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Normal Newborn: Processes of Adaptation Ch 19
Terms in this set (81)
First vital task the newborn must accomplish
Initiation of respirations
Development of Lungs
During fetal life, the alveoli produce fetal lung fluid that expands the alveoli and is essential for normal development of the lungs
Some of the fluid empties from the lungs into the amniotic fluid
The fluid is cont produced at a rate of 4-5 ml/kg/hr
As fetus nears term, the amt of fetal lung fluid produced decreases in prep for birth, when the fluid must be cleared for the infant to breathe air.
Absorption of lung fluid begins during early labor and by the time of birth only 35% of the original amt remains
During labor, the fluid begins to move into the interstitial spaces where it is absorbed
Absorption is accelerated by secretion of fetal epinephrine and corticosterioids, but may be delayed by cesarean birth without labor
Ther emoval of the fluid helps reduce pulmonary resistance to blood flow that is present before birth and enhances the advent of air breathing
Surfactant, a slippery, detergent-like combo of lipoproteins, is detectable by 24-25 weeks of gestation
Surfactant lines the inside of the alveoli and reduces surface tension within alveoli, allowing the alveoli to remain partially open when the infant begins to breathe at birth
Without surfactant, the alveoli collapse as the infant exhales
The alveoli must be re-expanded with each breath, greatly increasing the work of breathing and possibly resulting in atelectasis.
By 34-36 weeks of gestation sufficient surfactant is usually produced to prevent respiratory distress syndrome
Surfactant secretion increases during labor and immediately after birth to enhance the transition from fetal to neonatal life
Steroids given to a woman in preterm labor help increase surfactant production and speed maturation of the lungs
The fetus with intraauterine growth restriction (IUGR) or stressed by conditions such as maternal HTN, heroin addiction, preeclampsia, or infection; placental insufficiency, or premature rupture of membranes greater than 48 hours may also have accelerated lung maturation.
Infants of mothers with diabetes have slower lung maturation
Causes of Respirations
At birth, the infant's first breath must force remaining fetal lung fluid out of the alveoli and into the interstitial space around the alveoli to allow air to enter the lungs
This requires a much larger negative pressure (suction) than subsequent breathing.
Breathing is initiated by chemical, mechanical, thermal, and sensory factors that stimulate the respiratory center in the medulla and trigger respirations
Chemoreceptors in the carotid arteries and the aorta respond to changes in blood chemistry caused by the hypoxia that occurs with normalbirth
A decrease in the partial pressure of oxygen and pH and an increase in the partial pressure of carbon dioxide in the blood causes impulses from these receptors to stimulate the respiratory center in the medulla.
Occlusion of these vessels in the cord ends the flow of a placental substance that may inhibit respirations.
A forceful contraction of the diaphragm results, causing air to enter the lungs
However, stimulation of the respiratory center and breathing do not occur if prolonged hypoxia causes central nervous system depression.
During a vaginal birth the fetal chest is compressed by the narrow birth canal. Approximately one third of the fetal lung fluid is forced out of the lungs into the upper air passages during birth
The fluid passes out of the mouth or nose or is suctioned as the head emerges from vagina
When the pressure against the chest is released at birth, recoil of the chest draws a small amount of air into the lungs and helps remove some of the viscous fluid int he airways. This reduces the amount of negative pressure needed for the first breath after birth.
The temp change that occurs with birth also stimulates the initiation of respirations
At birth, the infant moves from the warm, fluid-filled uterus into an environment where the temperature may be much cooler.
Sensors in the skin respond to this sudden change in temp by sending impulses to the medulla that stimulate the respiratory center and breathing.
Tactile, visual, auditory, and olfactory stimuli occur during and after birth to stimulate sensors
Nurses hold, dry, place infants skin-to-skin with the mother or wrap them in blankets, providing further stimulation to skin sensors.
The stimulation of the light, sound, smell, and pain at delivery may also aid in initiating respirations
Continuation of Respirations
As the alveoli expand, surfactant allows them to remain partially open between respirations. About 20-30 ml of air from the first breaths remains in the lungs to become the functional residual capacity (FRC)
Within the first hour after 80%-90% of the FRC is established
Because the alveoli remain partially expanded with this residual air, subsequent breaths require much less effort than the first one
As the infant cries, pressure within the lungs increases, causing remaining fetal lung fluid to move into the interstitial spaces, where it is absorbed by the pulmonary circulatory and lymphatic systens,
Complete absorption may take several hours.
This explains why the lungs may sound moist when first auscultated but become clear a short time later.
During fetal life 3 shunts - the ductus venosus, formaen ovale, and ductus arteriosus - carry much of the blood away from the lungs and some blood away from the liver
High pressures within the collapsed, fluid-filled lungs permit only a small amt of blood flow into the narrow pulmonary vessels.
Oxygenated blood from the placenta enters the fetal circulation through the umbolical vein
About one third of the blood is directed away from the liver into the ductus enosus which connects to the inferior vena cava
The rest of the umbilical vein flow goes through the liver before entering the inferior vena cava
Near the end of pregnancy, the liver needs more perfusion, and 70%-80% of the oxygenated blood goes to the liver first and then to the ductus venosus
Blood from the ductus venosus or the portal system of the liver enters the IVC and joins blood from the lower part of the body
Little mixing of blood from the DV and the lower body occurs because it travels to the heart in separate streams within the IVC
As blood flows into the right atrium, a flap of tissue directs the blood from the more highly oxygenated stream across the atrium to the foramen ovale
A flap valve in the septum between tje roght and left atria of the fetal heart
As blood flows into the right atrium, 50% to 60% crosses the foramen ovale to the left atrium
In the left atrium it mixes with the small amount of blood entering from the pulm veins, flows to the left ventricle, and leaves through the aorta.
The majority of the blood in the ascending aorta flows to the coronary, left carotid, and subclavian arteries.
Therefore, most of the better-oxygenated blood bypasses the nonfunctioning lungs before birth and travels to the heart, brain, head, and upper body
Blood that does not cross the foramen ovale moves to the right ventricle, but flow to the lungs is restricted by the narrow pulmonary artery and pulmonary blood vessels, causing a high pressure in the right side of the heart
Pressure is low on the left side of the heart because little resistance occurs as blood leaves the left ventricle to travel to the rest of the body and into the widely dilated placental vessels.
This difference in pressures between the right and left atria allows blood to flow through the foramen ovale
Pulmonary Blood Vessels
Blood from the superior vena cava and the less oxygenated blood from the inferior vena cava flow into the right atrium, to the right ventricle, and into the pulmonary artery.
Most of the blood passes through the ductus arteriosus while 10%-12% of the blood goes to the lungs.
After 30 weeks gestation, the amount of blood to the lungs increases
Blood flow to the lungs is limited because the pulmonary artery and other blood vessels are constricted, causing high pulmonary vascular resistance.
Blood perfusing the lungs returns to the left atrium by the pulmonary veins.
Connects the pulmonary artery and the descending aorta during fetal life.
Dilation of the ductus arteriosus is maintained by prostaglandins from the placenta and low oxygen content of the blood.
Changes During Birth
At birth, the shunts close and the pulm vessels dilate
These changes occur in response to increases in blood oxygen and shifts in pressure within the heart, pulmonary, and systemic circulations, as well as clamping of the umbilical cord
The alterations necessary for transition from fetal to neonatal circulation occur simultaneously within the first few minutes
As the newborn takes the first breaths at birth, the rise in oxygen concentration causes the ductus arteriosus to constrict, preventing entry of blood from the pulmonary artery
The pulmonary blood vessels respond to the increased oxygenation by dilating
At the same time, fetal lung fluid shifts into the interstitial spaces and is removed by blood and lymph vessels
These changes decrease pulmonary vascular resistance by 80% and allow the vessels to expand to hold the suddenly increased blood flow from the pulmonary artery
At birth, pressures between the right and left sides of the heart are reversed. The sudden dilation of the vessels of the lungs allows blood to enter freely from the right ventricle and decreases pressure in the right side of the heart.
Clamping of the umbilical cord closes the ductus venosus and further decreases pressure in the right side of the heart.
Increased blood flow from the pulmonary veins into the left atrium causes pressure in the left side of the heart to build
Systemic resistance increases as blood flow to the placenta ends with clamping of the cord, and this also elevates pressure in the left heart.
Changes at Birth Cont.
The foramen ovale's flap valve closes when the pressure in the left atrium is higher than that in the right atrium.
This change forces the blood from the right atrium into the right ventricle and pulmonary artery.
Because the ductus arteriosus is lso closing, the blood continues into the lungs for oxygenation and returns to the left atrium through the pulmonary veins
Blood from the left atrium enters the left ventricle and leaves through the aorta to circulate to the rest of the body.
Thus blood flow through the heart and lungs changes from fetal to neonatal circulation and is similar to that in the normal adult
Conditions such as asphyxia and persistent pulmonary HTN however, may reverse the pressures in the heart and cause the foramen ovale to re-open
The ductus ateriosus closes gradually as oxygenation improves and prostaglandins, which helped keep it open, are metabolized.
Until closure is complete, a small amt of blood may shunt through the ductus arteriosus from the aorta to the pulm artery, a reverse of flow during fetal life.
This sequence occurs because pressure in the aorta has become higher than that in the pulm artery
A murmur may be heard as a result of blood flow through the partially open vessel
Low levels of oxygen in the blood may cause the ductus arteriosus to dilate and the pulm vessels to constrict, increasing resistance to blood flow to the lungs
The result may be opening of the foramen ovale to allow a right-to-left shunt of blood and flow from the pulmonary artery through the ductus arteriosus and into the aorta.
A patent ductus arteriosus may occur in the infant who experiences asphyxia at birth, becomes hypoxic, or is preterm
Study Table 19-1
Neurologic Adaptation: Thermoregulation
At birth, the infant must assume thermoregulation, the maintenance of body temp
Although the fetus produces heat in utero, the consistently warm temp of the amniotic fluid and the mother's body makes thermoregulation unnecessary.
The infant's temp may drop as much as 0.2-1 degree C (0.5-1.7 F) per minute if not kept warm at birth
Neonates must produce and maintain enough heat to prevent cold stress, which can have serious and even fatal effects
Newborn Characteristics That Lead to Heat Loss
Certain characteristics predispose newborns to lose heat.
The skin is thin, and blood vessels are close to the surface
Little subQ fat or white fat is present to provide a barrier to heat loss
Heat is readily transferred from the warmer internal areas of the body to the cooler skin surfaces and then to the surrounding air.
Newborns have 3 times mor surface area to body mass than adults, which provides more area for heat loss
Newborns lose heat at a rate 4 times greater than that of adults
The healthy full-term infant remains in a position of flexion, reducing the amt of skin surface exposed to the surrounding temp and decreasing heat loss
Sick or preterm infants have decreased muscle tone and are unable to maintain a flexed position
Preterm infants also have thinner skin and even less white subQ fat than full-term infants
Therefore, they are at increased risk for cold stress
Methods of Heat Loss
Heat is lost in 4 ways
1. Evaporation: air drying of the skin that results in cooling. Drying the infant, esp the head, as quickly as possible helps prevent loss of heat by evaporation. Insensible water loss from the skin and respiratory tract increases heat loss from evaporation.
2. Conduction: Movement of heat away from the body occurs when newborns have direct contact with objects that are cooler than their skin. Placing infants on cold surfaces or touching them with cool objects causes this type of heat loss. The reverse is also true: Contact with warm objects increases body heat by conduction. Warming objects that will touch the infant or placing the unclothed infant against the mother's skin helps prevent conductive heat loss.
3. Convection: Transfer of heat from the infant to cooler surrounding air occurs in convection. When infants are in incubators, the circulating warm ir helps keep them warm by convection. Providing a warm, draft-free environment avoids convective heat loss. "Draft, wind, open window"
4. Radiation: Transfer of heat to cooler objects that are not in direct contact with the infant. Infants in incubators transfer heat to the walls of the incubator. If the walls of the incubator are cold, the infant is cooled, even when the temperature of the air inside the incubator is warm. To combat this problem, incubators have double walls. Placing cribs and incubators away from windows and outside walls minimizes radiant heat loss. Newborns can gain heat by radiation, too. sing a radiant warmer transfers heat from the warmer to the cooler infant.
Nonshivering Thermogenesis p. 373
When adults are cold, they shiver, increasing muscle activity to produce heat
Shivering is not an important method of thermogenesis for newborns who rarely shiver except during prolonged exposure to low temperatures. Instead, they become restless and cry.
Their increased activity and flexion help generate some warmth and reduce heat loss from exposed surface areas of the body
Exposure to cool temperatures also results in peripheral vasoconstriction, decreasing flow of warm blood to the skin
This helps prevent heat loss from the skin and causes the skin to feel cool to the touch
Acrocyanosis (bluish discoloration of the hands and feet) may occur.
In addition, a drop in temp increases the metabolic rate as much as 200-300%, causing above-normal oxygen and glucose use.
The primary method of heat production in infants is nonshivering thermogenesis (NST), the metabolism of brown fat to produce heat
Newborns can increase heat production by 100% by using NST
Brown fat contains and abundant supply of blood vessels, which cause the brown color.
Brown fat is located primarily around the back of the neck; in the axillae; around the heart, kidney and adrenals; between the scapulae; and along the abdominal aorta
As brown fat is metabolized, it generates more heat than white subQ fat.
Blood passing through brown fat is warmed and carries heat to the rest of the body
NST begins when thermal receptors in the skin detect a skin temp of 35-36 C (95-96 F)
Thermal receptor stimulation is transmitted to the hypothalamic thermal center
As a result, norepinephrine is released in brown fat, initiating its metabolism
NST goes into effects even before a change occurs in core (interior) body temp, as measured with a rectal thermometer
Activating thermogenesis before core temp decreases allows the body to maintain internal heat at an even level.
NST may begin in an infant when skin temp has been cooled, even though core measurements show normal readings
A decreased core temp will not occur until NST is no longer effective.
Some infants have adequate bornw fat stores. It is accumulated mainly during the 3rd trimester, so preterm infants may be born before adequate stores of brown fat have accumulated.
IUGR may deplete brown fat stores before birth.
Hypoxia, hypoglycemia, and acidosis may interfere with the infant's ability to use bornw fat to generate heat
These infants are not able to raise their body temperature if they are subjected to cold stressand may have serious complications
Effects of Cold Stress
The increased metabolic rate and metabolism of brown fat that result from cold stress can cause a sig rise in the need for O2.
If an infant is having even mild resp distress, the problem may be exacerbated if added O2 is used for heat production
Cold stress also causes a diminished production of surfactant, impeding lung expansion and leading to more resp distress
Glucose is also necessary in larger amts when the metabolic rate rises to produce heat
When glycogen stores are converted to glucose, they may be quickly depleted causing hypoglycemia.
Cont use of glucose for temp maintenance leaves less available for growth
Metabolism of glucose in the presence of insufficient O2 causes increased production of acids
Metabolsim of brown fat also releases fatty acids
The result can be metabolic acidosis, which can be life-threatening
Elevated fatty acids in the blood can interfere with transport of bilirubin to the liver, increasing the risk of jaundice
As the infant's body attempts to conserve heat, vasoconstriction of the peripheral blood vessels occurs to reduce heat loss from the skin surface.
Decreased O2 concentration in the blood, however, may also cause vasoconstriction of the pulmonary vessels leading to further respiratory distress
Neutral Thermal Environment
An environment when the infant can maintain a stable body temp with minimal O2 need and without an increase in metabolic rate
The range of environmental temp that allows this stability is called thermoneutral zone
In healthy, unclothed, full-term newborns, an environmental temp of 32-33.5 C (89.6-92.3 F) orovides thermoneutral zone
When the infant is dressed it is 24-27 C (75.2-80.6 F)
The thermoneutral zone for each infant varies according to the infant's gest age, size, and postnatal age
Infants also respond poorly to hyperthermia
With an elevated temp the metabolic rate rises, causing an increased need for O2 and glucose and possible metabloic acidosis
In addition, peripheral vasodilation leads to increased insensible fluid losses
Sweating may occur but is often delayed because sweat glands are immature
Newborns may be overheated by poorly regulated equipment designed to keep them warm
When radiant warmers, warming lights, or warmed incubators are used, the temp mechanism must be set to vary the heat according to the infant's skin temp and thus prevent heat that is too high or too low.
Alarms to signal that the infant's temp is too high or too low should be functioning properly
Hematologic Adaptation: Factors that Affect Blood
The blood volume of the term newborn is 80-100 ml/kg but thus varies according to the time of the cord clamping, the gest age, and the position of the infant when the cord is clamped
Pre-term infants have a greater blood volume/kg than term infants.
Blood samples drawn from the heel, where the circulation is sluggish, show higher hemoglobin, hematocrit, and erythrocyte values than samples taken from central areas
Venous blood samples are more accurate and are taken when precise measurement is essential
1. Erythrocytes and Hemoglobin: At birth the infant has comparatively more erythrocytes and higher hemoglobin levels than the adult. This difference is necessary bc the partial pressure of oxygen in fetal blood is much lower than the normal adult level. Adequate oxygenation of the cells is possible bc fetal hemoglobin carries 20%-50% more oxygen than adult hemoglobin
2. Hematocrit: Normal newborn is 44%-70% for the first month. A level above 65% from a central site indicates polycythemia (high erythrocytes), whcih increases the risk of jaundice and injury to the brain and other organs as a result of blood stasis. Respiratory distress and hypoglycemia are more common in these infants
3. Leukocytes: The leukocyte (WBC) count at birth is 9,100/mm to 34,000/mm. the average WBC is 15,000 in term infants. In newborns an elevated WBC count does NOT necessarily indicate infection. In fact, the WBC count may decrease in infections.
Increased numbers of immature leukocytes are a sign of infection or sepsis in the neonate
The number of platelets may also decrease as a result of infections.
Risk of clotting Deficiency
Newborns are at risk for clotting deficiency during the first few days of life bc they have low levels of Vit K, which is necessary to activate several of the clotting factors.
Vit K is synthesized in the intestines, but food and normal intestinal flora are necessary for this process. At birth the intestines are sterile and therfore unable to produce Vit K
To decrease the risk of hemorrhagic disease of the newborn, Vit K is administered intramuscularly to most newborns in the United States during initial care.
Drugs such as Phenytoin, Phenobarbital, and Antituberculosis drugs taken by the mother during pregnancy interfere with clotting ability in the infant after birth.
The platelet (thrombocyte) count ranges from 84,000/mm to 478,000/mm at birth.
After the first week platelet levels are the same as in the adult - 150,000/mm to 400,000/mm
Although platelet counts in term newborns are neaar adult levels, platelet response to stimuli is decreased during the first few days of life.
Newborns must begin to take in, digest, and absorb food after birth because the placenta no longer performs these functions for them.
Newborn's stomach capacity is about 6 mL/kg at birth
Gastric emptying may be delayed at first
It is twice as rapid after ingestion of human milk than after formula and slower if the infant has swallowed mucus
The gastrocolic reflex is stimulated when the stomach fills, causing increased intestinal peristalsis.
Infants frequently pass a stool during or after a feeding
The cardiac sphincter between the esophagus and the stomach is relaxed, which explains the tendency to regurgitate feedings easily.
The intestines of the newborn are long in proportion to the infant's size and compared with those of the adult.
The added length allows more surface for absorption but makes infants more prone to water loss should diarrhea develop.
Air enters the GI tract soon after birth, and bowel sounds may be heard beginning at 15 minutes after birth
The digestive tract is sterile at birth
Once the infant is exposed to the external environment and begins to take in fluids, bacteria enter the gastrointestinal tract
Normal intestinal flora are established within the first few days
Maturation of the ability to digest and absorb occurs at different rates for various nutrients.
Pancreatic amylase, needed to digest complex carbs, is deficient for the first 4-6 months after birth.
Amylase is also produced by the salivary glands, but in low amts until about the 3rd month of life
Amylase is present in breast milk
The newborn is also deficient in pancreatic lipase, limiting fat absorption significantly.
Lipase present in the mouth and stomach helps with some digestion of fat
Lipase is present in breast milk, which may make it more digestible for the newborn than formula.
Protein and lactose, the major carbohydrate in the infant's milk diet, are both well digested.
Meconium is the first stool excreted by the newborn.
It consists of particles from amniotic fluid such as vernix, skin cells, and hair, along with cells shed from the intestinal tract, bile, and other intestinal secretions.
Meconium is greenish black with a thick, sticky, tarlike consistency.
The first meconium stool is usually passed within 12 hours of life, and 99% of neonates pass meconium within 48 hours
If meconium is not passed within that time, obstruction is suspected
Meconium stools are followed by transitional stools, a combination of meconium and milk stools.
They are greenish brown and of a looser consistency than meconium
Milk stools characteristic of of the type of feeding given to the infant occur next.
The stools of infants fed with breast milk are seedy and the color and consistency of mustard, with a sweet-sour smell.
The breastfed infant generally has more frequent stools than the infant who is formula fed.
A stool may be passed with each feeding.
Some older infants pass only one stool every 2-3 days.
the normal breastfed newborn should have at least 4 or more stools daily.
The formula-fed infant has pale yellow to light brown stools.
They are firmer in consistency than those of the breastfed infant
The infant may excrete several stools daily, or only one or two.
The stools have the characteristic odor of feces.
The important functions of the liver after birth include: Maintenance of blood glucose levels, conjugation of bilirubin, production of factors necessary for blood coag, storage of iron, and metabolism of drugs.
Blood Glucose Maintenance
Throughout gestation, glucose is supplied to the fetus by the placenta.
During the third trimester, glucose is stored as glycogen primarily in the fetal liver and skeletal muscles for use after birth.
These stores are almost completely depleted within 12 hours after birth
They are used for energy during the stress of delivery and for breathing, heat production, movement against gravity, and activation of all the functions that the neonate must assume at birth.
Until newborns begin regular feedings and their intake is adequate to meet energy requirements, the glucose present in the body is used,
As the blood glucose level falls, stored glycogen in the liver is converted to glucose for use.
Although the brain can use alternative fuels such as ketones and fatty acids if necessary, glucose is the primary source of energy,
Glucose concentration in the blood commonly falls to the lowest levels by 60 to 90 minutes after birth but rises and stabilizes in 2 to 3 hours after birth
In the term infant, lucose levels should be 40-60 mg/dL on the first day and 50-90 mg/dL thereafter
There is no general consensus about the level of blood glucose that defines hypoglycemia, but a level below 40-45 mg/dL in the term infant is often used
Many newborns are at increased risk for hypoglycemia.
In the preterm, late preterm (34-36 wks gestation), and SGA infant, adequate stores of glycogen or even fat for metabolism may not have accumulated.
Stores may be used up before birth in the postterm infant because of poor intrauterine nourishment from a deteriorating placenta.
LGA infants and those with diabetic mothers may produce excessive insulin that consumes available glucose quickly.
Infants exposed to such stressors as asphyxia or infection may exhaust their stores of glycogen.
The cold-stressed infant may deplete glycogen to increase metabolsim and raise body temperature
Conjugation of Bilirubin
A major function of the liver is the conjugation of bilirubin
The newborn;s liver may not be mature enough to prevent jaundice during the first week of life.
Jaundice results from hyperbilirubinemia, excessive bilirubin in the blood
It occurs in 60% of term newborns and 80% of preterm infants
Source and Effect of Bilirubin
The principal source of bilirubin is the hemolysis of erthryocytes
This is a normal occurrence after birth, when fewer erythrocytes are needed than during fetal life
The breakdown of RBCs releases their components into the bloodstream to be reused by the body
Only bilirubin remains as an unusable residue in the blood
This substance is toxic to the body and must be excreted
Bilirubin is released in an unconjugated form
Unconjugated bilirubin, also called indirect bilirubin, is soluble in fat but not in water
Before excretion can occur, the liver must change it to a water-soluble form by a process called conjugation.
The bilirubin is then known as conjugated, or direct, bilirubin
Conjugated bilirubin is not toxic to the body and can be excreted.
Because the unconjugated nilirubin is fat soluble, it may be absorbed by the subcutaneous fat, causing the yellowish discoloration of the skin called jaundice.
If enough unconjugated bilirubin accumulates in the blood, staining of the tissues in the brain may occur.
This may cause acute bilirubin encephalopathy, a neurologic condition resulting from bilirubin toxicity.
If this condition becomes chronic, it causes permanent neurologic injury known as kernicterus.
The level of bilirubin necessary to cause injury to the central nervous ssstem is unknown and may be different for various infants.
When unconjugated bilirubin is released into the bloodstream, it attaches to binding sites on albumin in the plasma and is carried to the liver.
If an adequate number of albumin-binding sites are not available, bilirubin circulates as unbound or free unconjugated bilirubin
Bilirubin can be displaced from albumin by some medications.
Free fatty acids, acidosis, and infection also decrease albumin binding of bilirubin
It is the freem unbound unconjugated bilirubin that can move into the tissues and cross the blood-brain barrier.
When the albumin-bound bilirubin reaches the liver, it is changed to the conjugated form of bilirubin by the enzyme uridine diphosphate glucuronyl transferase (UDPGT)
Conjugated bilirubin is excreted into the bile and then into the duodenum
In the intestines, the normal flora act to reduce bilirubin to urobilinogen and stercoblin, which are excreted in the stools
Some urobilinogen is excreted by the kidneys.
A small percentage of conjugated bilirubin may be deconjugated, or converted back to unconjugated state, by the intestinal enzyme beta-glucuronidase.
This enzyme is important in fetal life because only unconjugated bilirubin can be cleared by the placenta for the conjugation by the mother's liver.
In the newborn, deconjugated bilirubin in the intestines in reabsorbed into the portal circulation and carried back to the liver, where it again undergoes the conjugation process.
The recirculation of bilirubin is called enterohepatic circuit and it creates additional work for the liver.
Blood tests for biliruibin measure total serum bilirubin (TSB) and direct (conjugated) bilirubin the serum.
TSB is a combination of indirect (unconjugated) and direct bilirubin.
Factors in Increased Bilirubin
A number of factors lead to the production of excessive amts of bilirubin or interfere with the normal process of conjugation
These increase the incidence of jaundice during the first week of life
Approx 8-10 mg/kg of bilirubin is produced in newborns each day, a rate twice that in adults
Newborns have more RBCs per kilogram than adults
Red Blood Cell Life
Fetal RBCs break down more quickly than adult erythrocytes. They last 80-100 days in term infants and 60 to 80 days in preterm infants, as compared with RBCs in adults, which have a typical life span of 120 days
In addition, neonate erythrocytes are more fragile and susceptible to injury than those in the adult
Compared to adults, for their size neonates have more RBCs breaking down faster and producing greater amounts of bilirubin to excrete
Newborns have less albumin, decreased albumin binding capacity, and decreased albumin affinity for bilirubin than adults
The newborn's immature liver may not produce adequate amts of UDPGT and other substances during the first few days of life. This limits the amount of bilirubin that can be conjugated
Rh, ABO, OR OTHER INCOMPATIBLE BLOOD BETWEEN THE MOTHER AND THE INFANT MAY INCREASE RBC BREAKDOWN
Preterm and late preterm infants have immature conjugation abilities
At birth the intestines of the newborn are sterile.
Conjugated bilirubin cannot be reduced to urobilinobgen or stercobilin for excretion without the action of intestinal flora.
In addition,the newborn intestines have a large amt of the enzyme beta-glucuronidase, which changes bilirubin back to the unconjugated state.
Intestinal motiliy is decreased, allowing more time for the enzyme to act.
These factors may result in high levels of unconjugated bilirubin, which is reabsorbed into the blood circulation.
Feeding the newborn helps establish the normal intestinal flora and promotes passage of meconium, which is high in bilirubin.
When feedings are delayed or taken poorly, normal flora are not established, and passage of meconium, which is high in bilirubin, is delayed.
Delayed passage of stools allows more time for exposure to beta-glucuronidase, increasing the chance that conjugated bilirubin will be converted to the unconjugated state and absorbed into the blood.
Trauma during birth, such as bruising or a cephalhematoma, causes increased hemolysis of RBCs
As the RBCs in the traumatized areas break down, they add to the bilirubin load.
Fatty acids have a great affinity than bilirubin for the binding sites on albumin and bind to albumin in place of bilirubin
Fatty acids are released when brown fat is used to increase heat during cold stress.
during asphyxia, anaerobic metabolism also produces free fatty acids.
Therefore, the level of unbound unconjugated bilirubin is increased in these infants and jaundice may develop
Infants who are Asian, Native American, or Eskimo or have a sibling who had jaundice are more likely to be affected.
Infants of diabetic mothers are also at increased risk of jaundice
Some drugs (Sulfisoxazole) given to the mother during pregnancy or to the infant increase jaundice.
Blood swallowed during birth, hypoglycemia, infection, and hemolytic anemias also increase jaundice.
Transient hyperbilirubinemia and considered normal
Not present in the first 24 hours of life in term infants but appears on the second or third day after birth
Jaundice becomes visible when the bilirubin level is greater than 5 mg/dL
The rate at which the bilirubin level in the blood rises and falls is important bc it helps determine whether the rate for a particular infant is following the expected curve for age and birth weight
In physiologic jaundice, the bilirubin peaks at between the second and fourth days of life and falls to normal levels by 5 to 7 days
The bilirubin level rises higher and falls more slowly in Asian infants
Jaundice that is physiologic or normal must be differentiated from nonphysiologic or pathologic jaundice that requires further investigation
One of the most important differences is the time at which jaundice appears
Pathologic jaundice may occur in the first 24 hours
When bilirubin rises higher or more rapidly than expected or stays elevated for longer than expected, earlier treatment is needed to prevent severe hyperbilirubinemia
Nonphysiologic jaundice is a result of abnormalities causing excess destruction of RBCs or problems in bilirubin conjugation
These include incompatibilities between the mother's and the infant's blood types, infection, and metabolic disorders.
Nonphysiologic jaundice is often treated with phototherapy
Infants who are preterm may receive treatment for hyperbilirubinemia at lower TSB levels than full-term infants
Jaundice Assoc with Breastfeeding
The breastfed infant has a higher risk of developing jaundice which may begin early or late after birth
Breastfeeding or Early-Onset Jaundice
Bilrubin levels greater than 12 ml/dL develop in 13% of breastfed infants by 1 week of age
The most common cause of jaundice in breastfed infants is insufficient intake
Jaundice begins within the first week of life, and serum bilirubin may reach dangerous levels if intake is not increased
Infants who are sleepy, have a poor suck, or nurse infrequently may not receive enough colostrum - the substance that precedes true breast milk - to benefit from its normal laxative effect in eliminating bilirubin-rich meconium.
When meconium is not eliminated, the bilirubin may be deconjugated by beta-glucuronidase in the intestine, absorbed, and recirculated to the liver for conjugation again.
Lack of adequate suckling depresses production of breast milk and increases the problem further.
Helping the mother with breastfeeding to increase the infant's intake and stimulate milk production may be the most important treatment
Supplementing with formula interferes with the mother's milk production.
However, if breastfeeding is inadequate and the infant is dehydrated or losing excessive weight, supplements of expressed breast milk or formula may be necessary.
Glucose-water will not reduce bilirubin levels and should be avoided
True Breast Milk Jaundice
Occurs after the first 3-5 days of life
Lasts 3 weeks to aslong as 3 months for some infants
The TSB usually peaks at 5-10 mg/dL and falls gradually over several months
Some infants reach levels of 20-30 mg/dL
The exact cause of true breast milk jaundice is unknown
Substances in the breast milk may increase absorption of bilirubin from the intestine or interfere with conjugation
This may be a form ofphysiologic jaundice in breastfed infants.
Infant have no signs of illness
*Treatment of breast milk jaundice includes close monitoring of TSB and at least 8-12 feedings every 24 hours
Feed every 2-3 hours if jaundiced*
Interruption of breast feeding is generally not recommended
However, if the TSB levels are dangerously high, the HCP may order formula feeding be given for 1-3 days while the mother uses a breast pump to maintain milk supply
Temporarily switching to formula causes a rapid drop in bilirubin level
If the level rises while breastfeeding is interrupted, jaundice from another cause should be investigated.
The level may rise again when breastfeeding is resumed but generally not high enough to interfere with further breastfeeding
Prothrombin and coagulation factors are produced by the liver and activated by Vit K, which is deficient in the newborn
Iron is stored in the fetal liver and spleen during the last weeks of pregnancy
Full-term infants who are breastfeeding usually do not need added iron until 6 months of age
At that time, they should begin iron-containing foods or iron supplements
All infants who are not breastfeeding should be given iron-fortified formula
Metabolism of Drugs
The liver metabolizes drugs inefficiently in newborns
This must be considered when drugs are given to the neonate
A breast feeding mother should alert her HCP before taking medications, as harmful amounts may be transferred to the infant via the breast milk
By 34-36 weeks, the fetal kidneys have as many nephrons as an adult
Blood flow to the kidneys increases after birth, and resistance in the renal vessels decreases.
The improved perfusion results in a steady improvement in kidney function during the first few days of life
The newborn's kidney function is immature compared with that of the adult.
The ability of the glomeruli to filter and the renal tubules to reabsorb is considerably less than in adults.
The GFR doubles or triples during the first weeks of life but does not reach adult levels until 1-2 years of age
Therefore infants have a decreased ability to remove waste products from the blood
Small amts of substances such as glucose and amino acids may escape into the urine of the neonate
They disappear within the first few days of life as kidney function improves
Uric acid crystals may give a reddish color to the urine that is sometimes mistaken for blood
Voiding occurs within 12 hours for 50% of newborns, 92% within 24 hours, and 99% within 48 hours of life
Failure to void within that time may be a result of hypovolemia from inadequate intake of fluids
Absence of kidneys or anomalies that interfere with excretion of urine are usually discovered before birth because they cause oligohydramnios, low amniotic fluid volume.
This generally prompts investigation into the cause during pregnancy
Only 1-2 voidings may occur during the first 2 days of life, although a higher number is common.
The infant voids at least 6 times a day by the 4th day
Newborns have a lower tolerance for changes in total volume of body fluid than do older infants
This is because of the location of water within the newborn;s body and the inability of the kidneys to adapt to large changes in fluid volume
Fluid turnover rate is greater than that in adults
To maintain fluid balance, full-term infants need 60-100 mL/kg daily during the first 3-5 days of life and 150-175 mL/kg a day by 7 days of age
78% of the newborn;s body is composed of water
Intracellular water constitutes 34% of the body and extracellular water comprises 44% of the body
Interstitial water volume is 3 times greater than in adults
Although fluid within the cells is relatively stable, extracellular water is easily lost from the body
Because infants have more fluid for their size than adults, and because a larger proportion of it is located outside the cells, total body water is easily depleted
Conditions such as vomiting and diarrhea can quickly result in life-threatening dehydration.
At birth, normal diuresis causes a 5% to 10% weight loss as excess extracellular water is lost
Insensible Water Loss
Water lost from the skin and respiratory tract contributes to insensible water loss
These losses are increased in the newborn because of the large surface area of the body and the rapid respiratory rate
Fluid losses increase greatly when infants are placed under radiant warmers or phototherapy lights, which accelerate evaporation from the skin.
An elevated respiratory rate or low humidity in the air surrounding the infant raises insensible water losses even further.
Urine Dilution and Concentration
The ability of a newborn's kidneys to dilute urine is similar to that of adults, but they have only half the adult's ability to concentrate urine.
However, a newborn's kidneys cannot handle large increases in fluids, which result in fluid overload
This is most likely to happen if infants receive too much IV fluid
Normal urine output is 2-5 ml/kg/hr, and urine specific gravity is 1.002 to 1.01
When abnormal conditions such as diarrhea cause excessive loss of fluid, the newborn's limited ability to conserve water may result in dehydration more quickly than in the older infant or child.
Acid Base and Electrolyte Imbalance
The maintenance of acid-base and electrolyte balance is a primary function of the kidneys and may be precarious in neonates
Newborns tend to lost bicarbonate at lower levels than adults, increasing their risk for metabolic acidosis
The excretion of solutes also is less efficient in newborns
Although newborns conserve needed sodium well, they are limited in excretion of sodium; this is especially a problem if they receive excessive amounts.
The neonate is less effective in fighting infection than the older infant or child.
Leukocytes are delayed in moving to the site of invasion and are inefficient in destroying the invader
The infant's decreased ability to localize infection leads to a tendency toward generalized sepsis.
Fever and leukocytosis, which occur during infection of the older child, are often not present in the newborn with infection
This lack of response occurs because the hypothalamus and inflammatory responses are immature.
Nonspecific signs such as changes in activity, color, tone, or feeding may be the only signs of sepsis.
Because of their immature immune system, infants are susceptible to some pathogens that do not usually affect older children.
Full-term newborns receive antibodies from their mothers during the last trimester of pregnancy.
The mother continues to provide passive antibodies to the infant in her milk if she chooses to breastfeed
Immunoglobins (serum globulins with antibody activity) help protect the newborn from infection.
The major immunoglobins are IgG, IgM, and IgA, each of which performs a different function.
At birth the infant's total immunoglobin levels range from 55%-80% of the adult levels
Only immunoglobin G crosses the placenta with passage beginning in the first trimester
Preterm infants have less IgG because transfer is greatest during the third trimerster
IgG provides the fetus with passive temporary immunity to bacteria, bacterial toxins, and viruses to which the mother has developed immunity
The full-term infant has IgG levels that are as high as or higher than those of the mother
Although the fetus makes some IgG, significant production of IgG is delayed until after 6 months of age
The infant gradually produces larger quantities of the immunoglobin to replace IgG from the mother, which is being catabolized.
The passive immunity gradually disappears reaching the lowest level at 2-4 months of age
Immunoglobin M is the first immunoglobin produced by the body when the newborn is challenged
This immunoglobin helps protect against gram-negative bacteria
Rapid production of IgM begins a few days after birth as a result of exposure to environmental antigens
IgM cannot cross the placenta because the molecules are too large.
If IgM is found in cord blood, exposure to infection in utero has occured
Immunoglobin A also does not cross the placenta and must be produced by the infant
IgA is important in protection of the GI and respiratory systems, and newborns are particularly susceptible to infections of those systems.
*Secretory IgA is present in colostrum and breast milk.
Therefore, breastfed infants may receive protection that formula-fed infants do not*
In the early hours after birth, the infant goes through changes called periods of reactivity
The 2 periods of reactivity are separated by a period of sleep or decreased activity
First Period of Reactivity
Begins at birth and lasts for 30 minutes.
Infants are active at this time and appear wide awake, alert, and interested in their surroundings
Parents enjoy watching the infant gaze directly at them when held in the en face position
Infants move their arms and legs energetically, root, and appear hungry
If allowed to nurse, many infants latch on to the nipple and suck well.
The temperature may be decreased during this period
Respirations may be as high as 80 breaths per minute
The heart rate may be elevated to 180 beats/min
Crackles, grunting, retractions, and nasal flaring may be present
The pulse and respiratory rate gradually slow, and the infant becomes sleepy
Period of Sleep or Decreased Activity
After the first period of reactivity, infants become quieter or fall into a deep sleep
During this time the pulse and respirations drop into the normal range
Bowel sounds are audible and meconium may be passed
Second Period of Reactivity
Lasts 4-6 hours
Infants have alert periods, and parents may enjoy the opportunity to get to know their infant at this time
Infants become interested in feeding and may pass meconium
There may be tachycardia and rapid respirations
Mucous secretions increase, and infants may gag or regurgitate
6 gradations in the behavioral state of the infat have been indentified tanging from quiet sleep to crying
The amount of time infants spend in the different sleep-wake state varies and is a key to their individuality
Deep or Quiet Sleep State
During the quiet sleep state the infant is in deep sleep with closed eyes and no eye movement
Respirations are quiet, regular, and slower than in the other states
Although startles occur at intervals, the infant's body is quiet
The infant is very difficult to arouse and will not feed.
Light or Active Sleep State
The active sleep state is a lighter sleep in which infant;s eyes are closed
They move their extremities, stretch, change facial expressions, make sucking movements, and may fuss briefly
During this period, respirations tend to be more rapid and irregular and rapid eye movements occur
Infants are more likely to startle from noise or disturbances and may return to sleep or move to an awake state
Transitional period between sleep and waking similar to that experienced by adults as they awaken
The eyes may remain closed or, if open, appear glaxed and unfocused
Infants startle and move their extremities slowly
They may go back to sleep or, with gentle stimulation, gradually awaken
Quiet Alert State
Also called Alert Inactivity
Should be pointed out to parents because it is an excellent time to increase bonding time
Infants focus on objects or people, respond to the parents with intense gazing and seem bright and interested in their surroundings
they respond to stimuli and interaction with others
Body movements are minimal as infants seems to concentrate on the environment
Active Alert State
Infants seem restless, have increased motor movements, and may be fussy
Infants have faster and more irregular respirations, may hiccup or regurgitate, and seem more aware of feelings of discomfort from hunger or cold
Although their eyes may be open, infants seem less focused on visual stimuli than during the quiet alert state
May quickly follow the active alert state if no intervention occurs to comfort the infant
The cries are continuous and lusty, active body movements occurs, and the infant does not respond positively to stimulation
Respirations are irregular and rapid
It may take a period of comforting to move the infant to a state in which feeding or other activities can be accomplished
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