Paediatrics Notes-2017 Batch

Mithushaa Shanmugananthan
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Contents
Introduction & Infant Feeding………………………………………………01- 14
Growth and Development…………………………………………………….14- 23
Neonatal Septicaemia (Sepsis)…………………………………………….23- 24
Neonatal Jaundice………………………………………………………………24- 27
Hypoxic-Ischemic Encephalopathy (HIE)……………………………….27- 29
Paediatric Anemias……………………………………………………………..29- 40
Congenital heart disease………………………………………………….....40- 50
Bronchial Asthma………………………………………………………………..50- 55
Acute poststreptococcal glomerulonephritis………………………….55- 60
Nephrotic syndrome…………………………………………………………….61- 68
Tuberculosis………………………………………………………………………68- 76
Suppurative Meningitis……………………………………………………….76- 83
Infantile Diarrhea……………………………………………………………….83- 88
Pneumonia………………………………………………………………………..88- 94
Growth Hormone Deficiency……………………………………………….94- 97
Congenital Hypothyroidism，CH………………………………………….97- 100
Central Precocious Puberty………………………………………………..100- 102
01. Introduction & Infant Feeding

What is Pediatrics?
Paediatrics is a relatively new medical specialty, developing only in the mid-19th century. Abraham
Jacobi (1830–1919) is known as the father of American Paediatrics.
• As the first professor of pediatrics and the first President of The American Pediatric Society,
Jacobi was the primary pioneer in a field that is a relatively new medical specialty, one that at
the end of the 19th century “marked an epiphany in medicine: the recognition that children
deserved a cadre of professionals dedicated to their care, professionals who would advocate for
and protect children who could not speak for themselves.”
• Almost all of the history of American pediatrics during the second half of the 19th century is
reflected in Jacobi’s writings and work. He wrote extensively on numerous medical subjects.
Without the aid of Dictaphones or secretaries (or, of course, computers), he wrote thousands of
letters and hundreds of scientific papers.
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By Dr Ananya Mandal, MD
Pediatrics is the branch of medicine dealing with the health and medical care of infants, children,
and adolescents from birth up to the age of 18.
The word “paediatrics” means “healer of children”; they are derived from two Greek words:
(pais = child) and (iatros = doctor or healer).
• The young are often among the most vulnerable or disadvantaged in society and thus require
special attention.
• Facilitate optimal health and well-being for children and their family
• Focus on the growth and development of children
• Focus on the prevention of diseases of children
• Focus on the treatment of diseases of children
• Preventive Pediatrics
• Developmental Pediatrics
• Clinical Pediatrics
Aims:
• Raise child’s physical endowment
• Decrease the morbidity and mortality rate
• Improve the living quality of the children
Major causes of death:
Under 1y 1. perinatal conditions

intrauterine growth retardation
respiratory distress syndrome
2. congenital malformation
3. sudden infant death syndrome
4. pneumonia
5. gastrointestinal disorders
1 ～ 4y 1. accidental injuries
2. congenital malformation
3. malignant neoplasms
5 ～ 14y 1. accidental injuries
2. malignant neoplasms
• The infant mortality rate (IMR) is the ratio of the number of deaths among children less than
one year old during a given year to the number of live births during the same year.
• The death of an infant is often dependent on external factors, especially in developing
countries. Poor water quality, an inadequate food supply, substandard health services, and a
high level of infectious diseases such as malaria all contribute to a high IMR.
• The IMR is therefore considered a good indicator of the level of health in a community
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• The current worldwide average is just under sixty per thousand live births
• In the developed and developing world, poor children suffer a disproportionate burden of
morbidity and mortality.
• An estimated 70% of child deaths are preventable.
• Success has been achieved by identifying cost-effective best practices in child and infant
health.
Critical preventive care for young children (GOBI-FFF)
（UNICEF--United Nations International Children’s Emergency Fund）
G-- Growth monitoring
O-- Oral rehydration
B-- Breast feeding
I -- Immunization
F -- Food supplements
F -- Family spacing
F -- Female education
Growth Monitoring
With the help of a growth chart and basic advice on weaning, this helps mothers to prevent most
child malnutrition before it begins.
Oral Rehydration
Previously, the only effective treatment for dehydration was the intravenous feeding of a saline
solution - a cure beyond the physical and financial reach of most of those who need it. Now a child
can be rehydrated by drinking a solution of salts, sugar and water administered by the mother in the
home.
Breast feeding
Breast feeding can ensure that infants have the best possible food and a considerable degree of
immunity from common infections during the first six month of life. For infants, breast milk is more
nutritious, more hygienic, and provides a degree of immunity from infection.
Immunization
Immunizations can protect a child against measles, diphtheria, whooping cough, tetanus,
tuberculosis, and polio. At present, these diseases kill an estimated 5 million young children a year,
leave 5 million more disabled, and are a major cause of child malnutrition.
Female Education
A child born to a mother with no education has been shown to be twice as likely to die in infancy as
a child born to a mother with even four years of schooling.
Family Spacing
Infant and child deaths have been found to be, on average, twice as high when the interval between
births is less than two years.
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Food Supplements
A handful of extra food each day for at-risk pregnant women has been shown to reduce the risk of
low birth-weight—a risk which carries with it a two or three times greater likelihood of death in
infancy.
Genetic disorders
The recent decoding and sequencing of the human genome has expanded the horizon of possibilities
in the diagnosis of genetic disorders.
Pre-natal diagnosis.
Substantial progress has been made in the pre-natal epidemiology in order to identify the congenital
heart malformations and facilitate the appropriate treatment as early as possible
The traditional focus of neonatal screening for inherited metabolic diseases, which is responsible for
significant morbidity and mortality unless treatment is initiated early, is also moving toward a
genetic and mutational scan across the whole fetal genome in a non-invasive manner by analyzing
cell-free fetal DNA in the maternal blood as early as the 5th week of gestational age
Epidemiological, clinical, cellular, and molecular evidence suggests that the conditions during fetal
life play a critical role in developmental programing.
Prematurity.
As a consequence of the improvement of pre-natal screening and diagnosis, the recognition of high-
risk neonates allowed the referral for delivery in proximity of high level Neonatal Intensive Care
Units, with substantial benefits for the neonatal outcomes
Traumas.
Recent studies have shown the unexpected evidence that the burden of permanent disability
resulting from traumatic brain injuries among children is primarily accounted for by mild injuries,
rather than by severe injuries. As a result, efforts have to be addressed to prevent, not only severe,
but also mild injuries to decrease the levels of disability following traumatic brain injuries
Introducing new devices and new drugs.
The research and development of drugs and devices for pediatric patients is complicated due to
small patient populations, characteristics of pediatric physiology and pathophysiology, practical and
ethical difficulties in designing pre-clinical and clinical trials
Continuity of treatment from the pediatric age through the transitional age.
As a result of the advances in medical and surgical treatment during the pediatric age, most patients
are now expected to live to adulthood, with a significant increase in the population of adults with
congenital defects. Consequently, the transition from a pediatric primary care provider to an adult
primary care system has become a critical process in health care management plans, addressing the
medical, psychosocial, and educational needs of adolescents and young adults with chronic physical
and medical conditions.
Influence of the life style of the parents.

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Obesity and the associated and related complications such as diabetes, hypertension,
cardiovascular, and respiratory diseases represent the highest risk factor for mortality and
morbidity.
Childhood obesity, a disturbingly growing problem, is directly related to the number of parent
stressors. Parent-perceived stress is correlated to children’s fast-food consumption, an important
behavioral indicator of obesity risk. Addressing parent stressors and parent-perceived stress is
needed in future research in studying the prevention of child obesity
• Caring for children is distinctly different than caring for adults, since children have unique
medical conditions and issues which adults do not face, and their different body size poses
some unique treatment challenges.
Characteristics of Physiology
pediatrics HR: 1m-1y： 110-130bpm
>8y: 70-90bpm
BR: neonate: 40-45bpm
>8y: 18-20bpm
BP (mmHg): SBP: = age ×2+80
Pathology
Pneumococcal infection
Vitamin D deficiency
clinical medicine
disease pattern
clinical manifestation
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Age Period
Childhood Age Staging

• Fetal period
first trimester of pregnancy first 12 weeks
second semester of pregnancy 13~28weeks
third semester of pregnancy 29~40weeks
Neonatal period
the first 28 days of life
experience great changes from inside uterus to outside
the functions are not mature
the diseases usually caused by maladjustment
high mortality rate
Infancy
From birth to 1 year old
The most rapid growth period
High incidence of malnutrition, dyspepsia, infectious diseases, etc
Immunization
Toddler’s age
from 1 to 3 years old
Intelligence development is very fast
high incidence of accidental injury
Preschool period
from 3 to 6/7 years old
School age
from 6/7 to preadolescence
Adolescence
Biological changes – onset of puberty
Cognitive changes – emergence of more advanced cognitive abilities
Emotional changes – self image, intimacy, relation with adults and peers group
Social changes – transition into new roles in the society
• Early adolescence(10 -13yrs):
Spurt of growth of development of secondary sex.
 Middle adolescence(14-16yrs):
Separate identity from parents, new relationship to peer groups, with opposite sex and desire for
experimentation.
• Late adolescence(17-19yrs):
Distinct identity, well formed opinion and ideas
- mother’s medical history (chronic medical conditions, medications taken during pregnancy
thalidomide event)
- smoking, dietary habits
- occupational exposures to chemicals
- infections
ToRCH infection：
T Toxoplasma
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R Rubella
C Cytomegalovirus, CMV
H Herpes virus
O Others
Thalidomide Thalidomide was developed in the 1950s

The drug was marketed as a mild sleeping pill safe even for pregnant women
It caused thousands of babies worldwide to be born with malformed limbs
Animal tests did not include tests looking at the effects of the drug during pregnancy
Physical characteristics of children in •

Children are extremely active
preschool and kindergarten •
Children need frequent rest periods
•
Children’s large muscles are more developed than than those that control fingers
and hands
• Eye-hand coordination is still developing
• Children’s bodies are flexible and resilient
Cognitive characteristics of children in preschool and kindergarten
 Many children begin to develop a theory of mind
 Children are becoming quite skillful with language
 Children may stick to their own rules in using language
 Competence is encouraged by interaction, interest, opportunities, and signs of
affection
SMR(Sexual Maturity Rating)
Genitalia stage for boys(G1 to G5)
Pubic hair stage(PH1 to PH5)
Breast development for girls(B1 to B5)
Immunization
• Denotes the process of inducing or providing immunity artificially by administering an

immunologic substances
– Active
– Passive
• Routine immunization dramatically decreased morbidity and mortality from a variety of

infectious diseases
Vaccination
• Denotes the physical act of administrating any vaccine or toxoids
Immunobiologic Substances
• Vaccine - a suspension of live or inactivated microorganism or fractions there of

administered to induce immunity and prevent infectious disease or its sequela
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• Toxoid – modified bacterial toxin that has been made nontoxic but retains the ability to
stimulate the formation of antitoxins
• Antitoxins – a solution of antibodies derived from the serum of animals immunized with
specific antigens
• Passive immunization
• Diphtheria antitoxin
• Tetanus antitoxin
VACCINES
• Hepatitis B
• Bacille Calmette--Guerin BCG
• Diphtheria Pertussis Tetanus DPT
• Poliomyelitis
• Measels
Immunization schedule
age vaccine
<1d HB 1
1m HB 2
<2 m BCG
2m Polio 1
3m Polio 2 DPT 1
4m Polio 3 DPT 2
5m DPT 3
6m HB 3
8m Measles
Infant Feeding
Children need food of appropriate quantity and quality for optimal growth and development
The nutritional vulnerability
Infants and children are more vulnerable to poor nutrition than are adults
Low nutritional stores
High nutritional demands for growth
Rapid neuronal development
Illness
Category of nutrients（2000 Chinese Dietary Reference Intakes）
 Energy：
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 Macronutrients: PRO、FAT、CHO
 Micronutrients: minerals
vitamins
(Fat-soluble-vitamins,
water-soluble-vitamins)
 Other diet elements: cellulose, water
Macronutrients Energy produced
Gross Energy Intake
Infant feeding
Definition: Exclusive breastfeeding is fed no foods or fluids, even water.
Partial breast-feeding is defined as breast milk plus either solid foods or other milks.
Summary of differences between milks

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Two patterns for partial breast-feeding
To supply with formular within 4~6 months For deficient B.M intake
To replace B.M with formular after 4~6 months preparation for weaning
Components of human milk
Colostrum : “first milk"; immature milk produced in 4-5 days post-partum
Transitional Milk: 2weeks; The composition is midway between colostrum and mature milk .
Mature Milk:
The changes of the components during nursing (g/L)
colostrum middle maturity
PRO 22.5 15.6 11.5
FAT 28.5 43.7 32.6
CHO 75.9 77.4 75.0
Mineral 3.08 2.41 2.06
Ca 0.33 0.29 0.35
P 0.18 0.18 0.15
Colostrum
Property
• Antibody-rich
• Many white cells
• Purgative
• Growth factors
• Vitamin-A rich
Importance
• protects against infection and allergy
• protects against infection
• clears meconium; helps prevent jaundice
• helps intestine mature; prevents allergy, intolerance
• reduces severity of some infection (such as measles and diarrhoea); prevents vitamin A-
related eye diseases
Benefits of breastfeeding
• Provides superior nutrition for optimum growth.

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• Provides adequate water for hydration.
• Protects against infection and allergies.
• Promotes bonding and development.
• The primary benefit of breast milk is nutritional. Human milk contains just the right amount
of fatty acids, lactose, water, and amino acids for human digestion, brain development, and
growth
• IMMUNOLOGY- Breast milk contains valuable antibodies from the mother that can help the
baby resist infections. About 80 percent of the cells in breast milk are macrophages, cells
that kill bacteria, fungi and viruses.
Breast-fed babies are protected, in varying degrees, from a number of illnesses,

including pneumonia, botulism, bronchitis, staphylococcal infections, influenza, ear
infections, and German measles.
Breastfeeding is associated with a reduction in the risk of:
 acute otitis media
 non-specific gastroenteritis
 severe lower respiratory tract infections
 atopic dermatitis
 asthma (young children)
 obesity
 necrotizing enterocolitis
Benefits for Babies
 Positive Effect on Later Intelligence Tests
 Preterm Babies Breast Milk (plus Fortification)
 Protection Against Infectious Diseases.
 Protection Against Allergic Diseases
 Lower Prevalence of Inflammatory Bowel Diseases
 Blood Cholesterol
 Later Overweight and Obesity
 Blood Pressure
 Mothers produce antibodies to whatever disease is present in their environment,

making their milk custom-designed to fight the diseases their babies are exposed to
as well.
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Breastfeeding has psychosocial and developmental benefits
Benefits of breastfeeding for the mother
• Protects mother’s health
– helps reduces risk of uterine bleeding and helps the uterus to return to its previous
size
– reduces risk of breast and

ovarian cancer
• Helps delay a new pregnancy
• Helps a mother return to pre-pregnancy weight
The disadvantages of breast-feeding
• Unknown intake Volume of milk intake not known
• Transmission of infection HIV
• Breast milk jaundice self-limiting, unconjugated

hyperbilirubinaemia
• Transmission of drugs Antithyroid drugs

cathartics, antimetabolites
• Nutrient inadequacies Prolonged breast-feeding
• Vitamin K deficiency- insufficient vitamin K in breast milk to prevent hemorrhagic disease of

the newborn
• Potential transmission environmental contaminants nicotine, alcohol, caffeine, etc.
• Less flexible- Other family members cannot help or take part.

More difficult in public places
• Emotional upset if unsuccessful Breast-feeding can be problematic to establish

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Main points of breast milk promotion
 Early nursing
 Fed on demand
 Rooming-in
 Proper technique of feeding
 Nutrition ,rest, fluid intake of lactating mother
WHO Feeding Recommendations
 Breastfeed children for at least 2 years
 No bottle feeding
 Start breastfeeding immediately after birth
 Exclusive breastfeeding for first 6 months
 Introduce solid/mushy foods at 6 months together with breastfeeding
Risks of artificial feeding
• More diarrhoea and respiratory infections

• Persistent diarrhoea
• Malnutrition- Vitamin A deficiency
• More likely to die
• May become pregnant sooner
• More allergy and milk intolerance
• Increased risk of some chronic diseases
• Overweight
• Lower scores on intelligence tests
• Increased risk of anaemia, ovarian and breast cancer
• Interferes with bonding
Choice of breast milk substitute
 Fresh cow’s milk,other animal’s milk
 Milk powder,condensed milk
 Rice powder, bean powder
 Formula milk
Cow’s Milk
Although cow's milk contains most of the same components as breast milk, these components are
not in the same amounts
Contains too much protein and salt.It would create too high a solute to their immature kidneys ,
especially in babies below 6months.
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And infants are not generally able to concentrate urine well.
The infant can develop an allergy to dairy products if given cow's milk too early in life.
Cow’s milk can irritate the baby’s intestine, causing the baby to lose small amounts of blood.
Formula
• Modified cow’s milk to mimic the desirable qualities of breast milk such as a lower protein
and sodium content, a higher lactalbumin to casein ratio and emulsified fat are well
tolerated by most infants.
• The presence of enzymes and other bioactive components in breast milk that have beneficial
effects in digestion and metabolism have not, as yet, been replicated in formula. In addition,
breast milk contains enzymes that facilitate digestion.
• formula cannot copy breast milk exactly.
For example, the antibodies found in breastmilk, however, can never be added to formulas.
Complementary food
 cereal rice power
 egg yolk
 paste of fish,meat ,vegetable, fruit
The changes of food-taking behavior
 change of food quality : from liquid to solid
 change of feeding behavior: from sucking to chewing
 change of feeding utensils : from bottle to spoon
 change of foster: the feeding person
How to help the child adapt to the change
 Encourage the child take part in the process of feeding
 Give the child the opportunity to have many kinds of food
 Pay attention to the environment of eating ,concentrate child’s attention to eating
 Try a new food repeatedly until the child accept it
 To form good eating habit around 1-year old
Current Status of Infant Feeding Practices
 Initiation of breastfeeding is late
 Bottle feeding is common
 About half of infants below 4 months are breastfed exclusively, as recommended
 Introduction of solid or mushy food is much later than recommended for a majority of
children
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• Exclusive breast feeding until 6 months of age
• Introduce complimentary foods with continued breastfeeding
• Optimum to breastfeed for 2 years or longer
02. Growth and Development

Growth: Defined as an increase in size of body, biological growth of an individual takes place through
cell multiplication, this morphological growth can be measured clinically.
The enlargement of the organ and the system morphological growth can be measured by exact
values
Development: A gradual change and expansion; advancement from a lower to a more advanced
stage of complexity; increased capacity through growth, maturation, and learning
An increase in competence and adaptability A QUALITATIVE change Functioning at a higher level
Thus, since both processes are part of one whole, the combined terms growth and development
form an unitary concept that indicates the quatitative and qualitative of maturational changes of a
child
•Growth is a continuous and orderly PROCESS
Not all tissue or systems of the body grow at the same rate
Variability: Not everyone is alike in the way that they grow
Percentile growth/ standard deviation to the norm
Racial and ethnic differences
Boys vs Girls
Patterns of Growth and Development
 Cephalocaudal Pattern (head to toe)

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Cephalocaudal :most pronounced during the prenatal period (when the head may make up more
than half of the baby's length), decreases by birth (when the head comprises about 25% of the
neonate's body length), and gradually reaches adult levels by adolescence (when the head comprises
about 10% of the body's length). This pattern is largely complete by the beginning of adulthood,
though of course other aspects of development continues throughout life
 Proximodistal Pattern (from center outward)
Proximodistal: The second general pattern of physical growth consists in the tendency for growth to
start at the center of the body and work its way outward, toward the extremities. This is called the
proximodistal pattern. Thus, the head and trunk of the body develop (grow) first, followed by the
arms and legs
Factors Influencing Growth:
•Heredity
pattern, rate, rhythm and extent: governed by genes interplaying with environment
•Nutrition
Begins during the prenatal period Intrauterine life extremely important in growth and healthy
development of the child LBW/preterm and SGA can result from poor prenatal nutrition
•Disease
FOAD (Fetal origins of adult disease)>> IUGR / SGA>>> hypertention Coronary heart disease II DM
Insulin resistent Metabolic syndrome
•Environment –Hazards –Socioeconomic influences
family composition family position in society family socioeconomic status knowledge of the family
availability of healthy diets housing diseases present in family and child
Indices of Growth
Body weight (kg)
• the weight of a person’s body.
• the weight of all tissues, organs and body fluids.
• one indicator of the nutritional status of child.
• the basis of drug dosage and amount of infusion
Patterns of Weight Increment
The first growth spurt occurs in the first year of life (the increment is about 6kg).
Growth is not at the same rate in different age : The increment of weight during the first 3 months is
equal to that of the following 9 months.
Yearly increments increase slowly until the onset of puberty

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•Weight loss: Physiological weight loss: 3 - 9% recover at 7-10th day Loss of 3%~ 9% of birth weight
in the first few days of life is considered normal and is common for most newborns. (pass of
Meconium, the use of dry heat from radiant warmers and isolettes (incubators) causes insensible
fluid loss)
Height(cm) • The length from vertex to plantae • The index of long time nutritional status
The height for infants up to three years should be measured as recumbent length using a properly
constructed measuring device. Height measurements for children over three years of age should be
accomplished using vertical measuring board or fixed wall device
Length/Stature --- < 3y --- Supine Length ≥3y Stand Stature
Patterns of Length Increment
The first growth spurt occurs in the first year of life (the increment is about 25cm). Growth is not at
the same rate in different age : The increment of height during the first 3 months is equal to that of
the following 9 months. Yearly increments increase slowly until the onset of puberty.
• Shortness may be caused by malabsorption, chronic illness, psychosocial deprivation, hormonal

disorders, familial patterns, or syndromes with dwarfism. • Gigantism may be the result of pituitary
abnormalities.
Crown-rump/Sitting height
They give a measure of the length of the head and trunk. It is a measurement of the distance from
the highest point on the head to the base sitting surface.
<3y: Supine- Crown-rump, length
≥3y: Sit- Sitting, height
During the first year of life, spinal increase is faster than extremities. Later on, the extremities grow
at a faster rate than the trunk, which is contribute to the body length and leading to a gradually
change in relative proportions.
Head Circumference
HC is a measurement of perimeter of head,from eyebrows to occipital prominence. The change of

the HC is related with the growth of brain and skull.
Head circumference should be measured with a tape measure at each visit during the first two years
of life. A large head may be an early sign of hydrocephalus or an intracranial mass. A small head may
be a result of early closure of sutures or lack of brain development.
Abnormal of HC:
Small HC ——Cerebral dysplasia, Microcephaly
HC increase too fast—— Hydrocephalus
Growth on Puberty • At puberty, there is a marked growth spurt(The second peak of height
velocity,PHV), that is, a very rapid increase in size and weight
• Girls usually showing their pubertal growth spurt around age 9~11.
• For boys the same process begins at apx. age 11~13.

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• According to Tanner (1990), girls finish pubertal growth by about age 16 whereas boys continue to
grow until approximately 18 years of age.
Sexual Precocity：Secondary sexual characteristics appear before puberty. Girls<8y，Boys<10y
Delayed sexual maturity： Secondary sexual characteristics do not appear after puberty Girls>14y，
Boys>16y
Closure time of fontanel/suture
Fontanel/suture At birth Time of closure

Anterior fontanel 1.5-2cm ≦18m
Posterior fontanel 0.5-0.7 1-2m
Cranial suture Smallest 3-4m
Abnormality of anterior fontanel
Small size or early closure：Microcephaly
Large size or delayed closure：Hydrocephalus, Cretinism
Bulging fontanel：Intracranial hypertension( Encephalitis, Meningitis)
Sunken fontanel ：Dehydration
Bone development
Osteite (center of ossification), which is located near ends of long bones (epiphyses), with growth
plates. It is very important for bone’s growth in length.
Bone age Bone age is that the age should be according to the osteite number for normal child. The
most commonly used standards are those of Gruelich and Pyle, which require radiographs of the left
hand and wrist; knee films are sometimes added for younger children(usually less than 1 year old).
Abnormality of Bone Age
Retardation of BA Hypothyoidism, Hypopituism

Precocity of BA： Adrenogenital syndrome, Precocity
Dentition
Primary teeth:
•Primary teeth are 20 totally.
•The first eruption is at about 6 months(4~10 months) .
•The timing of tooth eruption is more variable than other developmental parameters
•Delayed eruption is usually considered when there are no teeth by approximately 12 months of
age.
•The last eruption of primary teeth is at 2~2.5 years of age.

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Abnormality of Dentition:-
Delayed eruption: Hypothyroidism, idiopathic
Failing to erupt : Ectodermal dysplasia,Mechanical blockage
Abnormality of dental enamel : Ectodermal dysplasia
Evaluation of growth
• Growth level: Every single measurement can be plotted on a growth curve which illustrates the
amount of growth in children within different age group.
• Growth velocity: Growth velocity can show the process of growth. Growth velocity is measured in
terms of how much a child grows within a specified period of time.
• Proportion
• Reliable and accurate data
• Single Value and series investigation
• reference
Evaluation of growth • mean standard deviation： cut-off point x ± 2SD • percentile：cut-off point
P3 --P97 • Z score Z score=( x - x )÷SD
Methods of assessment •Reference table •Growth curve

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Neuropsychological and Behavioural Development
Nervous system anatomically complete at birth,except: Myelination rapid for 2 years complete by 7
years
Primitive reflexes disappear in few months
Sensory and Perceptual capacities
Vision The infant is also able to elicit responses from the outside world through the
sensory capacity of sight.
Audition Audition is important because it relates language development. If a child has
hearing loss, the child will have impaired speech, language and learning and
behavioural problems stemming from difficulty in communication.
Taste and smell Newborns prefer sweet tastes over sour, bitter, and salty tastes. They can
distinguish odors right from birth and soon learn to know the smell of their
mother’s milk and bodies.
By late infancy, these senses are probably sharper than at any other time in the
entire life span. We recommend giving infants a wide variety of foods, not
because nutrition demands it, but because taste preferences develop so
rapidly that introduction of new foods becomes more problematic with each
passing year
Skin Sensory At birth, the dermal or touch system is the most mature of all the sensory
capacities. The skin sends a multitude of sensory messages to the brain. The
skin is the most extensive and basic of all sensory systems and contains
receptors for temperature, contact, and pain.
BEHAVIOR DEVELOPMENT
Four Attributes
 Gross motor
 Fine motor
 Language
 Personal—social skill
• Growth and Development Milestones Skills such as taking a first step, smiling for the first time, and
waving "bye bye" are called developmental milestones. Knowing the average age at which children
achieve certain neurodevelopmental milestones and encounter specific developmental tasks helps
to provide a conceptual framework for determining whether or not a child’s development is age-
appropriate. Developmental normality cannot be defined in absolute terms.
gross motor Physical skills involving large body movements such as lifting head, walking, and jumping.
4 ½ months (2-7months): rolls from back to side
7months (5-9 months): sits alone
7months (5-11months): crawls
8months (5-12 months): pulls to stand
Newborns usually can not lift their heads. When on their stomachs, their heads will turn to one
side. By 6 weeks of age he can lift his head and move it from side to side. By 3-4months of age, he
can, and hold his head upright when held sitting.
Rolling over: Rolling is defined as moving from supine to prone or from prone to supine position,
and it involves some aspect of axial rotation.
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Usually between 8 and 10 months after birth, most infants are crawling on “all four” , coordinating
the movement of their hands and knees in a smooth, balanced manner. Within a couple of
months, most infants also learn to climb up onto couches and chairs-as well as ledges, window
sills, and the like.
Walking shows a similar progression, from reflexive, hesitant newborn stepping to a smooth,
speedy, coordinated gait. On average, a child can walk while holding a hand at 9 months, can stand
alone momentarily at 10 months, and can walk well unassisted at 12 months.
A child who is 18 months subsequently learns to run, kick a ball, jump on two legs, hop on one leg,
go up and down stairs one leg at a time, and pedal a bicycle.
During infancy, great advances in physical abilities occur. Motor development proceeds in two
directions: (1) from the center of the body out to the arms, hands, and fingers (2) from the top of
the body downward.
Development in the outward direction is known as proximodistal ( “near” to “far” ) development;
this trend leads to ever-increasing skill in using the hands.
Development in the downward direction is known as cephalocaudal ( “head” to “tail”)
development; this trend eventually leads to using the legs to stand and walk.
Fine Motor Physical skills involving small body movements, especially with the hands and fingers, such as
picking up a coin and drawing
Newborn: Prereaching
3-4 months: reaching with ulnar grasp
4-5 months: transfer objects from hand to hand
9m0nths: pincer grasp
holds and grasps object 2-4months
5-6m (reach and grabs)
transfers object 6-8m
thumb-fingers grasps (pincer grasp) 8-12 月
Language Language is essential to our culture as it provides the symbolic code for communication and for
Development our thought process. Spoken language, that uniquely human achievement, emerges over the
course of the first few years of life.
Babies listen, attend to certain noises, show preference for certain tones, and soon begin to
produce the sounds of their native tongue.
Newborn reflexive communicationcries, movement, facial expression
3-6 months new sounds, including squeals, growls, croons, trills, vowel sounds.
6-10months Babbling, including both consonant and vowel sounds repeated in syllables.
10-12months Comprehension of simple words; simple intonations; specific vocalizations that have
meaning to those who know the infant well.
18months Vocabulary spurt – three or more words learned per week
If a child is suspected speech and/or language delay, you must have these key findings:
< 6m the absence of apparent response to sound
by 9-12m the absence of babbling
by 18 m the absence of any words
by 24 months the absence of meaningful phrases
at 3 years speech that is largely unintelligible to strangers an inability to use language
communicatively, and apparent difficulties with language comprehension.
Personal —Social Through rapid early maturation, the infant becomes more alert and utilizes his rapidly developing
Skill sensory systems to interact with both the animate and inanimate environment
In infancy, social development is mainly gauged by the infant’s ability to interact with his family.
Subsequently , he will need to acquire self-help skills and imitate adults behaviour patterns. He
also needs to learn to enjoy social interaction with other children
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Smile, Stranger wariness,

By 8 MONTHS:
•Searches for a hidden object •shows fear of falling from high places •imitates
sounds,actions,facial expressions •smiles at own reflection in the mirror •raises arms as a sign to
be held •recognizes family members’ names
By 12MONTHS:
•imitates adult actions •responds to their own name •offers toys to others •pushes away
unwanted objects
Developmental Surveillance
Periodic assessment of a child’s developmental progress with the aim of detecting pre-symptomatic
disability
• Longitudinal and multidimensional developmental monitoring.
• Over-reliance on isolated developmental scales and tests should be avoided
• Screening tests: Screening procedures should be brief, simple, cheap and reliable Screening tests
are by definition not diagnostic and, when abnormal, must be followed by a thorough diagnostic
evaluation
• Pediatric periodic health supervision
• Standardized developmental screening instruments
• Not diagnostic
• when abnormal, diagnostic evaluation should be done
• DDST children under 6 yrs • PPVT from 4 to 9yrs especially for children delayed in language
Denver Development Screening Test II (DDST) • Screening test – not a measurement of intelligence •
Used to - identify children whose development deviates significantly from that of other children
warranting further investigation to determine if there exists a problem requiring treatment. • Test
covers - four general functions: personal social (such as smiling), fine motor adaptive (such as
grasping and drawing), language (such as combining words), and gross motor (such as walking). •
Ages covered by the tests range from birth to six years
Diagnostic tests • When a developmental problem is suspected, a definitive diagnostic evaluation

should be undertaken to determine whether a delay is truly present and, if so, whether a specific
etiology can be identified with implication for prognosis, therapy, and subsequent offspring.
• A comprehensive developmental assessment should be obtained by trained personnel, using a

standardized age-appropriate instrument. • If a developmental problem is confirmed, it is important
to ascertain whether the delay is selective or global. For example, a problem primarily with language
may suggest a hearing problem, inadequate environmental stimulation, or autism.
• Gesell’s test from 4 weeks to 3yrs • Bayley from 2 to 30 months • WPPSI from 4 to 6.5yrs • WISC-R
from 6-to 16yrs
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What do we look for in developmental screening?
Normal growth pattern: Height, weight, head circumference
Achievement of developmental milestones (indicating neurological development)
Gross motor function
Fine motor function and vision
Hearing and speech
Social behaviour and play
Neonatology Introduction & Septicemia
Definition:
Newborn period: the first 4 weeks after birth (<28 days)
Newborn infants (neonates) : live infants within 28 days after birth
Classification of Newborns
1. Based on gestational age (GA):

A. Full term: Gestational age 37w≤GA＜42w
B. Preterm: Gestational age
C. Post-term: Gestational age GA＜37w GA≥ 42w
2. Based on birth weight (BW)]
A. Normal birth weight (NBW): 2500~4000g
B. Low birth weight (LBW): <2500g
C. Very low birth weight (VLBW): <1500g
D. Extremely low birth weight (ELBW): <1000g
E. Macrosomia: >4000g
3. Based on the relationship between GA and BW (GA+BW)
A. Appropriate for gestational age (AGA): BW: between 10th~90th percentile of average BW
of infants with same gestational age
B. Small for gestational age (SGA): BW: below the 10th percentile of average BW in infants
with same gestational age
C. Large for gestational age (LGA): BW: above the 90th percentile of average BW in infants
with same gestational age
4. Based on week age after birth
A. Early Newborn: The first week
B. Late Newborn: The 2nd to the 4th week

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5. High-risk infant
A. mothers a. society factors (age) b. abnormal pregnancy c. diseases
B. neonates a. preterm, post-term, LBW, SGA, LGA b. asphyxia, infection
03. Neonatal Septicaemia (Sepsis)

 Etiology
 Pathogens analysis
 Routes of infection
 Clinical manifestations
 Diagnosis
 Treatment
Introduction Sepsis: A serious systemic infection in neonates. One of the most common medical
problems during the neonatal period.
Pathogens>>> blood, grow, toxin>>>>> systemic infection
Etiology and Mechanism Routes of Infection Immune function

Pathogens 1. China Staphylococcus
2. North America, Europe Group B Streptococcus (GBS)
conditional bacteria: common
Routes of Three routes:
infection 1. Prepartum (antenatally) : A. mother’s infection (chorioamnionitis)
B. ruptured membrane
2. During labor (perinatally) : prolonged labor, etc. Pathogens: Gram-negative
bacterium
3. Postpartum (nosocomially): A. Skin infection, umbilical infection, respiratory
infection B. medical apparatus: catheterization,
stethoscope
Pathogens: both Gram-positive and Gram-negative bacterium
Skin problems: Omphalitis; Skin infection
Immune 1. Nonspecific immunities: A. skin, blood-brain barrier B. neutrophil,
function: phagocytes C. complement activities
immature 2. Specific immunities:
A. cell-mediated immunity: Deficiencies of neutrophil number and function.
Neutropenia ( (<2000/mm3) : premature infants
B. humoral immunity: 1. Antibody production ↓ 2. IgG, IgM, IgA: Low or none
Clinical Manifestations Categorized
1. early: 85% within 24 hours pathogens from the mother
2. late: after 7 days of birth from environment
Responses decrease: 1. Feeding 2. Crying 3. Movement 4. Temperature 5. Body weight 6.
Reaction
Systematic damages 1. Pathological jaundice: bilirubinemia 2. Bleeding 3.
aggravation (increase) Hepatosplenomegaly 4. Respiratory: tachypnea, apnea, 5.
Gastrointestinal: vomiting, diarrhea 6. CNS: seizure
Complications: 1. Meningitis 25% 2. Pneumonia 3. Liver abscess 4. Osteomyelitis
Diagnosis Laboratory tests: (specific test)
Cultures: blood A. Positive cultures: diagnosis can be confirmed B. Negative cultures: infection can
not be ruled out
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Laboratory tests: (nonspecific tests) 1. WBC: 20109 /L 2. C-reaction protein (CRP): ↑ in acute stage
3. Platelet < 100109 /L
Treatment The essentials of treatment:
1. antibiotic treatment: a. early initiation b. enough doze (highest dosage) c. whole therapeutic
course d. toward suspected bacteria (combination) e. injection through vein
Correct choice of antibiotics : A. Gram-positive : Staphylococci
B. Opportunistic bacteria  first-generation cephalosporin:
Cefradine  Vancomycin
C. Gram-negative bacteria : Escherichia coli  Third-generation
cephalosporin: Cefotaxime  Aminoglycoside: Gentamycin
The course of antibiotics treatment: 1) 10-14 days or 7days after culture (-) 2) 3-4 weeks for
meningitis
2. supportive therapy: 1. Monitoring the vital signs A. Maintenance of fluid and electrolytes
balance B. Oxygen support 2. Intravenous immune globulin (IVIG)
04. Neonatal Jaundice

Jaundice is quite common in newborns
Full term infants: at least 50%
Preterm infants: over 80%
When? In the first week of life
Where? Skin and sclera
What? Blood bilirubin concentrations is ≥5mg/dl.
The metabolic characteristics of bilirubin in newborns:
1. Bilirubin production 8.8mg/Kg/d in newborns 3.8mg/Kg/d in adults
2. Bilirubin-albumin complex formation a. preterm infants b. acidosis
3. Bilirubin metabolism in hepatocyte

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a. Hepatic uptake of bilirubin, Y, Z protein b. Bilirubin conjugation: UDPGT (uridine diphosphate

glucoronosyl transferase)
4. Enterohepatic circulation
Bilirubin toxicity
1. Conjugated bilirubin water-soluble
2. Unconjugated bilirubin
lipid-soluble bilirubin-encephalopathy (kernicterus)
Manifestations Evaluation of jaundice:

1. By eyes: face: 5mg/dl ( 85μmol/L ) abdomen: 10-15mg/dl limbs: 15-20mg/dl
2. By transcutaneous measurement : used for screening
3. By serum levels : standard
Classification:
Physiological jaundice Pathological Jaundice
1. Cause: relevant to bilirubin metabolism 1. Appears earlier (first 24 hours of life) Fades >2
2. Appears 2-3 days (>24h of age) weeks (term infants) >4 weeks (preterm infants)
peaks 4-5days 2. Accumulates >5mg/dl/d
fades <2 week (term infants) 3. Direct bilirubin >2mg/dl
<4 weeks (preterm infants) 4. Jaundice recurrence
3. Bilirubin accumulates <5mg/dl/d 5.Treatment: primary diseases
4. General condition is good Laboratory examination:
5. Treatment: early feeding, help pass meconium Pathological Jaundice ( peak value of bilirubin)
from the bowels 1. above 95th% of the Bhutani Guideline
Laboratory examination:
Physiological Jaundice ( peak Level of bilirubin)
1. Under 95th % of the Bhutani Guideline
2. reaching the Guidelines for Phototherapy
2. Under the Guidelines for Phototherapy
Bilirubin Encephalopathy & Kernicterus:

warning stage
convulsion stage
recovery stage
sequelae stage
Laboratory tests 1. Blood type incompatibility
2. Hyperbilirubinemia :
Unconjugated bilirubin level
3. Hemolytic tests
1) Hemoglobin level :
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2) Reticulocytes:
3) Nucleated RBC
Antibody test
1) Direct Coombs test (+) confirm
2) Antibody release test (+) confirm
3) Free antibody test (+) judge
Treatments 1) Phototherapy
Indications of phototherapy :
Unconjugated bilirubinemia
Bilirubin level >12mg/dl
Light source: Spectral outputs 425 to 475nm
Side effects of phototherapy :
a. fever
b. diarrhea
c. skin rash
d. bronze baby syndrome
(conjugated bilirubin>4mg/dl)
2) Exchange transfusion
a. Severe hemolytic disease
b. Refractory to phototherapy
Aims of transfusions:
a. Remove antibodies
b. Remove bilirubin
c. Correct anemia
Indication of transfusions:
one of the follows
a. 20mg/dl
b. >4mg/dl, Hb<120g/L
c. 0.7mg/dl/h
d. Bilirubin encephalopathy (Kernicterus)
Volume
150-180ml/kg (twice as much as the blood
volume of a newborn)
Method
Through peripheral blood vessels
Exchange transfusion>> Radial artery (out) >>>Dorsalis pedis vein (in)
3) Internal Medicine
Pharmacological agents: a. Albumin b. IVIG c. Probiotics
Preventions For ABO incompatibility: No
For Rh incompatibility
300 μg of human anti-D globulin
within 72 h of delivery
Hemolytic disease of newborn
- ABO: 85.3%
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the mother: type O
the infant: type A or B
- Rh : 14.6%
the mother: Rh (−)
the infant: Rh (+) D, E, C, d, e, c
- MN : 0.1%
ABO Rh
1.Jaundice mild 2-3 day Severe 24 h
2.Anemia mild (3-6 weeks) Severe
heart failure
3.Hepato-splenomegaly rare common
05. Hypoxic-Ischemic Encephalopathy (HIE)

Definition
Hypoxia: PaO2↓
HIE
Ischemia: Blood flow↓
Incidence: 3~9 per 1000 live births
1. Etiology Maternal Causes

1. Reduced maternal oxygen delivery Anemia Cardiovascular disease Hypotension/hypertension
2. Reduced uterine blood flow Abnormal uterine contractions
Placental Causes
1. Early placental separation
2. Placental dysfunction Prematurity，Postmaturity Placentitis Placental edema
Umbilical Causes
Reduced umbilical blood flow
Excessive length of umbilical cord
Short of umbilical cord
Knots of umbilical cord
Neonatal Causes
1. Preterm，Low birth weight，SGA，LGA
2. Diseases Asphxia，Septicemia Pulmonary diseases Congenital cardiovascular diseases
2.
Pathophysiology
3. Clinical Depending on HIE severity

manifestations
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4. Laboratory Auxiliary tests

tests Electroencephalogram (EEG)
1. Assess the severity of the injury
2. Evaluate for subclinical seizures
3. A suppressed seizure activity of EEG>>>> A poor prognosis
Cranial computed tomography scan
1、Cerebral edema
2、Hemorrhage
Potentially harmful radiation
CT: Cerebral edema
Brain MRI
1、Accurately demonstrate the injury pattern (edema) hyperintensity
2、Diagnosis and follow-up of infants with moderate-to-severe HIE
5. Treatment Therapeutic window
1. Clinic: No direct evidence
2. Studies: Animal models
3. When: 6h
Management aims at:
1. maintaining adequate perfusion
2. stopping the processes of ongoing injury
3. promoting recovery
Supportive treatment
1. Adequate ventilation:
50mmHg<PaO2<100mmHg
30mmHg<PaCO2<60mmHg
pH: 7.35~7.45
2. Adequate perfusion
Blood pressure: 70/50 mmHg
Echocardiography (ECHO)： cardiac output Fluids: 60~80 mL/kg .d Dopamine: 2.5～5μg/kg. min
3. Adequate glucose
Aim: Avoidance of hypoglycemia/hyperglycemia
Maintain the glucose: 40~90mg/dl
Maintain the normal electrolytes: K+, Na+, Cl
Specific treatment
Recovery treatment (rehabilitation)
To promote recovery In the recovery stage: rehabilitation training 3 month, 6 month, 12 month
Symptomatic treatment
1. Treatment of seizures: Drug: Phenobarbitone (first line treatment)
20 mg/kg, intravenously
repeate once as needed
daily dosing 5 mg/kg/day
(target level 40–
2. Treatment of intracranial pressure
Fluids: 60~80 mL/kg .d
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Furosemide ？
Mannitol
Current potential specific treatment: Hypothermia
Hypothermia is used for the following:
≥ 35 weeks gestational age
≥ 1800g
moderate to severe encephalopathy
intrapartum hypoxia indicated as following: (1) Apgar score ≤ 5 at 10 minutes (2) blood gas with pH ≤ 7.00
Optimal timing of initiation
Within 6 hours, the earlier the better Temperature
3~4℃ below baseline temperature, 33.0~34.0℃ Optimal duration
72h, the more serious, the longer Methods
Selective head / whole body cooling
6. Prognosis Death: 15~20% in neonatal period
Neurodevelopmental abnormalities: 25~30% survivors
06. Paediatric Anemias

OUTLINE
1 Hemopoietic characteristics of normal children
Hematopoiesis: 1. In fetus 2. After birth
1. Fetal Hematopoiesis 2.Hematopoiesis after birth

Occurs in three anatomic stages: – Medullary hematopoiesis
– Mesoblastic Hematopoiesis – Extramedullary hematopoiesis
– Liver/Spleen Hematopoiesis Postnatal Hematopoiesis
– Medullary Hematopoiesis Medullary hematopoiesis
A red marrow (activity hematopoiesis)
B yellow marrow (fatty tissue)
<5y: full of red marrow
5-7y:more red marrow
SITES TIME CELL less yellow marrow
>18y and adult: less red marrow
Mesoblastic Yolk 0-14th day 3- Erythroid
more yellow marrow
hematopoisis Sac 4wk:primitive blasts
Extra-Medullary Hematopoiesis
10-12wk:ceased
Cause: Acute hemolysis Leukemia Trauma acute
Hepatic Liver 6-8wk:appear 12- Erythroid
hemorrhage
hematopoiesis Spleen 16wk:active
Signs: Hepatosplenomegaly, Enlargement of the
6mo:diminish/ stop
liver,spleen,lymph nodes, Erthrocytoblast and blast cell
at birth
in peripheral blood, Reversible if the cause removed
Medullary Bone 4mo:start Erythroid
hematopoiesis marrow 6mo:increase/steady Neutrophils
after birth: major Macrophages
Normal characteristics of peripheral blood cells
A. Red blood cell:
– Birth :RBCs ：5.0-7.0× 1012/L，Hb ：150-220g/L
– Physiological hemolysis（1w after birth）：Hb/RBC decrease
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– Physiological anemia（2-3m after birth）： RBC 3.0 × 1012/L Hb 100g/L

– Etiology ：（1）EPO decrease （2）Physiological hemolysis （3）Red blood cell diluted
3m after birth RBC、Hb recovery
12y equate to adults
• Reticulocyte 3d：0.04-0.06 × 1012/L 7d：0.005-0.015 × 1012/L 1m：0.02-0.08 × 1012/L 5m：
0.01-0.015 × 1012/L
Hemoglobin types • Hb=Hemo（Protoporphyrin+ Fe）+ globin （two pairs of polypeptid)
Polypeptide Chains Dysfuction OR Iron deficiency Anemia
• Types of polypeptid: • polypeptid ：α、 ζ β、γ、δ、ε
• Types of hemoglobin: • Fetus Hb： Gower1: ζ2 2
Gower2: α2 2
Potland：ζ2 γ2
HbF ：α2 γ2
HbA ：α2 β2 （98%）
HbA2：α2 δ2 （<3%）
B. White blood cell
C. platelet
D. Blood volum
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2 Definition and criteria of pediatric anemia
Definition : Anemia is an absolute decrease in hematocrit , hemoglobin concentration, or the

RBC count. Anemia is not a diagnosis, but a sign of underlying disease.
Criteria of anemia
Age Hb concentration
< 28 days < 145 g/L
1～4 months < 90 g/L
4～6 months < 100g/L
6 months～6 years < 110g/L
6～14 years < 120g/L
Many factors affect baseline Hgb levels
Age
Gender
Race
Pregnant
Altitude
Heredity
Degree of anemia
Newborn Children
Minor 120-145 90-110
Intermedia 90-120 60-90
Severe 60-90 30-60
Very severe <60 <30
3 Classify anemia based on RBC size and mechanism
Classification
1） Morphology of RBC
2）Mechanism： lost blood , hemolysis nutritional deficiency
Morphological classification
mean corpuscular volume(MCV), means corpuscular hemoglobin (MCH), mean corpuscular

hemoglobin concentration(MCHC)
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Anemia classification by RBC size
Microcytic Normocytic Macrocytic

• Iron deficiency • Anemia of inflammation • DBA
• Thalassemia • Acute blood loss • Fanconi Anemia
• Anemia of inflammation • TEC • Other BMF
• Lead poisoning • Hereditary Spherocytosis • Down’s
• Other unstable • DBA • Hypothyroid
hemoglobinopathy • AIHA • B12/Folate Deficiency
• Sickle cell anemia
• G6PD def. /Enzymopathies
• Statistical
Mechamism of Anemia
A. Decreased RBC
Production • Nutritional Iron Deficiency
• Megaloblastic Anemia
• Aplastic anemia、leukemia
• Infection、 Chronic nephritis
• Cancer cells infiltration bone marrow
B. Increased RBC 1. Intrinsic Cause :
Destruction 1). RBC membrane: hereditary spherocytosis
2). RBC enzyme deficiency: Glycolysis pyruvate kinase

Glucose-6-phosphate
dehydrogenase deficiency (G6PD)
3). Dysfunction of globin synthesis: Thalassemia
Sickle cell anemia
2. Extrinsic Cause :
1)Immune: ABO incompatible hemolytic disease
Autoimmune hemolytic anemia
2) Non-immune: Medicine, Toxic,
Chemotherapy, Physicality
C. Increased RBC Loss • Acute： trauma, fracture, spleen rupture
• Chronic ： Hookworm infection
Idiopathic pulmonary hemosiderosis
Functional uterine bleeding
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Digestive tract tumor

Aplastic anemia
•bone marrow hypocellularity
•peripheral pancytopenia
•absence of abnormal infiltration
•no increase in reticulin
Disfunction of globin synthesis-----Thalassemia
• β-thalassemia
– >1% in Mediterranean basin, northern
Africa, SE Asia, India, Indonesia
– >20% in some villages in Greece
– Rare in No. Europe, Korea, Japan, and No. China
β-thalassemia: Phenotypic variability Common β-globin mutations • Mutations affecting both

the β-globin gene and its regulators / promoters • Cause anywhere from 0% production to
99.9% of normal production – β 0 = 0% production – β+ = 1-99% production
• α-Thalassemia
– Most common single gene disorder in the

world?
– Frequency: 5-10% in Mediterranean basin
– 20-30% in West Africa
– 68% in SW Pacific
– <1% in Britain, Iceland, and Japan
• Mutations affecting α-globin gene
– Differ from β-thalassemia
– Tend to be whole gene deletions
Thalassemia – Clinical Picture
• Presentation
– Family History
– NB screen
• Bart’s (2 or 3 gene α deletion)
• Hgb F only (β thal major)

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– Microcytic anemia, target cells, ↑ RBC
– Elevated Hgb A2
– Extramedullary hematopoiesis
– bony expansions
– skeletal changes, Cooley’s face
– poor growth
– infection
Classification of anemia by mechanism
4 Understand the presentation, diagnosis, and treatment of anemia
Symptoms of anemia
• Asymptomatic: particularly if the anemia develops over a long time.
• General manifestation: pallor of the skin and mucous membranes, lethargy, malnutrition,
growth retardation
• Liver, spleen and lymph nodes enlarged
• Digestion system: anorexia, nausea and constipation
• Cardiovascular and respiratory system: tachycardias, increased artery pressure, wheeze and
increased pulse. Severe anemia may cause heart expansion and congestive cardiac failure.
• Nervous system: vertigo, tinnitus, irritability, and disorders of attention.
Diagnosis of anemia
• Most anemias can be diagnosed with history, physical exam, and minimal laboratory testing
• History: fatigue, pallor, jaundice, poor diet/feeding blood loss
• PE: pallor, jaundice, tachycardia, heart murmur, splenomegaly, congenital anomalies

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• Labs: – CBC, retic, peripheral blood smear
• Norms specified by individual labs may be inaccurate
• Sampling (cap vs. venous)
– Bone marrow biopsy
Treatment
• Elimination cause
• General
• Medicine
• Transfusion blood
• Transplantations : BMT , HSCT
• Other
5 Nutritional iron deficiency anemia
Nutritional iron deficiency anemia
• Definition
• Anemia associated with either Inadequate absorption or Excessive Loss of Iron. • The most
common cause of anemia in Children. • It’s most common cause by Microcytic Hypochromic
Anemia. • It is Chronic Anemia.
• Iron content and distribution
• Iron content and distribution: 2/3 of the iron is present in HB and 1/3 in tissue and transport
form.
Content of elemental iron (mg/kg)

Adult females 40
Adult males 50
Newborn 75
DAILY REQUIREMENT
Adult male : 17mg/d
Adult female : 21 mg/d
Pregnant female : 35 mg/d
Lactating female : 21 mg/d
Children : 1mg/kg/day
• Iron metabolism
- The fetus absorbs iron from the mother across the placenta.
- Term infants have adequate reserves for the first 4 months of life.
- Preterm infants have limited iron stores and because of their higher rate of growth, they
outstrip their reserves by 8 weeks of age.
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- At birth, because of “physiological haemolysis”, much iron is released to plasma and

little iron is absorbed from food
- During the second stage (about 2 months old), hematopoiesis is increased and more iron
is absorbed from food, so iron deficiency is rare in this stage.
- After 4months, development increase, iron in food is deficient and iron stores exhaust,
so most iron deficiency anemia occurs in 6 months to 2 years or 3 years old child.
• Causes of IDA in children
• Premature birth
• Growth and development quickly
• Malabsorption chronic diarrhea
• Nutritional – Excessive Cow’s Milk Intake
• Chronic low grade hemorrhagic enteropathy
• Low iron content
• Prevention of eating iron-rich foods –

Vegan/Poor Meat Intake
• Blood Loss – Menorrhagia – GI (celiac, IBD) –

Parasite/Worm (#1 cause of GI blood loss
worldwide)
Iron transfer
 Transferrin, Tf：
Iron vehicles ,produced by liver，WT 80Kd ，1 Tf binding 2 Fe+++ (Ferric iron)
 Serum Iron, SI：
Fe++ （Ferrous iron） -- ---
 Ferritin
Fe++ （Ferrous iron） + Apo-ferritin ---
 Unsaturated Iron Binding Capacity, UIBC：
Transferrin still can binding Fe+++ capacity
 Total Iron Binding Capacity, TIBC= SI + UIBC

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TIBC indicates the maximum amount of iron necessary to saturate all available transferrin
ironbinding sites.
transferrin saturation, TS = （SI / TIBC）
Different stage of iron deficiency
1. Iron Deficiency , ID
Storage Iron Ferritin
2. Iron Deficiency Erythropoiesis , IDE
SI 、TIBC TS
Percent sideroblasts 、FEP
3. Iron Deficiency Anemia, IDA
Hb MCV 、MCH、MCHC
• Clinical manifestation and diagnosis
• Main signs may be pallor of the skin and mucous membranes.
• Severe anemia may cause congestive cardiac failure.
• IDA in infancy and early childhood is associated with developmental delay and poor growth.
laboratory test: 1. Blood smear • Microcytosis & Hypochromia anemia • Reticulocyte is normal
or slightly decreases • WBC and platelets are normal
2. Bone marrow smear
3. Iron metabolism
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• Treatment and Prognosis
Treatment • Decrease milk intake: 16-24 oz/day • Promote iron rich foods (mg) •
Control/evaluate for blood loss • If stable, no transfusions necessary • Ferrous Sulfate 4-6 mg/kg
elemental Fe per day (divided once or BID) – MVI with iron is inadequate – Take with juice, meat
to enhance absorption (NOT MILK!) – Constipation, metallic taste, teeth staining • IV iron if
malabsorption suspected – Anaphylaxis, hypotension
6 Nutritional megaloblastic anemia
• Definition Megaloblast –abnormally large cells of Erythroid series

Caused by defective DNA synthesis due to deficiency of Vit B12 & Folic acid
• Vit B12 & Folic acid metabolism Vit B 12 Daily need – 1-2 μg Sources – Milk, Meat, Liver of Animals. Also synthesized by
bacterial Flora
Folic Acid Daily requirement –100 μg. Sources – leafy veg, pulses, yeasts, liver. From
breakdown of Polyglutamate to Monoglutamates.
• Causes of MA in children • Premature birth
• Growth and development quickly
• Malabsorption: chronic diarrhea, Medicine, small intestinal resection
• Nutritional
–Goat Milk Intake
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• Chronic low grade hemorrhagic enteropathy

• Low Vit B12 content
• Prevention of eating folate-rich foods
– Poor Meat Intake
• Excessive Consuming
– Infection
– Antibiotics
• Clinical manifestation and General features of Anemia:
diagnosis Pallor, Weakness, Lethargy,
Breathlessness on exertion
Palpitations heart failure pedal edema
Special features :
Angular cheilitis, Atrophic glossitis,
Oesophageal atrophy , Dysphagia, tremble
Koilonychia, brittle nails, gastric atrophy.
Lab finding: Blood smear :Hb Decreased

Megaloblastic Red cell– MCV,MCH& MCHC Increase
VB12: ＜100ng／L
Folic acid：＜3ug/L
LDH : serum lactic dehydrogenase(LDH) is increase
Diagnosis • History • Clinical manifestation • Blood smear • Bone marrow • Vitamine
B12 / folic acid level measure
• Treatment and Prognosis Treatment 1. A healthy diet should be encouraged 2. Dietary teaching sessions should be
individualized 3. Remove etiology 4. Replacement therapy vit B12 folic acid
IDA Megaloblastic anemia
age 6m-2y 6m-2y

Cause iron ↓ VtB12/folic acid↓
Clinical pallor puffiness
manifestation
extramedullary ↑ ↑
Nervous system slight striking
Blood smear micro-hypochromia macrocytosis
Bone marrow cytoplasm falls behind nucleus Megaloblastic changes
Iron metabolism abnormal N
VtB12/ folic acid N ↓abnormal
07. Congenital heart disease

Definition of congenital heart disease
• Also named as congenital heart defects, is a heart abnormality present at birth, even it might
be discovered much later, that occur as the baby's heart is developing during pregnancy.
• The most common type of birth defect

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• Some defects require no treatment, but some require treatment soon after birth.
• With the diagnosis and treatment of CHD improved, more babies are surviving and now many
adults are living with congenital heart defects.
Lymphocinesia
Circulatory system
Blood circulation
Pump: heart
Artery
Vein
Capillary
Basic Concepts
The heart is the first organ to form and functions to support the rapidly growing embryo before
it establishes the shape of a four-Chambered organ.
Fetal Circulation
One pathway: ovale foramen
Two Ducts: arterial duct (ductus arteriosus)
venous duct
Three vessels: umbilical artery
umbilical vein
Changes at birth: • Decrease of the pulmonary vascular resistance as a result of expansion of the
lungs
• Closure of the Foramen Ovale
• Closure of the Ductus Arteriosus
The Closing Time of Fetal Pathway
Functional close Anatomical close

Quctus Arteriosus (DA) After birth Less than 1Y
Ovale Foramen (OF) After birth 5-7 M
Epidemiological Features
 7~8/1000 living neonates

 150,000 new cases in China per year
 20-30% die just after labour
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 1 from 2005, CHD became the first in birth defects in China (Chinese Birth Defect
Monitoring Center, CBDMC)
Etiology
 Multiple factors play synthetic roles in the early pregnancy. Only about 10% could be
detected now, including genetics and circumstance Factors.
- Genetics: 8%
Chromosomal disorders: 5% DiGeorge Syndrome
Down Syndrome
Turner Syndrome
Single-gene disorders: 3% Marfan Syndrome

Noonan Syndrome
- Circumstance Factors:
 2% Smoking during pregnancy
 Taking some medicines-such as angiotensin-converting enzyme (ACE)
inhibitors for high blood pressure and retinoic acids for acne treatment-
in the first trimester
 Diabetes before pregnancy or in the first trimester
 Phenylketonuria
 Rubella virus Infection during pregnancy (PDA)
DiGeorge Syndrome: The deletion occurs near the middle of the chromosome at a
location designated q11. Characteristic signs and symptoms may include congenital
heart disease, defect the palate, mild differences in facial features, hypoplastic thymus
and recurrent infection.
Down Syndrome (Trisomy 21 syndrome): A chromosomal disorder caused by the

presence of all or part of an extra 21st chromosome.
Physical features includes
• congenital heart defects.
• Flattened face
• Short neck
• Protruding tongue (microgenia) Upward slanting eye lids (palpebral fissures)
• Poor muscle tone
• Broad, short hands with a single crease in the palm
• Relatively short fingers and small hands and feet
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• Intellectual disabilities
Turner Syndrome: All or part of one of the sex chromosomes is absent.
Marfan Syndrome: Fibrillin ( FBN1 ) mutation affects the body's connective tissue
Skeleton system: typically very tall, slender, and loose jointed slender tapering fingers
Eye: dislocation of one or both lenses, 50%
Cardiovascular system: faulty connective tissue in the aorta wall (dissecting aortic
aneurysm, bicuspid or tricuspid insufficiency)
Noonan Syndrome: Noonan syndrome is a developmental disorder characterized by

unusual facial characteristics, short stature, heart defects (pulmonary stenosis, septal
defects).
CHD
Yes shunt No shunt (noncyanotic)
direction
Left to Right to
right left shunt
shunt (cyanotic)
( potential
cyanotic)
History Clinical manifestation:

Physical retardation
Repeat respiratory infection
Decreased Activity Tolerance
Cynosis
More blood in pulmonary circulation
Less blood in systemic circulation
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Physical Inspiration: • Precordial bulge Other abnormalities

examination Palpation: • Thrill Peripheral pulses
Auscultation: Different Grades of murmur
Laboratory
findings
ECG Enlarged atrium or ventricle

Conduction block
Ectopic rhythm
X-Ray Position: postero-anterior view
left-anterior oblique view
Right-anterior oblique view
Observation: Pulmonary field
Heart shape
Cavity volume
UCG Classification: M type
two dimensional
Doppler
Most valuable diagnostic non-invasive Examination
Treatments Internal therapy: prevent complications
Surgical treatments: Intervention
ASD, VSD, PDA, PS
Surgery
Cyanotic CHD
Atrial Septal Defects (ASD)
Definition • Defined as opening in the atrial spectum permitting shunting between two atria.
• More frequent in females than males by about 2:1
Classification  Secondary ostium defect is the most common type, accounting for 50-70%.
 Primary ostium defect occurs in 30% of cases. 15%: Part of complete endocardial cushion defect; 15%:
Isolated (partial endocardial cushion defect)
 Sinus venous defect is about 10%. Most located at the entry of SVC, some located at the entry of IVc. Often
associated with anomalous pulmonary venous connection.
Anatomy
Hemodynamic RA↑→RV↑→PA↑→Pulmonary circulation↑

Features ↑
ASD
↑
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LA↑→LV↓→AO↓
EISENMENGER SYNDROME (RIGHT TO LEFT SHUNT)

RA→RV↓→PA↓→Pulmonary circulation
↓
ASD
↓
LA↑→LV↑→AO↑
Clinical  Usually asymptomatic
manifestation  Poor growth, fatigue, dyspnea, and recurrent pulmonary infection in patients with large shunt
 Spontaneous closure to some very small defect
 Sometimes transient cyanosis while crying or pneumonia
 Eisenmenger syndrome, heart failure occurs after 30-40 y/r
Physical Typical Murmur: II~ I SM: 2nd left intercostal space
examination This murmur is not caused by the shunt, because the pressure gradient is small. It originates from the
pulmonary valvular stenosis because of the increased flow.
Mid-diastolic murmur: at the lower left sternal border because of relative tricuspid stenosis.
Wide and fixed split of S2 ( a split of S2 can be detected in normal people)
Common Pneumonia
complication Congestive heart failure
Cerebrovascular accident due to paradoxical embolization through ASD
Test X-Ray Pulmonary congestion
Cardiomegaly
Prominent PA
Enlarged RA and RV
ECG Right axis deviation
Incomplete RBBB: V1 rSR; QRS<0.12sec
RV hypertrophy
Echo Show the location and size of the ASD, the flow of the shunt.
Measure the increased dimensios of RA and RV
catheterization Pressure: RV; PA
Oxygen saturation: vena cava, RA, RV, PA
Angiography Anomalous pathway- interatrial
Treatments Surgery: 3 to 5 /Y
Intervention is recommended as the first choice in many cases: needs: the site of defect; the margin of the
defect
Ventricular Septal Defect (VSD)
Definition  Defined as the opening in the ventricular septum permitting shunting between two ventricles
 Most common CHD Phathological classification
Pathological The ventricular septum is divided into : a small membranous portion
classification a large muscular portion
 the inlet septum
 the trabecular septum
 the outlet septum
Membranous defect: most common (70%)
Outlet defect: about 13 to 15%
Large Moderate Small
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Area/body surface area >1.0 0.5 to 1.0 <0.5

(cm2/m2)
Area/aortic roof area 0.5 to 1.0 0.25 to 0.5 <0.25
(cm2/cm2)
Hemodynamic RA→RV↑→PA↑→Pulmonary circulation↑
features ↑
VSD ↑ LA↑→LV↑→AO↓
Pulmonary circulation reaction
1. vascular constriction
2. 2. Vascular wall remodelling
Eisenmenger Syndrome
It is so-called pulmonary vascular obstructive disease, because of the right-to-left shunt, persistent
cyanosis appears clinically. Vascular remodeling become irreversible. No regular treatments are
effective.
RA→RV↓→PA↓→Pulmonary circulation
↓
VSD
↓
LA↑→LV↑→AO↑
Clinical - The blood into pulmonary circulation is increased.
Manifestations - The blood into systemic circulation is decreased.
- Cardiac murmur
- small: asymptomatic, Roger disease
- moderate to large: delayed growth and development sweaty, decreased exercise tolerance, tachypnea
repeated pneumonia, congestive heart failure
- Spontaneous closure occurs in about 20% cases most often within 2 y/r
- A few cases have aortic insufficiency
- Infectious endocarditis: a main complication
- Large VSDS suffer from Eisenmenger Syndrome in earlier stage
Physical Enlarged cardiac border
Examination Increased P2 intensity
Grade 3-6 SM is audible at 3-4 left sternal border Systolic thrill
A diastolic murmur at the apex due to relative mitral stenosis
Common • Pneumonia
complications • congestive heart failure
• Infectious endocarditis
Test X-Ray Pulmonary congestion
cardiomegaly
Prominent pulmonary marking
Enlarged LV Rv
Enlarged LA
Almost normal heart size
Enlarged RV
Prominent pulmonary artery segment
Right inferior pulmonary artery dilated
ECG Small: LV hypertrophy
Large: biventricular hypertrophy
Depressed ST-T
Echo Provide accurate diagnosis of the location and size of the VSD, the flow of the shunt.
Measure atrial and ventricular diameters.
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Catheterization Pressure: RV, PA

Angiography Anomalous pathway intercentricular
Treatments Medical therapy for complications:
CHF : digoxin diuretics vasodilators
No exercise restriction is required in absence of PH
Antibiotic prophylaxis to IE
To close the VSD, according to the age, symptoms, complications and pulmonary artery pressure:
Surgical repair
Interventional catheterizatic
If Eisenmenger's syndrome is present, the only remedy is heart-lung transplantation.
Patent Ductus Arteriosus
Anatomy • Ductus Arteriosus is a normal pathway during the fetal circulation.

• After delivery, the functional closure will happen at once.
• Anatomical closure will occur in one year in 95% infants. • If DA remains open, we call it PDA.
Hemodynamic RA→ RV →PA↑→Pulmonary circulation↑
features ↑
PDA
↑
LA↑→LV↑→AO↓
With development of PAH: left to right shunt; no shunt silent duct; right to left shunt
When Eisenmenger Syndrome…
When cyanosis…
Differential cyanosis: the appearance of cyanosis in both lower extremities with a pink right upper
extremity
Clinical The magnitude of the left to right shunt is determined by the size of the ductus, and the differences in
Manifestations systemic and pulmonary vascular resistance.
Symptoms is similar to VSD.
Asymptomatic when the ductus is small.
Physical examination Enlarged cardiac order
Thrill
Machinery (continuous) murmur in the left infraclavicular area
Mid-diastolic murmur at the apex because of relative mitral stenosis with the large shunt
Bounding peripheral pulses with wide pulse pressure as the result of runoff of blood into the pulmonary
circulation during diastole.
Common •Pneumonia
complications • Congestive heart failure
• Infectious endocarditis
(The same as VSD)
Test Xray • Pulmonary congestion (increased pulmonary vascular markings)
• Prominent PA segment
• Enlarged LA and LV
Severe PH
Eisenmenger syndrome (marked prominence of the MPA and hilar vessels)
ECG Earlier stage: LV hypertrophy
Late stage: Biventricular or RV hypertrophy
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Echo Show the location and size of the PDA, the flow of the shunt.
Measure the increased dimensions of LA, LV & Aorta
Estimate the pressure of PA
Catheterization Pressure: RV, PA
Angiography Anomalous pathway intercentricular
Treatments Medical:
Complication treatments
Drug closure: indomethacin for premature neonates
Surgical, according to..
Tetralogy of Fallot
Definition • The most common cyanotic CHD， accounting for 12-14％ of all CHD
• The association of four cardiac abnormalities： VSD, PS, overriding aorta and RVH
Hemodynamic RA→RV→PA↓→Pulmonary Circulation↓
features ↓
VSD
↓
LA→LV→AO↑
Hemodynamic Features:
• With restrictive VSD, systolic pressures in RV and LV are identical.
• With the severity of pulmonary stenosis, the cyanosis becomes more prominent. Severe TOF is similar
to pulmonary atresia.
• The change of resistance of systemic circulation is the common reason of the shunt change, for
pulmonary circulation, the resistance is stable.
Clinical manifestations Hypoxemia
It is the basic of all manifestations.
Direct consequences
Compensatory consequences
Complications
Direct consequences
Cyanosis
Increased respiration
Growth retardation
Direct consequences
"Tet speil (also called 'hypoxic spel')
• characterized by paroxysm of hyperpnea, marked increased cyanosis, then syncope, convulsion, and
even death.
• Mechanism: increased resistance to blood flow to the lungs and the increased right to left shunt;
• hypoxia to increase pulmonary resistance;
• vicious circle
Common Causes: Crying, Defecation, Feeding, Awakening from naps, Fevers, Dehydration
Squatting: a special posture which can temporarily increase the resistance of systemic circulation to
gain more saturated oxygen.
Polycythemia
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bone marrow stimulated thrombosis Sharp increase in the viscosity of blood

Clubbing of the nails:
soft tissue under the nail grows fast
cerebral abscess: thrombosis
other complications: infectious endocarditis
Physical examination: A long loud ejection-type SM with 3-5 grade is heard at left upper sternal borders
P2 decreased or disappeared
The more severe the pulmonary stenosis, the shorter and softer the murmur prensents.
Tests X-Ray  Normal heart size
 Decreased pulmonary vascular marking (black lung)
 A concave PA segment
 Boot-shaped heart
ECG Right axis deviation
RVH
Echo Show almost all abnormalities, including VSD, PS, overriding aorta and RVH
Treatments Medical:
General treatment to prevent complications:
• Prevent dehydration
• Deal with infection timely to prevent IE and cerebral abscess
Emergency treatment of hypoxic spell :
• Oxygen
• In a knee-chest position
• Morphine, 0.1-0.2mg/kg IM, suppressing the respiratory center and abolishing to hyperpnea
• Beta-blocker (propranolol), reducing heart rate and subpulmonary muscular obstruction
• Sodium bicarbonate, IV for acidosis
Surgical: Palliative procedures: To increase pulmonary blood flow in patients with severe cyanosis and
hypoplastic PA
Complete repair surgery
Pulmonary Stenosis（PS）
Classification of PS
Pulmonary valve stenosis is the most common type.

Pathophysiology • Pulmonary stenosis increases resistance to flow from the right ventricle.
• To maintain blood flow to the lungs, the right ventricle must pump harder to generate higher
pressures.
• So RVH, then right heart failure.
• When severe PS, the increased pressure of RA may result in a right to left shunting through the
foramen ovale and cyanosis.
Clinical Manifestations - Usually asymptomatic with mild and moderate PS Symptoms become more common with
increasing age in patients with moderate to severe PS
- Exertional dyspnea, easy fatigability, chest pain, syncope and occasionally right heart failure with
severe PS
- Neonates with critical PS are cyanotic and tachypneic.
Physical examination Typical Murmur
IIV systolic ejection murmur at 2nd left intercostal space with or without systolic thrill
• S2 may split widely, and P2 may be diminished in intensity.
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• An ejection click may caused by valvular PS.

• The louder and longer the murmur, the more severe is the stenosis
Test X-Ray  Normal heart size
 Prominent PA (poststenotic dilation)
 Decreased pulmonary vascular markings
ECG Normal in mild PS
Right axis deviation and RV hypertrophy in moderate PS
Echo Two-dimensional echo show thick pulmonary valves with restricted systolic motion.
Doppler can estimate the pressure gradient across the stenosis.
catheterization Identify the position of PS
Measure the pressure gradient
Angiography Show valvular PS and post stenotic dilation.
08. Bronchial Asthma

Outline
 Introduction
 Definition
 Etiology, Pathogenesis and Pathology
 Clinical manifestation
 Laboratory tests
 Diagnosis
 Differential diagnosis
 Assess, Treat and Monitor Asthma
Introduction  Asthma is a major cause of chronic morbidity and mortality throughout the world.
 There is evidence that its prevalence has increased considerably over the past 20 years, especially in
children.
 Health care expenditure is very high, total estimated cost of asthma was $ 6.2 billion/year in the world.
Definition Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation.
It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness
and cough that vary over time and in intensity, together with variable expiratory airflow limitation.
Key points:
 A heterogeneous disease
 Chronic airway inflammation
 airway allergic inflammation
 Inflammation≠Infection
 Many cells and cellular elements play a role
 eosinophil, mast cell, T cell (Th2), B cell, basophil, neutrophil
 resident cells: epithelial cells, fibroblasts
 This inflammation is associated with increase airway hyperresponsiveness that leads to recurrent
episodes of wheezing, ,shortness of breath, chest tightness, and coughing, particularly at night or in
the early morning .
 These episodes are usually associated with widespread but variable airflow obstruction that is often
reversible either spontaneously or with treatment.
Etiology, Etiology
Pathogenesis and • Genetic factors an inheritable disorder
Pathology
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• Atopy: the production of abnormal amounts of IgE antibodies in response to common

environmental allergens, is the strongest identifiable predisposing factor for developing asthma.
• Airway hyperresponsiveness: the tendency of the airways to narrow too much and too easily in
response to various stimuli
 Environmental factors (triggers)
- Allergens:
- Air Pollutants
- Respiratory infections
- Exercise
- Weather changes:
- Food, additives, drugs
- Other:
Pathogenesis: Cells and Mediators
Pathology of Asthma
Inflammation of the airway wall
 Eosinophils, mast cells, T lymphocytes
 Patchy necrosis of epithelium
 Sub-mucosal glandular hyperplasia
 Hypertrophy of bronchial smooth muscle
 Mucous plug
Clinical Symptoms
manifestation  Recurrent wheezing: musical, high-pitched, whistling sound
 Coughing: worse particularly at night, chronic and recurrent cough may be the only symptoms in
children
 Chest tightness
 Dyspnea
Physical findings
 Varying with the absence or presence of an acute episode and its severity.
 During acute episode: dyspnea, three depressions sign, prolongation of the expiratory phase,
expiratory wheezing, coarse crackles, emphysema, “silent chest”
 Other sign: allergic rhinitis, eczema, etc
Laboratory tests Chest radiography
 Typical findings: hyperinflation, increased bronchial markings
 Helpful in the differential diagnosis: parenchymal disease, atelectasis, pneumonia, congenital
anomaly, foreign body aspiration
Measurement of allergic status
 Elevated serum specific IgE
 Skin prick test: positivity to common antigens
 Eosinophil count
Pulmonary function test
 ≥5 years old: Spirometry FEV1>80%
Peak expiratory flow (PEF)
PEF variation= highest PEF- Lowest PEF ×100% 1/2 (highest PEF+ Lowest PEF)
 <5 years old: Impulse oscillometry system (IOS)
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Measurement of airway responsiveness

 Methacholine challenge test:
Other laboratory tests: FENO, induced sputum
Diagnosis  Is it Asthma?
- Recurrent episodes of wheezing
- Troublesome cough at night
- Cough or wheeze after exercise
- Cough, wheeze or chest tightness after exposure to airborne allergens or pollutants
- Colds “go to the chest” or take more than 10 days to clear
 History and symptoms: atopy, age, triggers, family history
 Symptoms:
 Coughing, wheezing, shortness of breath, chest tightness
 recurrent, episodic often occur at night or in the early morning , reversible either spontaneously or
with treatment
 Physical examination:
 Diffusing, expiratory wheezing
 Prolonged expiration
 Measurements of pulmonary function
 PEF and FEV1 is lower than predicted
 >13% PEF variability (AM:PM)
 >20% decrease in FEV1 after 6 minutes of exercise or inhalation of specific agents
 >12% increase in FEV1 15 minutes after inhalation of a short acting 2 agonist
 Measurement of airway responsiveness
 Measurements of allergic status to identify risk factors
 Other laboratory examination:
 Blood tests: EOS
 Arterial blood gas analysis
 FENO
 Sputum studies
 Chest X-ray
 Exclude other causes of wheezing
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Differential  Respiratory disorders

diagnosis  Viral infection: RSV, RN, bronchiolitis
 Congenital abnormality: Congenital laryngeal stridor, tracheomalacia, bronchopulmonary dysplasia
 Foreign body in airways
 Tracheobronchial tuberculosis
 Cardiac asthma: congenital heart disease
 GI disorders: gastroesophageal reflux
Ascess, Treat and Assessment of asthma

Monitor Asthma 1. Asthma control - two domains
 Assess symptom control over the last 4 weeks
 Assess risk factors for poor outcomes, including low lung function
2. Treatment issues
 Check inhaler technique and adherence
 Ask about side-effects
 Does the patient have a written asthma action plan?
 What are the patient’s attitudes and goals for their asthma?
3. Comorbidities
 Think of rhinosinusitis, GERD, obesity, obstructive sleep apnea, depression, anxiety
 These may contribute to symptoms and poor quality of life
Goals of Long-term Management
 Symptom control: to achieve good control of symptoms and maintain normal activity levels
 Risk reduction: to minimize future risk of exacerbations, fixed airflow limitation and medication
side-effects
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 Achieving these goals requires a partnership between patient and their health care providers
o Ask the patient about their own goals regarding their asthma
o Good communication strategies are essential
o Consider the health care system, medication availability, cultural and personal preferences
and health literacy
Global Strategy for Asthma Management and Prevention Clinical Control of Asthma
The focus on asthma control is important because:
the attainment of control correlates with a better quality of life, and
reduction in health care use
Determine the initial level of control to implement treatment (assess patient impairment)
Maintain control once treatment has been implemented (assess patient risk)
Asthma Management
 Depending on level of asthma control, the patient is assigned to one of five treatment steps
 Treatment is adjusted in a continuous cycle driven by changes in asthma control status. The cycle
involves: - Assess - Adjust treatment (pharmacological and non-pharmacological) - Review the
response
 A stepwise approach to pharmacological therapy is recommended
 The aim is to accomplish the goals of therapy with the least possible medication
 The choice of treatment should be guided by:
- Level of asthma control
- Current treatment
- Pharmacological properties and availability of the various forms of asthma treatment
- Economic considerations
- Cultural preferences and differing health care systems need to be considered
Medications for Asthma
Controller Medications Reliever Medications
- Glucocorticosteroids - Rapid-acting inhaled β2-agonists
- Leukotriene modifiers - Systemic glucocorticosteroids
- Long-acting inhaled β2-agonists - Anticholinergics
- Theophylline - Theophylline
- Cromones - Short-acting oral β2-agonists
- Anti-IgE
Commonly used drugs
 Inhaled glucocorticosteroids (ICS)
 Budesonide
 Fluticasone
 Systemic glucocorticosteroids
 oral predinisolone: 1-2mg/kg.d
 Methylpredinisolone: 1mg/kg ivgtt q12h-6h
 β2-agonists
 Short-acting β2-agonists: - inhaled: 2puffs salbutamol or 2.5mg salbutamol by nebulizer; - oral:
meptin 1.25ug/kg bid
 Long-acting inhaled β2-agonists in combination with inhaled glucocorticosteroids - formoterol –
salmoterol
 Leukotriene modifiers
 Montelukast : 2-5 years old 4mg qn 6-14 years old 5mg qn >14 years old 10mg qn
 Anticholinergics
 Ipratropium
 Theophylline
 Cromones
 Anti-IgE
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Choosing an inhaler device for children

Device Pressurized PMDI plus face Dry power inhaler Nebulizer with
metered-dose mask face mask
inhaler ( PMDI)
with mouthpiece
Age group >7 yrs All age group > 5yrs All age group
Manage Asthma Exacerbations
 Exacerbations of asthma are episodes of progressive increase in shortness of breath, cough,
wheezing, or chest tightness
 Exacerbations are characterized by decreases in expiratory airflow that can be quantified and
monitored by measurement of lung function (FEV1 or PEF)
 Severe exacerbations are potentially life-threatening and treatment requires close supervision
 Treatment of exacerbations depends on:
 The patient
 Experience of the health care professional
 Therapies that are the most effective for the particular patient
 Availability of medications
 Emergency facilities
 Primary therapies for exacerbations:
 Repetitive administration of rapid-acting inhaled β2- agonist
 Early introduction of systemic glucocorticosteroids
 Oxygen supplementation
 Closely monitor response to treatment with serial measures of lung function
Summary
Asthma is a persistent chronic inflammatory disorder of the airways that causes recurrent
episodes of wheezing, breathlessness, chest tightness, and coughing.
Airway inflammation, hyperresponsiveness and airway remodeling are major

pathophysiological changes of asthma.
A stepwise approach to pharmacologic therapy is recommended. The aim is to accomplish

the goals of therapy with the least possible medication
09. Acute poststreptococcal glomerulonephritis
1.Introduction  It has been known for a long time that some children, after suffering from scarlet fever, can
develop edema and gross hematuria.
 This disorder has been known as acute poststreptococcal glomerulonephritis (APSGN).
 Since the advent of antibiotics and better public health, the incidence of this disease has
decreased dramatically in developed countries.
 In developing countries (include China), however, PSGN remain as a common form of
glomerulonephritis in children.
 Fortunately, the disease is self-limiting in most children and the recovery is complete, but
occasional it may lead to acute renal failure.
 Acute glomerulonephritis (AGN) follows an infection with a nephritogenic strain of group A
beta-hemolytic streptocci.
 AGN is one of the most common forms of renal parenchymal disease in childhood.
 A favorable outcome is likely in most patients.
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 The associated morbidity of the early stages of the disease is of little consequence when
acute complications respond to recommended forms of therapy
2.Etiology  APSGN may follow an infection of the throat or skin with one of the few nephritogenic strains
of group A beta-hemolytic streptococci.
 Tonsillitis ,pharyngitis ,sinusitis and media otitis precede 75% to 80% the cases of APSGN.
 The factors that allow only certain strains of streptococci to be nephritogenic remain unclear.
Etiology---  During cold weather, APSGN commonly follows streptococcal
respiratory tract respiratory tract infection ,such as Tonsillitis ,otitis and pharyngitis .
infection  A latent period of 7 to 10 days occurs between streptococcal infection
of the upper respiratory tract and the onset of clinical manifestation of
APSGN.
Etiology---skin  During in summer and early fall (warm weather ),the
infection glomerulonephritis generally follows streptococcal skin infection or
pyoderma.
 The peak incidence lags approximately a month behind that of
pyoderma.
3.Epidemiology  Epidemics of nephritis have been described in association with both throat (serotype 12) and
skin (serotype 49) infections.
 The disease is most commonly sporadic.
4. Incidence  The incidence of APSGN is difficult to assess.
 Many patients with acute nephritis are not diagnosed because they are either asymptomatic
or have such mild symptoms that the disease is not suspected and the urine is not examined .
 A peak incidence between 6 and 7 years old .
 age  60 percent of cases occurring between age 5 and 10.
 About 90% of cases between 2 and 12 years of age
5. Pathology  As in most forms of acute glomerulonephritis, the kidneys appear Syllmaetrically enlarged
 Large red kidney
 Typical change :diffusive ,exudative and proliferative glomerlonephritis
 Endocapillary proliferative glomerulo
 nephritis
light microscopy  All glomeruli appear enlarged and relatively bloodless
 Diffuse mesangial cell and endothelial cell proliferate with an
increase in mesangial matrix
 Polymorphonuclear leukocytes (WBC) are common in glomeruli
during the early stage of the disease
 Crescents and interstitial inflammation may be seen in severe
cases.
Immunofluorescence  lumpy-bumpy deposits of immunoglobulin and complement on the
microscopy glomerular basement membrane (GBM) and in the mesangium
electron microscopy  On electron microscopy, large electron-dense deposits or “humps”
are observed on the epithelial side of the GBM
6. Pathogenesis nephritogenic streptococci
immune complex formation
complement activation through the alternatives pathway
cell proliferation GBM damage
GRF↓ Hematuria and proteinuria

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salt and water retention oliguria
expanded extracellular fluid volume edema hypertension

7. Clinical  The typical case of APSGN is difficult to define because of the varied and diverse nature of
characteristics the individual present
 At one extreme is the child who is incidentally discovered to have APSGN.
 At the other extreme is the child who presents with severe systemic manifestation
 Between these two extremes lies the so-called typical case
latent period  Clinical manifestations of acute glomerulonephritis usually occur after an
asymptomatic period following infection.
 But microscopic hematuria and proteinuira are occasionally observed
during the latent period
 The latent period varied from a few days to three weeks,averaged about
10 days.
 Latent periods in excess of three weeks are uncommon,and an interval
of four weeks suggests a doubtful diagnosis
 Within 1 to 4 days of the onsetof the infection suggestpreexisting
glomerulonephritis or IgA nephropathy
 The latent period is about 10 days in the upper respiratory tract infection
such as tonsillitis, otitis media, or cervical adenitis.
 The latent period averages 3 weeks after the skin infections (notably
impetigo)
initial  The initial symptoms usually have an abrupt onset
symptoms  With the two most common complaints:edema and hematuria
 Accompanying these two featuresmaybe varying degrees of nonspecific
synptoms:malaise,lethargy ,anorexia,fever,abdominal
pain,weakness,and headaches
main  The usual clinical manifestations of acute nephritis are a mild degree of
manifestation edema, urinary abnormalities ( hematuria, proteinuria, and cylindruria),
and varying degree of hypertension.
 Acute nephritic syndrome
edema Edema is the most common symptom ,and most often involves the face,with particular
involvment of the periorbital area
In the majority of patients the edema is mild
hematuria Gross hematuria,often described as smoky,coke colored,tea colored,rusty ,or
reddish-brown,
occurs at the onset in 30% to 50% of those children who required hospitalizationand
is often the presenting symptom.
Microscopic hematuria is present in all children .
Gross hematuria clears within a few days ,but it has been observed for up to 4 weeks.
hypertension Hypertension is the third of the cardinal features
The Bp elevation is variable and maybe mild or severe
The Bp elevation may persist for one or two weeks
Persistence of BP elevation past 3 to 4 weeks usually indicates chronic disease or
rapid progression of the APSGN
BP（mmHg）
Preschool >120/80
School >130/90
Oliguria Reduced urine output is observed in the majority of hospitalized childre
Anuria is un common
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age normal oliguria anuria

Infant 500-600 <200 <30-50
preschool 600-800 <300
School 800-1400 <400
Non-symptom case nephrotic syndrome There is marked variation in the intensity and
distribution of symptoms and signs at the onset and during the early stage of acute nephritis.
In many instances the symptoms and the urinary findings are so mild that unless
they are specifically looked for, the disease goes unrecognized.
It is probable that the number of such unrecognized cases greatly exceeds those
recognized
Severe case The early phase of acute nephritis in children is made perilous by three possible
complications:hypertensive encephalopathy, cardiac failure, and acute renal failure.
Early recognition and prompt treatment of these complications are of greatest
importance.
Although usually present soon after the onset of disease they may develop several
days later(during 1 to 2 weeks) , a fact that need close observation.
Severe overload o Symptoms and signs referable to the heart occur in many patients
of circulation with acute nephritis, and heart failure dominates the clinical picture
in some.
o Paroxysmal or persistent dispnea, orthopnea,apical gallop rhythm,
cardiac enlargement, venous engorgement, enlarged liver, and
pulmonary edema may appear suddenly during the course of the
disease or may be the first manifestation of the disease.
o Radiographic evidence of pulmonary edema is seen in up to 60% of
cases.
o The cause of heart failure in acute nephritis is not certain, but it is
probably attributable to an increase in blood volume secondary to
retention of sodium and water.
o Although cardiac overload may be increased by accompanying
hypertension, it seems clear that failure is not due to hypertension.
o Evidence for myocarditis is lacking
Hypertensive o Hypertensive encephalopathy is characterized by headache, vomiting,
encephalopathy irritability or apathy,convulsions, transitory paralyses, and coma.
o Temporary complete blindness occurs occasionally.
o Papilledema may or may not be present.
o Blood pressure may be as high as 160 to 200mmHg (systolic) and 100
to 140mmHg (diastolic).
o The cause of the elevated blood pressure is unknown.
o The hypertension of acute nephritis is attributed to expanded
vascular volume or to vasospasm, the cerebral symptoms being
caused by cerebral ischemia and anoxia.
Acute renal failure o Severe renal failure is a less common complication of acute nephritis
in children.
o It is characterized by marked oliguria or anuria.
8. Laboratory Urinalysis; Bacteriologic and serologic examination; Renal functional test; Hemogram;
investigations Complement C3; Renal biopsy
Urinalysis hematuria
Gross or microscopic hematuria is almost always present, the urine usually
being reddish brown or smoky in appearance.
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The supernatant usually is brownish, indicting hemolysis and release of

hemoglobin that has been converted to acid hematin.
proteinuria
Proteinuria is nearly always present but typically in the subnephrotic range.
Nephrotic range proteinuria may occur in as many as 20% of patients
cast
The urinary sediment also contains many white blood cells and epithelial
cells and hyaline,granular, and red blood cell casts.
Renal function The BUN concentration is elevated in 75% of patients and may result from
examination a reduction in GFR and from prerenal factors such as cardiac
decompensation and continued dietary intake of protein.
The serum creatinine concentration, a more reliable indicator of renal
function, is abnormal in more than one half of the patients with APSGN.
Bacteriology Throat or skin culture may reveal group A beta - hemolytic streptococci
The sensitivity and specificity of these tests are likely affected by the
methodology of obtaining a throat culture and the test used
Such cultures may be less satisfactory than serological studies to evaluate
the presence of recent streptococcal infection
Serology Serology --- Streptozyme The antibodies used are antistreptolysin (ASO) ,
antibyaluronidase, anti-DPNase, antiDNase B, and antistreptokinase.
Of these ,the most commonly used test is the ASO.
Serology ---ASO Elevated ASO titer above 200units may be found in 90% of
patients with pharyngeal infection.
Serial ASO titer measurements with twofold or greater rise in titer are
highly indicative of a recent infection.
Serology ---C3 Early in the acute phase,the level of complement C3 is
usually reduced.
C3 levels return to normal within 6 to 8 wk .
The presence of persisitent of depression of C3 levels may be indicative of
another diagnosis ,such as MPGN ,SLE.
Hematology A mild to moderate anemia, secondary to hemodilution rather than blood
loss, is common at the outset of PS- AGN and may persist until diuresis
occurs.
Leukocytosis with a shift to less mature forms is noted in those patients
who present during or soon after a streptococcal infection.
The erythrocyte sedimentation rate is almost always elevated in APSGN.
Ultrasonography differentiate acute disease (usually normal or slightly enlarged kidneys)
from an exacerbation of chronic disease (small kidneys).
9. Key point of  Urine routine: Protein ,RBC Cast
diagnosis  In a child with an acute nephritic syndrome (Edema , Oliguria , Hematuia, Hypertension)
 evidence of recent streptococcal infection(A recent infectious history(7-14day))
 a low C3 level
10. Differential • It is important, however, to preclude(1) an acute exacerbation of chronic
diagnosis glomerulonephritis ,(2)anaphylactoid purpura with nephritis;(3)idiopathic hematuria(e.g IgA
nephropathy),(4)lupus erythematosus and. (5)familial nephritis.systemic .
• Renal biopsy is often necessary to distinguish similar presentations
Indication of renal biopsy

Considerations for renal biopsy would include the development of acute renal failure or nephritic
syndrome, the absence of evidence for streptococcal infection, the absence of
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hypocomplementemia, or the persistence of marked hematuria or proteinuria or both,

diminished renal function or a low C3 level for more than 3 months after onset.
11. Treatment  Bed rest :
- Although traditional therapy of acute glomerulonephritis has included prolonged bed
rest, a much less restrictive policy is now generally recommended.
- Bed rest is indicated as long as there are clinical manifestations of active disease, such as
significant edema, hypertension, or gross hematuria.
- These usually subside within 2 or 3 weeks, after which the patient feels quite well.
- At this state the patient may be allowed out of bed, with activity gradually being
resumed.
- Within a few weeks ,most children are back in school, but exhausting and competitive
activities are prohibited until the Addis count returns to normal.
 Diet
- It appears the only time that protein needs be restricted in if acute renal failure occurs
during the initial stage of acute nephritis.
- The same principle applies to the salt content of the diet, which should be that of a
normal diet except during the period of hypertension, edema, and oliguria.
 Antibiotics
- Antibiotic therapy is indicated only for the patient who has evidence of persisting
streptococcal infection demonstrated by a positive culture.
- A 10-day course of antimicrobial therapy is indicated to ensure eradication of the
streptococcus, which may be transmitted to susceptible persons.
- Treatment of established infection does not prevent the development of post-
streptococcal glomerulonephritis, but may lessen its severity.
 Treatment for complication
- Restriction of salt and water intake is mandatory in the management of each child with
APSGN from the time the diagnosis is suspected.
- Fluids are not given to the hypertensive child until the blood pressure is brought under
control.
- Thereafter, 300 ml/(m2.24h) can be allowed until the patient's dry weight is reached,
assuming blood pressure remains normal.
- Antihypertensive medications (diuretics, angiotensin-converting enzyme inhibitors) are
indicated to treat hypertension and to avoid hypertensive complications.
- Severe renal failure may warrant dialysis
Principle of therapy
- No therapeutic measure has been demonstrated that can favorably influence the course
of acute glomerulonephritis.
- Treatment of APSGN is largly supportive care.
- Immunosuppressive drugs are ineffective, and corticosteroids may worsen the condition.
- Prompt recognition and treatment of the early complications, based on sound
understanding of the disturbed physiology, constitute the most urgent aspects of
treatment.
12. Prognosis and  The acute clinical episode of post-streptococcal glomerulonephritis is usually self-limited
natural course  The prognosis for complete recovery is excellent in children, even in patients with the
nephrotic syndrome or crescentic disease at presentation.
 complement levels return to normal within 8 weeks.
 In most patients hematuria disappears by 6 months but proteinuria may persist for two years
in a third of patients
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10. Nephrotic syndrome

1. how to  Nephrotic syndrome (NS) is characterized by heavy proteinuria [ greater than
understand the 50mg/( kg .24h) ], hypoalbuminemia (less than 25g/L), often associated with
concept of hypercholesterolemia ,edema.
nephrotic  It must be recognized that heavy proteinuria represents only one manifestation of various
syndrome types of glomerular pathology.
 NS is the clinical state that results from persistent heavy proteinuria.
 Proteinuria resulting from increased permeability of the glomeruli to serum proteins is the
most essential feature.
 The classic features, namely hypoalbuminemia and edema, are the direct consequence of this
loss of protein through the kidneys.
2. Clinical  Idiopathic NS: unassociated with systemic disease.accounts for over 90 %of all cases in
classification of childhood
NS  Secondary NS: found in association with a systemic illness and is usually preceded by other
manifestations of this underlying disease.
Causes of secondary NS Systemic lupus erythematosus, viral hepatitis and Henoch - Schonlein
( anaphylactiod) purpura are the most common.
 Congenital NS: present at birth,or begin shortly after thereafter,rare and most patients die
before 1 year old.
3. Histopathologic Pathology of MCNS
classification of  In minimal change nephrotic syndrome , the glomeruli appear normal or show a minimal
NS increase in mesangial cells and matrix.
 Findings on immunofluorescent microscopic studies are typically nondiagnostic.
 Electron microscopy reveals fusion of the epithelial cell foot processes.
 More than 95% of children with MCNS respond to corticosteroid therapy.
Pathology of mesangial proliferative glomerulonephritis
 The mesangial proliferative group (5%) is characterized by a diffuse increase in mesangial
cells and matrix.
 The frequency of mesangial deposits containing Ig G and C3 by immunofluo rescence is not
different from that observed in minimal change disease.
 Approximately 50-60% of patients with this histologic lesion respond to corticosteroid
therapy.
Pathology of focal segmental glomerulosclerosis
 In biopsy specimens from patients having the focal sclerosis lesion (10%), the majority of
glomeruli appear normal or show mesangial proliferation. Others, especially those close to
the medulla (juxtamedullary), show segmental scarring in one or more lobules.
 The disease is frequently progressive, ultimately involving all glomeruli, and leads to
endstage renal failure in most patients.
 Approximately 20% of such patients respond to prednisone or cytotoxic therapy or both.
4. Pathophysiology Pathophysiology of NS ---proteinuria
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 The most common cause of proteinuria is increased permeability

of the glomerular capillary wall.
 The cause remains unknown.
 Because in some cases antigen-antibody complex and C3
complement deposit in the basement membrane had been found.
The causes may be the abnormal T cell function and immunal
complex formation.
 The glomerular filter barrier is composed of 4 major components,
the endothelial cells, the visceral epithelial cells or podocytes, the
mesangium and the capillary loop basement membrane.
 The capillary wall carries a net negative charge, and acts as both a
charge-selective and size-selective filter.
 Glomerular proteinuria may been termed selective or
nonselective.
 Electrostatic barrier damage results in albumin excretion (selective proteinuria).
 Molecular barrier damage results in nonselective proteinuria
Pathophysiology of NS--- hypoproteinemia
 It is generally agreed that proteinuria is the major cause of
hypoproteinemia
 Increased rates of catabolism of protein and protein loss
through the gastrointestinal tract also contribute to the observed
hypoproteinemia.
Pathophysiology of NS--- hypercholesterolemia

 Serum cholesterol, phospholipids, and triglycerides are all elevated
 The cause of the hyperlipidemia remains obscure.
 Hypoproteinemia stimulate the protein synthesis in the
liver,including the synthesis of lipoproteins. All of the serum
lipids exist in association with proteins such as lipoproteins,
which is carrier to cholesterol.
 Lipid catabolism is reduced due to decreased level of
lipoprotein lipase. It is the major enzyme that removes lipids
from the plasms
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Pathophysiology of NS--- edema

 Hypoalbuminemia results in a reduction in colloid osmotic
pressure of the plasma, permitting a shift in plasma water into
the interstitial space with resultant decrease in plasma volume
and edema formation.
 Increased tubular absorption of sodium chloride and
water leads to continued increase in edema. This increase in
tubular reabsorption of sodium has been attributed to activate
the RAS system.
 Antidiuretic hormone release in response to vascular
volume contraction contributes to water retention.
 Decreased renal plasma flow and glomerular filtration rate
occur in a few patients and may contribute to sodium and water
retention.
 Ultimately due to decreased osmotic pressure, reabsorbed
sodium and water are lost in interstitial space and increase the edema.
5. Clinical age and gender

Manifestations  The idiopathic nephrotic syndrome is more common in boys than in girls (2:1) and most
commonly appears between the ages of 2 and 6 year.
 It has been reported as early as the last half of the first year of life and in adults.
predisposing cause
 The initial episode and subsequent relapses may follow an apparent viral upper respiratory
tract infection
edema
 The disease usually presents as edema, which is initially noted around the eyes and in the
lower extremities, where it is "pitting" in nature with time
 The onset of edema is usually insidious, but it may be abrupt.
 The first evidence of periorbital edema is often attributed to a cold, although frank
respiratory symptoms are usually wanting.
 It may be misinterpreted as allergic in origin.
 the edema becomes generalized and maybe associated with weight gain, the development
of ascites or pleural effusions, and declining urine output.
 The edema acqumulates in dependent sites and appears to shift from the face and back to
the abdomen, perineum, and legs as the day progresses.
 The large abdomen produced by ascites is common, and scrotal swelling is often seen.
 The degree and duration of edema are very variable.
 The edema may progress slowly or rapidly;not uncommonly, however, it tends to subside
and reappear over a period of weeks.
 More severe degrees of edema may be associated with dilated veins of the anterior
abdominal wall, umbilical hernia, and rectal prolapse.
Gastrointestinal disturbances such as diarrhea not associated with infections are frequently
observed.
Respiratory difficulty resulting from abdominal distention with or without plural effusion may
occur.
Even in the presence of massive edema, which may appear so uncomfortable to others, many
children remain remarkably good in spirits.
6. Complication of  Infection
NS  Electrolyte disturbance and hypovolemia
 Thrombosis
 Acute renal failure
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 Physical growth retardation

Infection  Proposed explanations include decreased immunoglobulin levels, the
edema fluid acting as a culture medium, protein deficiency decreased
bactericidal activity of the leukocytes, immunosuppressive therapy,
decreased perfusion of the spleen due to hypovolemia, and loss in the urine
of a complement factor (properdin factor B) that opsonizes certain bacteria.
 Infection is the major complication of nephrosis
 Upper respiratory tract and urinary tract infection are common.
 Spontaneous peritonitis is a frequent type of infection. The presence of
ascites may mask the classic signs of peritonitis, which may be suspected
whenever an edematous child develops fever and looks sick.
 Sepsis, pneumonia, cellulites, and urinary tract infections may also be
noted.
 Fever and physical findings may be minimal in the presence of
corticosteroid therapy.
 Accordingly, a high index of suspicion, prompt evaluation ( including
cultures of blood and peritoneal fluid), and early initiation of therapy that is
effective against both gram - positive and gram - negative organisms are
critical to prevention of life threatening illness.
Electrolyte  Hypokalemia, hyponatremia, hypocalcemia, and hypochloremiamay occur.
disturbance The causes may be long term restriction of salt intake, excessive diuresis,
and infection, vomiting, diarrhea, etc.
hypovolemia  Some patients are susceptible to hypovolemia shock. It may result from
hypoproteinemia, reduction of plasma colloid pressure and apparent edema
thrombosis  Additional complications may include an increased tendency to develop
arterial and venous thrombosis owing at least in part to elevated plasma
levels of certain coagulation factors and inhibitors of fibrinolysis, decreased
plasma level of antithrombin III, and increased platelet aggregation.
 Excessive diuresis causing hypovolemia and steroid therapy stimulating
hypercoagulatory state also play a role.
 Venous thrombosis are more common than arterial thrombosis.
 Renal venous thrombosis is the most frequent type, manifesting sudden
lumbodynia, hematuria or exacerbated hematuria, oliguria or acute renal
failure.
acute renal  It easily occur when the patient has predominant water retention, long -
failure term oliguria, elevated BUN, decreased specific gravity of urine, and mass
casts.
 The possible reason may be renal interstitial edema or protein casts causing
infection.
Physical  The reason is complex.
growth  Malnutrition, steroid therapy, growth hormone resistance caused by
retardation nephritic disease, decreased level of insulin and thyroid hormone
7. Diagnosis  to defines NS
 to define primary nephrotic syndrome
 to define simple or nephritic NS
 to define the pathological type
 to confirm the complication
 to define the renal function
step 1 --- to defines NS
The combination of edema, proteinuria, hypoproteinemia, and hyperlipidemia
Urinalysis
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During the active stage of the disease, urine protein excretion may be greater than 50
mg/( kg.24h), +++~++++
The most important clinical feature is heavy proterinuria
Blood chemistry
Total serum protein concentrations :less than 25g/L.
Cholesterol concentrations :over 5.7mmol/L.
step 2 --- to define primary nephrotic syndrome
To exclude the secondary nephrotic syndrome and the congenital nephrotic syndrome
For new diagnosed cases, serum examination about evidence of streptococcal infection, and
hepatitis viral infection, anti nuclear antibody, anti -Smith antibody, etc should be performed.
step 3 --- to define simple or nephritic NS
Simple type NS
Nephritic type NS: For the diagnosis of nephritic type NS, besides four main features of nephrotic
syndrome, one of the following features is necessary : hematuria ( RBC in the urine > 10/HP, 3
times in 2 weeks), recurrent or persistent hypertension ( preschool child > 120/80 mmHg, school
child > 130/90 mmHg,exclude the use of glucocortcoid), or azotemia (BUN > 10.7 mmol/L) or
persistent decreased complement C3
step 4 --- to define the pathological type
Most children with nephrotic syndrome do not need renal biopsy.
The purpose of renal biopsy is to define diagnosis, estimate prognosis, and guide therapy.
Indications of renal biopsy
The indications of renal biopsy in children with nephoitic disease are as follows :
(1)steroid -resistant, frequent relaps,
(2)nephritic NS,
(3)secondary NS or congenital NS.
step 5 --- to confirm the complication
Infection
Electrolyte disturbance and hypovolemia
Thrombosis
Acute renal failure
Physical growth retardation
step 6 --- to define the renal function
8. Treatment  General measures :diet ,activity,and diuretic therapy
 Adrenocorticosteroids treatment
 Immunosuppressant therapy and cytotoxic drugs
 ACEI
 anticoagulator
 Others -Immune regulator
General management
diet and activity
control of edema
exposure to and treatment of infection
immunizations
psychological support of patients and their families
treatment of the important complications of nephrotic syndrome
---to prevent and treat infection
- Serious intercurrent infections are a real hazard for the nephrotic child.
- Continuous prophylaxis with antibiotics is not recommended
- It is advisable to administer antibiotics after definite exposure to bactcerial infection
and the use of these agents promptly and more liberally for therapy of possible
bacterial infection.
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- To keep the skin clean

Diet
- In general , the diet should be normal for child’age.
- The child should be fed according to his appetite.
- Sodium restriction is advisable when edema is present,but only to the extent that it
does not interfer seriously with the child’s appetite
- Food with very high salt content should be excluded and salt shouldnot be added to
food at the table.
- Fuilds are given as desired.
- No attempt should be made either to restrict or to increase protein intake.
--activity
- Children should be permitted to lead lives as normal as possible.
- Fear of infection should not prevent children from having normal schooling and normal
socialization
- There is no evidence that restriction of general activity favorably influence the
subsequent course or outcome of the disease.
- It seems clear that the psychological benefits of relatively normal activity outweigh any
benefits of restriction
- For this reason and because of enforcing bed rest in young children,no attempt should be
made to restrict activity
- During peroids of extensive edema ,there is a certain amout of selfiposed limitation of
activity
--- diuresis---indication
- Since the majority of patient exhibit satisfactory diuresis within 2 to 3 weeks after
beginning adrenocorticosteroid therapy, diuretic agents are not given initially.
- But in refractory patients, or before diuresis has occurred in very edematous patients
who become more edematous during treatment, diuretic may provide important
symptomatic relief.
--- diuresis---usage
- Hydrochlorothiazide, in a dosage of 2 to 4 mg/(kg ~ d), is the agent used initially in
patients whose edema is not severe.
- The thiazide drugs are relatively nontoxic. Hypokalemia is usually not seen if a child is
eating a normal diet, but it may be avoided by giving potassium supplements.
- In hypoalbuminemic patients, low - salt human albumin is given first, in a dosage of
0.5g/kg for patients whose serum albumin is between 1.5 and 2.0g/dl, and 1 g/kg if the
serum albumin is lower.
- The albumin is infused slowly over the course of 1 hour.
- Furosemide is given by intravenous injection after an additional 30 to 60 minutes of
equilibration, in a dose of 1 mg/kg.
Steroid therapy
steroid therapy is the specific therapy and the first choice of inducing NS remission.
the basic aim of all regimens is to maintain the patient free from proteinuria with the
minimal dosage of adrenocorticosteroids.
the presence or absence of proteinuria is the best indicator of disease activity, and
changes in therapy are based on these tests.
Initial dose of prednisone should be full
- Prednisone, 1.5 -2mg/(kg .d) in three divided doses,is given orally for 8 to 12
weeks once the diagnosis has been confirmed.
- The maximum prednisone dose should not exceed 60 mg/d
Dose of prednisone should be reduced slowly
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- Most steroid -responsive patients will clear their proteinuria during the 8 weeks of
prednisone therapy.
- When: Two weeks after the urine becomes protein free (negative)
- How:the regimen of prednisone is changed to 60mg/m2 body surface area, taken
every other day as a single dose with breakfast. Prednisone is then tapered,
reduced every 2 -4 weeks, and the patient's urine is monitored for evidence of
recurrent proteinuria. This alternate day regimen is continued for 3-12 months
Prolonged use of prednisone
- Short - term therapy ( 8 weeks)
- Middle - term or long - term therapy (6 - 9 months)
Short - term therapy
- The total course is 8 weeks.
- Prednisone at a dosage of 2mg/( kg ~ d) ( maximum60 mg/d), tid for 4 weeks,
followed by 1.5mg/kg given as a single morning dose on alternate days for an
additional 4 weeks.
- This regimen has less side effect but relapses are common.
- Not used in China
Middle-term or long-term therapy
- The total course is 6 - 9 months
- Prednisone at a dosage of 1.5 - 2mg/kg .d ( maximum 60mg/d), tid, is given orally
until the patient has protein free urine for 2 weeks,which needs 4 - 8 weeks,
followed by 2mg/kg given as a single morning dose on alternate days for an
additional 4 weeks.
- If the urine examination is persistent on protein free, then gradually decrease the
prednisone dose.2.5-5mg every 2 to 4weeks
- The total course of treatment for 6 months is regarded as middle-term therapy,
for 9 months is regarded as long-term therapy.
Why we need alternate day therapy ?
- The purpose of alternate day therapy is to maintain the remission using a
relatively nontoxic dose of prednisone, thus avoiding frequent relapses of the
disease and the cumulative toxicity of frequent courses of daily administration of
corticosteroids.
- Adequate experience indicates sufficient recovery of pituitary-adrenal axis
function that patients are not at risk for adrenal insufficiency after abrupt
withdrawal of alternate-day prednisone.
How to Judge the curative effect of corticosteroids (after 4 weeks)
- Steroid -responsive NS: edema extinction, protein in the urine is negative.
- Steroid -resistant NS: the quality examination of protein in the urine is + - + + + +.
- Steroid - dependent NS : patients respond well to daily divided doses of steroids
but have relapse in alternate day regimen or patients respond well to adequate
steroids but have relapse during tapering.
Immunosuppressant therapy and cytotoxic drugs
---indication
 The indications of immunosuppressant therapy include frequent relapser (frequent relapser
is regarded as a patient who relapses more than twice in a 6-month period of time) ,
unaccepted steroid side effect(cushingoid appearance, hypertension, growth failure ), steroid
- resistant eases, and steroid-dependent cases.
---drug and usage 
• The use of drugs such as nitrogen mustard, cyclophosphamide, chlorambucil, methotrexate, 6
-thioguanine, and azathioprine has been advocated in the treatment of patient's refractory to
other forms of therapy.
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• Cyclophosphamide:most common
cytotoxic drugs---- Cyclophosphamide
 Cyclophosphamide has been shown to prolong the duration of remission and to
prevent relapses in children with frequently relapsing nephrotic syndrome.
 The potential side effects of the drug (leukopenia, disseminated varicella infection,
homorrhagic cystitis, alopecia, sterility)should be reviewed with the family.
 The dose of cyclophosphamide is 10-12mg/kg.d for 2 days,every 2 week
 Total dose :less than 150-200mg/kg
 Alternate day prednisone therapy is often continued during the course of
cyclophosphamide administration. During cyclophosphamide therapy, the white blood
count must be monitored weekly and the drug withheld if the count falls below
5,000/mmL
other therapy
--- ACEI
 Benefit: is considered to delay glomerulosclerosis, and to decrease proteinuria
 Routine used, especially adapted to NS accompanied with hypertension
 Drug: such as captopril, enalapril, and fosinopril.
--- Anticoagulant
 sodium heparin [ 1mg/(kg.d) + GS50 - 100ml iv drip for 2 ~4 w]
 urikinase (30 000 -60 000 U/d + GS100 - 200ml iv drip for 1 -2 w)
 Role:another choice for patients with high coagulation state
9. How to treat the  A relapse is defined as the recurrence of edema and not simply of proteinuria, as many
relapse of children with this condition have intermittent proteinuria that resolves spontaneously.
nephrosis  Each relapse of nephrosis is treated in a similar manner.
 A small number of patients who respond to daily divided dose therapy have relapses shortly
after switching to or after terminating alternate - day therapy. Such patients are termed
steroid dependent.
10. Tuberculosis
Objectives
• Overview global epidemiology
• Information of Childhood TB
• Diagnostic methods
• Common clinical types in Childhood TB
• Treatment for childhood TB
Tuberculosis • One third of the world’s population is infected

A Global • TB kills 5,000 people a day – 2-3 million each year
Emergency • HIV and TB co-infection is producing explosive epidemics
• Multidrug-resistant (MDR) threatens global TB control
Information of • In 2017, an estimated 1 million children became ill with TB and 230 000 children died of TB
childhood TB • TB is major cause of childhood morbidity and mortality worldwide
• Limited information on epidemiology, diagnosis and treatment of TB in children TB in Children
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TB in children • In high burden TB 15-20% of TB among children whereas only 2-7% in low burden TB
• The reported absolute rate of TB is only 0.8% for children under 14 years Challenges for Surveillance
Challenge of • Difficult diagnosis of childhood
surveillance • Lack of standard case definition
• Increased extrapulmonary disease
• Low public health priority of childhood TB
Etiology • pathogen
1. Mycobacteriaceae
2. Acid-fast bacilli
3. M tuberculosis and M bovis
4. growing slowly, culture 4-6 weeks Some current concepts on pathogenesis
Transmission of Mode of spread
tuberculosis in • Respiratory tract
children • Intestinal tract
• Skin
• vertical transmission (congenital tuberculosis)
TB germs can spread when a contagious person: coughs, sneezes, shouts, sings
You can get TB infection if you spend a lot of time indoors with this person
1)the number of organisms
2)concentration of organisms
3)length of time and distance
4) the immune status
Three forms after contact M. Tuberculosis in children
TB
Exposure Infection Disease

Clear bacteria Limit bacteria Bacteria break limitation
Exposure
• Exposure (close contact) TB, PPD negative
• No any lesion
TB infection
Person:
• Not ill
• Not contagious
Germs:
• Sleeping but still alive
• Surrounded (walled off) by body's defense system
Latent TB Infection
LTBI is a huge pool of active TB
• The TB skin test is usually positive (over 10 mm)
• Chest x-ray = normal
What causes TB infection to become TB disease?

- HIV-positive persons
- Immunosuppression
•Organ transplants, Severe kidney disease or other conditions need corticosteroids treatments or
immunosuppression therapy.
- children <4years of age
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- diabetes, tumor, malnutrition

Wall breakdown due to a weakened immune system
Risk of Progression • Age
to Disease 43% in infants (children < 1year)
25% in children 1-5 years
15% in adolescents
• Total 10% risk over a lifetime
Classification Primary TB: exposure disease

Secondary TB: exposure LTBI disease
In active TB
• The TB skin test is usually positive (over 10 mm)
• Chest x-ray = abnormal %3D
Germs:
• Active and multiply
• Cause damage
Person:
• May feel sick
• May be contagious
• Children be rarely infectious
• In active TB, the person has symptoms:
- Fatigue
- Weight loss (unexplained) or failure to thrive
- Loss of appetite
- Loss of appetite
- Cough
- Night sweats
Common clinical types of childhood TB:
Pulmonary Primary tuberculosis
1. Three manifestations: primary lesion, Lymphangitis, and lymphadenopathy
2. With or without of Symptoms of TB
3. X-ray ----initial complex, hilar enlargement
outcomes • Lesion absorb, left calcification • Blood dissemination, miliary TB or extrapulmonary TB •
Spread by bronchus, PTB
Diagnosis Childhood TB diagnosed by:
Combination of :
• Medical History
• Positive tuberculin skin test
• Serology
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• Suspicious CXR ·
• Bacteriological confirmation
Medical Types of evidence Evidence to be collected
History History of collection Careful history (including TB contacts; symptoms consistent
with TB)
Symptoms of disease Physical examination (including growth assessment), HIV
testing (in high HIV prevalence areas)
Positive There is a test for TB injection The PPD(Purified Protein Derivative) Skin Test
tuberculin • Read reaction 48-72 hours after intradermal injection
skin test • Measure only induration, not erythema
• Record reaction in millimeters
Interpreting Tuberculin Skin Tests
Positive-PPD
TB Active TB
infection
Degree of risk Risk factors Positive reaction
High • HIV-positive persons >5mm
• Recent contacts of TB case
• abnormal chest X-rays
• Immunosuppression
Medium  Recent arrivals from high- >10mm
prevalence countries
 Injection drug users
 Residents and employees of high-
risk congregate settings
 Myčobacteriology laboratory
personnel
 Pérsons with clinical conditíons
that place them at high risk
 Children <4 years of age, or
children and adolescents éxposed
to adults in high-risk categories
Low  Persons with no known risk >15mm
factors for TB
 Targeted skin testing programs
should only be conducted among
high-risk groups
Factors that may affect the skin test

Type of reaction Possible cause
False-positive BCG vaccination
Nontuberculous myobacteria
False-negative Recent TB infection (in 4-6weeks)
Overwhelming TB disease
Live-virus vaccination
Use of corticosteroids
Serology Serodiagnosis:
Serological detection:
purified and recombinant antigens
monoclonal antibodies
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Children have lower antibody titers since they make distinction from natural exposure
antibodies more difficult.
Little value !
TB blood tests
• enzyme-linked immunospot assay, T.SPOT
• interferon-gamma release assays (IGRAS).
• specific antigen of Mt : combinations (ESAT-6 and CFP-10)
• Results with little influence by BCG or NTM
PCR
• Traditional PCR methods- False positive and negative
• Xpert MTB/RIF is a rapid and high effective PCR method
Xpert MTB/RIF
• Xpert MTB/RIF is an automated, cartridge-based nucleic amplification assay
• simultaneous detection of TB and rifampicin resistance under two hours
• Detect directly from sputum, gastric aspirate, and other fluid samples.
Suspicious Chest Radiograph

CXR there is a prominent node in the left hilum of the lung
tuberculous lymphadenopathy.
CT Scan
patchy shadows with bronchial lymph nodes and mediastinal lymph nodes enlarged
miliary tuberculosis
evenly distributed miliary nodules with same size and density in pulmonary CT scan
Bacteriological Smear Examination (Gastric aspirate )
confirmation • Sputum
• Gastric aspirates
AFB smear results
•Lower sensitivity, less than 10%
•a negative smear by no means excludes tuberculosis
Diagnosis of TB on children
• To find TB you must
- Suspect TB (thìnking of it )
- Screen for TB(TST X- ray)
- Confirm TB (bacteria, follow up) (Combination of list)
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TB can be found in all parts of your body: Brain, Eye, Lymph node, Throat, Lung, Bone, Spine, Kidney, Skin,
Abdomen
Tuberculous meningitis
• TB of the centre nervous system.
• Young children, especially those under 4 years, are high at risk for TBM.
The most fatal form of TB. What clinical signs would suggest TBM?
Stage Weeks Symptoms Signs

1 1-2 Vague; weight loss; vomiting; irritability; personality Non-specific
changes
2 1-2 incapable of play, confusion, headache, fever, vomiting, With neurological findings
neck stiffness, disorientation, slurred speech...
3 1-2 consciousness falls facial weakness, blindness. hemi- or Marked decrease in mental status
quadriplegia with neurologic findings
CT scan: hydrocephalus and basal enhancement; tuberculomas and infarcts
What is a helpful clue to diagnosis of TBM ?
• Failure to thrive or weight loss
• evolving meningitis
• Evidence of primary TB and miliary TB (chest X-ray change)
• TB infection evidence: Positive TST or TSPOT gastric aspirate -- acid fast bacilli
• Typical Radiographic appearance of brain
Keypoint: CSF in TBM
• the leukocyte count: the range of 50-500/mm3 and lymphocytes predominate
• protein concentration: markedly elevated
• glucose concentration: reduced
• chloride levels: reduced

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Pathogen confirm
• Bacteria are seldom detected in CSF with traditional culture or smear
• Xpert MTB/RIF detection has some value for diagnosing of TBM
Treating PTB disease: general principles
• Start TB chemotherapy immediately
WHO recommend: 2HRZE/4HR
isoniazid (H) 10 mg/kg (range 10-15 mg/kg); maximum dose 300 mg/day
rifampicin (R) – 15 mg/kg (range 10-20 mg/kg); maximum dose: 600 mg/day
pyrazinamide (Z)- 35 mg/kg (30-40 mg/kg)
ethambutol (E) – 20 mg/kg (15-25 mg/kg)
Prognosis of TBM
Stage 1: good
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Stage 2: 10% of children die and 20% of children disable
Stage 3: 30%-50% of children die and at least 60% of children disable
Military and TB abdomen
Tubercular lymphadenopathy
Adrenal tuberculosis:
Addison’s disease
TB bones: hip joint
Summary of Pediatric tuberculosis
1. The diagnosis of TB is more difficult in children due to non-specific or complete absence of

symptoms and difficulty in confirming the diagnosis microbiologically.
2. Young children suffer more extrapulmonary and disseminated TB
3. Children should be TB skin tested only if they have risks for TB infection, are likely to progress to
active TB, or are suspected of having active TB.
4. Unlike adults, all children should be treated for TB infection (<5y)
5. Young children are not contagious with active TB
TUBERCULOSIS QUIZ
Q. Which one is wrong to describe childhood tuberculosis infection?
A. The child is infectious to others.
B. TB germs exist in body
C. The child has asymptoms
D. TB skin test is positive
Q. Which group of signs and symptoms are characteristic of a child with tuberculosis:
A. Sleeplessness, cough, and chest pain
B. Productive cough, fever, night sweats, weight loss
C. Fever, enlarged lymph nodes, and nasal drainage
D. Fast heart rate, shortness of breath, and fatigue
Q. As an airborne microbe, tuberculosis is spread by all of the following activities EXCEPT:
A. Singing
B. Coughing
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C. Needle-sharing
D. Sneezing
Q. which one is wrong to diagnose Tuberculin skin test:
A. Read reaction 48-72 hours after injection
B. Measure only erythema
C. Record reaction in millimeters
D. Taken by intradermal injection
Q. For which child would preventive therapy for Tuberculosis (TB) be implemented:
A. the child has productive cough and a negative TB skin test
B. the child had BCG vaccination and has a positive TB skin test
C. the child has recently converted to positive TB skin test
D. The child has a cough over more than two weeks
Q. If a child has a positive reaction to PPD, the possible cause is
A TB infection
B Active TB
C BCG vaccination
D Nontuberculous mycobacteria infection
E Overwhelming TB disease
11. Suppurative Meningitis

Outline of suppurative meningitis:
 Epidemiology, anatomy, pathophysiology, pathology, pathogens.
 Symptoms and signs (PE), diagnosis (tips, LP)
 Treatment (antibiotics) and support, complications, sequala, prognosis, prevention
Definition-------- Purulent Meningitis

 Acute infection of central nervous system (CNS). 90% of cases occur in the age of 1mo-5yr.
 The inflammation of meningitis caused by various pathogens. Common features in clinical practices
include: fever, increased intracranial pressure, meningeal irritation.
One of the most potentially serious infections, associated with high mortality (about 10%) and morbidity
Meninges of the central nervous system: dura mater, arachnoid mater, and pia mater.
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Meningitis
 inflammation of the leptomeninges (the tissues surrounding the brain and spinal cord)
 Bacterial meningitis
 Aseptic meningits: infectious or noninfectious Viral, Rickettsiae, Mycoplasma Fungal, spirochetes: syphilis,
 Lyme Protozoa: malaria Malignancy Lupus erythematous Lead or mercury poisoning
Pathophysiology Inflammation of the meninges
Anatomy and How microbes enter the CNS:
physiology  Skull or backbone fractures
 Medical procedures
 Along peripheral nerves
 Blood or lymph
Routes of  Blood-borne infection (major form)

infection to the  Respiratory tract infections (U.R.I) / pneumonia
meninges  Skin lesion: furuncle, impetigo, cellulitis, inflammation of umbilicus
 Enteritis: salmonellae infection, etc
Infection of Adjacent tissue
 Nose infection: Rhinitis, Sinusitis
 Ear infection: Otitis media, Mastoiditis
 Injury of the skull or rupture of brain abscess
Common Staphylococcus
pathogens E-coli
Neisseria meningitides
Normally causes Listeriosis- Listeria monocytogenes
Streptococcus pneumoniae—a causative bacteria of meningitis
Other common pathogens  Haemophilus influenzae(HI)  Streptococcus pneumoniae(SP)  Pseudomonas
aeruginosa (PA)  Listeria monocytogenes
Causes Immune status Overall, the most common causes of bacterial meningitis in immunocompromised patients
are •S. pneumoniae •L. monocytogenes •Pseudomonas aeruginosa •Mycobacterium tuberculosis •N.
meningitidis •Gram-negative bacteria
Clinical Fever
Manifestation headache
vomiting
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convulsion
changes in consciousness
atypical in young infants (irritability, depressed mental status, poor feeding)
Features of Increased Intracranial Pressure

In infants In children
Bulging fontanelle Papilledema
Shrill cry Diplopia
Failure to thrive Nausea and vomiting
Large head (Hydrocephalus) Headache
Impaired upward gaze (setting-sun sign) Mental changes
Meningeal irritation signs:
 Neck stiffness (nuchal rigidity): keep the child with supine position without pillow, flex his head, if
resistance exists, it means the test is positive.
 Kernig sign: keep the child with supine position without pillow, flex the hip and knee joint at 90° , elevate
a leg, if the child raises his head or has painful expression, it indicates the test is positive.
 Brudzinski sign: keep the child with supine position without pillow, flex the head, if the child flexes his legs
involuntarily at the same time, it means the test is positive.
Laboratory  Blood test: Routine blood test reveals that the total white cell count is increased
investigations  CSF test: CSF color is cloudy, turbid, even purulent. Pressure is elevated
 a CT scan to check for any problems with the brain, such as swelling
“Blood Can Be Very Bad”—”BCBVB”, which stands for
B - blood C - cisterns B - brain V - ventricles B – bones
Lumbar puncture
Step 1: Body position
1. The patient is placed in a lateral recumbent position,
with the back as near the edge of the bed as possible.
2. The legs are flexed on the thighs, the thighs are flexed
on the abdomen, and the head and shoulders are bent
down, curving the spine convexly to afford the greatest
space between the vertebrae
Step 2: Puncture site

1. The interspace of the third and fourth lumbar vertebrae is selected.
2. The intersection of 2 lines, one is the middle line of the back and the other is the line connecting bilateral
posterior iliac crest, can be selected to be the puncture site.
Step 3: Sterilizing and anaesthesia
1. The skin over the interspace of the third and fourth lumbar vertebrae is cleaned and sterilized.
2. The operator puts on sterile rubber gloves.
3. A fenestrated sterile drape is placed over the back, the window over the puncture site.
4. Local anaesthesia with Lidocaine
Step 4: Puncture
1. The needle is inserted through the interspace to the subarachnoid space (about 4-6 cm deep from skin;
two times of “pops”), and the stylet is withdrawn.
2. If the needle is in the proper place, CSF will begin to drip out through the needle.
3. The pressure of the CSF may be measured with a manometer and CSF is sent to the laboratory for
chemical and bacteriologic analysis.
Step 5: After Puncture
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1. Withdrawing the needle after inserting the stylet and covering the puncture site with sterile gauze block.
2. The patient is usually kept flat in bed without pillow for 4-6 hours after the procedure.
Complication Common Complication of purulent meningitis
◆ Subdural Effusion
◆ Pyocephalus
◆ Syndrome of inappropriate secretion of antidiuretic hormone,
SIADH(hyponatremia , low plasma osmotic pressure and brain
edema)
◆ Hydrocephalus
◆ Other
Sequelae  Deafness  Blindness  Epilepsy  Paralysis
Diagnosis Orientation diagnosis
 Location diagnosis
 Qualitative diagnosis
Diagnosis for purulent menigitis  Orientation diagnosis  Location diagnosis  Qualitative diagnosis
Earlier diagnosis and prompt initiation of effective antibiotic treatment is critical for minimizing sequelae of
purulent meningitis.
 Suspected cases: febrile infants with seizure, meningeal irritability, increased intracranial pressure, altered
mental status
 Pay attention to the atypical symptoms and signs in neonate, infant and patient already received irregular
antibiotic therapy
Treatment  Symptomatic treatment
Antipyretics: Antipyretics will be given when the temperature is over 38.5°C. Anticonvulsion drugs: Sedative
should be given as soon as possible. Immediate therapy of anti-seizures includes diazepam(0.1-0.3mg/kg) or
5% chloral hydrate(0.5ml/kg) by enteroclysis. Reduce intracranial hypertension: 20% mannitol, diuretics,
and corticosteroids can be used. Anti-shock management
 Antibiotic therapy
Roles for antibiotics selection: 1) Use antibiotics as early as possible. Once the initial diagnosis is made, the
appropriate antibiotics should be given immediately. (penicillin;ceftriaxone) 2) If the pathogen is not sure,
use antibiotics which could kill both gram positive and negative bacteria 3) If the pathogen is known, select
sensitive antibiotics (antibiotic susceptibility test)
 Corticosteroids
Dexamethasone is used to decrease cerebral and cranial nerve inflammation and edema; it should be given
when therapy is started. Adults are given 10 mg IV; children are given 0.15 mg/kg IV. Dexamethasone is
given immediately before or with the initial dose of antibiotics and every 6 hours for 4 days.
Use of dexamethasone is best-established for patients with pneumococcal meningitis.
 Other measures
 The effectiveness of other measures is less well-proved.
 Patients presenting with papilledema or signs of impending brain herniation are treated for increased
ICP:
 Elevation of the head of the bed to 30˚
 Hyperventilation to a PCO2 of 27 to 30 mm Hg to cause intracranial vasoconstriction
 Osmotic diuresis with IV mannitol
 Usually, adults are given mannitol 1 g/kg IV bolus over 30 minutes, repeated as needed every 3 to 4
hours or 0.25 g/kg every 2 to 3 hours, and children are given 0.5 to 2.0 g/kg over 30 minutes, repeated as
needed.
 Additional measures can include
 IV fluids
 Antiseizure drugs
 Treatment of concomitant infections
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 Treatment of specific complications (eg, corticosteroids for Waterhouse-Friderichsen syndrome, surgical

drainage for subdural empyema)
course of treatment: • Depends on the clinical response

group B Streptococcus 10-14d
L monocytogenes 10-14d
uncomplicated meningococcal meningitis 4-7d
Gram-negative enteric meningitis >21d
Haemophilus disease 7-10d
Enterococcus meningitis 14-21d
pneumococcal meningitis >10d
Prognosis  For children < 19 years, the mortality rate may be as low as 3% but is often higher; survivors may be deaf
and neuropsychologically impaired. The mortality rate is about 17% for adults < 60 years but up to 37% in
those > 60. Community-acquired meningitis due to S. aureus has a mortality rate of 43%.  In general,
mortality rate correlates with depth of obtundation or coma. Factors associated with a poor prognosis
include  Age > 60 years  Coexisting debilitating disorders  A low Glasgow coma score at admission (see
tables Glasgow Coma Scale and Modified Glasgow Coma Scale)  Focal neurologic deficits  A low CSF cell
count  Increased CSF pressure (particularly)  Seizures and a low CSF:serum glucose ratio may also
indicate a poor prognosis.
SUMMARY
 Use antibiotics actively, carry out lumbar puncture as early as possible
 Empirical medication: ceftriaxone or cefotaxime, plus vancomycin, patients under three months
with ampicillin, meropenem for g- bacillus infection
 After the culture result comes out, the medicine is selected according to the drug sensitivity test
 Finishe the course of treatment according to the guidelines
 After the condition is stable, the patient is advised to return to the local hospital for further
treatment
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 Streptococcus pneumoniae and Neisseria meningitidis are the most common causes of bacterial
meningitis in infants and children older than one month of age.
 Certain host factors may predispose to bacterial meningitis with a particular organism . Additional
risk factors for bacterial meningitis include exposure to someone with meningococcal or
Haemophilus influenzae type b (Hib) meningitis, cochlear implantation device, recent neurosurgical
procedure, or anatomic defect (dermal sinus or urinary tract anomaly).
 Most patients with bacterial meningitis present with fever and symptoms and signs of meningeal
inflammation . However, the clinical manifestations of bacterial meningitis are variable and
nonspecific; no single sign is pathognomonic.
 Suspected bacterial meningitis is a medical emergency, and immediate diagnostic steps must be
taken to establish the specific cause.
 The laboratory evaluation of children with suspected meningitis should include a complete blood
count with differential and platelet count, two aerobic blood cultures, and serum electrolytes,
glucose, blood urea nitrogen, and creatinine. Evaluation of clotting function is especially indicated if
petechiae or purpuric lesions are noted.
 A lumbar puncture should be performed on any child in whom, after careful history and physical
examination, the diagnosis of meningitis is suspected unless specific contraindications to lumbar
puncture are present. Examination of the cerebrospinal fluid (CSF) should include cell count and
differential, glucose and protein concentration, Gram stain, and culture.
 If there is a contraindication to or inability to perform a lumbar puncture or if the lumbar puncture

is delayed by the need for cranial imaging, blood cultures should be obtained and empiric antibiotics
administered as soon as possible.
 Laboratory findings characteristic of bacterial meningitis include CSF pleocytosis with a

predominance of neutrophils, elevated CSF protein, decreased CSF glucose, the presence of an
organism on CSF Gram stain, and isolation of a pathogenic organism from the CSF and/or blood
culture .
 Isolation of a bacterial pathogen from the CSF (by culture or other diagnostic techniques) confirms
the diagnosis of bacterial meningitis.
 In children who were treated with antibiotics before CSF was obtained, increased CSF cell count,
elevated CSF protein concentration, and/or decreased CSF glucose concentration usually are
sufficient to establish the diagnosis of meningitis; blood cultures and/or rapid diagnostic tests may
help to identify the pathogenic organism.
 Empiric therapy for bacterial meningitis (a thirdgeneration cephalosporin and vancomycin) should
be initiated immediately after the results of lumbar puncture are received or immediately after the
lumbar puncture is performed if the clinical suspicion for bacterial meningitis is high.
 Common causes of acute bacterial meningitis include N. meningitidis and S. pneumoniae in

children and adults and Listeria species in infants and the elderly; S. aureus occasionally causes
meningitis in people of all ages.
 Typical features may be absent or subtle in infants, alcoholics, the elderly, immunocompromised
patients, and patients who develop meningitis after a neurosurgical procedure.
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 If patients have focal neurologic deficits, obtundation, seizures, or papilledema (suggesting

increased ICP or an intracranial mass effect), defer lumbar puncture pending results of
neuroimaging.
 Treat acute bacterial meningitis as soon as possible, even before the diagnosis is confirmed.
 Common empirically chosen antibiotic regimens often include 3rd-generation cephalosporins (for
S. pneumoniae and N. meningitidis), ampicillin (for L. monocytogenes), and vancomycin (for
penicillin-resistant strains of S. pneumoniae and for S. aureus).
 Routine vaccination for S. pneumoniae and N. meningitidis and chemoprophylaxis against N.

meningitidis help prevent meningitis.
NEUROLOGICAL EXAMINATION:
 The major areas of the exam, covering the most testable components of the neurological system, include: 1. Mental
status testing (covered in a separate section of this web site) 2. Cranial Nerves 3. Muscle strength, tone and bulk 4.
Reflexes 5. Coordination 6. Sensory Function 7. Gait
 A feature of disease in an anatomically important part of the nerve  Muscle disease - muscle weakness 
Neuromuscular joint disease - muscle fatigue, rest relief  Peripheral neuropathy - asymmetrical weakness, sensory
changes  Nerve root disease - root pain  Spinal cord disease -- sensory plane, positive pathological signs, cystorectal
dysfunction  Brainstem disease -- cranial nerve symptoms + long tract signs+cross paralysis  Cerebellar disease - ataxia
 Subcortical disease - primary sensory impairment, motor and sensory deficits involving the face, upper and lower
limbs, and visual field deficits  Cortical disease - inability to speak or ignore or deny consciousness, seizures, cortical
lesions involving the face and upper limbs, not the lower limbs, no visual field defects.
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12. Infantile Diarrhea
Definition ❖ Increases in fluidity, volume and number of stools.

❖ Multiple pathogens and complex origins.
❖ High incidence during age of 6 months to 2 years
Classifications ❖ Acute < 2 weeks
❖ Persisting 2 weeks ~ 2 months
❖ Chronic > 2 months
Predisposing ❖ GI system: underdevelopment
factor ➢ poor function and low digestive enzyme
➢ heavy digestive burden
❖ immune system: underdevelopment
➢ systemic immunity : low immunoglobulin
➢ local immunity of GI: low SIgA
Cause of infantile Ⅰ—infection
diarrhea
❖ Intra-enteric infection
①Virus: rotavirus, norwalk virus, coronaviruss
②bacteria: escherichia coli (E . Coli)
➢ invasive : EPEC, ETEC
➢ non-invasive: EIEC, EGEC
③others: fungus, tuberculosis, parasites
❖ Extra-enteric infection: symptomatic diarrhea
Ⅱ—non-infectious
❖ Inappropriate feeding :
➢ inappropriate supplementary food: dietary diarrhea
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➢ food intolerance: deficiency of disaccharidase, lactose intolerance

❖ Allergic cause: food allergy
➢ induced by IgE
➢ induced by IgG
❖ Weather
➢ cold→ gastrointestinal movement ↑
➢ hot → thirsty → overeating, dyspepsia
Pathomechanism Types according to pathophysiology：
of infantile ❖ Osmotic diarrhea: hyperosmosis in intestinal tract (eg. lactose intolerance)
diarrhea ❖ Secretary diarrhea: increased secretion of intestinal juice ( eg. Zollinger-Ellison Syndrome)
❖ Exudative diarrhea： Inflammatory exudate of intestines (eg. infectious diarrhea)
❖ Dynamic diarrhea: enhancement of intestinal motility (eg. irritable bowel syndrome)
Pathomechanism of infantile diarrhea Causes are usually not single but compound for each patient
Pathogenesis Non-infectious diarrhea
Infectious diarrhea
1. non-invasive bacteria, enterotoxin
2. invasive bacteria
Direct invasion>>> small intestine & colon>>> intestinal wall
mucous hyperemia, edema, Exudation, ulcer, haemorrhage
exudative diarrhea bloody pus stools rectal tenesmus RBC, WBC, pus cell , phagocyte in stools
3. Virus infection
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Clinical Diarrhea, vomiting abdominal pain change of stool>>> Gastrointestinal symptoms

manifestations of Dehydration, shock electrolyte disturbances metabolic acidosis metabolic disorder>>>> Dehydration
infantile diarrhea electrolyte disturbances Disorder of acid base
infective toxic symptoms Fever, depress toxic encephalopathy MORDS>>> Extraenteric Systemic Symptoms
Assessment ❖ Excessive loss of water and electrolyte, especially loss of extracellular fluid
of Dehydration of infants: easy, severe, develop soon and recover soon
dehydration
and
electrolyte
disturbances
Danger signs of dehydration
Types of dehydration according to osmotic pressure (sodium level) of plasma
Diagnosis of Establish diagnosis is not difficult According to clinical symptoms and physical signs stool changing and
infantile diarrhea laboratory examination Assessment is more important
cause dehydration disturbance
electrolytes
infection non- degree type
acid-base
infectious
Differential No or few WBC in stools

diagnosis ❖ Physiological diarrhea: breast feeding with normal growth
❖ Disorder of digestion: lactose intolerance, food allergy
❖ Symptomatic Diarrhea: pneumonia
Abundant WBC and RBC in stools
❖ Dysentery : invasive salmonella typhimurium
❖ NEC (Necrotizing enterocolitis)
❖ Secondary intestinal intussusception
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❖ Inflammatory bowel disease

Treatment Principle of Treatment
❖ Reasonable Diet
❖ Antibiotic treatment
❖ Intensive nursing care
❖ Liquid therapy
❖ Symptomatic treatment
Feeding during ❖ Continue feeding child
diarrhea ❖ Give as much as child want
❖ Give small frequent feeds with multiple times
❖ Encourage anorexic child to eat
❖ Rotavirus gastroenteritis and lactose intolerance: diarrhea milk powder (Lactose-free
formula)
❖ Food allergy: ➢ deep degradation of milk protein ➢ amino acid milk powde
Antibiotic ❖ Indication for antibiotic using
treatment ➢ newborn or weak infant with severe complications
➢ invasive bacteria infection: pus and blood stool, infective toxic symptoms
❖ Chose of antibiotic
➢ according to possible pathogen: Gram staining - or +
➢ according to bacterial culture and drug sensitivity test
Fluid ❖ORS (Oral rehydration salts)
replacement ➢ WHO recommended
➢ preferred treatment for mild to moderate dehydration
➢ Prevent for losses of fluid and electrolyte
❖Vein fluid replacement
➢ Severely dehydrated
➢ shock must receive immediate and aggressive intravenous fluid therapy
ORS ❖ osmotic pressure ：2/3 tonic
❖ preferred for mild to moderate dehydration
➢ mild dehydration 50~80ml/kg/day
➢ moderate dehydration 80~100ml/kg/day
➢ prevention dehydration 50ml/kg, small frequent oral
❖ supply physiological maintenance and ongoing loss of fliud and electrolytes : slowly
replace within 12~16 hours, should dilute to 1/3 tonic
Intravenous ❖ Severe dehydration
fluid therapy ❖ Shock must receive immediate and aggressive intravenous fluid therapy
Total liquid volume needed: three part of supplement
❖ Complete correcting of the deficit of past loss
❖ Replacing ongoing loss of water and electrolytes
❖ Supply the physiological maintenance
Common solution of liquid therapy
❖ Nonelectrolyte solution:
➢ Glucose: 5%GS or 10%GS, tonic is zero
❖ Electrolyte solution :
➢ NaCl (NS): 0.9%NaCl (1 tonic) and 10%NaCl
➢ NaHCO3 : 5%NaHCO3 and 1.4%NaHCO3 (1 tonic)
➢ KCl: 10%KCl (need to Dilute to 0.33%KCl)
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➢ CaGS: 10% calcium gluconate

Configuration of different tonic solution
Principle of intravenous rehydration

❖ three determination
➢ ① qualitation (tonic)；② quantification；③ speed
❖ three priority ➢ ① fast to slowly；② hypertonic to hypotonic；③ NS to glucose
❖ three observation ➢ ① acidosis for NaHCO3 ； ② convulsion for CaGS； ③urine
for KCl；
The first day intravenous transfusion(1)
❖ Quantification: total volume = past loss + ongoing loss + physiological maintenance
➢ mild degree of dehydration 9 0~120ml/kg
➢ moderate degree of dehydration 120-150ml/kg 30ml per level
➢ severe degree of dehydration 150-180ml/kg
❖ Qualitation: average tonic of all fluid
➢ isotonic dehydration 1/2 tonic solution
➢ hypertonic dehydration 1/3 tonic solution
➢ hypotonic dehydration 2/3 tonic solution
The first day intravenous transfusion(2)
❖ Speed (fast to slow; hypertonic to hypotonic)
➢ Rapid rehydration stage: shock patient, 2:1 isotonic fluid, 20ml/kg, within 30-60 min
➢ Replacement for past losing: give half of total dose within 8-12 hr, 1/2 ~1/3 tonic,
8~10ml/kg.h
➢ maintain rehydration stage: finish the remnant doses (ongoing loss and
physiological maintenance) within 12-16 hr, 1/3 ~1/4 tonic, 5ml/kg.h
Summary for the first day transfusion
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The second day rehydration

❖ Evaluate effects of treatment
❖ Assess degree of dehydration again
❖ If relief, change intravenous transfusion into ORS
Treatment for electrolyte disturbances-- hypokalaemia, hypocalcemia
❖ Calcium supplement
➢ Convulsion: indicate possible of hypocalcemia
➢ 10%CaGS 0.5~1ml/kg/time, slowly ivgtt
❖ Kalium supplement
➢ See urine supply Kalium: severe dehydration with on urine, KCl is forbidden
➢ physiological requirements: 10%KCl 2-3ml/kg.d
Treatment of metabolic acidosis
❖ Mild and moderate degree of acidosis
➢ can self-corrected once dehydration corrected and effective circulation volume restored
❖ Severe acidosis
➢ should use NaHCO3 according to analysis of arterial blood gas ( ABG)
➢ For full correction of acidosis, NaHCO3 required (mmol)= Base deficit x body weight x 0.3, the first dose
usually give half dose of total
symptomatic treatment
Common drugs used in diarrhea
❖ Micro-ecological therapy: probiotics, prebiotics and synbiotics
➢ lactobacilli
➢ Bifidobacteria
❖ Antidiarrheal agents
➢ Adsorbents: SMECTA
➢ Inhibit secretion of intestine: racecadotril granules
➢ Mucous membrane protectors
Principle for treatment of chronic diarrhea
❖ Eliminating etiology: bacterial culture and drug sensitivity test, enteroscope
❖ Adjusting diet: lactose-free formula and amino acid milk powder
❖ Careful using antibiotics: secondary infection of fungus
❖ Micro-ecological therapy: probiotics, prebiotics and synbiotic
13. Pneumonia
* A potentially serious respiratory infection
* Diagnosis requires both clinical presentation and diagnostic studies
Introduction • The most frequent diagnosis in pediatric inpatient department : 1/3-1/2

• The most important cause of death in children from developing country
• Incidence peaks :between 1 and 5 years of age
• The most important one of four common pediatric diseases in China : pneumonia, diarrhea, anemia and
ricket
Definition • Pneumonia is an inflammation of the parenchyma of the lungs.
Causes Microorganisms: viral，bacterial and atypical organisms
Non-infectious causes: aspiration of food or gastric acid, foreign bodies, hydrocarbons and lipoid substances,
hypersensivity reactions, drug-or-radiation-induced pneumonitis
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Risk factors for• Lung disease: asthma, cystic fibrosis, respiratory anormaly
the • Anatomical problems: tracheoesophageal fistula
development of • Gastroesophageal reflux
pneumonia • Neurologic disorders
• Diseases which alter immune system: immunodeficiency, hemoglobinopathies
Classification 1. based on pathological features
Parenchymal pneumonia
• Brochopneumonia
• Lobar pneumonia
Interstitial pneumonia
Mixed type of pneumonia
2. based on etiology
Infectious Noninfectious
• Bacterial (dependent on age) • Viral (majority of • Aspiration • Allergic • Radiation associated •
pediatric pneumonias) • Mycoplasma, Chlamydia Immunologic
• Fungus • Tuberculosis • other
3. based on course of disease
• Acute Pneumonia – within one month, most in 2-3 weeks – Most common
• Prolonged Pneumonia – 1 month to 3 months
• Chronic Pneumonia – over 3 months – hard to treat , must search reason
4. based on clinical manifestations
• Mild pneumonia: Mainly involves respiratory system, no generalized toxic symptoms
• Severe pneumonia:Besides respiratory system, other systems might be severely involved
Respiratory failure
Circulatory system: congestive heart failure
Digestive system: abdominal distention , toxic intestinal paralysis
CNS: toxic encephalopathy
Other: body fluid derangement ,disseminated intravascular coagulation (DIC)
5. based on onset time
Community acquired pneumonia, CAP
Hospital Acquired Pneumonia, HAP
Pathology Lobar pneumonia: congestion stage
Lobar pneumonia: red hepatization stage
Lobar pneumonia: gray hepatization and resolution
Etiology Pathogen
Bacteria Virus Atypical organism
Newborns group B Streptococcus, E coli
Infants B. pertussis, Streptococcus respiratory syncytial virus Chlamydia trachomatis,
pneumoniae, Haemophilus parainfluenza viruses, Pneumocystis carinii
influenzae influenza virus, adenovirus
Young Pneumococcus, mycobaterial parainfluenza viruses, Mycoplasma
children tuberculosis influenza virus, adenovirus pneumoniae
Older Pneumococcus, B. pertussis, Mycoplasma
children mycobaterial tuberculosis pneumoniae, Chlamydia
and trachomatis
adolescents
- In developed countries, virus is the most common cause
- In developing countries, bacteria are the most common causes
- Streptococci is the most common bacterial cause
Pathophysiology • Edema and accumulation of mucus→bronchiolar obstruction
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• Walls of alveoli →thicken  Alveoli are filled with inflammatory exudates→impairs the normal exchange
of gases in the lungs
• Diminished ventilation of the alveoli →hypoxemia and carbon dioxide retention →interfere normal
metabolic process and normal function of the chief organs
Clinical Prodromal symptoms

manifestations • Upper respiratory tract infection: rhinitis, cough
General condition
• diminished appetite, restless,
• gastrointestinal disturbance: vomiting, anorexia, diarrhea,
Fever
• Temperatures are generally lower in viral pneumonia than in bacterial pneumonia.
• Infants may have hypothemia.
Cough
• dry cough →wet cough
• Neonates and infants may present with choking cough, groan.
Tachypnea
• The most consistent clinical manifestation of pneumonia
• Increased respiratory rate: ＞60 breaths/min in neonate, ＞50 in infants 11 months of age or less, ＞40 in
children over 11 months
• Increased work of breathing accompanied by supraclavicular, intercostal, and subcostal retractions, nasal
flaring, and use of accessory muscles
Cyanosis
• Cyanosis will appear when SaO2 ＜85% and unoxygenated Hb ＞5g/dl
• location: face, finger nails.
Physical findings depend on the stage of pneumonia
• Early course:
diminished breath sounds, scattered crackles, rhonchi, wheezing
difficult to localize the source of these adventitious sounds in very young children
• Development of increasing consolidation or complications:
cyanosis:
dullness on percussion
abdominal distention: gastric dilation from swallowed air
liver enlargement: downward displacement of the diaphragm
Severe pneumonia
• Acute • Manifestation: breath difficulty, nasal flaring, tachypnea, cyanosis, cardiovascular
Respiratory and central nervous system disturbance • Critera  Noninvasive ventilation: Oxygen
Distress saturation index (OSI)=PaO2 /FiO2 ≤300  Invasive ventilation: OSI=FiO2 X mean
Syndrome airway pressure X 100/SpO2
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• Circulatory • Myocarditis: pallor, tachypnea, and arrhythmia, low and dull heart sound
system: • Heart failure – tachypnea, breath rate more than 60/min – tachycardia, heart rate is
congestive heart quicker than 160 -180 beats/min – suddenly extreme restless, obvious cyanosis, pallor
failure or grey complexion – heart sound decrease, gallop rhythm, high distention of jugular
vein occurs – liver enlarged rapidly, liver can be palpable 3cm at right subcostal region
– oliguria, facial edema and edema of lower extremity
• shock: gram negative bacillus , microcirculation dysfunction
• Central nervous • Change of degree of consciousness: - agitation and drowsiness
system: toxic • Cerebral edema – consciousness disturbance – Convulsion – irregular respiratory
encephalopathy rhythm – hypertonia anterior fontanel
• Digestive • Mild case : vomit, diarrhea, and abdominal distention
system: toxic • Abdominal distention – gastric distention – due to swallowed air or paralytic ileus
intestinal paralysis • Enlarged liver – downward displacement of right diaphragm – superimposed
congestive heart failure
• Severe case – toxic paralysis of the intestine – bowel sounds disappear –
hemorrhage : melena, hematemesis
• Disseminated • Anemia
intravascular • Bleeding tendency – bleeding at sites of vein puncture – scattered petechiae over
coagulation (DIC) the skin – gastric-intestinal bleeding
• Activation of clotting - microvascular and macrovascular thrombosis
Complications • Pleural effusions • Pneumatoceles • Empyema • Pneumothorax
Laboratory ---blood test
finding  White blood cell count(leukocyte)
• virus →normal or slightly elevated
• bacterium ↑ WBC may be normal : when the pathogen is bacterium if the patient is malnutrition or in very
severe condition
 C reactive protein (CRP)
– increase: in bacterial infection
– normal: in viral infection
--- Etiologic agent
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 Isolation of an organism
– nasopharygeal secretions (deep coughing, tracheal suction, or pleural fluid obtained at thoracentesis)
– Blood culture: bacteria pneumonia
– Sputum culture
– Pleural fluid
– Lung biopsy
– BALF
 Serologic testing：specific antibody to virus, mycoplasma pneumoniae
Radiological  Methodology:
finding • Chest X-ray
• Chest CT
 Findings:
• Viral: hyperinflation, segmental atelectasis, interstitial infiltrates
• Mycoplasma : various, lobar or bronchopneumonia
• Bacterial: Lobar consolidation, more common in the older child, diffuse infiltrates
Diagnosis • Symptoms：fever, cough and tachypnea.

• Signs：persistent moist rales in the lung
• Chest X-ray：spotted-like or patchy shadows over the lung field
• Severe case：Congestive heart failure， Toxic encephalopathy，Toxic intestinal paralysis， DIC
• Complications：empyema，pyopneumothorax and pneumatocele
Diagnostic Difficulties in Pediatric Pneumonia
• Sputum samples are often unobtainable
• Some common pathogens are not easily cultured: C. pneumoniae and M. pneumoniae
• Nasopharyngeal samples are unreliable due to high asymptomatic carriage rates
Differential ---Acute bronchitis
diagnosis • Symptoms：mild
• Breath sound：coarse，or a few rales (sputum) at the end of inspiration and early expiration.
• Chest X-ray：lung markings↑, no spotted or patchy shadows
---Bronchial foreign body
• History：foreign bodies aspiration, sudden onset of cough and wheezing
• Physical signs：bronchial obstruction -complete obstruction ：atelectasis -incomplete obstruction ：
emphysema.
---Pulmonary tuberculosis
• History: recent contact with TB
• Toxic symptoms of TB：fever，diminished appetite， weight loss, irritability， malaise，easy
fatigability，night sweating
• Laboratory test: -Radiogram -ESR↑ -Positive tuberculin test, T-SPOT, XPERT
Treatment Principles of treatment – Control infection – Improve ventilation – Prevent complications
General • Good and enough nutrition
treatment • Maintain good ventilation :
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– relieving hypoxia and CO2 retention

– when the secretion in airway is thick →intermittent ultrasonic inhalant therapy is
recommended.
– Sputum suction in time：the best way to keep normal ventilation of airway
• Oxygen if indicated: SaO2≤92% PaO2≤60mmHg
– oxygen inhalation can be administrated with nasal cannula, the flow is 0.5-1L/min.
– If the hypoxia continues ：Oxyhood may be used with a flow of 2-4L/min.
– when respiratory failure occurs ：intubation and ventilation needed
• Analgesics and antipyretics
• Expectorants
Anti-microbial  Empiric therapy is justified as initial management as the specific bacteriological
Therapy etiology is unknown and delaying therapy while trying to find a diagnosis may be
injurious to the patient
Choice of antibiotics
Factors to consider:
• The age and any underlying illnesses
• The degree of illness and the kinds of bacteria. (the best way →give the most sensitive
antibiotic to the bacteria by medicine sensitive test)
• Other: spectrum y of activity, pharmacokinetics, dosage, cost, frequency and route of
administration, adverse effects, development of resistance
• Palatability
• Chlamydia Macrolides- azithromycin
• Mycoplasm- azithromycin
• Staph aureus- clindamycin vancomycin
• S. pneumonia- penicillin
• H. influenza-amoxicillin
• E. coli- amoxicillin
Duration of Therapy
• Total of 7 to 10 days of Antimicrobial therapy
• Complications such as pleural effusion or empyema require 2 to 4 weeks of therapy
• Staphylococcal empyema is 3 to 4 weeks
Corticosteroids • Indications
- Apparent toxic symptoms, complicated with shock, sepsis,
- Severe wheezing, increased respiratory secretions
- Severe acute respiratory distress
- Pleural effusion
- High fever with excessive inflammatory reactions
• Medications:
- Dexamethasone 0.2-0.4mg/(kg.d) or Hydrocortisone 5- 10mg/(kg.d)
- Duration: 3-5 days
Flexible • Indications - Etiologic study - Therapeutic role： atelectasis,consolidation
bronchoscopy • Methods： -bronchoaveolar lavage - instill drugs - remove endogenic foreign body:
plastic bronchitis
Other • Treatment of complication:
treatment: – Pleurocentesis
– Surgery
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14. Growth Hormone Deficiency
Introduction of growth Growth hormone

hormon • Growth hormone (GH) is a single-chain protein of 191 amino acids with a molecular size of
approximately 22 kDa that is produced by the pituitary somatotroph cells
• GH production begins early in fetal life and continues throughout life
Chemical structure of GH
The image at left is a space-filling, all-atom
representation, and the image on the right is a ribbon
representation of the same protein
Hypothalamic-pituitary-growth axis
GH secretion is directly controlled by
• Hypothalamic growth hormone-releasing hormone (GHRH)
• Somatostatin 
Insulin-like growth factor-1 (IGF-1)
• The downstream product of growth hormone is IGF-1
• The predominant action of GH is to stimulate hepatic synthesis and secretion of IGF-1
• IGF-1 is the mediator of the majority of the growthpromoting actions of GH\
• In turn, IGF-1 directly inhibits GH secretion by a negative feedback regulation loop
GH secretion
• GH secretion is pulsatile
• Serum GH concentration may be undetectable between pulses unless an ultrasensitive assay is
employed
• Peak GH secretory activity occurs within an hour after the onset of deep sleep
As a result, random measurement of serum GH will likely not distinguish patients with GH deficiency
or GH excess from normal subjects
Specific effects of GH
 GH stimulates linear growth in children by acting directly and indirectly (via the synthesis of IGF-1)
on the epiphyseal plates of long bones.
 GH also has specific metabolic actions including:
• Increased lipolysis and lipid oxidation
• Stimulation of protein synthesis
• Antagonism of insulin action
• Phosphate, water, and sodium retention
Definition and etiology Short stature
of GHD Short stature is defined as a height that is more than 2 standard deviations (SD) below the mean
height for individuals of the same sex and chronologic age in a given population, which corresponds to
a height that is below the 2.3 percentile
Growth chart
Growth chart is an indispensable tool to know the child’s growth percentiles
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Growth Hormone Deficiency, GHD

• when a child is not following the normal, predicted growth curve, an evaluation for underlying
illness and central nervous system abnormalities is required
• GHD is a rare condition in which the body does not make enough GH
• Without enough GH, a child is likely to grow slowly and be much shorter than other children of the
same age and gender
Classification Cause
Primary forms
Genetics POU1F1, PROP1, GH-1, GHRHR, etc
Born Hypothalamic-pituitary dysplasia
Idiopathic Causes cannot be found
Acquired forms CNS tumors, trauma, inflammation, etc.
Transient forms Preadolosence, hypothyroidism, psychosocial
deprivation
Diagnosis Clinical manifestations + Auxiliary examination = Diagnosis
Clinical ✤ Clinical assessment of the growth-retarded child is the single most useful
manifestations parameter in diagnosing growth disorders
✤ The clinical significance of the short stature depends on
- height velocity
- severity of the short stature
- genetic potential
①Abnormal growth velocity--Growing slower than the following rates:
• <7cm/ year (under 3 years old)
• <5cm/ year (3 years old and prepubescent)
• <6cm/ year (puberty)
②Height ≤-2SD or 3 percentile

③ Symmetrical short stature with a childish face
④ Normal intellectual development
Auxiliary examination:
⑤Delayed bone age; e.g: Bone age of a 7-year-old GHD boy is only 3 years
⑥Low concentration of serum IGF-1
⑦GH stimulation tests—
▸ The stimulation tests are performed after an overnight fast
▸ After the pharmacologic agent is administered, serum samples are
collected at intervals designed to capture the peak stimulated GH level
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▸ most pediatric endocrinologists defined a “normal” response by a serum

GH concentration of >10 ug/L
• GH stimulation test is a valuable diagnostic tool when combined with
auxologic data and measurements of IGF-1 and IGFBP-3.
• The peak stimulated GH level less than 10ug/L suggests GH deficiency
⑧Magnetic resonance imaging (MRI)
After the clinical and biochemical diagnosis of GHD is made, it is essential to
obtain an MRI of the brain to exclude the possibility of a pituitary tumor and
find the possibility of morphologic abnormalities of pituitary gland, such as
anterior pituitary hypoplasia, pituitary stalk agenesis, and posterior pituitary
ectopia
Diagnostic point
Symmetrical short stature
Slow growth velocity
Normal intellectual development
Delayed bone age
low serum concentrations of GH, IGF-1
Rule out other diseases
Differential diagnosis ✧ FSS (Familial Short Stature)
✧ SGA (Small For gestational age)

• SGA is defined as a weight and/or length at birth below the 10th percentile for gestational age
• Most SGA infants display sufficient catch-up growth to attain a height above -2 SD by the age of 2
years, whereas 10 percent remain short throughout childhood and adolescence, which called SGA
continued short
✧ Turner Syndrome
• Turner syndrome is a sex chromosome disorder caused by loss of part or all of an X chromosome
• Short stature combined with a stocky appearance is the most common clinical feature of Turner
syndrome
• The diagnosis is confirmed by karyotype analysis
Type of chromosome abnormalities in Turner syndrome
• The main anomalies of turner syndrome are shown in the right picture,
including a short and webbed neck, low hairline, elbow deformity,
constriction of aorta, underdeveloped gonadal structures and no
menstruation, etc
• If left untreated, the adult height in Turner syndrome is approximately
20 cm below that of the general female population
Treatment GH replacement therapy

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• Treatment with GH is appropriate for children with GH deficiency GH replacement therapy

• The common dose of GH is 0.1 IU/kg/d
Administration of GH in the evening is frequently suggested, based on the rationale that this more
closely mimics the predominance of GH secretion during sleep
• The GH dose is adjusted based on growth response, serum IGF-1 levels and body weight
• When given for the treatment of GH deficiency, GH therapy is clearly effective
• Children who have an inadequate growth response to GH therapy should be reevaluated
Adverse effects of GH
• Treatment of children with recombinant human GH has generally been safe
• Acute effects
① headaches (the most common treatment-associated)
② insulin resistance and disorders of glucose intolerance
③ a slightly higher risk of developing idiopathic intracranial hypertension, increased intraocular
pressure, slipped capital femoral epiphysis, and worsening of existing scoliosis
Duration of therapy
• GH therapy is generally continued at least until linear growth decreases to less than 2.0 to 2.5
cm/year
15. Congenital Hypothyroidism，CH
Introduction of thyroid Thyroid gland

hormone The thyroid is a butterfly-shaped gland in the middle of the neck
• Thyroid is an endocrine gland situated at the root of the neck on either side of the trachea
• It makes two thyroid hormones, namely thyroxine (T4) as the major product and the active hormone
triiodothyronine (T3) as the minor product
• Most T3 is produced by deiodination of T4 in peripheral tissues
Thyroid Ontogenesis
• T4 and T3 synthesis and secretion occur from the 12th weeks of gestation
• Hypothalamic-pituitary-thyroid axis is functioning and independent of the maternal axis by the 30th
gestational weeks
Structure and Synthesis of thyroid hormone: Thyroid hormones are made from tyrosine and iodine. The
major form of thyroid hormone in the blood is thyroxine (T4), which has only a slight effect on
metabolism. T4 is converted to the active T3 (three to four times more potent than T4) within cells by
deiodinases (5'-iodinase)
Regulation of thyroid hormones
✧ The secretion of thyroid hormone is regulated within the hypothalamus-pituitary thyroid axis.
• The hypothalamus produces thyrotropin-releasing hormone (TRH)
• TRH stimulates the pituitary gland to produce thyroid stimulating hormone (TSH)
• TSH stimulates the thyroid gland to secrete the hormone thyroxine (T4)
Physiological role of thyroid hormones
✧ Thyroid hormones are primarily responsible for regulation of metabolism.
• Increase oxygen consumption
• Stimulate protein synthesis
• Influence growth and differentiation
• Affect carbohydrate, lipid and vitamin metabolism
What’s hypothyroidism ☞ Hypothyroidism results from deficient production of thyroid
hormone or a defect in thyroid hormone receptor activity
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What’s congenital ☞ Congenital hypothyroidism (CH) is defined as thyroid hormone

hypothyroidism deficiency present at birth
• The incidence is between 1:2000 to 1:4000 newborns worldwide
Etiology of congenital 1- Primary CH
hypothyroidism • Thyroid dysgenesis
• Disorders of thyroid hormone synthesis and secretion
2- Central CH
• TSH deficiency
• Defects in transcription factors associated with anterior pituitary development
• TRH secretion defect
• TRH resistance
3- Peripheral CH
• Resistance to thyroid hormones
• Transport defects in thyroid hormone
4- Transient CH
• Maternal antithyroid drugs
• Iodine deficiency or iodine exposure
• Maternal TSH receptor-blocking IgG antibodies
Manifestations symptoms and signs of CH
Newborns • Over 95% of newborns with CH are asymptomatic at birth to the trans-placental
passage of maternal T4
• Post maturity (gestation extends beyond 42 weeks)
• Birth weight and length are normal
• Head size may be slightly increased because of myxedema of the brain
over the • Lethargy
first few • Hoarse cry
months of • Feeding difficulties
life • Constipation
• Puffy (myxedematous) and/or coarse facies
• Macroglossia
• Umbilical hernia
• Large fontanels
• Hypotonia
• Dry skin
• Hypothermia
• Prolonged jaundice
Coarse facial features: 㽋 The eyes appear far apart 㽋 The bridge of the broad nose
is depressed 㽋 The palpebral fissures are narrow 㽋 The eyelids are swollen 㽋 The
mouth is kept open 㽋 The thick and broad tongue protrudes
If • Slow linear growth
undiagnosed • Loss of IQ
at a later • Ataxia
age • Gross/fine motor incordination
• Hypotonia and spasticity
• Speech disorders
• Attention deficit
• Strabismus
• Sensorineural deafness
Diagnosis Newborn screening
✧CH is one of the most common preventable causes of intellectual disability (mental retardation)
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✧Newborn screening programs allow for early identification and treatment of affected infants to
minimize complications
• Newborn screening is done using heel prick sample on dried blood spot filter paper at 2nd and 5th
days of life
Three approaches are being used for screening:
① Initial T4 assay, with follow up TSH assay
• T4 is measured first
• TSH is measured only if T4 is below a certain concentration
② Initial TSH assay
③ Simultaneous T4 and TSH assays
• It is the most sensitive approach but incurs higher cost
☆Either approach detects the majority of infants with congenital primary hypothyroidism, and each has
its advantages and disadvantages
Normal range for neonate screening
T4 84-210nmol/L 6.5-16.3ug/dl
FT4 12-28pmol/L 0.9-2.2ng/dl
TSH 1.7-9.1 mu/L 1.7-9.1 uU/ml
☆Abnormal values on screening should always be confirmed by a venous sample, using age appropriate
cut-offs
Serum tests of thyroid function
☆ To confirm or exclude the diagnosis of hypothyroidism, a blood sample should be obtained by
venipuncture to measure TSH, free T4, total T4 and T3
High TSH, low free T4- primary hypothyroidism
High TSH, normal free T4 or total T4- Subclinical hypothyroidism
Low or normal TSH, low free T4- Central hypothyroidism
Other auxiliary examination

☆ If the diagnosis of hypothyroidism is confirmed, other studies may be performed to identify the
cause.
• Thyroid ultrasonography and color flow Doppler -- to characterize thyroid shape, size, and location
• Thyroid radionuclide uptake and scan --Tc99m, I 123 to identify cases of thyroid dysgenesis
• X-ray --Retardation of osseous development
• Serum thyroglobulin(Tg) concentration --Tg can reflect the presence and activity of thyroid gland
tissue
• Thyroid autoantibodies
• Genetic test
✧It's worth noting that
• These auxiliary examination usually do not alter treatment
• They are considered optional
• They be done only if clinically indicated, if the results help make a management decision
Treatment Principle of treatment
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• Infants with low T4 and elevated TSH should be started on Levothyroxine (L-T4) as soon as the
diagnosis is made
• Preferred preparation is Sodium Levothyroxine. It has uniform potency, reliable absorption and good
bioavailability
• Daily dose should be crushed and placed directly on the tongue in the morning
• Initial dose of L-Thyroxine is 10-15 μg/Kg/day for free T4 in 2 weeks and TSH in 4 weeks to normalize
✧ Free T4 should be kept in the one-upper half of normal range with the TSH suppressed in the normal
range for age
Dose of L-T4
Age Ug/kg/d
0-6m 8.5-10
6-12m 5-8
1-5y 5-6
6-12y 4-5
12y to 2-3
adult
Monitoring
✧T4 and TSH should be monitored according to following schedule
The initiation of treatment 2 weeks later
0 to 1 year Every 1-2 months
1 year to 3 years Every 3 months
Beyond 3 years Every 6 months
Any dose change 4 weeks later
✧ At 2~3 years old, confirmation of diagnosis may be necessary for some infant to rule out the
possibility of transient hypothyroidism
Prognosis • Final outcome in CH is closely related to the :
--nature and severity of underlying thyroid abnormality
--age at diagnosis
--age of onset of treatment
--adequacy and regularity of treatment
• Worldwide neonatal screening programs for CH have a significant impact on reducing intellectual
deficits in hypothyroid infants diagnosed and treated early
• Early diagnosis and adequate treatment from 1st week of life leads to normal linear growth and
intelligence
16. Central Precocious Puberty

01. Normal pubertal development
Introduction of pubertal ✧The most visible changes during puberty are growth in stature and development of secondary
development sexual characteristics Introduction of pubertal development
✧ The mean age for the first signs of puberty
• Girls--10.5 years of age (8-12 years)
• Boys--11.5 years of age (9-13 years)
✧ Puberty is marked by an increase in the pulsatile secretion of gonadotropin-releasing hormone
(GnRH) from the hypothalamus
✧GnRH stimulates the the pituitary gland to release pulses of luteinizing hormone (LH) and
folliclestimulating hormone (FSH)
✧ LH and FSH stimulate the sex organs to produce estrogen and testosterone
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Sequence of pubertal Adolescents follow a predictable sequence of pubertal maturation

development ✧Girls
The earliest secondary sexual characteristic on physical examination is breast development
✧Boys
The earliest stage of maturation on physical examination is an increase in testicular size (volume
≥4 mL and length ≥2.5cm)
Stages of pubertal developntmet
• Sexual maturity ratings (Tanner stages) for pubic hair, breast, and male genitalia consist of five
categories, with stage 1 representing prepuberty and stage 5 representing adult development
02. Precocious puberty

Definition of precocious • Precocious puberty is traditionally defined as the onset of secondary sexual characteristics
puberty before the age of eight years in girls and nine years in boys
Classification of precocious 1- Central precocious puberty (CPP)
puberty 2- Peripheral precocious puberty
3- Benign or nonprogressive precocious variants
Mechanism of precocious Type Etiology Mechanism
puberty CPP Idiopathic, Secondary to CNS lesions Activation of hypothalamic-
pituitarygonadal axis with
GnRH secretion leading to
increased LH and FSH
secretion
Peripheral Adrenal, ovarian, testicular tumors; Excess sex steroid production
precocious Autonomous gonadal activation, such as (↑estradiol or testosterone)
puberty McCune-Albright syndrome, congenital with suppression of
adrenal hyperplasia hypothalamic-pituitary-
gonadal axis (↓LH and FSH)
Benign or Premature thelarche; Premature Unknown but not associated
nonprogressive adrenarche; isolated premature menarche with full activation of the
precocious hypothalamic-
variants pituitarygonadal axis
03. Central precocious puberty

Definition of CPP ✧ Central precocious puberty (CPP; also known as gonadotropindependent precocious puberty) is
caused by early maturation of the hypothalamic-pituitary-gonadal axis
Characteristics of CPP • CPP is characterized by sequential maturation of breasts and pubic hair in girls and of testicular
and penile enlargement and pubic hair in boys
• CPP children have accelerated linear growth for age, advanced bone age, and pubertal levels of LH
and FSH
Causes of CPP ① Idiopathic --80% to 90% of girls with CPP and 25% to 60% of boys with CPP are idiopathic
② Secondary to CNS lesions --eg, hypothalamic hamartomas, CNS tumors and lesions, cranial
radiation
③ Post-early exposure to sex steroids --after treatment for peripheral precocity (eg, Treated
congenital adrenal hyperplasia, McCune- Albright syndrome, Familial male precocious puberty)
How CPP affects the • Children with CPP usually do not achieve their full height. They may be taller when younger
children compared to their peers but when older they are short
• Girls can become more emotional, moody, and irritable at a younger age
• Boys can become more aggressive and develop a sex drive that is very inappropriate for their
young age
Symptoms of CPP ⭐ Symptoms in girls
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• Breast development
• Menstruation at a young age
⭐ Symptoms in boys
• Testicles enlargement
• Voice deepening
• Excess facial hair
⭐ Common symptoms in girls and boys
• A growth “spurt” before their peers
• Pubic or underarm hair development
• Acne
• mature body odor
Auxiliary examination Laboratory evaluation
Basal serum LH, FSH, estradiol/testosterone > LH concentrations greater than 0.2 to 0.3 mIU/mL
suggest CPP
GnRH agonist stimulation test > Stimulated LH concentration post-GnRH agonist greater than 3.3 to
5.0 mIU/L suggest CPP
Imaging
Bone age: Bone age of children with CPP is significantly advanced for chronologic age (eg,≥2
standard deviations)
Pelvic ultrasound: Pelvic ultrasonography may be a useful investigation to help differentiate
between CPP and benign pubertal variants
Brain magnetic resonance imaging (MRI): Brain MRI is recommended to rule out CNS abnormalities
Treatment ✧ Goals of treatment
• A primary goal of treatment for CPP is to allow a child to grow to a normal adult height
• Another goal of therapy is to relieve psychosocial stress
✧ pubertal progression in CPP can be treated by administration of a GnRH agonist
mechanism
GnRH agonist administration results in an initial transient stimulation of gonadotropin secretion

from the pituitary, followed by a complete, but reversible, suppression of the pituitary-gonadal axis
✧ Decision to treat
• The decision of whether to treat CPP with a GnRH agonist depends upon the child’s age, the rate
of pubertal progression, height velocity, and the estimated adult height

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Mithushaa Shanmugananthan

Introduction & Infant Feeding………………………………………………01- 14

Growth and Development…………………………………………………….14- 23

Neonatal Septicaemia (Sepsis)…………………………………………….23- 24

Hypoxic-Ischemic Encephalopathy (HIE)……………………………….27- 29

Congenital heart disease………………………………………………….....40- 50

Acute poststreptococcal glomerulonephritis………………………….55- 60

Growth Hormone Deficiency……………………………………………….94- 97

Congenital Hypothyroidism，CH………………………………………….97- 100

Central Precocious Puberty………………………………………………..100- 102

01. Introduction & Infant Feeding

• Focus on the growth and development of children

• Focus on the prevention of diseases of children

• Focus on the treatment of diseases of children

• Raise child’s physical endowment

• Decrease the morbidity and mortality rate

• Improve the living quality of the children

Major causes of death:

Under 1y 1. perinatal conditions

3. sudden infant death syndrome

Critical preventive care for young children (GOBI-FFF)

（UNICEF--United Nations International Children’s Emergency Fund）

G-- Growth monitoring

O-- Oral rehydration

B-- Breast feeding

Introducing new devices and new drugs.

Influence of the life style of the parents.

Childhood Age Staging

Thalidomide Thalidomide was developed in the 1950s

Physical characteristics of children in •

Genitalia stage for boys(G1 to G5)

Pubic hair stage(PH1 to PH5)

Breast development for girls(B1 to B5)

• Denotes the process of inducing or providing immunity artificially by administering an

• Routine immunization dramatically decreased morbidity and mortality from a variety of

• Denotes the physical act of administrating any vaccine or toxoids

• Vaccine - a suspension of live or inactivated microorganism or fractions there of

• Bacille Calmette--Guerin BCG

• Diphtheria Pertussis Tetanus DPT

The nutritional vulnerability

Low nutritional stores

High nutritional demands for growth

Rapid neuronal development

Category of nutrients（2000 Chinese Dietary Reference Intakes）

 Other diet elements: cellulose, water

Macronutrients Energy produced

Gross Energy Intake

Definition: Exclusive breastfeeding is fed no foods or fluids, even water.

Summary of differences between milks

Two patterns for partial breast-feeding

Components of human milk

Colostrum : “first milk"; immature milk produced in 4-5 days post-partum

The changes of the components during nursing (g/L)

colostrum middle maturity

PRO 22.5 15.6 11.5

FAT 28.5 43.7 32.6

CHO 75.9 77.4 75.0

Mineral 3.08 2.41 2.06

Ca 0.33 0.29 0.35

P 0.18 0.18 0.15

• Many white cells

• protects against infection and allergy

• protects against infection

• clears meconium; helps prevent jaundice