to the brain and
spinal cord; therefore the condition is classified as a medical emergency.
Etiology:
1) Bacterial: E-coli, Proteus, Klebsiella, Pseudomonas, group B Streptococci,
pneumococci, Hemophilus influenza, Nisseria Meningitidis,..etc.
2) Viral: herpes simplix, mumps, varicella,..etc.
3) Fungal: Cryptococcus, Histoplasma , Candida species, …etc.
4) Protozoa, helminths, spirochetes, rickettssia.
Classifications of meningitis:
1) Septic meningitis: caused by bacteria only and bacteria can be isolated or detected on
direct smear or ordinary culture media from the CSF and CSF shows increased
neutrophil
2) Aseptic meningitis: No organism can be detected from CSF by ordinary culture media
and CSF shows predominantly increased lymphocytes. Its caused mainly by: virus,
mycobacterium TB, fungi, …etc. but not bacteria.
Pathophysiology:
 It is almost always preceded by an upper respiratory infection, bacteria circulating in the
blood invade the CSF.
 May occur as an extension of a local bacterial infection such as otitis media or
mastoiditis.
 Also gain direct entry through a penetrating wound, spinal tap, surgery or anatomic
abnormalities.
 The infective process results in inflammation, exudation and varying degree of tissue
damage in the brain.
Signs and symptoms are variable depending on the patient's age, the etiologic agent and the
duration of the illness when diagnosed.
 Infant less than 1 month of age:

o Hypothermia or fever, irritability, lethargy, weight loss, seizures, jaundice, cyanosis,
apnea, poor suckling, vomiting, full tense and bulging fontanel, neck usually supple.
 Infants and up to 2 years of age:
o Neck rigidity, bulging fontanel, fever, vomiting
o The infant with bacterial meningitis may rest in the opisthotonos position (head and
neck are hyperextended to relieve discomfort).
o Positive Kernig's sign: with the child in the supine position and knees flexed at the
hip so that the thigh is brought to a position perpendicular to the trunk. An attempt is
then made to extend the knee. If meningeal irritation is present, this can't be done and
attempts to extend the knee results in pain.
o Positive Brudzinski's sign: spontaneous flexion of the lower limbs following passive
flexion of the neck.
 Children over 2 years:
o Vomiting, headache, mental confusion, lethargy, neck rigidity, positive Kernig's and
Brudzinski's signs, seizures, agitation, hallucination, drowsiness, coma, fever and
chills.
Brudziniski's Kernig's
Sign Sign
 History.
 Physical examination.
 CBC (elevated WBCs).
 Serum glucose, urea, creatinine, electrolytes
 Blood culture.
 ESR, CRP
 Lumbar puncture (LP) to examine the CSF (diagnostic).

Lumbar puncture
 LP is a diagnostic and at times therapeutic procedure that is performed in order to collect a
sample of cerebrospinal fluid (CSF) for biochemical, microbiological, and cytological
analysis.
 A spinal needle is inserted between the lumbar vertebrae L3/L4 or L4/L5 and passed to
reach the subarachnoid space to collect CSF.
 The patient is positioned in sitting or side lying position.
Contraindications for LP:
1) Increased intracranial pressure: if LP performed , brain stem herniation will result with
sequel of cardiopulmonary arrest.
NB: To detect ↑ ICP early, Fundus examination for children who have close anterior
fontanel is essential. If there is ↑ ICP, fundus examination will reveals swollen optic
discs, or papilledema.
opisthotonos
2) Bleeding tendencies such as ↓ platelet and coagulopathy.
3) Skin infection at puncture site
4) Abnormal respiratory pattern
5) Hypertension with bradycardia and deteriorating consciousness
6) Vertebral deformities (scoliosis or kyphosis)
Normal Septic meningitis Aseptic meningitis

Color & Colorless & clear Turbid, may be milky Clear or turbid
turbidity white
Pressure 80-120 cm H2O Increased Increased
Cells 0-5 Increased mainly Increased mainly
lymphocytes/ml polymorphs (Neutrophil) lymphocytes
Sugar 1/2-2/3 of blood Marked decrease Mild decrease
sugar at time of
analysis
Protein 20-40 mg/dl Increased markedly Mild to moderate
increase
Gram stain Negative Positive Negative
Ordinary Negative Positive Negative
culture
Complications:
◊ Seizures ◊ Cerebral edema ◊ Subdural effusion ◊ Hydrocephalus
◊ Brain abscess ◊ Deafness ◊ Mental retardation

Management:
1. Prevention: Isolate the patient
2. Treatment of the patient:
 Antipyretic: such as paracetamol and cold compresses.
 Anticonvulsant: to control convulsions that may occur
 Managemnt of increased ICP: such as Furosemide and Mannitol
 Dexamethazone: IV 0.15 mg/Kg/dose every 6 hours for 4 days to prevent neurological
complications such as deafness.
 Antibiotics: till the result of culture sensitivity is available:
o Ampicillin + Chloramphenicol
o Ampicillin + Cefotaxime
o Ceftriaxone + Vancomycin
NB: The antibiotic therapy is discontinued when the patient is clinically free and afebrile for 5
days and the CSF is sterile
3. Treatment of complications:
o Subdural collection: daily tapping by neurosurgeon
o Hydrocephalus: Shunt operation by neurosurgeon
4. Anti-shock measurements:
 IV fluids
 Blood and plasma transfusion
 Hydrocortisone IV
 Inotropic drugs: Dopamine
Meningococcemia
o Meningococcemia is an acute and potentially life-threatening infection of the bloodstream

caused by bacteria called Neisseria meningitidis (also called meningococcus) which is gram
negative, aerobic diplococcus.
o The bacteria frequently lives in a person's upper respiratory tract without causing visible
signs of illness.
o Meningococci are transmitted by aerosol droplets (sneezing or coughing) or through contact
with respiratory secretions, such as through kissing or sharing a drinking glass.
o When the bacteria infect the meninges, the infection is called meningococcal meningitis.
o When the infection remains in the blood, but does not infect the brain or spinal cord, it is
called meningococcemia.

o An infection by Neisseria meningitidis, whether it becomes meningitis or meningococcemia,
is considered a medical emergency and requires immediate medical attention.
o Meningococcemia is characterized by a rapidly spreading petechial rash which may precede
other symptoms. The rash consists of numerous small, irregular purple or red spots
"petechiae" on the trunk, lower extremities, mucous membranes, conjunctiva, and
(occasionally) the palms of the hands or soles of the feet.
o The rash is typically non-blanching: the redness does not disappear when pressed with a
finger or a glass tumbler. Skin smear to detect the organism in the petechial rash is necessary
o Early treatment of meningococcal infections by antibiotics may prevent serious
complications, but timely early diagnosis is often difficult in the absence of petechial
rashes.
Prevention:
o Restrict Isolation
o Prophylactic antibiotics for contact with Meningococcemia:
Rifampicin (for 2 days):
 Infants <1 mo: 5 mg/kg PO every 12 hr
 Children >1 mo: 10mg/kg PO every 12hr
 Adults: 600 mg PO every 1 2 hr
Ceftriaxone (single dose):
 Children <15 yr 125 mg IM
 Children >15 yr 250 mg IM
Ciprofloxacin: Persons >18 yr 500 mg PO (single dose)
Treatment:
o Early treatment of meningococcal infections by antibiotics may prevent serious
complications, but timely early diagnosis is often difficult in the absence of petechial
rashes.
o Antibiotic includes:
 Penicillin G IM or IV 250,000-300,000 U/kg/day divided every 4 to 6 hours
 Ampicillin IM or IV 200-400 mg/kg/day divided every 6 hours
 Cefotaxime IM or IV 200-300 mg/kg/day divided every 6 to 8 hours
 Ceftriaxone IM or IV 100 mg/kg/day divided every 12-24 hours

Neisseria meningitidis (Diplococci)
If a glass is pressed firmly against a

rash, the rash will not fade. It will
remain visible through the glass
A: Purpuric rash in a 3 yr old with meningococcemia B: Purpura fulminans in an 11 mo old
Neural tube defects
 During pregnancy, the neural tube develops into the brain and the spinal cord.
 A neural tube defect is the failure of the neural tube to close within 28 days after conception
in an area of the neural tube or the entire length of the neural tube resulting in a neurologic
disorder in the fetus.
 The cause of neural tube defects is unknown; however, there is a link between inadequate
intake of folic acid prior to pregnancy and during the first trimester. Also its link to maternal
exposure to teratogenic agent as radiation, malnutrition and infections at early of pregnancy
 The most common neural tube defects are:
۞ Anencephaly: No cerebral hemispheres (only small vascular mass attached to the base
of the skull).

۞ Encephalocele: a rare disorder in which the bones of the skull do not close completely,
creating a gap through which cerebral spinal fluid, brain tissue and the meninges
protrude into a sac-like formation.
۞ Spina bifida
Spina Bifida
Refers to a malformation of the spine in which the posterior portion of the laminae of the
vertebrae fails to close. Bifida is a Latin word means (divided spine)
Types of spina bifida:
1. Spina bifida occulta:
 A mild form of spina bifida in which the spinal cord and the surrounding structures
remain inside the baby, but the back bones in the lower back area fail to form normally.
 There may be a hairy patch, dimple, or birthmark over the area of the defect.
 Other times, there may be no abnormalities in the area.
2. Meningocele:
 Consists of a sac-like cyst of meninges, filled with spinal fluid, but involves no nerves or
neurological defects.
 The cyst is usually covered with skin. The defect may occur anywhere on the cord
usually from the thorax and up.

 Surgical correction is necessary to prevent rupture of the sac and subsequent infection.
 Hydrocephalus may be an associated finding.
3. Meningomyelocele:
 A severe form of spina bifida in which the spinal cord and nerves develop outside of the
body and are contained in a fluid-filled sac that is visible outside of the back area.
 These babies typically have weakness and loss of sensation below the defect.
 Problems with bowel and bladder function are also common.
 A majority of babies with meningomyelocele will also have hydrocephalus.
Etiology:
 Unknown
 Genetic predisposition
 Environmental.
Prevention:
 Increased intake of folic acid.
 Prenatal detection is now possible through amniocentesis and measurement of alpha-
fetoprotein.
Surgical Intervention: Laminectomy "usually at birth"
Nursing Care:
1. Risk for infection R/T presence of infective organisms.
Goal: To prevent infection.
Interventions:
• Position infant on abdomen to avoid pressure on the sac and prevent contamination from
urine and stool
• Cleanse the sac carefully with sterile normal saline
• Apply sterile dressings and moisten with sterile solution
• Administer antibiotics as prescribed
• Monitor closely for signs of infection as elevated body temperature
• Administer similar care to operative site postoperatively
• Carry out meticulous perineal hygiene to remove infective organisms.
• Monitor urinary output for signs of stasis
• Ensure adequate fluid intake
Expected Outcome: meningeal sac remains clean, intact and exhibits no signs of infection.
2. Risk for trauma R/T delicate spinal lesion.
Goal: will not experience trauma to spinal lesion or surgical site
Interventions:

 Handle infant carefully to prevent damage to meningeal sac or surgical site
 Place infant in prone position or side lying if permitted.
 Apply protective device around sac such as a plastic surgical drape.
 Modify routine nursing activities e.g. feeding and bed making to prevent trauma.
 Don't place a diaper or other covering directly over the sac.
Expected Outcome: meningeal sac remains intact, surgical site heals without trauma-
3. Risk for impaired skin integrity R/T paralysis.

Hydrocephalus with sunset
Goal: will not experience skin irritation. eyes
Interventions:
 Change diaper as soon as soiled to keep skin dry and free
of irritation
 Keep perineal area clean and dry
 Place child on pressure reducing surface
 Gently massage skin during cleansing to increase stimulation
 Provide passive range of motion exercises.
Expected outcome: skin remains clean and dry with no evidence of irritation.
4. Risk for trauma " hydrocephalus" R/T impaired CSF circulation.
Goal: will not experience increased intracranial pressure.
Interventions:
 Measure head circumference daily to detect increased intracranial pressure and
hydrocephalus.
 Observe for signs of increased intracranial pressure, which might indicate developing
hydrocephalus e.g. irritability, lethargy, increased head circumference, separated sutures,
change in level, of consciousness, tense fontanel and vomiting.
Expected Outcome: evidence of increased intracranial pressure and hydrocephalus is detected
early and appropriate intervention is implemented.
Other nursing interventions:
1. Provide adequate nutrition and hydration.
2. Monitor infant's weight pattern.
3. Provide emotional support to the family, encourage talking, encourage participation in
infant's care.

Hydrocephalus
 Refer to accumulation of CSF in the ventricular cavity of brain causing ventricles to dilate
and increase intracranial pressure.
 Hydrocephalus occurs in approximately one out of 500 births.
 The following are the primary reasons why hydrocephalus occurs:
1) Blockage of the CSF flow
2) Lack of CSF absorbing
3) Overproduction of the CSF
Types of hydrocephalus:
1) Congenital hydrocephalus is present at birth and is often due to environmental influences
during fetal development or a genetic disposition as in myelomeningocele
2) Acquired hydrocephalus develops at the time of birth or later. It can occur at any age and
can result from:
 Tumor  Infection (meningitis)
 Prematurity  Birth injury
 Bleeding inside the head (subarachnoid hge)
3) Obstructive (non-communicating) hydrocephalus: occurs when CSF is unable to pass
between the ventricles and spinal cord due to physical mass.
4) Non-obstructive (communicating) hydrocephalus: occurs due to impaired cerebrospinal
fluid reabsorption.
Pathophysiology:
 Cerebrospinal fluid (CSF) is produced by the choroid plexus in the paired lateral, third, and
fourth ventricles (ventricular system) and circulates through the subarachnoid space and is
reabsorbed primarily by the arachnoid villi to be excreted into circulation.
 The excess CSF causes the ventricles to expand. As a result, pressure is increased on the
brain at the skull, causing neurological problems.
 The normal rate of CSF production is approximately 20 mL per hour.
Infants:
 Abnormal rapid head growth, bulging fontanel.
 Delayed closure of anterior fontanel, thinning of skull, bones, dilated scalp veins,
separated sutures.

 Signs of increased intracranial pressure: vomiting irritability, high pitched cry,
convulsions, coma, lethargy, bradycardia and papillary changes.
 Later signs: prominent forehead, scalp appears shiny, sunset eyes, visible sclera, poor
feeding, infant has difficulty in holding head up.
Older children: (who have closed sutures) headache, vomiting, lethargy, double vision,
bradycardia, increased systolic blood pressure and irregular respiration
 History "infection or trauma".
 Physical assessment
 Diagnostic procedures
 Skull percussion "cracked pot sound".
 CT or MRI scanning.
 Brain Ultrasonography
Treatment:
Extra cranial shunt: divert fluid from the ventricular system to an extra cranial compartment,
frequently the peritoneum VP shunt or right atrium VA shunt

Cerebral Palsy (CP)
 Is a comprehensive diagnostic term applied to a disorder of motion, tone, coordination

and/or posture due to non-progressive (they don’t get worse overtime) brain insult or injury
during the period of early brain growth (generally under three years of age).
 It is generally characterized by paralysis, weakness, incoordination and/or ataxia.
 It may be associated with other evidences of brain damage involving other areas like sensory
changes (visual, auditory, speech), mental retardation, seizures, and behavioral changes.
 CP is a major cause of disability among children.
Etiology:
1. Prenatal factors:
 Hereditary: e.g. congenital cerebellar ataxia
 Intrauterine infection: rubella, toxoplasmosis, CMV, and other viruses.
 Maternal trauma, anoxia, anemia, abruption of placenta.
 Maternal bleeding, maternal toxemia, ABO or Rh incompatibility.
 Cord prolapse.
 Toxins and drugs.
2. Perinatal factors:
 Brain anoxia: resulting from anesthesia, prolonged labor, placenta previa or air way
obstruction.
 Cerebral trauma or hemorrhage during delivery due to malposition, cephalopelvic
disproportion, breech presentation, high forceps delivery, delivery by vacuum.
 Prematurity, hyperbilirubinemia, hypoglycemia, infection, R.D.
3. Postnatal factors:
 Head trauma.
 Intracranial infection: meningitis, brain abscess, encephalitis.
 Neoplasm.
 Vascular: thrombosis, embolism
 Kernicterus
Types of CP:
1. Spastic CP (70% of cases): Increased muscle tonicity due to cortical damage. Permanent
contractures develop without muscle training
2. Athetotic or dyskinetic CP (15% of cases): involuntary, uncoordinated, uncontrollable
movements of muscle due to damage of basal ganglia located in midbrain.

3. Ataxic CP (5% of cases): disturbance of balance result from cerebellar damage.
4. Mixed type (10% of cases) e.g. spasticity and ataxia are coexist.
 Asymmetry in motion, irritability, delayed gross motor development
 Poor suckling, feeding difficulties
 Feels stiff on handling or dressing
 Persistent infantile reflexes
 Evidence of mental retardation, delayed, or defective speech.
Common associated problems:
 Seizures, hearing deficiency, visual defects.
 Perceptual disorders, mental retardation, language disorders.
 History.
 Neurological examination
 CT scanning
 Psychological testing.
Management:
Requires coordination and integration of the contributions of numerous health care providers
and professionals (pediatrician, nurses, physiotherapists, orthopedists, surgeon, social worker,
psychiatrists) as well as family and societal institutions.
Nursing Care:
1. Impaired physical mobility R/T neuromuscular impairment.
Goal: will acquire locomotion within capabilities.
Interventions:
 Encourage sitting, crawling and walking at appropriate age
 Carry out therapies that strengthen and improve control to facilitate optimum
development
 Evaluate and incorporate play that encourages desired behavior, since this encourages
cooperation
 Ensure adequate rest before attempting locomotion activities to encourage success
 Carry out and teach family to perform stretching exercises to prevent deformities.
 Employ appropriate range of motion exercises to facilitate muscle development and
flexibility of joints
Expected Outcome: flexibility is maintained within child's limits.
2. Self-care deficits R/T physical disability.
Goal: will engage in self-help activities of daily living.
Interventions:
 Encourage child to assist with care as age and capabilities permit.
 Encourage unimanual and bimanual activities.
 Select toys and activities that allow maximum participation by the child.
 Encourage use of adapted utensils and clothing to facilitate help.
 Assist parents in toilet training child.
Expected Outcome: child engages in self-help activities.
Cerebral
Palsy

Seizure Disorders
 A seizure is an abnormal electrical discharge from the brain.

 Convulsion: involuntary contractions of muscles due to abnormal electric activity brain. The
terms convulsion and seizure can be used interchangeably.
 Epilepsy: is defined by having at least two unprovoked seizures occurring more than 24
hours apart. The seizures must be of an unprovoked cause (no apparent cause like
hypoglycemia, head trauma, hypocalcemia, fever,.. etc.)
 A postictal period of decreased responsiveness usually follows most seizures, in which the
duration of the postictal period is proportional to the duration of seizure activity.
 Status epilepticus refers to continuo us or recurrent seizure activity lasting longer than 30
minutes without recover y of consciousness.
Types of seizure:
Seizures are generally divided into 2 main types according to the area affected in the brain:
1) Partial: also called focal or local which involve a limited brain region
2) Generalized: involving the entire brain. Therefore always associated with loss of
consciousness
Classification of seizures:
A. Generalized Seizures: involve the whole of both hemispheres of the brain. Therefore
always associated with loss of consciousness.
Types:
1. Tonic-clonic (Older term: grand mal):

 Generalized tonic-clonic seizures are the most common type of childhood seizure.
 Involve an initial contraction of the muscles (tonic phase) which may involve tongue
biting, urinary incontinence and the absence of breathing. This is followed by
rhythmic muscle contractions (clonic phase).
 Tonic-clonic phase takes from few seconds to 30 minutes.
 Postictal state: appears to relax, may remain semiconscious and difficult to arouse,
remain confused, severe headache, no recollection of entire event.
2. Myoclonic:
 Brief rapid jerks of the muscles, only lasting a second or two.
3. Atonic or akinetic:
 These attack are ch.ch.by sudden transient loss of postural tone with sudden fall to
the floor and transient loss of consciousness.
4. Absence (Older term: petit mal):
 Characterized by a sudden cessation of motor activity and brief loss of consciousness.
and unresponsive for a short period of time (usually up to 30 seconds).
 The attack may be associated with rhythmic movements of eyelids, eyebrows or lower
jaw
 May occur many times in a day and go unrecognized.
 Rarely appear before 5 years of age.
B. Partial Seizures: when only a small part of the brain is involved in the seizure
1. Simple: (Without loss of consciousness). They may be with:
 Motor signs (muscle contraction)
 Sensory symptoms (numbness, flashes of light)
 Autonomic signs or symptoms (sweating, tachycardia, abdominal pain)
 Psychic symptoms (auditory hallucination)
 Seizure episodes persist for 10-20 seconds.
2. Complex: (With loss of consciousness). They may be:
 Simple partial onset, followed by impairment of consciousness
 With impairment of consciousness at onset
NB: Both simple and complex partial seizure may spread to become generalized.
Pathophysiology:
 During a seizure, cerebral blood flow, oxygen and glucose consumption, and carbon dioxide
and lactic acid production all increase.
 Early systemic changes include tachycardia , hypertension, hyperglycemia, and hypoxemia.

 Brief seizures rarely produce lasting effects on the brain .
 Prolonged seizures, however, can lead to lactic acidosis, hyperkalemia, hyperthermia, and
hypoglycemia, all of which may be associated with permanent neurologic damage.
 Airway management and termination of the seizure are the initial priorities in patients who
are actively seizing.
Causes of seizures:
Seizures may be classified according to the causes into:
a) Epileptic seizures: is caused by epilepsy
b) Non epileptic seizures: isn't caused by epilepsy but looks the same.
It may be due to:
a) Fever: a significant rise in body temperature results in occurrence of convulsion called
Febrile convulsion or seizure or fit.
 They most commonly occurs in children between the ages of 6 months and 5
years of age.
 They are more common in boys than girls.
 There is little risk of neurological problems
b) Intracranial infections: such as Meningitis, encephalitis, brain abscess
c) Intracranial hemorrhage: e.g. subarachnoid , subdural hemorrhage
d) Toxic: Drugs, tetanus, lead encephalopathy, Shigella infections, carbon monoxide
e) Anoxia
f) Metabolic: hypoglycemia, hypocalcemia, hypomagnesemia, hypo/hypernatremia
g) Renal and hepatic failure
h) Space occupying lesion: e.g. brain tumor
 History & Physical examination.
 Procedures: skull x-ray, CT scanning, EEG,
blood chemistry, serum glucose, electrolytes.
Management of status epilepticus:
A Airway patency by: suctioning, oropharyngeal airway if needed
B Breathing should be adequate, so oxygen by mask, or use Ambu bag if needed or use
assisted ventilation.
C Circulation: establish IV line, administer IV glucose. Avoid over-hydration to prevent brain
edema
D Drugs: Diazepam → Phenytoin → Phenobarbital → general anesthesia and intubation.
Drugs used for the control of epilepsy in children:
 Phenobarbital (Luminal).
 Phenytoin (Dilantin).
 Diazepam (Assival, Valium).
 Clonazepam (Rivotril)
 Carbamazepine (Tegretol)
 Sodium Valproate
Nursing Care plan:
1. Risk for injury R/T type of seizure.
Goal: will not experience injury.
Interventions:
Administer antiepileptic medications and teach family how to do.
 Stress importance of complying with therapeutic regimen
 Avoid situations that are known to precipitate seizure as fatigue
 Be aware of and teach family to recognize side effects of medications
 Encourage good dental care during Phenytoin therapy
 Provide companionship during permissible activities as swimming
 Recommend showering or close supervision during bathing
 Educate teachers and other persons who are associated with child regarding correct
assistance during and after seizure.
Expected Outcome: child remains free of seizure activity.
2. Risk for injury R/T motor activity and loss of consciousness.
Goal: to prevent injury.
Interventions:
 Time seizure to determine duration of possible hypoxia
 Don't attempt to restrain child or use force to prevent injury
 If child is standing, ease child to floor to prevent falls
 Don't put anything in child's mouth
 Remove eye glasses.
 Loosen clothing that may restrict movement or breathing
 Remove hazards as furniture.
 Pads objects as side rails
 If child begins to vomit, carefully turn to side
 Call emergency medical services
Expected Outcome: child exhibits no signs of injury.

Review questions
1. ................................................ Is inflammation of the protective membranes covering the

brain and spinal cord
2. ............................. meningitis caused by bacteria only and bacteria can be isolated or detected
on direct smear or ordinary culture media from the CSF and CSF shows increased neutrophil.
3. .................................... meningitis in which no organism can be detected from CSF by
ordinary culture media and CSF shows predominantly increased lymphocytes. Its caused mainly
by: virus, mycobacterium TB, fungi, …etc. but not bacteria.
4. ...................................... head and neck are hyperextended to relieve discomfort in meningitis
5. ................................................ with the child in the supine position and knees flexed at the
hip so that the thigh is brought to a position perpendicular to the trunk. An attempt is then
made to extend the knee. If meningeal irritation is present, this can't be done and attempts to
extend the knee results in pain.
6. ......................................... spontaneous flexion of the lower limbs following passive flexion
of the neck.
7. Contraindications for LP:
1. .......................................................2. ............................................. 3. ........................................
4. ......................................................5. ................................................
8. Why fundus examination should be done before LP especially when anterior fontanel
is closed?
.......................................................................................................................................................
.......................................................................................................................................................
9. Complications of meningitis:
1........................................................2.............................................. 3. ........................................
4. ......................................................5. ................................................
10. ................................................ Inflammation of the brain tissue.
11. ............................................ No cerebral hemispheres (only small vascular mass attached to
the base of the skull).
12. ............................................... : a rare disorder in which the bones of the skull do not close
completely, creating a gap through which cerebral spinal fluid, brain tissue and the meninges
protrude into a sac-like formation.
13. .................................................... malformation of the spine in which the posterior portion of
the laminae of the vertebrae fails to close.

14. ....................................... A mild form of spina bifida in which the spinal cord and the
surrounding structures remain inside the baby, but the back bones in the lower back area fail to
form normally.
15. ................................................. Consists of a sac-like cyst of meninges, filled with spinal
fluid, but involves no nerves or neurological defects.
16. ................................................... A severe form of spina bifida in which the spinal cord and
nerves develop outside of the body and are contained in a fluid-filled sac that is visible outside
of the back area.
17. ............................................ is accumulation of CSF in the ventricular cavity of brain causing
ventricles to dilate and increase intracranial pressure.
18. .................................................. hydrocephalus occurs when CSF is unable to pass between
the ventricles and spinal cord.
19. ........................................................... hydrocephalus is caused by impaired cerebrospinal
fluid reabsorption in the absence of any CSF-flow obstruction between the ventricles and
subarachnoid space.
20. Hydrocephalus can be caused by ..........................., ......................................., .........................
21. Clinical manifestations of hydrocephalus: 1. .................................... 2. ................................
3. .......................................4. .........................................5. .................................6........................
22. ............................................... a tube inserted in the brain ventricles and extend to drain CSF
into peritoneum.
23. ....................................... continuo us or recurrent seizure activity lasting longer than 30
minutes without recover y of consciousness.
24. Causes of convulsions without fever in children include:
1. ................................................ 2............. ..................................... 3. .......................................
4. ................................................. 5. ...................................................6........................................
25. Nursing care for child undergo convulsion:
1. ......................................................... .................... 2............. ............................................
3. ............................................................................. 4. ..........................................................
Normal Septic meningitis Aseptic meningitis
Color &
turbidity
Pressure
Cells
Sugar
Protein
Gram stain
Ordinary culture

Chapter (10)
Child With a genetic and metabolic Disorder
Learning objectives
 Define rickets and describe the clinical manifestations of
rickets
 Explain the type of inheritance for phenylketonuria
 Recognize the importance of screening for PKU among

newborn infants
 Explain the predisposing factors for down syndrome
 Formulate an appropriate nursing process for baby with

down syndrome, rickets and PKU

Rickets
 Rickets is a softening and weakening of bones in children due to deficiency vitamin D,

calcium or phosphorus, potentially leading to bone fractures and deformity.
 Vitamin D is required for proper calcium absorption from the gut.
 Vitamin D is absorbed from food or produced by skin when exposed to sunlight, especially
ultraviolet light, which convert vitamin D from an inactive to active state.
 When calcium and phosphorus levels in the blood are imbalanced, then calcium is released
from the bones into the blood, resulting in loss of the supportive bony matrix.
Causes:
 The predominant cause is a vitamin D deficiency or inability to utilize vitamin D
 Inadequate intake of calcium of phosphorus
Higher risk for developing rickets include:
 Age. Children 3 to 36 months old are most at risk of rickets because their skeletons are
growing so rapidly.
 Dark skin. Dark skin doesn't react as strongly to sunshine as does lighter colored skin, so it
produces less vitamin D.
 Geographical Location. Children who live in places where there is less sunshine
 Premature birth because calcium is primarily laid down in the bones of the fetus during the
third trimester.
 Anti-seizure medications. Certain types of anti-seizure medications (phenytoin,
phenobarbital) appear to interfere with the body's ability to use vitamin D.
 Exclusive breast-feeding. Breast milk doesn't contain enough vitamin D to prevent rickets.
 Chronic diseases that result in loss of or poor absorption of calcium and vitamin D such as
chronic kidney diseases.
 Bone pain or tenderness
 Dental problems, delayed closure of anterior fontanel, large head, soft skull
 Muscle weakness (rickety myopathy or "floppy baby syndrome" Widening of
wrist
 Easily broken bones especially greenstick fractures
 Skeletal deformity e.g. Bowed legs
 Cranial, pelvic, and spinal deformities
 Hypocalcemia (low level of calcium in the blood)
 Tetany (uncontrolled muscle spasms all over the body)
 Costochondral swelling

 Widening of wrist
Bow
leg
 Serum calcium may show low levels of calcium
 Serum phosphorus may be low
 Serum alkaline phosphatase may be high.
 Arterial blood gases may reveal metabolic acidosis
 X-rays of affected bones may show loss of calcium
from bones or changes in the shape or structure of the bones.
 Bone biopsy is rarely performed but will confirm rickets
Therapeutic Management:
 Treatment of the underlying cause
 Vitamin D-fortified dairy products
 Foods high in calcium
 Foods high in vitamin D, such as fatty fish, liver, egg yolk, and green vegetables
 Supplements of vitamin D, calcium, and other minerals
spinal deformity of rickets

Knock Knee

Down Syndrome (Trisomy 21)
 Down syndrome is a genetic disorder caused when abnormal cell division results in extra
genetic material from chromosome 21 causes the characteristics associated with Down
syndrome.
 Discovered By: Dr. John Langdon Down
 This genetic disorder, which varies in severity, causes lifelong intellectual disability and
developmental delays, and in some people it causes health problems.
 Down syndrome is the most common genetic chromosomal disorder and cause of learning
disabilities in children.
Etiology:
 Is an error in cell division
 Isn't inherited disease.
 Human cells normally contain 23 pairs of chromosomes. One chromosome in each pair
comes from father, the other from mother.
 Down syndrome results when abnormal cell division involving chromosome 21 occurs.
These cell division abnormalities result in extra genetic material from chromosome 21,
which is responsible for the characteristic features and developmental problems of Down
syndrome.
 Associated with advanced maternal age over 35 years of age.
Incidence: 1 in every 600 - 800 live birth.
Common functional and structural abnormalities in down syndrome:
 Respiratory system: Recurrent respiratory infections
 CHD is present in 50% of cases: The common abnormalities include VSD, ASD, PDA,
TOF
 GIT: Imperforated anus, Duodenal atresia, Tracheoesophageal fistula, Congenital
megacolon.
 Hematology: the risk for leukemia is greater than normal people.
 Endocrine: hypothyroidism, DM. Hypotonia
 Skin infections
 Facial characteristics include:
o Small rounded skull, flat occiput, Short neck
o Prominent inner epicanthal folds with slant eyes
o Small nose with flat and depressed nasal bridge

o Protruding tongue due to a small mouth and large tongue
o Wide distance between both eyes with apparent squint
Protruded tongue
o Low set ear
 Excessive joint flexibility
 Extra space between big toe and second toe
 Marked Hypotonia with floppiness
 Protruding abdomen, umbilical hernia
 Neck is short.
 The hands are short and broad. A single transverse palmar crease (simian crease).
 Delayed motor and mental development, Speech problem
 Male are infertile.
 Malformed fifth finger
 Shorter than normal height
1. Chromosomal study.
2. Low maternal serum alpha fetoprotein.
3. Neonatal screening is possible.
Treatment:
o No treatment is available to cure
o Down syndrome. Attention is focused on treating associated problem and supportive care
to increase learning abilities and self-care
Nursing care:
 Support parents at time of diagnosis.
 Inform both parents, as soon as possible after birth.
 Give them reading material about the syndrome.
 Home care is better than hospitalization.
 Encourage parent to meet other families who have children with Down syndrome.
 Assist parents in preventing physical problems
 Hypotonicity of muscle and hyper-extensibility of joints complicate positioning and
flaccidity of the limp makes it difficult to hold the body.
 Respiratory infections, underdeveloped nasal bone cause chronic problems of inadequate
drainage of mucus, mouth breathing, dries oropharyngeal membranes.
 Rinsing the mouth with water after feedings.
 Use cool-mist vaporizer to keep the mucus membrane moist.
 Postural drainage and change the child position frequently.

 Promote optimum development
 Assess developmental progress.
 Encourage learning of self-care skills as soon as the child achieves readiness.
 Encourage day care program and education classes.
 Emphases on play, discipline, social interaction.
 Encourage vocational training.
 Speech and language therapy, occupational therapy, and physical therapy will be
important in promoting the child’s growth and development.
 Special education should be congruent with the child’s individual needs, and the child
should be integrated into mainstream education whenever possible.
Phenylketonuria (PKU)
o Is an inborn error of amino acid metabolism.

o It is a genetic disease inherited as an autosomal recessive trait and caused by the absence of
phenylalanine hydroxylase enzyme in the liver resulting in failure in hydroxylation of
phenylalanine to tyrosine and accumulation of phenylalanine in the blood and body fluids.
o High serum phenylalanine level reaches the brain and results in progressive brain damage.
 Vomiting, mousy/musty odor of urine and sweat
 Fair skin, blue eyes and fair, blond hair
 Hyperactivity, seizures
 Mental retardation.
Guthrie test: to detect the increasing phenylalanine levels.
The screening test is most reliable if blood sample is taken after the infant has ingested a source
of protein.

Management:
o The cornerstones of therapy are dietary protein restriction combined with dietary
substitution of proteins containing a balanced mixture of amino acids, including a large
supply of tyrosine.
o Regular assay of plasma phenylalanine level, along with levels of its metabolites, are
used to assess and monitor response to therapy.
o Low phenylalanine diet" phenylalanine can't be eliminated because it is an essential
amino acid for tissue growth.
o This diet should be started as early as possible and continued throughout childhood and
adolescence.

Review questions
1. Clinical manifestations of rickets:

1. ......................................................... .................... 2............. ............................................
3. ............................................................................. 4. ..........................................................
5. .................................................................................6. ...................................................
2. Higher risk for developing rickets include:
1. ......................................................... .................... 2............. ............................................
3. ............................................................................. 4. ..........................................................
5. .............................................................................. 6. ........................................................
3. Therapeutic Management of rickets include:
1. ......................................................... .................... 2............. ............................................
3. ............................................................................. 4. ..........................................................
4. Facial ch.ch. of dawn syndrome are:
1. ......................................................... .................... 2............. ............................................
3. ............................................................................. 4. ..........................................................
4. Common functional and structural abnormalities in down syndrome:
1. ......................................................... .................... 2............. ............................................
3. ............................................................................. 4. ..........................................................
5. .............................................................................. 6. ........................................................
5. ................................................. is failure of the liver to hydroxylate phenylalanine to tyrosine
6. …………………. Test is used to detect the increasing phenylalanine levels.
7. Management of PKU include:
1. ......................................................... .................... 2............. ............................................
3. ............................................................................. 4. ..........................................................

Chapter (11)
Child With an emergency Disorder
Learning objectives
 Describe the possible causes of poisoning in children
 Explain the emergency management for child with

poisoning
 Describe the clinical manifestation for Paracetamol and

aspirin poisoning
 Differentiate between symptoms of acute and chronic aspirin

poisoning
 Explain the pathophysiology for parathion poisoning
 Specify the appropriate antidote for the specific poison

Poisoning
Ingested poisons
 Poisoning by ingestion refers to the oral intake of a harmful substance to body functions and
cause possible death.
 The most common agents ingested by young children include cosmetics, personal care
products, analgesics, and cleaning solutions.
 Fatal childhood poisonings are commonly caused by analgesics, antihistamines,
sedative/hypnotics, and fumes/ gases/vapors.
Etiology:
 Improper or dangerous storage.
 Poor lighting (cause error in reading).
 Human factors: failure to
 Read label properly.
 Return poison to its proper place.
 Recognize the material as poisonous.
Diagnostic evaluation: Analysis reveals presence of toxic substances in:
1. Blood. 2. Urine. 3. Gastric washing. 4. Vomitus. 5. Stool.
Corrosives substances poisoning
Corrosives substances “strong acids or alkali” e.g. Drain or toilet cleanness, detergents, etc.
Clinical manifestation:
 Severe burning pain in mouth, throats and stomach.
 White swollen mucous membranes.
 Edema of lips and tongue and pharynx (respiratory obstruction).
 Violent vomiting and drooling and inability to clear secretions.
 Anxiety and agitation and signs of shock.
Treatment:
 Inducing vomiting is contraindicated “vomitus will re-damage the mucosa.
 Dilute corrosive with water; not milk unless vomiting occurs.
 Provide patent air way if needed.
 Administer analgesics and don’t allow oral intake.

Hydrocarbons Poisoning
e.g. Kerosene, Lamp oil, Turpentine and paint remover.

 Gagging, choking and coughing.
 Nausea, vomiting, lethargy and weakness.
 Respiratory symptoms (tachypnea, cyanosis and grunting).
N.B. Immediate danger is aspiration lead to chemical pneumonia.
Treatment:
 Never induce emesis after the ingestion of a low-viscosity hydrocarbon (eg, gasoline,
kerosene, furniture polish, mineral spirits) because the aspiration risk is high.
 Regarding gastric lavage, the risk and complications of aspiration outweigh the benefits.
Lavage is useful in cases in which the hydrocarbon has an inherent systemic toxicity or
contains additives with known toxicity.
 Activated charcoal has a limited role in the management of hydrocarbon ingestion.
Charcoal poorly adsorbs most hydrocarbons. Furthermore, charcoal tends to distend the
stomach and cause vomiting, increasing the aspiration potential.
 Symptomatic treatment of chemical pneumonia as oxygen therapy, humidification and
hydration.
 Antibiotic for secondary infection.
Acetaminophen Poisoning
 Most common in children and toxic dose is 150 mg/kg.

Clinical manifestations: occur in 4 stages:
1. Initial period (2-4 hours after ingestion) nausea, vomiting, sweating and pallor.
2. Latent period (24-36 hours), patient improves.
3. Hepatic involvement (last up to 7 days), pain in right upper quadrant, jaundice,
confusion stupor, coagulation abnormalities.
4. Recovery stage (gradual recovery) for patient who doesn’t die in hepatic stage.
Treatment:
 Emesis, lavage and activated charcoal.
 Antidote N-acetylcystine given by N.G. tube or I.V. because of its offensive odor
“rotten eggs”.
Aspirin Poisoning
 Acute ingestion toxic dose 300-500 mg/kg and chronic ingestion toxic dose 100 mg/kg for 2
or more days.
 Acute poisoning: nausea, vomiting, disorientation, dehydration, diaphoresis, hyperpnea,
hyperpyrexia, oliguria, tinnitus, coma and convulsions.
 Chronic poisoning: as mention above and bleeding tendencies.
Treatment:
 Home use of ipecac for moderate toxicity and hospitalization for severe toxicity.
 Emesis, lavage, activated charcoal, sodium bicarbonate to overcome metabolic acidosis.
 Diazepam for seizures.
 Oxygen and ventilation for respiratory depression.
 Vitamin K. for bleeding.
 Dialysis for severest toxicity.
Organophosphorus Poisoning
“Parathion poisoning”
 Parathion inhibits acetylcholinesterase enzyme result in accumulation of acetylcholine.

◊ Miosis (pinpoint pupils) ◊ Salivation ◊ Lacrimation
◊ Urination ◊ Bronchospasm ◊ Diaphoresis
◊ Bronchorrhea (frothy secretions) ◊ Bronchospasm ◊ Convulsions
◊ Confusion or even Coma ◊ Bradycardia ◊ Muscle weakness
Diagnosis:
Signs of OPP:
 History and physical examination “clinical manifestations”. (SLUDGE BB)
 Salivation,
 Serum Cholinesterase level: decreased
 Lacrimation,
 Atropine test  Urination,
 Diaphoresis,
Treatment:  Gastrointestinal motility
 Remove clothes and wash skin ▪ Gastric lavage.  Emesis
 Bradycardia
 Give specific antidote:  Bronchospasm
a. Atropine sulfate: acts by blocking acetylcholine action
Dose: 0.05–0.1 mg/kg IV/ET, repeat every 5–10 minutes as needed until atropinization
(tachycardia, dilated pupil, flush face and dry mouth).

Prevention of Injury
Injuries are a major cause of death during infancy, especially for children 6 - 12 months old.
1) Aspiration of foreign objects:- Asphyxiation by foreign material in the respiratory tract,
such as small objects obstruct the airway, balloons, small beaches of rattles, broken rattle,
food items (candy, nuts), pacifiers and baby powder may be another aspirated substance.
2) Suffocation: asphyxiation by covering the mouth and nose or, by pressure on the throat
and chest. This might occur in several situations such as heavy covering blanket, plastic
bags, anything tied around the neck.
3) Burns: scalding from hot water, excessive sunburn, house fire, electrical wires socket
and heating elements such as radiators, registers.
4) Drowning: can occur in only inches of water, in a bathtub, swimming pools are not
recommended.
5) Bodily damage: By kitchen utensils, fork, knife must be kept away from the infant reach.
6) Motor vehicle injuries: infant restraints are very necessary such as seat belt.
7) Falls: common after 4 months of age when the infant has learned to roll over, areas for
falling are a crib, changing table, infant seat, high chairs, walker and swing. Avoid
slippery socks, long pants and pajama.
8) Poisoning: especially when infant start to crawl, improper storage of poisoned materials,
such as drugs, creams, ointments, cleanser or detergent materials poisoning result from
ingestion or inhalation etc.
POISON ANTIDOTE
1. Acetaminophen (Acamol) Acetylcysteine (Mucomyst)
2. Anti-cholinergic agents, Physostigmine (Antilirium)
Antihistamines, Atropine.
3. Benzodiazepines Flumazenil (Annexate)
4. Calcium channel blockers calcium chloride
6. Digoxin Digoxin immune Fab (Digibind, Ovine)
7. Heparin Protamine sulfate
8. Iron Deferoxamine (Desferal)
9. Opiates, narcotics Naloxone hydrochloride (Narcan)
10. Organophosphate insecticide  Atropine sulphate
Cholinergic agonists  Pralidoxime (Protopam)
11. Warfarin "Coumadin" Phytonadione (Vitamin K)
12. Carbon Monoxide Oxygen
13. Methemoglobinemia Methylene Blue
14. Chlorpromazine "Largactil" Diphenhydramine
15. Lead EDTA (Ethylene Di Amine Tetra acetate)
16. Cyanide Sodium nitrate and Na thiosulphate

Review questions
1. Clinical manifestation of parathion poisoning:

1. ......................................................... .................... 2............. ............................................
3. ............................................................................. 4. ..........................................................
5. ............................................................................. 6. ..........................................................
2. Signs of atropinization:
1. ......................................................... .................... 2............. ............................................
3. ............................................................................. 4. ...........................................................
3. What are the treatment of corrosives substances poisoning?
4. Paracetamol poisoning is most common in children and toxic dose is …………… mg/kg.
5. …………………..is the body organ which is damaged by Paracetamol poisoning
6. ……………………………. Is antidote for paracetamol poisoning
7. Chronic poisoning of Aspirin causes …………………………..
8. What are the treatment for Aspirin poisoning?

References
 Al-Khateeb, A (2010). Pediatric nursing. UCAS library. Palestine
 Hatfield, N (2008). Broadribb’s Introductory Pediatric Nursing, 7th edition. USA:
Lippincott Williams & Wilkins
 Joyce, J. & Keogh, J. (2010). Pediatric Nursing Demystified .USA, New York: McGraw-
Hill
 Kliegman, R, et al (2011). Nelson Textbook of Pediatrics, 19th edition. USA: Elsevier
 Kyle, T.,& Carman, S. (2013). Essentials of pediatric nursing, 2nd edition. USA: Lippincott
Williams & Wilkins
 Miall, L., Rudolf, M., & Levene, M. (2003). Pediatric at Glance. USA: Blackwell Science
 MOH (2010). Neonatal Care Pocket Guide for Hospital Nurses. Egypt
 MOH (2010). Neonatal Care Pocket Guide for Hospital Physicians. Egypt.
 MOH (2016). Annual report of Health of Palestinians. Gaza. Palestine
 Polin, R., & Lorenz, J. (2008). Pocket clinician Neonatology. USA, New York: Cambridge
University Press.

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Essentials of

Mr. Ramadan Ali Hassan

To my dear mother that the secret of my success is her du'aa.

Palestine and Al-Aqsa.

Essentials of Pediatric Nursing 2018 1

Essentials of Pediatric Nursing 2018 2

Essentials of Pediatric Nursing 2018 3

Essentials of Pediatric Nursing 2018 4

 Define health, mortality, morbidity, infant mortality rate,

 Explain the developmental milestones for different ages

 Discuss the appropriate use of growth charts.

 Describe the methods used for assessing body temperature for

 Explain the child reaction for hospitalization

 Describe the safety measures that should be taken for

Essentials of Pediatric Nursing 2018 5

Roles of the Pediatric Nurse

Essentials of Pediatric Nursing 2018 6

Measurement of Children's Health Status

Essentials of Pediatric Nursing 2018 7

Growth and development

Essentials of Pediatric Nursing 2018 8

Developmental Age Period

1. Prenatal period: From conception to birth, divided into:

Essentials of Pediatric Nursing 2018 9

Factors affecting growth and development

Essentials of Pediatric Nursing 2018 10

Anthropometric measurements (Weight, Height, Head circumference, Chest circumference)

 Between 7-12 years: 2.5 kg/y

Weight in kg = (Age in years x 7) – 5

Length in cm = Age in years x 5 + 80

Essentials of Pediatric Nursing 2018 11

 A growth chart is used to follow a child's growth over time.

Essentials of Pediatric Nursing 2018 12

Essentials of Pediatric Nursing 2018 13

Essentials of Pediatric Nursing 2018 14

Age Respiratory Rate Heart Rate Blood pressure

Essentials of Pediatric Nursing 2018 15

 Development is intimately related to the maturation of the nervous system.

Essentials of Pediatric Nursing 2018 16

Essentials of Pediatric Nursing 2018 17

The nurse’s role in caring for hospitalized child :

Essentials of Pediatric Nursing 2018 19

Safety Measures for hospitalized child

Essentials of Pediatric Nursing 2018 20

Essentials of Pediatric Nursing 2018 21

Answer the following questions

Essentials of Pediatric Nursing 2018 22

Essentials of Pediatric Nursing 2018 23

 Explain the neonatal adjustment to extrauterine life

Essentials of Pediatric Nursing 2018 24

Essentials of Pediatric Nursing 2018 25

Essentials of Pediatric Nursing 2018 26

Methods of Heat Loss

Essentials of Pediatric Nursing 2018 28

1. Conjugation of bilirubin with glucourinic acid leading to physiological jaundice.

Breast milk is a relatively poor source of vitamin K

Gastrointestinal System Adaptations

Essentials of Pediatric Nursing 2018 29

Essentials of Pediatric Nursing 2018 30