BACHELOR OF SCIENCE IN NURSING:

CARE OF MOTHER AND CHILD AT RISK OR

WITH PROBLEMS (ACUTE AND CHRONIC)

COURSE MODULE COURSE UNIT WEEK

2 6b 8
Newborn Screening

✔Discuss the course and unit objectives

✔ Comprehend study guide prior to class attendance
✔ Read required learning resources; refer to unit terminologies for jargons
✔ Actively participate in classroom discussions
✔ Accomplish and submit assigned course unit tasks on time
✔ Participate in weekly discussion board (Canvas) Answer and submit course unit tasks

At the end of this unit, the students are expected to:

Cognitive:
1. Identify the significance of Newborn Screening
2. Describe the most common disorders identified in newborn screening
3. Discuss the benefits of participating in newborn screenings.
4. Recognize the symptoms of the most commonly diagnosed disorders from the newborn screen.
5. Identify the follow-up necessary for patients with positive screening results.

Affective
1. Listen attentively during class discussions
2. Demonstrate tact and respect of other students opinions and ideas
3. Accept comments and reactions of classmates openly.
Psychomotor:
1. Perform a systematic assessment of a high-risk newborn.
2. Integrate knowledge on the disorders that can be assessed through newborn screening.
3. Provide nursing care that meets the immediate and long-term needs of the family.

Newborn Screening Center, Institute of Human Genetics, National Institute of Health,University of the
Philippines Manila) https://www.jica.go.jp/project/philippines/0600894/04/pdf/ppt_13.pdf

NEWBORN SCREENING

Newborn screening (NBS) is a simple procedure to find out if a baby has

congenital metabolic disorder that may lead to mental retardation and even
death if left untreated.
This public health program detects treatable disorders in newborns, allowing
treatment to begin often before symptoms or permanent problems occur.
Newborn screening not only saves lives but can also improve the health and
quality of life for children and their families.

Within the first 24 to 48 hours after birth, babies undergo a simple heel stick
and a few drops of blood are collected on a special paper card. Providers test
those dried blood spots for a variety of different congenital disorders, or
conditions that are present when the baby is born. Newborns are also screened
for hearing disorders and certain serious heart problems using methods other
than dried blood spots.

● The Department of Health (DOH) Advisory Committee on Newborn Screening (ACNBS) has approved
the implementation of the expanded newborn screening program. The trial for expanded newborn
screening is currently being conducted in selected hospitals in Metro Manila and its implementation will
start on January 2014.

● Newborn screening program in the Philippines currently includes screening of six disorders: congenital
hypothyroidism (CH), congenital adrenal hyperplasia (CAH), phenylketonuria (PKU), glucose-6-
phosphate dehydrogenase (G6PD) deficiency, galactosemia (GAL) and maple syrup urine disease
(MSUD). The expanded screening will include 22 more disorders such as hemoglobinopathies and
additional metabolic disorders, namely, organic acid, fatty acid oxidation, and amino acid disorders. The
latter are included in the standard care across the globe.

● The expanded NBS will be offered as optional to parents in all participating facilities. First option is the
screening of six disorders at ₱550, which is included in the newborn care package for Philhealth
members and the second option is the full complement of disorder at ₱1500. At present, there is on-
going discussion with Philhealth to increase subsidy for expanded newborn screening.
 ● The formal recommendation to expand the coverage of the NBS program was prompted by the results
of the study Enhancing case detection of selected inherited disorders through expanded newborn
screening in the Philippines by Dr. Carmencita Padilla and Dr. Tomas Aguirre of University of the
Philippines Manila. The data of Filipino newborns screened through the California newborn screening
program (CNSP) from 2005 to 2009 revealed that serious disorders were detected from CNSP which
are not included in the existing program of the country.

● The screening of more disorders will save more lives and reduce unnecessary negative health
outcomes of Filipino newborns.

● Newborn screening is a procedure intended for early identification of infants who are affected by certain
genetic, metabolic, or infectious conditions that may lead to mental retardation or morbidity if left
untreated. The NBS was integrated into the public health delivery system with the enactment of
Republic Act 9288 or Newborn Screening Act of 2004.

● In the Philippines, the mandate for performing Newborn Screening on every baby is RA 9288 known as
the “Newborn Screening Act of 2004” with its Implementing Rules and Regulations.

Why is it important to have newborn screening?

Most babies with metabolic disorders look normal at birth. One will never know that the baby has the
disorder until the signs and symptoms are manifested. By this time, irreversible consequences are already
present.

When is newborn screening done?

– Ideally done on the 48th to 72nd hour of life (first 2 to 3 days of life).
– May also be done 24 hours from birth since some disorders are not detected if the test is done earlier
than 24 hours from birth.

How is newborn screening done?

• Using the heel prick method, a few drops of blood are taken from the baby’s heel
• Blotted on a special absorbent filter card
• Blood is dried for 4 hours and sent to the Newborn Screening Center

Who may collect the sample for newborn screening?

A Trained
• physician
• nurse
• midwife or
• medical technologist

Where is newborn screening available?

• Available in participating Newborn Screening Facilities that includes
– hospitals
– lying-in centers
– RHU’s
– health centers.
• If babies are delivered at home, the baby may be brought to the nearest Newborn Screening Facility.

When are newborn screening results available?

• Seven (7) working days from the time the newborn screening samples are received parents should claim
the results from their physician, nurse, midwife or health worker.
• Any laboratory result indicating an increased risk of a heritable disorder (i.e. positive screen) shall be
immediately released, within twenty-four (24) hours, so that confirmatory testing can be immediately done.
• A positive screen means that the newborn must be referred at once to a specialist for confirmatory testing.
and further management.
Out of Range Results
If the screening detects one or more conditions, the result is "positive" or, more accurately, "out of
range." The child's health care provider or someone from the state health department will notify the
parents, usually within 2 to 3 weeks, if the results are out of range.

This result does not mean the child definitely has the condition detected. Sometimes, the tests produce a
"false positive," meaning that even though the test result was positive, the infant does not actually have
the disease.

If the test result is positive, it is very important for the infant to undergo additional testing right away to
confirm and diagnose any specific condition(s). Screening tests and diagnostic tests are not the same. If
a baby is diagnosed with a condition, his or her health care provider and other providers will recommend
a course of treatment.

What are the roles of the RHU staff?

• Advocacy for the newborn screening of every baby. This starts during pregnancy. The family is also
advised to start saving for the Php550.00 that is needed for the screening. The savings must start
during pregnancy.
• Sample collection
• Assures transport of specimen to the nearest Newborn Screening Facility within twenty-four (24) hours
following collection of the sample
• Advice and counsel parents upon receiving the screening results

The Importance of Following Up

Newborn screening is used to detect serious medical conditions. If not treated, some of these conditions
can cause lifelong health problems; others can cause death.

If your child’s health care provider or the state health department calls you about your infant’s newborn
screening results, it is important to follow up quickly. Follow their instructions to get care for your baby.

Newborn screening makes early diagnosis possible so that treatment can begin immediately—before
serious problems can occur or become permanent. This approach helps to ensure the best possible
outcomes for babies.
What are the most common newborn screening tests?

1. CONGENITAL HYPOTHYROIDISM
● Congenital hypothyroidism may have a number of causes and can be either permanent or transient.
Transient CH is frequently associated with maternal Graves disease that was treated with antithyroid
drugs.
● The majority of cases are sporadic (nonhereditary), but approximately
15% of all cases are transmitted as an autosomal dominant trait.
● The most common pathogenesis is thyroid dysgenesis, mostly with
unknown causes. Worldwide, the most common cause of CH resulting in
hypothyroidism is iodine deficiency.
● In some conditions, the thyroid deficiency is severe, and manifestations
develop early; in others, the symptoms may be delayed for months or
years.
● Early detection and prompt initiation of treatment are essential because
their delay will result in various degrees of cognitive impairment, in which
the IQ loss has a direct relationship to the time treatment is initiated.
● If treatment is implemented from 0 to 3 months of age, the mean IQ
attained is 89 (range, 64–107); if treatment begins at 3 to 6 months,
mean IQ will reach 71 (range, 36–96); treatment initiated after 6 months
of age will result in a mean IQ of 54 (range, 25–80).
● It affects all races and ethnicities, but it is more prevalent among Hispanic
and American Indian or Alaskan Native people (1 in 2000 to 1 in 700
newborns) and less prevalent among African Americans (1 in 3200 to 1 in
17,000 newborns).
● Infants with Down syndrome have a much higher rate of either permanent or transient forms of the
disorder (approximately 1 in 140 newborns).
 ● Also, a higher incidence of other congenital abnormalities has been observed in infants with CH.
Many preterm infants have transient hypothyroidism (hypothyroxinemia) at birth as a result of
hypothalamic and pituitary immaturity. Infants born before 28 weeks of gestation may require
temporary thyroid hormone replacement.

Diagnostic Evaluation
● Because CH is one of the most common preventable causes of cognitive impairment, early
diagnosis and treatment of this disease are essential interventions. Neonatal screening consists of
an initial filter paper blood spot thyroxine (T4) measurement followed by measurement of thyroid-
stimulating hormone (TSH) in specimens with low T4 values
● Tests are mandatory in all U.S. states and territories. Although a blood sample obtained by heel stick
for the spot test is best obtained between 2 and 6 days of age, specimens are usually taken within
the first 24 to 48 hours or before discharge as part of a concurrent screen for other metabolic
defects. Early screening can result in overdiagnosis (false-positives) but is preferable to missing the
diagnosis.
● For screening results that show a low level of T4 (<10%), obtain TSH levels, and if these are
elevated (>40 mU/L), further tests to determine the cause of the disease should be carried out.
● Additional tests include serum measurement of T4, triiodothyronine (T3), resin uptake, free T4, and
thyroid-bound globulin. Tests of thyroid gland function (thyroid scan and uptake) usually involve oral
administration of a radioactive isotope of iodine (131I) and measurement of iodine uptake by the
thyroid, usually within 24 hours. In CH, protein bound iodine, T4, T3, and free T4 levels are low, and
thyroid uptake of 131I is decreased.
● Skeletal radiography is used to assess age
● In newborns, thyroid function studies are elevated in comparison with values in older children;
therefore, it is important to document the timing of the tests. In preterm and sick full-term infants,
thyroid function tests are usually lower than in healthy full-term infants; a repeat T4 and TSH may be
evaluated after 30 weeks (corrected age) in newborns born before that time and after resolution of
the acute illness in sick full-term infants.

Therapeutic Management
● Treatment involves lifelong thyroid hormone replacement therapy as soon as possible after
diagnosis to abolish all signs of hypothyroidism and reestablish normal physical and mental
development.
● The drug of choice is synthetic levothyroxine sodium (Synthroid, Levothroid). Optimum dosage of L-
thyroxine should be able to maintain blood TSH concentration between 0.5 and 2.0 mU/L during the
first 3 years of life (AAP and American Thyroid Association, 2006).
● Regular measurement of thyroxine levels is important in ensuring optimum treatment. Bone age
surveys are also performed to ensure optimum growth.

Nursing Care Management

● The most important nursing objective is early identification of the disorder. Nurses caring for
neonates must be certain that screening is performed, especially in infants who are preterm,
discharged early, or born at home.
● Parental remarks about an unusually “quiet and good” baby and demonstrated symptoms such as
prolonged jaundice, constipation, and umbilical hernia should lead to a suspicion of hypothyroidism,
which requires a referral for specific tests.
● The child should be referred to a pediatric endocrinologist for care. The importance of compliance
with the drug regimen for the child to achieve normal growth and development must be stressed.
● Because the drug is tasteless, it can be crushed and added to formula, water, or food. If a dose is
missed, twice the dose should be given the next day. Unless there are maternal contraindicative
factors, breastfeeding is acceptable and encouraged in infants with hypothyroidism.

2. PHENYLKETONURIA
● Phenylketonuria, an inborn error of metabolism inherited as an autosomal recessive trait (the PAH
gene is located on chromosome 12q24), is caused by a deficiency or absence of the enzyme
needed to metabolize the essential amino acid phenylalanine.
● Classic PKU is at one end of a spectrum of conditions known as hyperphenylalaninemia. Within the
spectrum of hyperphenylalaninemia are conditions with varying degrees of severity depending on the
degree of enzyme deficiency. Because rarer forms are a result of a deficiency in other enzymes and
are diagnosed and treated differently, the following discussion of PKU is limited to the severe, classic
form.
● The hepatic enzyme phenylalanine hydroxylase, which normally controls the conversion of
phenylalanine to tyrosine, is deficient. This results in the accumulation of phenylalanine in the
bloodstream and urinary excretion of abnormal amounts of its metabolites, the phenyl acids.
● One of these phenylketones, phenylacetic acid, gives urine the characteristic musty odor associated
with the disease. Another is phenylpyruvic acid, which is responsible for the term phenylketonuria.
● Tyrosine, the amino acid produced by the metabolism of phenylalanine, is absent in PKU. Tyrosine
is needed to form the pigment melanin and the hormones epinephrine and thyroxine. Decreased
melanin production results in similar phenotypes of most individuals with PKU, which is blond hair,
blue eyes, and fair skin that is particularly susceptible to eczema and other dermatologic problems.
● The prevalence of PKU varies widely in the United States because different states have different
definition criteria for what constitutes hyperphenylalaninemia and PKU. The reported figures for PKU
in the United States is one case per 15,000 live births. The disease has a wide variation of incidence
by ethnic groups. In Europe, the incidence is 1 in 10,000 births; in Asia and Africa, the prevalence is
quite low (Blau, van Spronsen, and Levy, 2010).

Clinical manifestations in untreated PKU

➢ failure to thrive (growth failure);
➢ frequent vomiting;
➢ irritability;
➢ hyperactivity;
➢ unpredictable, erratic behavior.
Cognitive impairment is thought to be caused by the accumulation
of phenylalanine and presumably by decreased levels of the
neurotransmitters dopamine and tryptophan, which affect the
normal development of the brain and CNS, resulting in defective
myelinization, cystic degeneration of the gray and white matter, and
disturbances in cortical lamination.
Older children commonly display bizarre or schizoid behavior
patterns such as fright reactions, screaming episodes, head
banging, arm biting, disorientation, failure to respond to strong
stimuli, and catatonia-like positions.

Diagnostic Evaluation
● The objective in diagnosing and treating the disorder is to prevent cognitive impairment. Every
newborn should be screened for PKU. The most commonly used test for screening newborns is the
Guthrie blood test, a bacterial inhibition assay for phenylalanine in the blood. Bacillus subtilis,
present in the culture medium, grows if the blood contains an excessive amount of phenylalanine. If
performed properly, this test detects serum phenylalanine levels greater than 4 mg/dl (normal value,
1.6 mg/dl), but it will not quantify the results. Other methods for testing include quantitative
fluorometric assay and tandem mass spectrometry, which will give an absolute value. Only fresh
heel blood, not cord blood, can be used for the test.
● Because of the possibility of variant forms of hyperphenylalaninemia, PKU cofactor variant screen
should be performed in all children diagnosed with PKU.. Give special consideration to screening
infants born at home who have no hospital contact and infants adopted internationally.

Therapeutic Management
● Treatment of PKU involves restricting phenylalanine in the diet. Because the genetic enzyme is
intracellular, systemic administration of phenylalanine hydroxylase is of no value. Phenylalanine
cannot be eliminated because it is an essential amino acid in tissue growth
● Dietary management must meet two criteria: (1) meet the child’s nutritional need for optimum growth
and (2) maintain phenylalanine levels within a safe range (2–6 mg/dl in neonates and children up to
 12 years, 2–10 mg/dl through adolescence, and 2–15 mg/dl in adults) (Kaye, Committee on
Genetics, Accurso, and others, 2006).
● Infants with PKU who have blood phenylalanine levels higher than 10 mg/dl should be started on
treatment to establish metabolic control as soon as possible, ideally by 7 to 10 days of age. The daily
amounts of phenylalanine are individualized for each child and require frequent changes on the
basis of appetite, growth and development, and blood phenylalanine and tyrosine levels.
● Because all natural food proteins contain phenylalanine and will be limited, the diet must be
supplemented with a specially prepared phenylalanine-free formula (e.g., Phenex-1 for infants or
Phenex-2 for children and adults).† The phenylalanine-free formula is an amino acid–modified
formula essential in the low phenylalanine diet to provide the appropriate protein, vitamins, minerals,
and calories for optimal growth and development.
● To achieve optimal metabolic control and outcome, a restricted phenylalanine diet, including medical
foods and low-protein products, most likely will be medically required for virtually all individuals with
classic PKU for their entire lives. To evaluate the effectiveness of dietary treatment, frequent
monitoring of blood phenylalanine and tyrosine levels is necessary
● Phenylalanine levels greater than 6 mg/dl in mothers with PKU affect the normal embryologic
development of the fetus, including cognitive impairment, cardiac defects, and LBW. It is
recommended that phenylalanine levels below 6 mg/dl be achieved at least 3 months before
conception in women with PKU.

Nursing Care Management

● The principal nursing considerations involve teaching the family regarding the dietary restrictions.
Although the treatment may sound simple, the task of maintaining such a strict dietary regimen is
demanding, especially for older children and adolescents.
● Foods with low phenylalanine levels (e.g., vegetables; fruits; juices; some cereals, breads, and
starches) must be measured to provide the prescribed amount of phenylalanine. High-protein foods,
such as meat and dairy products, are eliminated from the diet.
● The sweetener aspartame (NutraSweet) should be avoided because it is composed of two amino
acids, aspartic acid and phenylalanine, and if used will decrease the amount of natural phenylalanine
that is prescribed for the day
● Maintaining the diet during infancy presents few problems. Solid foods such as cereal, fruits, and
vegetables are introduced as usual to the infant.
● A decreased appetite and refusal to eat may reduce intake of the calculated phenylalanine
requirement. The child’s increasing independence may also inhibit absolute control of what he or she
eats. Either factor can result in decreased or increased phenylalanine levels.
● The assistance of a registered dietitian is essential. Parents need a basic understanding of the
disorder and practical suggestions regarding food selection and preparation.* Meal planning is based
on weighing the food on a gram scale; a less accurate method is the exchange list. As soon as
children are old enough, usually by early preschool, they should be involved in the daily calculation,
menu planning, and formula preparation.
● Preparation of the phenylalanine-free formula can present some challenges. The formula tends to be
lumpy; mixing the powder with a small amount of water to make a paste and then adding the rest of
the required liquid, helps alleviate this problem. A blender or mixer dissolves the powder more easily;
a rechargeable hand mixer can be used when traveling.
● Formula bars are convenient for active adolescents. Formula capsules are also available, but the
patient would need to take 20 or more capsules per day.

3. GALACTOSEMIA
● Galactosemia is a rare autosomal recessive disorder that results from various gene mutations
leading to three distinct enzymatic deficiencies.
● The most common type of galactosemia (classic galactosemia) results from a deficiency of a hepatic
enzyme, galactose 1-phosphate uridyltransferase (GALT), and affects approximately 1 in 50,000
births. The other two varieties of galactosemia involve deficiencies in the enzymes galactokinase
(GALK) and galactose 4′-epimerase (GALE); these are extremely rare disorders. All three enzymes
(GALT, GALK, and GALE) are involved in the conversion of galactose into glucose.
● As galactose accumulates in the blood, several organs are affected. Hepatic dysfunction leads to
 cirrhosis, resulting in jaundice in the infant by the second week of life. The spleen subsequently
becomes enlarged as a result of portal hypertension.
● Cataracts are usually recognizable by 1 or 2 months of age; cerebral damage, manifested by the
symptoms of lethargy and hypotonia, is evident soon afterward. Infants with galactosemia appear
normal at birth, but within a few days of ingesting milk (which has a high lactose content), they begin
to experience vomiting and diarrhea, leading to weight loss. E. coli sepsis is also a common
presenting clinical sign.
● Death during the first month of life is frequent in untreated infants. Occasionally classic galactosemia
is seen with milder, chronic manifestations, such as growth failure, feeding difficulty, and
developmental delay.

Diagnostic Evaluation
● Diagnosis is made on the basis of the infant’s history, physical examination, galactosuria, increased
levels of galactose in the blood, and decreased levels of GALT activity in erythrocytes. The infant
may display characteristics of malnutrition; hypoglycemia, jaundice, hepatosplenomegaly, sepsis,
cataracts, and decreased muscle tone (Bosch, 2006). Newborn screening for this disease is required
in most states. Heterozygotes can also be identified because heterozygotic individuals have
significantly lower levels of the essential enzyme.

Therapeutic Management
● During infancy, treatment consists of eliminating all milk and lactose containing formula, including
breast milk. Traditionally, lactose-free formulas are used, with soy-protein formula being the feeding
of choice; however, some research suggests that elemental formula (galactose-free) may be more
beneficial than soy formulas.
● However, the AAP recommends the use of soy protein–based formula for infants with galactosemia,
and it is considerably less expensive than elemental formula (Bhatia, Greer, and Committee on
Nutrition, 2008).
● As the infant progresses to solids, only foods low in galactose should be consumed. Certain fruits
are high in galactose, and some dietitians recommend that they be avoided. Food lists should be
given to the family to ensure that appropriate foods are chosen.
● If galactosemia is suspected, supportive treatment and care are implemented, including monitoring
for hypoglycemia, liver failure, bleeding disorders, and E. coli sepsis.

Prognosis
● Follow-up studies of children treated from birth or within the first 2 months of life after symptoms
appear have found long-term complications, such as hypogonadism, cognitive impairment, growth
restriction, and verbal and motor delays (Bosch, 2006).
● These findings have revealed that eliminating sources of galactose does not significantly improve the
outcome. New therapeutic strategies, such as enhancing residual transferase activity, replacing
depleted metabolites, and using gene replacement therapy, are needed to improve the prognosis for
these children.

4. Glucose-6-phosphate dehydrogenase deficiency

● The most common enzyme deficiency worldwide, causes a spectrum of disease including neonatal
hyperbilirubinemia, acute hemolysis, and chronic hemolysis. Persons with this condition also may be
asymptomatic.
● This X-linked inherited disorder most commonly affects persons of African, Asian, Mediterranean, or
MiddleEastern descent. Approximately 400 million people are affected worldwide.
● Homozygotes and heterozygotes can be symptomatic, although the disease typically is more severe
in persons who are homozygous for the deficiency
● Epidemiology: G6PD deficiency occurs with increased frequency throughout Africa, Asia, the
Mediterranean, and the Middle East. In the United States, black males are most commonly affected,
with a prevalence of approximately 10 percent. Prevalence of the deficiency is correlated with the
geographic distribution of malaria, which has led to the theory that carriers of G6PD deficiency may
incur partial protection against malarial infection.
 Pathophysiology
● G6PD catalyzes nicotinamide adenine dinucleotide phosphate (NADP) to its reduced form, NADPH,
in the pentose phosphate pathway.
● NADPH protects cells from oxidative damage. Because erythrocytes do not generate NADPH in any
other way, they are more susceptible than other cells to destruction from oxidative stress.
● The level of G6PD activity in affected erythrocytes generally is lower than in other cells. Normal red
blood cells that are not under oxidative stress generally exhibit G6PD activity at approximately 2
percent of total capacity. Even with enzyme activity that is substantially reduced, there may be few or
no clinical symptoms. A total deficiency of G6PD is incompatible with life.
● Genetics: The gene mutations affecting encoding of G6PD are found on the distal long arm of the X
chromosome. More than 400 mutations have been identified, most being missense mutations. Most
of the variants occur sporadically, although the G6PD Mediterranean and the G6PD A– variants
occur with increased frequency in certain populations.

Diagnosis
● The diagnosis of G6PD deficiency is made by a quantitative spectrophotometric analysis or, more
commonly, by a rapid fluorescent spot test detecting the generation of NADPH from NADP. The test
is positive if the blood spot fails to fluoresce under ultraviolet light.
● Tests based on polymerase chain reaction detect specific mutations and are used for population
screening, family studies, or prenatal diagnosis.
● In patients with acute hemolysis, testing for G6PD deficiency may be falsely negative because older
erythrocytes with a higher enzyme deficiency have been hemolyzed. Young erythrocytes and
reticulocytes have normal or near-normal enzyme activity.
● G6PD deficiency is one of a group of congenital hemolytic anemias, and its diagnosis should be
considered in children with a family history of jaundice, anemia, splenomegaly, or cholelithiasis,
especially in those of Mediterranean or African ancestry.

Treatment
● The main treatment for G6PD deficiency is avoidance of oxidative stressors. Rarely, anemia may be
severe enough to warrant a blood transfusion. Splenectomy generally is not recommended.
● Folic acid and iron potentially are useful in hemolysis, although G6PD deficiency usually is
asymptomatic and the associated hemolysis usually is short-lived.
● Antioxidants such as vitamin E and selenium have no proven benefit for the treatment of G6PD
deficiency.6,31 Research is being done to identify medications that may inhibit oxidative-induced
hemolysis of G6PD-deficient red blood cells.

5. Congenital adrenal hyperplasia

● is an inherited disorder that affects the production of certain hormones and causes the adrenal
glands to become too big (hyperplastic).
● a group of rare inherited autosomal recessive disorders characterized by a deficiency of one of the
enzymes needed to make specific hormones. CAH affects the adrenal glands located at the top of
each kidney.
● Hormones involved in CAH:
A. Cortisol (stress hormone): Helps control blood pressure, blood sugar and heart function. The body
uses more cortisol during times of stress, injury and infection. Not having enough cortisol can be
life threatening because it can lead to shock (dangerously low blood pressure), which is also
known as an ‘‘adrenal crisis.’’
B. Aldosterone (salt-saving hormone): Helps balance water, sodium and potassium in the body.
Without enough aldosterone, the body can’t hold on to sodium and water.
C. Androgens (male hormones, such as testosterone): Both males and females have androgens. A
male fetus needs androgens for normal genital development. However, a female fetus should not
have androgens or her genitals may not form normally (they may become more male in
appearance).

Types of CAH
1. Classical CAH
 ●In classical CAH, the body produces more androgens (male hormones) than it needs. At the
same time, there is too little cortisol (stress hormone) and sometimes too little aldosterone (salt
saving hormone). This type of CAH occurs in about 1 out of every 15,000 births.
● There are two forms of classical CAH:
- Salt-wasting CAH is the more common------and severe------form. With salt-wasting CAH, too
much sodium and water are lost through urine, and the amount of potassium in the body
increases, causing dehydration (loss of fluids) and very low blood pressure.
- Simple-virilizing CAH does not cause the body to lose sodium and water. Therefore, it is
less severe than salt-wasting CAH. Like salt wasters, simple virilizers produce too many
androgen
● Diagnosis in girls:
- In girls, both kinds of classical CAH tend to be detected at birth because the genitals may
not look normal. (Often they look more like boys’ genitals.) This is because their adrenal
glands produced too many androgens (male hormones) in the womb. A typical female fetus
does not produce this many androgens.
● Diagnosis in boys:
- In the male fetus, the testes already produce androgens. So if a few more androgens come
from the adrenal glands, the genitals may look only slightly different at birth. (The scrotum
may be more brownish in color, and the penis may be a little larger). Newborn screening is
of particular value in boys, because they have no outward signs of the disease, and yet are
at risk of "adrenal crisis" which can be prevented by early diagnosis and medical treatment.
2. Non-classical CAH
- Non-classical CAH (NC-CAH) is milder than classical CAH. It is often referred to as “lateonset”
CAH, because symptoms do not appear until later in life. Currently, this type of CAH is not
detected through newborn screening of infants.
- Newborns with NC-CAH do not have genital changes. Instead, the disease is diagnosed when
the effects of excess androgen appear in childhood (rapid growth, early puberty) or during the
teenage or adult years (too much face and body hair, severe acne, irregular periods).

Treating CAH
● Treatment involves replacing hormones that the body cannot produce itself and keeping the body
from making too much of other hormones. This means that the child will need to take medicine
regularly for the rest of his or her life. While this appears simple, long-term success requires
teamwork between the family and the doctors.
● Make sure that your child takes the medicine faithfully.
● Keep all appointments with your child’s doctors.
● See a pediatric endocrinologist (a children’s doctor who specializes in hormones) to make sure the
medicine is working.
● Because each person is different, treatment is tailored to each patient. Your child will need to take
medicine two to three times a day. This will ensure that your child maintains normal energy levels,
the right balance of sodium and water, and normal growth and development.
● Medicines: Children who have classical CAH need extra steroids during periods of increased
physical stress. (Emotional stress does not require extra medicine.) The extra dose of steroids is
called a stress dose. It can range from two to three times the normal daily dose depending on the
severity of the stress to the body.
● Regular doctor visits: The child should see his or her endocrinologist every three to four months for
blood tests, Xrays and an exam. As the child gets older, he or she will not have to go to the doctor as
often.
● Psychological counseling and support:
- With any lifelong condition, family counseling is helpful. Counseling should begin as soon as the
diagnosis is made. It will also help to meet with other families who have a child with CAH.
- Parents may feel a range of emotions when learning about their child’s CAH, from shock and
confusion to shame, anxiety, anger and sadness. Addressing these feelings will help the family
accept the diagnosis and act in the child’s best interest.
- Other challenges may include body image concerns, insecurity with dating and sexuality, and
concerns about possible infertility. All of this requires the support of parents, peers and health
 professionals. Specialized counseling may be useful throughout the person’s life.
● Surgery : In cases of some females with CAH, a question may arise about possible surgery to
change the look of the child’s genitals. Patients and parents should make this decision with the help
of a psychologist and surgeon. Your doctor should offer you detailed medical information and all
available options.
6. Other Disorders:
● Hemoglobinopathies are inherited conditions that affect the number or shape of the red blood
cells in the body. These conditions can be very different from one another. Some
hemoglobinopathies can cause life-threatening symptoms, while others do not cause medical
problems or even signs of the condition. Mild hemoglobinopathies may require no medical
treatment. However, when severe cases are left untreated, they can cause a shortage of red
blood cells (anemia), organ damage or even death. Fortunately, when severe
hemoglobinopathies are identified and treated early in life, affected children often can lead
healthy lives.
● Organic acid disorders are a group of inherited metabolic conditions. Each organic acid
disorder is associated with a specific enzyme deficiency that causes the accumulation of organic
acids in blood and urine. The accumulated compounds or their metabolites are toxic, resulting in
the clinical features of these disorders.
● Fatty acid oxidation disorders are lipid metabolism disorders that are caused by a lack or
deficiency of the enzymes needed to break down fats, resulting in delayed mental and physical
development. Fatty acid oxidation disorders occur when parents pass the defective genes that
cause these disorders on to their children.
● Amino acid disorders are a group of rare, inherited conditions that affect infants from birth.
They are caused by enzymes that do not work properly. Protein is made up of smaller
building blocks, called amino acids. A number of different enzymes are needed to process
these amino acids for use by the body.
● Biotinidase deficiency is a genetic disorder that is found in a few babies born each year.
When a baby has biotinidase deficiency, he or she cannot use biotin, a vitamin that is found
in foods, including breast milk and infant formula. Without biotin, the baby will not grow and
develop properly.
● Cystic fibrosis (CF) is an inherited disorder that causes severe damage to the lungs,
digestive system and other organs in the body. Cystic fibrosis affects the cells that produce
mucus, sweat and digestive juices. These secreted fluids are normally thin and slippery.
● Severe combined immunodeficiency (SCID) is an inherited primary immunodeficiency
disease (PIDD) that typically presents in infancy and results in a profound immune
deficiency condition resulting in a weak immune system that is unable to fight off even mild
infections. It is considered to be the most serious PIDD.
● Critical congenital heart disease (CCHD) is a term that refers to a group of serious heart defects
that are present from birth. These abnormalities result from problems with the formation of one or
more parts of the heart during the early stages of embryonic development. CCHD prevents the heart
from pumping blood effectively or reduces the amount of oxygen in the blood. As a result, organs
and tissues throughout the body do not receive enough oxygen, which can lead to organ damage
and life-threatening complications. Individuals with CCHD usually require surgery soon after birth.

Infant and Young Infant

1. GROWTH FAILURE (FAILURE TO THRIVE)

● Growth failure, or failure to thrive (FTT), is a sign of inadequate growth resulting from an inability to
obtain or use calories required for growth. FTT has no universal definition, although one of the more
common criteria is a weight (and sometimes height) that falls below the fifth percentile for the child’s
age.
● Another definition of FTT includes a weight for age (height) z value of less than −2.0 (a z value is a
standard deviation value that represents anthropometric data normalizing for sex and age with
greater precision than growth percentile curves [Markowitz, Watkins, and Duggan, 2008]).
● A third way to define FTT is a weight curve that crosses more than 2 percentile lines on a
standardized growth chart after previous achievement of a stable growth pattern. Weight for length is
reported to be a better indicator of acute undernutrition (Cole and Lanham, 2011).
● Growth measurements alone are not used to diagnose children with FTT. Rather, the finding of a
pattern of persistent deviation from established growth parameters is cause for concern. In addition
to lack of consensus on the precise definition of FTT, some advocate for a change in terminology;
thus, terms such as growth failure and pediatric undernutrition are used in the literature for FTT
(Locklin, 2005).
● Another term seen in the literature is weight or growth faltering. According to Cole and Lanham
(2011), approximately 5% to 10% of children in primary care in the United States have FTT with the
majority presenting before the age of 18 month.
● FTT be classified according to pathophysiology in the following categories (Krugman and Dubowitz,
2003):
- Inadequate caloric intake—Incorrect formula preparation, neglect, food fads, excessive juice
consumption, poverty, breastfeeding problems, behavioral problems affecting eating, or central
nervous system problems affecting intake
- Inadequate absorption—Cystic fibrosis, celiac disease, vitamin or mineral deficiencies, biliary
atresia, or hepatic disease
- Increased metabolism—Hyperthyroidism, congenital heart disease, hyperthyroidism, or chronic
immunodeficiency
- Defective utilization—Genetic anomaly such as trisomy 21 or 18, congenital infection, or
metabolic storage diseases.
● The cause of growth failure is often multifactorial and involves a combination of infant organic
disease, dysfunctional parenting behaviors, subtle neurologic or behavioral problems, and disturbed
parent–child interactions (Block, Krebs, and Committee on Child Abuse and Neglect and Committee
on Nutrition, 2005). However, the primary etiology is inadequate caloric intake, regardless of the
cause.
● Other factors that can lead to inadequate caloric intake in infancy include poverty, health or
childrearing beliefs such as fad diets, inadequate nutritional knowledge, family stress, feeding
resistance, and insufficient breast milk intake. In infants younger than 8 weeks of age, breastfeeding
problems as a result of inadequate latch or uncoordinated sucking and swallowing may occur.
● Besides showing signs of malnutrition and delayed social development, children with FTT may
exhibit altered behavioral interactions. They may display intense interest in inanimate objects, such
as toys, but much less interest in social interactions. They are often watchful of people at a distance
but become increasingly distressed as others come closer. They may dislike being touched or held
and avoid face-to-face contact. However, when held, they protest briefly on being put down and are
apathetic when left alone.
● Children with growth failure may have a history of difficult feeding, vomiting, sleep disturbance, and
excessive irritability. Patterns such as crying during feedings; vomiting; hoarding food in the mouth;
ruminating after feeding; refusing to switch from liquids to solids; and displaying aversion behavior,
such as turning from food or spitting food, become attention-seeking mechanisms to prolong the
attention received at mealtime.

Diagnostic Evaluation
● Diagnosis is initially made from evidence of growth failure. If FTT is recent, the weight, but not the
height, is below accepted standards (usually the fifth percentile); if FTT is longstanding, both weight
and height are low, indicating chronic malnutrition. Perhaps as important as anthropometric
measurements are a complete health and dietary history (including perinatal history), physical
examination for evidence of organic causes, developmental assessment, and family assessment.
● A dietary intake history, either a 24-hour food intake or a history of food consumed over a 3- to 5-day
period, is also essential. In addition, explore the child’s activity level, parental height, perceived food
allergies, and dietary restrictions.
● An assessment of household organization and mealtime behaviors and rituals is important in the
collection of pertinent data. It is often helpful to obtain the growth patterns of the affected child’s
parents and siblings; these can be compared with norm-referenced standards to evaluate the child’s
growth (Markowitz, Watkins, and Duggan, 2008).
 ● An assessment of the home environment and child–parent interaction may be helpful as well.

Therapeutic Management
● The primary management of FTT is aimed at reversing the cause of the growth failure. If malnutrition
is severe, the initial treatment is directed at reversing the malnutrition. The goal is to provide
sufficient calories to support “catch-up” growth—a rate of growth greater than the expected rate for
age.
● In addition to adding caloric density to feedings, the child may require multivitamin supplements and
dietary supplementation with high-calorie foods and drinks. Any coexisting medical problems are
treated.
● In most cases of FTT, an interdisciplinary team of physician, nurse, dietitian, child life specialist,
occupational therapist, pediatric feeding specialist, and social worker or mental health professional is
needed to deal with the multiple problems. Make efforts to relieve any additional stresses on the
family by offering referrals to welfare agencies or supplemental food programs. In some cases,
family therapy may be required.

Prognosis
● The prognosis for FTT is related to the cause. If the parents have simply not understood the infant’s
needs, teaching may remedy the child’s limited caloric intake and permanently reverse the growth
failure. Inadequate or infrequent feeding periods by the infant’s primary caretaker, in conjunction with
family disorganization, are often observed to be the cause of FTT.

Nursing Care Management

● Nurses play a critical role in the diagnosis of FTT through their assessment of the child, parents, and
family interactions. Knowledge of the characteristics of children with FTT and their families is
essential in helping identify these children and hastening the confirmation of a diagnosis.
● Accurate assessment of initial weight and height and daily weight, as well as recording of all food
intake, is mandatory. The nurse documents the child’s feeding behavior and the parent–child
interaction during feeding, other caregiving activities, and play. One available feeding observation
instrument is the Nursing Child Assessment Satellite Training (NCAST) Feeding Scale, which is
designed to assess the feeding interaction of infants up to 12 months of age.
● The nurse should assess the approximate developmental age on admission by administering an
appropriate developmental test.
● Some parents are at increased risk for attachment problems because of (1) isolation and social
crisis; (2) inadequate support systems, such as teenage and single mothers; and (3) poor parenting
role models as a child. Other factors that should be considered are lack of education; physical and
mental health problems such as physical and sexual abuse, depression, or drug dependence;
immaturity, especially in adolescent parents; and lack of commitment to parenting, such as giving
priority to entertainment or employment. Often these parents and their families are under stress and
in multiple chronic emotional, social, and financial crises.
● Four primary goals in the nutritional management of children with FTT are to (1) correct nutritional
deficiencies and achieve ideal weight for height, (2) allow for catch-up growth, (3) restore optimum
body composition, and (4) educate the parents or primary caregivers regarding the child’s nutritional
requirements and appropriate feeding.
● Because maladaptive feeding practices often contribute to growth failure, give parents specific step-
by-step directions for formula preparation, as well as a written schedule of feeding times. Avoid
juices in children with growth failure until adequate weight gain has been achieved with appropriate
milk sources; thereafter give no more than 4 oz/day of juice.
● Behavior modification techniques may be used with older infants and toddlers to interrupt poor
feeding patterns. Feeding times may actually involve “struggles of will” in cases of maladaptive
feedings that result in FTT. These behaviors are different from the occasional toddler behavior of
food refusal, which is primarily developmental, not pathologic. The association of appropriate food
with good or bad behaviors and consequent rewards may be part of the complex problem. In severe
cases of malnourishment, tube feedings or intravenous therapy may be required.

2. COLIC (PAROXYSMAL ABDOMINAL PAIN)

● Colic is reported to occur in 15% to 40% of all infants (Morin, 2009), yet it has no particular affinity in
regard to gender, race, or socioeconomic status (Ellett, 2003). An organic cause may be identified in
fewer than 5% of infants seen by physicians because of excessive crying (Roberts, Ostapchuk, and
O’Brien, 2004).
● The condition is generally described as abdominal pain or cramping that is manifested by loud crying
and drawing the legs up to the abdomen. Other definitions include variables such as duration of cry
greater than 3 hours a day occurring more than 3 days per week and for more than 3 weeks and
parental dissatisfaction with the child’s behavior.
● Some studies report an increase in symptoms (fussiness and crying) in the late afternoon or evening
(Morin, 2009); however, in some infants, the onset of symptoms occurs at another time. Colic is
more common in infants younger than 3 months than in older infants, and infants with difficult
temperaments are more likely to be colicky.
● Despite the obvious behavioral indications of pain, the infant with colic gains weight and usually
thrives. There is no evidence of a residual effect of colic on older children except perhaps a strained
parent–child relationship in some cases. In other words, infants who are colicky grow up to be
normal children and adults. Colic is self-limiting and in most cases resolves as infants mature,
generally around 12 to 16 weeks of age.
● Among the theories investigated as potential causes are too rapid feeding, overeating, swallowing
excessive air, improper feeding technique (especially in positioning and burping), and emotional
stress or tension between the parent and child. Although all of these may occur, there is no evidence
that one factor is consistently present.
● Parental smoking, strained parent–infant interaction, lactase deficiency, difficult infant temperament,
difficulty regulating emotions, overstimulation, central nervous system immaturity, and
neurochemical dysregulation in the brain have also been proposed as potential causes of colic
(Ellett, 2003; Neu and Robinson, 2003). A positive association between consumption of fruit juices
(carbohydrate malabsorption) and colic has been demonstrated in some cases (Duro, Rising,
Cedillo, and others, 2002).

Therapeutic Management
● Management of colic should begin with an investigation of possible organic causes, such as CMA,
intussusception, or other GI problem. If a sensitivity to cow’s milk is strongly suspected, a trial
substitution of another formula such as an extensively hydrolyzed (Nutramigen, Alimentum,
Pregestimil), whey hydrolysate, or amino acid (Neocate, EleCare) formula is warranted. Soy
formulas are usually avoided because of the possibility of sensitivity to soy protein as well (AAP,
2009). Oral administration of Lactobacillus reuteri to colicky breastfed infants decreased symptoms
within 1 week of initiation in one small study.
● An extensive review of a wide variety of interventions for colic indicates no specific safe remedies
are available to alleviate symptoms of colic in every infant. Dietary changes, such as eliminating
cow’s milk protein from the lactating mother’s diet, and behavioral interventions were shown to be
effective in helping parents reduce stimulation and respond to the infant’s crying, yet these
interventions are perceived only as moderately effective.
● Administering sucrose was effective at reducing crying in colicky infants for a short period (3–30
minutes)

Nursing Care Management

● The initial step in managing colic is to take a thorough, detailed history of the usual daily events.
Areas that should be stressed include (1) the infant’s diet; (2) the diet of the breastfeeding mother;
(3) the time of day when crying occurs; (4) the relationship of crying to feeding time; (5) the presence
of specific family members during crying and habits of family members, such as smoking; (6) activity
of the mother or usual caregiver before, during, and after crying; (7) characteristics of the cry
(duration, intensity); (8) measures used to relieve crying and their effectiveness; and (9) the infant’s
stooling, voiding, and sleeping patterns. Of special emphasis is a careful assessment of the feeding
process via demonstration by the parent.
● If cow’s milk sensitivity is suspected, breastfeeding mothers should follow a milk-free diet for a
minimum of 3 to 5 days in an attempt to reduce the infant’s symptoms. Caution mothers that some
non dairy creamers may contain calcium caseinate, a cow’s milk protein.
 ● One important nursing intervention (before or after an organic cause has been eliminated) is
reassuring both parents that they are not doing anything wrong and that the infant is not
experiencing any physical or emotional harm. Parents, especially mothers, become easily frustrated
with their infant’s crying and perceive this as a sign that something is horribly wrong.

3. SUDDEN INFANT DEATH SYNDROME

● Sudden infant death syndrome (SIDS) is defined as the sudden death of an infant younger than 1
year of age that remains unexplained after a complete postmortem examination, including an
investigation of the death scene and a review of the case history. Since 1992, the incidence of SIDS
in the United States has decreased by 53% to an all-time low of 0.57 per 1000 live births in 2002
(AAP, Task Force on Sudden Infant Death Syndrome, 2005).
● The dramatic decrease is attributed to the Back to Sleep campaign.* SIDS is the third leading cause
of infant deaths (birth to 12 months) and the leading cause of postneonatal deaths (between 1 and
12 months). SIDS claimed the lives of 2145 infants in the United States in 2006; preliminary data
from 2007 indicate there were 2461 deaths from SIDS.
● Other terms have been developed to explain sudden deaths in infants. Sudden unexpected early
neonatal death (SUEND) and sudden unexpected infant death (SUID) share similar features but
differ in regards to the timing of death: whereas SUID is considered a death in the postneonatal
period, SUEND occurs in the first week of life. The AAP, Task Force on Sudden Infant Death
Syndrome (2011) policy statement considers SIDS to be a component of SUID.

Etiology
● There are numerous theories regarding the etiology of SIDS; however, the cause remains unknown.
One hypothesis is that SIDS is related to a brainstem abnormality in the neurologic regulation of
cardiorespiratory control. This maldevelopment affects arousal and physiologic responses to a life-
threatening challenge during sleep.
● Abnormalities include prolonged sleep apnea, increased frequency of brief inspiratory pauses,
excessive periodic breathing, and impaired arousal responsiveness to increased carbon dioxide or
decreased oxygen. However, sleep apnea is not the cause of SIDS.
● A genetic predisposition to SIDS has been postulated as a cause. In one study, a genetic mutation
on chromosome 6q 22.1-22.31 was positively linked to a syndrome of SIDS and dysgenesis of the
testis (Puffenberger, Hu-Lince, Parod, and others, 2004).

Risk Factors for SIDS

● Maternal smoking during pregnancy has emerged in numerous epidemiologic studies as a major
factor in SIDS, and tobacco smoke in the infant’s environment after birth has also been shown to
have a possible relationship to the incidence of SIDS. It has been postulated that 12% of all SIDS
deaths could be prevented with prenatal maternal smoking cessation. Increased nicotine
concentrations in lung tissue were found in children who died from SIDS compared with a group of
control children.
● Cosleeping, or an infant sharing a bed with an adult or older child on a noninfant bed, has been
reported to have a positive association with SIDS. One survey found a high association between
infant deaths, nonstandard beds (sofa, day bed), and bed sharing; a large percentage of infants
were found dead on their backs when bed sharing, suggesting suffocation.
● Prone sleeping may cause oropharyngeal obstruction or affect thermal balance or arousal state.
One study found that healthy full-term infants had significantly impaired arousal from active and quiet
sleep states when sleeping prone (Horne, Ferens, Watts, and others, 2001). Rebreathing of carbon
dioxide by infants in the prone position is also a possible cause of SIDS. Infants sleeping prone and
on soft bedding may not be able to move their heads to the side, thus increasing the risk of
suffocation and lethal rebreathing.
● Soft bedding such as waterbeds, sheepskins, beanbags, pillows, and quilts should be avoided for
infant sleeping surfaces. Bedding items such as stuffed animals and toys should be removed from
the crib while the infant is asleep. Head covering by a blanket has also been found to be a risk factor
for SIDS, thus supporting the recommendation to avoid extra bed linens and other items.

Protective Factors for SIDS

 ● One study indicated that breastfeeding during the first 16 weeks of life decreased the likelihood of
SIDS.
● Some studies have found pacifier use in infants to be a protective factor against the occurrence of
SIDS; the data for pacifier use in infants in the first year of life are said to be more compelling than
data linking pacifier use to the development of dental complications and the inhibition of
breastfeeding.
● The AAP, Task Force on Sudden Infant Death Syndrome (2011) emphasizes that medically stable
preterm infants and infants diagnosed with gastroesophageal reflux (GER) be placed in a supine
sleep position unless there is a specific upper airway disorder wherein the risk of death from the
condition is greater than the risk of SIDS.
● Updated childhood immunization status has also been shown to be protective against SIDS.
● Although the cause of SIDS is unknown, autopsies reveal consistent pathologic findings, such as
pulmonary edema and intrathoracic hemorrhages, that confirm the diagnosis.

Infant Risk Factors

● Certain groups of infants are at increased risk for SIDS:
• Low birth weight
• Low Apgar scores
• Recent viral illness • Siblings of two or more SIDS victims
• Male sex
• Infants of American Indian or African-American ethnicity
● No diagnostic tests exist to predict which infants, including those in the above groups, will survive,
and home monitoring is no guarantee of survival. Whether subsequent siblings of one SIDS infant
are at increased risk for SIDS is unclear. Even if the risk is increased, families have a 99% chance
that their subsequent child will not die of SIDS.

Nursing Care Management

● Nurses have a vital role in preventing SIDS by educating families about the risk of prone sleeping
position in infants from birth to 6 months of age, the use of appropriate bedding surfaces, the
association with maternal smoking, and the dangers of cosleeping on noninfant surfaces with adults
or other children. Additionally, nurses have an important role in modeling behaviors for parents to
foster practices that decrease the risk of SIDS, including placing infants in a supine sleeping position
in the hospital.
● Nurses must be proactive in further decreasing the incidence of SIDS; postpartum discharge
planning, newborn discharges, follow-up home visits, well baby clinic visits, and immunization visits
provide excellent opportunities to educate parents on these matters.
● Nurses must continue to take every opportunity to advocate for infants by providing information for
parents and caretakers about the modifiable risk factors for SIDS which can be implemented to
prevent its occurrence across all sectors of the population.
● Nurses must continue to take every opportunity to advocate for infants by providing information for
parents and caretakers about the modifiable risk factors for SIDS which can be implemented to
prevent its occurrence across all sectors of the population.

EBSCO HOST http://search.ebscohost.com Usersname: OLFU PW: #fatima2020

http://dbctle.erau.edu/initiatives/seven/ Iowa State Center for Excellence in Learning and Teaching.

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1. What is the role of a Nurse after identifying the different disorders of an Infant?
2. What should be the focus of your health teachings on the parents who have a baby with failure to
thrive? Formulate a Plan that you can use for this case.

Hockenberry (2019). Wong’s Nursing Care of Infants and Children, 11th edition. Elsevier.

Frank, J.Diagnosis and Management of G6PD Deficiency, October 1, 2005 Volume 72, Number 7
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