Clinical Nursing Module

Module for
Clinical nursing students

(Designed for TVET program)

Hawassa Ethiopia 2001 E.C
1
Chapter 1. Introdaction to child health
1.1 Defintion of child health (paediatrics)
Is a study and care of children in sickness and health.
The word paediatrics comes from the Greek and means child cure
This field is one of the most broadest of all medical specialities b/c it includes:
A study of growth and devt of a total person from conception to adolescence
Prevention, diagnosis and Rx of disorders affecting children during their growing years
Defintion of termes
Foetu s From conception to birth (From 9 months of conception in the mothers
Womb to birth
Neonate- The first month of life (birth to 28 days)
Infant The first years of life p birth (From 1 month of 1 years)
Preschool child Under five year-old
School child From 5 year to 15 year old
Puberty The period from about 9 years to 15 years
Nearly 50% of the population of Africa are children (From birth to 15 years old)
Almost all born healthy, but approximately 180 out of every 1,000 children born alive die
before the age of 5 years
Infant mortality (death before 1 years of age) = 110 per 1,000 live births; and an
additional 60 deaths per 1,000 children b/n their frst and fifth birth days.
General Facts and Rationales of Child Health
Child- Include all the stages that a human being goes through before he/she
becomes a full-grown adult
Nearly 50% of the pop
n
of Africa are children (From Birth to 15 years old)
Almost all of them are born healthy, but
2
Approximately 180 out of every 1,000 children born alive die before the age of 5 years
(Under five mortality rate= CMR = 180/1,00)
Death before 1 year 7 age = 110 per 1,000 live births
Additional 60 deaths per 1,000 children b/n the first and fifth birthdays
Sever malnutrition in under 5=34%
These (the above) figures can decrease dramatically when:
1- The general standard of living rises
2- Preventive measures are introduced
3- Basic curative services become available to every child
A bout 65% of child death are preventable at low cost
1.2 Safe mother hood in relation to child health (SMI)
SMI IS a program, which was emerged in 1987 at Nairobi conference
and encompasses:
1. Safe pregnancy
2. Safe and clean delivery
3. Safe postnatal care
4. Basic obstetric care
5. Family planning
6. Equity for women
The aim of SMI was to enhance the quality and safety of girls and womens lives through
combination of health and non-heath strategies the program of SMI was based on the risk
approach.
i.e. most needed family planning or detecting warning signs of pregnancy, delivery and postnatal
period.
Elements of safe mother hood initiative include the following:
A. Advancement of the status of women
B. Birth planning/preparedness
C. Prenatal service for all pregnant women
3
D. Safe delivery
E. Essential obstetric care
SMI had four priorities, which help to enhance the equality of womenslife.
Priority: I Ensure access to medical treatment for obstetric emergencies
N.B. Receiving appropriate medical care depends on:
Socioeconomic and cultural factors
Geographic location/distances
Quality of cane
Priority: II Reduce exposure to the risk of unwanted pregnancy.
Provide accessible and acceptable FP.
Provide safe abortion.
Priority: III-Improve/Establish other maternal health services
Establishing and equipping community maturities (Health post)
Training TBA`S too treat or refer women
Establishing maternity waiting homes
Priority: IV Re address social inequalities
Any implementation strategy attempting to improve access to medical care still
depends on the states of women
Therefore, one of SMI intervention aim was to improve
o Womens access to education
o Womens employment opportunities
o Basic human rights and freedom
There are also four pillars of SMI:
a) Family planning
b) Antenatal care
c) Safe and clean delivery
d) Essential obstetric care
4
The 4 pillars of SMI; source: who MBP 1996
+ Since the health of children, directly or indirectly depends on the quality of life or
health of womens (mothers), the implementation of the strategies of SMI are
important for the wellbeing of children.
1.3 Age and Disease pattern
The following lists summarize the most important disease pattern that will be
encountered at different age.
a) Intrauterine Fetal life
- Maternal infection - other maternal disease
- Maternal toxaemia - congenital and inherited abnormalities
- Maternal malnutrition - many as yet unknown causes
b) Birth to one month (Neonatal period)
- Obstetric complications and birth injuries
- Asphyxia (Failure to bearthe at birth)
- Low birth weight babies
- Congenital abnormalities
- Infection leading to septicaemia
- Neonatal tetanus
- Death of the mother
c. First year of life (Period of infancy)
- Respiratory disease
- Malaria
- Diarrheal disease
- Measles
- Sudden weaning and deprivation
-PEM (especially marasmus)
d. Second to Fifth year of life
- Malnutrition (marasmus, kwashiorkor or both)
- Pneumonia (often caused by measles or whooping cough)
5
- Diarrheal diseases
- Malaria and measles
- Anaemia (sometimes caused by hook worm)
- Tuberculosis and AIDS
- Accidents
e. After 5 years
- Infectious diseases - Malaria
- Intestinal parasites - Skin diseases
- Malnutrition - Respiratory diseases
- Deprivation and neglect
NB- Most of the above childhood diseases are preventable; so agreat emphasis
must be put on preventive programmes.
Eg - Education on nutrition
- Immunization
- Environmental sanitation
I ndicator of child health
Perinatal mortality rate
Neonatal mortality rate
Postnatal mortality rate
Infant mortality rate
Child mortality rate

1.4 Health priority in children
Communicable diseases and malnutrition are the most common source of child ill health and
mortality.
* The components of child health service are:
Care of the healthy child
Care of the sick baby
Care of the disabled
*Activities in child health services include
6
Screening
Growth monitoring]
Immunization (IMCI)
CDD and ARI includes:
*Care of the healthy child includes:
General health states (i.e. growth monitoring and V/S)
Immunization states
Neglect and physical abuse
*Care of the sick child include:
Management of the childs problem(s) based on the principles of IMCI.
Malnutrition
Vitamin A deficiency
Vaccine preventable diseases
*Care of the disabled child include:
Education of society on the concept of disability
Early detection and intervention to prevent secondary problems.
Prevention of infection, proper nutrition and immunization
Collaboration with other ministries (MOE)
Make basic health services avail able at all levels.
*Selective health strategies for child survival (GOBI FEE)
Growth monitoring
Oral dehydration
Breast feeding
Food
Female Education
Family Planning
Immunization
*Epidemiology of illness and specific intervention strategies.
35,000 children die each day in developing countries (12.9 million children
die/year)
Pneumonia accounts 28% of deaths
Diarhoeal diseases 23% of deaths
Vaccine preventable diseases 16%
* Simple and affordable intervention strategies are:
Vaccines
Essential drug use
ORT
Contraception
About 65% child deaths are preventable at low cost.

7
The at-Risk child

I. Socio-economic Risks
Most diseases are poverty associated than Puberty tropical disease4s in developing
countries. These include diseases like:-
- Diarrhea
- Malnutrition
- Measles
- Polio
- Tuberculoses
- Helminthes
- Trachoma
- Vitamin deficiencies
- Health service delivery system inaccessibility, health workers shortage and mal distribution of
health institution.
- Illiteracy (low educational status).
II. ii. Biologic Risks
Age:-childrens less than five years of age are at risk because of low immunity.
Sex: - comparatively female are at risk
Poor environmental conditions
Children who live at poor environmental conditions are at higher risk of developing
diseases
The ante partum Intrapartum and Neonatal risk factors contribute for the high risk
of children
Childrens of the following conditions are generally at special risk.
-Children in poverty
-Children of migrant farm workers
-Children of immigrants
-Homeless children and
-Runaway and thrown away children
III. Cultural factors
- The child is acculturated by the family to the traditional views and practice s of their
culture.
- Culturally derived health beliefs influences how the child and family respond to
preventive ,maintenance and restorative
- Culture influences every aspects of human developments and is reflected in
childrearing belief and practices designed to promote healthy adaptations.
8
Chapter 2 History taking and physical examination in
children
2.1- History taking
The pt, usually comes with his/her mother, and your task is to pick out from all the
different information the mother is giving, what is important
Always believe what the mother tells you, but try to be realistic a bout the importance the
symptom she is mentioning.
History of the child includes the following points
9
Identifying Data -Name of child
-Age
-Sex
Mother and father
Ethnicity
Occupation
Religion
2.2 Chief complaint (C/c)
One or more symptom (s) for which the pt, seeking medical care or advice E.g.-
fever, cut wound, vomiting etc
2.3History of present illness (HPI)
- Chronologic description ,duration and onset of the disease/symptom
- Severity
- Aggravating and relieving factors
- Associated symptoms
- Any Rx and response to Rx. Etc
2.4 Past medical and surgical History
Illness the child/pt has had in the past
Medical Hx of pediatrics contains:
- Past medical illness
- Child hood illness
- Prenatal history
- Birth history
2.5 Social and family Hx
This include the parental occupation and current
living condition
Poverty and ignorance are major sources of ill health
2.6 Immunization status
Ask both mothers and her childs immunization status
10
If not properly immunized, take the opportunity of minor illness to prevent
major disease by advice and vaccination
= Allergic and medication Hx
- Particular attention should be given to the allergies that are more prevalent
during infancy and child hood. E.g. Allergic rhinitis, asthma, insect
hypersensitivity.
2.7 Nutritional Hx
Particularly important in the first two years of life
Methods of feeding- Breast feeding, bottle feeding or combination
Duration of Breast-feeding
When and what type of complementary feeding is started
Review of system-- It is best organized from the head down to the extremities
N-B In children, special emphasis should be given on symptoms related to
respiratory, gastro intestinal and genitor-urinary systems.
2.8 Physical examination
Technques of physical examination
In case of small child you should make it a habit undress the child and examine the
whole body
To examine the whole body we start with the head and end at the feet
Do unpleasant procedures last and quickly
Examine the child according to what you expect to find from the Hx.
The most important method of examination is inspection of the child
N.B- The most important tools for medical examination are your eyes and fingers and not the
stethoscope
Chronological stepes physical examination
This consist of 4 parts
1. General appearance
11
2. Vital sign
3. Anthropometric measurements
4. Evaluation of various body systems
2.8.1General Appearance
This is what you observe, while examining your patient
Mental status of the pt
General physical state of the pt
2.8.2- Vital sign
Vital sings are signs that reflect changes in the functions of the body. There are very important signs of
the condition of the pts they tell you much information about the disease. So, always take vital signs of
every patient who has a serious illness.
2.8.3 Defintion each vital sign (v/s)
Vital signs are also called cardinal signs
They include P/R, R/R, B/P and T
0
(Body temp.)
Assessing V/S provides a very quick over view of a persons/children physiological
status.
2.8.4 Measuring body temperature
In healthy state, core body temperature remains relatively constant with minor
fluctuation (+0.5
0
C)
2.8.5 Route and Sites of body temperature
Rectum (Rectal)
Mouth (oral )
Axilla
2.8.6 Indication and contradicatien sites body temperature
Rectal measurement is considered most accurate and it should be
used in:
Under 6 year children
Any confused patient
12
Any person who is prone to seizure
Comatose person
Rectal measurement is contraindicated in the following case:
Abdomino-perineal resection
Haemorrhoidectomy
Oral method can be used in clients who are:
Alert and conscious
Cooperative clients
Children over 6 years
During this time the pt should breath through the nose
Oral method is contraindicated for pts with:
Oral pathology
Recent oral surgery
Axillary method is considered least accurate but is preferred for infant b/c it is
safer than other method
2.8.7 Measuring Pulse Rate
Refers to the number of pulse beat counted in 1 minute
Normal P/R in adult ranges from 60-100
In children: - Babies 100-140 beats/minute
Children 80-100 beats/minutes
Arterial pulse is examined by auscultation and/or palpation to determine the
pulse rate and rhythm
2.8.8 Common pulse sites:
- Carotid -Femoral
- Brachial -Popliteal
13
- Radial -Posterior tibial and dorsal pedis
Apical pulse may be auscultated or palpated over the apex of the heart
Radial pulse is the common site for counting pulse in adults and child, while
temporal and apical pulses are preferable in newborn and infants

2.8.9 Pulse characteristics /quality rhytm and rate
The pulse may be classified according to;
a. Rate
b. Rhythm
c. Volume
d. Tension
a) Rate means the rate at which heart is beating.
Normal rate is considered to be between 100-140beat/min.in children, average is
90b/m.
*Bradycardia: a decrease in pulse rate below 100 beats/min
*Tachycardia: an increase in the pulse rate above 140 beats/min.
* Based on above one
Pathological alterations in pulse rates;
The pulse rate decreased due to;
- Heart muscle disease
- Cerebral tumours
- Opium poisoning
- Drugs such as digitalis
- Heart block
The pulse rate increase due to;
- Fevers
- Thyrotoxicosis
- In take of drugs like caffeine, atropine & alcoholism
- Fear & worry
- Haemorrhage
- heart failer

b) Rhythm- It is a regularity with which the heart beats.
Normal or regular rhythm; is a regular pattern of beats & intervals. The heart beat is felt at
the pulse at regular intervals with the distance b/n beats also regular. For this reason the pulse
should be counted for one full minute to detect any arrhythmias (irregularities).
Irregular rhythm (arrhythmia) or intermittent rhythm; when the irregular beat may occur at
longer or shorter intervals. The beats are not uniform

14
c) Volume strength of the pulse.
Variation volume is the force or strength of the pulse depending on the volume of blood
in the arteries
The blood volume is decreased either by haemorrhage or by heart failer the pulse will
become weak, feeble & threads.
d) Tension- tension depends up on the resistance of the walls of the artery whether the artery is easily
compressible or if excessively resistant & firm as in arteriosclerosis
2.8.10 Respiratory Rate
The respirator rate and pattern may be observed visually by watching persons
chest rise and fall during inspiration and expiration.
- Normal Respiration Rate:
Less than 2 month < 60 breath/min
2 month- 12 month < 50 breath/min
12 month-5 years < 40 breath/min
V/S indicate the over all status of a no of body systems and human responses,
Assessing V/S provides cues to the following Nursing Dx:
-Hypothermia -Ineffective airway clearance
- Fluid volume excess -Activity intolerance
- Altered tissue perfusion - Hyperthermia, etc
2.8.11 Blood pressure
The techniques used to measure blood pressure are auscultation and palpation.
Normal B/p range is:
Neonate = 88/50 mmHg.
Infant = 96/66 mmHg
6- 12 liars = 110/60 mmHg
N.B The B/P cuff should be paediatric size
2.8.12 Head to toe examination
= Start from the head then down to extremities
Assessing child nutritional status
15
1. Anthropometric assessment
Refers to measurements of variations of physical dimension and gross composition of human
body at different levels and degrees of nutrition
- Weight -Mid upper Arm circumference(MUAC)
- Height -Skin fold
- thckness -HC
Interpretation ; Wt/age - Ht/age
- Wt/ht or length
Anthropometric measurements indicate the variation in physical growth at
different ages and the degree of nutrition.
It is a widely used, simple, accurate, rapid & inexpensive measure of the
general nutritional status of an individual or population group.
It can be carried out in clinical set up and/or field work.
The major pitfalls are it cannot detect nutritional status of short duration nor can it identify specific nutrient deficiencies.
Weight
The average birth weight is around 3.25kg.
The new born loses up to 10% during the first wk of life. It is
however regained by the age of 10 days.
After this, weight gain occurs at a rate of 25 to 30g a day for the
first 3months and 40g a month during the rest of first year or life.
At 5 months of age it becomes double the birth weight.
At 1 year of age it triples the birth weight.
At 2 year it increases to 4 times of the birth weight.
At 3 year it increases to 5 times the birth weight.
At 5 years it increases to 6 times the birth weight.
At 10 years it increases to 10 times the birth weight
Wt in kg at 3 to 12 months = age (months) + 9
2
Wt in kg at 1 to 6 years = age (yrs) x 2 + 8

Wt in kg at 7 to 12 years = age (yrs) x7 - 5
2
Growth monitoring chart
It is a chart by which we put a serial record of the childs weight
periodically.
It indicates where the child failed to grow and leads to take action
immediately
16
It is the most powerful tool in growth assessment.
The chart is used to:
- Make growth a tangible visible attribute
- Create a felt need, a demand for growth
- Detect the earliest signs of faltering growth
- Reinforce effective behavior resulting in growth
- Illustrate the adverse effects of various negative events or
circumstances on growth.
- Facilitate the transfer of information to the mother.
HEIGHT
The average height of a full term infant at birth is 50cm
- At 3 month it rises to 60cm
- At 9 month it rises to 70cm
- At 1 year it rises to 75cm
- At 2 yrs it rises to 85cm
There after the child gains about 5cm every year until the onset of puberty.
- Length at birth is 50cm
- Length at 1yr is 75cm
- Length at 2-12yrs = age (years) x 6 + 77
Weight for height
It is calculated by dividing the actual weight by the weight corresponding to
the height and multiplies by 100.
Weight for height = Actual wt x 100
Wt corresponding to height
Weight for age
It is the chart which indicates the weight in kg of the child plotted on the Y
axis to the corresponding age in months plotted on the X axis.
Children below 80% of Harvard standard are labeled as malnourished.
According to Harvard standard (welcome) procedure, a child having:
Edema and Wt forage 60-80% is said to have
kwashiorkor.
Edema and Wt for age <60% is said to have marasmic
kwashiorkor.
No edema and Wt for age 60-80% is diagnosed as
underweight.
17
No edema and Wt for age <60% is diagnosed to be
marasmus.
Disadvantages of welcome system are:
- Relies on age
- Does not consider height
- Does not differentiate acute Vs chronic malnutrition.
HEIGHT FOR AGE
It is the chart which indicates the height in cm of the child to the
corresponding age in months.
- It shows linear skeletal growth.
- It reveals stunting and chronic malnutrition
The water low system for measuring nutritional status
Wt for Ht
Nutritional
status
Height for age
Nutritional
status
90-100% Normal >95% Normal
85-90% Mild wasting 90-95% Normal
75-85% Moderate 85-90% Moderate
<75% Severe wasting <85% Severe stunting

Based on water low assessment:
Wasting suggests acute malnutrition
Stunting suggests chronic malnutrition
This system has the following advantages.
It is the best method for screening malnutrition in the
community.
It can detect mild forms of PEM
It can distinguish acute from chronic malnutrition
It does not rely on age.
Disadvantage
It does not differentiate severe forms of PEM
HEAD
Head circumference at birth is about 35cm
Head circumference at 3month is about 40cm
Head circumference at 6 months is about 43cm
18
Head circumference at 1 year is about 45cm
Head circumference at 2 years is about 48cm
.
Mid upper arm circumference (MUAC)
Is measured by putting the tape measure at midway between the acronium
and olecranon process after the arm hanged freely to side.
In preschool children <12.5cm means significant malnutrition.
Body mass index (BMI)
BMI = Weight (kg) =Kg/m
2
Height (cm)
2

BMI remains constant up to the age of 5years. BMI >30kg/m
2
suggests obesity
but <15kg/m
2
points to malnutrition.
2. Biochemical measurements
Involves measurement of a nutrient or its metabolites in reselected biological
material (blood, body fluids, urine) E.g Serum ferritin level
Serum HDL
Erythrocyte folate
Tissue store of vit A, and D
3. Clinical methods
Used to detect deviations from normal state of nutrition (by observation and
interpretation of clinical data- sign and symptom) E.g. PEM (especially sever
PEM)
Marasmus
Kwashiorkor
Marasmic- kwashiorkor
Signs of marasmus include:
- Wt/age < 60% -Lass of interest in the envt
- Extreme wasting -Irritable
19
- Old man face -Good appetite
- Skin wrinkling -Usually occurs in the 1
st
2 years of life
Signs of kwashiorkor include:
- wt/age 60-80% -anorexic
- puffy face -pale spares hair with weak roots
- skin lesion -Oedema of face, arm and leg
Signs of marasmic kwashiorkor:
- The combination of the signs of the two with wt/age <60% with oedema
4. Dietary data
include assessment of past or/and current intake of nutrients
could be gathered at the national, household or individual levels
2.9.3 Theories of growth and development
There are d/ft theories about human development. But we only consider the two
dominantes theories of human development
1. THE COGNITIVE THEORIES.
The frst cognitive view of human development it basically grounded in the
theory of jean piaget.
At each of the stages, each person is seen striving for equilibrium, striving for
the sufficiency of mental concepts (schemas) to explain their expeience.
Thus intelligence for piaget involves the organization of idea s and adaptation
of existing schemas to include new perception
Accommodation- refers to the process the altering schemas in order to take
new information in to account
20
These all processes occur in four stag of development
1) The sesory motor stage of infancy
2) The Preoperetional stage of early childhood
3) The concrete operational stage of late childhood
4) The formal operational stage of adolescence and adulthood
1. The sensory motor stage of infancy
Covers from birth to two years
Infant uses sensory and motor abilities to understand the world
This stage begins with reflex actions and ends with complex coordinations of
sensory motor skills
The major acquisitions of this stage are learning the existence of a disappearing
object from the sight (objecte permanence ) and remembering and imagining ideas
and experiences (mental representation)and causation (understanding of the child
about means to ends.)
2. Preoperational stage
-Covers from 2-6 years
The child uses symbolic thinking including language to understand the world
Most thinking is egocentric which means the children understand the world from only
once own point of view.
3. Concrete operational stage
Coveres from 7 to 11 years
The child understands and applies logical operation or principles to interpret specific
experience or perceptions.
Major acquisition of this stage are application of logical abilities, understand basic
idea of conservation, number, classification of and many other specific or concrete
ideas.
4. Formal operational stage.
Covers approximately from 12 on words
T he adolescent or adult is ableto think about abstract and hypotheticl
21
Major acquisition of the period is the evaluation of an idea of ethics, politics and
social sciences become the interest of them.
Major contributions of the cognitive theory
1. The cognitive theory has revolution ized development psychology by focusing
attention on active mental processing.
2. It has had a major impact on education, allows teachers to know their students
2- The psychoanalytic theory:-
*The founder and proponent of this theory is Sigmund freud
*S. Freud psychoanalytic theory is view human behavioral development in five
psychosexal stages.
*According to Freud s theory of infantile sexuality, children have sexual pleasures
and fantasies long before the reach of adolescence
*In general the following are the five stages of psychosexual
development
1) The oral stage (0-1)
According to Freud infant obtains sensual pleasure firt by sucking and later by biting
and hence the center of gratification is the oral (mouth) region.
If baby given too little or too much opporch unity to stimulate his mouth region.
(It could be through food staffs or play materials) it may acquire an oral fixatioin,
which in adult hood may foster excessive oral behavior (talking, alcoholism, smoking,
chwing and the like). This means that dissatisfaction during that stage ends the child
to stop or stunk on the psychosexual development to satisfay these of the oral stage
through the stimulation of the mouth in d/ft ways.
2) The Anal stage (2-3)
The center of gratification shifts from mouth to anal region during this stage.
The Major concern of the child during these stagesa is how to control his/her bowel.
There fore, the parents should provide adequate and smooth toilet training and also
instruct what is right and wrong. Otherwise, if the parents are too harsh in the baby
toilt training effort, the baby becomes likely to be anally fixated or stunk to the anal
stage, and the child become stubborn, over conformist and exaggerated self-control
in the later adult life
22
3) The phallic stage (4-6)
In this stage genitals become the major focus of sexual excitement.
During this stage children develop sensual feeling of love to wards parents of the
opposite sex and hate parent s of the some sex. Freud called this feeling as Oedipus
complex for boys and Elecra complex for girls. As a result the child begins to identify
with the same sex [identifications].
Therefore, the smooth resolution of these needs of the child will lead the child to
positive and optimist view of world in later adult life but the mistreatment of child
during this stage (like harsh punishment being less affectionate will lead the child to
the negative view of the world and will have a pessimist view of the world in general.
4, Latency Stage (7-11)
During this stage sensual feelings are dormant or latent or repressed and then the
ego expands
5, The Genital Stage from 12 to on wards)
After five or six-year period of sexual latency, the individual enters the fifth stage
called the genital stage which lasts through out adulthood.
During this stage the center of gratification is the genital organs In general
according to S. Freud. The early child hood experiences are significant for an
individuals late adult hood personality
2.9.3 Developmental stages (mile stones)
The devt of child can be assessed from different point of view
It can be classified into four stages
1- Gross motor development
2- Fine motor development
3- Cognitive development
4- Psychosocial development
1- Gross motor development
At about 3 month- the infant exhibits almost no head lag
At 5 month, the infant sits with out support
At 8 month, the infant sits with out support
23
At 9 month, stand with support
At 12 month (1 year) the infant can walk with support
2- Fine motor development
The infant has strong grasp at 1 month
The infant can grasp voluntarily at 5 month
The infant develops pincer gasp at about 9mnths
3- Cognitive development
In the sensory-motor stage b/n birth and 18 month, intellect develops and the infant
gains knowledge of the environment through the senses devt progress from reflexive
activity to purposeful acts.
Language crying is the 1
st
means of comm.
- Laughing, babbling and constant sound begins b/n 3 and 4 month
- Combining syllables (ma-ma) begins by 8 month
- Infant says and understand mama and dada in correct context by 10
month
- By 12 month the infant can says b/n 12 and 14 words in correct context
4- Psychosocial development
- Stranger anxiety typically begins around 6 months
- Social smile at 2 month of age
- Enjoys social interaction at 4 months
- At 12 months the infant shows emotion such as jealousy and affection.
The various skills the baby and young child learn are called mile stones
All children are different some walk early, others late
- The average at which children reach various milestones is given below
Summary of Normal Development Mile Stones
Average
Age
Motor devt Language and social behaviours
1 month Can lift head when prone Can fix with eyes, often smiles
24
3-6 month Good head control Can follow an object with eyes, play
with hands
6-9 month Can sit unsupported Grasps actively, makes loud noises
9-12 month Able to stand Understands a few words, tries to use
them
12-18 month Able to walk Grasps small objects with thumb and
fingers
2 years Able to run around as
much as he/she wants
Can say several words or even some
sentences
3 years Actively playing, clever
in climbing and jumping
Starts talking a lot, curious and
inquisitive
In watching development, we can notice at what age the child learns to do certain things,
such as smiling at his mother, sithing with out support, grasping objects with his hands
etc

2.9.5 Growth measurments
The best way to measure growth is by weighing, other ways include: measuring
height, arm circumference and head circumference
1) Height
Height growth is faster in the 1
st
6 month of life and again in early
puberty than the rest of childhood
From 0-6 month an infant grows 2.5 cm/month
Average 6month old infant is 63.8 cm
Average 12 month is 72.5 cm
2) Weight
25
Average birth weight is 3.5 kg
Weight doubles at 4-5 month
Weight triples at one year
Daily wt gain is 20-30 gm/d for 1
st
3-4 mo and 15-20 gm/d for the rest 5 years.
3) Head circumference
35 cm at birth
change 1cm/month for the 1
st
1 year, and than 10cm for the rest of life
head grows 12cm in circumference in the 1
st
12 mo (6 cm in the 1
st
3 mo, 3 cm in the
next 3month, 3 cm in the rest of the month)
In normal infant, Hc > CC up to 1 year, but equal for another 6month, and then, after
18 mos of age, the CC > HC.
N.B The Hc is measured by taking the greatest distance around the forehead and
the back of the head above the ears (maximum fronto-occipital
Circumference)

4) Arm circumference
- The circumference of the middle of the upper arm es fairly rapidly to about 16
cm by the age of 1 year.
Remains nearly constant from 1 to 5 years (increases only about 1cm, to 17cm)
5) Tooth eruption
Lower central incisors erupt at 6 month of age
By 2 and years all the 20 deciduous teeth erupt
Permanent teeth start to appear at the age of 6 years
2.9.6 Factor affecting growth and development
a) Nutrition Good nutrition is the base for normal growth and devt
b) Prenatal condition
c) Postanatal environment
d) Hereditary
26
2.9.7 Measuring Childs hearing ability
The hearing ability of a child may be tested in a no of ways:
a) Voice test c)- Tuning fork test
b) Finger fraction test d)- Audiometery
c) Watch test e)- simple tests in paediatric
a) Voice Test
Conversational Voice (C.V) Can be headed up to a distance of 12 meters inquite room
Whispered Voice (W. V) If W.V is not audible but the pt can hear C.V, he may have
mild deafness
b) Finger Friction Test
Is a quick screening method for testing hearing
Make the pt (child ) hear sounds made by rubbing fingers or snapping a thumb& a finger
held near the ear of the child,
c) Watch Test
Easily carried out c any watch
But the test can not be considered to be a standard test.
(Because the laudness of the ticking of d/f watches is variable)
d) Tuning fork test
There are three types of tuning fork tests
1- Rinne test
2- Weber test
3- Absolute Bone conduction test (ABC)
Measures inner ear function
Compare the ABC of the pt with the examiner
e) Simple Test
27
A) Reflex (Age< 1year) the child blinks or turns its eyes & head on
hearing voice, bells, drums pure tone.
B) Distraction Test (age 1to 2years)
- By the sound of a rattle or clinking of the feeding cup, child gets distracted
C) Performance Test
- Older children are asked to perform actions like closing the door.
N.B In Otoscopic examination for infant and Young children, restrain may be necessary
to accomplish safe& effective assessment.
- Otoscopic examination should be postponed until last in infants & young children
2.9.8 Screening child for visual
Examination of the eye is routine part of the paediatric assessment beginning from the newborn
period.
This assessment includes:
- Evaluation of visual acuity - Colour vision testing
- Inspection of the eye - Ophthalmoscopic examination
- Light perception
A- Visual Acuity
Records the acuteness of central vision for distance and near, or reading
vision
Even though many visual acuity tests exists, their use depends on the childs
age and ability to cooperate.
The most important and common visual acuity test in infant is an assessment of their ability to
fixate and follow a target
Sheridan Test A simple comparison test with the examiner indicating letter on a
familiar toys on a board and asking a child to indicate a similar object on the board
held by the mother
Used to test children of 2 -3 years.
The E Test Is the most widely used visual acuity test for pre school children.
28
Can be performed by age 3-4 years in which a child points in the direction of the
letter
Snellen acuity chart
Can be used at about 5-6 years, if a child knows letter
B- General Inspection
Requires good light (light is important to inspect the eyes)
Inspect or observe the following
Shape and size of each eye
Symmetry of the orbits positions
Movement of the eye lids
Symmetry of the globs
C- Light perception
Can be tested by papillary examination
Includes evaluation of both the direct and consensual rx
n
s to light
D- Ophthalmic Examination
Is used to examine the inner part of the eye (Exam, of the fundus)
Best done when pupil is dilated
Requires dark room for good inspection
2.9.10 - Screening the child for speech and language devt
Expected characteristics in Relation to Age
Speech At 9 month babbling with a series of syllables
At 1 year the first words used with meaning appear
At 2 year three word sentences are used
- By the time infants speak their 1
st
words, around 12 months, they already
respond appropriately to several simple statements, such as: no, bye-bye
and give me.
- By 15 months, the child points major body parts
- Age 18-24 month- is the most dramatic devt of linguistic
29
Communication and Language
- The child smiles in response to face and voice at 6 month (6 month)
- Monosyllabic babble at 7 month (7 month)
- Inhibits no and follow one-step command with gesture at 7 month
- Follow one step command with gesture at 10 month (e.g. give it tome)
- The child can speaks first real word at 12 month
- The child speaks 4-6 words at 15 month and 10-14 words at 18 months.
- The child can speaks two-words sentences (e.g. Mommy shoe)

Summery of language Development

Age in months Language development
15 Jargon; follows simple command; may name familiar objects (ball)
18 10 words (average); name pictures, can identify one or more parts of body.
24 Can put three words together (subject, verb, object)
30 Refers to self by pronoun I knows full name
36 Knows age and sex, counts 3 objects correctly, repeat 3 no or a sentence of 6 syllables
48 Counts 4 pennies accurately; tells a story
60 Names 4 colours, repeats sentence of 10 syllables; counts 10 pennies correctly
Screening for language delays is particularly important b/c of the strong links
b/n language and cognitive devt ant later performance.
Assessment Technique
The most widely used and researched test is the Denver II Developmental
screening Test
The test generates pass-fail ratings in 4 domains of development.
1- Personal-social
30
2- Fine motor-adaptive For children from birth to 6 years
3- Language
4- Gross-motor
- It can be administered in 20-30 minutes with expensive training or expensive
equipment.
- Originally published in 1969 as the Denver Developmental screening Test
(DDST)
The Early language milestone (ELM) scale provides pass-fail ratings in expressive,
receptive and visual language, using a format similar to that of the Denver.
Administration takes 2-3 minute
Most items can be completed by parental reporting
Sensitivity for language and cognitive deloys is high compared with golden
standard diagnostic tests
Identifies many children even before their parents report being concerned
The clinical linguistic and Auditory Milestone saves (CLAMS) is a sequence of language
milestones that can be quickly administered
Has been validated in infants and toddlers suspected of language delay, and in
those with known motor delays
Correlates well with standard diagnostic tests
The test correlates well with a golden standard test of mental retardation
The Ages and stages Questionnaires (ASQ) are a series of 11
Questionnaires
designed to be completed at home by parents at several time points from 4 to 48
month
- Validity and reliability are established, with over all agreement with standard
developmental tests of 76-91% However;
- ASQ may fails to identify up to 13% of children with developmental delays
- Scoring and interpretation are quick.
31
N.B Denver II screening tests may fails to identify children with subtle delays and its ability to
predict cognitive delay at a later age (predictive validity) is modest.
- It offers clinicians 125 well standardized, easily administered developmental test items,
presented in a convenient one-page format (questionnaire)
Generally the techniques, which are used to assess language development in children, are.
- Denver II- test (DDST)
- Early language milestone scale (ELM)
- Clinical linguistic and Auditory milestone scales (CLAMS)
- Ages and stages Questionnaires (ASQ)
- Others (E.g.- Draw- a person test and the kinetic family drawing)
Chapter 3 providing care for a child with
therapeutic and diagnostic procedure
3.1 Medications administration
- The giving of medication to the child is a serious responsibility of a nurse
- The need for accuracy in pouring and giving medication is greater than adult pts.
- The dose varies with the size, surface area and the age of the child; and the nurse
has no standard dose as customary for adult pts.
Since the dose is relatively small, a slight mistake in the amount of drug given makes a
greater proportional error in terms of the amount ordered than with the adult dose
- The possibility of error in the giving of medication to children is greater than to
adults
The child reaction to a dose ordered by a physician is less predictable than adults Rx
n
, the
nurse must be alert to recognize undesired effects of the medication given.
3.1.1 Routes of drug administration
Most of the routes of drug administration in children are similar to that of
adults, and includes the following:
32
A) Oral administration
- Infants generally accept the medication put into their mouth, provided that it is in
a form that they can easily swallow
- Medication should be given slowly in order to prevent choking
- The nurse should:
Sit down and hold the infant, or
If he/she can not be remove from his/her crib, raise the child to sitting
position, or
If this is contraindicated, elevate his/her head and soulders
- If so there is less danger of choking
Medication can be given to a child by
Glass
The tip of a teaspoon, or
A rubber tipped medication dropper
- If the medication is immediately vomited, the nurse should notified this to the
physician
- A child as young as two years of age can be thought to swallow drugs
Tell the child to place tablet near the back of his/her tongue and to drink the
water, fruit juice or milk (to wash down the tablet)
- For younger and seriously sick children, tablets should be crushed and dissolved
in water; can be given by spoon or through NGT.

B) Intramuscular injections
- The procedure of using an Im injection is the same as for the adults
- In children and infants, the anterior lateral thigh is often used for IM injection to
reduce the risk of vascular and peripheral nerve (sciatic) injury (As well as the
less devt qluteal muscle)
33
- Use long needle for Im injection (This helps to give deep Im injection for better
and proper absorption)
The purpose and procedure of IM injection for paediatrics or children is similar with
administration of Im medication in adults.
C) Intravenous administration (IV)
- Many medications are delivered intravenously, either by infusion or directly into
the vein
- Intravenous administration circulates to the body rapidly
- The ability to gain access to the venous system for administering fluid and
medications is an expected nursing skill in many settings
- Nurses are responsible for selecting the appropriate vein puncture site and being
proficient in the technique of vein entry
Ideally both arms and hands should be carefully inspected before a specific vein puncture
site is chosen
The following factors are to be considered when selecting a site for vein puncture
o Condition of the vein
o Type of fluid/medication to be infused
o Duration of the therapy
o Patients age and size
o Skill of the health care provider
Other medication administration routes
In addition to the above mentioned routes, medication can be administered
by other routes, and these includes:
o Intra dermal injection (ID)
o Hypodermic or subcutaneous injection (sc)
o Rectal administration
o Topical application of drugs
34
o Inhalation of drugs
3.1.2 Site of administration
Intramuscular injections
o -anterior lateral thigh
Possible sites for IV drug administration includes:
o Scalp veins
o Femoral veins
o External jagular veins
o Ante cubital fossa
3.1.3 Paediatric drug dosage
There are various drugs which are commonly used in the treatment of young
children
Local variation in dosage may be necessary and strength of a vailable tablets
and mixture must be known
Treatment should always be as simple as possible
Great care must be taken to make sure the mother really understand when
and how to give drugs on return home
The weight of a child is important for calculating the amount of drug that should be
admistered to the child
To give some understanding of how to calculate drug dosage, we will see some common
types of drugs used in paediatrics.
Type of Drugs Dosage of the drugs
Penicilline G
(crystalline pencillin)
New born= 60,000 untli/kg/24hrs
Older children= 25,000-500,000 unit/kg 24 hours
Oral Im,IV in 4 divided dose
Benzanthine pencillin 0.6-1.2 million unit Im once a month
Cloxacillin 50 mg/kg/24 hours in 4 divided dose
35
Ampicilline Moderate infections = 50-100 mg/kg/24hrs
Severinfection = 200 mg/kg/24hrs
Pyogenic meningitis = 400 mg/kg/24hrs
Chloramphenicol 50mg/kg/24 hours given 6 hourly
sever infection 200 mg/kg/24hrsbut reduce other 48
hors
in new born, reduce to 25 mg/kg/24 hours for 1
st
month
Cotrimoxazole 48mg/kg/24hrs by mouth in two doses
Mbendazole 100 mg daily for 3 days
do not give children under 2 years of age
Metronidazole 15-50 mg/kg/24hrs orally in three doses
Frusemide (lasix) 1mg/kg/24hrs in single dose; may be repeated
Ephedrine 2.5mg/kg/24hrs in three doses
Paracetamole 15mg/kg per dose; not more than 4 doses in 24 hours
Chloroquine 0-1 years = 1/4 tabs/day/for 3d
1-5 years = 1/2 tabs/day/for 3d
6-10 years = tabs/day/for 3d
over 10 years 2 tabs/day/for 3d
N-B- The precaution, contraindication and the nursing Responsibilities are similar to
administration of drugs in adults (But it depends on each specific drug)
3.1.4 Precaution
Precautions- Cautions that should be taken before drug administration
Eg. - Maintaining rate of flow of injection
- Monitoring rate of flow of injection
3.1.5 Contraindicion
3.1.6 Nursing responsibility
Why we need pharmacology in nursing?
- It is the nurse who follows patients status most closely
- 1
st
member of health care team to observe and evaluate drug responses and intervene if required
36
- It is must to know the responses that a medication is likely to elicit.
- A nurse is patients last line of defense against medication errors
Dosage may differ for drugs
- Having more than one indication
- Adminstered by more than one route
Basic guidelines to ensure correct administration
- Read medication order carefully
- Verify identity of patient
- Read medication label carefully (identity, amount and suitability for intended route
- Verify dosage calculation and timing of doses
- Implement special handling the drug may require
3.2 Performing scalp vein puncture
3.2.1 Definition
Vein puncture is the procedure of using a needle to withdraw or administer drugs and
infusion from the vein and to the vein respectively
(i.e. Withdraw blood from the vein)
o Administer drugs and infusion to the vein
- The type of infusion, duration of infusion and age of the patent determine the
location or site of the vein
- Because infants do not have large veins in the antecubitalfossa, blood specimen
for exam jugular vein and femoral vein
- Superficial veins puncture is the easiest of vein puncture
- Veins of choice in infants are the following
1- External Jugular vein
2- Femoral vein
3- Scalp vein The head is turned to 45
0
and the veins in the fronto-parietal
region are traced which are usually the most prominent
- The area should be shaved
- A 24 guage short bevelled needle with its butterfly flap is used
37
- Insert the needle into the vein by holding it in the fingers and threaded for some
distance
- As soon as the vein wall is entered blood can be seen flowing into the polythene
tubing
- If blood appears in the tubing, allow some fluid to run and secure the tubing in
place with tape
N-B- All other procedures and nursing responsibilities are similar with adult vein puncture and
blood with draw and Iv medication administration
3.2.2 Indication of scalp vein puncture
To with draw bloods for different lab investigation
To administer drugs for treatment and investigation
To administer Iv infusion for the Rx of dehydration and hypotension and
shock
3.2.3 How to differentiate vein from Artery?
- Blood from a vein puncture is dark-red in appearance
- There is bounding pulse on artery on palpation (pulsation of artery)
- The blood from the artery is bright-red and the speed of the bleeding is high from
the side of the puncture
- Mostly veins are superficial (visible)
The best veins for scalp vein puncture are:
- Frontal ----------------------------- In the midline of the fore head
- Temporal --------------------------- In front of the ear
- Posterior auricular -----------------Behind the ear
- Supraorbital ------------------------ Above the eye
3.2.4 Contraindication
3.2.5 Precaution
-Ensure a good light and comfortable position
38
-Before puncturing the vessel, make sure that it is not an artery by feeling whether it
is pulsating or not
3.2.4 Nursing responsibilities and procedure
- Ensure the presence of special scalp vien needle shave the area over the vein
carefully and clean with antiseptics
- Rub the skin over the vein or apply compression with the finger or a rubber band to
make the vein more visible
- Strech the skin and introduce the needle close to and parallel to the long axis of the
vein, about 0.5 cm from the place where you ain to puncture the vein
- Puncture the vein and push the needle a few millimetres into it; check whether you
are inside the vein or to
- With draw the blood or fix the needle in this position by putting a strip of plaster
over the tubing and on to the skin near the top of the needle
- Inject small amounts of fluid from the syringe during the fixing procedure to avoid
blood clothing in the needle
- Make sure that the needle and the tube are securely fixed in place in case of Iv
infusion
3.3 Inserting Nasogastric tube
3.3.1 Definition
- NG tube insertion means an introduction or passage of a tube into the stomach
through the nose
- The tip of the nose is pressed upwards and the tube is passed into the nostrile along
the base of the nose, aiming towards the occipute
- If the tube coils in the mouth or the patient begins to cough, with draw the tube to
the nasopharynx and re-insert
- In infants and small children, it is necessary to immobilize the jaw
- The tube is passed to the posterior pharynx and advanced into oesophagus and then
pushed into the stomach
39
- Position the infant on his side or back with a nappy roll placed under his shoulder
- Measure feeding tube and mark with tape
For preterm infants and neonate measure from bridge of nose to just beyond tip of
sternum
For older children measure from tip of nose past ear to tip of sternum
- Lubricate the tube with water. Do not use oil, because of danger of aspiration
- Insert through nares, do not push against resistance
- In infants, especially observe for vegal stimulation (i.e. Bradycardia and apnea)
Test for correct positioning of the tube in the stomach by:
- Putting the external end of the tube into a cup of water (If air bubbles appear, it
indicates that the tube is in respiratory tract)
- Aspirating gastric content with syringe
- Auscultating the bowel (Abdomen) while injecting air into the tube with syringe.
N.B - Failure to obtain aspirate does not necessarily indicate improper placement of the tube, there
may not be any stomach content or the tube may not be in contact with fluid
- Avoid inserting the NG tube into the infants trachea
- The feeding position should be supine or side lying with head and chest slightly
elevated
- The flow of feeding should be slow. Do not apply pressure
- Irrigate the tube with clean water and clamp it before air enters the stomach with
feeding is completed

40

3.3.3 Purpose
- To provide a method of feeding or administering medication that requires minimal
patient effort (when the infant is unable to suck or swallow, e.g. in preterm)
- To provide a route that allows adequale kilojule or fluid intake
- To prevent fatigue or cyanosis which is apt to occur from bottle feeding
- To provide a safe method of feeding for unconscious child or one who is too limp
or weak to feed normally.
3.3.4 Indications
- Prematurity or preterm infants; cleft palate
- Weak or severly ill child; respiratory distress
- When sucking and swallowing causes distress, such as with breathing distress
ordifficulties or tetanus, particularly neonanatal tetanus
- Unconscious child and Neurologic disorders, sever PEM
Hazards of NG- tube insertion includes
- Placement of the tube in the traceobronchial tree
- Ulceration of the nasal mucosa
- Perforation of the stomach
- Epistaxis due to trauma
3.3.6 Precaution

41
3.4 Performing cardiopulmonary resuscitation
Definition
- CPR- is the re-establishing of heart and lung action after cardiac arrest or apparent
sudden death resulting from electric shock, drowning, respiratory arrest and other
causes
Resuscitation means restoration to life or consciousness of one apparently dead
Purpose
The goal of Resuscitation in paediatrics is to maintain adequate oxygenation and perfusion of
blood throughout the body while steps are taken to stablize a child and establish long-term
homeostasis
Resuscitation process/Technique/
The two major components of CPR are:
1) Artificial ventilation
2) Closed chest cardiac massage
Emergency measure must be done with in 3 to 5 minutes
The steps for resuscitation can be remembered as A,B,C,D, where A is for
airway, B for berating and C for circulation and D for drug administration
The following three techniques will provide adequate oxygenation to major body
parts or organs for an extended period of time
1- Clearing the air way
2- Ventilating the lungs
3- Circulating blood by cardiac compression
Respiratory support
- Look and assess the presence of obstruction by foreign body
42
- If no obstruction, but the child has no spontaneous respiration, steps should be
immediately taken to breathe for the child
- A Common cause of airway obstruction in an unresponsive child is the tangue
occluding the airway.
Assessment of respiration includes
- Opening the airway (head tilt/chin lift or jaw thrust if the cervical spine is unstable)
- Looking for the rise and fall of the chest
- Looking for the presence of foreign body
- Listening at the nose and mouth for breathing
- Feeling air existing the childs airway
This should be done in less than 10 seconds.
Rescue breathing should be done by
- Mouth-to- mouth breathing
- Mouth to- nose breathing
- A mask over the pts mouth and nose and mouth-to-mask breathing, or
- Bag- mask respiration
Cardiovascular support
- Support of circulation should be provided to sustain adequate blood flow to deliver
oxygen to the tissues
- If there is no pulse or if the pulse < 60 beats/min with poor perfusion, chest
compressions must be given
Chest compressions are given without interruption of ventilations
- Effectiveness of chest compression is determined by the presence of palpable pulse
- Chest compression in infants (small infants) and newborns may be performed by
Placing two thumbs on the midsternum with the hands encircling the thorax, or
Placing two fingers over the midsternum and Compressing the chest; or
Holding the child in the supine posture on ones lap
43
N-B- The resuscitation effort should pause periodically to make an assessment of the possible
return of spontaneous
- Heart rate
- pulse and
- Respiration
Chest compression: ventilation Relationship
Neonate 1-8 Yrs > 8 years
Compression rate 120 At least 100 100
Compression to
ventilation ratio
3:1 5:1 15:2
Pulse check Umblical artery Brachial Carotid
N.B- Ventilation should be given without interrupting chest compressions. It is asynchronous
Some medication therapy are used in cardio pulmonary resuscitation
E.g. epinephrine
- Continuous follow-up and monitoring of the childs condition is mandatory
both in the process of the resuscitation and afterwards
- Follow-up and monitoring helps to assess the effectiveness of the procedure
Precaution
- Do not over blow or over inflate the child during ventilation (mouth-to- mouth
breathing)

3.4 Providing care for a child with Tracheostomy
3.4.1 Definition - Tracheostomy is an opening made in to the trachea
for various purposes (Opening an airway into the trachea)
3.4.2 Purpose:
To bypass the obstruction and to gain easy access to tracheal secretions
To create patent airway in case of upper airway obstruction (to provide
adequate airway)
44
To maintain oxygen supply to the tissue
The nurse should assess the child with Tracheostomy and provide
adequate care
3.4.3 Assessment Reasons for performing Tracheostomy
Laryngotracheo bronchitis
Congenital anomalies/abnormalities) e.g. Congenital stenosis
Lodged foreign body
Sever chest trauma
Burn of the head and neck
Laryngeal edema

3.4.4 Precaution
3.4.5. Care of the Tracheostomy
Provide adequate humidity
Aspirate secretion whenever indicated by
Noisy respiration
Intercostals retraction
Poor colour or change in V/S
Observe closely for rising pulse rate and restless ness
Monitor respiration frequently and observe for unequal chest expansion
Keep the area around the tube clean and dry
Clean with an applicator dipped in hydrogen peroxide
Observe the site for bleeding and irritation
Place sterile dressing around the tube and under the tapes that holds the tube in
position
Observe the child closely to prevent accidental removal of the tube, and make
sure that the tape which hold the tube in place are tie
45
Have necessary equipment available at the bedside (e.g. suction machine,
Tracheostomy set, materials for cleaning
Never immerse the child in a full bath
Position the infant with his neck extended
Provide psychological care and reassurance of the child and the family
3.4.6 Suctioning the Tracheostomy,
Tracheal suctioning due to decreased cough mechanism patient is unable to clear
= Tracheal suctioining is performed when adventitious breath sounds are detected
or when ever serections ae obviously present
= Unnecessary suctioning can intitate bronchospasm and cause mechanical trauma
to the tracheal mucosa.
-Use sterile equipment
3.4.7 follow- up and monitoring
It is Post operative nursing intervention
- Continous monitoring and assessment
- Keep the tracheostomy patient by suctioning ofsecetions
- Positioing the patient in semi fowlers position
- Promote drainage
- Minimize edema
- Prevent strain on the suture lines.
- Analgesic drugs are administered
- Sedative are not given b/c they may cause respiratory center depratioin and aggravetes the
respirtory problem.
3.4.8 Nursing Responsibilities
- Tell the procedure to the family and get informed consent
- Prepare the necessary equipment for performing the procedure
- Assist the physician/surgeon/ during the procedure
- Maintain sterility of the procedure
46
- Care of the Tracheostomy and suctioning
- Follow-up and monitoring the childs condition
3.5 Oxygen administration (0
2
Therapy)
Oxygen therapy is the administration of oxygen at a concentration of pressure greater than that
founding in the environmental atmosphere
Oxygen transport to the tissues depends on the following factors, and these factors must be
considered when oxygen therapy is considered
- Cardiac out put
- Arterial oxygen content
- Adequate concentration of Hgb
- Metabolic requirements
3.5.1 Indication
Hypoxemia, while decreasing the work of breathing and the stress on the
myocardium
- Pneumonia
- Carbon monoxide poisoning
-Sever asthma
-Heart failure or MI
3.5.2 Dose (oxygen concentration)
=Simpl mask -Used for low to moderate concentration of oxygen (40-60% range),
with a flow rate of 6 to 10 lit/min
=Tent (o
2
tent) - It also supply 30% - 55% oxygen concentration with a flow rate
of 4 to 8 litters/min
=Nasal cannula (nasal pronges) -It can deliver 24% to 44% of oxygen at a flow
rates of 1 to 6 LPM
3.5.3 Way or methods of oxygen administration
- Oxygen is dispensed from a cylinder or from a piped in system
- Reduction gauge is necessary to reduce the pressure to a working level
47
- Flow meter regulates the control of oxygen in L/min
- Oxygen is monitored and moistens by passing it through a humidification
system (To prevent mucous membrane of the respiratory tree from becoming
dry)
- When a patient/child is unable to take enough oxygen, he/she must get oxygen
by the following ways/methods:
a. Tent (oxygen tent)
- Traditionally, the oxygen tent was a clear plastic canopy placed over the upper
half of a bed.
- A motor unit that circulate oxygen in the tent is attached to it
- The face tent is an adaptation of the oxygen tent, which is a clear plastic molded
to fit under the chin and in front of the mouth and nose
- Face-tent can supply high humidty with the 0
2

- It also supply 30% - 55% oxygen concentration with a flow rate of 4 to 8
litters/min
- Nurses should pay special attention to care of the childs facial skin when caring
for a child using face tent.
b. Simple mask Is a transparent mask with a simple nipple adaptor
- It fits over the clients nose, mouth and chin
- Used for low to moderate concentration of oxygen (40-60% range), with a flow
rate of 6 to 10 lit/min
- Simple mask requires a minimum oxygen flow rate of 6 LPM to prevent C02
build up
c. Nasal Cannula (Nasal Prongs)
- A device used to deliver small to moderate increases in
0
2 concentration
- The Cannula has two short tubes that fit into the nostrils
- It can deliver 24% to 44% of oxygen at a flow rates of 1 to 6 LPM
Is relatively simple and allows people (patient) to move about in bed, talk, cough and eat
without interruption of
0
2 flow.
48
- Use Cannula with caution for clients who have irregular breathing patterns
(Rationale- The percentage of
0
2 that reaches the lung depends on the rate and
depth of respiration)
+ Goals of O
2
Therapy are
- Reverse Hypoxemia
- Decreases the work of respiratory system
- Decreases the hearts work in pumping blood.
3.5.4 Equipment and Accessories
- Oxygen cylinder with valve and pressure tubing
- Safety pin
- Glass connector
- Wolffs bottle
- Fine catheter, mask, Cannula or tent
- No smoking sign
- Hanger for the tent
- Atray with gallipot of saline or water
3.5.5 Monitoring Administration of 0
2
- Whenever a client/a child is receiving
0
2, the childs respiratory status must be
continually monitored to ensure that Rx has the desired effect
- For monitoring
0
2 administration, consider the following points
A- Observe the clients respiration. (rate, depth, character)
B- Document difficulty in breathing
- Abnormal movements
- Retraction
- Irregular breathing pathern
- Abnormal breathing sounds
C- Assess lung sounds-Document abnormal lung sounds
D- Assess the clients/childs level of comfort
E- Measure the clients pulse rate often
49
F- Assess for evidence of cyanosis
G- Monitor the
0
2 delivery device for proper fit and usage
H- Closely observe the child whose
0
2 has been discontinued
3.5.6 Complication/
0
2 Toxicity/ and sign and symptom
0
2 is a drug and can cause serious side effects such as:
-
0
2 induced hypoventilation (which can be prevent by giving low flow 02 at a
rate of 1-2 LPM)
- Atelectasis
The most serious and insidious hazard is 02 toxicity
- Caused by too high concentration of 02 for an extended period of time
0
2 toxicity is believed to cause the following two conditions
- destruction and decrease of surfactant
- Development of pulmonary edema
Signs and symptoms of 0
2
toxicity include
- Substantial distress
- Paresthesias in the extremities
- Dyspnea and anorexia
- Flaring of nares
- Restlessness, fatigue and malaise
- Progressive respiratory difficulty
3.5.7 Precaution of
0
2 Administrations
Oxygen will not by itself burn or explode, but it does facilitate combustion
The greater the concentration of
0
2, the more rapidly fires start and burn
There fore, the staff, the patient and visitors must take safety precautions.
The nurse ensures safety by
1- Placing cautionary No smoking:
0
2 in use sign on the childs/patients door, at the foot or
head of the bed and on the
0
2 equipment
2- Removing matches and cigarette lighters from the bedside
50
3- Requesting other people in the room and visitors to smoke in areas provided elsewhere in
the hospital
4- Removing and storing electrical equipment (in case short-circuit sparks occur)
5- Avoiding materials that generate static electricity (E.g.-woolen blanket, synthetic fabrics)
6- Avoiding the use of volatile, flammable materials near pts receiving
0
2
e.g. Oils, greases, alcohol or ether
7- Grounding electrical monitoring equipment, suction machines and portable
diagnostic machines
- 02 therapy should be discontinued temporarily if portable diagnostic radiographic)
equipment is required
- Monitoring and suction equipment needs to be placed on the bed side opposite to the 02
source
8- Making known the location of fire extinguishers and making sure personnel
are trained in their use.
3.5.8 Nursing responsibility and mgt of 0
2
toxicity
Management- Prevention of
0
2 toxicity is achieved by using oxygen only as
prescribed
- If high concentrations of
0
2 are necessary, the duration of administration is kept to a
minimum and reduced as soon as possible.
- Positive End Expiratory pressure (PEEP) or continuous positive Airway pressure (CPAP)
is used in conjunction with 02 therapy to reverse or prevent microatelectasis
Nursing Responsibilities during O
2
Administration
1- Explain the procedure to the child and allow him/her to feel the equipment, the
0
2 flowing
through the tube, mask, etc
2- Maintain clear airway by suctioning if necessary
3- Provide humidification to moisten the dry
0
2
4- Measure
0
2 concentration every 1 to 2 hours
5- Observe the childs response to
0
2 therapy
Decrease restlessness -Improved colour
51
Decreased respiratory distress -Improved V/S
6- Keep combustible materials and potential source of fire a way from the
0
2 equipment
7- Ensure and maintain the safety precaution of
0
2 administration
Chapter 4 Providing elimination care
4.1 Catheterization
4.1.1 Inserting urinary catheter
Defintion: - Urinary catheter is inserting a small tube, called catheter, through the
urethra in to a bladder.
Purpose:-
Provide a means of collecting urine & controlling incontinence with out the risk of
infection
To help patients with urinary retention
To measure the urine out put
For bladder irrigation
For instilation
CATHETERIZATION

4.1.2 Indication
1- Urinary retention
52
2- Lower urinary tract obstruction
3- Incontinent patient
4- To collect sterile urine specimen
5- To empty bladder before,during&after surgery
6- For bladder irrigation
7- For bladder instilation

Classification
1. Female catheterization
2. male catheterization

4.1.3 Types of catheter
1. Rubber, plastic or nylon based on made of substance
2. Single lumen vs. double lumen based on no of lumen
3. Indwelling/retention vs. in-and-out catheterbased on time of stay
4.1.4 Precaution
Use strict aseptic technique
Clearly identify the urethral opening.
If you are catheterizing a distended bladder, allow 300 500cc of urine to pass and clamp the
catheter for 20 minutes to allow the bladder to regain its muscle tone.
Have adequate light during the procedure.
Ensure that catheter drainage system is closed sterile system.
Observing the urine flow for proper functioning of drainage system.
Plaster the tubing to the bed and not kinked.
Observe the quality and characteristics of urine
The client can go into shock it too much urine is removed from the bladder too fast.
4.1.5 Contraindication and complication
Contraindication
Urethral trauma,injures ,pelvic fracture
Non sterile technichque
Complication of catheterization
UTI due to contamination
53
Retention
Obstruction
Damage to bulb urethral gland and bleeding
Irritation and pressure sensation
Tissue trauma
Removal of catheter
-Removal of the indwelling urethral catheter is a simple procedure using medically aseptic
technique.
Care must be taken to avoid trauma to the urethra & discomfort for the client. - -Remove
the tape that has secured the catheter tubing to the clients body.
-Put on gloves, insert the syringe in to the entry part of the lumen of the catheter that was
used to fill the balloon, & then aspirate all fluid from the balloon.
-After aspirating the fluid from the balloon, instruct the client to inhale deeply & then
remove the catheter slowly & care fully.
-The client should be encouraged to drink plenty of liquids to distend the bladder & should
expect to void with in the next 6-8 hrs.

1. Procedure for female catheterization
Explain the procedure to the chiled (patient) family.
Wash hands
Assemble the equipment after checking the physician order.
Keep the sterile equipment on the top shelf and unsterile on lower shelf.
Put up screen for privacy close the door
Pull the bed and adjust the bed to a comfortable working height.
I.e. left handed stand on left of patient
Right handed stand on right side of patient.
Assist the patient dorsal recumbent position and with bath blanket drape the client.
Place rubber sheet under patients buttocks
Put on clean glove wash the womens perinea area with soap and water, rinse and dry the area.
54
Remove the glove and wash the hand again.
Open sterile trolley or pack and pour the cleaning solution in to the cup.
Put on sterile glove
Put up sterile drape and gently shake it to open.
Place the cotton balls in to cup.
Remove the plastic coverage of catheter and attached to prefilled syringe syringe to the balloon
inflation part, inflate the balloon to test for function, and then aspirate all fluid/air back to the
syringe.
Lubricate the chatheter 2.5 5cm long
Clean both labial folds and then the meatus.
N.B:- use each swab only once clean with forceps by using cotton balls.
Separate vulva with the gauze held by two fingers of your dominant hand until the opening is exposed.
Make sure the opening is urinary meatus.
Pick up the catheter with dominant hand
Insert the catheter gently in to urinary meatus advanced 4-6cm or until urine begins to drain. Never force in
sertion of the catheter it any indwelling, allow the urine flow into the basin, then remove the catheter after
urine drained.
But in indwelling catheter inflate the balloon
Pull gently on the catheter inflate the balloon balloon is inflated and that the catheter is secured.
Connect the catheter to drainage bottle or bag position the bag below the level of the bladder.
Tape the catheter to the patient upper thigh
Dry the patient perinea area if needed
Measure the urine out put
Remove the rubber sheet and other equipment.
Make sure the patient is comfortable
Wash the equipment and return
Wash the hands
Record the size, type of catheters inserted client response, amount of urine obtained its appearance
and specimen and send.
55
2. Male catheterization
The procedure is the same as above except
Cleaning the penis with antiseptic solution from the center to outer part.
Position the client/him lie on his back with the legs lightly a part, no need to flex his leg.
Drape the sterile fenestrated towel on the client
Hold the penis with sterile gauze upright or a 60
0
C angle and gently pressing the end of the penis
from two sides may help to open the meatus.
Lubricate the catheter up to 12cm of tip of catheter.
Insert it 16 18cm or until urine flow.
Then follow the same steps as in female.
4.2. Administering an enema
4.2.1 Defintion: - An enema is the cleansing of a portion of the large
bowel by insertion of fluid rectally.
Purposes
1. To relief gas, constipation /Fecal impaction/
2. To clean the bowel in preparation for diagnostic or surgical procedures, example x-ray,
Anastomosis ---
3. To evacuate feces in patients with Hemiplegia, quadriplegia or paraplegia ---
4.2.2 Indication
faeces prior to a surgical procedure or a delivery
For incontinent patients to keep the colon empty
For diagnostic certain X-ray exam
e.g.:- Before certain X-ray exam
Equipments
Enema container with appropriately sized tubing, i.e. -for children size 14-18frand for
infants 12Fr.
Solution like tap water, soap solution, normal saline ---
Disposables gloves & water-soluble lubricant
Water proof bed protector
Clean bed pan & toilet paper

56
4.2.3 Types of enema
It is of two types depending up on the amount of fluid to be used. These are:
A. Small volume: enemas are used when rapid stool evacuation is preferred. It contains
laxative medication approximately 150ml. Are usually prepackaged.
B. Large volume enemas cleanse the bowel of stool by distending the bowel with up to 1000
ml fluid for adults, 150-160ml for infant, 240-360ml for older children.
4.2.4 Precaution
Care is needed in children especially those with poor cardiac function
The procedure should not take > 2hrs.
Should be finished 1 hr before exam or x-ray to give time for the large intestine to
observe the rest of the fluid.
Give cleansing enema hr before the rectal wash out
Allow the fluid to pass slowly.
Prolapsed haemorriods
Anal fissure
Inflammatory bowel disease
Tumor in sigmoid colon
4.3 Colostomy
4.3.1 Defintion: Colostomy is a temporary or permanent opening of the colon
through the abdominal wall.
Ostomy: the surgical creation of a new opening on the surface of
the body in to the colon is a colostomy; in to the ileum, an ileostomy.
Ostomy is surgically created for infants who are born with an
imperforate anus, intestinal atresia, Hirschsprugs disease (aganglionic
mega colon) congenital lack of intestinal musele nerve in the rectal and
sigmoid segment of the bowel.
Ileostomy is not irrigated because the fecal content of the ileum is
liquid which can not be controlled, but colostomy is irrigated.
Purpose of colostomy irrigation:
57
1. To encourage a bowel motion in a recently established
colostomy and to ensure that the opening is patent.
2. To relieve constipation in patients who has difficulty in
managing their colostomy.
3. To teach the patient how to establish regularity of
evaluation through colostomy.
4. To reduce distention before closure of colostomy.
Indications:-
follow- up and monitoring Imperforate anus
Abd-rectal atresia
Intestinal volvulus, /mal rotation/
Extensive trauma /car/
Narcotizing enter colitis
Cancer of rectum
Colo rectal anastomosis
Recto-vesical or recto-vaginal fistula to promote healing
4.3.2 Care of colostomy
Skin care- frequently wash with mild soap and apply powder to reduce irritation
- apply protective skin barrier
- As a rule colostomy bags are not necessary. Usually simple dressing of disposable tissue often
covered with plastic wrap is used and is held in place by an elastic belt.
- To prevent passage of flatus and feces a colostomy plugs are available
- The drainage appliance is 1/3-1/4 full it should be changed
- Regulating the passage is achieved by irrigating the colostomy or allowing the bowel to evacuate
naturally without irrigation.
- Educate the family members about care of the stoma.
- Most of the time performing the procedure is decided by the patients life style and it is better to be
performed after meal.
- Give education about feeding habit i.e discourage eating foods that cause excessive odor and gas
like cabbage, egg, fish, peanut, beansetc
- Give psychological support about body image disturbance and change in life style.
N: B-the function of colostomy will begin 3-6 days post operatively.
4.3.3 Irrigation colostomy
PURPOSE-to empty the colon gas, mucus& feces
Equipment- dressing set, drawer sheet, sleeve/sheath
58
- micropore tape, dirt receiver
- Solution for irrigation, glove
Procedure for irrigating a colostomy
- Explain the procedure
- Wash hand
- Assemble the necessary equipment
- Position the pt in a sitting position
- Apply an irrigation sleeve or sheath to the stoma place the end in the commode
- Allow some solution to flow through the tubing and catheter
- Lubricate the catheter and gently but firmly insert it against the stoma
- Hold the shield in place 10 sec after the water has been instilled and gently remove it
- Allow 10-15 min for most of the drainage to return
- Leave the sleeve/sheath in place about 30-45min while pt gets up and moves around
- Cleanse the area with mild soap and water
- Replace the colostomy dressing or pouch
4.3.4 Precaution
COMPLICATIONS OF COLOSTOMY
prolapse of the stoma
perforation
stoma retraction
Skin irritation
Pulmonary complication
4.1.5 Nursing mamagement
Observation of a stoma & surrounding tissue
Looking for abdominal distention & should be reported if an irrigation of faces.
Care of skin around the stoma
Maintain an ostomy bag in place to collect liquid stool
Look for any colonic prolase via the stoma
Changing an ostomy bag at least once/wk
59
Chapter 5 Assisting hospitalized child

5.1 Admitting a child to the health care unit
5.1.1 Definition of The age of the child, the severity of the signs & the symptoms of
illness the length of the time they have been present determine whether or not the infant or child
requires immediate care /admission/.
60
5.1.2 Steps in admission
While admitting a child, the following suggestions should be kept in mind:
1. Orient the pt & parents to the facilities in the ward such as water source, bed rails, light,
toilets
2. A comfortable bed should be provided
3. Explain the rules & regulations of the hospital e.g. visiting hrs
4. pts Ht, Wt, T
0
, PR, RR, B/P should be measured on admission
5. Give support to the child parents if possible
6. Have consent from parents for any surgical & special diagnostic procedures like biopsy,
L.P. thoracentesis, post mortem exam.
The pediatric unit
The pediatric unit must meet the needs of children & of their parents, childrens needs can be
classified as adequate provision for care, protection from physical danger e.g. infection, & accident
and protection from a psychologically threatening envt. In the pediatric unit, the surroundings
should be home like & cheerful.
When children are permitted to wear appropriate clothing rather than hospital gowns, they tend to
feel more as though they were at home.
Pediatric intensive care unit
New born infants or children requiring intensive care include those with congenital
anomalies, major illnesses of new born, coma, status asthmaticus, sever bronchitis, & sever
pneumonia, CHD with failure as well as those undergoing major cardiovascular or neurological
procedures, & seriously ill form poisoning or trauma.
Emotional reactions on admission of a child to the hospital
It is natural that when the infant is admitted to the hospital they feel anxiety, anger, fear, and
disappointment & possibly quit. Specific causes of parental anxiety are.
a. Fear of the strange envt in the hospital
b. Fear of the unknown & of what will happen to the child immediately & in the future.
c. Fear than the condition is infectious & may spread to other family members
61
d. Fear that society will look up on the illness as a reflection of something wrong with the
problems.
Nursing responsibilities
Thorough reliable explanation about the condition of a child
Reassurance
Listening to complaints patiently to provide relief from anxiety.
Health talks for children in school about hospital experience
Introduce the head nurse, dietitian & other appropriate personnel to the child/ parents
The admission procedure should be carefully explained, & all questions asked by the parents
should be answered clearly, fully & in a way that will not cause them anxi

5.2 Bathing
5.2.1 Defintion
is a cleaning sponge bath given to a patient in bed patients or an ambulatory patient.

5.2.2 Purpose
To cleanse the body
To prevent multiplication of bacteria on the skin
To stimulate circulation
To improve general muscle tone
Give a good opportunity to observe his condition & establish friendly
communication with him. .
Teach the patients the essentials of health
To keep the skin surface dry, thus helping to prevent bed sores.
62
5.2.3 Types of bed bath
+ There is two type of bed bath
Complete bed bath and partial bath
Complete bed bath: - Taking a bath of whole body.
Partial bath: - The face, arms, hands and back are washed; a complete daily bath
is not advisable for all pts. Elderly pts have a decrease in production of
perspiration and natural oils w/c keeps the skin moist as a result, these pts. Need
not wash as frequently.
5.2.4 Method of bath
A- Bed bath - A bed bath is a cleaning sponge bath given to a
patient in bed patients
B- Tub bath (shower) - This type of bath is given to an
ambulatory patient.
5.2.6 Precaution and contra indication
- Change the water frequently whenever it is dirty/cold
- Do not go to opposite side of bed during bath, as all work can be done from one side
- Put up screen to protect the pts privacy
- Close the door and the window to prevent draft
- Re port to ward supervisor any undesirable symptoms, such as rash, swelling, pressure
sores or discoloration.
A. Give bed bath
-A bed bath is a cleaning sponge bath given to a
patient in bed patients
Equipment
-Two wash clothes
-Two bath towels
-Two linen cloths
-One draw sheet & rubber sheet if necessary
-Two basins & jug with water
63
Soap with soap dish
-Pyjamas as night clothes
-Comb
-Back care tray
-Mouth care tray
-Scissors for nail care
-Screen
-Bed pan or urinal
-Toilet paper
-Waste receiver
Procedure
Wash hands& collect the equipment
Greet the patient & explain the procedure
Bring the necessary articles to the bed side.
Close the door & window
Screen the unit
Offer bed pan or urinal empty & clean be for preceding with bath, wash hands.
Loosen top bed covers at sides & foot.
Remove bed spread & blanket & place them on a chair. Leaving the top sheet to
cover the patient & remove gown or pyjama.
Prepare the water & check the temperature of the water the back of your hand,
water at temp. of 105-115*F(41-46*C)
Place towel under the chin, wash face, eyes, ears& neck.
Ask the patient if he likes to have his face washed with soap or with out soap.
First wash eyes from inner to outer corners, then the for head, down the face to the
neck, then rinse& dry well.
Place the towel under the arm further away from the nurse.
Place your hand under the arm to give support.
Soap the wash towel, wash & rinse the arm & hand, repeat the other arm.
64
Cover the chest with both towel & turn blanket down to abdomen, put the towel
under the patient, wash, rinse& dry well.
Re cover the chest
Re covers the abdomen, protect the matters wash rinse& dry the abdomen.
Observe the patient & communicate during the bath.
UN cover far leg & drape with bath blanket arranging bath towel under the foot.
Flex knee, wash leg, rinse& dry well.
Repeat the same with near leg.
Change water now & whenever it is dirty or becomes cold
Turn patient on side, with back to wards you. Wash back & dry well. Rub the back
with oil. Observe condition of skin, especially over pressure points.
Put towel under the hip & give him the wash towel if he is able to wash the
genitalia area. if the patient is unconscious or un able complete the bath by the
nurse.
Put on a clean gown on the patient & comb patients hair while protecting the
pillow with a towel.
Cut & clean nails of the fingers & toes.
Prepare occupied bed & re move the screen.
Take care of the used equipment & re turn to its proper place, leave everything tidy
open the window & door.
Wash hands & report on chart any finding.

B. Giving tub bath-
- This type of bath is given to an ambulatory pt.
o The nurse should assist the pt. into and out of the tub. Anyone can fall during this procedure.
The pt. may become tired or dizzy, and slip causing injury. Some pts require the nurses
help through out the bath
o Special precautions must be taken to avoid having the pt. slip in the shower or tub
o The nurse should place a nonskid bath mat in the tub or shower
o Even though pts seem strong and alert they should be checked at least every five minutes
65
o Showers and tub baths do not need to last more than ten minutes
o Pt who are taking a shower or bath after prolonged bed rest, need to be watched care fully
for dizziness. These pt may also tire easily
Assisting with a shower
+ A pt. must show no signs of weakness before a shower is permitted. The doctor
will indicate when the pt. is ready for this activity however; the nurse should also
use judgment to decide whether a pt is able to shower.

+ The pts condition may vary throughout the day. A pt. may have medical
permission, how ever, signs of weakness, dizziness, or fatigue may require
postponement of the shower, and safety precautions explained at the beginning of
the unit should be reviewed. Observing safety rules in the shower helps prevent
injuries.
Purpose
To arrange the pt. during admission
To refresh and relaxed the admitted pt.
precautions and contraindications
- Have water at correct temperature
- Avoid chilling the pt.
- Do not leave pt alone in bathroom
- Always keep bathroom door unlocked
- Check pt. frequently for signs of exhaustion
- Do not allow the pt. to remain in the shower longer than ten minutes
Equipment
- Soap with soap dish
-Wash cloth
-Bath towel and face towel
-Gown or pajama
-Slipper
-Chair
66
-Bath blanket if it is needed
-Bath mat to avoided slipping of pt.
-Bath powder or lotion
-Bath thermometer
Procedure
- Explain procedure to the pt.
- Assemble equipment and take to the bathroom
- Close windows
- Help pt to undress
- Help pt to bath himself or her self assisting as necessary
- Assist pt. out of tub or shower vary and put a gown on the pt
- Clean the tub or shower and leave room in order
- Return pt. to room and put to bed
- Do not allow the pt. to remain in the shower longer than ten minutes

5.3. Applying restraints:-
5.3.1 Definition
All infants & children have physiologic & psychological needs to be mobile children may need to
be restrained /control/.
5.3.2 Purpose
for some diagnostic procedure, therapeutic procedure, or during the physical examination & some
time to protect from an injury.
5.3.3 Types of restraints
1. Jacket restraint
Used to help the child remain flat in bed in a supine position
The jacket is put on with the strings in the back
2. Mummy restraint
Used to immobilize the arms & legs
67
Used when the Childs head, or neck is to be examined/treated, scalp vein puncture is
to be inserted, gastric lavage/gavage is to be done,
3. Elbow restraint :-
Used to hold the elbow in an extended position so that the infant cant reach to face
Important when the child has had surgery on head eg. For cleft palate, repaired, or
scalp vein needle is in place.
4. Abdominal restraint
Holds the infant in a supine position on the bed.
Complication
Impairment of circulation
Physiologic loss of muscular strength & flexibility if prolonged
Psychological effects
5.4 Feeding a hospitalized child
An ill child can be given fluid & nutritional supports to avoid the problems of sever depletion
in several ways:-
Oral, gavage, IV, gastrostomy feedings, hyper-alimentation ---, the choice of method depends on
the age & abnormal condition of the child.
A. Oral feeding
If the GIT is functioning normally, liquid soft, or solid feedings by mouth are preferable from
a physiologic standpoint to other methods of feeding.
Infants & young toddlers can usually be encouraged adequate amounts of fluid from a bottle,
dropper, syringe or medicine cup if they are physiologically well enough to do so.
Pre-school & school age children can be encouraged to take fluids if the f/f suggestions are
followed.
1. Offer fluids that the child enjoys.
2. Use straws if the child is able & permitted to drink in this manner
3. Encourage school-age children to compete with each other to see who can drink the most
fluids each day.
68
B. Gavage feeding:
Definition: - Is the instillation of specially prepared nutrients in to the digestive tract through a tube that
is inserted through one of the nostril, down the nasopharynx and into the alimentary tract.
Purpose
1. To feed Unconscious patient
2. To administer medication
3. To introduce food in to the stomach when the patient can not take food in usual manner
4. When the patient unable to swallow as in paralysis of throat
5. After surgery on mouth, throat or fractured jaw
6. In babies when the baby is too weak swallow specialize premature babies
Equipment
- Correct amount of feeding solution
- Basin
- Calibrated plastic feeding bag
- Measuring container from which to pour the feeding
- Water
- NGT with all equipment
Procedure
- Wash hands and Prepare equipment
- Explain the procedure to the client or family
- Secure NGT
- Prepare client & feeding - Fowlers position
- Assess tube placement
- Administer the feeding
- Hang bag on IV pole (30cm)
- Clamp tubing & add the formula to the bag
69
- Open clamp. Run the formula through the tubing
- Attach the bag to the nasogastric tube & regulate the drip by adjusting the clamp to drop factor
on bag (e.g. 20 drop / ml)
i. Rinse the feeding tube immediately before all of the formula has run through the tubing.
- Instill 60 ml of water through the feeding tube
ii. Clamp & cover the feeding tube
iii. Ensure client comfort & safety
- Remain in fowlers position for at least 30 minutes.
iv. Dispose equipments appropriately
v. Document all relevant information
- Feeding amount kind, duration of feeding & assessment of client
- Record volume of feeding & water administered on I/O chart
To check the position of the tube
I. If patient cough, the tube may be in trachea
II. If the end of the tube is dipped in bowl of water air bubbles are seen if it is in trachea
III. If the end of the tube is brought near the ear, a whistling sound is heard if it is in trachea &
gurgling sound if it is in stomach
IV. Attach to the syringe & aspirate. If it is in stomach the stomach content will come out
C. Gastrostomy feeding
If the ill child has an upper GIT anatomic abnormality, requires prolonged gavage feeding or
has side effects from gavage feeding, feeding may be given by gastrostomy or jejunostomy.
- Gastrostomy is an opening in to the stomach through the abdominal wall, in to a self-retaining
catheter/tube.
Indications:
I. For infants with esophageal atresia requiring a temporary gastrostomy feeding purpose.
II. For infants with an esophageal stricture due to ingestion of corrosive solutions or fibrosis
or and anastomosis.
III. For infants requiring prolonged artificial feeding.
70
The procedure for feeding a child through a gastrostomy is similar to that used when gavage
feedings are given. The tube (funnel) should be held 20-25cm above the level of the stomach to
allow the food to run slowly. After the gastrostomy feeding the tube may be left open & suspended
or clamped depending on the childs condition.
D. Total parentral nutrition /TPN/ or hyper alimentation
TPN or intravenous alimentation fills the total nutritional needs of those who cannot receive
feedings by ways of the GIT. It is used for example, in small premature infants; infants who have
sever GIT anomalies & infants & children who have intractable vomiting & diarrhea, extensive
burns, etc
The usual IV solution contains electrolytes & sugar but not protein & fat, which are necessary for
the growth & maintenance of body tissue. The highly concentrated solution used in TPN contains
hypertonic glucose, electrolytes, vitamins, and minerals----.
This solution is given continuously by means of an infusion pump through a catheter placed in the
superior vena cava, which is reached by way of jugular vein or sub clavian vein.
These wide diameter central veins are used because they have a high rate of blood flow, which is
necessary to dilute the concentrated solution that is given.
The catheter doesnt have to be changed unless sepsis occurs or unless it is occluded by blood.
Nursing management/responsibilities
1. Careful assessment of the infant or child receiving TPN is necessary b/se of the danger o
sepsis, hyper glycemia or hypoglycemia.
2. TPN should not be discontinued suddenly b/se of fear of rebound hypoglycemia
3. Frequent record of input & out put.
4. Replace the tubing if the central venous line becomes discontinued accidentally.
5.5 Preventing transmission of infection in an acute care setting
The only source of infection before birth is through the mothers blood stream & her body
protected the fetus from injury, but p birth many portals of infection & sources of injury exist. The
neonate has little resistance to infection & no self-protection against injury, so is dependent on
health team members & parents for safe care.
71
Nursing responsibilities
1. Keep the babys and the familys envt clean
2. maintaining the four cleans in delivery and labor
3. Give vit-k im injection 1ml
4. Prophylactic Rx to prevent new born gonococal ophtalmia by TTC, silver nitrate 1%,
erythromycin 0.5%
5. Cord should be kept clean & dry.

Chapter 6 Neonatal care
6.1 care for normal new born
6.1.1 Immediate new born care
Immediately child births the nurse give special care like
- Maintaning of air way
- Siken car
72
- Masuring APGAR scor
- Cord care
-Physical examination
-Start berste feeding
6.1.1.1. Assessment of air way
- Immediately after birth, the birth attendant should assess the air way of the newborn
- If the baby does not breath with in 3 seconds or is blue (cyanosed) after delivery, do not
wait for a minute
Inspect for: - Shape of the chest it is cylindrical
- Symmetric / Assymetric movement of chest
- Respiratory distress sign (tachypnea, granting, chest in drawing, flaring of alae nasi, cyanosis)
- Ausculatate for added sound & air entry.
6.1.1.2 Maintaining an open air way
- Clear the airway quickly and thoroughly, especially if the amniotic fluid is meconium-
stained
- Place the neonate on his/her back in horizontal position with head down ward slightly
extended, so that the mouth, pharynx and nose clear of fluid, mucus, blood and meconium
by gravity
- Gently suck out mucus with a bulb syringe or soft rubber or plastic mucus extractor (1
st
mouth, then the nose)
- Ventilate the baby by Ambu bag or other available bag and mask:
The mask should cover mouth and nose
Push the lower jaw a little forward with your thumb and open the mouth
through slight pressure of a finger and the mask on the chin
Prevent air leak around the babys face
Start 02 (100% at a rate of 40 LPM)
Allow the baby to breath out
- Chest and abdomen must be moving with ventilation
- Proper breath sounds should be heared over the chest
73
If not: did you clear the airway properly, readjust the mask and check if the
head is not too flexed (bent forward) or the mouth closed?
- Apply external cardiac massage if there is no breath (unfortunately, external massage is
rarely of value in the new born, so concentrate on clearing the airway and ventilating the
baby)
+ Most infants will respond to the above measures if they are correctly done
- If there is no response after 3-5 minutes, give a combination of:
- 5% or 10% glucose 2ml/kg and 8.4% (7.5%) sodium bicarbonate 2ml/kg very slowly
IV
- If the heart rate is very slow, 0.2 ml/kg of a 1 in 10,000 (0.01%) dilution of adrenaline can
also be given IV
NB- Never give bicarbonate before adequate ventilation
- Vigorous and unnecessary prolonged suctioning can cause reflex apnea
- Asphyxia is a common cause of death and long-term disability
- Failure to resuscitate usually is failure to ventilate
Structural and functional difference with adult:
The structure and function of a neonate is not well developed during this period (i.e. during
the neonatal period)
- An infants intrauterine to extra uterine transition requires many biochemical and
physiological changes
- No longer dependent on maternal circulation via the placenta, a newborns pulmonary
function is actuated for self-sufficient respiratory changes of 02 and Co
2
.
Newborn infants are also become dependent on
Gastrointestinal tract function for absorbing nutrient
Renal function for excreting wastes and maintain chemical homeostasis
Hepatic function for neutralizing and excreting toxic substances
Immune system for protecting against infect
74
Unsupported by the maternal placental system, the neonatal cardiovascular and
endocrine systems also adapt for self-sufficient functioning
Generally all cells, tissues, organs and system of the newborn are not well developed
structurally as well as functionally, and hence risk for injury and infection
6.1.2 - Measuring Apgar score
6.1.2.1Defintion - It is a practical method of systematically assessing the newborn
infant immediately after birth to help identify infants requiring resuscitation for hypoxic-acidosis
- Assessment at birth is by the APGAR score is done routinely at 1 and 5 minutes
after delivery
6.1.2.2 Purpose To help identify infants requiring resuscitation for hypoxic-
acidosis (Asphyxia) or not
6.1.2.3 APGAR score measurement
- A low score doesnt necessarily signify fetal Hypoxic-Acidosis
- APGAR score may be normal in most patients who subsequently develop cerebral
palsy
- The incidence of cerebral palsy is very low among infants with scores of 0-3 at 5
minutes
- The 1- minute APGAR score signals the need for immediate resuscitation
- The 5minute score indicates the probability of successfully resuscitating the
newborn
- APGAR scores of 0-3 at 20 minute predict high mortality and morbidity
What to do if the APGAR score is:
1- Apgar 7-10
- Dry the baby and keep him/her warm
- Using suction is not necessary if the baby cries vigorously
75
2) Apgar 4-6
- Most of these babies are breathing
- If so and have HR> 100/minute, quick and gentle clearing of the airway and
stimulation by slapping the buttocks, with 02 by mask
- If there is no improvement, or getting worse and the HR<100/minute
Move on immediately to vigorous Rx as follows below (see Apgar 0-3)
2- Apgar 0-3
- Proceed in the following order as quickly and as carefully as possible
Note the time
Dry and cover the baby
Supply heat from above the baby
Apgar scoring system
Score
Sign 0 1 2
Appearance (colour) Blue, pale grey Body pink blue extremities Completely pink
Pulse (HR) Absent Slow <100/min >100/min
Grimace (Response to
stimuli)
No response Grimace (slight) Cry, cough sneezing
Activity (Muscle tone) Limp Some flexion of extremities Active motion
Respiratory effort Absent Slow irregular gasping Good crying
Classification of APGAR score according total score (interpretation)
1) Apgar 7-10 = Normal
2) Apgar 4-6 = Moderate Asphyxia
3) Apgar 0-3 = Sever Asphyxia
Factor affecting APGAR score
- There are different factors that affects the APGAR score and results in False
positive scoreauma and/or False negative score
False positive score (No fetal Acidosis or Hypoxia; Low Apgar)
o Immaturity
76
o Analgesics, narcotics, sedatives
o - Lung anomaly (Diaph. Hernia)
o Magnesium sulphate
o Congenitalmyopathy/Neuropathy
o Acute cerebral trauma
o Precipitous labour/delivery
o -Spinal cord trauma
CNS anomaly
o -Congenital atresia
-Congenital pneumonia
False Negative score (Acidosis; Normal score)
Maternal acidosis
High fetal catecholamine level
Some full-term infants
6.1.3 Eye, skin and Umblical cord care of a new born baby (to
Prevent infection)
6.1.3.1 Nursing care of Eye
- Immediately after the head is born, the babys eyes should be cleaned with a sterile
guaze. (Eyes should be gently wiped with a swab)
- The eyes of all infants must be protected against gonococcal infection by applying
1% silver nitrate drops-the best proven therapy
0.5% erythromycin or 1% tetracycline ointment (alternative measures)
2.5% povidone-iodine-may be effective at one time prophylactic agent
+ Instil 2drops of 1% silver nitrate solution into each conjactiva sac shortly after birth
- Infants born to mothers with active gonorrhoea are at high risk for developing
gonococcal ophthalmitis and should be given:
A single 125 mg/im injection of ceftriaxone for prophylaxis
For low birth weight infants, the dose is 25-50mg/kg
77
6.1.3.2 Nursing care of Skin
- To reduce the incidence of skin and periumblical colonization with pathogenic
bacteria and infection (omphalitis), the entire skin and cord should be cleansed,
once an infants temperature has stabilized.
- Clean with sterile cotton soaked in warm water or mild, no medicated soap solution
- Rinse the neonate in warm water near or at body temperature
- Keep the child wrapped in a dry cloth at a warm place (Temperature of 30-35
0
C
)
-Excess vernix and any blood on the babys body is removed using a soft cloth soaked in
lukewarm water
- Do not scrub the babys skin with a rough sponge immediately after birth
- Avoid any form of powder, and the cord is left exposed
- A void bandaging around the abdomen, as it may interfere with breathing and give
rise to asphyxia
6.1.3.3 Nursing care of umbilical cord
- Use sterile cored clamp or autoclaved cord ties and tie well
- The Umblical stump is examined again for any bleeding and is re-tied if necessary
- If necessary, paint the Umblical stump with an antibacterial preparation
Triple dye (a mixture of gentian violet, brillian green and proflavine)
Antibiotic spray (a mixture of neomycin, bacitracin and polymyxine), in the absence
of triple dye
There fore, care of the skin, eyes and cord of the newborn is vital to prevent infection
- The nurse is responsible to give the care
6.1.4 Temperature Regulation
6.1.5 Feeding neonate
- Successful infant feeding requires cooperation b/n the mother and her baby
- Promptly establishing comfortable, satisfying feeding practices contributes greatly
to the infants and mothers emotional well-being
78
- Feeding should be initiated to maintain normal metabolism and growth during the
transition from fetal to extra uterine life
To promote maternal infant bonding
To decrease risks of
- Hypoglycemia - Hyperbilirubinaemia and
- Hyperkalemia - Azotemia
- Neonates should start breast-feeding immediately after birth (with in 30 minutes)
- The neonate should feed the breast milk frequently and as much as he/she wants
(Every 3-4 hour/day= day and night)
EBF- is giving breast milk alone for the first 6 months of life except medication
WHO recommended that every infant should exclusively breast-fed until 6 months of age
Advantages of EBF
- Breast-feeding is essential for the survival of the infant in most situations in
developing countries
- It has overwhelming advantages anywhere in the world
Colostrums - produced during the first few day of lactation is particularly beneficial in preventing
infections
- Human-milk is exactly right nutritionally for the young infants needs, and, even in
less than well-nourished women
Generally breast-feeding has the following advantages:-
a) Breast-milk is the natural food for full-term infants during the 1
st
months of life
- Always readily available at proper temperature
- Needs no time for preparation
- Fresh and free of contaminating bacteria
b) Allergy and intolerance to cows milk create significant disturbances and feeding
difficulties
79
- these are not seen in breast-fed infants
c) Human-milk contains bacterial and viral antibodies
d) Macrophages normally present in human colostrums and milk may be able to synthesize
complement, lysozyme and lactoferrine
e) Supply the necessary nutrients to the infant
f) It has psychological advantage for both the mother and infant
g) Prematurely born baby usually thrive on breast milk
NB- The low vitamin K content of human-milk may contribute to hemorrhagic disease of the
newborn, so, 1 mg of vit k administration is recommend for all infants, especially for those who
will be breast-fed
Formula- milk is used if the mother could never breast feed for various reasons
- Animal milk and numerous modified formulas are widely available, but are very
expensive
- Whatever is fed to the non-breast-fed infant, is extremely dangerous because of
Likelihood of over dilution
Bacterial contamination
- The feeding-bottle is especially risky as it is very difficult to clean
Advise the mother to use cups or spoons for feeding her infant

6.1.5.1 Baby Mother R/Ship
Mother- Baby emotional togetherness and the beginning of mutual love and
attachment start after delivery
- Ideally in the first few hours
Early attachment activities (Bonding) have a significant effect on the long-term
mother child relationship
Developing R/ship b/n the infant and the mother in the initial hours of life (Beginning
immediately after birth) is Maternal sensitive period
-More contact at this time increases the attachment of mother to baby
80
-Touch is a highly significant part of the attachment process
Offering the opportunity for skin-to-skin contact b/n mother and infant is important
Touching provides warmth, comfort and a sense of security all very real needs of
the vulnerable newborn
6.1.5.2 Encourage Breast-Feeding
- Explain for the mother that breast-milk is the best for the baby
- Discuss the importance/Advantage/ of breast feeding for the mother
- Describe that Breast-feeding helps for the psychological and physical bonding of
mother to-child
- Discuss to the mother what EBF mean and the time of weaning
- Describe the signs of good attachment and effective sucking during Breast Feeding
6.1.5.3 Teaching a bout Baby care
- Develop the mothers knowledge, ability and confidence to care for the baby at home
Feeding and bathing
Cord, skin and genital care
Recognition of illness
Infant safety
- Teach the mother how to maintain body heat.
- Teach about the importance of immunization of the infant
- Teach the mother about growth monitoring
Give special emphasis on preventive and promotive health behaviour concerning the care
of the newborn
6.1.5.4 Encourage mother-to-baby Eye-contact
-Mother and infant establish eye-contact in the same vertical plane as touching
Mutual gazing
- An infants initial quiet alert state provides the opportunity for eye-to eye contact
Particularly important in stimulating the loving and possessive feeling of many
mothers for their babies
81
- Nurses and other health professionals should teach and encourage mother-to infant
eye contact
- Hospitals routines should be designed to encourage mother-infant contact
+ Generally, facilitating mother-to-baby relationship is an important factor for the physical
and psychological development of the infant.
6.1.5.5 Show good positioning and attachment
- If an infant is not well attached, the result may be: pain and damage to the nipples
or: The infant may not take enough milk (breast-milk) effectively ,may cause
engorgement
- If the infant is not well attached
He/she may be unsatisfied after breast feeds; want to feed very often or for a very
long time
The infant may get too little milk and not gain weight
The breast-milk may dry up
All the above problems may improve if attachment can be improved
The following four signs indicates good attachment
1- Chin touching breast (or very close)
2- Mouth wide open
3- Lower lip turned outward
4- More areola visible above than below the mouth
- If all of these four signs are present, the infant has good Attachment
If attachment is not good, you may see
Chin not touching breast
Mouth not wide open, lips pushed for word
Lower lip turned in or
More areola (or equal amount) visible below infants mouth than above it
- If you see any of these signs of poor attachment, the infant is not well attached
+ attachment process is affected by many factors, such as:
82
Mothers emotional and physical conditions after labour
The infants condition and behaviour
The comparison of the real infant with the fantasy infant, that the mother
has imagined since she became a ware of her pregnancy.
Baby mother R/ship is facilitated by
Encouraging Breast-Feeding
Teaching about baby care
Encouraging mother to-baby eye contact
Breast Hygiene
- Advice on the care of the breasts is particularly important in any primigravida who
might not come into the maternity unit for delivery
- The nurse and/or other health workers should advise the nursing mother to use
simple cleanliness procedures
She should wash her hands with soap and water
Wash the nipples with plain water, avoiding all soap
Her nipples should be kept dry; expose to air and sunlight if possible
6.1.5.6 Making General Observation and physical
assessment of Newborn:
The initial examination of a new born infant should be performed as soon as possible after
delivery to
- Detect any abnormalities or injury
- Establish a baseline for subsequent examinations
The following should be monitored every 30 min after birth for 2hours or until stabilized
- Temperature
- Pulse
- Respiration rate and type
- Colour
- Muscle tone and activity
83
- Level of consciousness
A second and more detailed examination should be performed with in 24 hours of birth
The main objectives of examination of the newborn
A) To ensure and assess that the lungs have expanded and that the air passage are obstructed
B) To make an early diagnosis of life threatening condition and birth injuries
C) To assess the gestational age, so that we can classify as appropriate or not appropriate for
gestational age
D) To assess whether the baby has any sign of infection or metabolic disorders
Preconditions for examination of the neonate
- Make sure the baby is warm and comfortable
- Prewarm the room and place baby on flat surface
- Undress the baby with clean and warm hand
- Good source of light
- Do gentle, rapid and sufficient examination
Approaches for neonatal examination:
1- General appearance
- observe whether the baby has normal colour, activity, crying or not
2- Assessment of postnatal age
3- Look for congenital anomalies
4- Vital signs and Anthropometry and classify accordingly
5- Systemic examination
Assessment of postnatal Age
1) Physical criteria/External characteristics /
A) Skull hardness- soft hard bone
B) Ear cartilage and Form soft pinna and folded firm and incurved
C) Breast nodule and nipples None 7mm and barely visible to raised areola
D) Genitalia Testis undescended to descended and complete rugae of scrotum
- Labia majora widely separated, prominent clitoris to labia minora and clitoris
well covered
84
E) Sole creases None whole sole creases.
2) Neurological signs
A) Posture resting: Hypotonia- Total flexion
B) Heel to ear maneuver: No resistance impossible
C) Trunk elevation: Absent, slight, or good
Look for congenital malformation
Inspect the cut end of the cord for number of vessels:
- Normally 2 arteries and 1vein
- Single Umblical artery in 0.8%
- Internal organ congenital anomaly (oesophageal atresia, imperforated anus, Gus
anomalies)
- Check imperforated/closed anus by Thermometer (closed anus patency)
- Check Oesophageal atresia by NGT.
N.B- The patency of oesophagus and anus should be cheeked for all newborns but
especially.
Small for dates babies
single Umblical artery
History of Polyhydraminous
Maternal diabetes mellitus
If excessive frothiness and drooling of saliva is observed
- Cleft palates and cleft lip
- Mid line lesions of the back (Spinal bifida, meningomyelocele)
- Genitalia: Ambiguous genitali, hypospadias, epispadias
- Abdomen: Exomphalus, Omphalocele, gastrochsis
- Talipes equinovarus (club foot) and congenital hip dislocation
Anthropometry and vital signs
- Weight
85
- Height
- Head circumference
- Chest circumference
- Heart rate
- Respiratory rate
- Temperature
- Blood pressure
Systemic Examination of the newborn
HEENt
*H-Head Look for caput succedaneum
- Cephalohematoma
- Shape of the head
- Size of head (micro/macrocephaly)
- Fontanels: Anterior/posterior, bulged, or flat, size
*E-Eye- Look for Conjunctivitis
- Corneal opacity
- Pupilary size
*E-Ear -Look for Shape and size (large/small or malformed)
- Low set ears- If only<10% of the ear lies above a straight line drawn from inner and
outer cantus of the eye
*N-Nose Check for patency of nares
- Look for nasal snuffle (cong. Syphilis)
- Look for nasal discharge
*M-Mouth Look for cleft lips/palate
- Tongue: Macroglossia, glossoptosis
- Excessive saliva
- Micrognathia and retrognathia
*N-Neck-Look for any swelling (congenital goitre, cysts)
86
- Neck to body ration/ ratio
- Webbed neck (significant skin fold over the neck) E.g. Turners syndrome
Respiratory system
Inspect for shape of the chest
- Symmetric/Asymetric movement of the chest
- Respiratory distress signs e.g. tachypnea, granting, chest indrawing, flaring of alae nasi,
cynosis)
Auscultate for Added sounds (rales/crepitations)
- Air entry (pneumothorax, effusion)
- Perstalistic sounds (Diaphragmatic hernia, left side)
Normal RR= 30-60 breaths/minute
CVS Always start neonatal examination from the heart b/c once the newborn is disturbed it is
difficult to ausculeate the heart
Look for-cyanosis
Count pulse rate > 160/min = Tachycardia
<80/min = Bradycardia
< 50/min = mostly in Av-dissociation
Feel the pulse: Weak or bounding
Femoral pulsation (For coarction of aorta)
Unplapable (Shock)
PMI- At the 5
th
ICS at the midclavicular line
o Shifted or displaced in cases of
Dextrocardia
Diaphragmatic hernia
Pneumothorax
Auscultated for murmurs and heart sounds
Normal pulse of the newborn = 120-160/min
GIS- Abdomen Normally flat and not distended
87
- Scaphoid in diaphragmatic hernia
- Distended in paralytic ileus, necrotizing entrocolitis, in obstruction, imperforated anus
etc.
Liver May be palpable up to 2cm below Rt costal margin at the MCL
+ Enlarged liver is suggestive of:
Storage diseases
Congestive heart failure
Neonatal hepatitis
Congenital TB
Spleen Tip of spleen may be palpable normally
+ Enlarged spleen is suggestive of
- Storage disease in the majority of cases
Kidneys- In the 1
st
2 days of life both kidneys may be palpable, especially the lower pole of the
Right kidney could be palpable in early neonatal life
+ Enlarged kidney is suggestive of
- Polycystic kidney
- Renal vein thrombosis
- Congenital hydronephrosis
Skin The colour of the skin is normally pink and few cases have acrocynosis
Pigmentations: Mongolian spot (brown pigmented naive scattered around any area
of the body, most commonly on the back)
- Vernix caseosa and Lanugos are the usual finding
- Pitechail rash
- Erythema toxicum
Neurological Examination
Routine examination in a healthy term baby is unnecessary
Assess for skull and spine abnormalities
Sensorium:- Level of consciousness
88
Irritable/consolable
Cry (normal or high pitched)
Assess for symmetry of spontaneous movement of limbs on the two sides
Look for facial deviation and abnormal movement of the eyes
Neonatal Reflexes
A- Sucking and Rooting Reflex
Touch the upper lip on lateral side with a nipple or clean little finger- Neonates
turns towards the touch and open their mouth - Hunger and more vigorous neonate
has intense Rooting Reflex
Put little finger in new born mouth- sucking response (Absent in septic neonate)
B- Grasp reflex
Palmar reflex till 3 months and plantar reflex till 9-12 months
Put your finger in the infants palm or plantar surface Reflex flexion
C- Moro-Reflex
Drop the flexed head suddenly bay about 30
0
. a positive response is abduction and
extension of upper limbs and opening of hands followed by slower adduction and
flexion
Unilateral in brachial injury, hummers or clavicular fracture
D- Stepping Reflex (until 6 weeks)
Hold infant upright with feet on mattress and then leaning the baby way forward-
motion with alternate stepping action
E- Glabellar Tap
Tap the glabella closure of the eyes
N-B- It is not of great help to write detail Hx and to do meticulous PE in neonates, like what we
are used to do in older children, hence a format with pricises and relevant information that could
help to arrive at the diagnosis is essential.
89
6.1.5.7 Providing an Identification Brace late
Defintion- A Bracelet is a small encircling band, denoting, in the plural, transverse markings
across the palmer surface of the skin of the wrist
- An ornamental band or chain worn around the wrist
Purpose Helps to identify ones newborn in the hospital from others
- Before the infant is transferred from the delivery room or birthing room, an
identification bracelet identical to the one on the mothers wrist is placed on the babys
wrist
Site- Apply on the wrist of the newborn
- In some hospitals, hand prints and foot prints are also taken and become part of the
infants chart
Sometimes with addition of the mothers right index finger print
- If the father has not been permitted in the delivery room, it is important that he have
the opportunity to see and touch his infant before transferring the newborn to the
nursery, if possible
Documentation
During applying the identification bracelet, you have to document the following
- Name of the mother
- Time of birth
- Date of birth
- Identification tag number

90
6.2 Providing care for neonate with congenital Abnormalities
Congenital Anomalies- are abnormal malformations existing at, and usually
before birth
- Refer to conditions that are present at birth, regardless of their causation
Congenital malformation gross structural defect present at birth
+ Congenital defects which are not detectable as gross structure, like microscopic defects,
inborn errors of metabolism, etc are included in the broader term congenital anomalies
+ Congenital malformations are the causes of death especially in the intrauterine life, and of
considerable disability
20% of death during 3
rd
trimester of pregnancy
15% of death during the neonatal period
The causes of congenital malformations in man are largely unknown, but the etiological
factors could be roughly divided into three :-
A. Genetic Factor
- Dominant traits, recessive traits, sex linked recessive traits, variable and some mal
formations (cleft lip, clubfoot, congenital heart diseases etc) are some of congenital
malformation associated with genetic abnormalities
B .Chromosomal Aberrations
- Downs syndrome - Gonadal dysgenesis
- D1-trisomy syndrome - Klienefelters syndrome
- E-18 trisomy
These are Congenital malformations resulted from chromosomal abnormalities
C. Environmental Factors
91
+ Maternal infection with Rubella during pregnancy can cause congenital malformation
of the
- Heart and eye - Mental retardation
- Deafness - Dental defect
+ Cytomegalovirus infection of the fetal brain in utero can causes
- Mental retardation - Cerebral calcification
- Chorioretinitis - Hydrocephalus
+ Toxoplasmosis involving the fetus in the utero can produce
- Hydrocephalus - Mental retardation
- Eye defects - Chorioretinitis
- Microcephaly
+ Maternal syphilis in pregnancy can cause
- Mental retardation
- Deafness
+ Irradiation of the fetus through irradiation of the maternal pelvis in utero can produce
- Mutation leading to malformation
- Fetal and neonatal death
- Microcephaly with mental retardation
+ Thalidomide administration to the mother in pregnancy can cause
- Haemangioma - Facial paralysis
- Malformation of ear -Malformation of alimentary canal
+ Hepatitis has a relationship with increase incidence of congenital disorder
- Mongolism
- Hydrocephalus
+ Surgical anesthesia Hypoxia and hypercapina
+ Advanced maternal and paternal ages

6.2.1 Providing care for a neonate with cleft palate and lip
92
6.2.1.1 Definition
- Cleft palate and lips are congenital deformities due to the failure of various parts of the
upper lip and palate to fuse in the normal manner
Which is most common facial deformations
- Both cleft palate and cleft lip may be present together
Cleft lip is a congenital anomaly involving one or more clefts in the upper lip
ranging from a slight dimple to a large cleft involving nasal structures
Cleft palate is a congenital anomaly consisting of a cleft ranging from soft
Palate involvement a lone to a defec including the hard palate and
Portion of the maxilla in severe cases
6.2.1.2 Etiology and Incidence
- Causes include genetic, heredity, environmental and teratogenic factor
- Cleft lip occurs in approximately 1 in every 1.000 births, most commonly in boys.
- Cleft palate occurs in 1 in every 2,500 births; incidence in girls is double that in boys
6.2.1.3 Pathophysology
- The defect occur during embryonic development
o Cleft lip results from failure of fusion of lateral and medial tissues forming the
upper lip
o Cleft palate resulted from failure of fusion of tissues forming the palate
- These defects may occur separately or in combination to produce complete unilateral
or bilateral cleft form the lip through the soft palate
- Depending on the defects severity and the childs general health, surgical correction
of cleft lip and palate are done
- Early correction of cleft palate enables development of more normal speech pattern
- Delayed closure or large defects may require the use of orthodontic devices
A) Cleft lip-
It may be unilateral or bilateral
o May be extended up into the nostrils
Etiology Not entirely clear (unknown) but it appears to be influenced by genetic
93
and other environmental factors
- This defect results from failure of the maxillary and premaxillary process to fuse
during the 5
th
to 8
th
week of intrauterine life
Dx- Physical examination
Management
The child should be admitted several days before the operation,&
Observed for signs of cold- if present the operation should be delayed and
throat swab should be taken
- The child should be trained in spoon feeding, putting the food well to the back of the
tongue
- Surgery is the best mgt for cleft lip, usually performed by plastic surgeon
- Cleft lip is operated on a bout the age of three month
Nursing care
- Little preoperative preparation for the infant who has surgery during the 1
st
few days of
life
- Elbow restraints has to be worn several days following surgery
- The nurse should learn how to feed the infant with an Asepto syringe or teach the
mother
- For the first few hours, the infant must never be left alone b/c he/she can quickly and
easily aspirate the mucus
- The suture line is left uncovered after surgery and must kept clean and dry to prevent
infection with subsequent scaring
- Crying must be prevented by good nursing care and let the mother to spend much of
her time
- Do not allow visitors with cold to come and see the child
- The stitches may be removed on the 3
rd
to 5
th
days
Soft foods is given by spoon well back on the tongue and followed by sterile water
Techniques of feeding
- Parents should be told that this baby can be fed and treated as any other person
94
- The baby is able to suck after the lip repair and should progress normally until ready
for palate surgery
- Have sterile Asepto syringe with tip protected by apiece of sterile rubber tubing
- Place the syringe and warmed formula on the bedside stand with in easy reach
- Hold the infant in your arms in upright position
- Pour the formula into the syringe and place the rubber-covered tips in the childs
mouth a way from the suture line
The formula usually drips quickly enough without squeezing the bulb
Regulate the drops to the infants breathing and swallowing
Allowed 30 minutes for feeding
The infant should be watched carefully after feeding

B) Cleft palate
- It is treated similarly with cleft lip by pairing the edges and suturing other cutting on
either side
- The child born with a cleft palate, but with an intact lip does not have the external
disfigurement that may be so distressing to the new mother
o But it is more serious
- Although a cleft lip and palate frequently appear together, either defect may appear
alone
o In embryonic development the palate closes at a later time than does the lip,
and the failure to close is for some what different reasons
- At about 8wks of the embryo, there is still no roof to the mouth
95
- The tissues that form the palate are two shelves running from the front to the back of
the mouth, and projecting vertically downward on either side of the tongue
o The shelves move from a vertical position to a horizontal position, and their
free-edges meeting and fusing in midline
o Normally the palate is intact by the tenth week of fetal life
Etiology Exactly what happens to prevent the closure of the palate is not known
with certainty
o Relatives/heredity Plays role a
o Environmentalfactor
- A cleft palate may involve the soft palate alone, or it may extend into the nose and into
the hard palate
- It may be bilateral or unilateral, an isolated defect, or in conjunction with the cleft lip
Management-The goal is to give the child a union of the cleft parts that would
allow intelligible and pleasant speech and to avoid injury to the maxillary growth.
Surgery- Timing of surgery individualized according to the size, the placement
and degree of deformity
Optimal time b/n 6 months and 5 years
Mgt of cleft lip and palate needs members of the professional teams which
include:
- Paediatrician - Speech therapist
- Plastic surgeon - Social worker
- Orthodontist - Public and clinical nurse
Counselling Explanation and counselling concerning the childs diet
o Counsel on speech training and immunization including general supervision
o Answer questions and misconceptions
96
o Counsel on dental caries of the deciduous teeth
Nursing care
- Preoperative and immediate postoperative nursing care are similar with the care of an
infant with cleft lip
- Allow the child to take clear fluids after nausea has ceases
- Allow the child to drink from a cups but not from a spoon or a strows
- Allow clear fluids for a period of 3 to 5 days followed by full liquids for approximately
10 days
- Care must be exercised to keep anyone with a suspicion of a cold or a cough a way
from the infant/child
- Provide water or clear liquid after a milk drink
6.2.2 Providing care for a neonate with Hernias
/Diaphragmatic Umblical and Inguinal Hernias/
6.2.2.1 Diaphragmatic Hernia
Definition Herniation of abdominal contents into the thoracic cavity
- May occur as a result of a congenital or traumatic defect in the diaphragm
- Acquired/traumatic herniation is not common in children, but the congenital one is
common
Cause Not well understood
- Exposure to drugs
- Disrupted developing thoracic mesenchyme
Clinial manifestation Majority of infants with CDH experiences sever respiratory distress with
in the 1
st
hours of life with in 24 hours
- Dyspnea
- Cyanosis
- Vomiting
97
- Intestinal sounds (peristaltic sounds especially on the left side) of the chest on
auscultation with evidence of Mediastinal shift
- Incarceration of the intestine will proceed to ischemia with sepsis and cardio
respiratory collapse
N.B Unrecognized CDH has been the cause of sudden death in infants and
toddlers.
Dx - Ultra Sonography is a common diagnostic procedure during prenatal
period
- X-ray films and C/Ms
Management
- Infants has to be nursed in the sitting position/posture/
- Provide small frequent feeds
- Intubation and gavages feeding may be given
- Emergency surgery may have to be done if condition allows
Recognition of the role pulmonary hypertension in addition to pulmonary hypoplesia and
the adverse effects of operative repairs on pulmonary function prompted critical re-
evaluation of that strategy.
- The availability of extracorporeal membrane oxygenation (ECMO) and utility of
preoperative stabilization have been the major stimuli to aggressive therapy.
ECMO- Is a form of cardiopulmonary bypass that augments systemic perfusion and provides
gas exchange
6.2.2.2 Umblical hernia
Definition It is the protrusion of the abdominal content through the Umblical ring produced
by its incomplete closure
- The swelling is covered by skin and is noticeable when the baby cries, coughs or
strains
- If the Umblical ring does not admit the tip of the index finger, the hernia tends to close
spontaneously by one to two years of age
- In case of a wider ring the hernia may close in 5 to 6 years or may require surgery
98
Cause Not well known, but believed to be caused by incomplete closure of the Umblical ring
due to congenital defects
Clinical manifestation
- Protrusion at site of umbilicus, which is covered with skin
- The protrusion or swelling disappears when child lying on his/her back
- The protrusion is visible when the child is in a sitting position, when the baby cries,
coughs or strains.
Dx- Based on P/E and C/M
Management-
If the ring of the umbilicus is small, it may be closed spontaneously
- Psychological support of the family
- Surgical repair if the ring is wide
. Inguinal Hernia
Defintion - It is the protrusion of the intestine through the inguinal wall or canal
An inguinal hernia is the most common condition requiring operation in paediatric age
group
- Incidence of inguinal hernia in children is estimated to be b/n 10 and 20/1,000 live
births
- A bout 50% will present before 1 year of age (most are seen in the first 6 month of life)
- Indirect inguinal hernia is the most common type of inguinal hernia in children
- 60% of inguinal hernia are on the right side
- 30% of inguinal hernia are on the left side
- 10% of inguinal-hernia are bilateral
N.B Premature infants have the higher incidence of inguinal hernia = 30%
Cause Failure of obliteration of the layers of the processes vaginalis (This
results in a persistent patency of the process vaginalis)
99
- Obliteration distally with patency proximally leads to An indirect inguinal hernia
obliteration proximally with patency distally leads to an isolated Hydrocele (Hydrocele
of the tunica vaginalis)
- Obliteration of the processus vaginalis proximally and distally but patency in the mid
portion of the spermatic cord leads to Hydrocele of the cord
- A complete failure of obliteration of the processus vaginalis leads to a complete
inguinal hernia
An inguinal hernia usually appears as a bulge in the inguinal region and
extends towards the scrotum
- swelling of the scrotum without a prior bulge in the inguinal region
- The bulge may be present only during crying or straining
- During sleep, rest or relaxed the hernia reduces spontaneously with a noticeable bulge
or enlargement of the scrotum
The Hx. of intermittent groin, labial or scrotal swelling that spontaneously reduces is
classic for an indirect inguinal hernia
- Distinguish b/n hydrocele of the cord and incarcerated inguinal hernia (in the later
there is s/s of intestinal obstruction)
P/E Reveals an inguinal bulge at the level of the internal or external ring or a scrotal swelling
that is reducible or fluctuates in size
- Lie the infant supine with extended legs and arms over the head (this usually causes
the infant to cry-raise intra abdominal pressure demonstrates a bulge over the pubic
tubercle (external ring) or swelling with in the scrotum
- Examine older children while they are on a standing position, which increases intra-
abdominal pressure and demonstrates the hernia
- Distinguish retractile testes from inguinal hernia with a bulge over the external ring
(palpate the testes before palpating the inguinal bulge)
100
- Distinguish a complete inguinal hernia from that of an isolated hydrocele (Take careful
Hx- in case of complete inguinal hernia, the scrotal swelling varies during the day-
large while the child cry or strains and disappear or become much smaller during
relaxation), this is not true in case of isolated hydrocele
N.B- In difficult diagnostic dilemma, a rectal examination can be extremely
helpful in differentiating acute groin abnormalities
- First examine the internal ring on the uninvolved side, and then can sweep the index finger
or fifth digit toward the internal ring on the involved side (Intra-abdominal organ can be
palpable extending through the external ring in case of indirect inguinal hernia)
Dx- Based on care full Hx, P/E and C/M
Mgt The treatment of choice is operative repair
- The operation should be carried out electively shortly other diagnosis
- Operation is not indicated for isolated hydrocele except hydrocele of the cord
- Most paediatric surgeons recommend bilateral inguinal exploration in
All boys younger than 1 years
101
Patients with conditions associated with an ed risk of inguinal hernia
All girls younger than 2 year
- Antibiotic for infants with congenital heart diseases and ventriculoperitoneal shunts
before operative repair
Complications
1- Incarcerated Hernia A condition which occurs when the contents of the hernia sac can not
be reduced back into the abdominal cavity
2- Postoperative Apnoea A life threatening complication of hernia repair in premature
infants
- The cause of this apnoea is unknown, but it may be due to immaturity of the brain stem
ventilator mechanism
6.2.3 Care of a child with gastroschisis and omphalocecele
6.2.3.1 Definition
Is a herniation or protrusion of the abdominal contents into the base of the
umblical cord.
In contrast to the more common Umblical hernia, the sac is covered with peritoneum, with
out overlying skin.
The size of the sac that lies outside the abdominal cavity depends on its
contents.
Herniation of intestines into the cord occurs in about 1/5,000 births
Herniation of liver and intestines occurs in about 1/10,000 birth.
The translucent, avascular covering consists of peritoneum inside and amniotic
membrane outside separated by whartons jelly
The stomach, all the small intestine and large intestine, and large intestine, most
of the liver, pancreas, spleen, bladder, etc may be outside the abdomen.
In omphalocele minor, the diameter of abdominal wall opening is less than 5cm
and in omphalocele major the diameter is more than 5cm.
6.2.3.2 Cause
102
- Similar with that of umblical hernia
Not well known, but believed to be caused by incomplete closure of the Umblical ring due to
congenital defects
6.2.3.3 Sign and symptoms
Protrusion of abdominal organ at the umblical area which is covered by peritoneium sac.
Transparent covering membrane at birth, but changed into opaque and with few
hours of birth.
After 24 hours, the sac dries and tend to crack or rupture causing evisceration
Abdominal skin may stop at the neck of the omphalocele or may extend for a
distance
6.2.3.4 Diagnosis-
Based on P.E and C/M
6.2.3.5 Management
Cover the omphalocele with saline soaked sterile dressing
Continuous Ryles tube suction is done to prevent vomiting and abdominal
distension
Administration of antibiotics to control infection
If the above technique is successful, the defect in linea alba should be closed in layers
when the child is older.
Surgery is essential if the sac is ruptured
Congenital anomalies commonly associated with omphalocele include:
o Beckwith weide mann syndrome
o trisomies 13 and 18
o Cardiac anomalies
o Malrotation of intestine
6.2.3.6 Nursing responsibilities
103
6.2.4 Care of aneonate with Esophageal Atresia (EA) and
Tracheo-esophageas Fistula (TEF)
6.2.4.1 Definition
Esophageal Atresia- is absence of a normal body opening or the abnormal closure
of a body passage
EA is the most frequent congenital anomaly of the esophagus, affecting about 1 in
4,000 neonates
- Of these more than 90% have an associated TEF
In the most common form of EA, the upper oesophagusend in a blind pouch and TEF is
connected to the distal esophagus

6.2.4.2 Etiology
6.2.4.3 Types
- There are five most commonly encountered forms of EA and TEF
I. Atresia of upper esophageal end with fistula of lower end to trachea (87-90%)
II. Both esophageal ends are atresia with no fistula (8%)
III. H-Type TEF- Recurrent pneumonia
IV. Upper end fistula with treachea and lower end blind loop (massive aspiration with 1
st
feeding) (<1%)
V. Both ends form TEF (<1% )
6.2.4.5 Pathophyiology
6.2.4.5 C/M
Atresia of esophagus should be suspected if:-
A) There is maternal polyhydraminoas
B) A catheter or NGT cant pass into stomach
104
C) Infant has excessive oro-pharyngeal secretions (Frothing and bubbling at the
mouth and nose)
D) Chocking, coughing or cyanosis occurs during feeding
6.2.4.6 Diagnostic evaluation
- By clinical manifestation
- Resistance to nasol (NGT) catheter 10-11cm passage
- Recoiled NGT after X-ray
- Contrast studies, Fluroscopy, bronchoscopy
6.2.4.7 Medical and surgical Management
- Surgical correction (ligation) of the TEF and primary end to end anastomosis
of the esophagus are performed when feasible
6.2.4.8 Nursing management
Preoperatively
Maintaining a patent airway and preventing aspiration of secretion
Basic supportive care, keep NPo, open IV line, elevate head and chest 300
Frequent oro-pharyngeal suctioning (Every 10-15 minutes)
Post operatively
Initially small quantities of normal saline feeds through gastrostomy or by indwelling
polythene tube
If tolerated well, replaced by milk feeds in gradually increasing quantities
It is possible to start oral-feeds in 7-10 days time
Observe any s/s that indicates complication
6.2.4.9 Prognosis: - is guarded (prematurity and associated
anomalies) but survival is possible.
6.2.5 Care of a child with imperforate anus
6.2.5.1 Definition
Imperforate anus:- is a congenital malformation in which the rectal pouch
ends blindly at a distance above the anus and there is no anal orifice
105
- There may be a fistula b/n the rectum and the vagina in females or
b/n the rectum and the urinary tract in males
Incidence varies from 1 in 3,000 to 1 in 5,000 live births
Imperforate anus can be classified into four:-
1) Type I- Although there is patency, a stricture of anus is present
2) Type II- The anus is separated from rectum by an intact thin bulging
membrane
3) Type III- The rectum ends blindly or by fistulous tract, at a varying
distance above the perineum
4) Type IV- The top of the anal canal is separated from the rectum by a
gap of varying distance.
6.2.5.2 Causes
-25.6% to 80% of imperforate anus is associated with fistula
-39% to 59 % of imperforate anus is also associated with other congenital
malformation
E.g.-Down syndrome
6.2.5.3 C/M
- No meconium passage (> 24 hours)
- Abdominal distension
- Rectal thermometer resistance
- Anal dimple only
- No flatus
- Based C/M and PE
- X-ray
6.2.5.5 Management
Surgical correction colostomy
-Toilet training to avoid faecal impaction
106
6.2.6 Congenital pyloric stenosis
6.2.6.1 Definition
Pyloric stenosis is the narrowing or stricture of the pyloric sphinicter (gastric outlet)
This disorder occurs mostly in body, most commonly form the age of 2 Wks up to 3 months
The condition first causes spasm and later hypertrophy of the pyloric muscle
The offspring of a mother and to alesser extent the father who had pyloric stenosis are at a
higher risk for pyloric stenosis
It develops approximately 20% of thealse and 10% of the female descendants of a mother
who had pyloric stenosis
The incidence of pyloric stenosis is ed in infants with type B andlood groups
It is usually associated with other congenital defects eg. Tracheoesophageal fistula
6.2.6.2 Etiology- The cause of pyloric stenosis is unknown, but many factors have be
implicated
More concordant in monozygotic than dizygotic twins (Genetic factor)
Abnormal muscle innervations
Elevated serum levels of prostaglandins
Reduced pyloric nitric oxide synthase etc..
6.2.6.3 Sign and symptoms
The spasm and hypertrophy of the pyloric muscle results in stenosis or narrowing of the
gastric outlet. this inturn results in the inability of the stomach to empty its content properly
Non- bilious vomiting is the initial symptiom
The vomiting may or may not be projectile initially but is usually progressive occurring
immediately after a feeding
The infants is hungry and wants to feed/suck well/ after vomiting
The vomiting consists of gastric contents only and may be blood stained, but never bile
stained
Prominent peristaltic movements of the contracting stomach
- Originate in left upper Quadrant and progress to and beyond the midline
107
Olive shape tumor is felt in the upper abdomen (epigastrium) Just lateral to the right rectus
muscle in 70-90% of cases
Jaundice with hyperbilirubinemia has been found in approximately 5% of affected infants
Loss of weight and signs dehydration
Failure to thrive, constipation
Malnutrition, especially s/s of marasmus
6.2.6.4 Dx- Based on Hx, C/M and PE.
Palpating pyloric mass
Firm, movable, olive shaped, hard, approximately 2cm in length
- Best palpated from the left side and located above and to the Rt of the umbilicus
Ultrasonography confirms the diagnosis in the majority of cases (95% sensitivity)
6.2.6.5 Sergical management
Ramstedt pyloromyotomy is the surgical procedure of choice for the surgical mgt of p.stenosis
-The procedure is performed through a short transverse incision or laparoscopically
Preoperatively
Correction of fluid, acid-base and electrolyte losses
IV-fluid therapy with the addition of potassivm chloride (Rehydration can be successfully
takes place with in 24 hours)
Preoperative correction of alkalosis is essential to prevent post operative apnea, which may
be associated with anesthesia
Postoperatively
Vomiting may occur in half the infants and is thought to be 2
0
to edema of the pylorus at the
incision site
Initiate feeding with in 12-24 hours other surgery and advanced to maintenance oral feeding
with in 36-48 hrs of surgery
Persistent vomiting postoperatively, suggests:
- Incomplete pyloromyotomy
108
- Gastritis
- Gastroesophageal reflux disease or
- Another cause of the obstruction
6.2.7 Providing care for a neonate with clubfoot
6.2.7.1 Definintion - Club foot is a congenitally deformed foot, which is twisted
out of the shape or position
- rsiflexion (Talipes calcareous)
- May be plantar flexion (Talipes equines)
- Abducted everted (Talipes valgus)
- Abducted inverted (Talipes varus)
6.2.7.2 Types There are many types of club foot (Talipes;
these includes
Talipes equinovarus
Talipes calcanovalgus
+ Talipes equinovarus is the most common type of clubfoot, in which the toes pointing
downward, the foot is turned in and the deformity can not be easily corrected by hand
6.2.7.3 Causes- Not clear; a hereditary factor is observed
- An arrested growth of germ plasma of the foot during the 1
st
trimester of pregnancy
Congenital clubfoot is a deformity in which the entire foot inverted, the heel is drawn up
and the forefoot is adducted
- It may appear as a single anomaly or in combination/connection with other defects E.g.
Spina bifida
- Clubfoot may be unilateral or bilateral
109
6.2.7.4 Pathophysiology
6.2.7.5Dx- Easily detected in a newborn infant
- But must be differentiated form a persisting fetal position of comfort assumed in
utero
N.B- Positional deformity can be easily corrected by the use of passive exercise, but the true
clubfoot deformity is fixed
6.2.7.6 Medical and surgical management
Non- surgical Mgt
- Manipulation, bandaging or applying cast during early neonatal period
110
- An alternative method involves the use of a Denis Browne splint Composed of a
flexible, horizontal metallic attached to two foot plates, the childs foot is attached to
the foot plates with adhesive tape (the attachment of the horizontal bare permits
changing the r/ship of the bar to the plate as necessary
Surgical m anagement
- Used for children who do not respond for non-surgical measures, usually older
children
- Involves several procedures depending on the age of the child and up on the degree of
deformity
- Lengthening of the Achilles tendon
- Capsulotomy of the ankle joint
- Release of medial strictures
- Operation on bony structures (for a child> 10 Years of age)
6.2.7.7 Nursing care
Preoperative care as cleft lip and palate, especially psychotherapy
Postoperative care
- Check vital signs until they are stable
- Observe the cast for signs of bleeding
- Elevate the affected leg
- Observe circulation and temperature of the toes
- Be alert for any signs of infection
Continuing care
The infant or small child in a cast can not explain to the nurses that his/her cast is too tight
impairing circulation or irritating his/her skin, so the nursing observation should include
the following
Checking the colour and temperature of the toes at frequent intervals
Preventing the child from banging and denting his/her cast before it is dry
111
Holding and comforting the child when possible (Better if mother or father is present to do
this)
If a Denis Browne splint is used instead of a cast, check the foot for
Irritation from adhesive tape
Swelling or for any other indication of circulation impairment from the tight
strapping
- Check frequently for the position of the foot on the foot plate
6.2.8 Caring for a child with congenital abnormalities of
Cardiovascular system
6.2.8. Defintion
Congenital heart diseases are conditions that affect the anatomical structure of the heart at birth
or shortly before birth
It is an inborn abnormalities or malformation of the cardiovascular system
Umbilical vein carries oxygenated blood to the fetus from placenta at average of 175 ml
per kg and at a pressure of 12 mmHg.
Roughly half of this blood bypasses the liver by way of ductus venosus into the inferior
vena cava where it mixes with the rest of the blood coming from the caudal part of the
body
- This stream of blood entering the atrium from the inferior venacava which has the
highest
0
2
concentration passes through foramen ovale to left atrium, then to left ventricle
ascending Aorta Supplying coronary arteries, cerebral arteries the upper
limbs
Blood stream from superior vena cava passes to right ventricle and then on to the
pulmonary artery and most of this passes to descending aorta through Ductus arteriosus
and supplies the caudal part of the body and the placenta via the Umblical arteries
At birth, dramatic changes take place as the fetal circulation adapts to extra uterine life
and gas exchange is transferred from the placenta to the lungs of the infant
112
After birth the foramen ovale, the Ductus arteriosus and Ductus venosus are no longer
required
- Cardiovascular malformation varies b/n 1 to 3.2 per 1,000 and accounts for more than 50%
of deaths by all congenital defects in the first year of life

6.2.8.2 Types and causes
Most of the causes of congenital heart diseases are unknown
Maternal infection, drugs, radiation
Types No classification of congenital heart disease can be entirely satisfactory
- For the purpose of conveniency, it is important to divide congenital heart disease into
two
1- A cyanotic congenital heart disease (with left to right shunt)
- This is a condition in which there is no central cyanosis (cyanosis is absent)
- Abnormal communication in the heart or between the big vessels is one of the defect. This
condition is seen in the following defects
Atrial septal defect
Ventricular septal defect
Patent Ductus arteriosus
- In the above conditions, due to the higher pressure in the left heart, there is a shunt from left
to right heart with an increased blood load in the lesser circulation in the lungs. No cyanosis
A- Ventricular septal Defect (VSD)
The ventricle is divided into two chambers by a septum, which grows upwards along the
anterior and posterior margin in the 2
nd
month of intrauterine life
A bout 90% of cases of VSD is due to the failure of closure of the inter ventricular foramen
and is associated with abnormality in the division of truncus arteriosus into aorta and
pulmonary artery
Because of the higher pressure in the left ventricle, the blood is shunted from left to right
ventricle
113
As the systolic blood is not contaminated by venous blood there is no cyanosis
In severe cases the pulmonary blood flow is ed 3 to 5 times the systemic flow, the work of
both ventricles is ed, specially of the left ventricles
Hyperkinetic pulmonary hypertension due to huge blood flow relative to the capacity of
pulmonary vascular bed
Increased pulmonary arteriolar resistance
Obstructive vascular lesions may contribute to pulmonary
Hypertension
C/M Majority of cases with small shunts are asymptomatic
- In moderate left to right shunt
Mild exercise intolerance
Repeated respiratory infection
- In severe left to right shunt (large defect)
Pan systolic murmur with maximum intensity in the left 3
rd
and 4
th
interspaces
A thrill accompanies the murmur in 90% of cases
Audible 3
rd
heart sounds
+ Dx- X-ray Shows enlargement of left ventricle with prominent pulmonary artery
Enlargement of left atrium
+ ECG- Shows incomplete right bundle branch pattern in large defects
- Left ventricular hypertrophy
- Biventricular hypertrophy in sever cases
+ Cardiac catheterization and Angiocardiography
Mgt- Small defects may close spontaneously
- Repair of other defects under direct vision (suture for bigger defects)
- Pulmonary banding as a palliative measure
- Pre and postoperative nursing care
-
114
B- Atrial septal Defect (ASD)
At the end of the 1
st
month of fetal life, the posterior superior portion of the common atrium
a septum divide into left and right (Septum primum)
A defect in the lower portion of septum primum is ostium primum
An opening which also appears in the upper portion of ostium primum is ostium
secondum
Ostium secondum is later embraced by a membrane arising from the right side called
septum secondum, but still leaving a small aperture called Foramen ovale
+ Atrial septal defect is a common form of congenital heart disease comprising nearly 10% of
all such cases
Secondum types of defect comprises 90% of all such cases
Ostium primum constitute 10%
- In ASD, the shunt is usually from left to right due to more pressure in the left atrium even
though it is only 3-5mm of Hg.
- In large ASD, the pressure in both atria may be equal and flow will depend up on the
relative resistance offered by pulmonary and systemic circulation
- The resistance offered by the pulmonary circulation is less than that of the left ventricle and
as such the shunt is from left to right.
- Reverse of shunt occurs if there is:
Pulmonary hypertension due to ed pulmonary arteriolar resistance
Obstruction to right ventricular flow as in pulmonary stenosis
- Right atrium and right ventricle are hypertrophied and pulmonary artery gets dilated
C/M There may be no symptom during child hood; however, the following are
present
115
Dyspnea on exertion
Palpitation and weakness
In infants
Feeding difficulties
Growth retardation
Recurrent respiratory infection
- Skeletal abnormalities, ejection systolic and mid diastolic murmur
- Wide split 2
nd
heart sound, which is characteristically fixed in respiration
Dx. X-ray- Shows cardiomegally (enlarged right ventricle and right atrium)
- Enlarged pulmonary artery
ECG- Show right axis deviation
- Incomplete right bundle branch is seen in 90% of cases
Cardiac catheterisation and Angio cardiography
Mgt Surgical treatment
- Repair of the defect by direct vision and by cardio pulmonary bypass is necessary in
most of the cases
- Preoperative and postoperative nursing care
C- Patent Ductus Arteriosus
The Ductus arteriosus connects the main or the left pulmonary artery near its origin with
the descending aorta just beyond the origin of the left subclavian artery
R.A R.V Pulmonary ArteryDuctus Arteriosus Descending Aorta
systemic circulation
Immediately after birth, due to expansion of lungs and establishment of pulmonary
circulation very little blood goes through the Ductus
Anatomically the Ductus closes by the 3
rd
month
The patent Ductus is usually 1cm long and 1mm to 7.5 mm in width
A higher pressure in the aorta shunts blood from that vessel into the pulmonary artery which
continues throughout the cardiac cycle
116
The pulmonary artery dilates and pulsation may be exaggerated
Degree of shunt is directly proportional to the calibre of duct and inversely proportional to
the length
Increased pulmonary resistance because of persistence of foetal state and arteriolar
hypertrophy causes reversed shunt pulmonary artery to Aorta
C/M Repeated chest infections common complaints
- Dyspnea on exertion
- Tiredness
CHF in large shunts
Collapsing pulse due to Left to Right shunt
Continuous or machinery murmur, which is best heard in 1
st
and 2
nd
interspaces
- In infants may be heard only during systole
Dx- Chest X-ray findings shows
Dilatation of pulmonary artery
Pulmonary plethora
Left a trial and Left ventricular enlargement
Enlarged and pulsatile aorta
Electrocardiogram (ECG)
Normal in mild cases
Left ventricular hypertrophy
Deep Q wave and inverted T-wave (Indicates diastolic over load)
Cardiac catheterization
Reveals arise of 0
2
saturation a bout 5% in pulmonary artery over that of right
ventricle
Mgs Surgical ligation and exclusion of the duct as early as possible, usually
results in a complete cure
117
- Restores the cardiac size to normal and abolishes the risk of complications
D- Coarctation of Aorta
- The stricture in the majority is just below the origin of left subclavion artery (pre-ductal
coarctation)
- Sometimes the coarctation is distal to the Ductus (post-ductal coarctation)
- The constriction may extend superiorly to the left subclavian artery
The following congenital anomalies may be associated with coarctation of aorta
Aortic stenosis
Patent ductus arteriosus
Bicuspid aortic valve
+ The patent ductus arteriosus is the most commonly associated anomaly chiefly of the pre-
ductal type
- Due to resistance to the flow of blood, the left ventricle hypertrophies in all cases
- The blood bypasses the constricted segment via collateral circulation, chiefly form:
Branches of subclavian artery
The superior intercostals
The internal mammary with its intercostals
Superior epigastric and musculo-phrenic branches
+ The thoracic and sub scapular branches of the axillary artery may also enlarge as collateral
channels
These in turn unit with the intercostals branches of descending aorta and inferior epigastric
branches of the femoral to form alternate channels
C/M May be asymptomatic until late in life
- Occasional headache or epistaxis
- There may be Left ventricular failure
- Small femoral pulse
118
- Visible or palpable pulsation of collateral vessels is best appreciated Posteriorly in
relation to intercostals arteries
Dx- X-ray finding may show
- Left ventricular enlargement
- Prominence of ascending aorta
- Elongated aortic knuckle resulting from dilatation of Left sub-clavian artery
- Post Steno tic dilatation of short segment of descending aorta
Aortogram will reveal the site of coarctotion and collaterals
Mgt In case of CHF- immediate and energetic Rx is indicated
- Surgical Rx consists of resection of coarcted segment with end to end anatomises with or a
graft as early as possible
+ Complications of coarctation of aorta includes:
Congestive Heart Failure
Bacterial Endocarditis
Rupture of the Aorta
Cerebral haemorrhage
E- Aortic stenosis
Congenital aortic stenosis accounts for about 5% of all cardiac malformations
More common in males, which is 3:1 ratio
In majority the stenosis is valvular
+ It may be sub-valvular (sub aortic) or in small percentage supravalvular, which may be
associated with:
Mental retardation
Abnormal facies
Hypercalcaemia of infancy
As there is obstruction to the left ventricular emptying, there is increased pressure and work
load for the Left ventricle
119
- With minor lesions, however, there are no changes. In severe cases the lumen may be
so narrow as not to permit a catheter
C/M It may be asymptomatic
- Signs of CHF in sever stenosis
- Angina pectoris and syncope
- Ejection systolic murmur at the aortic area
Dx. Chest X-ray
- In valvular stenosis, there may be prominence of ascending aorta and valvular calcification
- Evidence of Left ventricular enlargement
Electrocardiogram
- May be normal in mild cases
- Show left ventricular hypertrophy
- Serial ECG may help in assessment for surgery
- Show the gradient b/n the left ventricle and aorta
- Shows elevated systolic pressure in the left ventricle
Mgt Surgery is indicated in sever cases of aortic stenosis
- Children should be left along in mild cases (But restrict them from strenuous exercise)
- Proper preoperative and postoperative cares

2- Cyanotic congenital heart Diseases with Reversed (Right to left) OR
Bidirectional shunt
Cyanotic congenital heart diseases are congenital anomalies in which there is a central
cyanosis, largely due to shunts of blood from the right to the left side of heart
A- Fallo ts Tetra logy
120
+ In this congenital anomaly, extensive hemodynamic studies showed that there are two
fundamental lesions
Obstruction to Rt. Ventricular out flow
A ventricular septal defect
+ Other less significant lesions includes
Rt. Ventricular hypertrophy (2
0
lesion)
Dextroposition of Aorta
Due to pulmonary stenosis, there is decreased flow through the lungs and unsaturated blood
from the Rt. Ventricle is shunted through the high ventricular septal defect into the
overriding aorta
- The amount of Rt. to left shunt depends on the resistance in pulmonary and systemic
circulation
In case of sever pulmonary stenosis, the lungs are supplied by collaterals from the brachial
arteries
In some cases the pulmonary stenosis is less severe and give rise to acyanotic fallots
C/M Cyanosis- A prominent feature appear during infancy
Clubbing
Dyspnea on exertion
Retarded growth and development
Syncope which is characterized by:
- Irritability
- Crying
- Sudden Dyspnea to hypoxic attack, and occurs
- ed cyanosis commonly in 2 month to 2years
- convulsion
Quiet cardiac pulsation and slight Rt. Ventricular pulsation
121
Pulmonary systolic thrill
Grade III to V ejection murmur
CHF is a rare c/m but if present, it may suggest, some complications
E.g.- Anaemia
- AGN
- Rheumatic fever or bacterial endocarditis
DX - -X-ray
- Normal size heart
- Narrow base and concavity of the left border of the heart
- Rounded a pex and tilted upwards= Boot shaped heart
+ Electrocardiogram
- Right ventricular preponderance pattern with Rt. Axis deviation
- Prominent p-wave may be found
+ Angiocardiography
- Shows simultaneous filling of the aorta and pulmonary artery after a Rt. Ventricular dye
injection
- May show stenosis in the region of outflow tract of the Rt. Ventricle and pulmonary value
- Shows ventricular septa defect
+ Cardiac catheterization and dye studies
- Catheter directly pass into the ascending aorta from the Rt.ventricle
- Rarely the catheter may enter the left ventricle revealing the interventricular shunt
- Similar systolic pressure b/n the Rt. Ventricle and systemic arteries
- Low pulmonary artery pressure
The dye injection in the Rt. Ventricle demonstrates an earlier appearance of the dye in the
systemic circulation
122
Mgt During an attack of syncope, give morphine
- 0
2
during syncope attacks
- surgical Rx-systemic artery anastomsis with pulmonary artery = Blalock Taussing
water shunt operation
+ Complication includes the following:
- Anoxia
- CVA(cerebro vascular Accidents)
- Brain abscess
- Bacterial endocarditis
- Pulmonary haemorrhage or infections
B- Tricuspid Atresia
+ In this congenital anomaly, there is no outlet from the right atrium to the right ventricle
The entire systemic venous return enters the left side of the heart by means of the
foramen ovale or an associate ASD
+ Left ventricular blood usually flows into the right ventricle via a ventricular septal defect
(VSD)
The pulmonary blood flow and the degree of cyanosis depends on the size of the VSD and
the presence and severity of pulmonic stenosis
Pulmonary blood flow may be augmentd by or totally depend on a PDA
+ If the ventricular septum is intact, the Rt. Ventricle is completely hypoplastic and
pulmonary atresia is present
+ The only outlet from the Rt. Atrium involves shunting Rt to left across an atrial septal defect
or patent foramen ovale to the left atrium
Here, desaturated blood mixes with saturated pulmonary venous return
+ Blood enters the left ventricle and is ejected either through the aorta or via a ventricular
septal defect into the Rt. Ventricle
Most patients with Tricuspid Atresia are recognized in the early months of life by decreased
pulmonary blood flow and cyanosis
123
C/M Cyanosis is evident at birth
- Increased left ventricular impulse
- Holosystolic murmur, audible along the left sternal border
- Exertional dyspnea
- Easy fatigability
- Polycythemia
Dx . Roentgenographic studies
- Show either pulmonary under circulation or over circulation
Electrocardiogram
- Show left axis deviation and left ventricular hypertrophy, except in those with transposition
of the great arteries
N.B - The combination of cyanosis and left axis deviation is highly suggestive of
Tricus pid Atresia
- Biphasic or inverted T-waves
- Fibro muscular membrane in place of a tricuspid value
- Variably small Rt. Ventricle, VSD, and the large left ventricle and Aorta
- Indicated if questions remains after echocardiography
- Shows normal or slightly elevated Rt. Atrial pressure with prominent a wave
Rt Atrial Angiography shows immediate opacification of the lft atrium from the Rt.
Atrium followed by left. Ventricular filling and visualization of the aorta
Mgt Depends on the adequacy of pulmonary blood flow
- Severly cyanosed neonates should be maintained on an infusion of prostaglandin E1,
until a surgical aortopulmonary shunt procedure can be performed
Blalock Taussing procedure or a variation is the preferred anastomosis
Infants with just adequate pulmonary blood flow who are well balaced b/n cyanosis and
pulmonary overcircualtion can be watched closely for the development of increasing
124
cyanosis, which may occur as the VSD begins to get smaller and is an indication for
surgery
Creation of an anastomosis b/n the superior venacava and the pulmonary arteries =
Bidirectional Glenn shunt
Preoperative and post operative nursing care is an important responsibility of nurses
C- Transposition of Great vessels
+ Transposition of great vessels is a congenital anomaly in which the pulmonary artery arise
from left ventricle, while the aorta arise from right ventricle
Thus, there are two independent circulations
- Blood from the left ventricle going to the pulmonary artery and return to the left atrium via
the pulmonary vein
- Blood from the Rt. Ventricle goes into the aorta and returns via the systemic veins into the
Rt. Atrium
- In the absence of a shunt at ventricular, a trial or patent Ductus level, survival is not
possible
C/M Cyanosis is deep at birth
CHF usually after three weeks of age
Progressive Rt. Ventricular enlargement
Plethoric lungs
Development of Rt. Ventricular failure
- Rt. Ventricular type cardiac impulse
- Murmur of a VSD or an ejection systole murmur of pulmonary stenosis
Dx- Rt. ventricular hypertrophy on Electrocardiogram
- X-ray shows narrow base and cardiomegally
6.2.9 Care of a child with Hydrocephalus
6.2.9.1 Definition
125
Hydrocephalus is the term used for enlargement of the ventricular system due to
accumulation of CSF
- As a result of imbalance b/n production and absorption of CSF
May be hypertensive or normotensive, which occur with increased intracranial tension, and
cerebral athrophy respectively
Normally CSF is produced by the choroid plexus from where it flows through the ague duct
of sylvius, the 4
th
ventricle, and via the foramina of magendie and luschka reaches the
subarachnoid spaces, from where it is reabsorbed in the venous circulation
CSF from choroid plexus (lateral ventricles) Aqueduct of sylvius 4
th
ventricle
Foramina of magendie and luschka subarachnoid space venous circulation
N.B Hydrocephalus is almost always due to interference in the above pathways
o CSF production
o CSF circulation
o CSF absorption
6.2.9.2 Cause- Abnormality of the aqueduct or a lesion in the 4
th
ventricle
- Aqueductal steneosis
- Aqueductal glioosis due to the following condition
Neonatal meningitis
Subarachnoid haemorrhage
Intrauterine viral infection
Mumps & meningoencepnalitis
Classificatien
- Hydrocephalus can be distinguished or classified as:
1-Obstructive /non communicating hydrocephalus
Due to the obstruction to the flow of CSF with in the ventricular system
Is the commonest cause of congenial hydrocephalus.
Dilatation of the ventricular system proximal to the sit of obstruction.
2- Communicating Hydrocephalus
126
There is interference of absorption of CSF
May be due to either acclusion of subarachnoid cisterns around the brain stem or
obliteration of the subarachnoid spaces over the convexities of the brain
6.2.9.3C/M The clinical presentation of hydrocephalus is variable and depends on many factors
including
Age of onset
The nature of the lesion causing obstruction
The duration and rate of increase of the ICP
Enlargement of the head (HC> + 2 SD)
Widely opened and bulged anterior fontanel
Dilated scalp veins and soft skull
Broad and prominent forehead
Sun setting eye sign- Eyes may deviate down ward b/c of impingement of the dilated suprapineal
recess on the tectum
Wide suture lines
Babinski sign
Irritability, lethargy, poor appetite and vomiting
* Cracked-pot or macewen sing- A sign produced on percussion of the skull, which indicate
separation of the sutures.
DX- HX (Familial cases suggest X-linked hydrocephalus 20 to a queductal stenosis)
- Prematurity with intracranial hemorrhage
- Meningitis or mumps ence phalitis
P/E Inspection, palpation and auscultation of the skull and spine
- Measurment of occiptofrontal head circumference
- Size of the head, condition of the anterior and posterior fontanells
- Signs of intrachanial pressure
Plain skull films, typically show separation of the sutures, erosion of the posterior clinoid in
older child and es in convolutional markings (Beaten-siliver appearance)
127
CT scan, ultrasongraphy and MRI studies identify the specific causes of hydrocephalus.
Mg.t therapy for hydrocephalus depends on it causes
Medical Mgt includes the use of acetazolamide and furosemide
Provide temporary relief by reducing the rate of CSF production
Extra cranial shunts (Ventriculoperitoneal shunt)
Ventricles a trial shunt (modified spitz Holter valve) connects the lateral ventricle to the Rt.
Atrium through the jugular veins
6.2.9.6 Pre &post operative care
Prognosis prognosis of hydrocephalus is usually poor
Complication- Bacterial infection (staphylococcus epidermidis), proteus
Kinking, plugging, displacement of the shunt tubing
Pulmonary emboli
A cute shunt failure cause progressive increase in intracranial pressure
N.B- A gradual change in personality change and deterioration in academic productivity suggest a
slowly progressive form of hydrocephalus.
6.2.10 Care of a neonate with spinabifida
6.2.10.1 Definition
Spina bifida and meningomyelocele is a condition due to the failure the areches which
forms the brain and the spinal cord to join together in early fetal life.
Results if the closure of the spinal canal is incomplete
Defect in the neural arch, in lumbosacral region
Is a failure of posterior laminea of the vertebral to close
Opening Protrusion of the spinal meninges or spinal cord may accur
meningocele or myelomeningocele
Everything depends on the extent of the failure in normal development
128
If the vertebral failed to close but the overlying skin is normal, the lesion usually will not
even be detected
Meningocele and Myelomeningoceles occur due to a midline defect in the skin, vertebral
column and the neural tube
6.2.10.2 Occurance- The incidence of spina bifida is 1 in 1,000 births in USA
6.2.10.3Types
A) Meningocele - The meninges can be seen from outside but the spinal cord is developed
normally
B) Myelomeningocele A condition in which both the meninges and the spinal cord tissue
can be seen involved
C) Spina Bifida occulta
Common anomaly consists of a midline defect of the vertebral bodies with out protrusion of
the spinal cord or meninges.
Causes * Unknown
- Neural tube defects due to genetic predisposition
- Nutritional and environmental factors
E.g. Folic acid supplementation decrease neural tube defect
- Trimethoprim and anticonvulsants (carbamazepine, phenytoin, Phenobarbital) increases
the risk of myelomeningocele.
C/M Asymptomatic and lack of newologic signs
- Patches of hair, alipoma, discoloration of the skin
- Dermal sinus in the midline of spine (lower back)
- Aredish swelling at the back which is covered by transparent membrane
C/M depends on the extent and location of the lesion
- Bowel and bladder incontinence
- Saclike cystic structure covered by a thin layer of partially epithelialized tissue
- Flaccid paralysis of lower extremities.
129
- Absence of deep tendon reflexes
- Lack of response to touch and pain
- High incidence of postural abnormalities of the lower extremities
DX- Based on C/m and PE
Spine roentgenography, ultrasonography, CT-scan and MRI
6.2.10.4 Surgical Mgt Spinal bifida with only a membranous covering should always be covered
with asterile dressing
It the child is not obviously cerebrally damaged or handicapped by other
major congenital malformation and
If paralysis of the leg is doubtful or absent
Sent the child to theatre immediately
-Generally, surgical correction of the defect as early as possible birth is advised
-If the child has the following problems which are associated with spinal bifida,
the need of surgery depends on the surgeons preference and the prognosis is
poor.
Paralysis of the lower extremites
Incontinence of urine and stool
Clubfeet (Talipes)
Hydrocephalus
Neurosurgery, orthopaedic support
Physiotherapy, braces for support and crutches
6.2.10.5 Nursing responsibility
6.2.11 WILMS TUMOR and extrophy of the bladder
6.2.11.1 Definition
Wilms Tumor (Nephroblastom) Is a complex mixed embryonal neoplasm of the kidney
composed of three elements:
1- Blastema
130
2- Epithelia
3- Stroma
The incidence is approximately 8 cases/million children younger than 15 years of age.
Usually occurs in children b/n 2-5 years of age
Comprises approximately 6% of paediatrics cancer and is the second most common
malignant abdominal tumour in childhood.
- May arise in one or both kidneys
- Incidence of bilateral wilms tumour is 7%
- May be associated with hemi hypertrophy and other congenital anomalies.
The majority of wilms tumours cases are sporadic, although 1-2% of pts. have a family Hx.
Wilms tumour patients with associated congenital anomalies, frequently carry germ line
WT1 mutations.
Histologically, two broad categories have been recognized:
1. Favourable wilms tumour
2. Unfavourable wilms tumour
The favourable type is considered to be the Conventional form and usually carries a good
prognosis
Characterized by blastema, epithelia and stromal elements devoid of ectopia or anaplesia
The unfavourable type is characterized by marked enlargement of the nuclei,
hyperchromatis os the enlarged nuclei and multipolar mitotic figures
- Areas of anaplesia may be focal or diffuse and predict probable high rates of tumour
relapse and death
Clear cell sarcoma- is a subtype of unfavourable form and usually metastasizes to bone
Rhabdoid tumor, which may metastasize to the brain, is no longer classified as asubtype of
wilms tumor
Several syndromes, congenital abnormalities and chromosomal aberrations are
commonly reported in wilms tumour.
The most common genitourinary anomalies associated with wilms tumours are:
131
- Hypoplesia, fusion and ectopia of the kidney
- Duplication of the collecting systems
- Hypospadia and cryptorchidism
6.2.11.2 Cause- Chromosomal aberrations
- Genetic defect
6.2.11.3 C/M Abdominal mass
- May be identified during a well child clinical examination
- The mass is usually firm, smooth and occationally may cross the midline
- There may be abdominal pain and vomiting
- Infrequent hematuria
- Hypertension, probable due to renal ischemia
- Rapid abdominal enlargement and anemia
DX- Any abdominal mass in a child must be considered malignant until diagnostic imaging and
laboratory findings define its true nature
Biopsy, or excision and histologic verification
Complete physical examination
Complete blood cell counts
Kidney and liver function studies
Ultrasonograph, CT-scan and MRI
Chest radiography to determine the presence of pulmonary metastases
- Surgical extirpation of the tumour should be performed
- Establish patency of inferior venacava before resection, if it is not patent
- Preoperative chemotherapy should be administered
- Examination of collateral kidney during operation to exclude bilateral wilms tumour
132
- Administration of chemotherapy for a pt with inoperable wilms tumour and bilateral wilms
tumour
6.2.11.5 Nursing maagement
Prognosis- Major prognostic factor depends on the tumours:
Size
Stage
Histology
- The prognosis is worse in patients with
Large tumour, which > 500gm
Advanced stage (III and IV)
Unfavourable histologic subtype
More than 60% of pts with all stages of wilms tumour generally survive
Stages I through III have a cure rate varying from 88-98%
EXTROPHY OF THE BLADDER
EXTROPHY- The luring inside out of an organ
EXTROPHY OF BLADDER- Congenital absence of a portion of the lower
abdominal wall and the anterior vesicle wall, with aversion of the posterior vesicle wall
through the deficit and with an open pubic arch and widely separated ischial connected by a
fibrous band.
EXTROPHY CLOACA- A developmental anomaly in which two segments of
bladder (hemi bladders) are separated by an area of intestine with a mucosal
surface.
Appears as a large red tumour in the midline of the lower abdomen.
Extrophy of urinary bladder occurs about 1 in every 35,000 to 40,000 births.
The male to female ratio of extrophy of the urinary bladder is 2:1
133
- The severity of this anomaly ranges from a small vesicocutaneous fistula in the
abdoextrophy of the cloaca involving exposure of the entire hindgut and the bladder.
The extent of this failure determines the degree of the anomaly
C/M Protrusion and exposure of the bladder through the abdominal wall.
Downward displacement of the umbilicus
Widely separated pubic rami in the midline
Separated rectus muscle
Complete epispadias with a wide and shallow scrotum in males
Undescended testes and inguinal hernia are common
Separation of two sides of the clitoris and wide separation of the labia
The anus is displaced anteriorly in both sexes, and there may be recall prolapse
Urinary incontinence and increase incidence of bladder cancer Adenocarcinoma.
Sexual disability and broad based gait.
In classic bladder extrophy, the upper urinary tracts usually are normal.
DX- Based on C/M (Hx and PE)
Mgt Mgt of extrophy of bladder should start at birth
Cover the bladder with plastic wrap to keep the bladder mucosa moist
Closure of the extrophic bladder is the preferred treatment.
- During this procedure the abdominal wall is mobilized and the pubic rami are brought
together in the midline
If the bladder closure is performed during the 1
st
48 hours of life, there is sufficient mobility
of the pubic rami to allow approximation of the pubic symphysis.
Early bladder closure can be applied to almost all neonatal infants with classic bladder
extrophy
Total reconstruction include:
Closure of the bladder
Closure of the abdominal wall
134
Correction of epispadias using the technique of penile disassembly.
Monitor upper urinary tract for hydronephrosis and infection postoperatively.
The majority of such infants have Vesicourethral reflux and should receive antibiotic
prophylaxis.
In male, if the epispadias is not corrected at birth, then epispadias repaire is generally
performed b/n 1-2 yrs of age
- At this point child has total urinary incontinence b/c there is no external urinary sphincter
The final stage of reconstruction involves creation of a sphincter muscle for bladder control
and correction of the Vesicourethral reflux
Preoperative, postoperative and psychosocial nursing care
6.2.12. CARE OF ANEONATE WITH HYPOSPADIASIS AND EPISPADIASIS
6.2.12.1 Definition
HYPOSPADIAS - Refers to a urethral opening that is on the ventral surface of the penile shaft
Affects 1 in 250 male newborn
- There is incomplete development of the prepuce, termed a dorsal hood, in which the
foreskin is on the sides and dorsal aspects of the penile shaft and absent ventrally.
- Some boys, particularly those with proximal hypospadias, have chordee, in which there is
ventricle penile curvature during erection.
- The incidence of hypospadias may be increasing, possibly b/c of in utero exposure to
estrogenic or antiandrogenic endocrine disrupting chemicals
E.g. Polychlorbiphenyls
- Phytoestrogens
Cause- Endocrine disrupting chemicals
Unknown in some cases
CLASSIFICATION: Hypospadias is classified according to the position of the urethral meatus
after taking into account whether chordee is present.
1- Granular (an the glans penis)
2- Coronal hypospadia
135
3- Subcoronal hypospadia
4- Midpenile hypospadia
5- Penoscrotal hypospadia
6- Perineal hypospadia
Approximately 60% of cases are distal, 25% are sub coronal or Madeline and 15% are
proximal
In the more severe cases, the scrotum is bifid and sometimes extend to the dorsal base of the
penis (scrotal engulfment)
MEGAMEATAL VARIANT In this case the fore skin is normally developed, but the
there is either distal or sub coronal hypospadias with a fish mouth meat us
Hypospadias is usually an isolated anomaly, however, it is common in boys with multiple
congenital anomalies
Approximately 10% of boys with hypospadias have an undescended testes
Congenital inguinal hernias are also common
C/M Urethral meatus or opening on the ventral surface of the penile shaft
DX- Based physical examination and HX
Mgt Begins in the newborn period
Avoid circumcision, b/c the foreskin is used in the repair
The ideal age for repair in a healthy infant is 6-12 month. This age is chosen because:
- There is no greater risk of general anaesthesia at this age than at 2-3 yrs
- Penile growth over the next several years is low
- The child does not remember the surgical procedure
- Analgesic needs are less than in older children
The goal of hypospadias surgery is to correct the functional and cosmetic deformities
The incidence of hypospadias may be increasing, possibly b/c of in utero exposure to
estrogenic or antiandrogenic endocrine disrupting chemicals
E.g. polychlorbighenyls
136
Phytoestrogens
Hypospadias repair is recommended for boys with midpenile and proximal hypospadias
o Some boys with distal hypospadias will have no functional abnormality and do not
need any surgical corrections
Complications of untreated hypospadias include:
1- Deformity of the urinary stream, either ventral deflection or sever splaying
2- Sexual dysfunction 20 to penile curvature
3- Infertility if the urethral meatus is proximal
4- Meatal stenois (congenital) Extremely rare
Postoperative complications of hypospadias repair include:
1- Urethrocutaneous fistula
2- Hematoma
3- Wound infection
4- Meatal stenosis
5- Urethral diverticulum
6- Wound dehiscence
Epispadiasis
A condition in which the opening (urethral meatus) is on the dorsal (top) surface of
the penis
It is a congenital malformation, and commonly occurs with extrophy of the bladder
In boys:
- The prepuce is distributed primarily on the ventral aspect of the penile shaft and the urethral
meatus is on the dorsum of the penis
In girls:
- The clitoris is bifid
- The urethra is split dorsally
Distal epispadias in boys usually is associated with normal urinary control and upper
urinary tracts
137
- Should be repaired by 6-12 month of age
In severe cases of epispadias, both in male and female
o The sphincter is incompletely formed
o There is total incontinence
o Usually there is separation of pubicrami
N.B- DX, Mgt and nursing care of a child with epispadias is similar with that of a child with
hypospadias
Duty 6.3- CARE FOR ANEONATE WITH NEONATAL PROBLEMS
6.3.1 Low birth weight and preterm babies
LBW - infant is a baby whose birth weight is less than 2,500 gm.
VLBW -infant is low birth weight baby whose birth weight is <1,500 gm
ELBW-infant is a LBW baby whose weight is less than 1,000 gm (Immature
neonate)
Premature/preterm-infant is live born infant delivered be fore 37 weeks from
the 1
st
day of LMP
Post-term infant An infant born after 42 weeks of gestation from LMP,
regardless of birth weight
LBW infants are premature if they only have gestational age < 37 weeks.
CHANCE OF SURVIVAL OF LBW INFANTS
Birth weigh Chance of survival in %
400gm-1000 gm 10%
1,000 gm-1,500 gm 40%-50%
1,500 gm- 2000 gm 75-85%
- In developing world approximately 70% of LBW infant have IUGR
- VLBW infants account for > 50% of neonatal deaths
Many LBW infants are also preterm
138
The majority of infants above 2,000 gm do not need specialized care and can be kept
comfortably with their mothers
- Make sure they can feed and keep them warm
Infants below 2,000gm, and especially those less than 1,750 gm, do need specialized
care, which in most cases can be provided only by hospitals
IDENTIFIABLE CAUSES OF PRETERM BIRTH AND/OR IUGR
Generally the causes of LBW/Preterm/IUGR are classified into five categories:
1- Fetal- Fetal distress due to lung immaturity, infection or aspiration
- Multiple gestation
- Erythroblastosis
- Non- imunehydrops- chromosomal disorders
- Chronic fetal infections
- Congenital malformations
- Radiation injury
2- Placental Placenta praevia
- Abruptio placenta
- Small weight, decreased surface area, infarction
- Infection, tumor
4- Uterine Bicorunate uterus
- Incompetence cervix
4-Maternal Pre-eclampsia/eclampsia
- Chronic illness (cardiac, renal, pulmonary)
- Infections (GBS,UTI, chorioaminionitis)
- Drug abuse, alcohol, cigarette, cocaine
- Malnutrition or low socio-economic status
5-Others PROM
- Polyhydramnious
139
- Iatrogenic
PROBLEMS OF THE LBW/PREMATURE INFANTS
The problems of the LBW/Premature infants are mostly associated with anatomical
and physiological immaturity of the various organs of the infant
1- Respiratory system problem
Respiratory distress is common in very immature babies, especially the VLBW infants and those
with a gestation of < 32 weeks.
o Mainly due to lung immaturity, but it may be caused by infection or aspiration
Apnea/cyanosis
Prone to Atelectasis
Respiratory distress syndrome (HMD)
Poor gag and cough reflex
Poorly developed lungs
Poorly developed respiratory muscles
Lack of chest-wall stability
Poor/reduced surfactant production
DIGESTIVE SYSTEM
The GIT though physio9logically mature has not had opportunity to function till after birth.
Small stomach (likely to vomit)
Gastroesophageal regurgitation
Decreased food tolerance or absorption, especially fat, vit D and all fat soluble
vitamins
Do not express hunger by crying- not feed at regular intervals Hypoglycemia-
Brain damage
Abdominal distension due to poorly developed muscles
Hypoglycemia, hypo albuminemia and hypoprothrombinaemia due to hepatic
immaturity
140
3- POOR THERMAL STABILITY (HYPOTHERMIA)
Body temperature determines survival as well as postnatal growth
Small infants are unable to maintain normal body temperature unless the environment is
warm enough
Cold stress
Hypoglycemia
Hypoxia-acidosis
Little subcutaneous fat
Poor vasomotor control of blood flow to the skin (poor shivering)
Large surface area to body wt ratio
Decreased sweat glands cant perspire
Less active with decreased muscle and fat deposits
4- POORLY DEVELOPED RENAL AND HEPATIC FUNCTION
Poor electrolyte and fluid regulation
Liver unable handle or conjugate bilirubin- high rate of jaundice and Hyperbilirubinaemia
Liver Vit-k store or production not developed
Liver do not store glucose (hypoglycaemia)
A steady decrease in Hgb after birth and in production of blood- anemia
5- CNS Slow response to stimuli
Uncoordinated sucking and swallowing which may lead to aspiration
Poorly developed vital centres
6-Increased risk of infection
LBW infants, particularly those born very prematurely, have a very low resistance against
all infections of the newborn
o Infection is a major cause for death
Increased risk of infection in LBW/preterm infants is due to:
Dont receive enough antibodies from the mother
No IGM present
141
Decreasing, chemotaxis, opsonization and phagocytosis
POST-TERM IMFANT/NEONATE
Are infants whose gestation exceeds the normal 280 days by 7 days
25% of all pregnancies are born on or after 287 days
Cause- unknown
Large size doesnt correlate with late delivery, but correlates with:
Large size of either parents
Multigravida
Pre diabetic or diabetic state of mother
Characteristics of post-term/post maturity
Looks 1-3 weeks of age (old)
Large birth weight
Absence of lanugos
Decreased or absent vernix caseosa
Long nails
Abundant scalp hair
White parchment like or desquamating skin, cracked and wrinkled skin
Increased alertness
Only 20% of neonates with placental insufficiency are post term
When delivery is delayed more than 3 weeks beyond term, there is
a significant increase in mortality Three times riskier than term
The risks are:
- Placenta insufficiency (fetal hypoxia, and distress)
- Meconium aspiration syndrome
- Hypoxic encephalopathy
142
- Birth injury
- Congenital malformation
CHARACTERSTICS OF PREMATURE INFANTS
1) Premature infants are tiny, scrawny and red
2) Have thin extremities with very little muscles and subcutaneous fat
3) Have disproportionately large head and abdomen
4) Have thin, relatively translucent and usually wrinkled skin
5) Have more visible abdominal and scalp veins
6) Have plentiful lanugos aver the extremities, back and shoulder
7) Their ears are soft with minimal cartilages
8) Have soft bones of skull, which have
9) Ribs yield with each labored breath
10)Undescended testes in male, and quiet prominent labia and clitoris in female
11) Soles of the feet and palms of the hands have few creases
12)Many of the typical newborn reflexes are weak or absent
The above characteristics of pre-term infant helps for diagnoses purpose, and
to differentiate from term-infants.
Nursing care for premature infants
+ The physical handicaps of premature infants demand the finest nursing care, emphasizing.
1) Cleanliness
2) Continuous electronic monitoring
3) Frequent manual monitoring of vital signs
4) Maintenance of adequate oxygenation, hydration and nutrition
5) Sensory stimulation for the infant and emotional support for the parent
Prevention of low birth weight
+ The association b/n LBW and socio-economic status indicates that the ultimate solution to
this problem of LBW will result from socioeconomic development including appropriate
health care.
1) Improved socio-economic status
143
2) Appropriate Health care
3) Prevention of maternal malnutrition and illness during pregnancy
4) Prenatal care and effective practice of FP, leading to child spacing, improved general health
and nutritional status.
6.3.2 CARE OF ANEONATE WITH SEPSIS AND MENINGITIS
Neonatal sepsis- is a clinical syndrome characterized by systemic signs and symptom, and
bacteraemia during the first month of life.
The incidence is relatively low (1 to 8 cases 1,000 live births)
o The risk of mortality is approximately 25%
Meningitis in the neonate is usually a sequel a of bacteraemia, however, it is discussed with
neonatal sepsis, because the commonly share etiology and pathogenesis
o The incidence of meningitis is usually a fraction of number of infants with sepsis,
varying in different settings from 1/4
th
to 1/3
rd

Neonatal sepsis
There are two major forms (subtypes) of neonatal sepsis:
1-Early onset sepsis (disease)
Presents as a fulminant, multi systemic illness during the first 72 hours or 5-7 days of life.
Mostly caused by organisms prevalent in the genital tract or in labour room and maternity
operation theatre.
Common pathogens
Group B streptococci
Escherichia coli
Staphylococci aurous
Klebsiella
Pseudomonas
Entrobacter species
C/M Majority manifest with respiratory distress due to an intrauterine pneumonia) fever, failure
to feed etc
144
Route of infection:
infection (PROM)
Passage of baby through infected birth canal
During resuscitation in labour room
Risk factors of Early-onset of Neonatal sepsis
Birth Asphyxia
Unclean vaginal examination
Foul smelling liquor
Duration of labour > 24 hours
Birth weight < 2000 gm (2500gm/&/or gestation <37 weeks
Premature rupture of membrane > 24 hours
Maternal pyrexia
When at least two or more of the above high-risk factors are present, the body is considered
to be infected and should be investigated properly for sepsis and treated with appropriate
antibiotics
2- Late-anset of neonatal sepsis
Is more commonly recognized after the first week of life or after 72 hours of
life (Delayed by a minimum of 4 days)
Acquired as nosocommunal infection from the nursery or lying in ward
In most cases symptoms appear by the end of first week of life
Common pathogens are:
Klebsiella pneumoniae
Entrobacteria
Eschercia coli 2/3
rd
cases are caused by gram negative bacilli
Pseudomonas
Salmonella
145
The rest are caused by gram- positive organism:
Staphylococci aurous
Staphylococci albus/epidermitis
Source of infection includes
Incubators
Resuscitation equipments
Feeding bottles
Catheter, face masks, infusion sets,
Clinical features of neonatal sepsis
The clinical presentation could be silent in a very small baby who suddenly may die with
out exhibiting any s/s of infection.
o Behavioural changes and feeding changes (poor or failed sucking)
o Gradually or suddenly becomes lethargic, inactive, unresponsive and may refuse to
suck, then become pale.
o Hypothermia/Fever, RD
o Episodes of apnoeic spells
o Hepato-splenomegally
o Cyanosis
o Failure to gain weight or unexplained wt. loss
Localized features of organ and system involved
Diagnostic work up and interpretation of Neonatal sepsis
ESR (Value more than 10mm/hr is suggestive of infection)
Absolute Neutrophils count (ANC)
- Do WBC and differential count 1
st

ANC= TLC x percentage of PMN cells
Abnormal value <1,500 or >7,500
Ratio of immature to total Neutrophils if I/T > 0.89, it is suggestive of sepsis
Gastric Aspiration for polymorphs
146
Collect with in 1hours of birth
Mix with 1 drop of heparin
Drop on slide and thick smear
Leishmans stain
(If>5 PMN/HPF Infected amniotic fluid)
Blood culture and sensitivity
CSF analysis
CXR, U/A and urine culture
Management of Neonatal sepsis
-First-line drugs:
Crystalline pencillin or Ampicilline + Gentamycine
Crystalline pencillin 50,000-1000- IV/Kg/day 2 doses for <1 weeks of age and 4 doses if >1
weeks of age
Gentamycine 5mg/kg/day (2 doses)
Ampicilline 100 mg/kg/day (2 dose for <1 wk age and 3 dose if >1 wk age)
- If there is meningitis, double the dose of cry. Pencillin and Ampicilline
-Second Line drugs
Hospital acquired infection or if the mother has gram negative infection, give the following
Cefotaxine or ceftriaxone + Amino glycoside
Supportive blood transfusion in DIC, sclerema and Hyperbilirubinaemia
Increase peripheral and pulmonary perfusion
Corrects coagulation abnormality
Removes toxins
Preuention of infection
Hand washing (2min before examination and 30 sec b/n examination)
Nursery Attire (Gown, shoes, baby gown) should be clean
Avoid health personnel, if they are sick
147
Patient placement
Feeding-preparing formula/feeding materials
General maintenance of labour room or neonatal unit
Care of equipment (baby cots, tubes, thermometer should be clean)
Skin and cord care
N.B Better over treat than under treat, but do not overdose.
Neonatal Meningitis
Meningitis:- is an inflammation of the meninges, the membrane that covers the brain
It may be caused by bacteria, less commonly by tubercle bacilli or viruses, or especially in
immuno suppressed children by fungi or parasite
Bacterial meningitis
Out of all neonatal sepsis cases, 1/3 may have co-existing neonatal meningitis
Purulent meningitis is a serious disease, caused by meningococci or pneumococci, or other
bacteria entering the meninges.
In neonates clinical signs of meningeal irritation are absent
In a neonate with septicaemia, the following s/s should arouse the suspicion of neonatal
meningitis
Presence of fever
Onset of convulsion or twitching
Staring look
Bulging anterior fontanel
Abnormal high pitched cry or excessive crying
+ Lumbar puncture should be performed in:
All newborns with suspected septicaemia or
Those with above fractures
Abnormal CSF
More than 30 WBC per cubic millimetre
148
More than 60% of WBC being polymorphs
CSF glucose to blood glucose ratios< 50%
Protein concentration > 150mg /dl in term baby and > 175 mg/dl in preterm baby
Positive gram stain and /or presence of micro-organisms in CSF culture
Management
Crystalline pencillin 300mg(500,000 IV) /kg/day given IV or Im in 3-hourly doses, until
the temperature is stable and normal, there after in 6 hourly doses for 14days
Plus
CAF 100mg/kg/day Im in 6-hourly doses for 3-5 days and then change to oral CAF for a total
of 14 days
Ampicilline 200-400mg/kg/day
In neonatal meningitis, the three best combinations of antibiotic are:
CAF 25-50 mg/kg/day for babies > 2 kg of birth weight
May be ed to 50-75 mg/kg/day p 14 days
Plus
Pencillin 200,000-300,000 IV/kg/day Im or IV slowly
2- Ampicilline 200mg/kg/day in two to three doses
Plus
Gentamycine 5mg/kg/day in two doses Im or Iv- slowly
3- Ampicilline 200mg/kg/day in two to three doses
Plu s
Cefotaxim 200mg/kg/day initially Iv or Im in four divided dose for 3 to 5 days then
orally for 14 days after that the CSF has cleared.
Give phenobarbitone 5mg/kg/day in 3 divided doses with a minimum of 10mg three
times a day for children who have had a convulsion.
149
Fluid If the child cant drink, an NGT should be passed and fluid / ORS should be
gives
150ml /kg/day in children up to 10kg and 100ml/kg/day in bigger children up
to a maximum of 2 lit/day.
For very sick child or if vomiting, give maintenance IV fluid
100ml/kg/24hours up to 10kg, 50-75ml /kg/24 hours in bigger children.
N.B. Provide appropriate nursing care
6.3.3 MANAGING AND PREVENTING NEONATAL TETANUS
Tetanus- Is an acute, often fatal, disease caused by an exotoxin produced by the bacterium
clostridium tetani
Neonatal tetanus- is an acute, spastic paralytic illness in the newborn (neonatal) period caused by
tetanospasmin (neurotoxin) produced by clostridium tetani.
It is characterized by generalized rigidity and convulsive spasms of skeletal muscles.
- The muscle stiffness usually involves the jaw (lockjaw) and neck and ten becomes
generalized.
Epidemiology:
Occurs worldwide and endemic in 90 developing countries
Neonatal tetanus is the most common form and kills about:
+ 500,000 infants each year (un-immunized mothers)
+ Over 70% of these deaths occur just in 10 tropical Asian, and African countries
15,000-30,000 un-immunized mothers die world wide each year from maternal tetanus
(postpartum, postabortal, or post surgical wound infection with c. tetani)
Etiology
Oclostridium tetani
A slender, gram-positive, and anaerobic rod
May develop a terminal spore, giving it a drumstick appearance
Sensitive to heat and cant survive in the presence of oxygen
The spores are very resistance to heat and the usual antiseptics
150
Route of infection
Umblical stump
Injection site (Drugs, vaccines)
Circumcision
Pathogenesis
C.tetani, usually enters the body through the wound (route of entry) In the presence of
anaerobic (low oxygen) conditions, the spores germinate and produce toxins
The toxins disseminated via blood and binds at the neuromuscular junction Endocytosed
by motor nerves Axonal transport and goes to spinal inhibitory interneurons and prevents
neurotransmitter release.
- Blocks normal inhibition of antagonistic muscles that is the basis of voluntary coordinated
movements.
As a result, the affected muscles sustain maximal contraction
The toxins act at several sites with in the CNS, including:
Peripheral motor endplates
Spinal cord
Brain
Sympathetic nervous system
C/M The typical clinical manifestation of tetanus are caused, when tetanus toxins interferes with
release of neurotransmitters, blocking inhibitor impulses
This leads to unopposed muscle contraction and spasm.
Muscle spasm, Trismus or lockjaw
Facial expression Risussardonicus
Sustained spasm of the back muscle opisthotonus position
Tonic titanic seizure like activity
Suddenly fails to suck, irritable
Paralysis or diminished movement
Diagnosis By clinical signs
151
Un-immunized patient (and /or mother) born with in the preceding
2 wks with trismus, rigid muscles and clear sensorium.
Mgt
1- Remove source of tetanospasmin
Clean and debride wounds
Leave wounds open
Cleanse Umblical stump with antiseptics in newborns
Antibiotics
Pencillin G 100,000 IV/kg Im bid for 5 days
2- Neutralize circulating toxins by TAT 5000 IV Im
3- Provide supportive cares
A-Muscle relaxants and sedatives
- Diazepam 0.3 mg/kg Im or IV every 6 hourly, alternating with:
- Chlorpromazine 2mg/kg po or Im or
- Phenobarbitone 5mg/kg every 6 hourly po or Im
B-Meticulous nursing care
- Quiet environment
- Avoid a auditory or visual stimuli
- Respiratory, oxygen, suction and Tracheostomy equipment should be available
- Meticulous care of mouth, skin, bladder and bowel.
Prognosis
Quality of supportive care determines the outcome
Mortality is highest in:
- The very young and the very old
- short incubation period (<1wks)
- Short period of onset (< 3 days)
* Hypoxic insult to brain may result in:
-Cerebral palsy
152
-Mental retardation
-Behavioural disorders
Prevention
Maternal immunization (TAT)
Prompting clean delivery and nursery and cord cut
TAT for home delivery
Active immunization after that an episode of tetanus at should be given
Strengthening disease report
6.3.4 MANAGING AND PREVENTING RESPIRATORY DISTRESS
SYNDROME (RDS)
RDS is also known as hyaline membrane disease (HMD), occurs almost exclusively in
premature infants
The presence of two out of the following five features is defined as respiratory distress
- Respiratory rate> 60/min
- Chest-indrawing
- Grunting
- Flaring of alaenasi
- Cyanosis
The incidence and severity of RDS are related inversely to the gestational age of the infant
Common causes of RDS or HMD are classified into two:
1-Pulmonary causes:- They are again subdivided into three:
A-Lung parenchymal disease:
o Hyaline membrane disease
o Meconium aspiration syndrome
o Congenital pneumonia
o Transient tachypnea of newborn
o Air leak
o Pulmonary haemorrhage
153
o Bronchopulmonary dysplesia
B-Congenital Airway obstructions:
o Nasal or nasopharyngeal: choanal atresia, nasal edema
o Oral cavity: macroglosia, micrognatia and retrognathia
o Neck: congenital goitre, cystic hygroma
o Larynx: Web, subglottic, stenosis, haemangioma and laryngomalacia
o Trachea: Tracheomalacia, congenital tracheal stenosis
C-Intrathoracic malformations
o Pulmonary hypoplesia or agenesis
o Diaphragmatic hernia
o Intrathoracic cysts
o Congenital lobar emphysema
2-Extrapulmonary causes of RDS: These are also further divided into four:
A-Cardiac and circulatory causes
Congenital heart diseases
Hypervolemia
Cardiac arrhythmia
B-Metabolic causes
Hypoglycemia
Hypocalcaemia
Hypothermia
Metabolic acidosis
C-Neurological causes
Neonatal meningitis
Neonatal seizure
154
Hypoxic-ischemic encephalopathy
Extreme immaturity
Intracranial haemorrhage
D- Haematological causes
Anemia
Polycythemia
PATHOPHYSIOLOGY OF RDS
A relative deficiency of surfactant, which leads to decrease in lung compliance and
functional residual capacity with increased dead space, causes RDS
The resulting large ventilation-perfusion mismatch and right to left shunt may involve as
much as 80% of cardiac out put.
Macroscopically, the lungs appear airless and ruddy (i.e. liver like). Thus the lungs of these
infants require a higher critical opening pressure to inflate
Microscopically, diffuse Atelectasis of distal airspaces along with distension of some distal
airways and per lymphatic areas are observed
GENERAL APPROACH TO A NEONATE WITH RDS
Proper history is most important; ANC and perinatal detailed Hx.
A-For Hyaline membrane disease
Gestation
Previous preterm babies
Antenatal steroid prophylaxis
APH and maternal DM
B-For congenital pneumonia: Ask for
PROM
Duration of labour
Maternal fever
Unclean vaginal examination
155
Four smelling liquor
C-For meconium aspiration syndrome
Meconium stained liquor
Hx of interapartum or postnatal suctioning
Gestation
D-For congenital airway obstruction
Polyhydramnious
Excessive salivation since early neonatal period
Difficulty of feeding
Hx of traumatic delivery and birth asphyxia should be asked in all patients
Do meticulous physical examination of the newborn
C/M Progressive signs of respiratory distress are noted soon after birth and include:
Tachypnea
Expiratory grunting (from partial closure of glottis)
Sub costal and intercostals retractions
Cyanosis
Nasal flaring
Dx- Hx, C/M and physical examination
Analysis of blood gases (Respiratory and metabolic acidosis along with hypoxia)
Chest Radiographs of an infant with RDS exhibits
o Bilateral diffuse reticular granular or ground glass appearance
o Air bronchograms
o Poor lung expansions
Echocardiographic evaluation in selected infants
o For diagnosing PDA
o For determining the direction and degree of shunting
156
Mgt Strategies to prevent premature birth and prudent use of antenatal steroids to mature fetal
lungs may decrease the incidence and severity of RDS
Give Vit-k, if not given at birth
Give basic supportive cares
- Keep them in the thermo neutral zone
- Maintain adequate oxygenation
- Maintain adequate circulation
(make sure that there is normal urine out put and normal capillary filling time and normal weight)
Delivery and resuscitation
Surfactant replacement therapy
Initiate specific treatment for specific problems
Correction of metabolic abnormalities metabolic abnormalities
Chest tube for air leak
Mgt - of cardiac failure
Volume expander for hypovolemia
Antibiotic for congenital pneumonia
Surgery for congenital structural anomalies
N.B- The outcome of RDS has improved with increased:
Use of antenatal steroids to improve pulmonary maturity
Early postnatal surfactant therapy to replace surfactant deficiency
Gentle techniques of ventilation to minimize damage to the immature lungs
6.3.5 PROVIDING CARE FOR ANEWBORN WITH HEMORRHAGIC
DISORDERS
Classical hemorrhagic disease of the newborn presents from the second to fifth day of the
life or by 48 72 hours after birth
It is due to failure of maturation of the coagulation mechanism of the newborn
The disease results from deficiency of the prothrombine complex, especially:
157
Prothrombine
Factor-Vll
This is probably due to Vit.K deficiency and occurs as the childs intestinal flora is not
established and hepatic function is immature
A moderate decrease in factors II, VII, IX and X normally occurs in all newborn infants by
48-72 hours after birth; with a gradual return to birth levels by 7-10 days of age
Bleeding tendency can be caused by a deficiency of factors normally involved in clotting of
blood and sealing of the injured vessels
1) Lack of thrombocytes
2) Lack of clotting factors
3) Abnormal vessels
Hemorrhagic disease of the newborn responsive to vitamin K therapy:
Exclusively breast-fed infants
Premature infants
Hemorrhagic disease of the newborn which is unresponsive to vitamin K therapy:
Disseminated intravascular coagulopathy (DIC)
Congenital deficiencies of one or more of the other clothing factors
Classification
EARLY-ONSET LIFE THREATENING Vit-K deficiency- induced bleeding
Onset from birth to 24 hours
Occurs if the mother has been treated with drugs
E.g. Phenobarbital Interferes Vit K function
Phenytoin
LATE-ONSET HEMORRHAGIC DISEASE OF THE NEWBORN
Onset after one week (> 1wk)
158
Is after associated with vitamin K mal absorption
E.g. Neonatal hepatitis or
Biliary atresia
Hemorrhagic disease of the newborn resulting from severe transient deficiencies in Vit- K.
dependent factors is characterized by bleeding that tends to be:
Gastrointestinal
Nasal
Subgaleal
Due to circumcision
Vitamin K facilitates post-transcriptional carboxylation of factors II, VII, IX, and X
Cause Vitamin K deficiencies
Deficiency of coagulating factors
Risk-Factor- Exclusive Breast-fed infants
prematurity (premature infants)
Infants born to mothers receiving anticonvulsive medication
Infants with severe hepatic disease
A particularly sever form of vitamin K-dependent coagulation factors has been reported in
infants born to mothers receiving anticonvulsive medication during pregnancy.
Other forms of bleeding may be clinically indistinguishable from hemorrhagic disease of the
newborn responsive to Vit-K.
o But they are neither prevented nor successfully treated with Vit-K
Clinical pattern identical to that of hemorrhagic disease of the newborn may also result from
any of the congenital defect in blood coagulation.
DIC in newborn infants results in consumption of coagulation factors and bleeding
The clinical course is frequently characterized by
Hypoxia
Acidosis
159
Shock
Haemangioma
Infection
Widespread subcutaneous ecchymosis in premature infants at or immediately after birth are
apparently a result of:
Fragile superficial blood vessels rather than a coagulation defect
C/M The presenting clinical manifestation is hemorrhagic tendency, manifesting in any system, but
most marked in the:
GIT
Skin and
Mucous membrane, nose
Prolonged blood coagulation time
Prolonged partial thromboplastin time
Haematomas, Melena, post circumcision and Umblical cord bleeding
Clinically apparent deficiency of factor viii and IX in the newborn period
Injection site bleeding
Intracranial bleeding
Decreased factor II, VII,IX and X
Subgaleal haemorrhage.
N.B-Hemorrhagic disease of the newborn is mainly due to deficiency of vitamin K
Dx- Based on C/M and PE
Laboratory investigation
History of taking anticonvulsive medication during pregnancy
Mgt - Vitamin K1 1-5 mg IV (or VitK 2.5mg IV, 2.5mg Im) once cessation of
bleeding with in few hours
Old bloods may continue to come from the stomach or in the stool, but fresh bleeding
should stop with in 6 hours (if not, refer urgently)
160
Children with a general bleeding tendency, or continuing bleeding from one place only
should be referred to hospital for diagnosis
Meticulous nursing care for the newborn infant
N.B- Infants with CNS or other bleeding posing an immediate threat to life should receive fresh
frozen plasma, Vit K and blood
Administration of 1mg of Vit .K Im for all newborn infants at birth, especially:
Exclusively breast-fed infants
Premature infants
All difficult deliveries
All infants of diabetic mothers
7- Providing care for a neonate with jaundice (Neonatal Hyperbilirubinaemia)
Jaundice is yellowish discolouration of skin, sclera and mucous membranes due to high
bilirubin level in the blood
Jaundice is observed during the first week of life in approximately 60% of term infants and
80% of preterm infants
The yellowish pigment responsible for jaundice is bilirubin
Bilirubin is formed from haemoglobin when
6.3.6 Providing care for a neonate with Jaundice (Neonatal Hyperbilirubinaemia)
Jaundice is yellowish discolouration of skin, sclera and mucous membranes due to high
bilirubine level in the blood
Jaundice is observed during the first week of life in approximately 60% of term infants and
80% of preterm infants
The yellowish pigment responsible for jaundice is bilirubin
Bilirubin is formed from haemoglobin when this is set free in the plasma from red blood
cells that have been broken down or haemolysed
Bilirubin normally is combined in the liver cells with other substances to form
conjugated or direct bilirubin, which is then excreted in the bile and responsible for the
brown or green colour of the stools.
161
Before bilirubin passes through the liver cells, it is called unconjugated or Indirect
bilirubin
Damages brain cells, if it rises above a certain level in the blood, especially in the
premature or newborn infants. (Neurologic damage)
The skin pigmentation is due to accumulation of unconjugated (indirect, lipid soluble)
bilirubin.
Indirect bilirubin rises when large numbers of red cells are broken down as,
In haemolytic anaemia of the newborn
When the liver cells are too immature to combine bilirubin into the direct bilirubin that
is harmless to brain cells.
Direct bilirubin rises when its outflow from liver cells into the intestine is obstructed, as in:
Neonatal hepatitis
Congenital obstruction (atresia) of the bile duct
+ Classification of Neonatal Jaundice based on their causes
Based on their causes neonatal jaundice can be divided into two groups
1- Physiological Jaundice
It is also known as Icterus Neonatorum
Appears around the 2
nd
to 3
rd
days in an otherwise well baby
Under normal circumstances, the level of indirect-reacting bilirubin in umlical cord serum is
1-3 mg/dl, and rises at arate of less than 5mg/dl per 24 hours
Peak levels are reached b/n the 2
nd
and 4
th
days at 5-6 mg/dl and decreasing to below 2mg/dl
b/n 5
th
and 7
th
days of life.
Bilirubin levels are never higher than 12 mg/100 ml (most of it is indirect bilirubin)
Physiologic jaundice is believed to be the result of increased bilirubin production after the
break down of fetal red blood cells combined with transient limitation in the conjugation of
bilirubin by the liver.
In utero, the foetal bilirubin passes through the placenta to be dealt with in the mothers
body
162
after birth, the liver cells of the baby take a few days to take over this task
ed bilirubin production from the fetal red blood cell Jaundice for a few days until the
liver cells are fully functional
prediction of which neonatal infants are at risk for exaggerated physiologic jaundice can be
based on hour-specific bilirubin levels in the 1
st
24-72 hours of life
Persistent indirect Hyperbilirubinaemia beyond 2 weeks, suggests:
Haemolysis
Hereditary glucuronyl transferase deficiency
Breast-milk jaundice
Hypothyroidism or
Intestinal obstruction
Reasons for physiologic Hyperbilirubinaemia are:
A) Physiologic polycythemia and short lifespan of neonatal RBC Bilirubin
B) He patic uptake, conjugation and excretion of bilirubin is limited due to transient enzyme
deficiency (especially in preterm)
C) Due to paucity of bacterial flora in gut of the neonate, and also over activity of
glucoronidase enzyme Unconjugation and circulation of bilirubin
2- Pathological Jaundice
Jaundice in the newborn noticed in the 1
st
24 hours after birth
Or
- Which does not start to decrease after 5 days should be taken seriously
There are a number of excessive breakdown of red blood cells in the blood of the newborn
which can lead to the production of more bilirubin than the babys liver cells can deal with
+ Causes of pathological Hyperbilirubinaemia
1- Clinical Jaundice appearing with in 24 hours of birth Hemolytic disease of the
newborn due to feto-maternal blood group incompatibility in the Rhesus, ABO, &
minor blood group system.
2- Intravterine infection
163
3- Deficiency of RBC enzymes
E.g. G6 phosphate dehydrogenase- Pyruvate kinase, hexokinase
4- Administration of large amount of drugs to the mother during pregnancy
E.g. Sulfonamides, Diazepam, oxytocin, Nitrofurantoin
5- Hereditary spherocytosis
A- Clinical Jaundice Appearing at 24-72 hours of age:
- This is the time for physiologic Jaundice, but can be aggravated and prolonged by:
- Prematurity - Hypoglycemia
- Birth Asphexia - Drugs
- Hypothermia - Cepholohematoma & bruising
- Polycythemia
C- Jaundice Appearing after 72 hours and with in first 2 weeks of life
1- Septicemia
2- Neonatal hepatitis
3- Extrahepatic biliary atresia
4- Breast-milk Jaundice
5- Metabolic disorders
6- Hypertrophic pylomic stenosis and intestinal obstruction
N.B- Jaundice in the first 24 hours after birth is serious.
C/M- Jaundice in newborn progresses in Cephalo-caudal direction, and thus the extent of
yellowness of the skin can correspond to bilirubin level.
- Face ------------- 5.7 mg/dl
- Chest ------------ 10 mg/dl
- Lower Abdomen --- 12 mg/dl or thigh
- Sole/palm -------- 15 mg/dl
164
Holrever it is always mandatory to determine TSB by laboratory before one takes action for
hyperbilirubinemia
DX- Based on C/M and lab. Investigation
Mg.t- Principles of management of neonate with hyperbilirubinemia
1- Avoid any drug, which may interfere with bilirubin metabolism
2- Correct any factor which makes CNS more susceptible to bilirubin toxicity
E.g. Hypoxia, Hypoglycemia, Acidosis
3- Adequate feeding should be confirmed
4- Drug therapy is required as areplacement therapy in hypothyrodism or to
stimulate liver enzymes
E.g. Phenobarbitone
5- Lowering serum bilirubin by exchange transfusion and phototherapy
Make sure the baby gets adequate feeds
Find the cause and treat infection if present
Phototherapy should be started at a bilirubin level of:
- 10mg/100ml in preterm or sick full-term babies
- 15-19 mg/100ml in full-term babies
Exchange transfusion is considered if
- Bilirubin is rising very fast
- Initial levels of bilirubin are very high
- The babys haemoglobine is lower than normal or fallingshowing haemolysis is
severe
Danger signs in newborn Jaundice:
- Mothers who had a previously affected baby
- Jaundice appearing in the first 24hours
- Jaundice becoming rapidly more severe
- Increasing pallor and jaundice continuing to increase after 5 days
N.B- Kernicterus or Bilirubin Encephalopathy is due to indirect bilirubin toxicity
165
to the brain
- Occurs if the bilirubin level > 20 mg/100dl
- Usually occurs 2-5 days in term and as late as 7
th
day in preterm after birth
6.3.7 Managing Neonatal Hypothermia and Hyperthermia
- If babys temperature falls below 36.5
0
c, this is called Hypothermia or cold injury
- Due to certain characterstics, newborns, especially LBW babies are at increase risk
of heat loss
- Large body surface area in relation to weight
- Large head in proportion to body
- Little subcutaneous fat
- When heat loss exceeds the babys ability to produce heat, its body temperature
drops below the normal range and it becomes hypothermic
Classification of Hypotermia
1- Mild Hypothermia
- The newborn with a temperature of 36-36.4
0
c
- The newborn is under cold stress. Which should give rise to concern
2- Moderate Hypothermia
- A baby with a temperature of 32.0-35.9
0
c
3- Severe Hypothermia
- A temperature below 32
0
c
The newborn is most volunerable to hypothermia during the first few hours after birth
although the condition may occur later too.
Causes Situations contributing to excessive heat loss
1- External factors
Cold environment
Wet or naked baby
Cold linen
During transport
166
Various procedures (e.g.- bathing, surgery)
Increased air flow current with low humidity
2-Poor ability to conserve heat in LBW infants
3-Poor metabolic heat production
Several factors interfere with metabolic heat production, which includes
A) Deficiency of brown fat, eg. Preterm and SGAS
B) CNS damage due to anoxia and CNS malformation
C) Hypoxia
D) Hypoglycemia
Hypothermia of the newborn is due to more of lack of knowledge than to lack of
equipment
Incorrect car of the baby at birth is the most important factor influencing the occurrence of
hypothermia
Cold delivery room
Newborn is often left wet and uncovered after delivery until the placenta is delivered
Weighing the newborn naked and washed soon after delivery
Delayed initiation of breast-feeding
The baby is kept in a nursery, a part from the mother
Hypothermic newborns have decreased sucking ability, impaired feeding, will lead to
decreased heat production and worsening hypothermia
Consequences of hypothermia
- Hypoxia
- Hypoglycemia due to consumed glucose during thermogenesis
- Metabolic acidosis
- Bradycardia and Hypotension
- Depressed immunity (sepsis)
Mechanisms of Heat-Loss
There are for four (4) principal mechanism of heat loss:
167
1- Convection: loss of heat energy to surrounding cool air (From skin to moving
air)
Loss of heat depends on:
- Temperature difference b/n skin and air
- speed of air movement
- the surface area exposed
The cooler the air and the higher speed of velocity, the greater is the heat loss
2- Conduction: Loss of heat energy to cooler materials where neonate lies or
resting
- Conductive heat loss is less since it is unusual to keep a newborn on a cool surface
3- Radiation: Transfer of heat b/n objects of higher temperature to next solid
object of lower temperature. (Body to cooler object)
4- Evaporation: A major source of heat loss from the newborn
Greater surface area of contact, increased velocity and thinner skin layer, leads to an
increase evaporative loss of heat either from skin or lungs
C/M Cold feet to touch
- Cold skin all over the body (If hypothermia continued)
- The baby is less active, suckles poorly and has weak cry (If hypothermia allowed to
continue)
- Face and extremities may develop a bright red colur (in severely hypothermic
babies)
- Sclerem (hardening of the skin associated with reddening and oedema) may occur
on:
The back and limb or
Over the whole baby
- Lethargic, slow, shallow and irregular breathing
- Slow heart rate (Bradycardia)
- Low blood sugar and metabolic acidosis
168
- Gereralized internal bleeding (especially in the lungs) and respiratory distress
NB- It is important to realize, however, that all these signs (the above) are non-specific and may
indicate other sever diseases, such as bacterial infection in the newborn boby.
Dx- Based C/M and Hx, as well as P/E
Mgt Newborns found to be hypothermic must be rewarmed as soon as possible.
- Keep infants and room warm
- Over head radiant heater
- 10% dextrose and oxygen
- treatment of infection
The rewarming process should be continued until the babys temperature reaches the normal
range.
- The temperature should be checked every hour
- The temperature of the device being used or the room adjusted accordingly
- The baby should continue to be fed
Once the babys temperature reaches 34
0
c, the rewarming process should be slowed down to
avoid overheating
Prevention
- Watch out for a falling temperature, especially in a preterm and LBW baby
- Keep every newborn dry and properly clothed
- Keep the delivery and nursery room warm
- Feed the newborn properly
NB- Due to poor heat regulating mechanism of the newborn, the infant or premature babies tend to
develop moderate to high fever (Hyperthermia) and is just as dangerous as hypothermia of the
newborn.
6.3.8 Managing Neonatal Hypoglycemia
169
Hypoglycemia is defined as blood glucose level less than 40mg/dl irrespective of gestation and
day of life
A plasma glucose level of less than 30mg/dl in the first 24hours of life and
less than 45 mg/dl thereafter constiventes hypoglycemia in the newborn
Patients with Hypoglycemia may be asymptomatic or may present with sever
CNS and cardiopulmonary disturbances
Sustained or repetitive Hypoglycemia in infants and children has a major
impact on normal brain development and function.
There is eveidence that hypoxemia an dischemia potentiate hypoglycemia
causing brain damage that may permanently impair neurologic development
Cause
Hyperinsulinism or persistent hyperinsulinemic Hypoglycemia of infancy (PHHI)
Limited glycogen stores (e.g.- Prematurity, IUGR)
Depleted glycogen stores (Eg.- Asphexia per inatal stress, starvation)
Increased glucose utilization (e.g. hyperthermia, polycythemia, sepsis, growth hormones
deficiency)
Decreased glycogenolysis, gluconeogenesis, or utilization of alternate fuels
e.g. Inborn errors of metabolism, adrenal insufficiency)
Pathophysology
Normal blood glucose is regulated very narrowly, usually from 80-90 mg/dl
Glucose is the major energy source for fetus and neonate
The newborn brain depends upon glucose almost exclusively
Up to 90% of total glucose used is consumed by the brain
Alternate fuels (e.g.- ketones, lactate) are produced in very low quantities
The usual rate of glucose utilizaiton is 4-8 mg/kg/min
Glucose regulatory mechanisms are sluggish at birth. Thus the infant is susceptible to
hypoglycemia when
- Glucose demands are increased, or
170
- Exogenous or endogenous glucose supply is limited
Severe or prolonged hypoglycemia may result in long term neurologic damage
In the newborn serum glucose levels decline after birth until age 1-3 hours, then they
spontaneously increase
Liver glycogen stores become rapidly depleted with in hours of birth; and gluconeogenes is
primarily from alanine can account for 10% of glucose turnover in the newborn infant by
several hours of age.
Generally Neonatal Hypoglycemia is due to:
- Inappropriate change in hormone secretion
- Inadequate substrate reserve in the form of hepatic glycogen
- Inadequate lipid stores for the release of fatty acids
C/M - Are broad and can be from a combination of adrenergic stimulation or from decreased
availability of glucose for the CNS
A) Infants of the 1
st
or 2
nd
day of life may be asymptomatic or have life-threatening CNS and
cardiopulmonary disturbances
- Hypotonia - CHF
- Lethargy and Apathy - Cyanosis
- Poor-feeding - Apnea
- Seizures - Hypothermia
B) C/Ms associated with activation of the autonomic nervous system
- Anxiety, tremulousness - Pallor
- Diaphoresis - Hunger, nausea, and vomiting
- Tachycardia
C) C/Ms of hypoglycorrhachia or neuroglycopenia
- Headache
- Mental confusion, staring, behavioural changes difficulty concentrating
- Visual disturbances (e.g. decreased acvity, diplopia)
171
- Dysarthria
- Seizures
- Ataxia, somnolence, coma
- Stroke (hemiplegia, aphasia), paresthesias, dizziness, amnesia, decerebrate and/or
decorticate posturing
Dx- Based on C/M and PE
- Laboratory studies
- Serum or plasma glucose lever
- Serum insulin
- Urine for ketone and organic acid analysis
Mgt
- Manage both symptomatic and Asymptomatic cases similarly
- Treat associated problems, like polycythemia, sepsiz etc
- Mini bolus: 200 mg/kg of dextrose (10%2 ml/kg) over 1 minute, then followed by
10% dextrose, 6ml/kg/minute
- Check blood glucose after 15 minutes, if normal (>40mg/dl), continue the same
infusion, but if it is low, increase infusion rate by 2 mg/kg/min an dif still low keep
on increasing the glucose infusion rate by 2ml/kg/minute Q 15 minute
To maximum of 12-14 ml/kg/min. while doing this, take care of fluid over
load
- Once blood glucose is normal recheck Q 15 minute for two more times. If normal
check at 1 hourly interval twice, then 2 hourly twice and the 4 hourly
- Start tube-feeding with expressed breast milk or formula feed simultaneously.
This avoids drastic fluctuation in blood glucose level
- If blood glucose level remains normal for 12 hrs or if it exceeds 100mg/dl, decrease
the infusion rate by 2mg/kg/minute every 6 hrly while checking blood glucose
Once the infusion is down to 4 mg/kg/minute, increase the feeds and taper off IV fluids
172
Prevention
1- Early feeding of Infants of Diabetic mothers and small for Dates
- Start 1 hour of age
- 3. feeds at 1 hour interval, 5ml/kg/feed
- If normal blood sugar continue feed 2 hrly
- All feeds should be breast milk or formula feeds
2- Once the baby is transferred to the mother, Breast-Feeding should be supervised
for adequate intake (IDMs, SFDs)
3- In babies on IV- fluids, ensure that there is no discontinuation of drip
6.3.9 MANAGING PERINATAL ASPHEXIA
Def
n
- It is an insult to the fetus or newborn due to lack of oxygen /hypoxia/and/or lack of
perfusion/ischemia/to various organs
It is a failure to establish efficient breathing at one-minute of age/APGAR-score 0-6%
In most of the case it is associated with lactic acidosis
The definition depending on APGAR-score is not applicable on preterm, birth trauma, and
babies with congenital neurological anomalies
Incidence- 1-1.5% in developing country
Directly related to GA and birth weight
9% of newborns < 36 WKS of gestation are prone to have PNA
PNA is responsible for 20% of perinatal death
Causes of PNA
90% PNA are due to placental insufficiency (due to inability of the placenta to provide
adequate oxygen and remove C
0
2
and hydrogen from the fetus)
10% of PNA are secondary to:
Cardiovascular anomalies
Pulmonary anomalies
Neurological anomalies
PATHOPHYSIOLOGY OF PNA
173
Fetus deprived of oxygen Initial period of rapid breathing- primary apnoea (responds to 0
2
and stimulation) If asphyxia continues, it leads to gasping respiration.
HR, BP and ed 0
2
, apnoea develops progressive brain damage with central respiratory
depression, which can only be improved by cerebral oxygenation and circulation
If asphyxia is not reversed on time, hypoxic damage leads to ischemic challenge to the
fetus.
Reflexes are initiated (diving reflex) causing shunting of blood to the most vital
organs (Heart, brain, adrenals) and away from lungs, GIT, liver, kidneys, spleen,
skeleton, muscle and skin
As asphyxia progresses with sever hypoxia and acidosis, there is a decrease in the
heart rate and decrease in cop which leads to decrease BP.
Anaerobic metabolic due to lack of 02 to the tissue leads to excessive production of
lactic acidosis and progressive hypoxia will lead to multi-organ damage.
Target organs of PNA includes
Kidneys ---------- 50% of PNAS
CNS ---------- 28% of PNAS
CVS ---------- 25% of PNAS
RS- --------- 23%of PNAS
- Death due to multi-organ failure
- Brain injury due to PNA is termed as hypoxic ischemic Encephalopathy (HIE)
Predisposing /Risk/factors for PNA
Hypoventilation during anesthesia
Cyanotic heart diseases
Respiratory failure or co-poisoning
Spinal anesthesia hypotension
Administration of excessive oxytocin
Compression or knotting of the cord
Drug addiction of the mother (e.g. cocaine)
174
Toxaemia and post maturity
Severe anemia (severe haemorrhage or haemolytic disease)
Severe shock (interfere 02 supply to vital organ)
Cerebral damage, necrosis or injury
C/M Intrauterine growth restriction
Slow heart rate during labour
Scalp blood analysis may show a PH< 7.20.
Presence of yellow, meconium-stained amniotic fluid at delivery (Fetal distress)
Depression and failure to breathe spontaneously at birth
Pallor. Cyanosis, apnoea, a slow heart rate and unresponsiveness to stimulation are also
signs of Hypoxic-Ischemic encephalopathy seizure
Congestive heart failure and cardio-genic shock
Persistent pulmonary hypertension
Respiratory distress syndrome signs
Gastrointestinal perforation with haemorrhage
Hematuria and acute tubular necrosis
DX- Based on clinical manifestation, P/E
Analysis blood for PH-value
Mgt Supportive and directed at the organ system manifestations
Careful attention to ventilatory status and adequate oxygenation
Blood volume
Hemodynamic status
Acid-base balance
Possible infection
+ Phenobarbital, allopurinal, calcium channel blockers may be given
+ Continuous electro encephalographic monitoring in case of seizure
Nursing care
175
Monitor the condition of the fetus
Maintaining patent airway, by suctioning or cleaning the mouth or nose and positioning
Provide ventilation and cardiac message (Resuscitation) ABCs
Place the asphyxiated infant immediately after that birth under radiant heater (to avoid
hypothermia)
Administration
0
2 and other medications as ordered
Monitor closely for signs of multi-organ hypoxic ischemic tissue injury.
DUTY 7. COMMON MEDICAL SURGICAL PROBLEMEM IN CHILDRN
7.1- PROVIDING CARE FOR A CHILD WITH RESPIRATIORY SYSTEM DISORDERS
7.1.1. Providing care for a child with Tonsillitis
7.1.1.1 Definition
- Tonsils are a ring of lymphoid tissue encircles the pharynx, forming a protective barrier
against upper respiratory infection
This ring consists of groups of lymphoid tonsils
- Facial Tonsils - Commonly known as tonsils, are two oval masses attached to the side walls
of the back of the mouth b/n the anterior and posterior pillars
- Pharyngeal Tonsils Known as adenoids, is amass ding from the roof of the nasal pharynx
to the free-edge of the soft palate
- Lingual Tonsils - Are two masses of lymphoid tissue at the base of the tongue
Tonsillitis is an inflammation and/or infection of the tonsils
- There is a normal progression of enlargement of lymphoid tissue in child hood b/n the ages
of two and eight or ten years, regressing during the pubertal period
- If the tissue itself becomes a site of acute or chronic infection, it may become hypertrophied
to the extent of interfering with breathing, causing partial deafness, or it may become in
itself a source of infection
7.1.1.2 Etiology Caused by a variety of bacteria and viruses
176
- Mild pharyngitis or tonsillitis with out much fever, pus, swelling of lymphglands is almost
always a viral disease no need of Antibiotics
- Moderate or severe tonsillitis, usually accompanied by pharyngitis with high fever, beads of
pus and often enlarged lymph glands in the neck is more often due to beta-hemolytic
streptococci Need Antibiotic Treatment
7.1.1.3Pathophysology
- Tonsils and Adenoids consists o lymphoid tissues and forms a protective barrier against
URT-infections
- In young children, tonsils commonly are enlarged, but they diminish in size with aging
- Enlarged tonsils are vulnerable to viral or bacterial infection
- When the tonsils are infected or inflamed by bacterial or viral pathogen, the protective
function is lost, and the infection may spread to other parts of the body
- Non- bacterial exudative tonsillitis is mild disorder characterized by gradual onset of low
grade fever, mild headache, sore throat, hoarseness and productive cough.
- Bacterial tonsillitis, most often caused by beta hemolytic streptococcal infection, is a more
dramatic disorder marked by rapid onset of high fever, headache, generalized muscle aches
and vomiting
- Sequelae of bacterial tonsillitis may include skin rash and extension of infection to other
parts of the body including peritonsillar abscess, middle ear infection and involvement of
mastoids and Meninges
Late sequelae of bacterial tonsillitis include:-
o Rheumatic fever
o Acute glomerulonephritis
Marked tonsils and adenoid enlargement may occlude the airway causing respiratory
problems
7.1.1.4 C/M Fever, Feeling unwell
- Sometimes vomiting, diarrhea and abdominal pain
- Refusal of food
177
- Difficulty of swallowing
- May or may not complain of sore throat
- Swelling and Redness of the tonsils and surrounding s on EP
- Sometimes beads of pus on the surface of the tonsils
- Swollen and tender lymph glands, especially the tonsillar gland at the angle of the jaw
Sometimes movement of the neck is painful (This should always be differentiated with TB
lymphadenitis)
Clinical Features of Chronic Tonsillitis and Adenoiditis
Recurrent rhinitis, tonsillitis, Otitis media
In case of marked adenoiditis
- Snoring
- Sleeping with open mouth
- Nasal speech
- Pus from infected adenoids dripping into the trachea (postnasal drip), caucusing coughing at
night
General symptoms of chronic infections
- Tired, poor appetite pale, inactive
7.1.1.5 Dx. Based on the C/m and P/E
- Laboratory investigation
7.1.1.6 Complication:- Complications of tonsillitis include the following
- Otitis media
- Peritonsillar abscess- in older children only
- Cervical lymphadenitis developing into abscess
- Rheumatic fever and or Acute glomerulonephritis other streptococcal infection
7.1.1.7 MEDICAL AND NURSING Mgt Cases of viral tonsillitis require not treatment except
symptomatic or supportive mgt
178
- Children with streptococcal tonsillitis should be given PPF 50,000 unitsn/kg/day at least, to
start with. It is important to continue this Rx with:
- Oral pencillin 50mg/kg for 7days or
- Benethamine pencillin as Triplopen single dose 0.5 gm for under fives, 1gm for older
children or
- Benzanthine pencillin
Symptomatic treatment: Gargles and paracetamole for high-fever
Surgical Removal- Removal of the tonsils and adenoids or both is indicated in chronic enlargement
that interferes with swallowing or breathing
- Generally Removal of tonsils/adenoids or Adenoidectomy and /or tonsillectomy is/are
indicated when there is:
Chronic enlargement of the tonsils/Adenoids
Recurrent Otitis media, tonsillitis or cervical adenitis (several times a year)
Peritonsillar abscess
Recurrent group A beta-hemolytic streptococci
Enlarged adenoids should be removed if
It gives rise to recurrent infection
There is loss of hearing
Nose breathing is continuously obstructed
N.B- Tonsils are only very rarely to be removed solely v/c they are enlarged
- Poor appetite, disobedience and other vague complaints are never a reason to remove
valuable lymph tissues
- To prevent rheumatic fever, treat streptococcal tonsillitis thoroughly with pencillin
- Big tonsils are not necessarily diseased tonsils
Preoperative and postoperative care for a child with tonsillectomy
- Prepare the child for hospitalization and surgery
- Observe for and report unusual bleeding
- Intervene for bleeding as appropriate
179
- Monitor vital signs and assess skin colour
- Observe for frequent swallowing and restlessness
- Help prevent bleeding by a voiding gargling and discouraging the child from coughing
- Position the child on the side or abdomen to facilitate drainage from the throat
- Avoid persons with infection, teach the importance of soft diet with adequate fluids and
liquids that can irritate the throat
7.1.2Providing care for a child with Croup syndrome
7.1.2.1 Definition Croup is a syndrome characterized by inspiratory stridor, hoarseness,
cough and signs of respiratory distress due to varying degree of laryngeal obstruction
- The obstruction being produced by edema and spasm
- The term croup refers to a heterogenous group of mainly acute and infectious processes
that are characterized by a barklike or breassy cough and may be associated with
Hoarseness
Inspiratory stridor
Respiratory distress
- Croup usually affects to some defgree the larynx, trachea and braonchi
7.1.2.2 Classification
- Croup syndrome includes the following four syndromes, which must be differentiated from
one another and from a variety of other entities that may present as upper airway
obstruction
1- Laryngotracheobronchitis
- It is also known as croup or obstructive laryngitis
- Is the most common form of acute upper respiratory obstruction
- It refers to viral infection of the glottic and subglttic regions
- Laryngotracheitis used for the most common and most typical form of croup
- Laryngotracheobronchitis is the term used for more severe form of croup that is considered
an extension of laryngotracheitis associated with bacterial superinfection
180
Occurs 5 to 7 days into the clinical course
- Most patients have an upper respiratory tract infection with some combination of
rhinorrhea, pharyngitis, mild cough, low grade fever for 1 to 3 days before the s/s of upper
airway obstructions become apparent
2- Acute Epiglottitis (supraglottitis)
- Is a dramatic, potentially lethal condition which is characterized by an acute fulminating
course of high-fever, sore lthroat, dyspnea and rapidly progressing respiratory obstruction
- With in a matter of hours, the patient appears toxic, swallowing is difficult and laboured
berating
- Drooling and hyperextended neck in attempt to maintain the airway
- A brief period of air hunger with restlessness, which may be followed by rapidly
increasing cyanosis and coma
- Stridor is alate finding and suggests near complete obstruction
- The diagnosis requires visualization of a large cherry-red swollen epiglottis by
laryngoscopy
- Classic radiographs of a child who has epiglottitis show the thumb sign
Establishing an airway by nasotracheal intubation, or less often by tracheostomy is
indicated in patients with epiglottitis regardless of the degree of apparent respiratory
distress
3- Acute Infectious laryngitis
- The onset is usually characterized by an upper respiratory tract infection during which sore
throat, cough, and hoarseness appear
- The illness is generally mild; and respiratory distress is unusual except in young infants
- Hoarseness and loss of voice maybe out of proportion to systemic signs and symptoms
- Evidence of pharyngeal inflammation on PE
- Laryngoscopy demonstrate inflammatory edema of the vocal cords and subglottic tissues
- The principal site of obstruction is usually the subglottic area
4- Spasmodic croup
- Occurs most often in children 1-3 years of age
181
- Clinically similar to acute larnygotracheo bronchitis, except that the history of aviral
prodrome and fever in the pt. and family are absent
- Laryngoscopy reveals pale, watery edema with preservation of the epithelium (unlike the
erythematous edema and destruction of the epithet lium of acute infectious
laryngotracheobronchitis
- Occurs most frequently in the evening or night time
- Spasmodic croup begins with a sudden onset that may be preceded by mild to moderate
coryza and hoarseness
- The child a wakens with a characterstics barking, metallic cough, nosiy inspiration,
respiratory distress, appears anxious and frightened
It may represent more of an allergic reaction to viral antigens than direct infection
7.1.2.2 Etiology of croup syndrome
- spasmodic croup often recur several times
- The majority of cases (over 85%) are due to viruses
Parainfluenza virus accounts for more than 2/3
rd
of cases
Influenza virus, adenovirus, respiratory syncytial virus, ECHO and coxsackie
viruses accounts less than 1/3
rd
of the cases
- Bacteria responsible for croup are
Corynebacterium diphtheriae
H.Influenzae type B-
The primary site of involvement in H.Influenzae croup is the epiglottis, which becomes
swollen, red and edematous
7.1.2.5 C/M of croup syndrome
- Cough which is harsh and croupy
182
- Considerable respiratory distress with tachypnea, inspiratory stridor, and retraction of
supraclavicular, epigastric and intercostals spaces
- Apprehension and agitation
- Pale or show intermittent cyanosis
- There may be difficulty of swallowing
- Red throat on examination
- Large, red and swollen epigllotis at the back of the tangue
- Sorethroat, hoerseness, dyspnea, fever
Barking and metallic cough; nosiy inspiration
- drooling and hyperextended neck may be present
In diphtheric croup, with in 2-3 days, pharyngeal examination reveals the typical gray-
white membrane is adherent to the tissue (forcible attempts to remove it cause bleeding)
7.1.2.6 DX- Based on Hx, C/M and PE
- X-ray (Radiography) or laryngoscopy
7.1.2.7 Complications of croup syndrome
- Complications occur in approximately 15% of patient with viral croup- The most common
is extension of the infectious process to involve other regions of the respiratory tract
(middle ear, terminal brochioles, pulmonary parenchyma)
Bacterial tracheitis
Pneumonia
Cervical lymphadenitis
Otitis media
Meningitis or septic arthritis (rarely)
- Mediastinal emphysema and pneumothorax are the most common complication of
tracheotomy
7.1.2.8 Medicl, Sugical and nursing Mgt The mainstay of treatment for children with croup is
airway management
- Steam, which liquefies the dry secretion
183
- Humidified oxygen administration
- Make sure the child drinks enough (Po, NGT or IV-fluid)
- Decrease the mucosal swelling
Prednisolone 2mg/kg day or hydrocortisone 100mg Im
- Administration of antibiotics
PPF 50.000 units (50mg/kg) and cotrimoxazole orally in three divided dose
Amoxicillin or CAF should be given in sever diseases (Especially if epiglottitis or
extension of the infection into the trachea or brochi is suspected)
- Tracheostomy or intubation can be life saving
- Mild sedation with phenergan 1mg/kg/day can be of help
7.1.3Providing care for a child with Bronchitis
Bronchitis refers to non-specific bronchial inflammation and is associated with a number
of child hood conditions
Acute bronchitis is a syndrome, usually viral in origin, with cough as a prominent feature
Acute bronchitis may be restricted almost solely to the main bronchi, without affecting the
lungs themselves
But usually associated with some upper respiratory infection
- Acute tracheobronchitis is a term used when the trachea is prominently involved
- Asthmatic bronchitis is an obsolete term; wheezing and bronchial inflammation are
integral findings of asthma
Asthma exacerbations are commonly triggered by upper respiratory tract infections
The existence of chronic bronchitis as a distinct entity in children is controversial.
However, like adults, children with chronic inflammatory diseases or those with toxic
exposures may develop damaged pulmonary epithelium
Chronic or recurring cough in children should guide the clinician to search for
underlying pulmonary or systemic disorders
7.1.3.2 Etiology Viruses and bacterial agents
Influenza, Pertusis, diphtheria
184
Any inflammatory reactions may cause bronchitis
7.1.3.3 Pathophysology
Acute bronchitis is commonly preceded by a viral upper respiratory tract infection
It is more common in the winter when respiratory viral syndromes predominate
The tracheobroncheal epithelium is invaded by the infectious agent, leading to
activation of the inflammatory cells and release of cytokines
The tracheobronchial epithelium may become significantly damaged or hyper
sensitized due to the inflammatory response, leading to a protracted cough lasting 1-3
weeks
Interleukin -8(Il-8), Macrophage inflammatory protein (MIP) 1 and RANTES
(Regulated on Activation Normal T-cell Expressed and secreted) are inflammatory
mediators which invoked in the pathogenesis of airway inflammation
In addition to above, altered regulation of surfactant proteins A and B may exacerbate
the abnormal lung function of infants with bronchitis and bronchiolitis
These cellular and pathologic process impair normal pulmonary gas exchange
The above findings suggest a complex cellular deregulation producing the
clinical syndrome
7.1.3.4 C/M Commonly, the child first presents with non-specific upper respiratory infectious
symptoms, such as rhinitis
Frequent dry, hacking cough with in 3 to 4 days of the onset of URIT s/s (may or may not
be productive)
Purulent sputum other several days
Chest pain may be a prominent complaint in older children
Low- grade fever, conjunctivitis and rhinitis on P.E
Coarse breath sounds (Harsh breath sounds)
Coarse and fine crackles and scattered high-pitched wheezing (but no obstructive
symptoms)
185
The initial dry cough becomes productive as the disease progresses
Dyspnea and cyanosis may be present
The mucus gradually thins usually with in 5-10 days and then the cough gradually a bates
The entire episodes usually lasts about 2wks and seldom longer than 3 wks
The principal objective of the clinician is to exclude pneumonia, which is more likely
caused by bacterial agents requiring antibiotic therapy
7.1.3.5 Dx- Based on Hx, C/M and PE
7.1.3.6 Complications
- Chronic bronchitis
- Bronchiectasis
- Bronchial asthma
- Pneumonia
7.1.3.7 Mgt- There is no specific therapy for acute bronchitis
The disease is self-limited, and anitibiotics although frequently prescribed. Do note hasten
improvement in uncomplicated acute bronchitis
Frequent shifits in position to facilitate pulmonary drainage
Treatment is symptomatic and supportive
Humidified atmosphere is helpful for loosing secretions
Antibiotics, like penicillin should given for preventing secondary infection
Expectorants are usefull for clearing the airway
7.1.4 Providing care for a child with pulmonary Tuberculosis
Pulmonary Tuberculosis is the disease that affects the lung parenchyma (alveoli and
alveolar duct)
Currently, 95% of tuberculosis cases occur in developing countries
WHO estimates that more than 8 million new cases of tuberculosis occur and
approximately 3 million people die of the disease world wide each year
Almost 1-3 million cases and 450,000 deaths occur in children each year
+ More than 1/3
rd
of the worlds population is infected with mycobacterium tuberculosis
186
7.1.4.2 Etiology Mycobacterium tuberculosis is the most important cause of tuberculosis disease
in humans
M.bovis may also cause tuberculosis in humans
The primary complex of tuberculosis includes local infection at the portal of entery and the
regional lymph nodes that drain the area
The lung is the portal of entery in over 98% of cases
The tubercle bacilli multiply initially within alueoli and alueolar ducts
The hilar lymph nodes are involved when the primary infection is in the lungs
The tissue reaction in the lung parenchyma and lymph nodes intensifies over the next 2-12
wks as the organisms grow in number and tissue hypersensitivity develops
The parenchymal portion of the primary complex often heals completely by fibrosis or
calcification after undergoing caseous necrosis and encapsulation
Occasionally, this protion continues to enlarge, resulting in focal pneumonitis and pleuritis
If the caseous is itense, the center of the lesion liquefies and empties into the a ssociated
bronchus, leaving a residual cavity
During the devt of primary complex, tubercle bacilli are carried to most tissues of the body
through the blood and lymphatic vessels
Erosion of aparenchymal focus of tuberculosis into a blood or lymphatic vessel may result
in dissemination of the bacilli and a mi8liary pattern with small nodules evenly distributed
on the chest radiograph
Progressive tuberculosis can occur either immediately following the initial infection or
some time later
Progressive (secondary tuberculosis) will occur
After massive infection or due to repeated infection
As when the child is in close contact with an untreated case of open
tuberculosis in the family
If infection like malaria, measles or whooping cough diminish the general resistance
187
In malnourished children
In children with HIV/AIDS
+ Generally tuberculosis can progress in three ways
1- Extension of the primary lung lesion to a tuberculosis pneumonia or even cavitation
The infection can also spread into the pleurae as tuberculosis pleurisy
2- Pressure of hilar glands on bronchi may cause collapse of a part or whole of alobe
(Atelectasis), or rupture of a gland into the bronchus may cause bronchial spread of the
disease
3- Lymphogenous or haematogenous spread to distant body parts
7.1.4.4 C/M More than 50% of infants and children with radio graphically moderate to severe
pulmonary tuberculosis have no physical findings and are discovered only by contact tracing
Nonproductive cough and mild dyspnea are the most common symptoms in children/Infants
Fever, night sweats, anorexia and decreased activity occur less often
Difficulty of gaining weight, falilure -to- thriuesyndrome
Localized wheezing or decreased breath sound
7.1.4.5 DX- The most specific confirmation of pulmonary tuberculosis is Isolation of
M.tuberculosis
Sputum for AFB and culture should be collected for adolescents and older children
For most children, the presence of the following is a dequate proof that the disease is
present
1- Positive tuberculin skin test
2- An abnormal chest radiography consistent with tuberculosis
3- History of exposure to an adult with infectious tuberculosis
7.1.4.6 Mgt - Scc regimen for children of 6years or below and seriously ill children 7-14 years
old 22(RHZ) /4(RH) or2 (RHZ)/4 (RH)
Children between 7 and 14 years old with any type of TB, who are not seriously ill. 2
(RHZ)/6(EH)
7.1.4.7 Nursing Mgt
188
Advise the family/the mother to provide adequate and balanced diet for the child
Provide health education on the disease process, Rx and prevention
Provide appropriate nursing care for the sick child
Prevention
Investigation of family and other close contacts of any case of TB
Treatment of pt. and follow-up of contacts
A newborn of a tuberculosis mother should receive isoniazid 10mg/kg for 3months
If the mantoux is Ve, give BCG
If the mantoux is +Ve, treated with isoniazide as above for another 9month to a total of 1
year
Continue breast-feeding
BCG after birth, or two mantoux negatives
In the absence of a small BCG scar other 3 months, BCG should be repeated
General public health measures aimed at improving hygiene, housing and nutrition.
N.B Investigate the family in each case of tuberculosis
Contact tracing is the key to the control and prevention of Tb
BCG, good nutrition (food) and hygiene do help to prevent Tb
The diagnosis of pulmonary Tb is most difficult when you need it most, in acutely ill
marasmic children
7.1.5 Providing care for a child with foreign body aspiration
Foreign bodies are frequently inhaled by children and may lodge in the nose, larynx, trachea
or the bronchus
The symptoms and clinical features will vary depending on the
Nature of the foreign body
Size of the foreign body and
Site of the obstruction
Most victims of foreign body aspiration are older infants and toddlers
189
Children younger than 3 years of age account for 73% of cases
Etiology One-third of aspirated objects are nuts, particularly
Fragments of raw carrot, apple, dried beans, popcorn and sunflower or watermelon seeds
are also common etiology
C/M A positive history must never be ignored
A negative history may be misleading
Chocking or coughing episodes accompanied by wheezing are highly suggestive of an
airway foreign body
Complete airway obstruction is recognized in the conscious child as sudden respiratory
distress followed by inability to speak or cough
Three stages of symptoms result from aspiration of an object into the airway
1) Initial Event Violent paroxysms of coughing, choking gagging and possibly airway
obstruction occur immediately when the foreign body is aspirated
2) Asymptomatic interval
The foreign body becomes lodged, reflexes fatigue, and the immediate irritating symptoms
subside
Most treacherous and accounts for a large percentage of delayed diagnoses and overlooked
foreign bodies
The health worker may minimize the possibility of a foreign body accident, being reassured
by the absence of symptoms that no foreign body is present
3) Complications
In this third stage, obstruction, erosion or infection develops to again direct attention to the
presence of a foreign body
Complications include fever, cough, hemoptysis, pneumonia and Atelectasis
Rx- The treatment of choice for airway foreign bodies is prompt endoscopic removal with rigid
instrument
190
Airway foreign bodies are usually removed the same day the diagnosis is first considered
Try to open the airway with the head-tilt/chin lift manoeuvre, and attempt ventilation
Use a combination of five back blows and five chest thrust are administered in the in the
infants younger than 1 year
Administer aseries of five abdominal thrust with a child standing or sitting for a conscious
child older than 1 year
If unconscious, this is done with the child lying down
A- Foreign bodies in the Nose
Foreign bodies of the nose are quite commonly encountered
The foreign bodies are impacted in the lower part of the nose (they are anteriorly impacted)
S/S Pain, and chronic purulent discharge
Unilateral nasal obstruction
There may be unilateral epistaxis
Mgt Gently placed small piece of cotton wool soaked in lignocaine with a drenaline in the nostrile
Try to remove gently by means of a small hook or nasal forceps
If the above is failed, refer the child immediately to hospital for removal with adequate
equipment
Always work under direct vision with the otoscope and never ty just to poke in the nose
blindly
B- Laryngeal Foreign bodies
A foreign bodies in larynx will cause sever inspiratory stridor
Complete obstruction asphyxiates the child unless promptly relieved with the Heimlich
maneuver
Objects that are partially obstructive are usually flat and thin
Lodge b/n the vocal cords in the saggital plane
S/S- Inspiratory stridor
Symptoms of croup
191
Hoarseness, cough and dyspnea
Mgt Turn the child upside down while firmly squeezing the chest
Then quickly inspect the mouth for foreign body large enough to be simply removed with
forceps
If the above method fails and the child is desperately dyspnoeic, have another try to remove
the foreign body with fingers or forceps
If possible, transfer to hospital for laryngoscopy
C- Tracheal Foreign bodies
Foreign body in the trachea may cause choking and aspiration in 90% of pts.
Stridor in 60% and wheezing in 50% of pts
Posteroanterior and lateral soft tissue neck radiographs (airway films) are abnormal in 92%
of children
Chest radiography are abnormal in only 58% of children
D- Bronchial Foreign bodies
Posteroanterior and lateral chest radiographs are indicated for the assessment of infants and
children suspected of having aspirated a foreing body
During expiration the bronchial foreign body obstructs the exit of air from the obstructed
lung, producing obstructive emphysema with persistent inflation of the obstructed lung.
Shift of the mediastinum toward the opposite side
Air traping is an immediate complication, in contrast to Atelectasis, which is a late finding
N.B- Foreign body must be suspected in all acute and chronic pulmonary lesions causing
Atelectasis, and obstructive emphysema, regardless of the Hx of foreign body aspiration
Laryngoscopic and Bronchoscopic examination are necessary for definite diagnosis and
treatment where the foreign body is removed
Simple advice on safety procedures, storage of small articles may prevent many of foreign
body aspiration accidents.
7.1.6Providing care a child with Bronchial Asthma
192
The term Asthma is used to describe a widespread narrowing of the air passages due to
spasm of the muscular walls and swelling of the mucous membrane
Asthma is a chronic inflammatory condition of the lung airways resulting in episodic
airflow obstruction
Etiology- Asthma is caused by various stimuli (Foreign protein called Allergens, to which the
becomes sensitized)
Viral respiratory infection
Vigorous exercise producing ed respiratory rate and depth
Cold air, smoke and emotional stress
Parasitic larvae travelling through the lungs
Pathophysiology
Normally the air passages should be intact for free exchange of gases
In Asthma, there is an intermittent airway obstruction as aresult of complicated interactions
b/n allergy, infection, emotional and environmental factors; causing
Over-reaction of the airways
Bronchospasm and
Obstruction to the passage of air through swelling of the smaller bronchi
Broncho constriction of the bronchiolar muscular bands restricts or blocks airflow
A cellular inflammatory infiltrate and other inflammatory cell types can fill the airways and
induce epithelial damage and desqamation into the airways lumen
Excess production of mucus into the airways and edema of the surrounding
tissues also contribute to blockage of airways
Asthmatic airways tissues have increased number of mast cells, activated Eosinophils and
activated helper T.lymphocytes
Helper Tlymphocytes produce proallergic and proinflammatory cytokines and
chemokines which mediates the inflammatory process
Airway inflammation is strongly linked to hypersensivity of airways smooth muscles
Airways hyperresponsiveness to irritant exposure
193
It also linked to less reversible airways changes:- Basement membrane thickening
Subepithelial collagen deposition
Smooth muscle and mucus gland hyper throphy and hyperplesia
Remodelling abnormality
Airflow obstruction during asthma exacerbations can become extensive, resulting life-
threatening respiratory insufficiency
Generally the pathogenesis of Asthma includes
1- Airways obstruction
2- Airways Inflammation, Hyperresponsiveness and Remodeling
3- Progression of sever asthma exacerbations
C/M Intermittent dry coughing and/or Expiratory wheezing are the most common chronic
symptoms of asthma
Older children and adult complain of shortness of breath and chest-tightness
Young children report intermittent, nonfocal chest pain
There may be marked intercostals and subcostal indrawing or recession
Respiratory symptoms are characteristically worse at night, especially during
prolonged exacerbations triggered by respiratory infections or inhalant allergen
Dx- Medical Hx. C/M, PE
Mgt The goals of childhood Asthma Mgt includes
Maintaining normal activity
Regular school or daycare attendance
Full participation in physical exercise, athletics and other recreational activities
Prevent sleep disturbance
Prevent chronic Asthma symptoms
Keep asthma exacerbation from becoming worse/severe/
Maintain normal lung function
Experience little to no adverse effects of treatment
194
Four components of optimal Asthma Mgt
1- Regular Assessment and monitoring
2- Control of factors contributing to Asthma severity
3- Asthma pharmacotherapy
4- Patient Education
7.2- Caring for a child with GIT and Metabolic disorders
7.2.1Managing intussueception
Defn- Intussuception is an invagination of asegment of a bowel into an adjoining and usually lower
segment
Occurs when a portion of the alimentary tract is telescoped into an adjacent segment
It is the most common caused of intestinal obstruction b/n 3mong and 6years of age
60% of patients are younger than 1 year, and 80% of the cases occur before 24 months
it is rare in neonates
Etiology The causes of most intussuscoptions is unknown
Meckers diverticulum, polyp, nodules of ectopic pancrease, reduplication of gut,
lymphoma may serve as alead point for intussusception
Intrauterine intussusception is associated with the development of intestinal atresia
Pathology- Intussusceptions are most often ileocolic and ileoileocolic, less commonly cecocolic,
and rarely exclusively ileal
The upper portion of bowel, the intussusceptum, invaginates into the lower, the
intussuscipiens, dragging its mesentery along with it into the enveloping loop
Constriction of the mesentery obstructs venous return; engorgement of the intussusceptum
follows, with edema and bleeding from the mucosa leads to abloody stool, sometimes
containing mucus
The apex of the intussusception may extend into the transverse, descending, or sigmoid
colon, even to and through the anus in neglected cases
This presentation must be distinguished form rectal prolapse
195
Most intussusceptions do not strangulate the bowel with in the 1
st
-24 hours, but may later
enventvate in intestinal gangrene and shock
C/M Sever paroxysmal colicky pain that recurs at frequent intervals
Straining effort with legs and knees flexed and loud cries
The infant becomes progressively weaker and lethargic
Shocklike state with fever
Weak and thready pulse and shallow and grunting respiration
Vomiting, failure to pass stool and flatus
Abdominal distension and passage of blood and mucus in stool (60% of infants pass a stool
containing RBC and mucus= The currant jelly stool)
Sausage shaped mass on abdominal palpation most often in the Rt upper quadrant of the
abdomen
Dx- Clinical Hx and physical findings
Plain Abdominal radiographs may show a density in the area of Intussuception
Barium enema shows an inverted cap and an obstruction to the further progress of the
barium
Ultrasonography is a sensitive diagnostic tool in the diagnosis of intussusceptions
Mgt Reduction of an acute intussusception is an emergency procedure and performed
immediately other diagnosis in preparation for possible surgery
This is done by gentl administration of Barium enema
If manual operative reduction is impossible or the bowel is not viable, resection of the
intussusception is necessary, with end to- end anastomosis
N.B Reduction should not be attempted in pts. with prolonged intussusception with signs of :
Shock
Peritoneal irritation
Intestinal perforation or
Pneumatosis intestinalis
Prognosis Untreated Intussuception in infants is always fatal
196
The chances of recovery are directly related to the duration of intussusception before
reduction
Most infants recover if the intussusception is reduced with in the first 24 hours
The mortality rate rises after 24hr, especially other the second (2
nd
) day
Complications of Intussuception include:
Intestinal perforation
Peritonitis and shock
Death
The longer the delay before the treatment, the higher the mortality rate.
7.2.2 Providing care for a child with hernia
7.2.3Providing care for a child with appendicitis
Acute Appendicitis is the most common condition requiring emergency
abdominal operation in childhood
It is the main causes of acute abdomen in children
Among children presenting with abdominal pain, 36% can be expected to have acute
appendicitis
Acute- Appendicitis in children has to be distinguished from the adult disorder by its
Rapid course
Variability of symptoms and
Rapid recovery on proper medical and surgical treatment
It occurs in all age groups, most common during later child hood and early adult life
Distinctly rare in infants below the age of two years
Etiology Clinically, obstruction of the lumen is the prime cause of Appendicitis
197
Obstruction of the lumen is caused by
Inspissated fecal material (Fecalith)
Obstruction resulting from mucosal edema may be associated with systemic or enteric viral
or bacteria infections
Abnormal mucus has been suggested as the cause of increased incidence of appendicitis, in
children with cystic fibrosis
Carcinoid tumours, foreign bodies and Ascaris have rarely been implicated as a cause of
appendicitis
Pathophysiology
Experimentally, ligation (obstruction) of the appendix result in a marked increase of
intraluminal pressure, which rapidly exceeds systolic blood pressure
The pathologic changes in appendicitis progress through three predictable phases
1- Luminal obstruction, venous congestion progress to mucosal ischemia, necrosis and
ulceration
2- Bacterial invasion with inflammatory infiltrate through all layers of the appendiceal wall
- Organisms can be cultured from the serosal surface before microscopic
perforation
3- Perforation and contamination of the peritoneum
- The perforation usually occurs at the tip of the appendix, distal to the obstructing
fecalith
Subsequent to perforation, the microbiologic fecal contamination may be confined to the
pelvs or the right iliac fossa by the:
Omentum and adjacent loops of small bowel
Spread or throughout the peritoneal cauity
Young children have a poorly developed omentum, and local perforation is not usually
confined
Bacterial invasion of the mesenteric veins may result in portal vein sepsis (pylephlebits)
and subsequent liver abscess formation
198
The inflammatory process associated with perforation may lead to intestinal obstruction or
paralytic ileus.
C/M- The clinical s/s depend on the pathologic phases of appendicitis at examination
The classic triad s/s of appendicitis consists of: Pain, Nausea with vomiting and Fever.
Anorexia is more common
The sequence of symptoms with pain preceding emesis and fever is important in
distinguishing appendicitis from infectious enteritis, which usually begins with vomiting
followed by the cramping pain of hyperperistalsis
Infrequent small and mucoid stools (diarrhea)
Vrgency and frequency of urination
The initial periumblical pain migrates to the area of peritoneal irritation Right lower
quadrant of the Abdomen
Generalized pain if there is perforation
Discrete abscess at the right lower quadrant when the contamination is well localized
Palpation of an abdominal or rectal mass indicates abscess formation
The progression from onset of symptoms to perforation usually occurs over 36-48 hrs
If diagnosis is delayed beyond 36-48 hr, the perforation rate exceeds 65%
The following are pertinent (key) aspects of the history favouring a diagnosis os
appendicitis
Onset of pain before vomiting or diarrhea
Loss of appetite
Migration of pain from periumblical to RLQ
Aggravation of pain during walking
Dx- Bsed on C/M, PE and HX
Laboratory findings CBC 30 WBC/HPF
20 RBC/HPF
199
U/A- Bacteria or pyuria greater than 30 WBC/HPE
Imaging studies
Plain radiographs of the abdomen
Ultrasonography
CT-Scan
Compliations Complications occur in 25-30% of children with appendicitis
Appendiceal perforation
Peritonitis (local or generalized)
Portal vein sepsis (pylephlebitis)
Wound infection
Multiple intra-abdominal abscess
Liver abscess
Intestinal obstruction and paralytic ileus
Infertility due to adhesions or obstruction of the distal fallopian tube (especially other
perforation)
Most of the above complications are 2
nd
ry to perforation fo the appendix
Mgt IV-fluids and antibiotic for nonperforated appendix
IV- morphine to manage pain
Fluid resuscitation and broad-spectrum antibiotics a few hours before appendectomy in case
of perforation
Nasogastric suction if the pt has significant vomiting or abdominal distention
Appendectomy should be done with in a few hours of establishing the diagnosis
Performed through a right lower quadrant incision
Laparascopic appendectomy has been used in children
Appendectomy for non-perforated appendicitis is associated with:- A low complication rate
Rapid Recovery and
Short Hospitalization (2-3 days)
200
Appropriate preoperative and postoperative Nursing care
1- Caring a child with pyloric stenosis
Pyloric stenosis is the narrowing or stricture of the pyloric sphinicter (gastric outlet)
This disorder occurs mostly in body, most commonly form the age of 2 Wks up to 3 months
The condition first causes spasm and later hypertrophy of the pyloric muscle
The offspring of a mother and to alesser extent the father who had pyloric stenosis are at a
higher risk for pyloric stenosis
It develops approximately 20% of thealse and 10% of the female descendants of a mother
who had pyloric stenosis
The incidence of pyloric stenosis is ed in infants with type B and E blood groups
It is usually associated with other congenital defects eg. Tracheoesophageal fistula
Etiology- The cause of pyloric stenosis is unknown, but many factors have be implicated
More concordant in monozygotic than dizygotic twins (Genetic factor)
Abnormal muscle innervations
Elevated serum levels of prostaglandins
Reduced pyloric nitric oxide synthase etc..
C/M The spasm and hypertrophy of the pyloric muscle results in stenosis or narrowing of the
gastric outlet. This inturn results in the inability of the stomach to empty its content properly
Non- bilious vomiting is the initial symptiom
The vomiting may or may not be projectile initially but is usually progressive occurring
immediately after a feeding
The infants is hungry and wants to feed/suck well/ after vomiting
The vomiting consists of gastric contents only and may be blood stained, but never bile
stained
Prominent peristaltic movements of the contracting stomach
- Originate in left upper Quadrant and progress to and beyond the midline
201
Olive shape tumor is felt in the upper abdomen (epigastrium) Just lateral to the right rectus
muscle in 70-90% of cases
Jaundice with hyperbilirubinemia has been found in approximately 5% of affected infants
Loss of weight and signs dehydration
Failure to thrive, constipation
Malnutrition, especially s/s of marasmus
Dx- Based on Hx, C/M and PE.
Palpating pyloric mass
Firm, movable, olive shaped, hard, approximately 2cm in length
- Best palpated from the left side and located above and to the Rt of the umbilicus
Ultrasonography confirms the diagnosis in the majority of cases (95% sensitivity)
Mgt - Preoperatively
Correction of fluid, acid-base and electrolyte losses
IV-fluid therapy with the addition of potassivm chloride (Rehydration can be successfully
takes place with in 24 hours)
Preoperative correction of alkalosis is essential to prevent post operative apnea, which may
be associated with anesthesia
Ramstedt pyloromyotomy is the surgical procedure of choice for the surgical mgt of p.stenosis
The procedure is performed through a short transverse incision or laparoscopically
Postoperatively
Vomiting may occur in half the infants and is thought to be 2
0
to edema of the pylorus at the
incision site
Initiate feeding with in 12-24 hours other surgery and advanced to maintenance oral feeding
with in 36-48 hrs of surgery
Persistent vomiting postoperatively, suggests:
- Incomplete pyloromyotomy
- Gastritis
- Gastroesophageal reflux disease or
202
- Another cause of the obstruction
7.2.4 .Caring a child with Diabetes Mellitus
Df
n
- Diabetes mellitus (DM) is a common, chronic metabolic syndrome characterized by
hyperglycemia as a cardinal biochemical feature
Types/classification of DM
The major forms of diabetes are divided into two
1- Type-1 DM: It is caused by deficiency of insulin secretion due to pancreatic B-cell damage
2- Type -2 DM- This is due to a consequence of insulin resistance occurring at the level of
skeletal muscle, liver and adipose tissue, with various degrees of B-Cell impairment
3- Other specific types of secondary DM
This includes the following
Genetic defect of B-cell function
Genetic defects in insulin action
Disease of the exocrine pancrease
Endocrinopathies
Drug or chemical induced etc..
Type -1 Diabetus Mellitus
- Is the most common endocrine metabolic disorder of childhood and adolescence
- Individuals with type -1 DM confronts serious lifestyle alterations that include
An absolute daily requirement for exogenous insulin
The need to monitor their own glucose control
The need to pay attention to dietary intake
- Morbidity and mortality stem from Acute metabolic derangements and from long-
term complications
Formerly called IDDM or Juvenile diabetes
Characterized by low or absent levels of endogenously produced insulin
203
Depends on exogenous insulin to prevent development of Ketoacidosis
- An acute life-threatening complication of type -1 DM
The onset occurs predominantly in childhood, with median age of 7 to 15 years, but it may
present at any age
Is characterized by autoimmune destruction of pancreatic islet B-cells
Bothe genetic susceptibility and environmental factors contribute to the pathogenesis of
type -1 DM
E.g. Major histocompatrability complex (MHC) class II gene expressing human leukocyte
antigens (HLAS)
Type -2 Diabetus Mellitus
Usually common in obese children or/and adolescents
Is not insulin dependent (NIDDM) and infrequently develop ketosis
This category includes the most prevalent form of diabetes in adults, which is characterized
by insulin resistance and often a progressive defect in insulin secretion
Formerly known as Adult-onset diabetes mellitus
Non-insulin dependent diabetes mellitus
Or - maturity-onset diabetes of the young
Is more insidious than that of type-1 DM
The incidence of type -2 DM in children has ed by more than 10-fold in many diabetes
centres, in part as a result of epidemic childhood obesity
Paediatric type -2 DM may account for as many as 30% of the new cases of diabetes
In MODY, there is no apparent autoimmune destruction of B-cell and no association with
HLAS.
This subclass of type -2 DM consists of specific genetic disorders involving mutations in
the gene encoding pancreatic B-cell and liver glucokinase or in the nuclear transcription
factors
Hepatocyte nuclear factor (HNF) -4 or
Hepatic nuclear factor (HNF) -1
204
Defect in the gene regulating glucose transport into pancreas B-cell, defect in glycogen
synthase, and insulin reseptor and a possibly apoliporotein C-III.
Pathophyiology Type -1- DM
Insulin performs a critical role in the storage and retrieval of cellular fuel
Its secretion in response to feeding is exquisitely modulated by the interplay of neural,
hormonal and substrate-related mechanisms to permit controlled predisposition of ingested
foodstuffs as energy for immediate or future use
In type -1- DM, there is a progressive low-insulin catabolic state in which feeding does not
reverse, but rather exaggerates these catabolic process
Glucose utilization by muscle and fat decreases and postprandial hyperglycemia appears
At lower insulin level, the liver produces excessive glucose via:
Glycogenolysis and fasting hyperglycemia begins
Gluconeogenesis
Hyperglycemia produces an osmotic diuresis (glucosuria) when the renal threshold is
exceeded 180mg/dl or 10 mmol/litre
The resulting loss of calories and electrolytes as well as the persistent dehydration, produce
a physiologic stress with hypersecretion of stress hormones
Epinephrine, cortisol, growth hormone, and glucagons
These hormones inturn contribute to the metabolic decomponsation by further impairing
insulin secretion (Epinephrine), by antagonizing its action (epinephrine, cortisol and growth
hormone), and by promoing glycogenolysis, gluconeogenesis, lipolysis and ketogenesis
(glucagons, epinephrine, growth hormone, and cortisol), while decreasing glucose
utilization and glucose clearance (epinephrine, growth hormone and cortisol)
The combination of insulin deficiency and elevated plasma values of the counter-regulatory
hormone is also responsible for accelerated lipolysis and impaired lipid synthesis
ed plasma concentration of total lipid, cholesterol, triglycerides, and free
fatty acids
formation of ketonbodies (B-hydroxybutyrate and acetoacetate)
205
metabolic acidosis (DKA) and compensatory rapid deep breathing in attempt
to excrete excess Co2 (kussmaul respiration)
fruity odor of the breath due to conversion of acetoacetate to Acetone
Ketones are excreted in the urine in association with cations and thus further es losses of
water and electrolytes
Because of progressive dehydration, acidosis, hperosmolality and diminished cerebral
oxygen utilization, consciousness become impaired, and the patient ultimately become
comatose.
C/M- Polyuria, polydipsia and hyperphagia
Female pts may develop monilial vaginitis
Loss of body fat (Wt. loss and diminished subcutaneous fat)
Signs and symptoms of ketoacidosis
Abdominal discomfort, N/V
Dehydration S/S
Kussmalul respiration (deep, heavyrapid breathing)
Fruity breath odor (Acetone)
Diminished neurological function, and possible coma
About 20 40% of children with new-onset diabetes progress to DKA before diagnosis
In infants, most of the wt loss is a cute water loss
In adolescents, the course is usually more prolonged (over months)
Most of the wt. loss represents fat loss due to prolonged starvation
But additional wt. loss due to acute water loss may occur before diagnosis
N-B- In any child, the progression of symptoms may be accelerated by the stress of an intercurrent
illness or trauma
Counter- regulatory (stress) hormones overwhelm the limited insulin secretary
capacity
206
Dx- The diagnosis of type -1 DM is usually straight forward if considered in the differential
diagnosis
Non- fasting blood glucose greater than 200 mg/dl (11.1 mmol/l) with typical
symptom is diagnostic with or without ketonuria
Fasting blood glucose that exceeds 126 mg/dl (7.0 mm) is accepted criteria for
diagnosing diabetes
+ Symptoms of DM (polyuria, polydipsia, unexplanined wt. loss with glucosuria
and ketonuria plus RBS> 200mg/dl or
+ FBS > 126 mg/dl or
+ 2 hour plasma glucose during the OGTT > 200 mg/dl
Mgt The excellent diabetes control involves many goals
To maintain a balance b/n tight glucose control and avoiding hypoglycemia
To eliminate polyuria and nocturia
To prevent the development of DKA
To permit normal growth and development with minimal effect on lifestyle
+ The therapy encompasses
Initiation and adjustment of insulin
Extensive teaching of the child and caretakers and
Re-establishing the routine of life
In acute phase, the family must learn the Basics, which includes:
Monitoring the childs blood glucose and urine ketones
Preparing and injecting the correct insulin dose subcutaneously at the proper time
Recognizing and treating low blood glucose reactions
Having a basic meal plan
7.2.5Caring for a child with Iodine deficiency
Iodine Is a chemical element and is essential in nutrition
207
Is necessary for the synthesis of the thyroid hormones thyroxine and triiodothyronine
Iodine Deficiency- Is lack of shortage; a condition characterized by presence of less than normal a
mount of iodine in the body.
- Leads to low thyroid hormone level
Iodine deficiency (Endemic goiter) is the most common cause of congenital hypothyrodism
world wide
Border line iodine deficiency is more likely to cause problems infants who depend on a
maternal source of iodine
- Lack of thyroid hormones damages the proper growth and development of the body and
brain
The earlier in life it occurs, the more serious and long-lasting are the effects
The most serious effects of iodine deficiency occure during fetal life, causing cretinism
Less sever iodine deficiency leads to mildereffect later in the childs life, producing
Hypothyrodism (child hood myxoedema)
Reduced growth and activity; mental slowness of the child
ed/lack of Thyroid hormone- Enlargement of the thyroid gland
low level thyroid hormones in the blood pituitary gland (TSH) stimulates the thyroid
gland to grow bigger in order to make more thyroid hormones from little iodine being
supplied to it.
Etiolog Lack of iodine in the diet (especially during growth) Iodine Deficiency
Some goitrogen chemicals in the soils that interfere the absorption and use of iodine in the
body
C/M Most infants with congenital hypothyrodism are asymptomatic at birth
Low serum levels of T4 and elevated level of TSH, makes possible to screen and detect
hypothyroid neonates
Head size may be slightly increased b/c of myxedema of the brain
Prolongation of physiologic icterus, due to delayed maturation of glucuronide conjugation
208
Feeding difficulties, especially sluggishness, lack of interest, somnolence and choking
spells during nursing
Respiratiory difficulties, due in part to the large tangue
Little cry, much sleep, poor appetites and constipation
- Large abdomen, umblical hernia may be present
- Subnormal body temperature (less than 35
0
c)
- Cold and mttled skin, particularly that of the extremities
- Edema of the genitals and extremities may be present
- Slow pulse, heart murmurs, cardiomegally and asymptomatic pericardial effusion
- Stunted growth, short extremities, widely opened anterior and posterior fontanels
- The eyes appear far apart and the bridge of the broad nose is depressed
Mouth is kept open and the thick and broad tangue protrude from it
Short and thick neck
Deposits of fat above the clavicle, b/n neck and shoulders
Broad hands and short fingers
Thickened scalp, coarse, brittle, and scanty hair
Retarded devt, lethargic, late in learning to sit and stand
Hoarseness of voice, do not learn to talk
Hypotonic muscle; delayed sexual maturation or absence
Retarded physical and mental growth and development
Dx- Based on C/M, Hx and PE
Laboratory findings
Serum T4 and TSH level
X-ray of the bone to assess osseous devt
Ultrasonograpy and ECG
Rx- Sodium L- thyroxine given orally is the treatment of choice
Because 80% of circulating T3 is formed by monodeiodination of T4
209
Removal of the thyroid gland (Thyroidectomy)
Prevention Iodine deficiency can be completely prevented by increasing iodine intake through
adding iodine to salt (salt iodization) or
Orall mass dosing with iodized oil annually or
In high- risk areas, injecting long-acting iodized oil twice yearly
Individual cases of goiter or hypothyroidism, both iodine supplementation and treatment
with thyroid hormones are needed
Iodization of local drinking water.
7.3- Care of a child with GUS Disorders
Diagnostic and Therapeutic procedures of GUS
A- Urine Analysis
The best urine for examination is that while comes shortly after starting Midstream urine
UTI may be suspected based on the symptoms or findings on U/A or both
Pyuria (Leukocytes in the urine) suggests infection, but infection can occur in the absence
of pyuria
Nitrites and leukocyte esterase are usually positive in infected urine
Microscopic hematuria is common in acute cystitis
WBC casts in the urinary sediment suggests renal involvement, but these are rarely
seen
With a cute renal infection
Leucocytosis
Neutrophilia and
Elevated ESR and C-reactive protein are common
With renal abscess, the WBC count > 20,000 to 25,000/mm3
Generally U/A includes the following:
Volume, reaction and concentration of normal constituents
210
Specific gravity
Presence of abnormal constituents E.g. albumin, sugar, casts, blood cells etc
B- Blood Tests ( BUN, Serum creatinine and uric acid)
Urea, which is the chief end product of nitrogen metabolism is completely filtered in the
glmerulus and reabsorb at the proximal and distal parts depending up on water reabsorption
at these sites.
There may be disproportionate increase in the BUN 2
0
to ed passive reabsorption of urea in
the proximal tuble due to appropriate renal conservation of Na and H20
Creatinine freely filtered at glomerulus and secreted in the proximal tubule
A significant elevation of the creatinine concentration suggests renal insufficiency
The serum creatinine level is primarily influenced by the level of glomerular function
The baseline normal creatinine concentration increase with age E.g. A normal a dult
creatinine concentration of 1mg/dl may indicate significant renal insufficiency in na infant
+ BUN and creatinine concentration are dependent on the timing of the disease process
Urea and creatinine are waste products that build up gradually with ed renal excretion
Uric Acid- is the end product of purine metabolism that completely filtered and actively
reabsorbed
The renal excretion of uric acid involves the following components:
Glomerular filtration
Reabsorption in the proximal convoluted tuble
Secretion near the terminus of proximal tuble
Limited reabsorption near these secretary sites
Uric acid is poorly soluble and must be excreted continuously to a void toxic accumulation
in the body
In renal insufficiency, the serum uric acid level increases markedly
Blood tests (analysis) helps to assess the serum concentration of BUN, uric acid and
creatinine
211
C- Radiographic studies
IVP (intravenous pyelogram) is ordered to help identify or diagnose problems in kidney
function
A contrast medium is injected intravenously and roentgenograms are taken at 5,10 and 15
minutes intervals other injection to determine integrity of kidneys, ureters, and bladder
Preparation includes
Laxatives
With holding solid foods
Cleansing enema
Renal Angiography- Roentgenography of the blood vessels of the kidneys after introduction
of a contrast medium is another diagnostic study
D- Renal Biopsy
Is a valuable tool in the evaluation of the his lological changes in different diseases E.g.
Nephrotic syndrome
Contraindications of Renal biopsy include
Bleeding disorders
Tumours
Single kidney
Infection and very low general condition of the child
E- CT- scan
CT of the abdomen and pelvis provides an excellent method of demonstrating whether a
calculus (calculi) is present, its location and whether there is significant proximal
hydronephrosis
F- Purposes of Diagnostic and therapeutic procedures
To identify abnormal values that may indicate impaired renal function
To help the recognition of the specific site of the tissue or organ affected
To determine the normal function of the urinary system
212
To diagnose or know the problem of specific structure or organ
For therapeutic purpose
The nursing responsibility is explaining the procedure to the client; and
Giving appropriate care
Assisting during the procedure
Observation and mgt of complication
Assisting A child with GU Disorder
A- Brief Review of Anatomy and physiology
The kidney liel in the retroperitoneal space sligntly above the level of the umbilicus
The kidney has an outer layer, the cortex, which contains the glomeruli, proximal and distal
convoluted tubles and collecting ducts; and an inner layer, the medulla, which contains the
straighr portions of the tubles, the loops of henle, the vaserecta and the terminal collecting
ducts
Blood supply to each kidney usually consists of a main renal artery that arises from the aort
+ Descending Aorta- Renal Artery- segmental branches- Interlobar artery- Arcuate arteries-
Interlobular arteries Afferent arterioles of the glomeruli glomerular capillary network
efferent arterioles
- Each kidney contains approximately 1 million nephrones (glomeruli and associated tubules)
- Because new nephrones can not be formed other birth, progressive loss of nephrones may
lead to renal insufficiency
The glomerular network of specialized capillary ies serve as the filtering mechanism of the
kidney
Function of Kidneys
1- Regulation of body fluid volume and osmolality
2- Regulation of electrolyte balance
3- Regulation of Acid-Base balance
4- Excretion of metabolic waste products, toxins and foreign substances
5- Production and secretion of hormones
213
6- B/P regulation and RBC production as a result of the above functions
7.3.1Giving care for a child with UTI
UTI is an infection of the urinary tract or urinary system and include both lower and upper
urinary tract
- The infection may mainly affect the lower urinary tract (urethra and bladder), especially in
girls
- A lower UTI can spread upward into the ureters and kidneys if not treated properly
- The infection may be also spread to the kidneys through the blood stream
UTIS occur 3-5% of girls and 1% of boys
Risk Factors facilitating UTI
- Female
- Uncircumcised male
- Vesicoureteral reflux
- Toilet training
- Voiding dysfunction
- Obstructive uropathy
- Urethral instrumentation
- Wiping from back to front
- Tight clothing (underwear)
- Pregnancy and sexual activity
Etiology
UTIS are caused mainly by colonic bacteria
In females 75-90% of all infections are caused by Escherichia coli, Followed by Klebsiella
and proteus
Some series report that in males older than 1 year of age, proteus is as common as E.coli
Staphylococcus saprophyticus and adenovirus
- UTIS have been considered an important risk factor for the devt of renal insufficiency or
End-stage renal disease.
214
Clinical manifestation and Classification of UTIS
There are there basic forms of UTI
1- Pyelonephritis It is characterized by any or all of the following
Abdominal or flank pain
Fever
Malaise
Nausea/vomiting
Occasionally diarrhea
Some newborns and infants may show non-specific symptoms such as:
Jaundice
Poor feeding
Irritability and
Weight loss
Indicates bacterial involvement of the upper UT
Involvement of the renal parenchyma is termed acute pyelonephritis, where as if
there is no parenchyma involvement, the condition may be termed pyelitis
- Acute pyelonephritis may result in renal injury, which is termed pyelonephritic
scarring
2- Cystitis Indicates that there is bladder involvement and symptoms include
Dysuria
Urgency
Frequency
Suprapubic pain
Incontinence
Malodorous urine
+ Cystitis does not cause fever, and does not result in renal injury
215
3- Asymptomatic Bacteriuria Refers to individuals who have a positive urine culture with out
any manifestations of infection
Occurs almost exclusively in girls
It is benign and does not cause renal in ury, except in pregnant women
Pathogenesis and pathology
Nearly all UTIS are ascending infections
The bacteria arises from the fecal flora, colonize the perineum and enter the bladder via the
urethra
In uncircumcised boys, the bacterial pathogens arise from the flora beneath the prepuce
In some cases, the bacteria ascend to the kidney to cause pyelonephritis
- Renal infection may occur by hematogenous spread rarely
An infected urine then stimulates an immunologic and inflammatory response
- The result may cause renal injury and scaring
The pathogenesis of UTI is based in part on the presence of bacterial pili or fimbriae on the
bacterial surface
Glycosphingolipid that is present on both uroepithelial cell membrane and RBS helps as
areceptor for Type-II fimbriae
Bacteria with P-fimbriae are more likely to cause pyelonephritis
Between 7694% of pyelonephritogenic strains of E.coli have p-fimbriae, compared with
19-23% of cystitis strains
Xanthogranulomatous pyelonephritis is a rare type of infection characterized by
granulomatous inflammation with giant cells and foamy histiocytes
Dx- A UTI may be suspected based on the symptoms or findings on urinalysis, or both
Urine culture is necessary for confirmation and appropriate therapy
The diagnosis of UTI depends on having the proper sample of urine
Rx- Acute cystitis should be treated promptly to prevent its possible progression to pyelonephritis
Cotrimoxazole 3 to 5 days is effective against most strains of E.coli. (Before the result of
(Before the result of culture)
216
Nitrofurantoin 5-7 mg/24 in three to four divided doses
- Effective against Klebsiella Entrobacter organisms
Amoxicillin 50 mg/kg 124 hr is also effective as initial treatment
In acute febrile infections suggestive of pyelonephritis, a 14-day course of broad-spectrum
antibiotics capable of reaching significant tissue levels is preferable
Parenteral Rx with ciftriaxone 50-75 mg/kg/24 hour, not to exceed 2gm or
Ampcillin 100mg/kg/24hr with an amino glycosides (eg. Gentamycine 3-5 mg/kg/45hr)
Do not use Nitrofurantion in children with a febrile UTI, because it does not achieve
significant renal tissue levels
Use ciprofloxacin for resistant micro-organisms, particularly pseudomonas, in patients older
than 17 yrs and
Younger children with cystic fibrosis and pulmonary infection 2
0
to pseudomonas
7.3.2Giving care for a child with AGN
A cute glomerulonephritis is a disease mainly affecting the children of school-age and is
uncommon below three years.
Acute poststreptococcal glomerulonephritis (APSGN) is an acute, self-imimiing
autoimmune disease that follows group A-betahemolytic streptococcal infection
Etiology ANG is secondary to URT or/and skin infection caused by group A-betahemolytic
streptococcal infection
Antigen- antibody complex interaction
Pathophysiology
The onset of AGN commonly occur with in 7-14 days after antecedent infection
Some theory states that streptococcal infection is followed by release of a membrane like
substance from the specific organism, which is antigenic in nature
In immune complex- mediated diseases, antibody is produced against that is usually
unrelated to the kidney
The immune-complexes accumulate /lodge/ in glomeruli and activate the complement
system leading to inflammation and obstruction
217
Subsequent decreased glomerular filtration and tissue injury
Results excretion of RBC and casts
The inflammatory reaction that follows immunology injury results from activation of one or
more mediators pathways. The most important of these is the complement system, which
has two initiating sequences
1- The classic pathway, which is activated by antigen-antibody immune complexes
2- The Alternative or properdin pathway , which is activated by polysaccharides and
endotoxins
These pathways converge at C3, from that point on, the same sequence leads to lysis of cell
membrane
The major noxious products of complement activation are produced after activation of C3
and includes
Anaphylatoxin which stimulates the contractile proteins with in vascular walls and increases
vascular permeability
Chemotactic factors (C5a), that direct Neutrophils and perhaps macrophages to the site of
complement activation, where the cells release substances that damage vascular cells and
basement membrane
Kidneys enlarged, and sodium and water are retained leading to edema
Protein is also excreted in urine
C/M Hematuria resembling tea or cola
Oliguria
Pallor
Fatigue, lethargy
Weight gain
Irritability
Periorbital and generalized edema
Mild to moderately elevated B/P
Dx- Hx, C/M, and physical examination
218
Laboratory investigation
U/A Presence of protein
RBC, WBC and casts
Increased urine specific gravity
Other Laboratory study data
Mild anemia (mildnormochromic anemia)
Leucocytosis
Positive anti-streptolysin O titer
Elevated ESR, BUN and creatinine levels
Reduced serum C3 levels
Complications Acute complications of this disease result primarily from hypertension and Acute
renal dysfunction
Hypertensive encephalopathy
Pulmonary edema
Heart failure
Acute renal failure
Hyperkalemia, hyperphosphatemia and hypocalcem
Acidosis, seizure and uremia
Signs and symptoms that show the impending complications includes
Marked elevation of B/P, headache, dizziness, abdominal discomfort and vomiting
Altered LOC possibly progressing to seizure - Hypertensive encephalopathy
Coughing, restlessness, paroxysmal noctural dyspnea pulmonary edema
Sever Oliguria or anuria Acute renal failure
Medical Mgt
Mgt is directed at treating the acute effects of renal insufficiency and hypertension
219
10-day course of systemic antibiotic therapy with penicillin
sodium restriction, Diuresis
pharmacotherapy with calcium channel antagonists, vasodilators or angiogenesis-
converting enzyme inhibitors
administration of medication, which may include
IV diazoxide and Furosemide to treat sever hypertension
Methyldopa or hydralizine, usually in conjunction with reserpin or furosemide to treat
moderate HPN
Oral hydrochlorothiazide to treat mild HPN
Antibiotics to treat existing streptococcal infection
Digitalis to combat circulatory overload
Diuretic, such as hydrochlorothiazide or furasemide for sever edema
Assess the fluid status by monitoring input and out put, taking and recording daily Wt and
observing for edema
Stimulate the child by provide quiet, ambulatory play activities
Maintain adequate caloric intake and good nutrition
Impose Na, K or fluid restrictions as ordered
Ensure early detection of complications by closely monitoring blood pressure and
respiratory rate
Explain and answer question about Dx, Rx and home care
Prevention
Early antibiotic treatment of every streptococcal infection of the skin and the throat
Family members of pts with AGN should be cultured for group, A.B, hemolytic
streptococci and treated if culture is positive
7.3.2 Giving care for a child with Nephrotic Syndrome
220
- It is a symptom complex commonly accompanying glomerular disease and characterized
by:
Sever proteinuria, leading to edema
Hypoalbuminemia
Hypercholesterolemia
Etiology Congenital Nephrotic syndrome
- Believed to be caused by autosomal recessive gene
- Secondary nephrotic syndrome
- Caused by after glomerular damage due to acute or chronic glomerulonephritis
The most common onset of age is between 1 to 3 years
Pathophysiology
Disturbance of the glomerular basement membrane leads to increased permeability to
protein
Protein leaks through glomerular membrane resulting in:
Loss of protein, especially albumin in urine (Hyperalbuminuria or proteinuria)
Decreased serum albumin level (Hypoalbuminemia)
Decreased colloidal osmotic pressure in capillaries lead to fluid shifting, causing fluid to
accumulate in the interstitial spaces and body cavities, particularly in the abdomen (Ascites)
Massive fluid shift leads to Hypovolemia, which stimulates the Renin-angiolensin system to
increase secretion of ADH and aldesteron
Leading to Na and H2
0
reabsorption and further increase edema
Hyperlipidemia occurs for a yet poorly understood reasons
C/M- Weight gain
Periorbital edema, ascites, peripheral edema, and edema in the labia or scrotum
Respiratory difficulty secondary to pleural effusion
Anorexia and diarrhea secondary to edema of the intestinal mucosa
221
Signs of malnourishment (may be masked by edema)
Dark frothy urine, faligue and lethargy
Oliguria, pallor, irritability
Increased susceptibility to infection
Dx- Hx, C/M and physical examination
Laboratory findings
Massille proteinuria (> 40mg/m2/hr) Hypoproteinemia (<2.5 gm/dl)
Elevated serum cholesterol
Microscopic hematuria
Complications
Infection is the major complication in nephrotic syndrome
Thromboembolism
Mgt Administration of prednisone at a dose of 2mg/kg/day to reduce proteinuria
Immunosuppressant therapy (eg- cyclophosphamide) for a child failing to respond to steroid
therapy.
Spironolactone in combination with hydrochlorothiazide to treat sever edema
Abroad spectrum antibacterial agents to reduce the risk of infection
Assess for fluid volume deficit by
Moniloring for increased edema
Taking daily measurements of abdominal girth, weight, I/O, BP and pulse
Prevent skin breakdown by:
Checking areas of edema for skin break down
Ensuring frequent position changes, using scrotal sport in boys and providing good skin
care
Maintain or improve nutritional status by:
Providing a high protein and calorie diet
Offer small frequent meals of preferred foods in the pleasant atmosphere
222
Monitor for signs of infection and take precautions to prevent infection
Conserve the childs energy by enforcing bed rest and encouraging quiet activities
7.3.4 Giving care for a child with Hydrocele
Def
n
- Hydrocele is an accumulation of fluid in the tunica vaginalis
It is the commonest cause of scrotal swelling in pediatric age group
One to two percent of male neonates have a hydrocele
Etiology obliteration of the process us vaginalis proximaley with patency distally
Isolated Hydrocele (scrotal hydrocele) or Hydrocele of the tunica vaginalis
Hydrocele of the cord results from obliteration of the processus vaginalis proximally and
distally but patency and retained fluid in the midportion along the spermatic cord
NB- Reasons for failure of closure of the processus vaginalis is unknown; but it is more common
in cases of testicular nondescent and prematurity
Classification
1- Non- communicating hydrocele: is one found in infants up to one year of age, having
residual peritoneal fluid in the tunica vaginalis
Is the most common type of hydrocele
The processus vaginalis was obliterated during development
The hydrocele fluid disappears by 1yr of age
If there is persistently patent process us, the hydrocele persists and becomes progressively
larger during the day and is small in the morning.
Abdominoscrotal hydrocele is a rare variant of a hydrocele in which there is large, tense
hydrocele that extends into the lower abdominal cavity
+ In some older boys, a non-communicating hydrocele may result from an inflammatory
condition with in the scrotum
E.g. Testicular torsion
Torsion of the appendix testis
Epididymitis or
Tumour of the testis
223
2- Communicating Hydrocele
Is a type of hydrocele encountered above one year of age
It is due to patent processus vaginalis, so that the fluid leaves the peritoneal cavity and
enters the sack
The swelling is usually non-tender and causes no symptoms though when very tense, may
cause embarrassment
The risk of a communicating hydrocele is the development of an inguinal hernia
C/M smooth and non-tender swelling in the scrotal sac; which is mobile
Transillumination of the scrotum confirms the fluid-filled nature of the mass
There is no palpable abdominal organ
If compression of the fluid-filled mass completely reduces the size of the hydrocele, an
inguinal hernia is the likely diagnosis
Mgt - Most hydroceles resolve by 12 month of age after reabsorption of the hydrocele fluid
If the hydrocele is large and tense, however, early surgical correction is recommended
because
It is difficult to verify that the child does not have a hernia and
Large hydroceles rarely disappear spontaneously
Hydrocele persisting beyond 12-18 month are usually communicating and should be
repaired
The surgical correction is similar to a herniorrhaphy
N.B- Hydrocele is commonly occur at the right side. This is may be due the persistent patency of
the processus vaginalis, which is as twice as common on the right side
- May be related to later descent of the right testis
7.3.5 Giving care for a child with undescended Testicle
Def
n
- Undescended Testiscle is a condition in which the testes are not descended or not reached to
the scrotum
Failure to find one or both testes in the scrotum may indicate that the testis is: Undescended,
absent or retractile
224
Quite a number of newborns and about 1/3
rd
of the prematures shows this condition
An undescended (cryptorchid) testis is the most common disorder of sexual differentiation
in boys
At birth, approximately 4.5% of boys have an undescended testis
Because testicular descent occurs late in gestations, 30% of premature male infants have an
undescended testis
The incidence is 3.4% at term
The majority of undescended testes descend spontaneously during the first 3 month of life
By 6 month, the incidence decreases to 0.8%
If the testes have not descended by 6 month, it will remain undescended
Unilateral failure of descent is four times more common than bilateral
Etiology The process of testicular descent is regulated by an interaction b/n: Hormonal and
mechanical factors including
Testosterone
Dihydrotestosterone
Mullerian- inhibiting factor
The gubernaculums
Intra-abdominal pressure and genitofemoral nerve
Disturbance of these factor leads to undescended testes
C/M- un descended testes are usually in the inguinal canal
Some boys have an ectopic testis- lies a way from its natural descent, typically in the
superficial inguinal pouch or perineum
Some testes are intra-abdominal, which are non-palpable
Approximately 10% of boys with cryptorchidism have nonpalpable testis
The testis is present in the abdomen or inguinal in 50%
Absent secondary to perinatal testicular torsion in 50%
225
The undescended testis is histologically normal at birth, but the pathologic changes may be
demonstrated at 6-12 month
E.g Delayed germ cell, maturation
Reduction in germ cell number
Hyalinization of the seminiferous tubules and
Reduced leyding cell numbers
Less sever changes of the above condition are found in the contra lateral descended testis
other 4-7 years
Complications
Infertility
Malignancy
Associated hernia
Torsion of the crptorchid testis
Psychological effect of an empty scrotum
Acquired or ascending undescended testes
Descended testis at birth, but during childhood (b/n 4-10 years) of age, the testis does not
remain in the scrotum
The testis often can be pulled into the scrotum and obvious tension on the spermatic cord on
P/E
Thought to result from incomplete disappearance of the processus vaginalis
Retractile testes often are misdiagnosed as undescended testes
It is due to hyperactive cremasteric reflex which pulls the testes up and can often be
confused with undescended testes
The testes can be milked into the scrotum
Boys should be examined with their legs in arelaxed Frog-Leg position
If the testis can be manipulated in to the scrotum comfortably, it is probably retractile
226
It should be monitored every 6-12 month with follow-up physical examinations, b/c it could
be an Acquired undescended testis
Mgt The undescended testis should be treated at 9-15 months
Most testes can be brought down to the scrotum with an operation Orchiopexy
This procedure involves
An inguinal incision
Mobilization of the testis and spermatic cord and
Correction of the indirect inguinal hernia
Orchiectomy should be considered in the more difficult cases or when the testis appears to
be atrophic
Prostheses for older children and adolescents
Hormonal treatment is used infrequently
Testicular descent is under androgen regulation human chorionic gonadotropin or LHRH.
7.3.6 Giving care for a child with phimosis
Phimosis is adherence of the foreskin to the glans penis (It refers to the inability to retract
the prepuce)
Constriction of the orifice of the prepuce, so that it can not be drawn back over the glans.
The prepuce of the penis in the male newborn child is normally tight
Before the age of 3 years, adherence of the foreskin (prepuce) is a normal finding
In 90% of uncircumcised males the prepuce becomes retractable by the age of 3years
Etiology Accumulation of the epithelial debris under the infantile perpuse
Inflammation and scarring at the tip of the foreskin
Secondary to circumcision
C/M Adherence of the foreskin to glans penis
Failure of retraction of the prepuce
Dribbling of the urine
Poor stream of urine and the prepuce ballon up on trying to pass urine
227
Dx- Hx and PE
Mgt - For persistent physiologic and pathologic phimosis, application of corticosteroids cream to
the foreskin Tid/day for 1 month loosens the phimotic ring, in 2/3
rd
of cases
Soap and water cleansing for minor irritation
Circumcision in repeated balanitis or sever phimosis
NB- Never forcefully retract the foreskin in early infancy- This may tear the elastic fibers at the tip
of the foreskin and cause bleeding
Paraphimosis occurs when the foreskin is retracted behind the coronal sulcus and the
prepuce can not be pulled back over the glans
Painful venous stasis in the retracted foreskin
Edema leading to severpain and inability to reduce the foreskin
Rx- Lubrication of the foreskin and glans and then compressing the glans and simultaneously
placing distal traction on the foreskin to try to push the phimotic ring beyond the coronal sulcus
Complications of circumcision includes
Bleeding (Hemorrhage)
Wound infection
Meatal stenosis
Secondary phimosis
Removal of insufficient foreskin
Dense penile adhesion
7.3.7 - Giving care for a child with Vulvo vaginal Infections
Vulvovaginitis is an inflammation of the vulva and vaginal mucosa
Is the most common child hood or a dolescent gynaecologic problem
Vulvovaginal irritation results from the lack of labial fat pads and pubic hair for
protection of the external genitalia
The labial minora tend to open when a child squats Exposure of the sensitive tissue
with in the hymenal ring
228
The close proximity of the anal orifice to vagina allows transfer of fecal bacteria to the
vulvovagina area
In the relatively low estrogenic prepubertal environment, the thin atrophic vaginal
epithelium is susceptible to bacterial invasion
Recurrent vulvovaginitis usually ceases once a girl reaches puberty, estrogen increases
and the PH of the vagina becomes more acidic
Increased production of acetic and lactic acids, a phenomenon accompanied by an
increase in superficial cell proliferation and glycogen as well as by enhancement of
normal bacterial flora
Etiology Although there are a number of causes of vulvovaginitis in pediatric patients, the more
common ones include:
Poor perineal hygiene
Candida infection
Foreign body
Classification of vulvovaginitis
A- Nonspecific vulvovaginitis
Patients with poor perineal hygiene often develop a condition known as a non-specific
vulvovaginitis
Accounts for 70% of all pediatric vulvovaginitis cases
The discharge characteristically brown or green
Has a fetid odor and is associated with vaginal PH of 4.7-6
In 68% of reported cases, this vaginitis is associated with coliform bacteria secondary to
fecal contamination.
The next most common bacterial organisms associated with nospecific vulvovaginitis
are:
Hemolytic streptococcus and
Coagulase positive staphylococcus (These organisms mainly transmitted
manually from the nasopharnyx)
229
Chemicals, clothing, cosmetics and soap products or detergents used for bathing or
laundry may also cause irritation Nonspecific vulvovaginitis
Tight-fittings clothing, such as jeans, leotards, and tights, as well as rubber pants or
plastic coated paper diapers have also been implicated
Nonspecific vulvovaginitis occasionally can result in chronic infection
May cause significant psychologic consequences for both the child and parents
B- Specific vulvovaginits
Gardnerella vaginalis is the most common organism cultured in pediatric or adolescent
patients with vulvovaginitis, followed by candida
Other identified organisms include
Enterococci and anaerobic bacteria E.g Peptococcus, peptostreptococcus,
veillonella parvula, Eubacterium, propionibacterium
Bacteroid species
Protozoa, helminths and viruses are also considered as etiologic agents
C/Ms of vulvovaginitis
The main clinical manifestations in order of frequency include:
Vaginal discharge
Erythema and
Pruritus
Vaginal discharge is a common presenting complaint in paediatric patients
It is often the primary symptom of vulvitis vaginitis or vulvovaginitis
Frequent urination
Dysuria or
Enuresis
Vulvitis is manifested primarily by dysuria and Pruritus and is associated with erythema
of the vulva
Has a more protracted course than vaginitis
230
Vaginitis is characterized by discharge without associated dysuria, Pruritus or erythema
Vulvovaginitis involves a combination of these manifestations
Dx- C/m and Hx with PE
+ Vaginal culture
+ Cytology and vaginoscopy
+ Leukocyte esterase dipsticks to identify:
- Trichomonads
- Candida
- Bacterial vaginosis
To evaluate cervical secretions for identification of gonococcal and
chlamydial infection
Rx- Successful treatment of non-specific vulvovaginitis include instructions in
Perineal hygiene
Switching from tight-fithing underwear
The use of sitz baths with mild soap, and air drying the vulva
Instruction for appropriate bowel and bladder habits
Emphasazing the need to wipe fecal material a way from the vulvovaginal aea
Recurrent vulvovaginitis should be treated with systemic antibiotics
E.g. Amoxicillin
Cepholosporins
Topical estrogen cream or polysporin ointment is often helpful
Treatment of specific vulvovaginitis depends on the offending organisms.
Organism Presentation Diagnosis Treatment
Entrobiasis
(pinworm)
Nocturnal perineal Pruritus
GI symptoms
Vulvovaginal Fecal
contamination
Adult worm in stool
eggs or in the
prianal skin
Mebendazole,
repeat in 3wks if
necessary
231
Giardiasis
Asymptomatic fecal
contaminant, vaginal discharge,
diarrhea
Protozoal flagellate
(cyst ortrophozoites
infeces
Metronidazole
or quinacrine
Staphylococcus
and
streptococcus
Vaginal discharge to
vulvovaginal area; spread from
primamary lesion
Positive culture
results of
appropriate
organism
Penicillin or
capholosporin
+ Other specific vulvovaginitis include
1- Molluscum contagiosum
C/M- Vulvar lesions
Nodules with umblicated area
White core of curdlike material
Dx- Isolation of poxvirus
Rx- Dermal curettage of papule
2- Phthirus pubis (pediculosis pubis)
C/M- Pruritus, excoriation inner thigh or lower abdomen
Sky- blue macules
Dx- Nits on hair shafts, lice- skin or clothing
Rx- Lindane lotion (kwell)
3- Sarcoptes scabiei (scabies)
C/M- Nocturnal Pruritus
Pruritic vesicles
Pustules in runs
Dx- mites; ovablack, dots of feces (microscopic examination)
Rx- 1% Lindane application
4- Shigellaspecies (shigellosis)
C/M Fever, malaise, fecal contamination
Diarrhia (bloody or mucoid)
232
Cramps and pus in stool
Dx- Stool examination
White blood cells and RBCS
Positive for shigella
Rx- Trimethoprim and sulfamethoxazole
Chloramphenicol
Ampicillin or Tetracycline
7.4- PROVIDING CARE FOR A CHILD WITH CAR DIOVASCULAR
DISORDERS
1- ASSESSING CVS OF A CHILD
- The CVS includes the heart, blood vessels, bloods and lymphatics
The heart is a hollow muscular organ located slightly to the left in midchest b/n the lungs
with its apex toward the diaphragm
The heart has three layers of tissue:
1- Pericardium An outer covering
2- Myocardium - A middle and thicker muscular layer
3- Endocardium An inner thin membraneous lining that forms the valves
The heart is divided into four chambers with a septum dividing the Rt and Lft sides:
1- Right Atrium Receives venous blood returning from the body
2- Left Atrium Receives oxygenated blood returing from the lungs
3- Right ventricle- Pumps venous blood through the pulmonary artery to the lungs
4- Left ventricle- Pumps oxygenated blood out through the aorta to all parts of the body
The heart also has four valves located in the inlet and outlet of each ventricles- keeps the
blood flowing in one direction.
1- Cuspid values- Two valves (mitral and Tricuspid), guard the atria and ventricles
2- Semilunar values- Two valves (Aortic and pulmonic values), which guard the exits inside
the pulmonary artery and aorta
233
Electrical conduction
- The heart contracts as a result of nerueimpulses going from the cardiac center in the medulla
of the brain through the vagus nerve to SA node and Av node, and onward to the heart
muscle cells by special neuromuscular fibers
- These impulses alter the cell membranes, allowing calcium, sodium, chloride and potassium
ions to creoss into the cells
- Electrical impulses can be picked up on the body surface through leads and viewed on a
cardiac monitor or recorded by an electrocardiograph machine
Function of Heart
- To pump blood in sufficient amounts to meet the varying needs of cells for the substances it
transports
Blood vessels
- Consists of a network of tubes that carry blood to and from the heart
As the left ventricle contracts, blood leaves the heart by way of the aorta
- Arteries branch off the aorta dividing and subdividing into arterioles, and finally, tiny
capillary vessels. The capillaries then unite to form venules, which unite form larger and
larger veins that finally empty into the right atrium of the heart
Arteries have smooth muscle in their walls, allowing them to contract or dilate
- This action affects the pressure (force) and rate of flow of the blood
Veins are membranous tubes equipped with values located at intervals to prevent backflow
Capillaries have thin walls, some only a single cell thick, making possible the exchange of
gases, nutrients and wastes
234
Function of Blood vessels
- To provide conduits through which blood flows to and from tissues in the body
Lymph vessels
- Lymph vessels begin among the cells as tiny channels similar to blood capillaries
- These capillaries unit to blood capillaries
These capillaries unit to form progressively larger ducts that unite to form two main vessels:
The thoracic duct and Right Lymphatic ducts
- These ducts extend up to the subclavian vein of the neck where lymph empities into the
venous blood
Lymphnodes are round bodies which distributed along lymph vessels at strategic points
throughout the body
- Acts as filters to remove dead cells, bacteria and intracellular waste
- Reticuloendothelial cells digest debris and couvert it into harmless breakdown
products
- Manufacture two kinds of white blood cells
Lymphocytes
Monocytes
- When there is an inflammation in body tissue, interstitial fluid from the area drains to near
by lymphnode and a defensive battle is waged againsts the invader.
As a result the node becomes enlarged and sometimes tender
235
Function of lymphatic system
- To drain excess interstitial fluid form b/n the cells and return it to the blood, and
- To provide a major defense system for the body
Blood
- It is a connective tissue which is composed of 55% plasma and 45% of formed elements
A) Plasma Is a clear liquid part of blood
Is a complex mixture of water, electrolytes, proteins, lipids, glucose vitamins, gases,
enzymes, hormones and antibodies
Its protein (Albumin, globulin and fibrinogen) play an important role in regulating body
fluid
B) Formed Elements
Consists of three types of blood cells:
1- RBCS (Eryghrocytes)
Are biconcave discs marked by the absence of a nucleus and the presence of an iron-
bearing red protein called haemoglobin
Haemoglobin makes up above one third of the cell= 14-16 gm/100ml of whole blood
Cellular volume percent (Hematocrit) reflects number of erythrocytes
-
Successive stages of development of RBC. Hemocytoblast Proerythroblast
Erythroblast Normoblast Reticulocyte Mature erythrocyte
2- Leukocytes Are colorless cells that averages about 7000/mm
3
of blood
Granular WBC (Neutrophils, Eosinophils and Basophils) are formed in the bone marrow
Non-granular WBC (Lymphocyte and monocyte) are formed in the lymphnodes
236
Unlike RBCS, leukocytes have nuclei and can squeeze through capillary walls, infiltrate the
tissue, and aid in fighting infection
3- Platelets (Thrombocytes)
Are disc-shaped bodies in the blood that number 300,000/mm
3

Essential components of the clotting process by which blood preserves itself
Not really cells, the are believed to be fragments of giant megakaryocytes found in red
bonemarrow
Functions of blood
Transport of oxygen and carbon dioxide to meet respiratory needs
Transportation of food and nitrogen wastes to meet nutritional and excretory needs disease
fighting for protective needs
Maintaining fluid balance and chemical equilibrium
Has its own mechanism for self-preservation (clotting)
Fetal circulation
During fetal life the baby does not need its liver to synthesize nutrients or its lungs for
gaseous exchange He/She uses his/her mothers
In the fetal circulation, the right and left ventricles exist in a parallel circuit, as opposed to
the series circuit in adults or in a newborn
Three cardiovascular structures unique to the fetus are important for maintaining this
parallel circulation
- Ductus venosus
- Foramen ovale
- Ductus Arteriosus
Oxygenated blood returning from the placenta flows to the fetus through the umblical veins
with a po
2
of about 30-35 mmHg.
Approximately 50% of umblical venous blood bypass the liver and joins the inferior
venacauavia Ductus venosus
237
Here the umblical venous blood partially mixes with poorly oxygenated inferior
venacava blood drived from the lower part of the fetal body
The combined lower body plus umblical venous blood flow enters the right atrium and is
preferentially directed acrass the Foramen ovale to the left atrium LV- Aorta
Fetal superior venacava blood, which is considerably less oxygenated (po
2
of 12-14mmHg),
enters the right atrium and preferentially traverses the tricuspid value, rather than the
foramen ovale, and primarily to the right ventricle
From the right ventricle, the blood ejected into the pulmonary artery
Only about 10% of right ventricular outflow enters the lungs
The major portion of the right ventricular outflow, which has a po
2
of about 18-22 mmHg
bypasses the lungs and flows through the Ductus Arteriosus in to the descending aorta to
perfuse the lower parts of the fetal body, after which it returns to the placenta via two
umblical arteries
The upper part of the fetal body, including the coronary and cerebral arteries and those the
upper extremities is perfused exclusivelyfrom the left ventricle
Total fetal cardiac output amounts to about 450 Ml/kg/min
During fetal life, the right ventricle is not only pumping against systemic blood pressure but
it also performing a greater volume of work than the left ventricle
Transitional circulation
At birth blood circulation changes dramatically
Mechanical expansion of lungs Rapid decrease in pulmonary
An increase in arterial Po
2
vascular resistance
Removal of the low-resistance Increase in systemic vascular
placental circulation resistance
The out put from the right ventricle now flows entirely into the pulmonary circulation.
The shunt through the ductus arteriosus reverses and becomes left to right.
238
Over the course of several days, the high arterial Po2 constricts the ductus arteriosus and it
closes ligamentum arteriosum
The increased volume of pulmonary blood flow returning to the left atrium es left atril
volume and pressure sufficiently to close the foramen ovale function ally
Removal of the placenta from the circulation also results in closure of the ductus venosus
Due to the high resistance systemic circulation, the left ventricle wall thickness and mass
begin to increase
The Right ventricular wall thickness and mass slightly decrease because of the low-
resistance pulmonary circulation
Now the left ventricle deliver the entire systemic cardiac output = 250 ml/kg/min; almost
200% increase in output
Significant differences b/n the neonatal circulation and that of older infants may be
summarised as follows.
1- Right to left or left to Right shunting may persist across the patent foramen ovale
2- In the presence of cardiopulmonary disease, continued patency of the ductus arteriosus may
allow left-to-right, right-to-left or bidirectional shunting
3- The neonatal pulmonary vasculature constricts more vigorously in response to hypoxemia,
hypercapina, and acidosis
4- The wall thickness and muscle mass of the neonatal left and right ventricles are almost
equal.
5- Newborn infants at rest have relatively high oxygen consumption, which is associated with
relatively high cardiac output
Assessment and Diagnostic Evaluation of CVS
HISTORY- A comprehensive cardiac Hx starts with details of perinatal period,
including presence of:
- Cyanosis
- Respiratory distress or
- Prematurity
239
Maternal complications such as
- Gestational diabetes - Medications
- Systemic lupus erythematous or - Substance abuse
The timing of the initial symptoms
Many of the symptoms of CHF in infants and children are age specific
Feeding difficulties in infants
Respiratory distress (rapid breathing, nasal flaring, cyanosis and chest retraction)
Exercise intolerance in older children
- Difficulty keeping up with peers during sports
- Need for nap after coming home from school
- Poor growth
Orthopnea and nocturnal dyspnea
Cyanosis at rest, during crying or exercise
Chest pain is unusual manifestation of cardiac disease in pediatric patients
Careful family history may reveal early:
- Coronary artery disease or stroke (familial hypercholesterolemia or thrombophilia)
Generalized muscle disease (muscular dystroph, dermatomyositis, familial or metabolic
cardiomyopathy)
Relatives with congenital heart disease
PHYSICAL EXAMINATION
After general assessment of the patient, specific attention is directed toward the presence
of:- Cyanosis
Abnormalities in growth
Any evidence of respiratory distress
Evaluation of murmur
240
Quality of pulse and measurement of BP
Accurate measurement of height and weight
Edema around the eyes and or over the flank in infants
Periorbital edema and pedal edema in older children and teenagers
Heart rate
o > 200 beats/min in neonate
o > 150 beats/min in infants Tachycardia
o > 120 beats/min in older children
wide pulse pressure with bounding pulse my suggest
o patent ductus arteriosus - Increased cardiac output
o aortic insufficiency - Fever
o arterial-venous communication
A narrow pulse pressure occurs with
o Heart failure
o Aortic stenosis (Lft ventricular outflow obstruction)
o Tachycardia
Inspection of the jugular venous wave provides information about central venous pulse and
right atrial pressure
Diagnostic tests (Evaluation)
A number of tests are performed on children with heart disease
o To confirm medical diagnosis
o To assess the course of the disease
o To evaluate the effect of treatment
1) Blood Tests Measurment of the concentration and proportion of cells and chemicals found
in blood provides significant data
+ Hemoglobin
+ Complete blood count
241
+ Haematocrit
+ Na, K, chloride and Co2 levels
+ Serum creatinine and BUN
+ Arterial blood gases and hydrogen ion concentration
+ Platelet count, prothrombine time and thrombo plastin time
2) Cardiographic studies
Data a bout the heart are collected by various studies
A) angiocardiography
Use of X-rays on film to record dye-marked blood flowing through the heart and vessels
- Performed in conjuction with cardiac catherization
B) Cardiac catherization
- Introduction of a cardiac catheter through the femoral or brachial vessels into chambers
of the hearty to measure the volume and direction of blood flow, oxygen concentration
and pressure
C) Digital subtraction Angiography
- Procedure to provide computerized images of dye-marked blood flowing through vessels
and tissues by subtracting non-dyed tissues
D) Echocardiographs
- Test that records a picture of sound waves bounced off heart structures
E) Electrcardiograph (ECG)
- Procedure that records the electrical potential generated by heart muscles
F) Fluoroscopy
- Use of X-rays to provide direct observation of heart size, position and contour
G) Radiography
- Use of X-ray on film to provide a permanent record
242
H) Ultrasonography
- Procedures that records a three dimensional picture of heart structures, synchronized
with ECG.
7.4.1 PROVIDING CARE FOR ACHILD WITH ANEMIA
7.4.1.1 Definition
ANEMIA: - is defined as qualitative and/or quantitative deficiency of haemoglobin
characterized by reduced oxygen carrying power of blood resulting in tissue anoxia
producing various symptoms
- It describes a circumstance where there is a lack of heme (oxygen-carrying, iron
containing molecule)
Heme is attached to a protein called globin to form haemoglobin, and contained with in
the RBCS
A child with an Hb below 11gm/dl (or 70%) is considered to be Anemic
- In a newborn 14 gm/dl is the lower limit
Anemia, like fever, is a symptom which can be the result of various causative factors
It is extremely common and constitutes a major segment of hematologic disorders and
responsible for considerable morbidity and mortality
Anemia results when total haemoglobin content of the blood is below normal, either
because of insufficient haemoglobin in the RBCS or because of lack of RBCS
Anemia develops if there is
1- Excessive blood loss
2- Deficiency in iron
3- Decreased blood formation
4- Abnormal blood distruction
5- Impaired formation of RBCS
243
7.4.1.2 Types of anaemia
A. Hemorrhagic Anemia
- It is a type anemia which is caused by bleeding or blood loss
- It can be classified in to two
1- Acute- Bleeding disorder including
- Bleeding from the cord or birth injury
- Hemorrhagic disease of the newborn
- Bleeding due to accidents
- Nose bleeding (Epistaxis)
- Bleeding due to acute peptic ulcer
- Bleeding from esophageal varices
- Bleeding after salycilates and /or steroid over dosage
- Bleeding after uvulectomy or circum cision
2- Chronic Chronic blood loss can occur secondary to the following conditions
- Hookworm infestation - Chronic peptic ulcer
- Chronic dysenteric ulcers - Ulcerative colitis
- Tubercle ulcers - Regional ileitis
B) Anemia Due to Decreased Blood Formation (Aplastic Anemia)
- It is a failure to manufacture enough redcells in the bone marrow
- Is a condition in which the formation of RBCs WBCS and platelets is depressed
- Usually results from an injury or destruction of stem cells in the bone marrow
- It may be congenital or acquired
Acquired a plastic anemia can be caused by irradiation, toxins, severe diseases
(Sepsis, immune deficiencies) or drugs (e.g. CAF)
Medical interventions include:
- Adminstration of blood transfusions
- Drugs to suppress autoimmune response
- Bone marrow transplantation
Nursing interventions include
244
- Taking measures to prevent infection and bleeding
- Preparing children beforehand
- Comforting children during painful diagnostic procedures
- Giving care related to transfusion
- Providing emotional support for terminally ill children and their families
C) Anemia Due to Blood Distructions
- These are called haemolytic anemias
- The RBCS can be damaged and destroyed by a number of causes
Those within the red cell itself
- E.g. Due to abnormal haemoglobin as in sickle cell anemia or thalassemia
Weakness in the red cell membrane
- E.g.- In congenital spherocytosis or
- G6 PD deficiency
Those coming from outside the red cells
- E.g. Malaria
- Other infections (Leptospirosis, septicemia)
- Toxins (snake-bites)
- Drugs or antibodies formed against the red cells in hemolytic anemia of the
newborn (ABO, rhesus incompatibility) or auto-immune hemolytic anemia
Sicle cell Disease (Anemia)
- Is a chronic anemic condition marked by physiological crises
- It is caused by an inherited recessive trait that follows mendels law
- People who have two sickling traits are homozygous and have the disease
- Person who have one sickling trait and one normal trait are heterozygous and may
exhibit symptoms under stressful circumstances
- The trait controls the type of haemoglobin found in the red blood cells
In homozygous persons haemoglobin S (Hbs) replaces all or part of the normal
haemoglobin (HbA)
245
- When oxygen is released from red cells, S homoglobin causes the cells to sickle or
change from round to crescent-shaped disks
- Red blood cells with Hbs live only one fourth of the days of those with Hbs live
only one fourth of the days of those with HbA and have a much smaller oxygen-
carrying capacity
+ A child with sickle cell disease may become acutely sick. This sudden illness is
called a sickle-cell crisis
- This condition is may be due to
A- Vasocclusive (Thrombocytic) crisis
- Red blood cells clump and block small blood vessels, causing deficiency of blood
(Ischemia) and tissue death (Infarction)
- Any area of the body may be affected, including:-
o Extremities - Producing severe pain and respiratory, Lungs
urinary or neuromuscular symptom
o Abdomen
o Brain
B- Sequestration (separation) crisis
Occurs in children 5 years of age
Sickling causes sudden pooling of blood in the spleen
Without treatment shock and death may result
C- Aplastic (Failure to develop) crisis
Red blood cells are destroyed by the bdoy faster than they can be produced
At first the body accelerates its production, but then it stops all production for 10 to 14 days,
resulting in profound anemia
Usually end spontaneously
S/s Pain is the primary symptom painful crisis
Weakness and fatigue
May be respiratory distress, reduced urinary out put
246
CNS involvement, abdominal distention, fever and hypotension
Symptoms hypovolemic shock, including pallor, tachycardia and dyspnea
Medical Interventions aimed at:
Maintaining hydration
Replacing electrolyte and blood
Controlling pain
Providing rest and
Administering antibiotics
Nursing interventions in clued:
Controlling pain by nursing measures
Administering ordered medications, blood, and fluids
Protecting the child from infections
Measuring, input and output
Giving skin care and ROM exercises
Providing diversion and comfort
Teaching about the stress reduction and other aspects of the disease
Anemia Due to Impaired Formation of RBCS
B- Thalassemia (cooleys anemia)
Thalassemia is a group of inherited hemolytic anemias that are caused by abnormal
hemoglo9bin formation
As a result, bone marrow over produces RBCS, which are fragile and easily destroyed.
The haemoglobin components that are affected are named alpha, beta and soon
B-thalassemia is the most common type of thalassemia and has two forms
Thalassemia minor
Thalassemia major
The minor form occurs when a child inherits one thalassemia gene and one normal gene
247
Produce a mild to moderate anemia
The major form occurs when both genes are abnormal causing severe disease, called
cooleys anemia
This form is an outosomal recessive disorder found among people who ancestors
lived near the Mediterranean sea
Thalassemia causes progressive, sever, hemolytic anemia beginning when an infant is about
6 month of age
Spleen enlarges causing a large abdomen
Bone marrow expands to overcome the anemia
Skeletal changes of the cranium and facial bones
Such bones are fragile and fracture easily
Growth retardation and enlargement of the heart
Skin and mucousmembrane becomes jaundiced from the bilirubin of destroyed RBCs.
Interventions
There is no cure for cooleys anemia
Frequent administration of blood (Blood transfusions)
Treatment of infection
For some children spleenectomy
Careful observations for blood reaction, and symptoms of transfusion-borne hepatitis
Supportive care for parents and child
Genetic counselling for family members who lack symptoms, but are carriers of the genetic
trait
D- IRON-DEFICIENCY ANEMIA
It is a type of anemia resulting from lack of sufficient iron for synthesis of haemoglobin
It is the most common hematologic disease of infancy and childhood
Its frequency is related to certain basic aspects of iron metabolism and nutrition
248
Iron-deficiency anemia is the most common nutritional deficiency in infancy and childhood
in the developing countries and can be prevented and treated
It occurs as a result of an inadequate supply or faulty absorption of iron
The body of a newborn infant conlains about 0.5 gm of iron, where as the adult content is
estimated at 5 gm
To make up for this discrepancy, an average of 0.8 mg of iron must be absorbed each
day during the first 15 years of life
a small amount of iron is also necessary to balance normal of iron by shedding of cells.
To maintain positive iron balance in childhood, a bout 1mg of iron must be absorbed
each day
Iron is absorbed in the proximal small intestine, mediated partly by a variety of duodenal
proteins
The absorption of dietary is assumed to be about 10%, so a diet containing 8-10 mg of iron
daily is necessary for optimal nutrition.
Iron is absorbed 2-3 times more efficiently from human milk than from cows milk.
Breast-fed infants may, therefore, require less iron from other foods
Adolescents are susceptible to iron deficiency because of:
High requirements due to the growth 5 spurt
Dietary deficiencies and
Menstrual blood loss
Etiology- Iron-deficency anemia results from
Inadequate intake of dietary iron
Defective or zmpaired absorption of iron or
Increased demands of iron
Iron-deficiency anemia is likely to occur in
LBW Infants- Because of small iron stress and fast growth (Anemia of prema
turity)
249
Twins Because of sharing of maternal iron
Anemia of mother during pregnancy- The child has a small iron store and
become anemmic
Other causes of iron-deficiency anemia include
Occult bleeding due to lesions of GI tract (eg- peptic ulcer, polyp, inflammatory bowel
disease etc)
Hookworm infestation in some geographic area
Pulmonary hemosiderosis
Chronic diarrhea in early child hood
Chronic intestinal blood loss induced by exposure to a heat-labile protein in whole cows
milk
Histologic abnormalities of the mucosa of the GIT
C/M- Iron-deficiency anemia is more commonly seen between the age of six
months to three years
Pallor is the most striking sign
Lower palpebral conjuctiva and mucous membrane of oral cavity at early stage and later
on nails, palms and the rest of the skin
Dyspnea on exertion
Failure to thrive
Restlessness, irritability, fatigue and anorexia
Parasthesia, dizziness and vertigo
History of pica and breath holding attack
Koilonychias (spoon-shaped nails)
The nails may show clubbing and are thin and brittle
Slate blue discolouration of sclera
Mild edema associated with hypoprotieinemia
He patospleenomegally in moderate to severe iron-deficiency anemia
250
Tachycardia, soft systolic murmur, loud first heart sound, enlarged heart
Decreased attention span, alertness and learning of both infants and adolescents
Lab- Findings
In progressive iron-deficiency, asequence of biochemical and hematologic events occur
Decreased levels of ferritin
Decreased serum iron levels
Serum transferring increases, but transferring saturation falls below normal
As the deficiency progresses, the RBCS become smaller than normal and their haemoglobin
content decreases
Reduced haemoglobin and Red cell count
Absent or scanty bone marrow-hemosiderin provides the most valuable early and consistent
evidence of iron-deficiency
It indicates depletion of body iron stores which as arule precedes haematological
changes/symptoms
Examination of stool for ova, cysts, occult blood, concentration method for hook worm
infestation
Rx- The regular response of iron-deficiency anemia to a dequate amounts of iron
is an important diagnostic and therapeutic feature
Oral administration of simple ferrous salts provides inexpensive and satisfactory therapy
Feso4 1 teaspoon Tid as pediatric syrup (5ml=60mg) in infants
2 teaspoons (10ml) Tid for aged 1-5 years
3 teaspoons (15 ml) Tid for aged 6-12 years or
Feso4, 1 tablet (200mg) Bid daily for small children and Tid in children over 6 years
In 3 wks the Hbg should be close to normal, if iron-deficiency was the sole cause of
the anemia
Continue the Rx for 1 month other that to replenish the iron stores
251
High-energy and high-protein diet and Rx of hookworm and other disease contributing to
the anemia
If haemoglobin is below 7gm.dl (45%), and especially if follow-up is not very reliable; IM
iron may be preferable
Iron dextran (Imferon) 20mg/kg (0.4 ml/kg) deep Im as a total dose (Give 1-2 ml~ 50
-100 mg per injection every day until the total dose is given)
The Hbg will start to rise within the next wks and should be close to normal other 3
weeks
A child with Hbg value below 5 gm/dl (35%) will need blood transfusion if:
Edema
Liver enlargement In dicates that the condition is serious
Tachycardia or
Dyspnea
Frusemide 1mg/kg Im or slowly IV should be given before transfusing blood
Prevention
Prevention and treatment of anemia in pregnancy
Give iron supplements to all children with a birth weight below 2000 gm during the 1
st
half
year (Feso4 60mg daily should be enough)
Provision of green vegetables starting from the six month, even if abundant breast milk is
available
especially stressed in twins; and make sure the diet contains enough energy and other
nutrients
Summary
Anemia describes a circumstance where there is a lack of haemoglobin, which is contained
within the red cells of the blood
Anemia may be caused by:
252
Haemorrhage or blood loss
Deficiency of iron, vit-B12 and/or folic acids
Decreased blood cell formation (A plastic anemia)
Blood destruction (Hemolytic anemia)
Impaired formation of red blood cells
Other congenital red blood cells haemolysis
As anemia increases due to any of the above Causes:-
Oxygen- carrying ability of the blood falls
Blood circulation has to increase to keep up with the needs of the body tissue for 02
If the Hbg level is < 5gm/dl, then the amount of blood supply to any tissue, including the
heart muscle itself, must double to keep up the oxygen supply
The heart enlarges, the apex beat moves laterally outside the line of the nipple into the
axilla, and the heart beats more strongly and rapidly
The amount of blood returning to the heart increases Distended neck veins and the
liver became enlarged
Enlargement of liver indicate signs of the heart
Neck veins distension adapting to the anemia
Progressive and further fall of the Hbg leads the heart begins to fail to adapt
Signs of adaptation rapidly merge into the signs of cardiac failure, with
Breathlessness at rest
Engorgement of veins in the neck
Engorgement of the liver, which become tender
Rising pulse and falling blood pressure
N.B- Cardiac enlargement and venous congestion do not necessarly mean cardiac failure,
but are warning signs
Clinical Features
Pallor of conjective, lips, fingernails, palms, tangue
253
Skin pallor is not noticeable in a dark skin, and so mother must be taught the
significance of mucosal pallor
Tiredness, weakness or fatigue
Unusual and increasing breathlessness on exertion
Rapid pulse rate
In severe anemia (Hbg less than 5gm/dl)
Edema
Enlargement of heart and later failure
Breathlessness at rest
Laboratory investigations
Haemoglobin level estimations
Thin blood film for color, size and shape of RBC, identifying parasites, and appearance of
WBC
Thick blood film for detecting and counting malaria parasites
Stool microscopy for ova and cysts
U/A for:- Protein
Bilirubin and uroblinogen
Microscopic for RBCS and WBCS
Schistosome ova
NB- Anemia is a sign, not a disease
Malnutrition, malaria, hookworm and other infections cause 8 out of 10 anemias in children
Anemia of prematurity and sickle-cell anemia account for most of the others
Hbg is produced from iron, protein and number of other nutrients; look to the diet as well as
giving out iron tablets
Immediately transfer any baby who is pale or jaundiced with in 24 hours of birth to hospital
Think twice before giving a blood transfusion : How safe is it? How necessary is it?
The classic blood picture of iron deficiency anemia is Hypochromic and microcytic
254
Mgt Aimed at restoring the haemoglobin to normal level
Prevention of complication
Most of the causes of anemia is preventable
7.4.2CARING A CHILD WITH CARDIAC FAILURE
7.4.2.1 DEF
N
- Heart failure, also called congestive heart failure, is a condition in which the heart
can not pump enough oxygenated blood to meet the needs of the bodys other organs
The heart keeps pumping, but not as efficiently as a healthy heart
It actually is not as much a specific diagnosis, but rather a collection of symptoms that can
be the result of a variety of different heart problems
7.4.2.2Types of cardiac failure
1- Right sided Heart Failure
When the right side of the heart begins to function less efficiently, it is unable to pump
much blood forward into the vessels of the lungs
Because of the congestion in the right side of the heart, blood flow begins to back up into
the veins
There is back up of blood and fluid into the liver and other organs leading into the heart
Eventually, swelling is noticed in the feet, ankles, eyelids and abdomen due to fluid
retention
2- Left sided heart failure
When the left-side of the heart fails, it is unable to pump blood forward to the body
efficiently
Blood begins to back up into the vessels in the lungs, and the lungs become stressed
Breathing becomes faster and more difficult
Body does not receive enough blood to meet its needs, resulting in fatigue and poor growth
3- Both side Heart Failure
It is common for both sides of the heart to fail at the same time
This causes back up of blood and fluid into the lungs and body (both systems)
simultaneously
255
7.4.2.3 Causes of CHF
Heart failure and CHF can be caused by a number of conditions, including
1- Congenital Birth Defects
In this situation, the heart muscle pumps well, but the route that blood takes is very
inefficient
It occurs when too-much blood goes to the lungs, which the lungs, and eventually the heart
find difficult to handle
When heart failure occurs in children it is usually due to a birth defect involving the heart
PDA- It is large and does not close; the baby will have an excessive amount of blood flow to the
lungs
Is a very common problem in premature infants
VSD It will cause CHF only if the hole is big enough to allow so much extra blood flow to the
lungs that the heart has to work a lot harder to pump blood out to the heart
Leads to excessive blood flow to the lungs (Large VSD)
Truncus Arteriosus It is a hole between the two main arteries leaving the heart
Babies with this defects are also at risk for having too much blood flow to the lungs
ASD Rarely cause problems with CHF no matter how large
2- Valvular Heart Disease
It is the general term applied to any dysfunction or disease of any of the four valves of the
heart
In healthy heart, the four valves keep the right amount of blood flowing in one direction,
either into or away from the heart, and at the right time
Problems due to valvular heart disease can increase the workload of the heart na dcause
CHF
Valvular stenosis valve narrows, hardens or becomes blocked, and interferes with blood
flow
Valvular Regurgitation
Valve does not close completely, allowing blood to leak in the wrong direction
256
Atresia Birth defect where the valves does not fully develop or is completely closed at
birth
Mitral valve prolapse
Mitral valve can not close properly and allows blood to leak back into the left atrium
3- High blood pressure
Hypertension is diagnosed when the systolic and diastolic numbers are consistently above
the healthy range
HPN increases the workload of the heart
The increased workload of the heart over a prolonged period period of time increases the
risk of developing CHF.
4- Coronary Artery Disease (CAD)
CAD refers to the narrowing or blockage of the coronary arteries of the heart
When narrowing or blockage occurs in one of the coronary arteries, the portion of the heart
that the coronary leads to fails to receive enough oxygenated blood
This causes angina pectoris (occur when the heart must work harder, causing the hearts
0
2
demand to be greater than the 0
2
supply
When the arteries narrow or become blocked, blood can not be pumped through and goes
back to the lungs
5- Heart Attack
It occurs when the blood supply to the heart muscle is stoped or decreased
It is an emergency situation, and needs medical attention at once to prevent further damage
to the heart or death
Damage to the heart incurred during a heart attack increases the risk of developing heart
failure
6- Others
Chronic lung diseases
Anemia
Haemorrhage (excessive bleeding)
257
Cardiac arrhythmias (Irregular heart beats)
Cardiomyopathies/or another primary disease of the heart muscles
Infection of the heart valves and/or muscles (ie. Endocarditis)
Inflammation of heart muscle (myocarditis)
7.4.2.4 Signs and symptoms of CHF
The following are the most common symptoms of CHF, however, each child may
experience symptoms differently
Weight gain, even when the appetite is poor
Fast breathing during rest or exercise
Shortness of breath or labored breathing
Weezing while breathing
Visible swelling of the legs, ankles, eyelids, faces and occasionally in the abdomen
Fatigue, nausea, lack appetite
A child needs to take requent rest breaks while playing with friends
Falling a sleep when feeding or becoming too fired to eat
Cough and congestion in the lungs
Sweating while feeding
Breathing difficulty while feeding
Loss of interest in feeding
Difficulty breathing while lying down
7.4.2.5 Diagnosis of CHF
CHF is a clinical diagnosis, the S/S descreibed above are important clues to the problems
A good physical examination is of a major importance
A complete medical History and physical examination:- Asking questions about
Childs appetite
Breathing patterns
258
Enenergy level
Chest X-Ray- To determine if the heart is enlarged and if there is extra blood flow or fluid
in the lungs
Very important in determining the progression of the heart failure (CHF)
Electrocardiogram- Helpful to indicate if the chambers of the hearts are enlarged
Can point to specific congenital heart diseases or rhythm disturbances that can causes heart
failure. (Measures the heart rate and regularity)
Detects problems with in the heart muscles
Echocardiogram
A non-invasive test that uses sound waves to produce a study of the motion of the hearts
chamber and valves
Confirms the diagnosis of structural problem of the heart
Used in evaluating the function of the heart muscles
Performed to further investigate the function of the heart
Cardiac MRI
Provides a useful means to evaluate heart function in some older children and adolescents
7.4.2.6 Medical management
There are three types of medication typically prescribed to CHF patients
1- Vasodilators Dilates or relaxes the blood vessels, making it easier for the heart to pump
blood
E.g. ACE (Angiotensine- converting enzyme) inhibitors. E.g Captopril;
2- Diuretics- Remove excess fluids from the body, easing the amount of liquid
collecting the lungs and elsewhere.

Furosemide (Lasix), which helps the kidneys to eliminate extra fluid in the lungs, is often
the first medicine given both in babies and other children
259
Potassium-sparing diuretics helps the body retain potassium, an important mineral that is
often lost when taking diuretics
Potassium supplements- Replaces the potassium lost when taking diuretics
3- Digitalis
A medication that helps strengthen the heart muscle, enabling it to pump more efficiently.
e.g. Digoxin
B- Blockers help to prevent the heart from working too hard to compensate and improves
some of the bodys counter-productive responses to the stress of heart failure
e.g. Propranolol
Some surgical procedures may be employed for the mgt of CHF
A) Valve repaire or value Replacement
If the condition is caused by a valvular heart disease or deformity
It may correct the situation
B) Coronary artery bypass surgery
If the coronary arteries are blocked or severly narrowed, surgery to restor circulation may be
required
C) Heart transplant
In the most severe cases, when other treatment has failed, a heart transplant may be the best
option for some pts.
7.4.3Caring for a child with rheumatic heart disease
7.4.3.1Def
n
- it is a condition in which permanent damage to the heart valves
Rheumatic heart disease is an acquired heart disease secondary to rheumatic fever
260
Rheumatic fever is an inflammatory disease related to streptococcal infection, affecting
mostly the heart and joints
It also affects other tissues, including the brain and skin
It occurs most commonly in children between 5 and 15 years
Who is at Risk for Rheumatic Fever?
Children who have had strep-infections that were untreated or inadequately treated
Children ages 5 to 15 years, particularly if they experience frequent strepthroat infection
7.4.3.2 Etiology- Rheumatic fever and Rheumatic heart disease are caused secondary to Group
a streptococcal upper respiratory tract infections
Patients with acute rheumatic fever of a recent group A streptococcal infection
World wide, rheumatic heart disease remains the most common form of acquired heart
disease in all age groups
Accounts for as much as 50% of all cardiovascular disease and as much as 50% of all
cardiac admissions in many developing countries
Pathogenesis
The pathogienic link B/n group A streptococcal infection of the URT and an attack of acute
rheumatic fever is still not clear
Several theories of the pathogenesis of acute rheumatic fever and rheumatic heart
disease have been proposed; but only two are seriously considered:
A) Cytotoxicity Theory- This theory suggests that a group a streptococcal toxin may be involved in
the pathogenesis of acute rheumatic fever and rheumatic heart diseases.
Group A streptococcus produces several enzymes that are cytotoxic for mammalian cardiac
cells.
E.g- Streptolysin O has a direct cytotoxic effect on mammalian cells in tissue culture, and
most of the proponents the cytotoxicity theory have focused on this enzyme
261
B) Immunologic Theory
An immune-mediated pathogenesis for acute rheumatic fever and rheumatic heart disease has been
suggested by the clinical similarity of acute rheumatic fever to other illnesses produced by
immunopathogenic processes and by the latent period b/n the group A streptococcal infection and
the acute rheumatic fever.
The antigenicity of a alarge variety of group A streptococcal products and constituents, as
well as the immunologic cross-reactivity b/n group A streptococcal components and
mammalian tissues, also lends support to this hypothesis.
Common antigenic determinants are shared b/n certain components of group A
streptococcus (E.g.- M protein, protoplast membrane, cell wall group A carbohydrate,
capsular hyaluronate) and specific mammalian tissues (Eg. Heart, Brain, Joint)
The involvement of group A streptococcal superantigens, such as pyrogenic exotoxins in
the pathogenesis of acute rheumatic fever has been proposed
+ Why is Rheumatic Fever a concern?
Rheumatic fever, an inflammatory disease
Can affect many connective tissues, especially in the heart, joints, ski or brain.
The infection often, causes heart damage, particularly scaring of the heart valves, forcing
the heart to work harder to pump blood
The damage may resolve on its own or it may be permanent- CHF- accumulation of blood
in the vessels leading to the heart and fluid in the body tissue.
7.4.3.3 Clinical manifestation
+ What are the symptoms of Rheumatic Fever?
The symptoms of rheumatic fever usually start about one to five weeks after the child has
been infected with streptococcus bacteria.
The following are the most common symptoms of rheumatic fever
262
+ Joint imflammation- Including swelling, tenderness, and redness over multiple joints.
Usually larger joints in the knees or ankles are affected.
The inflammation moves from one joint to another over several days.
Small nodules or hard, round bumps under the skin
A change in the childs neuromuscular movements
This is usually noted by a change in the childs handwriting and may also include jerky
movements
Rash- A pink rash with odd edges that is usually seen on the trunk of the body or arms and
legs.
Fever
Weight loss
Fatigue
Stomach pain
+ Diagnosis of Rheumatic Fever
There are five major and four minor criteria and an absolute requirement for evidence of
recent group A streptococcal infection for the diagnosis of rheumatic fever
The diagnosis of acute rheumatic fever can be established by the Joins criteria, when a pt.
fulfils:
Two major criteria or
One major and two minor criteria and
Meets the absolute requirement.
A) Major manifestations
The presence of two major criteria with evidence of (microbiologic or serologic)
recent group A streptococcal infection fulfils the joins criteria.
1- Migratory polyarthritis
Arthritis occur in a bout 75% of patients with rheumatic fever
Typically involves larger joints; particularly the knees, ankles, wrists and elbows.
263
Involvement of the spine, small joints of the hands and feet or hips is uncommon
Rheumatic joints are generally hot, red, swollen and exquisitely tender
The joint involvement is characteristically migratory in nature
Arthritis is the earliest manifestation of acute rheumatic fever
2- Carditis
Carditis and resultant chronic rheumatic heart disease are the most serious
manifestations of acute rheumatic fever
Accounts for essentially all of the associated morbidity and mortality
Rheumatic carditis is characterized by pancarditis, with active inflammation of
myocardium, pericardium and endocardium
Endocarditis (valvulitis), which is manifested by one or more cardiac murmurs, is a
universal finding in rheumatic carditis.
Most cases consist of either isolated mitral valvular disease
Serious and long-term illness is related entirely to balvular heart disease as a
consequence of a single or recurrent attacks of acute rheumatic fever.
Carditis occurs in a bout 50-60% of all cases of acute rheumatic fever
The major consequence of acute rheumatic carditis is chronic, progressive valvular
disease, particularly valvular stenosis.
3- Chorea
Sydenham chorea occurs in about 10-15% of patients with acute rheumatic fever.
Usually presents as an isolated, frequently subtle, neurologic behaviour disorder
Emotional liability, in coordination, poor school performance, uncontrable movements
and facial grimacing, exacerbated by stress and disappearing with sleep are
characteristics
The latent period from acute group A streptococcal infection to chorea is usually longer
than for arthritis or coarditis, and can be months
The clinical manifestation or maneuvers to elicit features of chorea include:
264
1- Demonstration of milk moids grip (irregular contraction of the muscles of the
hands while squeezing the examiners fingers)
2- Spooning and pronation of the hands when the patients arms are extended
3- Wormian movement of the tangues up on protrusion
4- Examination of handwriting to evaluate fine motor movements.
4- Subcutaneous Nodules
Are a rarely found in patients with acute rheumatic fever (<1% of pts)
Consists of firm nodules approximately 1cm in diameter along the extensor surfaces of
tendons near bony prominences
There is a correlation b/n the presence of these nodules and significant rheumatic heart
disease
5. Erythema Marginatium
It is also ararly seen in patients with acute rheumatic fever (<3% of pts)
It is characterstic rash of rheumatic fever
Iconsists of erythematous, serpiginous, macular lesions with pale centers that are not
pruritic
It occurs primarily on the trunk and extremities, but not on the face
It can be accentuated by worming the skin
B. Minor manifestation
There are two clinical and two laboratory minor manifestations associated with
rheumatic fever
1. Clinical Features
A- Arthralgia, in the absence of polyarthritis as a major criteria
B- Fever- Typically temperature > 102
o
F and occurring early in the course of illness
2. Laboratory Features
A- Elevated acute-phase reactants
E.g. ESR
265
- C-reactive protein
B- Prolonged PR interval on electrocardiogram (First degree heart block); However, a prolonged
PR interval alone does not constitute evidence of carditis or predict long-term cardiac sequelae.
7.4.3.5 Medical and nursing management
Specific treatment for Rheumatic heart disease will be determined based on:
The childs overall health and medical Hx
Extent of the disease
The childs tolerance for specific medications, procedures or therapies
Expectations for the course of the disease
+ The best treatment for rheumatic disease is prevention
A. Antibiotic can usually treat strep throat (a streptococcal bacterial infection) and stop acute
rheumatic fever from developing.
- Antibiotic therapy has sharply reduced the incidence and mortality rate of rheumatic
fever and rheumatic heart disease
Children who have previously contracted rheumatic fever are often given continuous (daily
or monthly) antibiotic treatments to prevent future attacks of rheumatic fever and lower the
risk of heart damage.
B. Bed rest- If inflammation of the heart has been developed
- Medications are given to reduce inflammation and antibiotic to treat streptococcal
infection
Other medications may be necessary to handle CHF
C. Surgical repair or replacement of the valves if heart valves are damaged
7.4.3.6 Complication
7.4.4Caring a child with hemophilia
7.4.4.1Def
n
- Hemophilia is a group of inherited bleeding disorder in which the ability of blood
to clot is impaired
It is a genetic disorder that often results in excessive bleeding
266
Characterized by a disturbance of blood clothing factors
7.4.4.2 Cause- Abnormal or Defective gene
Genes are chemical units that are present in all cells and tell cells what functions to
perform
A person inherits a defective gene from apparent
This defective gene carries no instructions or the wrong instructions, for performing
some function
Injury to a blood vessel is a serious problem for the body
Blood may begin to leak out of the injured area. The body has developed a mechanism
for protecting itself from this kind of damage
The mechanism involves the formation of a blood clot over the injured area to prevent
loss of blood
+ Blood clotting is a complex process which involves:
- Blood cells (platelets)
- At least twenty different chemicals compounds.
- The first step in the clotting process is the formation of a temporary plug by sticking the
platelets to the damaged area
- The plug is soon covered by amore permanent structure consisting of fibrin, a tissue that
acts like a permanent patch or bandage on the injured area
The production of fibrin takes place in aseries of steps that requires thirteen different
chemicals called clotting factors
Inorder for fibrin to form, all thirteen clotting factors must be present in the blood
+ Hemophiliacs or people who have hemophilia may:
Lack one or more cloting factors, or
Their bodies may not make enough of a clotting factor or
The clotting factor may not be made correctly
In any one of these cases, the patients body is not able to make fibrin
Bleeding from the damaged blood vessels
267
Currently, a bout 17,000 people in the united states have hemophilia
About 1 in every 8,000 boys is born with hemophilia; girls are more rarely affected by
this genetic condition linked to gender.
A male can not pass the gene for hemophilia to his sons, though all his daughters will be
carriers of the disease gene.
Each male child of child of a female carrier has a 50% chance of having hemophilia

7.4.4.4 Types of Hemophilia
- Various types of hemophilia have been discovered
- Each type results from problems with a particular clotting factor
1- Hmophilia A- It is also known as classichemophilia or known as factor VIII deficiency
- It is the most common form the disorder
- It is the cause of a bout 80% of cases
- It can range from relatively mild to very severe condition
- The severity of the disorder depends on how much factor VIII the patients body is able
to make
- Individuals with more than 5% of normal factor VIII have mild hemophilia
These individual likely to experience bleeding problems only when having surgery or
dental procedures
Individuals with 1 to 5% of normal factor VIII have moderate hemophilia
- They may experience bleeding problems if they have miner injury, such as falls
Individuals less than 1% of normal factor VIII have severe hemophilia
- They may begin bleeding for no reason at all
- Surgery and dental procedures can be very dangerous
About half of all hemophiliacs have this form of disorder
268
Hemophilia A occurs a cross all populations in the world, with all races being affected
equally
Hemophilia A is found almost exclusively in males, occurring in about 1 in every 10,000
live male births
2- Hemophilia B-
It is also known as Christmas disease
People with hemophilia B have a deficiency in coagulation factor IX
It is the second most common forms of the disorder and makes up the majority of the
remaining 20% of cases
It occurs across all populations in the world, with all races being affected equally
It is found almost exclusively in males, occurring in a bout 1 in 34, 500 men
+ Each cases of hemophilia is unique
- A patient with blood tests suggest severe hemophilia may only bleed occasionally, where as
another patient with a milder form may bleed more often
The reason for this variability may relate to other clotting factors or to differences in
behaviours that present risk of injury
7.4.4.5 Signs and symptoms
The signs and symptoms of hemophilia A and hemophilia B are similar
Varies depending the severity of the factor deficiency and the location of bleeding.
Fewbabies are diagnosed with hemoophilia with in the first 6months of life,
becausethey are unlikely to sustain injury that would lead to bleeding
Eg- Only abut 30% of males with hemophilia bleed excessively when
circumcised and anly 1 to 2% of newborns with hemophilia have bleeding with in the
skull (called an intracranial hemorrhage)
Once babies with hemophilia begin crawling and cruising, parents may notice raised
bruises on the stomach, chest, buttocks and back
The primary symptom of hemophilia is bleeding
The amount of bleeding that occurs depends on how serious the patients condition is
269
In the most severe cases, bleeding can cause serious health problems including dearth
Generally the s/s of Hemophilia include
- Prolonged nose bleeds, from minor cuts
- Excessive bleeding from biting down on the lips or tangue
- Excessive bleeding following a tooth extraction
- Excessive bleeding following surgery
- Blood in the urine (called hematuria)
- Spontaneous bleeding (bleeding that occurs apparently without cause)
- Pain and swelling resulting from bleeding into joints and muscles
- Blood in the stool
- Prolonged bleeding following circumcision
The most common type of bleeding in hemophilia involves muscle and joints
A child with hemophilia will usually refuse to move the affected joint or
muscle because of pain and swelling
Recurrent joint bleeding can also lead to chronic damage
- The severity and frequency of bleeding episodes vary from patient to patient and may
differ depending on whether the person has hemophilia A or Hemophilia B
7.4.4.5 DIAGNOStic evaluation
Abnormal bleeding patterns are usually the first clue that a person has hemophilia
Consider the clinical manifestation
Diagnosis of hemophilia is confirmed by Blood Tests, including:
Complete blood count (CBC)
Prothrombine Time (PT)
Activated partial thromboplastin time (PTT)
Factor VIII and factor IX levels
These tests are able to measure how much of various clotting factors are present in the blood
and how quickly they work to produce clots
270
These tests also helps to diagnose the type of hemophilia a person has and seriousness of the
condition
7.4.4.6 Medical and nursing management
Hemophilia can be treated with injections of missing clotting factors
Patients with hemophilia A receives injections of factor VIII and those with hemophilia B
get factor IX
The frequency of treatmenht depends on the severity of the disease
People with mild hemohilia may require treatment:
Only when they have been injured
Before surgery or dental procedure
Patients with more severe forms of disorder may require regular injections of the missing
factor
Avoiding or preventing risk factors for injury
- Avoid the most strenuous form of work and exercise that might result injury and bleeding
- Special preparations for surgery and/or dental procedures are necessary
PREVENTION
Adults can be tested to tell if they carry a defective X-Chromosomes
Use this information to make decisions about having children
7.4.5 CARING A CHILD WITH LEUKEMIA
7.4.5.1Def
n
. Leukemia is a progressive malignat disease of the blood-forming organs, marked by
distorted proliferation and development of leukocytes and precursors in the blood and bone
marrow
It is a malignant neoplastic disorder of the blood-forming tissues
7.4.5.2 Etiology and Incidence
- The exact causes is unknown
- Possible predisposing factors include:
A) Genetic Influence
271
- Children with Downs syndrome develop leukemia at arate 15 times higher than the general
popn
B) Familial predisposition
- Sibilings of a child with leukemia have a higher risk of developing leukemia themselves
C) Immunologic influence
- Immune deficiencies increase the risk of developing many cancers
D) Viral infection
- Research suggests the possibility of an ancogenic virus that facilitaties the development of
cancer, but no direct link has been proven
E) Environmental Influence
- Evidence suggests that radiation during pregnancy contributes to the development of
leukemia in childhood
- Leukemia accounts for about 31% of all childhood cancers in whites and about 24% in
blacks
- Peak incidence occurs at age 2 to 4 years
7.4.5.3 Classification and clinilal manifestations
- It can be classified according to its predominant cell types and level of maturity
A- Lympho- Involving the lymphoid or lymphatic system
B- Myelo- Originated from the bone marrow
C- Blastic and Acute- Involving immature cells
D- Cystic and chronic- involving mature cells
- Acute leukemia- Represents about 98% of cases of childhood leukemia
- Acute leukemia include the following
1- Acute lymphoblastic Leukemia (ALL)
Accounts for 80% of acute leukemia in children
Sub-classes of ALL include:
- T-Lymphocyte
- B-Lymphocyte
272
- Pre-B-Lymphocyte
- Null cells Account for 75% of cases of ALL
o Carries prognosis of all ALL
2- Acute Nonlymphoblastic Leukemia (ANLL)
- Accounts for 15% of acute leukemia in children
3- Acute undifferentiated Leukemia (AUL)
- It is the least common type of acute leukemia
+ Chronic Leukemia
- Accounts for only 2% of child hood leukemias
C/Ms
Signs and symptoms of Anemia
Pallor - Lethargy
Fatigue - Cardiac murmurs
Poor wound healing, fever, anorexia, lymphadenopathy
Petechiae, ecchymoses, purpura, epistaxis, easy bruising, blood in urine or emesis.
Bone and joint pain
Headache, vomiting, papilledema and other signs and symptom of ed ICP
Weight loss and S/s of infection
P/E Enlarged spleen and liver
- Enlarged lymphnode
- Bone tenderness
- Skin and M.membrane bleeding
7.4.5.4 PATHOPHYSIOLOGY
The malignant leukemic cells arise from the precursor cells in blood-forming organs
- These malignant levkemic cells accumulate and crowd out normal bone marrow elements,
spills into peripheral blood, and evenlually can invade all body organs and tissues
- The replacement of the normal hematopoietic elements by leukemic cells result in bone
marrow suppression, marked by decreased production of RBC, normal WBC and platelets
273
- Bone marrow suppression results in:
Anemia
Infection
Bleeding tendencies
- This puts the pt at ed risk of death from infection or/and haemorrhage
Infiltration of the reticuloendothelial cells or organ causes marked enlargement and
eventually fibrosis
Leukemic infiltration of the CNS results in increased ICP and other effects depending on
the specific area of involvement
Other possible sites of long-term infiltration include the:
Kidnyes - Ovaries
Testes - GI-tracts and
Prostate - Lungs
The hypermetabolic leukemic cells eventually depriue all body cells of nutrients necessary
for survival
Uncontrolled growth of leukemic cells can actually result in metabolic starvation
- Is based on Hx, C/Ms, P/E and Lab. Investigations
Laboratory Findings
- WBC is elevated, low or normal
- Neutropenia (< 1000/m3)
- Thrombocytopenia (<50,000/mm3)
- Anemia
- Blast cells on peripheral blood smear
- Bone marrow:
- Markedly hypercellular
274
- Lacking fat globules and bone particles
- Blast cells over 5% (25% needed for diagnosis, but usually 60-100% blasts
N.B- Extensive replacement of normal bone marrow elements by leukemic cells seen on bone
marrow examination, confirms the diagnosis.
-Leukemia treatment commonly involves a combination of chemotherapy and radiotherapy,
provided at 4 levels
1- Induction of remission
The goal involves reducing the no of leukemic cells
Drugs used commonly include acombination of:
Oral prednisone
Intravenous vincristine
Intravenous L-asparaginase
2- Sanctuary Therapy
The goal is to attack leukemic cells in the CNS, which are protected by the blood-brain
barrier or in the testes, which are protected by their peripheral location
The therapy consists of intrathecal chemotherapy, typically a combination of:
Methotrexate
Cytosine
Arabinoside and
Steroids
Or
Irradcation, usually beginning during the first 6 to 8 weeks after diagnosis and lasting for 2
weeks
N.B- Irradiation of testes remains controversial
3- Continuation (maintenance) therapy
The goal is to preserve remission and continue to reduce the no of leukemic cells
275
Therapy begins when CBC values approach normal levels and commonly lasts for 1
to 3 years
4- Reinduction therapy
- The goal is to reduce the number of leukemic cells in a child who has relapsed
- Chemotherapy commonly involves:
Predinson and vincristine --combined with other drugs not used preveiously in
therapy
Bone marrow transplanlation may be performed in children facing almost certain death with
out the procedure.
If it is successful, it destroys the leukemic cells and replenishes bone marrow with
healthy cells
Prognosis for long-term survival after transplantation is 25% to 50%
Prepare the child for diagnostic tests and treatment by:
Assessing the childs level of understanding
Addressing specific fears and misconceptions
Providing information appropriate to the childs age and developmental level
- Explaining what the child will see, smell, hear and feel rather than merely specifying what
will happen
Prevent complications related to bone marrow suppression, such as infection and sepsis
Scrupulous handwashing
Limiting the childs exposure to persons with infection
Promote optimum nutrition to maintain and rebuild healthy tissue
Serve small, frequent meals in apleasant, relaxed environment
Involve the child in food selection, as appropriate
Assess for blood transfusion reaction for a child receiving blood transfusions
276
Promote adequate rest by providing a calm, quiet environment and by clustering nursing
care activities
Take measures to prevent hemorrhage
Turn the pt. frequently to relieve pressure on bony prominences
Provide meticulous mouth care and good skin care
Measuring To via the oral or axillary routes only, a voiding rectal To measurement
Prevent or minimize constipation, hemorrhagic cystitis, renal damage, and alopecia
resulting from chemotherapy.
Duty 7.5- Providing Care for A child with Musculoskeletal Disorder
7.5.1 Assessment of Musculoskeletal Disorder
7.5.1.1Brief Anatomy and physiology of musculoskeletal system
The muscular and skeletal systems are inseparably related because together they provide the
body with shape and movement
The skeletal system of the body is a living, ever- changing structure made up of bones and
joints
The muscular system is made up of all the muscle tissue in the body, including that form the
walls of various internal structures, such as the heart and intestines
+ Skeletal system is composed chiefly of:
Fibrous connective tissue
Cartilage All of theses are connective tissue
Bone
Reticuloendothelial tissue
+ Fibrous connective tissue composes of
Ligaments
Tendons
Muscle sheaths
Deep fasciae b/n organs
277
Walls of large arteries
Cartilage tissue is an opaque, bluish white tissue that consists of a firm rubbery material
called a matrix
Matrix is secreted by chondrocytes
Cartilage is covered by a dense membrane called perichondrium, which serve to nourish
and repair the tissue by chondroblast cells
+ Bone tissue is composed of about:
Two-third (2/3
rd
) of inorganic matter (calcium)
One-third (1/3
rd
) of organic matter (bone cells and blood vessels)
- Embedded bone cells called osteocytes lie with in tiny spaces called lacunae and are
supplied with blood by an interconnecting system of Havarsia canals, each canal surrounded
by concentric Lamellae
Compact bone tissue is a type of bone tissue is which the rings of the matrix are put down
layer upon layer
Cancellous bone tissue is a type of bone tissue in which the rings form delicate lacy pattern
with spongy apprance
Most bones are hyaline cartilage that has turned to stone by the deposite of calcium in the
matrix.
The marrow within all bones is classified as Reticuloendothelial tissue
Red marrow- specialized hemopoietic tissue that generates millions of blood cells in
each day
Yellow marrow Is not hemopoietic, contains fat and is used for storage
+ A typical long bone consists of:
Diaphysis- It is the main shaft, which is composed of compact bony tissue
Epiphysis- It is the bulbous ends and composed of cancellous bony tissue to which muscles
are attached
Articular cartilage- a thin layer of hyaline cartilage, which cushions shock
278
Periosteum- a dense fibrous membrane that couers bone except joint surfaces at which the
articular cartilage forms the couvering
Marrow cavity A space that runs the length of the diaphysis and contains the bone marrow
Endosteum- The lining within the marrow cavity
The short, flat and irregular bones consist of an inner core of cancellous tissue in which
marrow is found, an outer layer of compact bone and a covering of periosteum.
Function- The function of the skeleton is:
To support, protect and permit positioning and movement of the body
Produce most of the blood cells of the body
Store and release calcium according to the bodys needs
There are three types of muscle tissue:
o Skeletal or striated muscle tissue
o Visceral or smooth muscle tissue
o Cardiac or branching muscle tissue
Because the special function of muscle tissue is contraction, its structure is suited to its
function
The cells are long and slender with numerous contractile fibres running length wise through
them
Skeletal muscle cells are bound into numerous small bundles by a membrane of connective
tissue called the sarcolemma
The visceral muscle tissue is made of tapering spindle-shaped cells that do not have stripes
and are not bound in bundles
Cardiac muscle cells have cross-striations, but are not separate and distinct fibres
Based on nerve supply, muscle tissues are classified into two:
1- Involuntary muscles- Tose innervated by autonomic nerve fibres
e.g. Visceral and cardiac muscle tissue
2- Voluntary musctes- those innervated by cerebrospinal nerves
279
Characteristics of muscle tissue that make them especially suited for their functions
include:
A) Irritability- The cells respond to stimulation independently of their nerve supply e.g. If
aparalyzed muscle is shocked with electricity, it will contract
B) Contractility- On stimulation, the muscle tissue contracts, causing it to shorten and then
become thicker
C) Muscle responds to excessive and continuous contraction by becoming fatigued
Complete muscle fatigue is the state which a muscle has lost its irrilability and contractility
and is unable to contract
Exercise of muscle tissue causes the cells to multiply and the musle to enlarge
(Hypertrophy).
Disuse of muscle causes atrophy
Each muscle consists of a central portion called the body and two ends; the origion and
insertion
Origion of a muscle is the end attached to the bone that remains stationary when the muscle
contracts
Insertion of a muscle is the end attached to the bone that moves when the muscle shortens
As the muscle contracts, one bone must remains stationary to act as on anchor for the
muscle to pull a gainst it draws the other bone toward it
Names have been given to the special function of each muscle as it relates to others in group
actions
Agonist contracting muscle whose contraction is opposed by another muscle
Antagonist Muscle that opposes the action of agonist muscle
Prime mover- the muscle or muscles whose controaction actually produces the movement
Synergist Muscle that contracts at the same time as the prime mover but acts on
neighbouring joints to steady them and thus helps the prime mover produce amore effective
movement.
280
Function- The outstanding characterstic of muscle tissue is its ability to contract
By contracting, the muscle tissue:
1- Provides external movement of body parts for locomotion
2- Provides internal movement of portion of body organs for their proper function
3- Maintains body posture by partially contracting the skeletal muscles
4- Produces alarge share of body heat as a result of chemical changes.
Development of musculoskeletal system:
The musculoskeletal system arises from the embryonic mesodermal layer, which appears
during the 2
nd
week of gestation
By the 8
th
week of gestation, all major bones are present in the cartilaginous skeleton
Bone formation occurs via ossification, which begins as early as the 8
th
week of gestation
and continues throughout gestation and childhood
Bone growth occurs in two dimensions:
Length occur at the epiphyseal plate, avas cular area of active cell division
Diameter- From the center to the periphery
Sometimes in adolescence, the epiphyseal plate converts to bone and growth stops.
7.5.1.2 Assessment of musculoskeletal disorder
The key to an accurate diagnosis of musculoskeletal disorder is:
A careful history
A thorough physical examination
Appropriate radiographic imaging and
Occasionally laboratory testing
A- History Taking
In the initial assessment of a childs musculoskeletal system, the nurse should obtain a
complete health history of problems pertaining to this system
The history of the complaint is often the most important part of the evaluation
History taking of the musculoskeletal problem focus on:
Trauma or in juries
281
Delayed walking or other developmental abnormalities
Pain (dull, boring or sharp with movement)
Structural abnormalities (e.g.- clubfoot, hip dysplasia, leg length discrepancy, scoliosis etc)
Any physical limitations or life style alterations imposed by the problem
Mobility aids used
Joint stiffness, gait disturbance, swelling and generalized muscle weakness
Location and duration of symptoms
Antecedent factors:
Fever - Radiation of pain
Trauma - Neurologic symptoms
Factors aggravating or alleviating the symptoms
Previous evaluation or treatment
Past medical history, especially in children with chronic symptoms
Prenatal or pregnancy history, which include:
Maternal disease or illnesses
Vaginal bleeding
Oligohydraminos
Ingestion of toxic substances or medications
Trauma
Birth History should determine:
Length of pregnancy
Duration of labour
Type of difficulty, if any, with delivery
Birth presentation
Birth weight and Apgar score
History of the child during the neonatal period
Evaluation of the presence and delay of developmental milestones for:
282
Locomotion - Social activities and
Dexterity - Speech
Family history may give clues to possible genetic musculoskeletal disorders:
E.g- Congenital syndromes
- Muscular dystrophy
- Skeletal dysplasia
B- Physical examination
The physical examination of a child with a musculoskeletal disorder must be thorough
It includes the careful evaluation of the musculoskeletal and neurologic system, as well as
an appropriate general P/E
Many common musculoskeletal disorders can be diagnosed by the Hx and P/E alone
Physical assessment of the musculoskeletal system should include examination for:
Structural abnormalities, including asymmetric limb lengths and spinal deformities
Posture and gait
Range of motion in all joints
Muscle symmetry, tone, strength
Color, temperature, sensation, motion, pain, pulses, capillary filling and edema in each
extremity
The examination of the musculoskeletal system includes four parts
1- Observation
The first part of the musculoskeletal examination begins with inspection of the body
inspection must be accomplished by observing the child undressed
Observation helps to evaluate or assess:
Posture and gait
Truncal alignment
Symmetry of the extremities
Cutaneous lesions
283
2- Palpation
The involved joint, area of the extremity or trunk that is of concern should be palpated for:
Tenderness
masses
Soft tissue swelling
Increased warmth
Abnormal joints should also be palpated for:
Effusion
Synovial thickening
Increased warmth and
Area of tenderness
3- Assessment of Joint Range of motion
The range of motion of the involved joint or joints should be assessed and recorded
If the opposite joint is normal, this range should also be recorded for comparison purposes
The range of motion of joints changes from infancy through childhood and into adolescence
4- Assessment of Gait in ambulatory children
Gait disturbances are one of the most common parental concerns in children
The gait cycle is the time between Right heed strike followed by Left toe off, Left heel
strive, and Right toe. Off and ends with Right heel strike
Right heel strike Left toe. OffLeft heel Right heel strikeRight toe offstrike
The five events describe one gait cycle and include two phases
1- Stance phase The period of time during which one of the two feet is on the ground
2- Swing phase- Is the portion of the gait cycle during which a limb is being advanced forward
without ground contact
Neurological maturation is necessary for the:
- Development of gait and
- Normal progression of developmental milestones
284
Common gait disturbances include:
1- Limping It is categorized into either painful (antalgic) or nonpainful (Trendelenburg gait)
on the basis of the length of the stance phase
In painful gait, the stance phase is shortened as the child decreases the time spent on the
painful extremity
In non painful gait, the stance phase is equal b/n the involved and uninvolved sides, but
the child will lean or shift the center of gravity over the involved extremity for balance.
2- Torsional variations
Torsional variations- in- toeing and out-toeing- are the most common gait disturbances that
cause parents to seek advice from their paediatrician
the presence of in-toeing and out toeing doesnot imply an abnormality of the foot, but
rather only the direction in which the foot is pointing during ambulation
the causes for torsional variation can occur from proximal (hip) to distal (foot) in the
involved extremity
3- Toe walking
Toe walking equines gait is a less common cause of gait disturbance
It can be a normal finding in children up to 3 year of age
Persistent toe walking thereafter or acquired toe walking at a later age is considered
abnormal and requires careful evaluation
A careful Neurologic evaluation must be performed and includes.
Muscle strength testing
Sensory assessment
Evaluation of deep tendon
Evaluation of pathologic reflexes
Assessment of the spine and identify the presence of deformity (scoliosis, kyphosis,
spinal mobility)
C- Radiographic Assessment
It is the principal method for the evaluation of the pediatric musculoskeletal system
285
It include routine radiographs and as well as special procedures such as
- Technetium bone scans
- CT scan
- MRI and
- Ultrasonography
Routine Radiography
The first step and consists of anteroposterior and lateral views of the
involved joint, bone or area
Comparison views of the opposite side, if uninvolved, may be helpful in
difficult situations
Technetium Bone scans
Are particularly useful in looking for occult lesions, when routine radiographs are
normal
Common indication for bone scans include:
Early septic arthritis or Ostemoyelitis
Neoplasia, such as osteoid osteomas and leukemia
Metastatic lesions
Occult fractures, such as child abuse or a toddler fracture of the tibia
Inflammatory disorders
Computed Tomography
Coronal and axial cross-section studies with CT can be beneficial in evaluating complex
disorders of the spine, pelvis and feet
It allows visualization of the bone anatomy and the relationship of bones to contiguous
structures with routine radiograpsh do not
Magnetic Resonance Imaging
286
This avoids ionizing radiation and is presumed not to produce biologically harmful effects
It produces excellent anatomic images of the musculoskeletal system; including the spinal
cord and brain
It is especially useful for soft tissue lesions, allowing distinction among different muscles or
muscle groups
In children, MRI can be useful in the evaluation of:
A vascular necrosis of bone, especially the capital femoral epiphysis or femoral head
Bone and soft tissue neoplasms
Intra-articular abnormalities of the knee joint
Assessment of intraspinal pathologic conditions
Deep tissue infection (Fasciltis, myositis)
Ultrasonography
It has no ionizing radiation, no contrast material to be administered
Has no biologically harmful effects and can be repeated as often as necessary
The major indications for wtrasonography are:
Fetal studies of the extremities and spines
Developmental dysplasia of the hip
Joint effusions
Occult neonatal spinal dysraphism
Foreign bodies in soft tissues
Popliteal cysts of the knee
The disadvantages of ultrasonography include
Bone is not penetrated
Static images are difficult to interprete
The results are operator dependent
D- Laboratory studies
287
Occasionally, hematologic tests are necessary in the evaluation of the pediatric
musculoskeletal system
The laboratory study may include:
CBC
ESR
C-reactive protein determination
Blood culure for infectious disorders
Rheumatoid factor, etc
Diagnostic Evaluation for Musculoskeletal disorder includes the following:
A) History taking C) Radiographic Assessment
B) Physical Examination D) Laboratory studies
7.5.2- Providing care for a child with Fracture [Traumatic injury]
7.5.2.1Def
n-
Fracture Is a break in a bone, usually accompanied by vascular and soft tissue
damage and characterized by pain, swelling and tenderness
Childrens fractures differ from those of a dults in that they are:
Generally less complicated
Heal more quickly
Usually occur due to different causes
The child has an urge to explore his/her environment, but lacks the experience and
judgment to recognize possible hazards
The bones most frequently fractured in childhood are the:
Clavicle - Humerus and
Femur - Wrist
Tibia
Types of Fracture
288
Classification of fractures reflects the kind of bone jury sustained
7.5.2.2 Types of fracture
Generally there are two types of fracture:
1- Complete # - A fracture in which the fragments of the fractured bone are separated
2- Incomplete # - A fracture in which the fragments of a fractured bone remain partially joined
Fracture can be classified into two based on the associated skin condition:
A- Compound or open # - Is a type of fracture in which a broken bone penetrates the skin
B- Simple or closed #- Is a single break in the bone without penetration of the skin
Greenstick #s- Are one kind of incomplete fracture common in children dueto incomplete
ossification
Fractures in the are of the growth plate (Epiphyseal plate) can cause permanent damage
and severilyimpair growth
Bones break because they can not with stand force placed up on them
o When they are weakened by lack of calcium or tumors, they are more susceptible to
the effects of forces
Biochemically, the paediatric skeletal sytem can absorb more energy before deformation
and fracture than can adult bone
Radiological evaluation and classification of pediatric fractures include the following
1- gitudinal Fracture line parallel to bony axis
2- Transverse Fracture line perpendicular to bony axis
3- Oblique- Fracture line at angle to bony axis
4- Spiral Fracture line runs curvilinear course to bony axis
5- Impacted- Fracture bone ends compressed together
6- Comminuted Fragmentation of bone into three or more parts
7- Greenstick Bending of bone with incomptete fracture of convex side
289
8- Simple # - Fracture with no penetration of the skin
9- Open # - Fracture with penetration of the skin
Assessment
Whenever children fall or are involved in traumatic accidents of any kind, they are
assessed for:
Pain or tenderness at thepossible # site
Loss of function or abnormal mobility
Deformity in alignment or swelling
Grating sensation (crepitus) at the suspected break paint
Discoloration of the surrounding tissue
Splinting of the nearby muscles
The diagnostic evaluation of fracture includes the following
History taking
Physical examination and
Radiographic examination
- The aim of emergency care is/are
To prevent further injury
Stabilize the affected part
Promote comfort and safely transport injured children to medical facilities for
The goal of surgical treatment for fracture bones and injured joints is to restore them
to their normal alignment and function with minimal danger and discomfort in the
shortest possible time
Most childhood fractures are treated by realignment and immobilization, using either:
A- Traction or
B- Closed manipulation and casting
290
A few patients with severe #s or othe injuries such as burns or other soft-tissue damage may
require:
C- Surgical Reduction and/or
7.5.2.5.1 Cast
Casts Is a mold used to immobilize and position body parts
Are applied over almost every area of the body
Children who are to have area of the body
Children who are to have casts applied may be inpatients or outpatient.
Whatever the status of the patient, preparation for casting consisting of:
Withholding food and fluids to avoid stress vomiting
Administering preoperative sedation to reduce fear and pain
Cleansing the skin and treating abrasions
+ Nursing care of a child with cast includes the following:
Checking color, sensation and motion of skin distal to the cast every half hour for the first
6 hours after application, then every 4 hours until discharge
Checking pedal or radial pulses of casted extremities
Checking cast for tightness by slipping finger under edge (If impossible, cast is too tight)
Inquire about pain, numbness, or burning sensation.
Assessment of the movement to toes and fingers of the pt. with cast
Elevation of the casted extremity
Handling of wet casts carefully so as not to cause indenlations
Checking cast for foul or musty a doors.
N.B- Always consider the 5 ps during care of a patient with cast
Pain - Paralysis
291
Pulse - Pallor
Paresthesia
7.5.2.5.2 Traction- Is a pulling force applied to an extremity or other part of the body
A system of weights, ropes and pulleys is used to:
Realign and Immobilize fractures
Reduce or eliminate muscle spasm
Prevent # deformity and joint contracture
Basically, there are two types of Tractons:
1- Skin Traction Pulls on tape, rubber or plastic materials attached to the skin
and indirectly exerts pull on the musculoskeletal system.
2- Skeletal traction
Exerts a pulline force directly on the skeletal structures by means of a pin, wire, tongs or
other devices surgically inserted through a bone.
Bryants Traction- Is often used for the treatment a fractured femur in children under the
age of 3 years.
Russells Traction- Is more effective with older children who have femoral #s.
Side-Arm Traction Is sometime used for fractures of the hemerus or elbow
+ Nursing care for children in traction involves:
Checking the attachment of the traction to the child, signs of infection or irritation of the
skin
Checking body alignment, special positioning, such as pillows under legs
Checking pulleys, knots, weights, presence of siderails and restraints.
Checking for the presence of circulation, sensation, motion, swelling and discoloration of an
extremity
Encouraging breathing and range of motion exercises ---
Internal fixation- Devices include rods, pins, screw and plates made of
insert materials that will not trigger an immune reaction.
292
External fixation- Divices are used primarily in four conditions
Massive open #s with extensive soft tissue and/or neurovascular damage
Infected #s that fails to heal properly
Acutely infected fractures
Multiple trauma with a number of #s, often accompanied by injuries to the head, chest or
burns.
7.5.3 PROVIDING CARE FOR AMPUTATED CHILD
7.5.4 PROVIDING ARE FOR A CHILD WITH INFECTION OF THE BONE
[ STEOMYELITIS]
7.5.4.1 Def
n
- steomyelitis is an infection and inflammation of the bone
Suppurative infection of bones and joint in children are important because of their potential
to cause permanent disability.
The frequency of skeletal infection is greater in infants and toddlers than in older children.
The risk is geatest if the physis (growth plate of bone) or the synovium is damaged
7.5.4.2 Etiology- Bacteria are the most common pathogens in acute skeletal infection
Staphylococcus aureus is the most common infecting organism of the bone in all age
groups, including newborns
Group B streptococcus and gram-negative entericbacilli are prominent pathogens in
neonates
Group A streptococcus is next in frequency but constituets less than 10% of all
causes.
After 6 years of age, most causes of Osteomyelitis are caused by:
- S.aureus
293
- Streptococcus or
- Pseudomonas aeruginosa
Salmonella and S.aureus are the two most causes of Ostemoyelitis in
children with sickle cell anemia.
Microbial etiology is confirmed in about ths of cases of
osteomyelitis and 2/3 rds of cases of suppurative arthrilis.
Mode of transmission of the pathogens
The causative organism of osteomyelitis reaches the bone by
two ways:
1) Directly- Direct infections of the bone can occur as a result of penetrating wound or open
fracture
2) Indirectly- Indirect infections are spread by the blood stream from infections elsewhere in
the body.
Injury of a bone makes it more susceptible to bacterial infection of the bone
7.5.4.3 Pathogenesis
The unique anatomy and circulation of the ends of long bones
results in the
predilection for localization of blood borne bacteria
In the metaphysic, the nutrient arteries branch into non-
anastomosing capillaries under the physis, which make a sharp loop before entering venous
sinusoids draining into the marrow
Blood flow in this area is sluggish and provides an ideal
environment for bacterial seeding
Once the bacterial focus is established, phagocytes migrate to
the site and produce an inflammatory exudates.
294
The generation of proteolytic enzymes, toxic oxygen radicals,
and cytokines result in decreased oxygen tension, decreased PH, osteolysis and lissue
destruction
As the inflammatory exudates progresses, pressure increases
spread through the porous metaphyseal space via the havarsian system and Volkmann
canals into the subperiosteal space
Purulence beanth the periosteum may lift the periosteal
membrane of the bony surface
Further impair blood supply to the cortex and metaphysis
In newborns and young infants, transphyseal blood vessels
connect the metaphysic and epiphysis
- So it common for pus from the metaphysis to enter the joint
space
- Extension through the physis result in abnormal growth and
bone or joint deformity
In latter childhood the periosteum becomes more adherent,
favoring pus to decompress through the periosteum
Once the growth plate closes in late adolescence, hematogenous
Ostemoyelitis more often begins in the diaphysis and can spread to the entire intramedullary
canal
-The signs and symptoms of skeletal infection are highly dependent on the age of the patient
The earliest signs and symptoms are often subtle
Neonates- May exhibit pseudoparalysis or
- Pain with movement of the affected extremity
- Half of the neonates do not have fever and may not appear ill.
Older infants and children
More likely to have fever and pain
295
Localized signs such as edema, erythema, and warmth
With involvement of the lower extremities, limp or refusal to walk is seen in approximately
half of patients
In acute osteomyelitis, there is finger-point tenderness over the bone with swelling and
fever
In septic arthritis, there is acute tenderness, and swelling over the joint with fever
- The child will refuse to allow any movement in the joint
Erythema and edema of the skin and soft tissue overlying the site of infection is seen earlier
in suppurative arthritis than in osteomyelitis. This is because of:
The bulging infected synovium is usually more superficial, where as the metaphysis is
located more deeply
Local swelling and redness with osteomyelitis may mean that the infection has spread out of
the metaphysic into the subperiosteal space, representing a secondary soft tissue
infelammatory response
N.B- Long bones are principally involved in Osteomyelitis
The femur and Tibia are almost equally affected and together constitute almost half of
all cases
Bones of upper extremities account for one-fourth of all cases
Joints of the lower extremity constitute th of all cases of suppurative arthritis
The elbow, wrist and shoulder joints are involved in about th of cases
Usually only a single site of bone or joint is involved
In chronic osteomyelitis, symptoms are not severe, but draining sinuses may be present
7.5.4.5 Diagnostic Evaluation
Aspiration of the infected site for Gram stain and culture, when Hx and P/E indicate a
strong likelihood of osteomyelitis and/or suppurative arthritis remains the definitive
diagnostic technique and provides the optimal specimen for culture to confirm the Dx.
Blood culture in all cases of suspected osteomyelitis and septic arthritis
Synovial fluid analysis for cell count, differential, protein and glucose
296
There are no specific laboratory tests for osteomyelitis and suppurative arthritis
WBC count and differential Are very sensitive, for bone and
ESR joint infections but are non-
C- Reactive protein specific
Non helpful in distinguishing b/n skeletal infection and other inflammatory processes
Radiographic Evaluation
Radiographic studies play acrucial role in the evaluation of osteomyelitis and suppurative
arthritis
Plain Radiographs
- Are often used for initial evaluation to exclude other cause, such as trauma and
foreign bodies
- Are taken within 72 hours of onset of the symptom of osteomyelitis
- Show displacement of the deep muscle planes from the adjacent metaphysic caused
by deep tissue edema
- Show widening of the joint capsule, soft tissue edema and obliteration of normal fat
fines
N.B- Lytic bone changes are not visible on radiographs until 30-50% of the bony matrix is
destroyed
- Tubular long bones do not show lytic changes for 7-14 days after the onset of infection
Ultrasonography:
Helpful in detecting joint effusion and fluid collection in the soft tissue and
subperiosteal regions
May guide localization for aspiration or drainage
Highly sensitive in the detection of joint effusion, particularly for hip joint, where
plain radiographs may be normal in more than 50% of cases of suppurative arthritis
Computed tomography
It can demonstrate osseous and soft tissue abnormalities
297
It is ideal for detecting gas in soft tissues
Magnetic Resonance Imaging
Is the best radiologic imaging technique for the identification of abscesses and for
differentiation b/n bone and soft tissue infection
Provides precise anatomic detail of subperiosteal pus and accumulation of purulent
debris in the bone marrow & metaphyses for possible surgical intervention
It is particularly useful in the evaluation of vertebral osteomyelitis and diskitis owing
to the clear delineation b/n the vertebral body and cartilaginous disk.
Radionuclide studies
Radionuclide imaging is also called three phase bone scan
Can be valuable to augment MRI< especially if multiple foci are suspected
Technetium-99 methylene diphosphonate (99mgc), which accumulates in areas of
increased bone turnover, is the preferred agent of choice
Osteomyelitis causes increased vascularity, inflammation and increased osteoblastic
activity, resulting in an increased concentration of 99mTC.
Any area of increased blood flow or inflammation can cause increased uptake of 99m
TC in the first pahse (5-10min) and second phase(2-4 hours)
But osteomyelitis causes increased uptake of 99mTC in the thrd phase (24hr)
The three-phase imaging with 99mTC has excellent sensitivity (84-100%) and
specificity (70-96%) in hematogenous osteomyelitis and can detect osteomyelitis
with in 24 to 48 hours after the onset of the symptoms
Advantages:
Infrequent need for sedation
Lower cost
Ability to image entire skeleton for detection of multiple foci and
Ability to scan multiple times after one injection.
Optimal treatment of skeletal infections requires collaborative efforts of:
298
Pediatricians
Orthopaedic surgeans
Radiologist
Psychiatrists and
Nursing staffs
The treatment of osteomyelitis mainly includes the following:
Administration of Antibiotics
Surgical therapy
Physiotherapy
Antibiotic Therapy
The initial empirical antibiotic therapy is based on the:
Knowledge of the likely bacterial pathogens at various ages
Result of the Gram stain of aspirated material and
Other additional considerations
In neonates Adminstration of antistaphylococcal pencillin is important
Eg- Nafcillin or oxacillin 150-200mg/kg/24hr divided every 6 hr IV. &
Abroad-spectrum cephalosporin, such as cefotaxime 150-200mg/kg/24hr divide
every 8hrs IV, provide coverage for the:
S.aureus
Group B streptococcus and
Gram-negative bacilli
In infants and children younger than 5yrs of age:
The principal pathogens are S.aureus, streplococcus and H.influenzae type b
Cefuroxime 200-300mg/kg/24hr divide every 8hrs IV
After 5 years of age. In the absence of special circumstances, virtually all cases of osteomyelitis
are caused gram-positive cocci
Antistaphylococcal antibiotics such as:
299
Nafcillin 150-200 mg/kg/24hr every 6hrs or
Cefazolin 100-150mg/kg/24hr divided every 8hrs IV
Broad-spectrum drugs (a third generation cephalosporine are generally administered,
unless gram-positive cocci are seen in the Gram stain of synovial fluid, in case of
septic arthritis
Surgical Therapy. It is indicated when:
Frank pus obtained from subperiosteal or metaphyseal aspiration
After a penetrating injury
A retained foreign body is possible
There is infection of the hip
There is chronic osteomyelitis
Physical therapy
The major role of physical medicine is preventive one.
The affected extremity should be kept in extension with sandbags, splints, or if
necessary with casts.
7.5.4.7 Nursing consideration
7.5.4.8 Prognosis
7.5.5 SYSTEMIC LUPUS ERYTHEMATOSUS /SLE/
7.5.5.1Def
n
- SLE - is a rheumatic disease which is characterized by auto antibodies directed
against self- antigens and resulting inflammatory damage to the target organs.
300
The name literally means Red wolf because of the characterstics butter fly rash that
appears on the cheeks and bridges of the nose of some individuals
7.5.5.2 Etiology The cause and the disease mechanisms of SLE remain unknown
Many factors are belived to be contribute to the development of SLE
Genentic factors
Hormonal factors
Environmental factors
The halmork is autoontibody production against many self-antigens, particularly
DNA, as well as other nuclear antigens
Ribosomes
Platelets
Coagulation factors
Immunoglobulin
Erythrocytes and
Leukocytes
With autoimmune disorders, the immune system of the body produces antibodies
against antigens within the person
The body mistakes cells within itself as enemies and goes about destroyed them.
7.5.5.3 Pathogenesis
The contributing factors for SLE initiates the production of autoantibody
Elevated levels of these autoantibodies, particularly anti-double-stranded DNA antibodies
are associated with circulating and tissue-bound immune complexes that lead to
complement fixation and recruitment of inflammatory cells and then tissue injury.
Polyclonal activation of B lymphocytes result in elevated immunoglobulin levels, which
may be one cause of elevated autoantibody levels.
Polyclonal activation of B-lymphocyte may be due to:
Non-specific response to an antigenic stimulus, as:
301
o Viral agent
o Loss of tolerance to self-antigens by loss of suppressor T-lymphocyte function
Defects in macrophages phagocytosis and handling of immune complexes have been
described in the pathogenesis of SLE.
Exposure to the ultraviolet rays in sunlight can exacerbate SLE manifestations, perhaps
through damage to nuclear material resulting in release of DNA, which complexes with
circulating anti-DNA antibody
Genetic association in SLE are suggested by the frequent findings of Antinuclear antibodies
(ANAS), Hypergammaglobulinemia and SLE or other autoimmune diseases in family
members of patients with SLE
o Some HLA-types may occur with ed frequency among patients with SLE,
depending on the racial and ethinic backgrounds of pts. studied
SLE has been associated with complement abnormalities and abnormal complement
receptors
Fibrinoid deposits are found in blood vessel walls of affected organs, whose parenchyma
may contain hematoxylin bodies, most likely representing degenerated cell nuclei.
Rheumatoid nodules and granulomas are also sometimes found in affected tissues.
- Patients can present with various manifestations
Symptoms develop slowly and diagnosis may be missed for sometime because the disease
tends to have periods of exacerbation and remising
Children most frequently present with fever, fatigue, arthralgia or arthritis and rash.
Cutaneous manifestations are frequently present
The characterstic malar or butterfly rash includes the nasal bridge and varies from an
erythematous blush to thickened epidermis to scaly patches
Presenting clinical manifestation of SLE
Target organ Clinical manifestations
302
Constitutional Fatigue, anorexia, weight loss, prolonged fever, lymphadenopathy
Musculoskeletal Arthralgia, arthritis, tenditis, myositis
Skin Malar rash, discoid lesions, levido reticularis,
Renal Glamerulonephritis, nephrotic syndrome, HPN, renal failure
CVS Pericarditis, myocarditis, cardiomegally, valvular thickening, conduction
abnormalities, endocarditis and heart failure
Neurologic Seizure, psychosis, stroke, cerebral venous thrombosis, aseptic meningitis, chorea,
mood disorders, peripheral neuritis
Pulmonary Plevritis pain, pulmonary haemorrhage,
Rheumatologic Hemolytic anemia, anemia of chronic disease, thrombocytopenia and Leukopenia
Dx- The diagnosis is confirmed by the combination of clinical and laboratory manifestations
revealing mullisystem disease
The proposed classification is based on 11 criteria for the clinical Dx of SLE
1- Malar rash 6- Serositis
2- Discoid rash 7- Renal disorder
3- Photosensitivity 8- Neurologic disorder
4- Oral ulcers 9- Hematologid disorder
5- Arthritis 10- Immunologic disorder 11- Antinuclear antibody
For the purpose of identifying patients in clinical studies, a person shall be said to have
SLE if any 4 or more of the 11 criteria are present
Laboratory findings:
Elevated ANA titers are often present in children with SLE
Elevated levels of anti-double-stranded DNA, which are more specific for lupus
Serum levels of total hemolytic complement (CH50), C3, & C4 are decreased in active
disease and provide a second measure of disease activity
Anti-smith antibody, found specifically in patients with SLE
So you have to consider both clinical and laborator manifestations for the diagnosis of
SLE
303
The treatment regimen depends on the affected target organs and disease severity
Nonsteroidal anti-inflammatory agents are used to treat arthralgia and arthritis in pts with
SLE
o These should be used with cautions because pts with SLE are more susceptible to
hepatotoxicity
The antimalarial agent hydroxyl-chloroquine may by used to treat mild manifestations,
including skinlesions, fatigue, arthralgia, and arthritis
Anticoagularnt medications for pts with thrombosis and antiphospholipid antibodies
Corticosteroids have been demonstraled to control symptoms and autoantibody production
in SLE
Patients with severe disease may require cytotoxic (immunosuppressive) therapy e.g.
Cyclophosphamide
Generally the treatment of SLE includes:
Non-steroidal anti-inflammatory drugs
Antimalarial medications
Corticosteroid (steroid)
Immunosuppressive therapy
Duty -7.6 - Providing care for a child with nervous system disorders
7.6.1 PROVIDING CARE FOR A CHILD WITH CONVULSIVE DISORDERS
(SEIZURES)
7.6.1.1 BRIEF REVIEW OF ANATOMY AND PHYSIOLOGY
The nervous system is made up of the central nervous system (Brain and spinal cord) and
the peripheral nervous system (nerves, and sense organs)
The CNS arises from the neural tube during embryonic development
By the 4
th
wk of gestation, the neural tube has developed
By the 8
th
to 12
th
wks, the cerebrum and cerebellum begin to develop
304
Two periods of rapid nerve development occur:
Between the 15
th
and 20
th
week of gestation and
From the 30
th
wk of gestation through the first year of extrautrine life
In the first year of extrauterine life, the number of brain neurons increase rapidly
Normally comprising about 12% of the body weight at birth
The brain doubles its weight by the end of the first year of extrautrine life and triples it by
age 5 to 6 years
CNS nerve myelinization, which enables progressive neuromuscular function, follows the
cephalocaudal and proximodistal sequence
Its rate accelerates rapidly other birth
The peripheral nervous system arises from the neural cresat, which originates from the
neural tube during embryonic development.
Function
The Neurologic system consists of three main division:
CNS (Central Nervous System)
PNS ( Central Nervous System)
ANS (Autonomic Nervous System)
Major CNS structures include the:
Cerebrum
Thalamus
Hypothalamus
Cerebellum
Brain stem and
Spinal cord
Cerebrum is the center for:
Consciouness
Thought
305
Memory
Sensory input and
Motor activity
Consists of two hemispheres (Left and Right) and four lobes, each with its specific
functions
A- Frontal lobe Controls voluntary motor movements and contains motor areas, including the
area for speech, center for personality, behavioural and intellectual functions.
For autonomic function and for emotional and cardiac responses
B- Temporal lobe- center for taste, hearing, and smell
In the brains dominant hemisphere, interpets spoken language
C- Parietal Lobe Coordinates and interprets sensory information form the opposite side of the
body
D- Occipital Lobe- Interprets visual stimuli
Thalamus- Further organizes cerebral function by transmitting impulse to and from the
cerebrum
It is also responsible for primitive emotional responses, such as fear, and for distinguishing
b/n pleasant and unpleasant stimuli
Hypothalamus- An autonomic center that regulates blood pressure, temperature, libido, appetite,
breathing, sleep patterns and peripheral nerve discharges associated with certain behaviour and
emotional expression
It also helps pituitary secretion and stress reaction
Cerebrum Controls smooth muscle movements
Coordinates sensory impulse with muscle activity and maintains muscle tone and
equilibrium
Brain stem Includes the mesencephalon, pons and medulla oblongata
Relays nerve impulses between th brain and spinal cord
Makes up the reticular formation (a nerve network that acts as an arousal mechanism) with
the thalamus and hypothalamus
306
Spinal cord- Forms a two-way conductor pathway b/n the brain stem and the peripheral nervous
system
It is also the reflex center for motor activities that do not involve brain control
PNS Consists of 31 pairs of spinal nerves and their intricate branches
Connects the CNS to remote body regions and conducts signals to and from these areas and
the spinal cord
ANS Regulates involuntary body functions, such as digestion, respiration and cardiovascular
functions
The Nervous system regulates and coordinates body activities in response to various
internal and external changes in the environment
7.6.1.2 Definiition
CONVULSIONS- Are paroxysms of involuntary muscular contractions and relaxations that results
from CNS irritation
They are never normal an dare a serious sign in any newborn infant
Seizure is an excessive, disorderly discharge of electrical impulses by neuronal tissue causing
sudden, transient alteration in CNS function
7.6.1.3. Etiology Most seizures and idiopathic with no known cause
There is some evidence of genetic factor, in which the seizure threshold is lowered in
affected persons
This is seen I children over age 3 (>3years)
Some seizures are acquired in direct relation to an event, such as:
Perinatal injury resulting from trauma
Hypoxia and/or toxins
Infectiosn
Hypoglycemia
Hypoglycemia
Convulsions are also may be caused by:
Congenital cerebral defects
307
Intracranial hemorrhage
Hyperglycemia
Fever
Seizures are more common before age 2 years than at any other period
Up to 5% of all children experience at least one seizure by adolescence
Epilepsy, which is chronic and recurrent seizure affects 1% to 2% of all children
7.6.1.4 Classification /Types/
Seizures are classified into three:
A- Partial seizure- Focal focus of abnormal electrical discharge, usually in the cerebral cortex
It include simple partial and complex partial
B- Generalized seizure- Multi focal, arising in the reticular formation and involving both
hemispheres of the brain
Types of this seizure include:
Tonic clonic (Grand mal)
Absence (petit mal)
Atonic
Akinetic and
Myoclonic (including infant myoclonic seizures)
C- Status Epilepticus Continuation of gradmal seizures with no recovery period or regaining of
consciousness b/n attacks; is a medical emergency
The clinical manifestation of simple partial seizures include
Twitching of face, hand or foot; may progress to entire side of the body (Jacksonian seizure)
Turning of eyes or head away from side of focus (Aversive seizure)
Weakness of affected muscle group persisting for hours to days other the seizure:
Tingling, numbness, warmth, or other altered sensation in affected body areas
Possible progression to complex partial or generalized seizures
308
C/Ms- Of complex- partial seizure may include:
prodromal aura of anxiety, nausea and unpleasant taste and smell
impaired consciousness, confusion, vaguestare, mumbling or incomprehensible speech
Repetitive motor activity (Automatism), such as lip- smacking, spitting, chewing, blinking,
picking at clothing, kicking, walking in circles
Possible aggressive response to attempts at restraints
Auditory and visual Hallucinations
Postseizure confusion and fatigue
Possible progression o generalized seizures
C/ms of Grand mal seizures include:
Possible short prodromal aura. Marked by peculiar sensations, often dizziness, but usually
occurs suddenly
Upward rolling of eyes
Loss of conscious ness
Characterstics piercing cry as air is forced through tightly closed vlosed vocal cords
Generalized and symmetric muscle rigidity lasting 10 to 20 seconds, ed salivation, possible
apnea and cyanosis (Tonic phase)
Violent jerking movements as muscle undergo rhythmic relaxation and contraction, possible
foaming at the mouth, biting of tongue and urinary and fecal incontinence (Clonic phase)
Usually lasting about 30 seconds, but possibly persisting for up to 30 minutes
Postseizure exhaustion, headache, confusion, inability to recall the episode.
Status Epileptics
Marked by grand mal seizures occurring in rapid sequence
The child does not regain consciousness b/n attacks
Untreated, a succession of uniterupted seizures can lead to respiratory failure and death
Manifestations of petit mal seizures include
309
Brief (5 to 10 second) loss of consciousness with minimal or no atteration in muscle tone or
behavioural changes
May appear to be daydreaming or staring
Possible minor signs, such as eye rolling, head nodding, lip smacking, facial twitching and
slight had movements
Postseizure, normal appearance and sensations, but with no a wareness of event
Atonic and Akinetic seizures
Sudden momentary loss of muscle tone and postural control causing the child to fall
Often cause serious injury
Transiet loss of consciousness
Myoclonic seizures
Marked by sudden, brief contractures of a muscle or muscle group, occurring singly or
repetitively with no alteration in consciousness
Infant myoclonic seizures
Primarily affects infants b/n age 3 and 6 months and are marked by:
Sudden forceful myoclonic contractions in the trunk, neck and extremities, either flexion (
salaam or Jack Knife seizure) or extension (spread eagle seizure); usually lasting no
more than 1 minute
Crying or grunting in severe attacks
Grimacing and giggling during and after the seizure
The primary objectives of Rx include:
Reducing the frequency of seizures
Correcting the underlying cause, if possible and
Promoting a normal lifestyle as much as possible
The therapeutic Mgt primarily involves drug therapy
E.g. Phenobarbital, phenytoin, ethosuximide, primidone, diazepam,
Carbamazepine
310
Diet- High-fat, low carbohydrate and low protein diet
Surgery- Indicated only for well-defined, surgically accessible epileptogenic focus, when excision
does not interrupt significant life function
Protect the child from injury during acteepisodes
During seizures, carefully observe and document events, including
Apparent triggering factors, if known or suspected
Behaviour before the seizure; Aura
Time seizure began and ended
C/Ms of seizures
Post seizure behaviour and symptoms
Help prevent seizures by preventing the childs exposure to factors or situation known to
precipitate an attack
Eg. Emotional stress -Blinking lights
Minimizing the childs anxiety by staying with him/her during the seizure activity
Implementation of seizure precaution measures
Dosage, administration and side-effects of drug
7.6.2 PROVIDING CARE FOR A CHILD WITH MENINGITIS
7.6.2.1 Def
n
Meningitis- is an inflammation of the meninges, the membrane covering the
brain
Meningeal tissue is invaded by organisms in the blood from other places in the body or
directly from infected ears or sinuses and from wounds or surgical incisions
7.6.2.2 Anatomy and physiology of mening
7.6.2.3 Etiology and pathophysiology
Etiology- The causative agents of meningitis are categorized based on the age groups
The most common infective organisms are
Neonates- Escherichia coli, and group B streptococci
3 months- 5 years Haemophilus influenzae type B is the common causative agent
Over 5 years Neisseria meningitides, streptococci pneumoniae, entrovirus spp,
311
staphylococci, mumps and measles
Generally, meningitis can be caused by the following organisms
Bacteria
Viruses
Fungia & Esspecially common in immunosuppressed children
Parsites
Prulent meningitis is a very serious disease, which is caused by meningococci, pneumococci, or
other bacteria entering the meninges, either
From Blood stream, or
As a complication of mastoiditis or meningomyelocele
Viral or Aseptic meningitis: Clinically, this is often the same as, but less severe than purulent
meningitis
Acute bacterial meningitis Beyond the neonatal period
Bacterial meningitis is one of the most potentially serious infection occurring in infants and
older children
Associated with a high rate of acute complication and risk of long term morbidity
The etiology of bacterial meningitis and its Rx during the neonatal period are generally
distinct from those in older infants and children
The incidence of bacterial meningitis is sufficiently high in febrile infants that it should be
included in the DDX of altered mental status or other neurologic dysfunction
The etiology of meningitis in the neonatal and pastneonatal period may overlap, especially
in 1-2 month old patients in whom:
Group-B streptococcus
Streptococcus pneumoniae (pneumococcus)
Neisseria menigitidis (Meningococcus)
Hemophilus influenzae type B
Bacterial meningitis in children 2 month to 12 years of age usually caused by:
312
S.pneumoniae
N.Meningitidis or
H. Influenzae type b.
Before the widespread use of H. influenzae type b vaccines, approximately 70% of cases of
bacterial meningitis among children younger than 5 yrs were due to H. influenzae type. B
Meningitis now is most commoly caused by S.pneumoniae and N.meningitidis
Alterations of host defense due to anatomic defects or immune deficits increase the risk of
meningitis from less common pathogens such as:
Pseudomonas aeruginosa
Staphylococcus aureus
Coagulase-negative staphylococci
Salmonella spp. And
L.monocytogenes
Epidemiology
A major risk factor for meningitis is the lack of immunity to specific pathogens associated
with young age
Other additional risk factors include:
Recent colonization with pathogenic bacteria
Close contact with individual having the discase
Eg- House hold, daycare centers, military barracks
Crowding, poverity
The mode of transmission is probably person to person contact through respiratory tract
secretion or droplets
The risk of meningitis is ed among infants and young children with occult bacteremia
Epidemiology of streptococcus pneumoniae
Is being dramatically altered by the widespread use of conjugated pneumococcal vaccine
313
This vaccine is recommended for routine administration to all children 23 month of age and
younger at 2,4,6 and 12 to 15 months of age
Immunization targets this puputation b/c the incidence of invasive pneumococcal infections
peaks during the first 2 yrs of life (reaching rates of 228/100,000) in children 6 to 12 months
of age
Risk factors
Children with anatomic or/and functional asplenia 20 to sickle cell anemia
Children those infected with HIV
Otitis media, sinusitis, pneumonia and
CSF otorrhea and/or rhinorrhea
Neisseria meningitides
Meningococcal meningitis may be sporadic or may occur in epidemics
Serogroup B,C and Y each accounts approximaterly 30% of cases in USA
Epidemic disease, especially in developing countries, usually is caused by serogroup A
More common in the winter and springer
Haemophilus Influenzae Type B
Before universal H.influenzae type b vaccination in the united states, invasive infections
occurred primarily in:
Infants 2 month- 2 yrs of age
Peak incidence was at 6-9 month of age
50% of cases occurred in the 1
st
year of life
Risk Factors
Family or day care center contacts of pts with H.influenzae type b.disease
Unvaccinated individuals
Children with HIV infections
Pathophysiology (Patogenesis)
N.Meningitidis and H.influenzae type b attach to mucosal epithelial cell receptors by pili
314
After attachment to epithelial cells, bacteria breach the mucosa and enter the circulation
Bacteria gain entry to the CSF through the choroid plexus of the lateral ventrictes and the
meninges and then circulate to the extra cerebral CSF and subarachnoid space
Bacteria rapidly multiply b/c CSF concentration of complement and antibody are inadequate
to contain bacterial proliferation
Chemotactic factors, then incite a local inflammatory response characterized by
polymorphonuclear cell infiltration
The presence of bacterial cell wall lipopolysaccharide (endotoxin) of gram negative bacteria
(H.influenza type b and N.meningitidis) and of pneumococcal cell wall components
(teichoic acid, peptidoglycan) stimulates a marked inflammatory response, with local
production of:
Tumor necrosis factor
Interleukin-1
Prostaglandin E and
Other cytokine inflammatory mediators
The subsequent inflammatory response is characterized by:
Neutrophilic infiltration
Increased vascular permeability
Alteration of the blood brain barrier and
Vascular thrombosis
These inflammatory process results in:
Inflammation of spinal nerves and roots as well as cranial nerves
Increased ICP and hydrocephalus
Damage to the cerebral cortex
- The onset of acute meningitis has two predominant patterns
315
A) The dramatic, and fortunately, less common presentation is sudden onset with rapidly
progressive manifestation of
Shock
Purpura Frequently resulting death with in 24 hr.
DIC
ed LOC
B) Mare, often, meningitis is preceded by several days of fever accompanied by URT or GIT
symptom, followed by non-specific signs of CNS infection
The signs and symptoms of meningitis are related to the
Non specific findings associated with systemic infection and
Manifestation of meningeal irritation
Non-specific Findings include:
Fever
Anorexia and poor feeding
Symptoms of URTI
Myalgias
Arthralgia
Tachycardia
Hypotension
Photophobia
Various culaneous signs (petechiae, purpura or an erythematous macular rash)
Meningeal irritation manifestation:
Nucheal rigidity
Back pain
Kerning sign Flexion of the hip 900 with subsequent painwith extension of the leg
Brudzinski sign Involuntary flexion of the knees and hips other passive flexion of the neck
while supine
316
NB- some children, particularly in those younger than 12-18 months, kerning and brudzinski signs
are not consistenlly present
Increased intracranial pressure is suggested by:
Head ache
Emesis
Bulging fontanel or diastasis of sutures
Oculomotor or abducens nerve paralysis
Oculomotor or abducens nerve paralysis
Hypertension with bradicardia
Apnea or hyperventilation
Decorticate or decerebrate posturing
Stupor, coma or signs of herniation
Focal neurologic signs, usually due to vascular occlusion (10-20% of pts)
Eg- Cranial neuropathies of the ocular, oculomotor, abducens, facial and
auditory nerves
Focal or generalized seizures due to:
Cerebritis Occur in 20-30% of pts with meningitis
Infarction or
Electrolyte disturbances
Alteration of mental status are common among pts with meningitis and may be due
to:
Increased ICP Responsible for the C/Ms of altered
mental status
Cerebritis or
Hypotension
Irritability
Lethargy
317
Stupor
Obtundation and
Coma
Dx- The diagnosis of acute pyogenic meningitis is confirmed byanalysis of CSF, which
typically reveals micro-organisms on Gram stain and culture, neutrophilic pleocytosis, elevated
protein and reduced glucose concentrations
CT-Scanning for evidence of brain abscess or ed ICP
Blood cultures should be performed in all patients with suspected meningitis
Reveals the responsible bacteria in 80-90% of case of meningitis
Gram stain is positive in most (70-90%) patients with bacterial meningitis
-The therapeutic approach to patients with presumed bacterial meningitis depends on the nature of
the initial manifestations of the illness
A child with rapidly progressing disease of less 24-hours duration in the absence of
increased ICP should:
Receive anitibiotics immediately other an LP is performed
If there are signs of increased ICP or focal neurologic findings:
Antibiotic should be give without performing LP and before obtaining CT-scan
Based on the substantial rate of resistance of S.pneumoniae to B-lactam drugs
recommended empirical therapy is: Vancomycin 60mg/kg 24hr, given every 6hrs in
combination with either of the third generation cephalosporins, cefotaxime 200 mg/kg/24hr,
given every 6 hrs, or ceftriaxone 100mg/kg/24hr administered once/day or 50mg/kg/dose,
given in every 12hr
Patients allergic to B-lactam antibiotics can be treated with Chloramphenicol,
100mg/kg/24hr, given every 6hr.
If L.monocytogens infection is suspected, as in infants 1-2 months old or patients with a T-
lymphocyte deficiency:
318
Ampicillin 200mg/kg/24 every 6hrs plus ceftriaxone or cefotaxime
If a patient is immunocompromised and gram-negative bacterial meningitis is suspected:
Initial therapy may include ceftazidime and an aminoglycoside
Corticosteroids and supportive medical and nursing cares are very important in the mgt of
pts with meningitis
DUTY-8 PROVIDING CARE FOR ACHILD WITH INFECTIOUS DISEASE
8.1PROVIDING CARE FOR A CHILD WITH OPHTHALMIA
NEONATRUM
8.1.1 DEF
N
- it is aform of comjuctivitis occurring in infants younger than 4 wk of age
It is the most common eye disease of newborns
It is an inflammation of the conjuctiva of newborn infants
8.1.2Etiology Neisseria Gonorrhea
Chlamydia trachomatis
Psevdomonas aeruginosa
Staph aureus
Epidemiology
319
Usually acquired during vaginal delivery
Reflects the sexually transmitted diseases prevalence in the community
2% siliuer nitrate application has changed the epidemiology in developed world from 10%
to 0.3%
also affected by maternal screening and Rx for STIS.
During the 20ht century, the incidence of gonococcal ophthalmia neonatorum decreased in
industrialized countries secondary to:
Widespread use of siluer nitrate prophylaxis and
Prenatal screening and Rx of maternal gonorrhea
Gonococcal ophthalmia neonatorum has an incidence of 0.3/1,000 live births in the united
states
In comparison, Chlamydia trachomatis is the most common organism causing ophthalmia
neonatorum in the united states, with an incidence of 8.2/1,000 births
8.1.3 Clinical manifestation
- The clinical manifestations of various forms of ophthalmia neonatrum are not specific enough to
allow an accurate diagnsosis
Regardless of its cause, ophthalmia neonatorum is characterized by:
Redness and chemosis (swelling) of the conjunctiva
Edema of the eyelids and
Eye discharge, which may be purulent
Ophthalmia neonatorum is a potentially blinding condition
The infection may also have associated systemic manifestations that require treatment
+ Any newborn infant who develops signs of conjunctivitis needs aprompt and comprehensive
evaluation to determine the agent causing the infection and the appropriate treatment
The onset of inflammation caused by silver nitrate drops usually occurs:
Within 6-12hrs other birth,
With clearing by 24 to 48 hrs
320
The usual incubation period for conjunctivitis due to gonococcal and Chlamydia infection is
2-5 days and 5-14 days respectively
Gonococcal infection (conjunctivitis) may also begin in infancy after inoculation by the
contaminated fingers of a dults
Gonococcal conjunctivitis begins with mild inflammation and a serosaguineous discharge
Within 42 hrs, the discharge becomes thick andpurulent, and tense edema of the eyelids,
with marked chemosis occurs
8.1.4 Diagnostic evalauation
Dx- Conjunctivitis appearing after 48hr should be evaluated for a possibly infectious cause
Gram-stain of the purulent discharge should be performed and the material cultured
Swab should be submitted in tissue culture media for virus isolation, if a viaral etiology is
suspected
Chlamydial conjunctivitis, the diagnosis is made by:
Examining Giemsa-stained epithetial cells scraped from the tarsal conjunctivae for the
characterstic intracytoplasmic inclusions
Isolating the organism for a conjunctival swab using a special tissue culture techniques
Immunofluorescent staining of conjuctival scrapings for chlamydial inclusions or
Tests for chlamydial antigens
8.1.5 Complications
Corneal ulceration and perforation
Iridocyclitis
Anterior synechiae
Rarely panophthalmitis
Blindness
8.1.6 Medical and Nursing management
-Adequate saline irrigation of the conjuctiva every 10-30 minutes initially and then every 2 hours
until the purulent discharge is cleared
Ganococcal
321
Ceftriaxone 25-50mg/kg/day for 7 days or 50mg/kg/day Im stat
Kanamycin 75-150 mg Im + gentamycin ointment for 3 days
Chlamydial
Erythromycin 50mg/kg/24hr in four divided dose for 2 wks
this cures conjunctivitis and may prevent subsequent chlamydial pneumonia
Pseudomonas
Systemic antibiotics, including aminoglycosides and
Local saline irrigation
Gentamicin ophthalmic ointment
If proper Rx is delayed, the infection may spread to involve the deeper layers of the
conjunctiva and cornea
Staph aureus
Parentral methicillin and
Local saline irrigation
8.1.7Prevention
Before the institution of topical ophthalmic prophylaxis at birth, gonococcal ophthalmia was
a common cause of blindness or permanent eye damage
If properly applied, this form of prophylaxis is highly effective, unless infection is present at
birth
Drops of 0.5% erythromycin or 1% silvernitrate (instilled directly into the open eyes at
birth, using wax or plastic single dose container)
Povidone-iodine 2% solution is also an effective prophylactic agent
Identify maternal gonococcal infection and appropriate treatment
Treat chlamydial infection in mothers with erythromycin
No topical prophylaxis for chlamydial trachomatis is effective
8.2 CARING A CHILD WITH CONGENITAL SYPHILIS
8.2.1 DEF
N
- Syphilis is one of STD or/and a systemic communicable infection. Congenital
syphilis is atransplacental infection of the fetus by the spirochetes Treponema pallidum.
322
Pregnant women with primary and secondary syphilis and spirochetemia are more likely to
transmit infection to the fetus than women with latent infection
Untreated or inadequately treated disease can result in fetal and neonatal disease with
multisystem involvement; including
Anemia
Thrombocytopenia
Hepatosplenomegally
Jaundice
CNS manifestations
The CNS manifestations and/or sequelae include:
Hydroce phallus
Cerebral infarction
Meningovasculitis
Seizure
Mental retardation
The incidence of congenital infection in the offspring of untreated infected women remains
highest during the first 4 year after acquisition of primary infection, secondary and early
latent disease
The transmission can occur at any stage of pregnancy
The risk factors most commonly associated with congenital syphilis are
Lack of prenatal care and cocain drug abuse, which is associated with:
Prostitution
Unprotected sexual contact
Trading of sex for drugs
Inadequate prenatal care of pregnant addicts
Syphilis during pregnancy has atransmission rate approaching 100%
323
Fetal or perinatal death occurs in 40% of affected infants
8.2.2 Description of cause, s/s, complicatons
Etiology- Treponema pallidum
C/M- Among the survivors, manifestations have traditionally been divided into early and
late stages
Early signs appear during the first 2 year of life, where as late signs appear gradually during
the first 2 decades
Early manifestations result from transplacental spirochetemia and are analogous to the
secondary stage of acquired syphilis
Approximately 2/3
rd
of infected infants are asymptomatic at the time of birth and are
identified only be routine prenatal screening
If they are untreated, symptoms develop within weeks or months
EARLY SIGNS Are varies and involve multiple organ systems
Hepatospleenomegally
Jaundice and elevate liver enzymes
Diffused lymphadenopathy
Characteristic coombs negative hemolytic anemia
Thrombocytopenia
Characterstic osteochondritis and periositis
Mucocutaneous rash, presenting with
Erythematous maculopaular or bullous lesions, followed by desquamation involving hands
and feet
Mucous patch, rhinitis (snuffles) and condylomatous features of mucous-m involvement in
congenital syphilis
Pseudoparalysis of parrot
CNS abnormalities
Failure to thrive
324
Chorioretinitis
Nephritis and nephrotic syndrome
The C/Ms of renal involvement include:
Hypertension
Hematuria
Proteinuria
Hypoproteinemia
Hypocomplementemia
Less common C/Ms of early congential syphilis include:
Gastroenteritis
Peritonitis
Pancreatis
Pneumonia
Eye involvement (glaucoma and chorioretinitis)
Nonimmunehydrops
Testicular masses
Late signs
Resuls primarily from chronic inflammation of bone, teeth and the CNS.
Olympian brow Frontal bossing, a bony prominence of the forehead
Higoumenakis sign Unilateral or bilateral thickening of sternoclavicular portion of the
clavicle
Saber shins- An anterior bowing of the mid portion of the tibia
Scaphoid scapula- A convexity along its medial border
All of the above are skeletal changes due to persistent or recurrent periostitis and associated
thickening of bones
Dental abnormalities are common and include
325
Hutchinson teeth- The peg or barrelshaped upper centeral incisors that erupt during the 6
th
year of life
Abnormal enamel- Which results in a notch along the biting surface
Mulberry molars- Abnormal 1
st
. lower (6yr) molars, characterized by a small biting surface
and an excessive no of cusps
Defects in enamale formation lead to repeated caries and eventual tooth destruction
Saddle nose- A depression of the nasal root, is a result of syphilitic rhinitis that destroys the
adjacent bone and cartilage
A perforated nasalseptum is an associated abnormality
Rhagades- linear scars that extend in a spokelike pattern from previous mucocutaneous
fissures of the mouth, anus and genitalio
Juvenile paresis- An uncommon latent meningovascular infection, typically presents during
adolescence with behavioural changes, focal seizures or loss of intellectual function
Juvenile tabes- Extremely rare condition which involves spinal cord and cardiovascular with
aortitis
Other late manifestations of congenital syphilis may represent a hypersensitivity
phenomenon and include:
Interstitial keratitis (unilateral or bilateral)
Intense photophobia and lacrimation
Corneal opacification and complete blindness
Less common ocular manifestations include:
Choroiditis
Retinitis
Vascular occlusion
Optic atrophy
Eighth nerve deafness
Clutton joint Represents a unilateral or bilateral synovitis involving the lower extremities,
usually the knee
326
Soft tissue gummas
Dx- Diagnosis of primary syphilis is made with certainity when T-pallidum is demonstrated by
dark-field micro scopy or direct immunofluorescence
Serologic tests for syphilis are the best and principal means for diagnosis
The treponemal tests, which measure antibody specific for T.pallidum include:
T-pallidum immobilization test (TPI)
Fluorescent treponemal antibody absorption test (FTA- ABS)
Microhemagglutination assay for antibodies to T-pallidum (MHA-TP)
Nontreponemal tests detect antibodies against a cordiolipin-cholesterol-lecithin complex,
not specific for syphilis, and include:
Veneral disease research laboratory (VDRL)
Rapid plasma regain (RPR)
CDC recommends that infants be treated if:
They were born to mothers who had untreated syphilis at delivery
There is physical evidence of active disease
There is radiologic evidence of syphilis
There is areactive CSF VDRL, or for infants born to seropositive mothers, an abnormal
CSF WBC cout or protein regardless of CSF serology
A serum quantitiative nontreponemal serologic titer in the infant is at least fourfold
greater than the mother
8.2.3 Medical management
- Aqueous crystalline penicillin G (100,000-150,000 u/kg/24hr; give as 50,000 u/kg IV Q 12hr the
first 7days and Q 8 hour thereafter for 10-14 days or
Procaine penicillin G (50,000 u/kg Im daily in a single dose for 10-14 days
8.2.4 Nursing management
8.2 .5 Prevention
Adequate maternal therapy should eliminate the risk of congenital syphilis
327
Routine prenatal screening for syphilis remains the most important factor in the
identification of infants at risk for development of congenital syphilis
Generally, prenatal screening and appropriate treatment of mothers is the mainstay for the
prevention of congenital syphilis
NB- Take all measures that decrease the incidence of acquired syphilis in adults
A serological test for syphilis in all pregnant women is a desirable aim for prevention
At least test all pregnant women with a history of risk of STDs
Congenital syphilis occurs with untreated syphilis of the mother; you must discover and
treat the syphilis during the mothers pregnancy
8.3 Providing care of child with trachoma
Trachoma is a chronic infection of the conjectiva and cornea the disease is caused by chlamy
dlatrachomatis
Trachoma is considered to be the most common human infection. If is a leading caused of
preventable blindness and second only to cataract world wide
Acute trachoma is seen in commuties with poor hygiene and inadequate sanitation.
Blinding trachoma is a major public health problem in parts of Africa, the middle east

Transmission
o Favored by Environmental factors
Use of common fomiter
Use of common bedding
Person to person contact
Eye to eye by musca domestieated
Trachoma is a common inflammatioin that leads to spontaneous resolution accompanyled by
extensive clcatrazilion of the conjactiva and the subconjuncitval tissues eventually heads to inward
devation of the eye lash and lid margin.
The trichlasls disrupts the anatomic intergrity of the corneal eplthelium , leading to ulceration and
may be cause permanent O pacitlcation
328
In hyperendemic area prevalence may reach 95%
Trachoma is commonly seen in rural communities of most developing countries.
Indicators of trachoma
1. Triciasis inadults
2. Active infection inchildren
3. Implementation of the stratege
Incubation period
5-14 days on Average
C/F
Initial symptoms
Irritation, redness, tearing, photoploble and mucoprulent discharege (wateary discharege)
Forign body sensation
Swelling of the eye lid
o Follicles
o Scarring of eye lids with ultimate entroplon and trichlasis (inversion of eyelashes)
o Prevent the closure of the eyelids
o Corneal trachoma and viceration
Simplities WHO classification of trachoma
The system recognizes eylid, cornea & conjeucntival signs each eye is examined and assessed separetly
Grade Tf Trachomatous inflammation (follicular)
- 5 or more fillices are seen
- Mild moderate trachoma)
Grade T1 Trachomatons Inflammation (intense)
- Several inflammation
- Obbcures visualization of vessels
- Many follicles may be seen
- Severe trachoma
Grade TT- (Trachomatous trichlasis)
- One or more eye lash are tauching the globe
Grade (Co-(corneal apacity)
329
- Visible comea scare and the pupil margin is blurred
- A decrease in vision is recorded
Complication
- Dry eye
- Scaring
- Nasolacrimauduct obstruction
Treatment
Tetracyclin area know considered the treatment of choice for pt. with trachoma
Erythromycin for children & pregnant women
Regiemen
Erythromycin 500mg Oraly Tid 3-4 wks
Doxycyclin 100mg or minocyclin 100mg orally bid -3 wks
Tteracyclin HCL 1.5 2 gm /day
Topical TTC HCL for 2 month
In children
Topical TTC % or erythromycin Oint 5mg/gm bid for 6.8wk
Erythromycin systemically 40 mg/kg 10 days for 3 wk
Prevention
Implementation of the safe strategy integrated with PHC.
1. Assessment to identify communitles with blinding trachoma.
2. Delivery of community based trichiasias surgery by traine dparamadical staff
3. Antibiotic treatment (TTC or Azithoomycin) for children with active trachoma
4. Promotion of faccal cleaness and environmental improvement including personal hygine &
community sanitation as part of PHC.
Safe strategy
S tereitiary prevention (surgery )
A secondary (antibiotic)
F & Primaty Prevention facial hygine
330
E and environmental change to improve sanitation. E also includes education, economic
development.
8.4 MANAGING AND PREVENTING CONJUNCTIVITIS IN CHILDREN
8.4.1 DEF
N
- Conjunctivitis is an inflammation of the conjunctiva of the eye
It is one of the common types of eye infections in children and may be infectious or non-
infectious
8.4.2Etiology- The conjunctiva reacts to a wide range of bacterial and viral agents, allergens,
irritants, toxins and systemic diseases
The risk of conjunctivitis in newborn depends on:
Frequencies of maternal infection
Prophylactic measures
Circumstances during labor and delivery
Postdelivery exposures to micro-orgnisms
Bacterial causes of conjunctivitis:
Hemophilus influenzae
Hemophilus aegyptius
Streptococcus pneumonia
Neisseria gonorrhea
Chlamydia trachomatis
Staphylococcus aureus
Common causes of neonalal conjunctivitis
Viral causes of conjunctivitis:
ECHO virus
Adenovirus
Coxsackie virus
Entro virus
Measle virus
331
Other causes of conjunctivitis:
Different types of allergens
Different types of irritants
Chemicals
Systemic diseases
8.4.3 CLINICAL MANIFSTATION
A- ACUTE PURULENT CONJUNCTIVITS
Characterized by more or less generalized conjunctival hyperemia, edema, mucopurulent
exudates and various degrees of ocular discomfort
It is usually a result of bacterial infection
Nontypable Hemophilus influenzae
Pneumococci
Staphylococci and
Streptococci
Brazilian purpuric fever due to Hemophilus aegyptius manifests as conjunctivitis and sepsis
N.gonorrhea and Chlamydia are relativiely common causes of acute purulent conjunctivitis
in children beyond the newborn period, especially in adolescents
Conjunctival smear and culture are helpful in differentiating specific causative organism
The common forms of acute purulent conjunctivitis usually respond well to:
Work compresses
Frequent topical instillation of antibiotic drops
Systemic antibiotics
B- VIRAL CONJUNCTIVITIS
Characterized by a watery discharge
Follicular changes (Small aggregates of lymphocytes) are often found in the palpebral
conjunctiva
Adenovirus is relatively a common cause and sometimes may involve the cornea
332
Entrovirus cause out breaks of conjunctivitis and may be hemorrhagic
Measle which is asystem viral infection also can cause self-limiting conjunctivitis
C- EPIDEMIC KERATOCONJUNCTIVITIS
Is caused by a denovirus type 8 and is transmitted by direct contact
Initially presents as a sensation of a foreign body beneath the lids, with itching and burning
Edema and photophobia occur rapidly and large oval follicles appear with in the conjunctiva
Preauricular adenopathy and a pseudomembrane on the conjuctival surface occur frequently
Subepithelial corneal infiltrates may develop and may cause bluring of vision.
No specific medical therapy is available to decrease symptoms or shorten the course of the
disease
Emphasis must be placed on prevention of spread of the disease
NB- Replicating virus is present in 95% of patients 10days after the appearance of symptoms
D- MEMBRANEOUS AND PSEUDOMEMBRANEOUS CONJUNCTIVITIS
Can be encountered in a number of diseases
The classic membraneous conjunctivitis is that of diphtheria, which is accompanied by:
A fibrin-rich exudates that forms on the conjunctival surface and permeates the
epithelium
The membrane is removed with difficulty and leaves raw bleeding areas
In pseudomembraneous conjunctivitis:
The layer of fibrin-rich exudates is superficial
Can often be stripped easily, leaving the surface smooth
Occurs with many bacterial and viral infections including staphylococcal,
pneumococcal, streptococcal, or chlamydial conjunctivitis and in epidemic
keratoconjunctivitis
It is also found in vernal conjunctivitis and in stevens-Johnson disease
E- ALLERGIC CONJUNCTIVITIS
Usually accompanied by intense itching, tearing and conjuctival edema
333
It is commonly seasonal
Cold compresses and decongestants drops may give symptomatic relief
Topical mast cell stablizers or prostaglandin inhibitor may also help
In selected causes, topical corticosteroids are used under an ophthalmologist supervision
F- CHEMICAL CONJUNCTIVITIS
Can result when an irritating substance enters the conjunctival sac.
As in the acute, but benign conjunctivitis caused by silver nitrate in newborns
Other common offenders include:
Household cleaning substances
Sprays, smoke and smog
Industrial pollutants
Alkalis tend to linger in the conjunctiva tissues and continue to inflict damage for hours or
days
Acid precipitate the protein in tissues and so produce their effect immediately
In either case, prompt, thorough and coupious irrigation is crucial
NB- Extensive tissue damage, even loss of the eye can result, especially if the offending
agent is an alkali
G- VERNAL CONJUNCTIVITIS
Usually begins in the prepubertal years and may recur for many years
Atopy appears to have a role in its origin, but the pathogenesis is uncertain
Extreme itching and tearing are the usual complaints
Large, flattened, and a milky conjunctival pseudomembrane are frequently present
- A stringy exudates and a milky conjunctival psevdomembrane are frequently present
Smear of the conjunctival exudates reveals many Eosinophils
Topical corticosteroid therapy and cold compresses afford some relief
Mast cells stablizers or prostaglandin inhibitors are useful when long-term control is needed
NB- The long-term use of corticosteroid should be avoided
334
Generally conjunctivitis may have the following clinical features:
Redness of the eye, usually greatest under the lids
There may be sticky or watery discharge that may contain mucus (white) or be purulent
(yellow)
There is discomfort (foreign body feeling) with or without pain
Normal visual acuity
There may be small hemorrhages in the conjunctiva or enlarge lymph glands in front of
the ear
Dx- Based on Hx, C/M, P/E and Lab investigation
Rx- Symptomatic
- Antibiotic, (topical, systemic or both)
- Corticosteroids
- Mast-cell stablizers or prostaglandin
NB- For Gonococcal and chlamydial conjunctivitis, refer the note on ophthalmia neonatorum
8.4.6Prevention-
-Prevention of conjunctivitis depend on its cause& mode of trensmisien

8.5 PROVIDING CARE FOR A CHILD WITH INTESTINAL PARASITOSIS
A- ASCARIASIS
It is an infestation of the intestine by the nematode or round worm called ascaris
lumbricoides
Adult worms of A.lumbricoides inhabit the lumen of the small intestine and have a life span
of 10-24 month
The reproductive potential of ascaris is prodigious in that a gravid female worms produces
200,000 eggs/24hr
After passage in the feces, the eggs embryonate and become infective in 5-10 days under
favourable environmental conditions
Etiology- Ascaris-lumbricoides
335
Epidemiology
Occurs globally and the most prevalent human helminthiasis in the world
Most common in tropical areas of the world where environmental conditions are optimal for
maturation of ova in the soil.
Approximately 1 billion persons are estimated to be infected, with 4 million cases in united
states
Key factors linked with a higher prevalence of infection include:
Poor socioeconomic conditions
Use of human faces as fertilizer
Geophagia
Even though infection can occur at any age, the highest rate is in children of preschood or
early school age
Transmission is primarily hand to- mouth, but may also involve ingestion of contaminated
raw fruits, and vegetables
NB- Transmission is enhanced by the high out eggs by the fecund female and resistance of ova to
the outside environment
Ascaris eggs can remain viable at 5-10
0
c for as long as 2 years
Pathogenesis Ascaris ova hatch in the small intestine after ingestion by the human host
Larvae are released, penetrate the intestinal wall and migrate to the lungs by ways of the
venous circulation.
The parasite then cause pulmonary Ascariasis as they enter into the alveoli and migrate
through the bronchi and trachea
They are subsequently swallowed and return to the intestines, where they mature into adult
worms
Femal ascaris begin to deposite eggs in 8-10 Wk
C/Ms The clinical presentation depends on the intensity of infection and the organ involved
Most individuals have low to moderate worm burdens and have no symptoms or signs
The most common clinical problems are due to:
336
Pulmonary disease and
Obstruction of the intestine and biliary tract
Allergic symptoms, fever, urticaria, and granulomatous disease
Transient pulmonary symptoms, such as cough and dyspnea, pulmonary infiltrates and
blood eosinophilia.
Vague abdominal complaints due to the presence of adult worms in small intestine
A more serious complication occurs when a large mass of worms leads to acute bowel
obstruction
- Vomiting
- Abdominal distension
- Abdominal cramps
Pancreatitis and cholecystitis signs/symptoms
Stone formation may occur
Dx- Microscopic examination of stool for ova
A high index of suspicion in the appropriate clinical context is needed to diagnose
pulmonary Ascariasis or obstruction of the GIT
Rx- Albendazole 400mg po once for all ages
Mebendazole 100 mg bid po for 3 days or 500mg po once for all ages
Pyrantel pamoate 11mg/kg po once; maximum 1gm
Piperazine citrate 150 mg/kg po initially, followed by six doses of 65 mg/kg at 12 hour
intervals po
Surgery may be required for cases with severe obstruction
B- HOOK WORM INFESTATION
Two major genera of hookworms, which are nematodes or roundworms, infect humans
Ancylostoma
Necator americanus
337
Ancylostoma duodenale is the major anthropophilic hookworm which causes classic hook
worm infection of man
Necator americanus, the only representative of its genus, is also a major anthrophilic
hookworm and causes classic hookworm infection
The infective larval stages of the anthropophagic hookworms live in a developmentally
arrested state in warm, moist soil
The larvae infect humans either by penetrating through the skin or when they are ingested
Epidemiology
Hookworm infection is one of the most prevalent infectious disease of humans
Affect an estimated 1 billion individuals world wide
Because of the requirement for adequate soil moisture, shade and warmth, hook worm
enfection is usually confined to rural areas, especially, where human feces are used for
fertilizers or where sanitation is inadequate
Hookworm is an infection associated with economic underdevelopment and poverty
throughout the tropics and subtropics
The ability of A . duodenale to withstand somewhat harsher environmental and climatic
conditionsmay reflect its ability to undergo arrested devt in human tissue
Pathogenesis
Larvae entering the human host by skin penetration undergo extraintestinal migration
through the venous circulation and lungs before they are swallowed
Orally ingested larvae may either undergo extraintestinal migration or remain in the
gastrointestinal tract
Adult hookworms adhere tenaciously to the mucosa and submucosa of the proximal small
intestine by using their teeth or cutting plates and a muscular oesophagus that creat negative
pressure in their bucal capsules
At the attachement site, hookworms down regulate host inflammation by releasing anti-
inflamatory polypeptides
338
Rupture of the capillaries in the lamina propria is followed by blood extravasation; some of
the blood is directly ingested by the hookworms
Each adult A.duodenale hookworm cause loss of an estimated 0.2 ml of blood/24hrs
Light hookworm infestation-very little blood loss- have hookworm infection but not
hookworm disease
Hookworm disease results only when individuals with moderate and heavy infections
experience sufficient blood loss to develop iron-deficiency and anemia
C/Ms Heavily infected children suffer from intestinal blood loss resulting in iron deficiency,
which can lead to anemia and protein malnutrition
Physical growth retardation
Cognitive and intellectual deficits
Dermatitis, sometimes refered to as ground itch
Cough, larygotracheo bronchitis and pharyngitis
Anorexia, diarrhea and sometimes pain
Children with chronic hookworm disease acquire a yellow-green pallor known as
Chlorosis
Dx- Detected by stool examination
Rx- The goals of therapy are removal of the adult hookworms with an antihelmintic drug
inaddition to nutritional support for children with hookworm-associated iron deficiency and protein
malnutrition
Albendazole 400mg po once for all ages achieves cure rates of up to 95%
Mebendazole 100mg bid po for 3days or 500mg po once for all ages
Pyrantel pamoate 11mg/kg po once daily for 3days; maximum 1gm
Iron salt preparation to correct hook worm-associated iron-deficiency
Prevention- Drug chemotherapy
Improved sanitation
Avoidance of human feces as fertilizer
339
Economic development
Health education
C- Enterobiasis
The cause of Enterobiasis, or pinworm infection is Enterobius vermicularis, which is a small
(1 cm in length), white, threadlike nematode or roundworm
Typically inhabits the cecum, appendix, and adjacent areas of the ileum and ascending
colon
Gravid females migrate at night to the perineal and perianal regions where they deposit eggs
Eggs embryonate within 6 hours and remain viable for 20 days
Human infection occurs by ingestion of embryonated eggs that are carried on fingernails,
clothing, bedding or house dusts
After ingestion, the larvae mature to form adult worms in 36-53 days
Epidemiology
Enterobiasis infection occurs in individuals of all ages and socioeconomic levels
The prevalence of pinworm infection is highest in children from 5-14 year of age
It is common in areas where children live, play, and sleep close together, thus facilitating
egg transmission
Because the life span of the adult worm is short, chronic parasitism is likely due to repeated
cycles of reinfection
Autoinoculation can occur in individuals who habitually put their fingers in their mouth
C/M Enterobius infection may cause symptoms by mechanical stimulation and irritation, allergic
reactions, and migration of the worms to anatomic sites where they become pathogenic
The most common complaints include itching and restless sleep secondary to nocturnal
perianal and perineal Pruritus
Perianal granulomas containing live or dead worms or eggs develop rarely, but may require
surgical excision
Aberrant migration to ectopic sites occasionally may lead to:
Appendicitis
340
Chronic salpingitis
Peritonitis
Hepatitis and
Ulcerative lesions in the large or small bowel
Dx- A history of nocturnal perianal Pruritus in children strongly suggests Enterobiasis
Definitive diagnosis is established by identification of parasite eggs or worms
Microscopic examination of adhesive cellophane tape pressed against the perianal region
early in the morning frequently demonstrates eggs
NB- Repeated examinations increase the chance of detecting ova
Rx- Anthelmintic drugs should be administered to infected individuals and their family members
A single dose of mebendazole 100mg po for all ages, repeated in 2 wk results in cure rate
90-100%
Alternative regimens include:
Asingle dose of Albendazole 400mg po for all ages, repeated in 2wk or
Asingle dose of pyrantel pamoate 11mg/kg po; maximum : 1gm
Prevention Repeated treatments every 3-4 months may be required in circumstances with
repeated exposure, such as with institutionalized children
Personal cleanliness as a general principle
D- Trichuriasis
Trichuriasis is caused by the whipworm, Trichuris trichiura, a nematode, or round worm
It inhabits the cecum and ascending colon of humans
The principal hosts of T.trichiura are humans who acquire infection by ingesting
embryonated eggs
The larvae escape form the shell in the upper small intestine and penetrate the intestinal villi
341
The worms slowly move toward the cecum, where the anterior three-fourths whip like
portion remains within the superficial mucosa and the short posterior end is free in the
lumen
In 1-3 month, egg deposition by the adult female worm begins producing 5,000-20,000
eggs/24hrs
After excetion in the feces, embryonic devt occurs within 2-4 wk with optimal temperature
and soil condition
Epidemiology
It accur throughout the world
Especially common in poor rural communities with:
Inadequate sanitary facilities
Soil contaminated with human or animal feces
It is one of the most prevalent human helminthiases, with an estimated one billion infected
individual worldwide
The prevalence of T.trichiura infection can be as high as 95% in many parts of the world
where PEM and anemia are common
The highest rate of infection occurs among children 5-15 years of age
Infection develops after ingesting embryonated ova by direct contamination of hands, food
(raw fruits and vegetables fertilized with human feces) or drink
Transmission can also occur indirectly through flies or other insects
C/M Most persons harbour low worm burdens and do not have symptoms
Some individuals may have a history of RLQ or vague periumblical pain
In heavily infected children
Chronic dysentery
Rectal prolapse
Anemia
Poor growth
342
Developmental and congnitive deficits
Dx- Because egg out put is so high, fecal smears frequently reveal the characteristic Barrel-shaped
ava of T.trichiura
Rx Mebendazole 100mg po Bid for 3 days or 500mg po once for all ages is asafe and effective
drug
Albendazole 400mg po once for all ages is an alternative, but with heavy infections the
daily dose may have to be administered for 3 days
Prevention- The disease can be prevented by:
Personal hygiene
Improved sanitary conditions and
Eliminating the use of human feces as fertilizer
F- STRONGYLOIDIASIS
It is caused by the nematode or roundworm, strongyloides stercoralis
Only adult female worms inhabit the small intestine
The nematode reproduces in the human host by parthenogenesis and releases eggs
containing mature larvae into the intestinal lumen
Rhabditiform larvae immediately emerge from the ova and are passed in feces, where they
can be visualized by stool examination.
The rhabditiform larvae either differentiate into free-living adult male and female worms or
metamorphose into infectious Filariform larvae
Humans are usually infected through skin contact with soil contaminated with infectious
larvae
Larvaeskinvenous circulationlungs Bronchial tree swallowed stomatch Small
intestine.
Egg deposition begins about 28 days after initial infection
NB- Hyperinfection syndrome Occurs when large numbers of larvae transform into infective
organisms during their passage in the feces and then reinfect (ie. Autoinfect) the host by way of the
lower GIT or perianal region
343
This cycle may be accelerated in immunocompromised persons, particularly those with
depressed T-cell function
Epidemiology
Prevalent in tropical and subtropical regions of the world
Transmission requires appropriate environmental conditions, particularly warm, mist soil
Poor sanitation and crowded living conditions are conducive to high levels of transmission
Individuals with the following conditions are at a higher risk of the hyperinfection
syndrome:
Hematologic malignancies
Autoimmune diseases
Malnutrition
Drug-induced immunosuppression
Patient with AIDS may experience a rapid course of disseminated strongyloidiasis with a
fatal outcome
C/M Approximately one-third of the infected individuals are Asymptomatic
The remaining two-thirds have symptoms that correlate with the three stages of infection:
Invasion of the skin
Migration of larvae through the lungs
Parasitism of the small intestine by adult worms
Larva currens is the manifestation of an allergic reaction to filariform larvae that migrate
through the skin, where they leave pruritic, tortuous, urticarial tracks
The lesions may recur and are typically found over the lower abdominal wall, buttocks or
thighs
Pulmonary disease secondary to larval magiration through the lungs; rarely occurs:
Cough
Shortness of breath
Transient pulmonary infiltrates accompanied by eosinophilia
344
Gastrointestinal S/S includes:
Indigestion
Crampy abdominal pain
Vomiting and diarrhea
Steorrhea
Weight loss
Edema of the duodenum with irregular mucosal folds, ulcerations and strictures can be seen
radiographically
NB- strongyloidiasis is potentially lethal b/c of the ability of the parasite to cause overwhelming
hyperinfection in immunocompromised persons
The hyperinfection syndrome is characterized by an exaggeration of the clinical features
that develop in symptomatic immunocompetent individuals.
He onset is usually sudden with generalized abdominal pain, distention and fever
Mulliple organs can be affected
Petechiae and purpura
Cough, wheezing and hemoptysis
Eosinophilia is a prominent feature of strongylodiasis in immunocompetent persons, this
sign may be absent in immunocompromised persons
Dx- Intestinal strongyloidiasis is diagnosed by examining feces or duodenal fluid for the
characterstic larvae
Examination of several stool either by direct smear or cncentraiton method
In children with hgyperinfection syndrome, larvae may be found in sputum, gastric
aspirates, and rarely in small intestine biopsy specimens
Enzyme-linked immunosorbent assay for IgE antibody to strongloides may be more
sensitive than parasitologic methods for diagnosing intestinal infection in
immunocompetent host
345
Its utility in immunocompromized subjects with hyperinfeciton syndrome has not been
determined
Rx- Treatment is directed at eradication of infection
Ivermectin 200mg/kg/24hr once daily po for 1-2 days for uncomplicated cases
Thiabendazole 50mg/kg bid po for 2 days; maximum 3 gm/24hr
Patients with the hyperinfection syndrome should be treated with Ivermectin for 7-10 days
and may require repeated courses
Reducing the dose of immunosuppressive therapy and treatment of concomitant bacterial
infections are essential in the management of hyperinfection syndrome
NB- Close follow-up with repeated stool examination is necessary to ensue complete elimination
of the parasite
Prevention
Sanitary practices designed to prevent soil and person-to-person transmission are the most
effective control measures
Wearing shoes is the main preventive strategy
Case detection and treatment
Using clean bedding to decrease fecal contamination of the environment in institutional
settings
8.6 Providing Care for a child with Entra-pulmonary Tuberculosis
8.6.1Definition
Tuberculosis (TB) is a chronic infectious disease caused in most cases by mycobacterium
tuberculosis, on acid-fast rod shaped bacillus.
Occasionally it can also be caused by mycobacterium bovis and mycobacterium
africanum
8.6.2 Classification
TB is a disease with diverse clinical manifestations. Accordingly, patients are broadly
classified into.
1- Pulmonary TB (PTB) Comprises 75-80% of all PTB cases
346
A) Smear-positive PTB- Comprises 75-80% of all PTB cases
B) Smear-negative PTB Comprises 20-25% of all PTB cases
2- Extra-pulmonary TB (EPTB) Comprises 20% of all TB cases
Source of Infection
Untreated pulmonary TB patients discharging bacillin are the main source of infection
Route of Transmission
Transmission of infection happens through an air borne spread of droplets containing bacilli
expelled by: coughing and sneezing and inhaled by healthy persons.
Persons living in the same household, or who otherwise are in frequent conlact with an
infectious patient have the greatest risk of being exposed to the bacilli
Inaddition, consumption of raw-milk containing m.bovis is a possible way of
transmitting TB in Ethiopia
Population affected
TB affects individuals of all ages and both sexes within every socio-economic group
amongst the population
There are, however, groups which are ore vulnerable to develop the disease:
Poverity
Malnutrition
Crowded living condition
HIV-infection
NB- TB is a major public health problem throughout the world, including Ethiopia, and is the
leading infectious cause of death.
EPTB is a category of tuberculosis infection that affects tissues or organs other than the lungs
parenchyma
The signs and symptoms of EPTB depend mainly on the organ(s) involved
The most common forms and their respective presentations are.
347
Tuberculous lymphadenitis
Slowly developing and painless enlargement of lymphnodes, followed by matting and
eventually drainage of pus.
Tuberculous pleurisy
Pain while breathing in, dull lower chest pain, sligh cough, and breathlessness on exertion
TB of Bones or/and Joints
Localized pain and/or swelling, discharge of pus, muscle weakness, paralysis, and stiffness
of joints
Intestinal TB
Loss of weight and appetite, abdominal pain, diarrhea or constipation, mass in the abdomen,
fluid in the abdominal cavity (Ascites)
Tuberculous meningitis
Headache, fever, vomiting, neck stiffness and mental confusion of insidious onset
NB- Whenever a person presents with s/s suggestive of EPTB, he/she should be referred to a
hospital
Diagnostic Methods
Microscopic examination of sputum smears
Radiological examination
Culture
Histo-pathological examination
Tuberculin test
NB- It is a major error to diagnose TB on X-ray findings and omit examining the sputum
Diagnosis in children
Diagnosis of TB in children is difficult b/c of the presence of a wide range of non-specific
symptoms
Symptoms and signs may be confusing in children co-infected with HIV
Diagnosis largely rests on the results of:
348
Management of Enlarged Lymphnodes Enlarged lymphnode
NB- Health workers should strictly
follow the above criteria for
diagnosis in order to a void over-
diagnosis of TB in children with PCM
RX- SCC regimen for children of 6 years of below and seriously ill children 7-14 yrs old
25(RHZ) /4(RH) or 2(RHZ) /4(RH)
Scc for new EPTB patients
who are seriously ill
25 (RHZ) /6(EH) or
2(ERHZ)/6(EH)
NB- Seriously ill includes:
Acule life threatening diseases, such as:
Acute disseminated miliary TB
TB meningitis or
TB peritonitis
+ Risk of severe disability, such as
Spinal TB
TB Pericarditis
Bilateral TB pleural effusion
Renal TB
349
Improved
Condition the same or worse
Discharge
Invesligate for other site of active
TB
Prsent
Absent Refer pt for Biopsy
Initiatanti TB Rx.
Lymphnodes are firm, hard and
appear fixed
Refer patient for Biopsy
Extra-inguinal site Inguinal site
Signs and/or symptoms of active TB Refer to OPD or STI clinic
No Yes
Broad-spectrum antibiotic for 3 wks Sputum AFB x3+clinical
investigation
Review after 4-8wks
Lymphnodes are mobile soft and fluctuant
Extensive X-ray lesions without cavitation in immunocompromized patients such as
Diabetics
HIV Positives or
Patients with other concomitant diseases
Clinical history
A history of TB- contact in the family
Clinical examination
X-ray examination
Tuberculin testing
Children should be strongly suspected of having TB when they have:
Contacts of aknown adult case of pulmonary TB
Clinical signs and symptoms, such as:
Recent weight loss or failure to gain weight and /or
Cough or wheezing> 2 weeks
In the absence of confirmation, the diagnosis of active TB can be made and treatment
commenced when any one of the following conditions is metr
Radiological picture of miliary pattern
Pathologic findings compatible with TB from a biopsy or surgically removed lesion
Critieria for the diagnosis of tuberculosis in children:
A- Suspected tuberculosis
An ill child with a history of contact with a confirmed case of pulmonary tuberculosis.
Any Child:
Not regaining normal health after measles or whooping cough
With loss of weight, cough and wheeze not responding to antibiotic therapy for respiratory
disease
B- Probable Tuberculosis
Positive (> 10mm in diameter) induration on tuberculin testing
350
Suggestive appearance on chest radiograph, such as:
Unilateral hilar/Mediastinal lymphnode enlargement with or other lobar or segmental
opacity
Miliary pattern
Pleural effusion
Infiltrate and cavitations
Suggestive histological appearance of biopsy materials
C- Confirmed Tuberculosis
Detection by microscopy or culture of tubercle bacilli from secretions or tissues
Identification of tubercle bacilli as mycobacterium tuberculosis by culture
NB- Health workers should strictly follow the above criteria for diagnosis in order
to avoid over-diagnosis of TB in children with PCM
Rx- SCC regimen for children of 6 years or below and seriously ill children 7-14
yrs old
25 (RHZ)/4(RH) or 2 (RHZ) /4(RH)
SCC for new EPTB patients who are seriously ill
25 (RHZ) /6(EH) or 2 (ERHZ) / 6(EH)
N.B Seriously ill includes:
Acule life threatening diseases, such as:
- Acute disseminated miliary TB
- TB meningitis or
- TB peritonitis
Risk of severe disability, such as
- Spinal TB
351
- TB Pericarditis
- Bilateral TB pleural effusion
- Renal TB
Extensive X-ray lesions without cavitation in immunocompromized patients such as
Diabetics
- HIV- Positives or
- Patients with other concomitant diseases
SCC for New adult patients with EPTB, children between 7-14 years old with any type of
TB, who are not seriously ill 2 (RHZ) /6 (EH)
Duty 9 PREVENTING CHILD HOOD ILLNESSES
9.1 Assessing and intervening on child hood health
Problems in community
9.1.1 Situational analysis
9.2Characteristics and management of EPI Target Disease
9.2.1 Measles
It is a highly contagious acute viral disease characterized by fever, runny nose, cough,
irritability, conjunctivitis, lacrimation, enanthema (or kopliks spots) on the bucal and labial
mucosa, and maculopapular rash appearing in a shower distribution over a period of 3 days
Mode of Transmission
By droplet spread or direct contact with nose/throat secretions of infected persons
352
Also spread by indirect contact with articles soiled by secretions
Predisposing actors include
Not being immunized
Overcrowding
Malnutrition
Magnitude and Distribution:
In countries with low immunization coverage, measles is common in children
In countries with effective childhood immunization programme, such as Europe and USA
measles is limited to older age groups
In Ethiopia, measles is among the most common causes of morbidity and mortality in
children
Major outbreaks with large attack rates resulting in as high as 15-20% case fatality rates
have been reported in Ethiopia
It is highly contagious disease affecting nearly 90% of susceptible household contacts
Epidemics occur every 2-3 years in population with large susceptible group
Etiology It is caused by measles virus
The essential lesion of measles is found in the skin; the mucous membranes of the
nasopharynx, bronchi and intestinal tract; and in the conjunctivae
Clinical Feature
The incubation period ranged from 7-18 days
The initial stage (catarrhal stage) starts with fever, cough, sneezing, runny nose and red,
runny eyes
Kopliks spots in the mouth occur before the rash
A characterstic red blotchy rash appears on the third to 7
th
day, beginning on the face
becoming generalized, lasting 4 to 7 days
Dx- It is mainly by clinical features and epidemiological grounds
Mgt Severe cases only are admitted to the hospital
Mothers are advised about care at home, which include
353
Reducing fever
Maintaining hydration
Maintaining nutrition
Serious complications are treated in hospitals
Complications
Pneumonia
Otitis media
Malnutrition
Encephalitis
Eye problems and blindness
9.2.2 Poliomyelitis/polio
An acute viral diseases with severity ranging from in apparent infection to paralytic disease
It is a crippling disease that can occur in a dults, but it is mainly common in children
Etiology It is caused by polioviruses type I,II and III
Mode of transmission:
Mainly feco-oral
Rarely airborne droplets
Predisposing factors include:
Not being immunized
Poor sanitation and hygienic practices
Overcrowding
Poverty
Etiology It is caused by polioviruses type I,II and III
Magnitude and Distribution
+ Poliomyelitis occurs in many regions of the developing world
Globally in 2001 were:
354
80% decrease in number of polio cases (From 2979 to 480)
50% decrease in endemic counties (From 20 to 10)
51 countries in Europe have been polio free for 3 years
No wild poliovirus type 2 isolated for the last 2 years
Pathogenesis
The virus affects the anterior horn cells of the spinal cord and several areas of the brain
Damage may be reversible with recovery, but it may go on to irreversible nuclear
destruction where muscle paralysis results
Clinical features
Incubation period is 6-14 days
Fever, malaise, headache, muscle pain
Nausea, vomiting sorethroat and stiffness of the neck and back with or without paralysis
Paralysis usually affects the legs, more often one
Dx- It is mainly by clinical features
Mgt the management of poliomyelitis depends on the three phases
Acute phase
Keep the limbs position cusions
Apply warm packs
Provide analgesics
Active and passive movements are assisted by physiotherapist other the acute phase ended
Recovery phase
Continue with full range of passive/active movement of the affected limb every day
Residual phase
Regular out patient supervision of physical, social and economic problems if needed
9.2.3 Diphtheria
355
an acute bacteria disease of tonsils, pharynx, larynx and nose
it occasionally affects the conjunctiva, genitalia and can damage the heart
Etiology It is caused by Gram-positive bacterium called corynebacterium diphtheriae
Mode of Transmission
By droplets and secretions from the nose, throat and eyes
Contact with skin ulcers
Clothing and other articles that have been contaminated with fluid from skin ulcers
Predisposing factors include
Overcrowding
Poor living conditions
Not being immunized
Malnutrition
Magnitude and distribution
It tends to be a disease of the colder months and of temperate climatic zones
Affects people of all ages, but mostly non-immunized children under 15 yrs old
Although incidence has decreased world wide, it remains endemic in many developing
countries.
Pathogenesis
The bacterium produces exotoxin which causes local tissue inflammation and necrosis
In cases where the pharynx is involved, there are patches of a grayish membrane with a
surrounding dull red inflammatiory zone, which may cause pharyngeal obstruction
Clinical Features
The incubation period is usually 2-5 days
Sore throat which may be followed by stridor
Grayish white membrane seen in oropharynx
Upper airway obstruction by the membrane
356
Dx- Clinical signs mentioned above
Microscopy Gram stain
Management
Diphtheria antitoxin if the diagnosis is strongly suspected clinically
Antimicrobial therapy with pencillin or erythromycin
Strict bed-rest and sedation
Intubations if needed
Complications
Airway obstruction
Toxic cardiomyopathy (50-60% of diphtheria deaths)
Vocal cord paralysis
9.2.4 Pertussis/Whooping coughs
An acute bacterial disease of the respiratory tract characterized by intense cough in
paroxysms and sometimes with forceful inspiratory gasp and absence of fever, tachypea,
sorethroat, hoarseness etc
It transmits or spreads form person to person by droplets, i.e. through coughing or sneezing
etc
Predisposing factors include
Not being immunized
Overcrowding
Poor ventilation
Malnutrition
60,000,000 cases of pertussis occur per year world wide, with morethan half a million
deaths
Etiology It is caused by a gram- negative bacterium called bordetella pertussis
Pathogenesis The organism produces exotoxin and affects the pharynx, larynx, trachea, bronchi,
bronchioles and sometimes the alveoli.
357
Clinical Features
Incubation period is 7-17 days
The symptoms of classical pertussis lasts about 6 weeks and are divided into 3 stage
A) Catarrhal stage
The onset is insidious
Sneezing
Runny nose
Anorexia lasts 1-2 weeks
Malaise
Night cough

B) Paroxysmal stage
Lasts 2-4 weeks following the infection
Characterized by rapid consecutive (5-15) cough before a breath is taken and followed by
deep hurried inspiration (whoop)
Post cough vomiting is common at all ages
Factors stimulating cough include
Fright
Anger
Sneezing
Inhalation of irritants
Over distention of the stomatch
C) Convalescent stage
It begins after 4 weeks of the illness, and is manifested by a decrease in the frequency and
severity of the paroxysms of coughing
Diagnosis
358
A- Clinical
The child is well appearing and playful between paroxysms of cough
Presence of children with similar illness in the family or vicinity
There is no chest finding on P/E
The diagnosis is usually made on the distinctive clinical feature of the cough
To observe the classic type of cough, put tongue depressor to stimulate the coughing
NB- Not all children with pertussis whoop. Whooping is uncommon in infants < 3 months
B- Laboratory
WBC 15,000-20,000/mm3 (rarely to 50,000/mm3)
60-80% lymphocytes
microscopy Gram stain
Culture to isolate the organism
Differential Dx.
Aspiration of foreign bodies
Viral pneumonia
Influenza
Acute bronchitis and Bronchiolitis
Management
A- Specific measures
Antimicrobials- Erythromycine
Ampcillin
Sedatives Promethazine Hydrochloride
Phenobarbitone (when there is seizure)
Steroids Predinsolone
B- General measures
Frequent small feeding and continue feeding if vomiting occurs soon after meal
Oxygen if required
359
Severe cases, especially infants are best managed in hospital
Prophylactic erythromycine for all house hold members and other contacts regardless of
age, history of immunization and symptoms
Complications
Apnea
Conjunctival hemorrhage
Otitis media
Pneumonia
Atelectasis
Encephalopathy
9.2.5 Tetanus
A neurological disease characterized by generalized increase inrigidity and convulsive spasms of
skeletal muscles from the bacterial toxin
Etiology- It is caused by a gram-positive anaerobic bacterium called clostridium tetani.
+ Mode of transmission:
Neonatal tetanus mainly occurs as a result of umblical cord contamination at birth
A person may become infected if contaminated soil or dung enters a wound or cut
+ Predisposing factors include
Cutting umblical cord with non-sterile instrument
Lack of adequate tetanus toxoid(TT) immunization of mothers
Applying cow dung, mud an dother contaminated materials on the umblical stump
Home deliveries attended by untrained traditional birth attendants
Harmful traditional health practices, like uvulectomy, tonsillectomy
+ Magnitude and Distribution
360
Occurs worldwide and is endemic in 90 developing countries, but its incidence varies
considerably
Neonatal tetanus is the most common form, which kills approximalely 800,000
infants each year
In developing countries, neonatal tetanus represents about half of all neonatal deaths
and about 25% of infant mortality
In Ethiopia, neonatal tetanus accounts for two thirds of all tetanus deaths
Pathogenesis Tetanus toxin, after germination of the cl-tetani spores in a contaminated umblical
stump or wound in other parts of the body, is released to the peripheral nerves and circulation. This
causes sustained excitatory neuronal discharge and muscle contraction.
Clinical Features
Tetanus occurs in several forms. One of the most important manifestations is neonatal
tetanus (NNT)
Its incubation period is from 1-14 days (in 90% of cases), but it can last up to 54 days.
The period of onset (the time between the first symptom and start of the spasm) ranges from
hours to days
The clinical features has two forms:
A- Local tetanus
Pain around the umbilicus
Dirt, dung and clotted blood are usually present
B- Generalized tetanus
It is the most common form of the disease and presents with early symptoms
Progressive difficulty in feeding (sucking and swallowing)
Hunger and crying, followed by paralysis or diminished movement
Lock jaw (clenched)
Stiffness to the touch and spasms with or without opisthotonus
Board like abdomen
361
Hyper-extended extremities
Dx- Diagnosis of neonatal tetanus is mainly by clinical features
+ Indicators of poor prognosis are:
Incubation period <7 days
Period of onset <48 hours
Presence of spasm
Autonomic nervous system disturbances
Complications
Respiratory arrest
Laryngeal spasm
Presence of autonomic nervous system disturbances
Prevention
Immunization of children and women
Health information on harmful practice
Training of Traditional Birth Attendants (TTBA)
9.2.6 Tuberculosis (TB)
It is a chronic mycobacterial disease with a wide variety of clinical forms; pulmonary
tuberculosis being the predominant form
Etiology
Pulmonary tuberculosis is caused by mycobacterium tuberculosis
Tuberculosis of the gastrointestinal tract is caused by mycobacterium bovis
Mode of transmission
Respiratory route
Airborne droplet nuclei from sputum of person with infectious tuberculosis
Alimentary route
Ingestion of infected raw or non-pasteurized milk
Predisposing factors
362
Poor nutritional status
Not being immunized
Infection with HIV/AIDS
Habit of drinking non-boiled/non-pasteurized milk
Overcrowding
Contact with pulmonary tuberculosis cases
Magnitude and Distribution
A bout one third of the worlds population is infected with tuberculosis
Every year 3 million people from tuberculosis, mostly in developing countries where it kills
one in five adults
Neary 75% of pulmonary tuberculosis cases in developing countries belong to the
economically active group of the population
In Ethiopia in 1993 E.C was the 3
rd
leading causes of out patient morbidity and the first
cause inhospital death
Pathogenesis
The tubercle bacilli infect the lung forming atubercle (lesion)
The tubercle:
May heal leaving scar-tissue
May continue as a granuloma
May eventually proceed to necrosis, liquefaction, sloughing and cavitations
The initial lesion may disseminate tubercle bacilli:
By extension to adjacent tissue
Via blood stream
Via lymphatic system
Through the bronchi
Clinical Features
363
The incubation period range 4-12 wks but the ifection may persist for months or years
before the disease develops
The clinical features of pulmonary tuberculosis are:
Persistent cough for more than 3 wks
Sputum production, which may or may not be blood stained
Weight loss
Chest- pain
Shortness of breath
Intermittent fever, night sweats
Loss of appetite
Fatigue and malaise
Dx- Clinical Features
Laboratory diagnosis
Sputum smear for AFB
Culture
Tuberclin skin testing
Chest X-ray
Management
Chemotherapy: there are two phase of Rx-
1- Intensive or Initial phase
The first two or three months of treatment
2- Continuation phase
The remaining duration of treatment
Drug Regimens: There are two recommended standard tuberculosis drug regiments
1- Directly observed Treatment short course (DOTS)
In DOTS the patients are given the drugs under observations by the health worker for the
firs two months
364
2- Long course chemotherapy (LCC)
LCC is given for 12 months
During the initial phase of short course therapy, the recommended regimen of
uncomplicated pulmonary tuberculosis is two months of INH, Rifampcin and
pyrazinamide followed by four months of Isonized and Rifampcin
9.2.7 Hepatitius B
9.2.8 Hemophilus Influenza
9.3 MANAGING EXPANDED PROGRAMME OF Immunization
9.3.1 Definiition of immuinization
Immunity- Refers to the many built-in defense mechanisms in the body and the complex
antigen antibody mechanisms
Vaccines Are substance that are used to produce immunity
To be immune Means to be out of harms way
To immunize means to make some one immune
Immunization is the process where by a person becomes immune, or is able to resist
diseases
Immune status indicates the degree or extent to which an individual or a community is
immune to a disease or a number of diseases
Immunization status is immunization coverage which refers to the degree or extent to
which the process of making people immune has progressed
There are two main types of immunity present in humans:
1- General Immunity
Refers to the many built in defense mechanisms in the body E.g. Skin
Secretions of the digestive tracts
Circulatory system with its lymph and WBCS
Good nutrition and positive mental attitude
2- Specific immunity
Involves the complex antigen-antibody mechanisms
365
The immune system of the body responds to the presence of antigens in two main ways
1- Antibodies Substances which circulate within the body and can act against antigen at sites
very far from where they originally were produced
Are produced by special cells called B-lymphocytes within the lymphatic tissues of the
body
Are complex chemical substances called immunoglobulins, which match the particular
antigen they were made for just like a key matches one particular lock only
This forms what is called the Humoral immune system
2- T-Lymphocytes and macrophages
Are special cells that circulates through the body and destroy micro-organixms or other cells
that the micro-organisms may have invaded
The special T-cells work in the same way as the antibodies to a particular infecting germ
They form what is called the cell mediated immune system
Both of the above systems, as well as being specific for aparticular infection or toxin are
capable of retaining the memory of the antigen
The response to specific antigens by both systems is the reason why immunity developed
against one disease, does not protect against other diseases
366
Graphic picture of the kind of Immunity present in Human
Immunity
9.3.2 Objectives
of expanded program on Immunization (EPI)
Immunization is aprotection of asusceptible host from a specific disease by administration
of:
367
General (Body Defence) Specific (Antigen antibody mechanism)
Acquired (Added)
Natural (Inheriled)
Passive (Received readymade
antibodies from source below)
Active (make own antibodies by
method below)
Placenta
Animals; other humans
Contracting Diseases Receiving vaccines and
toxoids
Aliving modified agent
A suspension of killed organism
An attenuated toxins
Objectives
1- To reduce morbidity and mortality from six-major diseases; by immunizing all children
throughout the world
2- To promote national self-reliance in delivering immunization services within the
comprehensive health services
3- To promote regional self-reliance in vaccine production and quality control
Activities outlined
Provide immunization or information about immunization at every health contact
Reduce dropout rates b/n the 1
st
and last immunizations
Increase the priority given to control of measles, polio and neonatal tetanus
Improve immunization services to the poor in urban areas
Use the special approaches such as national immunization days, where they strengthen the
health infrastructure and contribute to asustained improvement in coverage
9.3.3 Strategies to conduct EPI
1- Fixed (Static) Facilities
Offers immunization every day in all health institutions
Advantages
No additional costs for transportation
Easier to keep vaccines at proper temperatures
Personnel who can give injection and instructing parents are already available as is basic
medical equipment
Client records may be more easily established and kept up to date
368
Disadvantages
Parents must travel long distance to bring children to health centers
The further parents travel, the less likely they are to come for immunizations
Absence of integrated health service
2- Outreach services and mobile teams
Offers immunization outside the health institutions
It is important, especially for:
Children in remote rural areas and poor urbans
Children whose parents are unable or unwilling to come to health institutions
Disadvantages
Scheduling visits and adhering to scheduling are difficult
It can be expensive
Staff need to be paid perdiem
Vehicles must be bought and maintained
Strict reminding is necessary for parents to be available on the days of appointment
3- Intensive Immunization campaigns
This consists of regularly repeated mass campaigns which are mounted to stop epidemic by
quickly immunizing as many susceptible people as possible
Have sharply increased vaccine coverage, especially, those of single dose vaccines
Can involve non health workers for polio vaccination as it is given orally
9.3.4 Classification /type of immunization/
Three type of Classification
1. Live attenuated vaccines
2. Killed vaccines and
369
3. Toxoids
9.3.5 Target diseases of EPI in Ethiopia
In Ethiopia eighat (8) child hood target diseases
1. Measles
2. Tuberculosis (TB)
3. Tetanus
4. Pertussis/Whooping coughs
5. Diphtheria
6. Poliomyelitis/polio
7. Hepatitius B
8. Hemophilus Influenza
9.3.6 Types of Vaccines and their administration
vaccines are substances that are used to produce immunity; and are prepared from micro-
organism in special laboratories
there are three types of vaccines:
1- Live attenuated vaccines
These are made from weakened live bacteria or viruses that have been modified enough to
infect the body, but only cause very mild or local effects.
They lost the property called virulence, and there fore they can be called avirulent strains of
the original or wild bacteria or viruses
These vaccines include:
Measles
Polio
BCG
These vaccines should be deeply frozen, at around-20
0
c.
Since BCG is sensitive to ultra violet (UV) light and heat, it is packed in coloured vials and
they should be protected against the sunlight
These vaccines are very active in the body in stimulating antibody production
370
A- Measles vaccine
A live attenuated freeze-dried vaccine
Must be kept in a refrigerator, usually around 2-10
0
c or according to the instructions
If stored correctly it will remain active for around 6 months
A few days outside the refrigerator at room temperature will destroy the vaccine
It only remains active for 5-6 hours after it has been diluted and ready for use
One Im injection of 0.5 ml is recommended (lateral aspect of the thigh) or SC (Lft upper)
arm
Given at 9 months of age
The duration of immunity is probably lifelong
There are no contraindications to measles vaccinations
Measles vaccine requires special care
B- Polio (Poliomyelitis) Vaccine
Usually sabin live oral vaccine
It contains live attenuated virus form all three types of polio stains
Must be kept in the refrigerator, but not in the freezer compartment
In the refrigerator at 2-10
0
c, the active life of the vaccine is around 6 months
Outside the refrigerator, at room temperature, the life of the vaccine is a bout 2 days
Administer three doses of 2-3 drops peros (on to the tangue) at 4 wks apart
Given at birth or at 6 wks of age
In most African countries now, four doses are given as primary immunization in the first
year of life
Duration of immunity is around 6 years, booster doses are recommended at school entry and
upon complesion of primary school
OPV should not be given to a child with diarrhea and vomiting
Otherwise there are no contraindications, and there are almost no complications or reactions
to the vaccine
371
C- Bacillus calmette-Guerin (BCG) vaccine
A live attenuated bacterial vaccine that is usually freeze dried
Should be stored in aregular refrigerator (not in the freezing compartment), where is will
retain its activity for 1-2 years
Outside the refrigerator, at room temperature (22-25
0
c), the vaccine will remain potent for 1
month
Reconstituted vaccine loses its potency very rapidly and must be discarded after 2-3 hours
BCG is most sensitive to light and loses much of its potency other only 3-5 minutes
exposure to sunlight
Administer 0.05 ml of reconstituted BCG vaccine intradermally at the right deltoid
It is given at birth, and the duration of immunity lasts for many years
BCG is contraindicated in an infant or child with active HIV infection (AIDS)
Complications can occur if the injection is given subcutaneously instead of intradermally
2- Killed vaccines and Toxoids
The pertussis part of the triple (DPT) vaccine is made from killed bacteria
The diphtheria and tetanus in the triple (DPT) vaccines are made for toxoids (altered or
attenuated toxins) of these bacteria
DPT or triple vaccine, is a combination of vaccine against three different diseases:-
Diphtheria
Pertussis (whooping cough)
Tetanus
Substance called adjuvants, usually are added to toxoid vaccines, which prolong and
increase their activity
Because killed vaccines do not stimulate antibody production as well as live vaccines, DPT
is given at least two times and preferably three times to give adequate protection
372
When the 2
nd
and 3
rd
doses are given, the body remembers the earlier doses and quickly
produces higher level of antibodies
The longer the period b/n the successive doses, the less body remembers the previous dose
Killed and toxoid vaccines include DPT and TT, which should be kept just above freezing
point in the refrigerator (0-8
0
c)
A- Triple vaccine or DPT
Should be kept in the refrigerator, but not in the freezer compartment
Remains active for 2-3 years when kept at 2-10
0
c
At room temperature, the vaccine will lose its potency other 2-3 days
Administered at a dose of 0.5 ml deep Im on the thigh 3 times in 4 wks a part
After a full primary vaccination of three doses, immunity will last 4-5 years and even longer
if a booster dose is given at 1-2 years of age
B- Tetanus Toxoid
Absorbed on alum as an adjuvant, so that it can work in the body more powerfully for a
longer time
Should be stored in a refrigerator at 2-10
0
c, where it will remain active for 2-3 years.
It is a heat-stable vaccine (is not destroyed rapidly at room temperature = 22-25
0
c), and
remains active for at least 6 wks at 37
0
c
It is given as a deep subcutaneous or intramuscular injection at a dose of 0.5 ml
WHO advise that every women of reproductive age should have a primary course of two
doses of tetanus toxoid (TT
1
and TT
2
)
Ensure immunity for both the mother and her newborn baby
9.3.7 Storages of vaccines / Cold chain system/
Cold chain is the equipment and people that ensure vaccine potency by keeping caccine cold
all the way from the manufacturer to the child/mother or the consumer
373
Cold chain is the cold environment in which vaccines pass from manufacturer to the
vaccinator (mother or child)
Maintaining cold chain is one of the very few important activities that should be conducted
without any exception
By all concerned in the manufacturing of vaccines and delivery of immunization services.
The cold chain is concerned with the maintenance and monitoring of temperature as the
vaccines pass out along a chain of storage places
Consider the following important points in the administration of cold chain
Knowledge about the vaccines
Knowledge about the various refrigerator
Knowledge about temperature monitoring devices
Knowledge about ordering the right amount of vaccines
+ Levels of cold chain
Central store
Regional store
Zonal store
District store
Health institution store
At consumption site
N-B- The important and guiding concept behind cold chain is once vaccine potency is lost, it can
not be regained
A broken cold chain is worse than no immunization at all.
9.3.8 Target age groupes

9.3 .9 Management of EPI program
The following procedures should be followed in conducting and managing the EPI program
374
1- Know the catchement area
2- Know the target population through survey
3- Organize and conduct in-service training for the staff
- Allocation of resources
- Assign staff
- Procure the required amount of caccines, refrigerator and other supplies
- The necessary financial support (budget)
- Transportation etc
4- Management of cold chain
5- Identify the strategy to be used and their frequencies
6- Prepare and organize immunization schedule or session. E.g. How many outreach sites
7- Give appropriate information for the client
8- Collect and distribute materials for recording and reporting
9- Social mobilization to create awareness
10-Devise means of monitoring. Supervising and evaluation
11-Identify problems and give solutions
12-Identify those illegible who are not vaccinated and are listed as dropouts
9.3 .10 Immunization schedule
The various factors influencing the administration of vaccines have now been couered
The knowledge together with the goal of protecting children from these infections as
rapidly, effectively and cheaply as possible, give enough information schedule
Immunization schedule certainly will change as new developments come in future, and even
now it is modified in different areas and circumstances; But it does give a standard plan that
is widely used
The following are the recommended Immunization schedule
A. For those who start at Birth
Contact Age of child Vaccines
1
st
At birth BCG AND POLIO-0
375
2
nd
6 weeks OPV-1 AND DPT
1
3
rd
2
4
th
3
5
th
9 months Measles
A- For those who start later
Age of child Antigens
Less than 6 weeks BCG and OPV1
Above 6 weeks BCG if not given previously
OPV (3 doses)
DPT (3 doses)
Above 9 months BCG if not given previously
OPV, DPT
Measles
B- Tetanus Toxoid vaccine schedule for women (15-49 years)
Dose Minimum Interval Duration of protection
TT
1
- 0
TT
2
4 weeks 3 years
TT
3
6 months 5 years
TT
4
1 year 10 years
TT
1 year Life long

NB- All children should be fully immunized within the first year of life
If a woman was given 3 doses of DPT vaccine when she was a child, provided that a
written document of immunization is available, and the doses are given at the right
intervals, the three doses of DPT can be counted as two doses of TT.
9.3.11 Immunization campaigns
9.3.12 Charting, Recording and Reporting
376
Duty - 10 Assisting A child with normal-feeding pattern
1O.1 Assisting with Breast Feeding and Substitute
10.1.1 Definition of child feeding
Child Feeding is giving or providing foods in the form of liquid, semi-solid or solid to the child
The establishment of feeding practices that are comfortable and satisfying for both the
mother and the infant is crucial for the emotional well-being of both and for ensuring
adequate nutrient intakes for the infant
The successful feeding of infants requires practical interpretation of:
Specific nutritional needs and
The wide variability among normal infants in appetite and behaviour regarding food
10.1.2 Breast feeding
Breast-feeding is best for both the mother and the infant in many ways; so we should focus
on good positioning, sucking and attachment procedures for effective breast-feeding.
How to help a mother put her baby on to the breast in a good position
Let the mother sit or lie some where comfortable so that she is relaxed
Show her how to hold the baby so that he/she faces the breast
The babys head should be in a straight line with his/her body; his/her stomatech should be
against the mothers stomach
The whold body should faces the breast and the infant should not have to turn or bend his
head to suckle
The mother should lift her breast with her hand and offer the whold breast to the baby not
just the nipple
The mother should touch the babys lips with the nipple to stimulate the rooting-reflex
Aim the babys lower lip well-below the nipple, which helps the chin close to the breast and
the nipple touches and stimulates the palate.
377
Signs that a baby is suckling in a good position
The babys whole body is facing his/her mother and is close to her
The babys face is close up to the breast
Then babys chin is touching the breast
The babys mouth is wide open
The babys lower lip is curled outwards
There is more areola showing above the babys upper lip and less areola showing below the
lower lip
You can see the baby laking slow., deep sucks and sometimes pauses
The baby is relaxed and happy and is satisfied at the end of the feed
The mother does not feel nipple pain
You may be able to hear the baby swallowing
Signs that the baby is suckling in a poor position
The babys baby may be turned away form his mothers and not close to the breast
The babys chin is separated from the breast
The babys lips point forwards
You see too much areola, including below the lower lip
The baby takes many quick, small sucks
The babys cheek may be pulled in as he/she sucks
The mother may feel nipple pain
The babys mouth may make a smacking sound as he sucks
The baby may fuss or refuse to feed because he does not get, enough breast-milk
The nipple may look flattened at the end of a feed and it may have a line across the tip
Signs of good positioning
Infants neck is straight or bend slightly back
Infants body is turned towards the mother
Infants body is close to the mother
378
Infants whole body is supported
Signs of good attachment
There should be more areola above the infants mouth than below
Infants mouth should be wide open
Infants lower lip turned outward
Infants chin should touch the breast
If all of these signs are present, the infant has good attachment
Correct positioning and attachment for Breast-feeding is important for effective suckling
10.1.3 Commercial/Formula/Preparation
Artificial or Formula feeding is feeding baby milks other than human milk
The milks could be of cow, goat, camel or formula milk
Disadvantages of Artificial-Feeding includes
1) Contamination
Artificial-feeding is often contaminated with bacteria, especially if the mother uses a
feeding bottle
Bottles are difficult to clean and need to be boiled after every feed
Bacteria grow in artificial feeding very quickly especially in a feeding bottle which is left
around in the warm
2) Persistent diarrhea
In artificially fed babies, diarrhea is more likely to become persistent; that is, to continue for
14 days or more
Persistent diarrhea can be difficult to treat and may lead to severe malnutrition
It is sometimes necessary to stop giving the baby artificial milk feeds to cure the condition
Artificially fed babies are ill more often
3) Lack of Vitamins
Cow milk may not contain enough vitamins for a baby; especially vitamin C
379
So artificially fed babies may need fruit juices
4) Lack of Iron
The iron from cows milk is not absorbed as completely as the iron from breast milk
An artificially fed baby may developiron deficiency anemia
5) Too much salt
Cows milk contains too much salt which can sometimes cause hypernatraemia and
seizures; especially ifthe child has diarrhea
If the formula milk mixed incorrectly it contains too much salt
6) Too much calcium and phosphate, which may cause tetany (twitching and spasm of
muscles)
7) Unsuitable fat
Cows milk contains more saturated fatty acids than breast milk
For healthy growth, a baby needs more unsaturated fatty acids
Cows milk does not contain enough of the essential fatty acids called linoleic acid and it
may not contain enough cholesterol for the growing brain
8) Unsuitable protein
Cows milk contains too much of the protein Casein
Casein contain an unsuitable mixture of amino acids, which are difficult for a babys
immature kidneys to excrete
Breast-milk contains a protein called whey, which is suitable in every aspect (constitutes
75% of breast milk protein)
9) Indigestion
Cows milk is more difficult to digest. It does not contain the enzyme lipase to digest the fat
The casein forms thick, indigestible curds; fills the stomach for longer than breast milk- not
humgry- constipated
10) Allergy, suckling problems expense are also the common problems associated to cows
milk and formula milk
380
NB- formula is similar to cows milk. The more expensive brands are modified so that they are
more like human milk
If there is no breast milk for the infant, cows milk should be given to replace the missed
breast-milk
Preparation of cows milk
A- For Infants up to 3 months
2 parts boiled milk
1 parts boiled water
1 level teaspoon sugar perfeed
150 ml/kg per day or 25 ml/kg at least 6 meals per day
B- For Infants 3 monts or older
Undiluted boiled milk
1 level teaspoon sugar per feed
150 ml/kg per dya up to maximum of 1,000 ml, or zoml/kg, 5 meals per day
Preparation of powdered milk
Powdered milk is cows milk from which the water has been removed
Follow the instructions on the tin for preparing the feeds
Never give less powder than the instructions say
Wash hands before preparing milk feeds
Use clean cup an spoon
Fill a small cup with boiled water (30ml/kg per feed is enough)
Usually about 7 level teaspoons of full-cream dried milk are needed per meal (a little less
for younger infants, but read instructions)
Mix the powder with the boiled water in the clean cup
If the mother insists on feeding with a bottle, advise her to:
Use boiled water for preparing milk
381
Wash the bottle with a brush other the meal
Leave the bottle and teat in the water in the pan after boiling it
Add 2 teaspoon antiseptic to the pan and cover with a lid
Start using cup and spoon as soon as possible
10.1.4 Weaning period
Weaning is the process of expanding the diet of the infant to include foods and drinks other
than breast milk
Why complementary food is needed?
The amount of breast-milk that mothers can produce does not decrease, but it is no longer
enough by itself for fast growing infant; the baby needs other foods as well
To teach the baby the taste and feel of new, solid foods
To teach the child to take food from a spoon
To increase the supply of carbohydrates, fats, proteins, minerals (especially iron) and
vitamins in the diet
Proper weaning age
Most mothers have enough breast-milk for their babies for 6 months; some have enough for
9-10 months
But some babies begin to outgrow their mothers milk about 4-5 months
The average age that a baby needs to start other foods is a bout 6 months
The earliest they should be given is 4 months
Stages of weaning
There are three stages of weaning
Stage I (4-6 months of age)
Fluids and semisolid foods like cows milk, porridge and at mite once a day
Only one type of food should be given for few days and then other types are added when the
baby is accustomed to the first diet
Stage II (6-9 months of age)
382
At this stage (age) the child is able to chew mashed foods can be started
Stage III (9-12 months of age)
Similar food can be served for the family
Weaning foods should be
Easily available
Absorbable
Digestable
Low in cost
Used in the family or in community
Nutrient wise, weaning food should be:
Of high protein sources
Legumes
Animal foods
Of high energy sources
Oil and fat
Contains adequate vitamins and minerals
Vegetables and fruits
Keeping weaning foods clean and safe:
Wash Hands
Before preparing food
Before feeding a young infant (child)
After using toilet
After cleaning young childs buttock
After cleaning up childs feces
Wash the childs hands too
Boil water for the child to drink
Clean the plate or bowl for the childs food carefully
383
Protect food and utensils from dust, insect and rats
Disadvantages of Early and late weaning
Early weaning (weaning before the age of 4 months) is not advised b/c
Babies do not have the neuromuscular coordination needed to move food from the tip of the
tangue to the back of the mouth
Their GIT is too immature to digest and absorb the food
Gastric, intestinal and pancreatic enzymes are not fully developed
Their kidneys can not regulate the high solute load
The food or water may be contaminated so that they may get diarrhea
The baby may suckle less at the breast so he gets less milk and the mother is more likely
conceive again
Disadvantages of too late weaning:
1) Malnutrition
+ The custom in some places is not to give a child any other food until he is 1 year old
This is too late and may cause malnutrition
Children who do not start to eat other foods at 6 months of age stop growing
Some babies continue to grow on breast milk alone until they are 9-10 months old, but most
babies need more than their mothers milk supply some time b/n 4 and 8 months
2) Difficulty to Initiate Solid Food
If a child does not start to eat other food at a bout 6 months of age, it may be more difficult
to teach him/her to eat solid food.
Now a days, it is generally recommended that:
Up to 6 months of age, an infant should breast-feed as often as he wants day and night, at
least 8 times in 24 hours (Do not give other foods)
6 months up to 12 months:
Breast feed as often as the child wants
Give adequate servings of freshly prepared:
384
Shiro fitfit, merek fitfit, porridge made of cereal and legume mixes, mashed potatoes and
carrot, mashed gommen, egg and fruits
Add some extra butter or oil to childs food
Give these foods:
3 times per day if breastfed
5 times per day if not breastfed
12 months up to 2 years:
Breast feed as often as the child wants
Give adequate servings of freshly prepared:
Porridge made of cereal and legume mixes
Shiro, kik, merek fitfit, mashed potatoes and carrot, gommen, undiluted milk, egg
and fruits
Add some extra butter or oil to childs food
Give nutritious complementary foods or family foods 5 times a day
Recommendations for Ages 2 years and older:
Give family foods at least 3 meals each day
Also, twice daily, give nutritious foods b/n meals, such as: Eggs, milk, fruit, kitta, dabo:
Some of disadvantages of breast milk substitutes:
Reduces the breast milk production and intake
Predisposes the infant to infection
If dilute, it will lead to malnutrition
Difficulties in digesting and absorbing nutrients from breast milk substitutes
Could lead to allergic diseases
Could increase the risk of persistent diarrhea
Providing nutritional education concerning normal feeding patterns is an important task.
Explanation of nutritional education
Importance of adequate nutrition
385
Preparation of locally available nutritious food
Importance of attending a well baby clinic.
Organizing nutritional Rehabilitation center
A nutrition rehabilitation unit or center is the place where medical and health care interact
with mother family and community care
During the recovery of a child after malnutrition or severe infection or both, the child
catches up to the slope of healthy growth he was on before he became malnourished or ill
The slope of this recovery catch-up is one of the best indicators of the adequacy of the
nutrient intake of a child
Nutrition rehabilitation is a lot more than nutrition convalescence
Rehabilitation is a process that uses the cure to teach prevention
As the child gets better, medical care is replaced by lay care (As the child becomes better,
the more he will need lay or mothers care
Rehabilitation is the process of replacing medical care with informed lay care
More often medical and health-care workers treat and cure people, but totally neglect to
replace their care with informed lay care
The mother takes the child home with no idea of what the illness has been all about and
what she must and can do herself to prevent it happening again
NB- A they relationship has been allowed to develop (They have done it) rather than
a we relationship we have done it.
Amount of the laycare Amount of medical & health worker care
Small Laymother & family care Large Medium Becoming malnourished Large
Nutritional Rehabilitation during recovery medical and H. worker care medium well under
weight marasmus/kwashiorkor small very ill
Sharing knowledge, attitude and practice
Figure A The transfer of care form medical and health. Professionals to the community during
rehabilitation
386
A nutrition rehabilitation rehabilitation activities can best be described under the following
headings:
Identification
Involvement
Indigenous
Influencers
Instructions
Integrations
Individuals
A good way of measuring the success of a childs recovery from malnutrition is to compare
the catch-up slope of his/her weight during rehabilitation
NB- Adequately rehabilitated PEM leaves no scars behind, unless there are associated deficiency
diseases, such as blindness from keratomalacia in vitamin A deficiency
So establishment and organization of nutritional center is very important to save the life of
children (cure and prevent malnutrition)
Need assessment and identifying cases (<60% growth monitoring chart) is important in
order to organize the nutritional rehabilitation center.
Duty 11 Manage child hood behavioral disorder
HABITE DISORDERS
Habit disorders include tension-discharging phenomena, such as head banging, body rocking, thumb
sucking, nail biting, hair pulling (trichotillomania), teeth grinding (bruxism), hitting or biting parts of
one's own body, body manipulations, repetitive vocalizations, and air swallowing (aerophagia). Tics,
which involve the involuntary movement of various muscle groups, are also included. Many children at
387
various developmental points show repetitive patterns of movement that can be described as habits.
Whether they are considered disorders depends on the degree to which they interfere with the child's
physical, emotional, or social functioning. Some habit patterns may be learned by imitation of adults.
Many begin as a purposeful movement that, for some reason, becomes repetitive, with the habit losing
its original significance and becoming a means of discharging tension. For example, a child who has an
eye irritation or is attempting not to shed tears might try closing the eyelids several times in rapid
succession. This activity may become repetitive and incorporated into the child's behavior as an outlet
for tension. Such symptoms are often reinforced by attention from parents or others. Other movements,
such as rhythmic head banging and rocking in early life, can persist without parental reinforcement,
occurring when the child is put to bed or is alone; these movements seem to provide a kind of sensory
solace for the child. In many cases, children who exhibit head banging or rocking either have been
neglected or have developmental delays. These movements represent a kind of internal stroking. Some
children twist their hair or touch or play with parts of their bodies in repetitive ways. As these children
become older, they may learn to inhibit some of their rhythmic habit patterns, particularly in social
situations. In some cases, however, social anxiety can increase repetitive behaviors. The prevalence of
habit disorders is not known. In part, this is because habit disorders are a heterogeneous group of
disorders with varying causes. The natural course can vary, though children with mental retardation
may be more refractory to treatment.
Teeth grinding, or bruxism, is quite common, can begin in the first 5 yr of life, and seems to be
associated with daytime anxiety. Untreated bruxism may create problems with dental occlusion.
Helping the child find ways to reduce anxiety may relieve the problem, though studies of psychologic
treatment for bruxism are rare. Bedtime can be made more enjoyable and relaxed by reading or talking
with the child, permitting review of fears or angers experienced during the day. Praise and other
emotional support are useful at these times. To what degree bruxism is heritable is not known.
Persistent bruxism requires referral to a dentist and may present as muscular or temporomandibular
joint pain.
THUMB SUCKING
Thumb sucking is normal in infancy and toddlerhood. Older children who thumb suck may eventually
affect alignment of the teeth. Like other rhythmic patterns of behavior, thumb sucking can be seen as a
388
way of securing extra self-nurturance. The best strategy for dealing with thumb sucking is to provide
the child with praise for substitute behaviors. Parents should ignore thumb sucking, if possible, while
giving attention to more positive aspects of the child's behavior. When the child actively tries to restrain
thumb sucking, he or she should be given praise and encouragement. The use of noxious agents (e.g.,
bitter salves) to control thumb sucking is not well studied and should be considered a second-line
approach.
11.1 ENURESIS (BED-WETTING)
11.1.1 Definition
Enuresis is defined as the voluntary or involuntary repeated discharge of urine into clothes or bed
after a developmental age when bladder control should be established.
11.1.2 ETIOLOGY AND INCIDENCE
-Beyond genetic factors, the cause of enuresis likely involves a complex web of physiologic and,
perhaps, psychologic factors.
-Children with nocturnal enuresis, for instance, may both hyposecrete arginine vasopressin (AVP)
generally and be less responsive to the lower urine osmolality associated with fluid loading.
-Independent evidence suggests that tubular sodium-potassium exchange in the kidney, partly
influenced by AVP secretion, is associated with nocturnal enuresis. -Evidence also suggests that
AVP receptor function in the tubule may be a key factor in the pathophysiology of the disorder.
- On the other hand, there may also be associations between sleep and enuresis. Although enuresis may
occur at any stage of sleep, there is some support for a relationship between sleep architecture,
diminished capacity to be aroused from sleep, and abnormal bladder function in enuretics.
-The relationship between enuresis and psychologic functioning also appears complex. Large-scale
studies reveal that older enuretic children have a higher incidence of psychopathology generally than
non-enuretic children, though no single disorder accounts for the group differences. Smaller studies
suggest that children with attention-deficit/hyperactivity disorder more commonly are enuretic than
age-matched comparison children. Secondary enuresis is associated with life stress and/or traumatic
389
experiences, particularly in children who were late in first achieving nighttime dryness. The
pediatrician should inquire about stressful events with all children who present with secondary enuresis
-Most children with a mental age of 5 have obtained bladder control during the day and night. The
prevalence of enuresis at age 5 yr is 7% for males and 3% for females. At age 10 yr, it is 3% for males
and 2% for females, and at age 18 yr, it is 1% for males and extremely rare in females. Twin studies
show that there is a marked familial pattern: A 68% concordance rate in monozygotic twins and a 36%
concordance rate in dizygotic twins have been documented. However, linkage studies have implicated
multiple chromosomes, particularly chromosome 22, and varying patterns of transmission appear
likely.
11.1.3 Pathophysiology
CLINICAL MANIFESTATIONS
-Bed-wetting may be divided into the persistent (primary) type, in which the child has never been
dry at night, and the regressive (secondary) type, in which a child who has been continent for 6
mo or more then begins to wet the bed. --- - Primary enuresis represents approximately
90% of all cases. Further classification involves nocturnal enuresis (voiding urine at night), and
diurnal enuresis (voiding urine while awake).
-Primary nocturnal enuresis is the most common and well studied subtype. Diurnal enuresis is
more common in girls and rarely occurs after the age of 9 yr. The most common cause of daytime
enuresis in the preschool child is waiting until the last minute to void urine (micturition deferral).
In addition to micturition deferral, etiologic factors to consider in diurnal enuresis include a
urinary tract infection, chemical urethritis, associated constipation, diabetes, and giggle or stress
incontinence. Children with both nocturnal and diurnal enuresis, especially in the presence of
voiding difficulties, are more likely to have abnormalities of the urinary tract, and
ultrasonography or uroflowmetry is indicated for these cases. Otherwise anatomic abnormalities
are rarely associated with either nocturnal or diurnal enuresis and invasive or costly studies are
contraindicated. A urinalysis and urine culture will rule out both infectious cause and the
elevated urine osmolality associated with diabetes.
11.1.5 Diagnostic assessment
390
The diagnosis of enuresis is made when urine is voided twice a week for at least 3 consecutive months
or clinically significant distress occurs in areas of the child's life as a result of the wetting
11.1.6 Medical management
Management of the child with enuresis should begin with behavioral treatment.
General guidelines for a first-line approach would be as follows:
1. It is important to enlist the cooperation of the child to deal with the problem. Rewarding the
child for being dry at night is a useful step. The child or parent can chart the dry nights, and,
with each dry night, a small reward can be given. More substantial rewards should be given for
increasing success.
2. The child should void before retiring.
3. Waking the child repeatedly to take him or her to the bathroom is not generally useful and
may further engender or aggravate anger in child or parents. Some data indicate that enuretic
children are more difficult to awaken than age-matched peers. However, using an alarm clock to
wake the child once 23hr after falling asleep is indicated.
4. Punishment or humiliation of the child by parents or others should be strongly discouraged.
One study showed that consistent dry bed training (as earlier) with positive reinforcement has a
success rate of 85% or more. The use of conditioning devices (e.g., an alarm that rings when the
child wets a special sheet) also is often helpful in training the child to improve bladder capacity
and avoid enuresis. In effect, these devices provide a consistent mode for behavioral retraining.
Again, consent of the child should be a prerequisite for use of such a device. Bell and pad alarm
systems have a success rate of approximately 75% across many studies, with relapse rates that
are lower than those with pharmacologic intervention. These devices are simple and cost-
effective. However, psychotherapy for traumatized children with secondary enuresis may be
indicated, especially when behavioral training has failed and traumatic experiences temporally
associated with the onset of enuresis are noted.
Pharmacotherapy for enuresis is second-line treatment and should be reserved for those patients
who have failed behavioral treatment. Head-to-head comparison studies of the bell and pad
versus imipramine and desmopressin acetate (DDAVP) reveal significantly lower relapse rates
for the bell and pad, although the initial response rates are similar. Imipramine (Tofranil) at a
maximum dosage of 2.5mg/kg/24?hr before bedtime has shown a success rate of approximately
50%, with a relapse rate of 30% or more even after 6 mo of treatment. Imipramine is associated
with cardiac conduction disturbances and is deadly in overdose. DDAVP can be administered
orally or intranasally at bedtime. The fast action of DDAVP suggests a role for special occasions
(such as overnights) when rapid control of enuresis is desired. Unfortunately, the relapse rate
upon discontinuation of DDAVP is very high, and 1 month of treatment typically costs as much
as a bell and pad system (which can be used for several months as necessary). DDAVP is also
associated with rare side effects of hyponatremia and water intoxication, with resulting seizures.
391
11.2 TEMPER TANTRUMS
11.2.1 Definition
Temper tantrums are a normal part of child development. However, when children express anger
in outbursts of rage it is a significant challenge for parents.
Parents may blame their ineffective parenting skills when the problem may relate to individual
personality styles of children or triggering situations. Characterizing the type of temper tantrum
may help parents to understand, so that they may apply different approaches.
Types of temper tantrums include frustration or fatigue-related, attention-seeking or
demanding, refusal, disruptive, potentially harmful, or ragelike. If children experience temper
tantrums related to excessive fatigue or hunger, the most appropriate response should be to give
support, sleep, or food. Positive remarks made at the time of the tantrum may help mitigate
feelings of frustration. When a child is insistent and makes unreasonable demands, it is best to
ignore him or her and allow time for the child to regain composure. Tantrums manifest by
refusal to go to bed or to school should be approached with firmness and consistency. Parents
should be clear and consistent in their requests for compliance but they must allow sufficient
opportunity and time for children to respond. If this approach fails, it may be necessary to
intervene with physical restraint by moving the child into the bedroom or the automobile. When
behavior is disruptive, out of control, and occurring in a public place, such as the grocery store or
a parking lot, it is necessary to remove the child from the situation and impose a time-out. A rule
of thumb for the length of time-out is approximately 1?min per year of age. When significant
rage with the potential for physical injury occurs, the best intervention is holding and physically
restraining the child to allow time for the child to become calm and relaxed. Even though temper
tantrums are a normal part of childhood and parenting, it is important to assess families to
determine if there are contributing factors such as parental depression or family violence that
may require other referrals or interventions.
DISCIPLINE
This common aspect of parenting is one of the most controversial. Families often have little
knowledge about effective techniques of modifying child behavior. Parents have a tendency to
apply discipline strategies similar to those used by their parents. Primary care practitioners
should inquire about methods of discipline and offer practical advice and alternatives. Well child
visits provide observations that may serve as stepping-off points to a discussion about behavior
and discipline. The basis of all effective discipline is a positive, supportive, loving parent-child
relationship. Key elements include positive role modeling, praise, paying attention and listening
to children, and devoting special time to enhance parent-child relationships. Pediatricians should
instruct parents to maintain a positive atmosphere within their home and provide clear
expectations about desired behaviors. Consistency of parental behavior, open communication
within families, and mutual respect form the cornerstones for effective discipline. If there is
evidence of marital discord, family dysfunction, substance or alcohol abuse, or family violence, a
referral for counseling is the most important priority.
392
Time-out or removal of privileges should be distinguished from punishment. Time-out involves
the removal of positive reinforcement for unacceptable behavior; this technique requires
consistency and patience because its effect on behavioral change takes longer to achieve a desired
result. Often time-out provokes a reactive emotional response or a tantrum. Parents should
remain calm and impassive to avoid prolonging the incident or escalating the level of response.
This form of discipline, among the most reliable and enduring in changing child behavior,
requires parents to manage their own distress in order to be successful. Punishment involves
issuing a negative stimulus or verbal reprimand, or inflicting physical pain, to reduce or
eliminate an undesired behavior. Behavioral research on corporal punishment is inconclusive and
conflicting about the
ENCOPRESIS
Encopresis refers to the passage of feces into inappropriate places after a chronologic age of 4 yr
(or equivalent developmental level). Subtypes include encopresis with constipation and overflow
incontinence (retentive encopresis) and encopresis without constipation and overflow
incontinence (nonretentive). Encopresis may persist from infancy onward (e.g., primary) or may
appear after successful toilet training (e.g., secondary). About two thirds of encopresis cases are
of the retentive type and associated with chronic constipation; it is less clear what percentage of
cases are primary versus secondary. In children younger than 4 yr of age, the male:female ratio
for chronic constipation is 1:1. In the school-aged child, however, encopresis is more common in
males, though good epidemiologic studies are lacking.
The first consideration in managing encopresis is assessment of fecal retention. A positive rectal
examination is sufficient to document fecal retention, but a negative rectal examination in the
presence of encopresis requires plain abdominal roentgenograms. The presence of fecal retention
is evidence of chronic constipation, and treatment will require active constipation management.
Many children with encopresis present with abnormal anal sphincter physiology as documented
either by electromyography or difficulty in defecating a rectal balloon. The inability to defecate a
balloon at presentation is associated with poorer response to treatment. Abnormal anal sphincter
function is a marker for chronic constipation; children with this pathology do not appear to have
a higher incidence of behavioral or psychiatric disorders than those without. However, a chart
review study suggests that primary encopresis in boys is associated with global developmental
delays and enuresis, whereas secondary encopresis is associated with high levels of psychosocial
stressors and conduct disorder. Associated behavioral or psychiatric problems obviously may
complicate the treatment of encopresisespecially when parents respond to soiling with
retaliatory, punitive measures and children become angry, ashamed, and resistant to
intervention. School performance and attendance may be secondarily affected as the child
becomes the target of scorn and derision from schoolmates because of the offensive odor.
TREATMENT
393
The standard treatment approach to encopresis begins with clearance of impacted fecal material
and short-term use of mineral oil or laxatives to prevent further constipation. Concomitant
behavioral management is also indicated. The focus of behavioral treatment should be on
compliance with regular postprandial toilet sitting and adoption of a high-fiber diet. On some
occasions, manual disimpaction is required before the treatment can begin; rarely megacolon is
observed and referral to a gastroenterologist is required. Several studies suggest that once
impacted stool is removed, the combination of constipation management and simple behavior
therapy is successful in the majority of cases, though it is often a period of months before soiling
stops completely. However, compliance may wane and failure of this standard treatment
approach sometimes requires more intensive intervention with a special emphasis on adherence
to a high-fiber diet and family support for behavior change. Parents should be actively
encouraged to issue rewards for compliance to the child from the outset of treatment and to avoid
power struggles with the child. Keeping records of the child's progress is necessary. In cases
where behavioral or psychiatric problems are evident, group or individual psychotherapy may be
necessary.
Biofeedback, which is used to train the anal sphincter muscle, has been helpful in some cases but
controlled trials do not suggest higher rates of improvement as compared to the standard
treatment regimen. Long-term laxative use is contraindicated. Several case reports suggest
improvement in some children on tricyclic antidepressants, though there is not enough data to
warrant regular use of these drugs, particularly given their narrow therapeutic window and
association with cardiac dysrhythmias. Furthermore, tricyclic antidepressants often cause or
exacerbate constipation and should be avoided in children with retentive encopresis. The few
long-term follow-up studies suggest that encopresis eventually resolves in most children,
regardless of treatment approach.
VIOLENT BEHAVIOR
For surveillance and research purposes, the Centers for Disease Control and Prevention have
accepted a definition of a violent injury as a threatened or actual use of physical force against a
person or group that either results or is likely to result in injury or death. Youth are
perpetrators of violence, victims of violence, or observers of violence with varying severity of
impact on the individual. Violent acts may result in, or are contributed to by, mental health
problems or disorders. Child health workers are challenged to screen for these disorders and
counsel or refer adolescents with serious disorders to mental health professionals. The public
health and educational communities have launched a variety of violence prevention interventions
to increase youth prosocial behavior and reduce violence as a societal problem.
ETIOLOGY
The theories to explain violence come from the perspective of varying disciplines. The development
psychopathology model of Mofitt identifies two types of antisocial youth:
- One that is life coursepersistent and
394
- One that is life courselimited.
Adolescent-limited offenders have no childhood aberrant behaviors and are more likely to commit
status offenses such as vandalism, running away, and other behaviors symbolic of their struggle for
autonomy from parents.
Life coursepersistent offenders, in contrast, exhibit aberrant behavior in childhood, such as
problems with temperament, behavioral development, and cognition, and as adolescents participate
in more victim-oriented crimes.
The public health model emphasizes the environment and other external influences. It focuses
primarily on preventive strategies that view violence as amenable to systematic, science-based,
multidisciplinary, and sustained interventions.
A third theoretical model examines violent behaviors across the spectrum occurring within and
outside the family and is referred to as the cycle of violence. This hypothesis proposes that
precursors such as child abuse and neglect, a child witnessing violence, adolescent sexual and
physical abuse, and adolescent exposure to violence and violent assaults predispose youth to
outcomes of violent behavior, violent crime, delinquency, violent assaults, suicide, or premature
death.
An additional common paradigm for high-risk violence behavior poses a balance of risk and
protective factors at the individual, family, and community level. None of these theories successfully
explains violent behavior. Although the media influences violence through a strong effect on
aggressive behavior, many questions still remain about the causes of violent behavior.
There are several clinical entities directly associated with violent behavior that require
recognition and intervention. The most common behavioral diagnoses associated with aggressive
behavior in adolescents are
- Mental retardation, learning disabilities, moderately severe language disorders
- Mental disorders such as attention-deficit/hyperactivity, mood disturbance, anxiety, and
personality disorders.
- Inability to master prosocial skills such as the establishment and maintenance of positive
family and peer relations and the resolution of conflict may put adolescents with these
disorders at higher risk for physical violence and other risky behaviors.
- Conduct disorder and oppositional defiant disorder are specific psychiatric diagnoses
whose definitions are associated with violent behavior.
- They occur co-morbidly with other disorders such as attention-deficit/hyperactivity
disorder and increase an adolescent's vulnerability for juvenile delinquency, substance use
or abuse, sexual promiscuity, adult criminal behavior, incarceration, and antisocial
personality disorder.
DIAGNOSIS
395
The assessment of an adolescent at risk for, or with a history of, violent behavior or victimization
should be a part of the health maintenance visit of all adolescents. The answers to questions about
recent history of involvement in a physical fight, carrying a weapon, or firearms in the household,
as well as concerns that the adolescent may have about his or her personal safety may suggest a
problem requiring a more in-depth evaluation. The additional factors of physical or sexual abuse,
serious problems at school, poor school performance and attendance, multiple incidents of
trauma, and symptoms associated with mental disorders are indications for evaluation by a
mental health professional. In a situation of acute trauma, assault victims are not always
forthcoming about the circumstances of their injuries for fear of retaliation or police
involvement. Stabilization of the injury or the gathering of forensic evidence in sexual assault is
the treatment priority; however, once this is achieved, addressing a more comprehensive set of
issues surrounding the assault is appropriate.
TREATMENT
In the instance of acute injury secondary to violent assault, the treatment plan should follow
standards established by the American Academy of Pediatrics model protocol, which includes,
but is not limited to, the stabilization of the injury, evaluation and treatment of the injury,
evaluation of the assault circumstance, psychologic evaluation of the functioning of the victim,
rehabilitation of the injury, and outpatient follow-up of the behavioral and physical sequelae. The
American College of Emergency Physicians details the required examination and documentation
for sexual assault victims in a handbook, Evaluation and Management of Sexually Assaulted or
Sexually Abused Patient. Specific requirements for forensic evidence, as well as the management
of sexually transmitted diseases and pregnancy prevention, are key elements of these
recommendations. Specifically prophylactic treatment of chlamydia and gonorrhea as well as
postcoital contraception is recommended.
PREVENTION
Interventions to prevent violence must encompass individual and social factors. Violent behaviors
are influenced not only by characteristics of individuals, but also by characteristics of families,
such as cohesion and parent practices; characteristics of peers, such as delinquent behaviors;
characteristics of schools, such as teacher practices and school atmosphere; characteristics of
community organization, such as the frequency and type of youth activities; and characteristics
of the larger society, such as economic opportunity, misuse of firearms, or media exposure.
Violence-prevention efforts to date have emphasized individually oriented strategies, directed
toward students in school or patients in the clinical setting. These approaches should be
continued, but need to be complemented by activities designed to modify exposures at the family,
peer, community, and society level.
DUTY 19
IMN CI (INTEGRATED MANAGEMENT OF NEONATAL AND CHILD HOOD ILLNES)
Peditric- HIV intersaction/ADIS/
396
HIV human immuno deficenc and virus mainly protects aperion form disease comes weak &
unable to protact from different germs.
-Acquired--not in born
- Immune--(body defience)
-deficiencysomething esencial lacking
- Syndromagroup of symptoms or desase that define illness.
EPIDEMIOLOGY
-the first cases were describred in homo sexualin 1980
-in vaganda 1982
-currently it become world wide
-38 millipn people living & HIV worled wide
-2003-5 million newly infacted
-3 millon died
Africa
25 millon people living with HIV
Patern is non uniform.
*nearly 6 countries < 2%
*anatler 6 countries in the south prevalence > 20 %
*southern Africa > 17%
*central & Eastern A.4& 13%
*Wast Africa < 10
*N.Africa < 2%
Mail to temale ration 1:1
ETHIOPIA
million People estimated nation wide prevalence 4%
million children or phanedd
HIV CAUSES AIDS
397
AIDS is agroup of disease that occurs when aperson immumess system is damated severly by
HIV.
There are two types of HIV HIV-1 and HIV-2
-worled wide, the predominant virus is HIV-1
-sub type C is predominant
-most HIV infected children born in dereloping countries
Perinatally {14-25%USA & EUROP
13-42%developing nations}
Estimated data ie 2001- 160000
Transmission
Occurs via sexual contact
Parenteral exposure to blood
Vertical (MTCT)
-Vertical transmisiton
-Intra uterine (25-40%)
-Intra partum (60-70%)
-post partum Via BF (12-14%)
-MTCT is major means of in children about 600000 each year.
Cells Infected by HIV
CD4 T. Cell
B.Lymphocytes
Mcrophages
Dandritic cells
glient Cell
PATHOGENESIS
-nteraction
-HIV enters the body CD4 Cell
-Immune reaction
398
-deplation of CD4 Cells
-HIV is retro virus uses an enzyme
Known as revrse transcriptase to convert its RNA in to DNA
HIV DNA enters the CD4 NUCLEUS & inserts its self into the cells DNA
HIV DNA then instructs the cell to make several copies of the original vires
-with the help of protose enziyem now virus partiles are assembled.
These newly termed viruses leave the cell ready to infcted other CD4 cell.
C/M
-HIV classification used to cate gorize the stage of pediatric d/se include two parameters
* Clinical status
* Degree of immunologic impairnene
CATAGORIES
Catagories A (mild symptom)
LAP, parotiets, hepatomegally, spleenomegally
399

400

Clinical Nursing Module

Enviado por

Dados do documento

Descrição original:

Título original

Direitos autorais

Formatos disponíveis

Compartilhar este documento

Compartilhar ou incorporar documento

Opções de compartilhamento

Você considera este documento útil?

Este conteúdo é inapropriado?

Direitos autorais:

Formatos disponíveis

Clinical Nursing Module

Enviado por

Direitos autorais:

Formatos disponíveis

Module for

Clinical nursing students

1 year Life long

Você também pode gostar