Developmental Milestone
Developmental Milestone
Developmental Milestone
Developmental milestone are behaviors or physical skills seen in infants and children as they
grow and develop. Rolling over, crawling, walking, and talking are all considered milestones.
The milestones are different for each age range.
There is a normal range in which a child may reach each milestone. For example, walking may
begin as early as 8 months in some children. Others walk as late as 18 months and it is still
considered normal.
One of the reasons for well-child visits to the health care provider in the early years is to follow
your child's development. Most parents also watch for different milestones. Talk to your child's
provider if you have concerns about your child's development.
Below is a general list of some of the things you might see children doing at different ages.
These are NOT precise guidelines. There are many different normal paces and patterns of
development.
Toddler -- 1 to 3 years
Preschooler -- 3 to 6 years
Begins gaining skills for team sports such as soccer, T-ball, or other team sports
Begins to lose "baby" teeth and get permanent teeth
Girls begin to show growth of armpit and pubic hair, breast development
Menarche (first menstrual period) may occur in girls
Peer recognition begins to become important
Reading skills develop further
Routines important for daytime activities
Understands and is able to follow several directions in a row
Adolescent -- 12 to 18 years
Respiratory distress syndrome refers to a condition of surfactant deficiency and physiologic immaturity
of a thorax . The term respiratory syndrome and hyaline membrane disease are most often applied to
the severe lung disorder. It is seen almost exclusively in preterm infants but may also be associated with
multifetal pregnancies, infants of diabetic mothers, caesarean section delivery, cold stress, asphyxia and
a family history of RDS. The disorder are rarely observed in drug exposed infants or infants who have
been subjected to chronic intrauterine distress
Pathophysiology
Preterm infants are born before the lungs are fully prepared to serve as efficient organs for gas
exchange. This appears to be critical factor in the development of RDS. RDS results from a combination
of structural and functional immaturity of the lungs. The fetal lungs are deficient in surfactant, a surface
active phospholipid secreted by type II cells in the alveolar cells. Surfactant is first produced at about 24
weeks of gestational age, but the type II cells in the lung do not fully mature until about 36 weeks of
gestation. Pulmonary Edema observed in the early stage of RDS also contributes to impaired gas
exchange. Factors believed to facilitate this fluid accumulation in the lungs include renal immaturity or
insufficiency resulting firm hypoxemia, high fluid intake and PDA, left ventricular dysfunction associated
with papillary music necrosis, low serum protein concentration and low colloid osmotic pressure,
increased alveolar surface tension. Pulmonary interstitial emphysema (PIE) may develop in preterm
infants with RDS and immature lungs as a result of overdistention of distal airways. This condition
further complicates adequate oxygenation in the immature airways.
Clinical Manifestations
Infants with RDS can develop respiratory distress either accurately or over a period of hours, depending
on the acuity of pulmonary immaturity, associated illness factors and gestational maturity. The
observable signs produced by the pulmonary changes usually begin to appear infants who apparently
achieve normal breathing and color soon after birth. Infants may display retractions suprasternal or
substernal, and supracostal, subcostal or intercostal which compliant chest wall.
Therapeutic Management
The treatment of RDS includes all the general measures required for an y preterm infant, as well as
those instituted to correct imbalance. The supportive measures most crucial to a favorable outcome are:
1. Maintain adequate ventilation and oxygenation with CPAP, high-flow nasal cannula, or
mechanical ventilation
2. Maintain acid-base balance
3. Maintain a neutral thermal environment
4. Prevent hypotension
5. Maintain adequate tissue perfusion and oxygenation
6. Maintain adequate perfusion
The treatment of the infant with RDS requires one or more IV line to maintain hydration and nutrition,
monitor at=retrial blood gases, and administer medications.
Care of infants with RDS involves all the observations and interventions previously described for high
risk infants. In addition, the nurse is concerned the complex problem related to respiratory therapy and
the constant threat of hypoxemia and acidosis that complicates the care of patients in respiratory
difficulty.
The most essential nursing function is to observe and asses the infants response to therapy. Continuous
monitoring and close observation are key because an infant’s status can change rapidly and because
oxygen concentration and ventilation parameters are prescribed according to the infant’s blood gas
measurements and pulse oximetry readings. Changes in oxygen concentration are based on these
observations.
Meconium Aspiration Syndrome – occurs when a fetus has been subjected to asphyxia or there
intrauterine stress that causes relaxation of the anal sphincter and passage of meconium into the
amniotic fluid. Most meconium aspiration occurs with the first breath.
Pathophysiology
MAS involve the passage of meconium in utero as a result of hypoxic stress. It occurs primarily in full
term and post term infants but has been reported in infants at less than 37 weeks of gestation. A “ball-
valve situations exists wherein gas flows into the lungs on inspiration but is trapped there on exhalation
as a result of the small airway diameter. As the infant struggles to take in more air, even more
meconium may be aspirated. Hyperinflation, hypoxemia, and acidemia result In increased PVR.
Clinical Manifestations
Infants who have released meconium in utero for some time before birth are stained from green
meconium stools. Tachypneic, hypoxic and often depressed at birth. They developed expiratory
grunting, nasal flaring and retractions similar to those of infants. They may be initially be cyanotic or
pale, as well as tachypneic and they may demonstrate the classic barrel chest from hyperinflation.
Apnea of Prematurity – is a common phenomenon in the preterm infant. Rarely observed in full-term
infants, apneic spells increase in prevalence the younger the gestational age. Apnea usually resolves as
infant approaches 37 weeks of postmenstrual age, but in those born very prematurely apnea can persist
up to 43 weeks of postmenstrual age.
Pathophysiology – AOP reflects the immature and poorly refined neurologic and chemical
respiratory control mechanisms in preterm infants. These infants are not as responsive to hypercarbia
and hypoxemia and their neurons have fewer dendritic associations than those of more mature infants.
The respiratory reflexes of these infants are significantly less mature, which may be a contributing factor
in etiology. Secondary causes of Apnea should be investigated in infants with new-onset of apnea are
when there in new significant change on the frequency or severity of apneic episodes.
Clinical Manifestations
Factors that contribute to apnea in preterm neonates should be investigated and treated. Apnea can be
anticipated in infants with a variety of conditions conversely one of these disorders may be suspected in
in infants with persistent apneic spells. Although apnea is an expected event in preterm neonates it
should not be designated benign until all other causes have been ruled out.
Therapeutic Management
Caffeine is often effective in reducing the frequency of [primary apnea bradycardia spells in newborns.
Caffeine acts as a CNS stimulant to breathing. Caffeine has come to the forefront of pharmacologic
therapy for AOP because It has fewer side effects than previously used aminophylline or theophylline,
requires dosing once daily, has more predictable plasma concentrations, has slower elimination and has
a wider therapeutic range.
Sepsis or septicemia -refers to a generalized bacterial infection in the bloodstream. Neonates are highly
susceptible to infection because of diminished specific (inflammatory) and specific ( humoral ) immunity
such as impaired phagocytosis, delayed chemotactic response, minimum or absent IgA and
immunoglobulin M and decreased complement levels.
Pathophysiology
Sources of Infection
Sepsis in the neonatal period can be acquired prenatally across the placenta from the maternal
bloodstream or during the labor from ingestion or aspiration of infected amniotic fluid Prolonged
rupture of the membranes always presents a risk for maternal-fetal transfer of pathogenic organisms.
Early onset of sepsis is acquired in the perinatal period. EOS is defined as a positive blood culture in an
infant who is less than 72 hours. EOS remains an important cause of serious illness and death among
neonates of all birth weights and gestational ages. Late onset sepsis is primarily nosocomial (health care-
associated infect ion) and the offending organisms usually staphylococci, Klebsiella organisms,
enterococci, E-coli, and Candida species. Neonatal sepsis is most common in the “at risk infant,
particularly the preterm infant or the infant born after a difficult or traumatic labor and delivery, who is
least capable of resisting such bacterial invasion.
General Signs
Respiratory System
Irregular respirations
Cyanosis
Grunting
Dyspnea
Retractions
CNS
Diminished activity
Increased activity
Full fontanel
Increased or decreased tone
Abnormal eye movements
Gastrointestinal System
Poor feeding
Vomiting
Diarrhea
Abdominal distention
Hepatomegaly
Hemmocult-positive stools
Hematopoietic System
Jaundice
Pallor
Petechiae
Splenomegaly
Therapeutic management
Diagnosis of sepsis is often based on suspicion of initial clinical signs and symptoms. Antibiotic therapy is
initiated before laboratory results are available for confirmation and identification of the exact
organism. Treatment consists of circulatory support, respiratory support and aggressive administration
of antibiotics.
The prognosis for neonatal sepsis is variable. Severe neurologic and respiratory sequelae may occur in
ELBW and VLBW infants with early-onset sepsis. Late onset sepsis and meningitis may also result in poor
outcomes for immunocompromised neonates.
Nursing care of the infant with sepsis involves observation and assessment as outlined for any high-risk
infant. Recognition of the problem is of paramount importance. Awareness of the potential modes of
infection transmission also helps the nurse identify those at risk for developing sepsis. Knowledge of the
side effects of the specific antibiotic and proper regulation and administration of the drug are vital. Part
of the total care of infants with sepsis is to decrease any additional physiologic or environmental stress.
This includes providing and optimum thermoregulated environment and anticipating potential problems
such as dehydration or hypoxia. Precautions are implemented to prevent the spread of infection to
other newborns, but to be effective, activities must be carried out by all caregivers.
Pathophysiology
Bilirubin as one of the breakdown products of hemoglobin that results from red blood cell (RBC)
destruction. When RBCs are destroyed the breakdown, products are released into the circulation, where
are the hemoglobin splits into two fractions: heme and globin. The globin portion Is used by the body,
and the heme portion is converted to unc0mjugated bilirubin, an insoluble substance bound to albumin.
Physiologic factors
An association with breastfeeding or inadequate breast milk, especially unsuccessful
breastfeeding and/or weight loss
Excess production of bilirubin
Disturbed capacity of the lover to secrete conjugated bilirubin
Combined overproduction and underexcretion
Genetic predisposition to increased production
Clinical manifestations
The most obvious sign of hyperbilirubinemia is jaundice, the yellowish discoloration primary of the
sclera, nails or skin. As a rule, jaundice that appears within the first 24 hours is caused by HDN, sepsis or
one of the maternally derived diseases such as diabetes milletus or infections.
Therapeutic Management
The primary goals is the treatment of hyperbilirubinemia are to prevent bilirubin encelopathy and
kernicterus and as in any blood group incompatibility, to reverse the hemolytic process. The main form
of treatment of involves the use of phototherapy. Exchange transfusion is generally used for reducing
dangerously high bilirubin levels that occur with hemolytic disease. The pharmacologic management of
hyperbilirubinemia with phenobarbital has centered primarily on the infant with hemolytic disease and
is most effective when given to the mother several days before delivery. Phenobarbital promotes
hepatic glucuronyl transferase synthesis, which increases bilirubin conjugation and hepatic clearance of
the pigment in bile, and protein synthesis, which may increase albumin for more bilirubin sites.
Part of the routine physical assessment include observing for evidence of jaundice at regular intervals.
Jaundice is most reliably assessed by observing the infant’s skin color from head to toe and the color of
the sclerae and mucous membrane. There's no treatment for jaundice as such, but disease can be
managed by managing symptoms and causes of jaundice. In treating pre-hepatic jaundice, the objective
is to prevent the rapid breakdown of red blood cells that's causing the level of bilirubin to build up in the
blood.
Sudden Infant 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. Sudden unexpected early neonatal death and sudden
unexpected infant death share similar features but differ in regard to the timing of death: whereas SUID
is considered a death in the post neonatal period, SUEND occurs in the first week of life.
Maternal Smoking during pregnancy is major modifiable risk factor for SIDS. The incidence of SIDS is
approximately 3 times greater among infants whose mothers smoked during pregnancy, and risk of
death is progressively greater as daily cigarette increases, The effects of smoking of the father and
household members are more difficult to interpret because they are highly correlated with maternal
smoking.
Co sleeping or an infant sharing a bed with an adult or older child in a non-infant bed, is associated with
beds.
Prone sleeping may cause oropharyngeal obstruction or affect thermal balance or arousal state.
Rebreathing of carbon dioxide by infants due to sleeping in prone position is also a possible cause of
SIDS, infants sleeping prone and on soft bedding maybe unable to move their beds to the side, thus
increasing the risk of suffocation and lethal breathing.
Another potential cause of SIDS may be a prolonged Q-T interval or other cardiac arrhythmias. Recently
cardiac ion channelopathies, which occur as a result of gene mutations and may result in lethal
arrhythmias, have been proposed as a possible risk factor of SIDS.
Soft bedding 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 sleep.
Necrotizing Enterocolitis – is an acute inflammatory disease of the bowel with increased incidence in
preterm and other high-risk infants; it is most common in preterm infants. Because the signs are similar
to those observed in many other disorders of the newborn, nurses must constantly be aware of the
possibility of this disease.
Pathophysiology
The precise cause of NEC is still uncertain but it appears to occur in infants whose GI Tract has suffered
vascular compromise. Contributory factors for NEC include the following: intestinal maturity. Such as
gastrointestinal dysmotility; impaired digestive capacity; altered regulation of intestinal blood blow;
carrier dysfunction; altered anti-inflammatory control; and impaired host defense.
Clinical Manifestation
The prominent clinical signs of NEC area distended abdomen, gastric residuals and blood in the stools.
Because NEC closely resembles septicemia, the infant may “not look well” Nonspecific signs include
lethargy, poor feeding, hypotension, apnea, vomiting, decreased urinary output, and hypothermia. NEC
in full term infants almost always occur in the first 10 days of life. The early clinical signs of NEC are
subtle and nonspecific and may often be overlooked for other conditions
Therapeutic Management
Treatment of NEC begins with prevention. Oral feedings may be withheld for 24 to 48 hours from
infants who are believed to have suffered birth asphyxia. Medical treatment if confirmed NEC consists of
discontinuation of all oral feedings; institution of abdominal compression via nasogastric suction;
administration of IV antibiotics: and correction of extravascular volume depletion, electrolyte
abnormalities: acid-base imbalances and hypoxia.
Retinopathy of Prematurity
- is a disorder involving immature retinal vasculature. Formerly known as retrolental fibroplasia, ROP is a
term used to describe retinal changes observed in preterm infants. The incidence and severity of the
disease correlate with the degree of the infant’s maturity, the younger the gestational age, the greater
the likelihood pf ROP, with extremely preterm infants being most at risk
Pathophysiology
Severe vascular constriction in the immature retinal vasculature, followed by hypoxia in those areas, is
characteristic of ROP. This appears to stimulate vascular proliferation of of retinal capillaries into the
hypoxic areas, where veins become numerous and dilate.
A demarcation line (separates the avascular retina anteriorly form the vascularized
retina posteriorly)
A ridge (formed form the demarcation line with the height and width, occupies volume,
and extends beyond the plane of the retina.)
A ridge with extraretinal fibrovascular proliferation
Partial retinal detachment
Total retinal detachment
The nursing care if extremely preterm infants and those at risk for development of ROP should focus on
decreasing or avoiding events known to cause fluctuations in systemic blood pressure and oxygenation.
The infant’s oxygenation status should be carefully monitored and targeted SPO2 , ranges maintained.
Failure to Thrive (FTT) – is inadequate growth resulting from an inability to obtain or use calories
required for growth. FTT has no universal definition: however, the objective parameter is usually the
deceleration of growth - both height and weight. If FTT is severe, poor brain growth may occur as
evidenced by a smaller than normal head circumference.
Pathophysiology
The primary management of FTT is focused on reversing the cause if the growth failure The goal
is to provide sufficient calories to support “catch-up” growth which is rate of growth greater that the
expected rate for age
Knowledge of the characteristics of children wit FTT and their families is essential in the identification of
these children and the rapid confirmation of diagnosis. Children with FTT may have a history of difficult
feeding, vomiting, sleep disturbance, and excessive irritability. Nursing care of children with FTT
involves a “family systems” approach. Therefore, if the goal is for the entire family to become healthy,
all the members should be engaged in the change process. Nursing care pf the child’s parents is focused
on improving their self-esteem and supporting them as they acquire positive, successful parenting skills.
Initially, this necessitates providing an environment in which they feel welcomed and accepted.
Growth failure
Developmental delays
Undernutrition
Apathy
Withdrawn behavior
Feeding or eating behaviors
No fear of strangers
Avoidance of eye contact
Wide-eyed gaze and continual scan of the environment
Stiff and unyielding or flaccid and unresponsive
Minimal mailing
There are four primary goals in the nutritional management of children with FTT: