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2. Identification of At-Risk Newborns. HistoryMaternalSocio-economic statusEnvironmental exposureHealth history (age, parity)Maternal medical complicationsPregnancy complicationsNewbornBirth weightGestational age. 3. Care of the SGA or IUGR Newborn. Small for Gestational AgeIntrauterine growth restriction.
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1. 1 The Newborn at Risk: Conditions Present at Birth
2. 2 Identification of At-Risk Newborns History
Maternal
Socio-economic status
Environmental exposure
Health history (age, parity)
Maternal medical complications
Pregnancy complications
Newborn
Birth weight
Gestational age
History- this is one of the most important aspects of newborn care. Assessment of the history surrounding the newborn’s birth.
Low socioeconomic status often equates with limited availability or accessibility to prenatal healthcare. Potentially compromising health conditions will not be picked up and treated if knowledge of the disorder or access to healthcare is not made.
Environmental factors such as high altitude, roentegen exposure, exposure to teratogenic agents, smoke, and prescribed or illicit drugs place the newborn at risk.
Mothers who are on either end of the age spectrum are at risk for the delivery of a compromised newborn. Mothers who are young adolescents (less than 16) and mothers who are advanced for maternal age (greater than 40) are at risk for a compromised newborn. Placental factors affect fetal circulation.
Fetal factors such as congenital infections (rubella,TORCH), chromosomal abnormalities
Newborns are classified according to weight as SGA, AGA, or LGA.
SGA are those newborns who fall below the 10th percentile, LGA are those above the 90th percentile, and AGA are those who fall in between
Infants of smaller birth weight and gestational age are more at risk for mortality and morbidity.
Morbidity refers to associated conditions that are precipitated by certain events
These morbidities are listed on pp 686, figure 27-2.
Newborns at risk deserve and require special observation since the most subtle changes in the newborn can be the beginning of one of the listed morbidity. Sepsis for example, reveals itself in the very early stages as temperature instability, feeding intolerance, or irritability.
History- this is one of the most important aspects of newborn care. Assessment of the history surrounding the newborn’s birth.
Low socioeconomic status often equates with limited availability or accessibility to prenatal healthcare. Potentially compromising health conditions will not be picked up and treated if knowledge of the disorder or access to healthcare is not made.
Environmental factors such as high altitude, roentegen exposure, exposure to teratogenic agents, smoke, and prescribed or illicit drugs place the newborn at risk.
Mothers who are on either end of the age spectrum are at risk for the delivery of a compromised newborn. Mothers who are young adolescents (less than 16) and mothers who are advanced for maternal age (greater than 40) are at risk for a compromised newborn. Placental factors affect fetal circulation.
Fetal factors such as congenital infections (rubella,TORCH), chromosomal abnormalities
Newborns are classified according to weight as SGA, AGA, or LGA.
SGA are those newborns who fall below the 10th percentile, LGA are those above the 90th percentile, and AGA are those who fall in between
Infants of smaller birth weight and gestational age are more at risk for mortality and morbidity.
Morbidity refers to associated conditions that are precipitated by certain events
These morbidities are listed on pp 686, figure 27-2.
Newborns at risk deserve and require special observation since the most subtle changes in the newborn can be the beginning of one of the listed morbidity. Sepsis for example, reveals itself in the very early stages as temperature instability, feeding intolerance, or irritability.
3. 3 Care of the SGA or IUGR Newborn Small for Gestational Age
Intrauterine growth restriction SGA refers to the newborn who is small for gestational age, the newborn’s weight is below the 10th percentile for that particular gestational age
IUGR refers to the newborn who has encountered slow development in utero.This newborn typically has the resemblance of an older person trapped in a newborn body, the skin sags, weight is decreased, ability to regulate temperature and tolerate feedings are often delayed.
IUGR can be precipitated by intrauterine infection such as viral illnesses of the TORCH series. There are two types of IUGR, the better type to have is the asymmetric IUGR that suggest the insult in growth occurred late in the gestation.
Symmetric IUGR suggest the insult in growth occurred early in the gestation from chronic infection or insult of some king such as severe malnutrition, substance abuse, chronic hypertension
Symmetric IUGR has worse outcomes, such as long-term cognitive difficulties
Asymmetric IUGR suggest the insult resulting in growth restriction occurred late in the pregnancy. These newborns have a more favorable outcome. This is referred to head-sparing IUGR as the head is usually in the normal range, but the weight is below the 10th percentile.
The asymmetric IUGR newborn is at risk for asphyxia, pulmonary hemorrhage, hypocalcemia and hypoglycemia.
Both the IUGR newborn and the SGA newborn are at risk for hypothermia and hypoglycemia. The IUGR newborn is at risk also for aspiration syndrome and asphyxia, congenital malformation.SGA refers to the newborn who is small for gestational age, the newborn’s weight is below the 10th percentile for that particular gestational age
IUGR refers to the newborn who has encountered slow development in utero.This newborn typically has the resemblance of an older person trapped in a newborn body, the skin sags, weight is decreased, ability to regulate temperature and tolerate feedings are often delayed.
IUGR can be precipitated by intrauterine infection such as viral illnesses of the TORCH series. There are two types of IUGR, the better type to have is the asymmetric IUGR that suggest the insult in growth occurred late in the gestation.
Symmetric IUGR suggest the insult in growth occurred early in the gestation from chronic infection or insult of some king such as severe malnutrition, substance abuse, chronic hypertension
Symmetric IUGR has worse outcomes, such as long-term cognitive difficulties
Asymmetric IUGR suggest the insult resulting in growth restriction occurred late in the pregnancy. These newborns have a more favorable outcome. This is referred to head-sparing IUGR as the head is usually in the normal range, but the weight is below the 10th percentile.
The asymmetric IUGR newborn is at risk for asphyxia, pulmonary hemorrhage, hypocalcemia and hypoglycemia.
Both the IUGR newborn and the SGA newborn are at risk for hypothermia and hypoglycemia. The IUGR newborn is at risk also for aspiration syndrome and asphyxia, congenital malformation.
4. 4 Care of the IUGR Newborn Asphyxia
Aspiration syndrome
Hypothermia
Hypoglycemia
Polycythemia Asphyxia and aspiration syndrome occur in the IUGR newborn as the fetus is exposed to chronic episodes of hypoxia which elicits a gasp in utero.
It is important to remember that the newborn who experiences asphyxia or hypoxic events is placed further at risk. These newborns are at risk of developing intraventricular hemorrhages. Because the newborn has been with decreased supply of oxygen in utero, this lack of oxygenation to the tissues may result in other disorders such as NEC.
The NEC can be dealt with and the newborn recovered but IVH can have long-lasting effects when one considers the chronic hypoxic environment the fetus is in. The fetus doesn’t receive that much oxygen while in utero, however any depletion of what should be available can have detrimental effects.
The fetus who undergoes stress releases meconium in utero and is placed at risk for meconium aspiration syndrome.
The SGA and IUGR newborn have decreased subcutaneous tissue, the brown fat is typically used up early on in an effort to maintain or reach neutral thermoregulation state.
In a like manner, the IUGR and sometimes SGA newborn use glucose stores in an effort to produce the necessary energy to maintain an adequate temperature. The newborn in this category also has an increased metabolic rate so what glucose is available is used up rapidly.
Polycythemia occurs as a response to chronic hypoxia, the body attempts to put out more rbc’s which have an oxygen carrying capacity.
The placenta of the IUGR newborn is usually a display of calcification or decreased size or other signs of placental insufficiency.Asphyxia and aspiration syndrome occur in the IUGR newborn as the fetus is exposed to chronic episodes of hypoxia which elicits a gasp in utero.
It is important to remember that the newborn who experiences asphyxia or hypoxic events is placed further at risk. These newborns are at risk of developing intraventricular hemorrhages. Because the newborn has been with decreased supply of oxygen in utero, this lack of oxygenation to the tissues may result in other disorders such as NEC.
The NEC can be dealt with and the newborn recovered but IVH can have long-lasting effects when one considers the chronic hypoxic environment the fetus is in. The fetus doesn’t receive that much oxygen while in utero, however any depletion of what should be available can have detrimental effects.
The fetus who undergoes stress releases meconium in utero and is placed at risk for meconium aspiration syndrome.
The SGA and IUGR newborn have decreased subcutaneous tissue, the brown fat is typically used up early on in an effort to maintain or reach neutral thermoregulation state.
In a like manner, the IUGR and sometimes SGA newborn use glucose stores in an effort to produce the necessary energy to maintain an adequate temperature. The newborn in this category also has an increased metabolic rate so what glucose is available is used up rapidly.
Polycythemia occurs as a response to chronic hypoxia, the body attempts to put out more rbc’s which have an oxygen carrying capacity.
The placenta of the IUGR newborn is usually a display of calcification or decreased size or other signs of placental insufficiency.
5. 5 Care of the IUGR Newborn Congenital malformations
Gastroschisis
Omphalocele
Congenital heart disease
Intrauterine infections
Continued growth difficulties
Cognitive difficulties Congential malformations frequented by the IUGR newborn include gastroschisis, omphalocele, Tet, Tgvessels
http://heart.health.ivillage.com/congenitalheartdisease/tetralogyoffallot.cfm
Intrauterine infections that result in IUGR are usually of the TORCH variety, however any chronic insult/infection can result in an underdeveloped newborn
Continued growth difficulties are noted in this group.
Cognitive difficulties are a major issue of the IUGR newborn. Learning disabilities as well as behavioral disorders such as hyperactivity, short attention span, poor fine motor coordination, hearing loss, and speech deficits. One can clearly see how the interdisciplinary healthcare team has need to coordinate this newborn’s care.Congential malformations frequented by the IUGR newborn include gastroschisis, omphalocele, Tet, Tgvessels
http://heart.health.ivillage.com/congenitalheartdisease/tetralogyoffallot.cfm
Intrauterine infections that result in IUGR are usually of the TORCH variety, however any chronic insult/infection can result in an underdeveloped newborn
Continued growth difficulties are noted in this group.
Cognitive difficulties are a major issue of the IUGR newborn. Learning disabilities as well as behavioral disorders such as hyperactivity, short attention span, poor fine motor coordination, hearing loss, and speech deficits. One can clearly see how the interdisciplinary healthcare team has need to coordinate this newborn’s care.
6. 6 Care of the LGA Newborn Birth trauma
Hypoglycemia-IDM
Polycythemia-IDM
Hyperviscosity-IDM Most LGA or macrosomic newborns are born to two types of women: those who have diabetes or those who are genetically proportioned with large structure
Large babes are at risk for birth trauma
Because the baby is so large there is the potential for the baby to get stuck in the birth canal, different body parts can get stuck but the most common area involved is the shoulder- shoulder dystocia with resultant fracture of the clavicle is not uncommon
Vacuum application or forceps delivery may be needed to extract the fetus
The newborn also has hyperinsulinemia and will often have hypoglycemia. To further complicate matters this large newborn (fluffy not pudgy) is often a difficulty oral feeder, which compounds the hypoglycemia. Treatment of hypoglycemia is accomplished best by getting the newborn to feed
Breastfeeding is not impossible but caution the mother of an LGA newborn or an IDM- that formula supplementation will most likely be required to keep the babe in a euglycemic state. A blood sugar of less than 50 in an at risk newborn should prompt the caregiver to encourage early and frequent feedings, within the first two hours of life and every 2-3 hours after that.
Polycythemia is noted in the LGA newborn, the newborn appears ruddy, plethoric. This is believed to be caused by decreased ECF. Keep in mind the newborn who is not of average size may indeed just be a reflection of his or her lineage. Big people tend to have big babies.Most LGA or macrosomic newborns are born to two types of women: those who have diabetes or those who are genetically proportioned with large structure
Large babes are at risk for birth trauma
Because the baby is so large there is the potential for the baby to get stuck in the birth canal, different body parts can get stuck but the most common area involved is the shoulder- shoulder dystocia with resultant fracture of the clavicle is not uncommon
Vacuum application or forceps delivery may be needed to extract the fetus
The newborn also has hyperinsulinemia and will often have hypoglycemia. To further complicate matters this large newborn (fluffy not pudgy) is often a difficulty oral feeder, which compounds the hypoglycemia. Treatment of hypoglycemia is accomplished best by getting the newborn to feed
Breastfeeding is not impossible but caution the mother of an LGA newborn or an IDM- that formula supplementation will most likely be required to keep the babe in a euglycemic state. A blood sugar of less than 50 in an at risk newborn should prompt the caregiver to encourage early and frequent feedings, within the first two hours of life and every 2-3 hours after that.
Polycythemia is noted in the LGA newborn, the newborn appears ruddy, plethoric. This is believed to be caused by decreased ECF. Keep in mind the newborn who is not of average size may indeed just be a reflection of his or her lineage. Big people tend to have big babies.
7. 7 Care of the IDM Birth trauma
Hypoglycemia
Hypocalcemia
Polycythemia
Hyperbilirubinemia When one thinks of care of the LGA newborn, think also of the IDM.
Other events that may occur during the birth of an LGA newborn are brachial palsy, fractures, cephalahematomas, intracranial bleeds including subdural hematomas.
The IDM is in a fetal environment where the placenta provides all the glucose needed, it is the supplier.
Once the fetus becomes a newborn and the placenta is removed, the newborn needs a moment or a good while to adjust to the decreased glucose supply. The newborn has been in a fetal state of hyperinsulinemia in response to the mother’s high glucose status. In so doing, the babe when born has not converted to extrauterine life totally and continues to be in a hyperinsulin state as he or she was in utero. That translates into lots of insulin and not much glucose and hypoglycemia follows. These newborns need to be fed as soon as possible as previously mentioned. Bedside glucose or blood sugars need to be checked on a frequent basis as these newborns tend to bottom out on their blood sugars quickly. The astute nurse wants to detect this change in time to prevent any further complications. Jitteriness should prompt the nurse to check a blood sugar and/or a calcium since low levels of both of these chemicals will cause the newborn to be jittery. Remember a blood sugar of less than 50 should prompt the nurse to feed the baby. If the blood sugar is not responsive to the feeding or the baby is not in a position to feed (respiratory distress), then a bolus of D10W is given. The D10W bolus may be repeated. If improved results are not sustained then a maintenance infusion of dextrose is begun. The neonate may have up to D12.5 before having a central line place. If there is still no resolution, consideration of endocrine involvement should be made.
The calcium level is often decreased because diabetic women have less magnesium and an increased urinary excretion of calcium which causes secondary hypoparathyroidism.
HgbA1C is present in the GDM, which binds oxygen and leads to tissue hypoxia. Hypoxia leads to an increase in erythropoeisis. The increased red blood cell production results in polycythemia. With the increased rbc’s there is increased rbc destruction ( a newborn’s rbc’s survive for about 80-90 days). With the frequent breakdown of rbc’s there is an increase in the amount of bilirubin and subsequent hyperbilirubinemia.
When one thinks of care of the LGA newborn, think also of the IDM.
Other events that may occur during the birth of an LGA newborn are brachial palsy, fractures, cephalahematomas, intracranial bleeds including subdural hematomas.
The IDM is in a fetal environment where the placenta provides all the glucose needed, it is the supplier.
Once the fetus becomes a newborn and the placenta is removed, the newborn needs a moment or a good while to adjust to the decreased glucose supply. The newborn has been in a fetal state of hyperinsulinemia in response to the mother’s high glucose status. In so doing, the babe when born has not converted to extrauterine life totally and continues to be in a hyperinsulin state as he or she was in utero. That translates into lots of insulin and not much glucose and hypoglycemia follows. These newborns need to be fed as soon as possible as previously mentioned. Bedside glucose or blood sugars need to be checked on a frequent basis as these newborns tend to bottom out on their blood sugars quickly. The astute nurse wants to detect this change in time to prevent any further complications. Jitteriness should prompt the nurse to check a blood sugar and/or a calcium since low levels of both of these chemicals will cause the newborn to be jittery. Remember a blood sugar of less than 50 should prompt the nurse to feed the baby. If the blood sugar is not responsive to the feeding or the baby is not in a position to feed (respiratory distress), then a bolus of D10W is given. The D10W bolus may be repeated. If improved results are not sustained then a maintenance infusion of dextrose is begun. The neonate may have up to D12.5 before having a central line place. If there is still no resolution, consideration of endocrine involvement should be made.
The calcium level is often decreased because diabetic women have less magnesium and an increased urinary excretion of calcium which causes secondary hypoparathyroidism.
HgbA1C is present in the GDM, which binds oxygen and leads to tissue hypoxia. Hypoxia leads to an increase in erythropoeisis. The increased red blood cell production results in polycythemia. With the increased rbc’s there is increased rbc destruction ( a newborn’s rbc’s survive for about 80-90 days). With the frequent breakdown of rbc’s there is an increase in the amount of bilirubin and subsequent hyperbilirubinemia.
8. 8 Care of the IDM Respiratory Distress Syndrome
Congenital birth defects Surfactant is present in the IDM however it is inactivated. Insulin affects the amount of lecithin. Lecithin is responsible for lung maturity. Insulin inhibits the synthesis of lecithin. There is also a decrease in PG- phosphatidylglycerol which aids in surfactant stabilization. The lack of lecithin and PG increases the chance of the newborn acquiring RDS. Newborns whose moms are in the diabetic class A-C are more at risk of developing RDS than IDM’s whose mom is in the D-F class. Review table 14-4 before NCLEX exam.
IDM are prone to cardiac defects: TG vessels, VSD (most common), PDA, small left colon syndrome, and sacral agenesis.
Moms who monitor and control their diabetic state have newborns who fare better as far as birth defectsSurfactant is present in the IDM however it is inactivated. Insulin affects the amount of lecithin. Lecithin is responsible for lung maturity. Insulin inhibits the synthesis of lecithin. There is also a decrease in PG- phosphatidylglycerol which aids in surfactant stabilization. The lack of lecithin and PG increases the chance of the newborn acquiring RDS. Newborns whose moms are in the diabetic class A-C are more at risk of developing RDS than IDM’s whose mom is in the D-F class. Review table 14-4 before NCLEX exam.
IDM are prone to cardiac defects: TG vessels, VSD (most common), PDA, small left colon syndrome, and sacral agenesis.
Moms who monitor and control their diabetic state have newborns who fare better as far as birth defects
9. 9 Care of the post-term Newborn Hypoglycemia
Meconium Aspiration Syndrome
Polycythemia
Congenital anomalies
Seizures
Cold stress Post-maturity occurs when the gestation goes past 42 weeks. Every post-term newborn will not have postmaturity syndrome.
Postmaturity syndrome refers to the newborn with chronic intrauterine hypoxia, looks include parchment like skin without lanugo or vernix, long fingernails, lots of hair, the babe is long a skinny and demonstrates a depletion of subcutaneous tissue.
Hypoglycemia occurs because the placenta is not as well kept as it was up to 40 weeks gestation and the fetus does not receive as much nutrition
Meconium aspiration syndrome occurs in response to fetal hypoxia, a stressful intrauterine insult. If the pregnancy is complicated by oligohydramnios the newborn is at risk of aspirating thick meconium. Aspiration of meconium places the newborn at risk of developing PPHN-because the newborn fails to enter newborn circulation and maintains a fetal circulation where the pulmonary vascular resistance is high (HTN).
In transition from fetal to newborn circulation the ductus arteriosus, ductus venosus, and foramen ovale should all close- in the newborn with persistent fetal circulation also known as persistent pulmonary hypertension, these closures do not occur.
Another MAS complication is the pneumothorax-from the air trapping, and pneumonia from the meconium (this is more of a chemical pneumonitis than pneumonia). Because meconium is so very thick and tenacious, it blocks the alveoli and does not permit adequate gas exchange. Gas comes into the alveoli but gets trapped inside the alveoli because the meconium is so thick. The air trapping places the newborn at risk for an air leak of the pneumothorax variety. It’s like a balloon that gets too much air inside has the potential to burst. The most effective intervention to lessen the occurrence of meconium aspiration is to suction the newborn on the perineum as soon as the head delivers. Newborns have the potential to aspirate other substances, such as amniotic fluid, feedings-water, breastmilk, or formula. Impaired gas exchange occurs with these diagnoses as well.
Polycythemia and seizures occur from the fetal hypoxia
Congenital anomalies from unknown causes
Cold stress occurs because of the limited subcutaneous fat
Post-maturity occurs when the gestation goes past 42 weeks. Every post-term newborn will not have postmaturity syndrome.
Postmaturity syndrome refers to the newborn with chronic intrauterine hypoxia, looks include parchment like skin without lanugo or vernix, long fingernails, lots of hair, the babe is long a skinny and demonstrates a depletion of subcutaneous tissue.
Hypoglycemia occurs because the placenta is not as well kept as it was up to 40 weeks gestation and the fetus does not receive as much nutrition
Meconium aspiration syndrome occurs in response to fetal hypoxia, a stressful intrauterine insult. If the pregnancy is complicated by oligohydramnios the newborn is at risk of aspirating thick meconium. Aspiration of meconium places the newborn at risk of developing PPHN-because the newborn fails to enter newborn circulation and maintains a fetal circulation where the pulmonary vascular resistance is high (HTN).
In transition from fetal to newborn circulation the ductus arteriosus, ductus venosus, and foramen ovale should all close- in the newborn with persistent fetal circulation also known as persistent pulmonary hypertension, these closures do not occur.
Another MAS complication is the pneumothorax-from the air trapping, and pneumonia from the meconium (this is more of a chemical pneumonitis than pneumonia). Because meconium is so very thick and tenacious, it blocks the alveoli and does not permit adequate gas exchange. Gas comes into the alveoli but gets trapped inside the alveoli because the meconium is so thick. The air trapping places the newborn at risk for an air leak of the pneumothorax variety. It’s like a balloon that gets too much air inside has the potential to burst. The most effective intervention to lessen the occurrence of meconium aspiration is to suction the newborn on the perineum as soon as the head delivers. Newborns have the potential to aspirate other substances, such as amniotic fluid, feedings-water, breastmilk, or formula. Impaired gas exchange occurs with these diagnoses as well.
Polycythemia and seizures occur from the fetal hypoxia
Congenital anomalies from unknown causes
Cold stress occurs because of the limited subcutaneous fat
10. 10 Care of the Preterm/Premature Newborn Surfactant deficiency
Patent ductus arteriosus (PDA)
Cold stress
Feeding intolerance
Necrotizing enterocolitis
Decreased renal blood flow
Decreased immune system response
Minimal stimulation http://survanta.com/parents/signs_rds.asp,
A preterm newborn is one who is born before 38 weeks gestation.
Surfactant is necessary to keep the alveoli open and permits the proper exchange of gases.
The newborn in respiratory distress may exhibit nasal flaring, retractions, and abnormal ABG results. This will be discussed later.
Patent ductus arteriosus is another common finding in the preterm newborn. The pulmonary vasculature of a preterm newborn does not have the tone of the term newborn. Without pulmonary vasculature tone the pulmonary arterioles do not constrict as well as they should in response to changes in oxygen content. When exposed to increased levels of oxygen as occurs after birth, the term newborn’s ductus arteriosus responds by closing itself, vasoconstriction occurs. The pretermer’s pulmonary arterioles remain lax, there is decreased pulmonary vascular resistance, meaning the pulmonary vasculature system allows blood to continue to move across the ductus arteriosus- hence a patent ductus arteriosus.
The preterm newborn has a large body to surface ratio which explains why this newborn is subject to problems in thermoregulation and may experience cold stress. The preterm newborn has little subcutaneous fat and this puts the vessels closer to the skin surface. The preterm newborn conducts heat away from the core of the body to the surface of the body, placing the newborn at risk for hypothermia. In order to maintain the little heat the newborn has the term newborn will flex itself into the fetal position to maintain what heat is available. The preterm newborn does not have the muscular tone to do this and is often found in an extended position which just allows for more heat loss. By 36 weeks the newborn should be able to assume this position. Another problem is the newborn’s inability of vasoconstriction, remember the tone of the vascular system is lax, although heat can be found in the vascular system, it is lost to the newborn’s skin surface where the vessels are visible. The preterm newborn loses heat on two counts, heat is conducted from the core to the surface and then the superficial veins are close to the skin’s surface which is subject to heat loss from being exposed to the cooler environment.
preterm newborn does not have an appropriate gag reflex, the LES is lax allowing for reflux of gastric contents, absorption of nutrients is slowed. The preterm newborn has an increased basal metabolic rate and increased oxygen consumption in an effort to feed by mouth, this is another mechanism by which calories are expended and is why oral feedings in the newborn are limited to 30 minutes. After this point, more calories are expended than are taken in. Some providers will allow a newborn to feed for as long as 45 minutes. Feeding intolerance (regurgitation of feedings) and NEC occur sometimes as a result of decreased perfusion to the GI system from being exposed to a hypoxic environment prior to or during delivery. Nursing care of the newborn with NEC includes maintaining an NPO status, decompression of the abdomen via low intermittent suctioning (a replogle), administering antibiotics as ordered, vigilant monitoring of vital signs- deterioration in the newborn’s status indicates a need for surgical intervention.
Decreased GFR occurs because there is decreased renal blood flow in the newborn and this is exaggerated in the premature newborn. Because of the decreased renal blood flow and decreased GFR, the preterm newborn is less able to concentrate urine or excrete excess fluids which makes fluid balance a bit tricky, preterm newborns are also more subject to nephrotoxicity. Medications which are nephrotoxic are monitored through therapeutic drug levels- gentamicin and vancomycin- amnioglycosides.
Urine output should be 1-3 ml.kg/hr. The newborn at risk will have strict I&O performed rather than the subjective count of 6-8 wet diapers per day. Weight is one of the most sensitive indicators of fluid status. Signs of dehydration would include the sunken fontanelle, loose skin turgor, dry mucus membranes, decreased urine output, and increased specific gravity.
The newborn has an immature immune system when born, this is even more so when the newborn is born prematurely. Newborns with any suspicion of sepsis are started on broad spectrum antibiotics as a prophylatic. Gentamicin and ampicillin are common. The best intervention to be performed in prevention of infection in the newborn is handwashing by the caregivers. Make note of subtle changes, especially the emergence of hypothermia, as this suggest infection.
The preterm newborn has a more immature nervous system and is unable to tolerate stimulation. Tactile, auditory, and visual stimuli should be kept at a minimum. When touching the preterm newborn, approach the newborn with a solid contact rather than stroking the newborn. This is often difficult for parents and reminders about the inability to tolerate increased stimuli are sometimes needed. Noise control is also essential for the preterm or sick newborn. Conversations should be held away from the bedside as much as possible. Some intensive care units actually have noise monitors. Caregivers should refrain from writing or tapping on the isolette or incubator as the sound is amplified inside the newborn’s environment. Minimal stimulation is a key word in care of the preterm newborn. Care is clustered so that the newborn can grow, too much manipulation further increases the preterm or sick newborn’s metabolic rate and calories are lost and growth does not occur at an adequate rate. http://survanta.com/parents/signs_rds.asp,
A preterm newborn is one who is born before 38 weeks gestation.
Surfactant is necessary to keep the alveoli open and permits the proper exchange of gases.
The newborn in respiratory distress may exhibit nasal flaring, retractions, and abnormal ABG results. This will be discussed later.
Patent ductus arteriosus is another common finding in the preterm newborn. The pulmonary vasculature of a preterm newborn does not have the tone of the term newborn. Without pulmonary vasculature tone the pulmonary arterioles do not constrict as well as they should in response to changes in oxygen content. When exposed to increased levels of oxygen as occurs after birth, the term newborn’s ductus arteriosus responds by closing itself, vasoconstriction occurs. The pretermer’s pulmonary arterioles remain lax, there is decreased pulmonary vascular resistance, meaning the pulmonary vasculature system allows blood to continue to move across the ductus arteriosus- hence a patent ductus arteriosus.
The preterm newborn has a large body to surface ratio which explains why this newborn is subject to problems in thermoregulation and may experience cold stress. The preterm newborn has little subcutaneous fat and this puts the vessels closer to the skin surface. The preterm newborn conducts heat away from the core of the body to the surface of the body, placing the newborn at risk for hypothermia. In order to maintain the little heat the newborn has the term newborn will flex itself into the fetal position to maintain what heat is available. The preterm newborn does not have the muscular tone to do this and is often found in an extended position which just allows for more heat loss. By 36 weeks the newborn should be able to assume this position. Another problem is the newborn’s inability of vasoconstriction, remember the tone of the vascular system is lax, although heat can be found in the vascular system, it is lost to the newborn’s skin surface where the vessels are visible. The preterm newborn loses heat on two counts, heat is conducted from the core to the surface and then the superficial veins are close to the skin’s surface which is subject to heat loss from being exposed to the cooler environment.
preterm newborn does not have an appropriate gag reflex, the LES is lax allowing for reflux of gastric contents, absorption of nutrients is slowed. The preterm newborn has an increased basal metabolic rate and increased oxygen consumption in an effort to feed by mouth, this is another mechanism by which calories are expended and is why oral feedings in the newborn are limited to 30 minutes. After this point, more calories are expended than are taken in. Some providers will allow a newborn to feed for as long as 45 minutes. Feeding intolerance (regurgitation of feedings) and NEC occur sometimes as a result of decreased perfusion to the GI system from being exposed to a hypoxic environment prior to or during delivery. Nursing care of the newborn with NEC includes maintaining an NPO status, decompression of the abdomen via low intermittent suctioning (a replogle), administering antibiotics as ordered, vigilant monitoring of vital signs- deterioration in the newborn’s status indicates a need for surgical intervention.
Decreased GFR occurs because there is decreased renal blood flow in the newborn and this is exaggerated in the premature newborn. Because of the decreased renal blood flow and decreased GFR, the preterm newborn is less able to concentrate urine or excrete excess fluids which makes fluid balance a bit tricky, preterm newborns are also more subject to nephrotoxicity. Medications which are nephrotoxic are monitored through therapeutic drug levels- gentamicin and vancomycin- amnioglycosides.
Urine output should be 1-3 ml.kg/hr. The newborn at risk will have strict I&O performed rather than the subjective count of 6-8 wet diapers per day. Weight is one of the most sensitive indicators of fluid status. Signs of dehydration would include the sunken fontanelle, loose skin turgor, dry mucus membranes, decreased urine output, and increased specific gravity.
The newborn has an immature immune system when born, this is even more so when the newborn is born prematurely. Newborns with any suspicion of sepsis are started on broad spectrum antibiotics as a prophylatic. Gentamicin and ampicillin are common. The best intervention to be performed in prevention of infection in the newborn is handwashing by the caregivers. Make note of subtle changes, especially the emergence of hypothermia, as this suggest infection.
The preterm newborn has a more immature nervous system and is unable to tolerate stimulation. Tactile, auditory, and visual stimuli should be kept at a minimum. When touching the preterm newborn, approach the newborn with a solid contact rather than stroking the newborn. This is often difficult for parents and reminders about the inability to tolerate increased stimuli are sometimes needed. Noise control is also essential for the preterm or sick newborn. Conversations should be held away from the bedside as much as possible. Some intensive care units actually have noise monitors. Caregivers should refrain from writing or tapping on the isolette or incubator as the sound is amplified inside the newborn’s environment. Minimal stimulation is a key word in care of the preterm newborn. Care is clustered so that the newborn can grow, too much manipulation further increases the preterm or sick newborn’s metabolic rate and calories are lost and growth does not occur at an adequate rate.
11. 11 Care of the Preterm/Premature Newborn Nutrition
Full feedings
Methods of feeding
Bottle
Breast
Cup
Gavage
TPN
Special formulas
supplements The stomach is a muscle and without use it atrophies. Initiation of feedings may occur very early, even in the compromised newborn. Trophic feedings aka minimal enteral nutrition are sometimes initiated to prime the newborn’s stomach. Nutrition and respiratory status are what propels the newborn. The nutritional requirements are higher in the preterm newborn than in the term newborn. The preterm newborn needs more protein (for tissue growth) than the term newborn. Caloric requirements are higher in the preterm newborn. The preterm newborn may receive as much as 30kcal/oz formula or breastmilk compared to the 20kcal/oz term feeding. Preterm formula has been marketed so that it contains more MCT, cysteine and other amino acids, calcium, iron, phosphorus, and vitamin D.
The term newborn’s stomach holds about 50-60 ml.
50-60 ml of 20kcal/oz formula translates to 33.5 to 40 kcals.
In the preterm newborn, the stomach holds less and the caloric intake is less.
For growth term newborn needs 120 kcal/kg/day.
The goal for the preterm newborn is to gain 20-30 g/day- 95-130 kcal/kg/day.
The preterm newborn’s stomach holds less volume and the feedings need to be gradually increased to what is considered full feedings: 150-160 ml/kg/day. Weight gain may not be noticed at first, even in the term newborn.
Weight loss should not be more than 10-15% of the birth weight.
Various methods of feeding the preterm newborn are available:
Bottle feeding may begin when the preterm newborn demonstrates a readiness for feeding: coordinated suck, swallow, and breathing, rooting, strong suck, adequate respiratory effort (minimal retraction, no tachypnea, limited apnea or periodic breathing), temperature stability, cardiac stability- no bradycardia (HR less than 80). The very tiny preterm newborn can feed with a special nipple and may be tried on a small amount of feedings that are gradually progressed. A sample feeding increment schedule would be 10-20 ml/kg/day.
Breast feeding is strongly encouraged in the preterm newborn. If the preemie is not able to feed the mom is encourage to pump her breastmilk and store it so the preemie can feed when able. Frozen breastmilk in a regular house freezer last 3-4 months, in a deep freezer that is not opened frequently the breastmilk last up to 6 months. Breastmilk should be stored in plastic containers so the wbc’s don’t stick to the glass containers. Moms should be supported in whatever choice of feeding they suggest, just remember to remind mom the colostrum is really loaded with IgA and IgG which offer passive immunity.
Just a reminder about IgG- it is small enough to cross the placenta and does. IgG offers the baby passive immunity for the first few months of life. If you can talk a mom to at least give her preterm newborn who has an immature immune system and can use all the help he or she can get, you’ve been successful. After colostrum, transitional milk appears in about 3-5 days (2-4 days per some souirces). Mature milk is produced by about 10 days and of that mature milk there are 2 portions, foremilk that comes at the beginning of a feed. Hindmilk has a higher concentration of fat, in pretermers who are not gaining weight adequately a mom may be requested to pump and dump her foremilk and bring in her hindmilk. Preterm newborns can be put to breast when they show themselves ready. Feedings should be limited to 30 minutes (or 45 minutes). Encourage breast feeding unless the mom is HIV + since the virus does transfer through breastmilk.
Some moms prefer that their newborns not have nipples, not even a pacifier. These newborns may be fed via cup. A small medicine cup is placed at the newborn’s mouth and the babe laps up the milk as a cat would.
Gavage feeding is given when the baby is not ready for oral feedings as when the babe is progressing to full nipple feedings. A nippling schedule is made, the preemie will feed one feeding per day, and have the nipple feedings gradually increased as tolerated. The newborn may receive part of a feeding via bottle or cup or breast and have the remaining feeding gavaged in.
TPN is used until the newborn is receiving full feedings. If the newborn is very near to full feedings, dextrose water (D10W) may be used instead of the TPN.
There are special newborn formulas for newborns with GI absorption problems, reflux, familial cow-milk “allergies”/feeding intolerance.
Supplements are infrequent but may include human milk fortifiers, addition of powdered formulas to increase caloric intake, MCT oil, thickit- for reflux. Newborns who are breastfed often receive supplemental iron. Most prepared formulas have an adequate content of iron so bottle fed newborns rarely have additional iron unless they are anemic.
One other thing to remember about feeding is how to position the newborn. The newborn should be positioned on his or her right side following a feeding as this helps in the digestive process. Newborns who have Pierre Robin sequence where the tongue may fall back and occlude the airway are positioned on the abdomen. Those infants with GERD are also placed prone. Both these newborns are monitored with cardiopulmonary monitors to detect apnea and bradycardia when they are sent home. If the babe is positioned supine the head of the bed should be elevated aout 30 degreesThe stomach is a muscle and without use it atrophies. Initiation of feedings may occur very early, even in the compromised newborn. Trophic feedings aka minimal enteral nutrition are sometimes initiated to prime the newborn’s stomach. Nutrition and respiratory status are what propels the newborn. The nutritional requirements are higher in the preterm newborn than in the term newborn. The preterm newborn needs more protein (for tissue growth) than the term newborn. Caloric requirements are higher in the preterm newborn. The preterm newborn may receive as much as 30kcal/oz formula or breastmilk compared to the 20kcal/oz term feeding. Preterm formula has been marketed so that it contains more MCT, cysteine and other amino acids, calcium, iron, phosphorus, and vitamin D.
The term newborn’s stomach holds about 50-60 ml.
50-60 ml of 20kcal/oz formula translates to 33.5 to 40 kcals.
In the preterm newborn, the stomach holds less and the caloric intake is less.
For growth term newborn needs 120 kcal/kg/day.
The goal for the preterm newborn is to gain 20-30 g/day- 95-130 kcal/kg/day.
The preterm newborn’s stomach holds less volume and the feedings need to be gradually increased to what is considered full feedings: 150-160 ml/kg/day. Weight gain may not be noticed at first, even in the term newborn.
Weight loss should not be more than 10-15% of the birth weight.
Various methods of feeding the preterm newborn are available:
Bottle feeding may begin when the preterm newborn demonstrates a readiness for feeding: coordinated suck, swallow, and breathing, rooting, strong suck, adequate respiratory effort (minimal retraction, no tachypnea, limited apnea or periodic breathing), temperature stability, cardiac stability- no bradycardia (HR less than 80). The very tiny preterm newborn can feed with a special nipple and may be tried on a small amount of feedings that are gradually progressed. A sample feeding increment schedule would be 10-20 ml/kg/day.
Breast feeding is strongly encouraged in the preterm newborn. If the preemie is not able to feed the mom is encourage to pump her breastmilk and store it so the preemie can feed when able. Frozen breastmilk in a regular house freezer last 3-4 months, in a deep freezer that is not opened frequently the breastmilk last up to 6 months. Breastmilk should be stored in plastic containers so the wbc’s don’t stick to the glass containers. Moms should be supported in whatever choice of feeding they suggest, just remember to remind mom the colostrum is really loaded with IgA and IgG which offer passive immunity.
Just a reminder about IgG- it is small enough to cross the placenta and does. IgG offers the baby passive immunity for the first few months of life. If you can talk a mom to at least give her preterm newborn who has an immature immune system and can use all the help he or she can get, you’ve been successful. After colostrum, transitional milk appears in about 3-5 days (2-4 days per some souirces). Mature milk is produced by about 10 days and of that mature milk there are 2 portions, foremilk that comes at the beginning of a feed. Hindmilk has a higher concentration of fat, in pretermers who are not gaining weight adequately a mom may be requested to pump and dump her foremilk and bring in her hindmilk. Preterm newborns can be put to breast when they show themselves ready. Feedings should be limited to 30 minutes (or 45 minutes). Encourage breast feeding unless the mom is HIV + since the virus does transfer through breastmilk.
Some moms prefer that their newborns not have nipples, not even a pacifier. These newborns may be fed via cup. A small medicine cup is placed at the newborn’s mouth and the babe laps up the milk as a cat would.
Gavage feeding is given when the baby is not ready for oral feedings as when the babe is progressing to full nipple feedings. A nippling schedule is made, the preemie will feed one feeding per day, and have the nipple feedings gradually increased as tolerated. The newborn may receive part of a feeding via bottle or cup or breast and have the remaining feeding gavaged in.
TPN is used until the newborn is receiving full feedings. If the newborn is very near to full feedings, dextrose water (D10W) may be used instead of the TPN.
There are special newborn formulas for newborns with GI absorption problems, reflux, familial cow-milk “allergies”/feeding intolerance.
Supplements are infrequent but may include human milk fortifiers, addition of powdered formulas to increase caloric intake, MCT oil, thickit- for reflux. Newborns who are breastfed often receive supplemental iron. Most prepared formulas have an adequate content of iron so bottle fed newborns rarely have additional iron unless they are anemic.
One other thing to remember about feeding is how to position the newborn. The newborn should be positioned on his or her right side following a feeding as this helps in the digestive process. Newborns who have Pierre Robin sequence where the tongue may fall back and occlude the airway are positioned on the abdomen. Those infants with GERD are also placed prone. Both these newborns are monitored with cardiopulmonary monitors to detect apnea and bradycardia when they are sent home. If the babe is positioned supine the head of the bed should be elevated aout 30 degrees
12. 12 Care of the Preterm/Premature Newborn Apnea of prematurity
Patent ductus arteriosus
Intraventricular hemorrhage
Anemia of prematurity
Retinopathy of prematurity
Chronic lung disease
Neurosensory deficits Apnea refers to a cessation of breathing that last more than 20 seconds It is particularly concerning when cessation of breathing is accompanied by cyanosis, pallor or bradycardia. Another take on respirations is periodic breathing in which the newborn has brief cessations in respirations that last less than 20 seconds but is not accompanied by cyanosis, pallor, or bradycardia.
Newborns that are less than 34 weeks gestation are at increased risk because there respiratory center in the brain has not yet developed, so the newborn does not respond to changes in CO2 levels as would an older gestation newborn. Central apnea is true apnea, obstructive apnea is caused by events such as increased secretions, poor body alignment, reflux.
PDA occurs when the ductus arteriosus does not close because of decreased tone of the pulmonary arteriole and decreased oxygen content in the blood AKA hypoxemia. The newborn with a PDA may experience pulmonary congestion since there is increased blood volume to the lungs. This may be clinically displayed as increased respiratory effort and increased oxygen needs.
IVH occurs most often in small pretermers, those who are less than 1500 grams or less than 34 weeks- especially those less than 30 weeks. The germinal matrix is a very vascular area of the brain and the vessels tend to rupture in response to hypoxic events. The newborn who delivers less than 30-32 weeks has an increased likelihood of encountering a hypoxic episode (respiratory distress) in utero and/or hypoxemia after delivery. Cranial ultrasounds are performed on the at risk or symptomatic newborn after 7 days of life. If a bleed occurs, it most often occurs between days 2 and 7 of life. Some facilities make it a practice to screen babes via cranial ultrasound on day 3 and 7 or 10. Preterm newborns who are at risk for IVH are also at risk for PVL, a condition where the white matter of the brain begins to disintegrate. Newborns at risk undergo a cranial ultrasound at 30 days of life to reassess any IVH and to detect the presence of PVL.
Anemia of prematurity occurs because the life span of the newborn rbc is shorter than an adult rbc. Newborn rbc’s live for about 90 days whereas the adult rbc lives for 120 days. The rbc nadir is reached at about 2 months of age and last for 3-6 months.
Retinopathy of prematurity occurs in the VLBW newborn who is exposed to oxygen more than 28 days- this poses a risk for the newborn, not all newborns of VLBW will have ROP. ROP describes the aberrant changes in retinal vascularity. The newborn with ROP is at risk for retinal detachment and blindness. ROP occurs in various stages. The disorder is sometimes self-correcting and at other times requires surgical intervention.
Chronic lung disease is the new term for bronchopulmonary dysplasia. Chronic lung disease follows RDS that does not resolve. These newborns require long term oxygen and are at risk for increased respiratory infections the first few years of life.
Neurosensory deficits include cerebral palsy- Premature newborns are 30 times more prone to develop CP than term newborns. The actual diagnosis is made during the first 3-18 months of life, but not during the neonatal period (first 28 days of life). 03.Consider CP in the newborn who has poor head control or failure to smile after 3 months, clenched fist after 3 months, hypertonicity in arms or legs, is pushing away or arching back, is floppy or displays irritability, feeding difficulties.
Hydrocephalus may occur, consider hydrocephalus in the newborn at risk. OFC should be measured serially, a metal measuring tape should be used. Place the measuring tape under the infant’s head and measure at the brow. Growth that exceeds 0.5 cm per week is suspicious.
Consider a neurological deficit when the newborn does not respond appropriate to stimuli to evoke newborn reflexes. The newborn, you recall should have a positive Babinski, plantar, and moro for example. The newborn who illicits a response other than expected should be considered for further neurological evaluation.
Speech difficulty may manifest itself as delayed expressive ability.
Auditory deficits are also a risk of the preterm newborn. Audiology screening is performed on every newborn prior to discharge from the hospital or very shortly thereafter. The goal is to test every newborn prior to discharge and notation of this is now being made on the newborn screening form submitted to the state laboratory. The initial hearing screen may show that the newborn has failed the evoked otoacustic emissions (OAE) test or automated auditory brain response test (BAER). Sometimes this occurs because the newborn still has amniotic fluid in the ear, a follow-up test is performed within 1-3 months.Apnea refers to a cessation of breathing that last more than 20 seconds It is particularly concerning when cessation of breathing is accompanied by cyanosis, pallor or bradycardia. Another take on respirations is periodic breathing in which the newborn has brief cessations in respirations that last less than 20 seconds but is not accompanied by cyanosis, pallor, or bradycardia.
Newborns that are less than 34 weeks gestation are at increased risk because there respiratory center in the brain has not yet developed, so the newborn does not respond to changes in CO2 levels as would an older gestation newborn. Central apnea is true apnea, obstructive apnea is caused by events such as increased secretions, poor body alignment, reflux.
PDA occurs when the ductus arteriosus does not close because of decreased tone of the pulmonary arteriole and decreased oxygen content in the blood AKA hypoxemia. The newborn with a PDA may experience pulmonary congestion since there is increased blood volume to the lungs. This may be clinically displayed as increased respiratory effort and increased oxygen needs.
IVH occurs most often in small pretermers, those who are less than 1500 grams or less than 34 weeks- especially those less than 30 weeks. The germinal matrix is a very vascular area of the brain and the vessels tend to rupture in response to hypoxic events. The newborn who delivers less than 30-32 weeks has an increased likelihood of encountering a hypoxic episode (respiratory distress) in utero and/or hypoxemia after delivery. Cranial ultrasounds are performed on the at risk or symptomatic newborn after 7 days of life. If a bleed occurs, it most often occurs between days 2 and 7 of life. Some facilities make it a practice to screen babes via cranial ultrasound on day 3 and 7 or 10. Preterm newborns who are at risk for IVH are also at risk for PVL, a condition where the white matter of the brain begins to disintegrate. Newborns at risk undergo a cranial ultrasound at 30 days of life to reassess any IVH and to detect the presence of PVL.
Anemia of prematurity occurs because the life span of the newborn rbc is shorter than an adult rbc. Newborn rbc’s live for about 90 days whereas the adult rbc lives for 120 days. The rbc nadir is reached at about 2 months of age and last for 3-6 months.
Retinopathy of prematurity occurs in the VLBW newborn who is exposed to oxygen more than 28 days- this poses a risk for the newborn, not all newborns of VLBW will have ROP. ROP describes the aberrant changes in retinal vascularity. The newborn with ROP is at risk for retinal detachment and blindness. ROP occurs in various stages. The disorder is sometimes self-correcting and at other times requires surgical intervention.
Chronic lung disease is the new term for bronchopulmonary dysplasia. Chronic lung disease follows RDS that does not resolve. These newborns require long term oxygen and are at risk for increased respiratory infections the first few years of life.
Neurosensory deficits include cerebral palsy- Premature newborns are 30 times more prone to develop CP than term newborns. The actual diagnosis is made during the first 3-18 months of life, but not during the neonatal period (first 28 days of life). 03.Consider CP in the newborn who has poor head control or failure to smile after 3 months, clenched fist after 3 months, hypertonicity in arms or legs, is pushing away or arching back, is floppy or displays irritability, feeding difficulties.
Hydrocephalus may occur, consider hydrocephalus in the newborn at risk. OFC should be measured serially, a metal measuring tape should be used. Place the measuring tape under the infant’s head and measure at the brow. Growth that exceeds 0.5 cm per week is suspicious.
Consider a neurological deficit when the newborn does not respond appropriate to stimuli to evoke newborn reflexes. The newborn, you recall should have a positive Babinski, plantar, and moro for example. The newborn who illicits a response other than expected should be considered for further neurological evaluation.
Speech difficulty may manifest itself as delayed expressive ability.
Auditory deficits are also a risk of the preterm newborn. Audiology screening is performed on every newborn prior to discharge from the hospital or very shortly thereafter. The goal is to test every newborn prior to discharge and notation of this is now being made on the newborn screening form submitted to the state laboratory. The initial hearing screen may show that the newborn has failed the evoked otoacustic emissions (OAE) test or automated auditory brain response test (BAER). Sometimes this occurs because the newborn still has amniotic fluid in the ear, a follow-up test is performed within 1-3 months.
13. 13 Care of the Newborn with Congenital Anomalies Neural tube defects
Trisomies
Diaphragmatic hernia
Cleft lip/palate
TE fistula
Diaphragmatic hernia Neural tube defects occur within the first 3-4 weeks of gestation and include spina bifida,myelomeningocele, meningocele anencephaly, encephalocele. Intake of folic acid 0.4mg or 400mcg per day prior to conception and 0.5mg during pregnancy. Intake of 4mg or 4000mcg for the mom with a history of a newborn with a NTD. A good source of dietary folic acid is in green leafy vegetables, liver, peanuts, and whole-grain breads and cereals. The first trimester is a period when the maternal intake of folic acid is really important. Folate should be taken throughout pregnancy and after delivery.
Cleft lip and palate are often associated with “syndromes”, particularly the trisomies: The major concern is in preventing aspiration with feedings an promoting growth. The mom who elects to bottle feed needs to have a special nipple that covers the cleft palate, a breast feeding mom has the advantage of being able to cover the defect with her breasts. Newborns with cleft lip and palate will have the cleft lip repaired as soon as possible. This facilitates bonding within the family. The cleft palate repair typically occurs much later unless the defect is really huge.
TE fistulas should be suspected in the newborn who vomits with every feeding or chokes, gets cyanotic and gags during feeds, has constant drooling, or signs of aspiration like decreased or coarse (rhonchi) breath sounds, tachypnea, retraction. if you are unable to pass a nasogastric tubeNeural tube defects occur within the first 3-4 weeks of gestation and include spina bifida,myelomeningocele, meningocele anencephaly, encephalocele. Intake of folic acid 0.4mg or 400mcg per day prior to conception and 0.5mg during pregnancy. Intake of 4mg or 4000mcg for the mom with a history of a newborn with a NTD. A good source of dietary folic acid is in green leafy vegetables, liver, peanuts, and whole-grain breads and cereals. The first trimester is a period when the maternal intake of folic acid is really important. Folate should be taken throughout pregnancy and after delivery.
Cleft lip and palate are often associated with “syndromes”, particularly the trisomies: The major concern is in preventing aspiration with feedings an promoting growth. The mom who elects to bottle feed needs to have a special nipple that covers the cleft palate, a breast feeding mom has the advantage of being able to cover the defect with her breasts. Newborns with cleft lip and palate will have the cleft lip repaired as soon as possible. This facilitates bonding within the family. The cleft palate repair typically occurs much later unless the defect is really huge.
TE fistulas should be suspected in the newborn who vomits with every feeding or chokes, gets cyanotic and gags during feeds, has constant drooling, or signs of aspiration like decreased or coarse (rhonchi) breath sounds, tachypnea, retraction. if you are unable to pass a nasogastric tube
14. 14 Care of the Newborn with Congenital Anomalies A newborn with a neural tube defect needs to have the defect covered as soon as possible. This is often accomplished with a turkey bag or saran/plastic wrap over the defect once warm sterile saline soaked gauze is placed on the defect. It is most important not to cause damage to the defect, the same applies with gastroschisis or omphalocele or any other organ protrusion. Cover the defect and maintain sterility. The newborn is at high risk for injury and infection. Depending on the defect, the newborn will be positioned prone, as with a NTD, so as not to put undue pressure on the defect. Repairs of the defect occur depending on the involvement of the spinal cord. This will be discussed in more detail in the semesters to come.A newborn with a neural tube defect needs to have the defect covered as soon as possible. This is often accomplished with a turkey bag or saran/plastic wrap over the defect once warm sterile saline soaked gauze is placed on the defect. It is most important not to cause damage to the defect, the same applies with gastroschisis or omphalocele or any other organ protrusion. Cover the defect and maintain sterility. The newborn is at high risk for injury and infection. Depending on the defect, the newborn will be positioned prone, as with a NTD, so as not to put undue pressure on the defect. Repairs of the defect occur depending on the involvement of the spinal cord. This will be discussed in more detail in the semesters to come.
15. 15 Care of the Newborn with Congenital Anomalies http://trisomy18support.org/modules/xoopsgallery/view_album.php?set_albumName=albun84
http://www.onetruemedia.com/otm_site/view_shared?p=2f2ab118f022d17b8448d6
Trisomy 13 and 18 are considered lethal anomalies. Trisomy 21 or Down’s syndrome results in the newborn with varying degrees of mental retardation.http://trisomy18support.org/modules/xoopsgallery/view_album.php?set_albumName=albun84
http://www.onetruemedia.com/otm_site/view_shared?p=2f2ab118f022d17b8448d6
Trisomy 13 and 18 are considered lethal anomalies. Trisomy 21 or Down’s syndrome results in the newborn with varying degrees of mental retardation.
16. 16 Care of the Newborn with Congenital Anomalies A hernia occurs when there is a gap between one organ and another. Umbilical hernias are a connection between the intestines and umbilicus. Gentle pressure on the umbilicus will put the intestines back into place where they belong. An inguinal hernia has intestines in the inguinal canal,. Gentle pressure on the inguinal area will place the intestines back where they belong. Diaphragmatic hernia occurs when the intestines and sometimes the liver are in the thoracic cavity. This is problematic because depending on the timing of the insult, lung development may be compromised. If the intestines occupy the thoracic area, the lung involved will be hypoplastic. A clue that a newborn may have a diaphragmatic hernia is #1 a scaphoid abdomen, #2 bowel sounds are heard in the thoracic area, #3 the liver’s edge cannot be palpated-
The abdomen should be soft and round with bowel sounds heard in 30-60 minutes of life, the liver’s edge should be felt 2-3 cm below the right costal margin
A hernia occurs when there is a gap between one organ and another. Umbilical hernias are a connection between the intestines and umbilicus. Gentle pressure on the umbilicus will put the intestines back into place where they belong. An inguinal hernia has intestines in the inguinal canal,. Gentle pressure on the inguinal area will place the intestines back where they belong. Diaphragmatic hernia occurs when the intestines and sometimes the liver are in the thoracic cavity. This is problematic because depending on the timing of the insult, lung development may be compromised. If the intestines occupy the thoracic area, the lung involved will be hypoplastic. A clue that a newborn may have a diaphragmatic hernia is #1 a scaphoid abdomen, #2 bowel sounds are heard in the thoracic area, #3 the liver’s edge cannot be palpated-
The abdomen should be soft and round with bowel sounds heard in 30-60 minutes of life, the liver’s edge should be felt 2-3 cm below the right costal margin
17. 17 Care of the Newborn of a Substance-Abusing Mother Fetal alcohol syndrome/effects
Heroin
Cocaine/crack
Marijuana/tobacco
methampetamine There are a variety of substances that can be misused by the expectant mother. Most of these substances have the potential to have a detrimental effect on the newborn.
Fetal alcohol syndrome or fetal alcohol effects occur when the mom ingests an inordinate amount of alcohol during her pregnancy. The newborn has characteristic features: thin upper lip, broad nose, smooth philthrum (upper lip) wide spaced eyes (hyperteliorism), and microcephaly. The FAS or FAE newborn may have difficulty regulating his or her temperature, exhibit poor feeding, and won’t tolerate increased stimuli well at all. The consequences vary from normal intelligence to severe mental retardation. Impulsivity, cognitive impairment, speech and language problems are par for the course.
Heroin places the newborn at risk for IUGR, MAS, and hypoxia. A shrill cry, irritability, vomiting, seizures, fist sucking are found in the neonate born to a heroin abusing mom.
The use of cocaine also places the newborn at risk for IUGR, microcephaly, cerebral infarctions, short lengths, altered brain development, and GU malformations. The mom who uses cocaine/crack places herself at risk for placental abruption. Moms who use heroin or cocaine and have medication administered within 2 hours of delivery really place the newborn at risk- these newborns cannot have naloxone aka narcan administered because it can actually cause acute withdrawal symptoms.
Newborns may experience withdrawal symptoms as the placenta and mother’s ingestion of abusing-substances. That doesn’t condone the mom continuing the substances and breast-feeding. Although there are very few drugs/medications that have a detrimental effect or are transferred in significant amounts through breastmilk, the mom should be encouraged not to breastfeed as these substances have the potential to transfer through breastmilk.
Marijuana can cause the newborn to have impaired coordination, memory, and critical-thinking ability.Even smoking or chewing nicotine has an effect on the newborn. Newborns born to moms who smoke experience the need for nicotine and notable periods of irritability can be seen on a cyclical trend. Nicotine metabolites cause the newborn to be born small.
Neonatal abstinence syndrome can occur in the newborn whose mother abusing illicit or prescribed substances. Having the mom stop the drugs cold turkey is not advisable cause the fetus may experience withdrawal. The newborn may need to undergo a weaning phase after delivery. There are a variety of substances that can be misused by the expectant mother. Most of these substances have the potential to have a detrimental effect on the newborn.
Fetal alcohol syndrome or fetal alcohol effects occur when the mom ingests an inordinate amount of alcohol during her pregnancy. The newborn has characteristic features: thin upper lip, broad nose, smooth philthrum (upper lip) wide spaced eyes (hyperteliorism), and microcephaly. The FAS or FAE newborn may have difficulty regulating his or her temperature, exhibit poor feeding, and won’t tolerate increased stimuli well at all. The consequences vary from normal intelligence to severe mental retardation. Impulsivity, cognitive impairment, speech and language problems are par for the course.
Heroin places the newborn at risk for IUGR, MAS, and hypoxia. A shrill cry, irritability, vomiting, seizures, fist sucking are found in the neonate born to a heroin abusing mom.
The use of cocaine also places the newborn at risk for IUGR, microcephaly, cerebral infarctions, short lengths, altered brain development, and GU malformations. The mom who uses cocaine/crack places herself at risk for placental abruption. Moms who use heroin or cocaine and have medication administered within 2 hours of delivery really place the newborn at risk- these newborns cannot have naloxone aka narcan administered because it can actually cause acute withdrawal symptoms.
Newborns may experience withdrawal symptoms as the placenta and mother’s ingestion of abusing-substances. That doesn’t condone the mom continuing the substances and breast-feeding. Although there are very few drugs/medications that have a detrimental effect or are transferred in significant amounts through breastmilk, the mom should be encouraged not to breastfeed as these substances have the potential to transfer through breastmilk.
Marijuana can cause the newborn to have impaired coordination, memory, and critical-thinking ability.Even smoking or chewing nicotine has an effect on the newborn. Newborns born to moms who smoke experience the need for nicotine and notable periods of irritability can be seen on a cyclical trend. Nicotine metabolites cause the newborn to be born small.
Neonatal abstinence syndrome can occur in the newborn whose mother abusing illicit or prescribed substances. Having the mom stop the drugs cold turkey is not advisable cause the fetus may experience withdrawal. The newborn may need to undergo a weaning phase after delivery.
18. 18 Care of the Newborn of a Substance-Abusing Mother Drug dependency
Prescription medications Moms have drug dependency based on a psychological need. Newborns have drug dependency based on a physiologic need.
Remember that over-the-counter and prescriptions can be misused too.
Encourage the mom to participate in early intervention programs, drug cessation programs (including cigarettes).
Newborns with neonatal abstinence syndrome are at an increased risk for SIDSMoms have drug dependency based on a psychological need. Newborns have drug dependency based on a physiologic need.
Remember that over-the-counter and prescriptions can be misused too.
Encourage the mom to participate in early intervention programs, drug cessation programs (including cigarettes).
Newborns with neonatal abstinence syndrome are at an increased risk for SIDS
19. 19 Care of the Newborn Exposed to HIV/AIDS Maternal AZT
Newborn AZT
HIV-PCR
Breastfeeding Vertical transmission of HIV can be reduced by having the mom use AZT. Maternal treatment with AZT can reduce the transmission to about 6%. A mom who does not get treatment subjects the newborn to a 13-39% of HIV transmission. Even if the treatment for mom is started late, it helps to lower the likelihood of transmission.
Recall that testing the newborn for HIV is really testing the mom since the baby doesn’t actually produce antibodies until about 6 months, more specifically testing for HIV on the newborn occurs at birth, at two months, 6 months, and 15-18 months. If the newborn is HIV-DNA-PCR negative at 1 month and 4 months the baby is considered uninfected. Two negative tests after the 1st month of age is considered uninfected. CD4 counts are also measured but these values are higher in infants and children (CD4+ = 2500-3500/ml3 rather than the 700-1000/ml3 in adults. The newborn needs to receive AZT as a precaution in the interim, it should start as soon after birth as possible-within 8-12 hours is recommended, and continue for 6 weeks. AZT should not be given with ribovarin as it will cause therapeutic interference. You recall that opportunistic infection is what the client with HIV ultimately succumbs to. The peak of onset is 3-9 months. Also at about 4-6 months old, the infant should be started on a prophylactic for PCP-sulfa, some neonatal experts advocate starting TMP-SMX at 6 weeks. Trimethoprim Sulfamethoxazole.
HIV-DNA-PCR is the best testing that can be done on the newborn. The ELISA test will test for mom’s HIV status rather than the babe. HIV-DNA-PCR is the test of choice.
Breastfeeding should be discouraged as the virus can transfer through breastmilk.
The best practice when caring for the new born with a potentially infectious disease, is to treat the newborn as you would any other newborn- use standard precautions.
Blood soiled items should be placed in plastic bags and disposed of daily. Bleach solution should be used to clean the diaper changing area.
Monitor the newborn for signs of FTT and progressive encephalopathyVertical transmission of HIV can be reduced by having the mom use AZT. Maternal treatment with AZT can reduce the transmission to about 6%. A mom who does not get treatment subjects the newborn to a 13-39% of HIV transmission. Even if the treatment for mom is started late, it helps to lower the likelihood of transmission.
Recall that testing the newborn for HIV is really testing the mom since the baby doesn’t actually produce antibodies until about 6 months, more specifically testing for HIV on the newborn occurs at birth, at two months, 6 months, and 15-18 months. If the newborn is HIV-DNA-PCR negative at 1 month and 4 months the baby is considered uninfected. Two negative tests after the 1st month of age is considered uninfected. CD4 counts are also measured but these values are higher in infants and children (CD4+ = 2500-3500/ml3 rather than the 700-1000/ml3 in adults. The newborn needs to receive AZT as a precaution in the interim, it should start as soon after birth as possible-within 8-12 hours is recommended, and continue for 6 weeks. AZT should not be given with ribovarin as it will cause therapeutic interference. You recall that opportunistic infection is what the client with HIV ultimately succumbs to. The peak of onset is 3-9 months. Also at about 4-6 months old, the infant should be started on a prophylactic for PCP-sulfa, some neonatal experts advocate starting TMP-SMX at 6 weeks. Trimethoprim Sulfamethoxazole.
HIV-DNA-PCR is the best testing that can be done on the newborn. The ELISA test will test for mom’s HIV status rather than the babe. HIV-DNA-PCR is the test of choice.
Breastfeeding should be discouraged as the virus can transfer through breastmilk.
The best practice when caring for the new born with a potentially infectious disease, is to treat the newborn as you would any other newborn- use standard precautions.
Blood soiled items should be placed in plastic bags and disposed of daily. Bleach solution should be used to clean the diaper changing area.
Monitor the newborn for signs of FTT and progressive encephalopathy
20. 20 Care of the Newborn with Congenital Heart Defect Left ventricular outflow obstructions
Hypoplastic
left heart
Coarctation
of the aorta
PDA
TGA (or vein)
Tetralogy of
Fallot
VSD
ASD Congenital heart defects may be caused by genetic or environomental factors. They are classified as being cyanotic or acyanotic. Cyanosis that worsens with crying indicates a cardiac problem, whereas cyanosis that improves with crying indicates a pulmonary problem.
Left to right shunt moves blood from the left side of the heart where the pressure is higher to the right side of the heart where the pressure is lower, blood goes through the lungs and is oxygenated so there is no cyanosis.
Right to left shunt moves blood from the right side of the heart where the pressure is higher because of an obstruction to the left side of the heart where the pressure is lower, blood bypasses the lungs the lungs and so there is cyanosis.
Manifestations of cardiac defects include an audible murmur, cyanosis, and CHF signs which include tachypnea, diaphoresis, hepatomegaly, and cardiomegaly.
Left ventricular outflow obstructions include mitral stenosis, aortic stenosis, or atresiaCongenital heart defects may be caused by genetic or environomental factors. They are classified as being cyanotic or acyanotic. Cyanosis that worsens with crying indicates a cardiac problem, whereas cyanosis that improves with crying indicates a pulmonary problem.
Left to right shunt moves blood from the left side of the heart where the pressure is higher to the right side of the heart where the pressure is lower, blood goes through the lungs and is oxygenated so there is no cyanosis.
Right to left shunt moves blood from the right side of the heart where the pressure is higher because of an obstruction to the left side of the heart where the pressure is lower, blood bypasses the lungs the lungs and so there is cyanosis.
Manifestations of cardiac defects include an audible murmur, cyanosis, and CHF signs which include tachypnea, diaphoresis, hepatomegaly, and cardiomegaly.
Left ventricular outflow obstructions include mitral stenosis, aortic stenosis, or atresia
21. 21 Care of the Newborn with Congenital Heart Defect Left ventricular outflow obstructions
Hypoplastic
left heart
Coarctation
of the aorta
PDA
TGA (or vein)
Tetralogy of
Fallot
VSD
ASD Hypoplastic left heart syndrome is an underdevelopment of the left side of the heart. The left ventricle is hypoplastic and there is aortic artresia. These newborns appear normal until the ductus arteriosus closes. The aorta in LHHS receives blood via the PDA which supplies systemic blood flow. When the ductus closes, the supply is cut off and cardiac abnormalities manifest themselves as cyanosis, decreased cardiac output, cardiovascular collapse and death within months if there is no intervention. The first step in intervening is to keep the ductus open, this is done with PGE1. Keeping the PDA allows for systemic perfusion. This is followed by a cardiac surgical procedure called the Norwood that allows another temporary fix. This is followed by a bi-directional Glenn shunt at 6-9 months and then the final repair is a modified Fontan.
Coarctation of the aorta should be suspected when there is marked difference in pulse intensity between the upper and lower extremities or if femoral pulses are absent. The body and lower extremities will have a weaker pulse compared to the head and upper extremities. Pulses will be bounding in the arms and weak in the femoral area. The lower extremities will be decidedly cooler and blood pressure will be lower. Correction is through cardiac surgery.
Transposition of the Great vessels (artery or vein) occurs when the pulmonary artery leaves the left ventricle, the aorta exits from the right ventricle and there is no communication between the systemic and pulmonary circulations. There MUST be another cardiac defect present in order for the newborn to survive until repair can be made surgically. Associated defects (compensatory defects) are PDA, PFO, VSD. In this newborn a pulse oximtery reading of 75% is optimal. PGE1 may have to be given to allow systemic and pulmonary blood mixing. A balloon atrial septostomy or Rashkind procedure is one step, followed by the Senning or Mustard procedures. The Senning using the baby’s atrial septum, the Mustard uses a prosthetic.
Tetralogy of Fallot involves 4 defects: VSD, pulmonic stenosis, over-riding aorta, and right ventricular hypertrophy. Acute episodes of cyanosis and hypoxia occur after crying or feeding and are termed Tet spells. The surgical procedure for this cardiac defect correction is called the Blalock. FYI An African American by the name of Viven Thomas, Blalock’s assistant was most instrumental in developing this procedure, see the movie Something the Lord made during your leisure.
VSD is an opening between the ventricles. Congestive heart failure is common. Management begins with diuretics and digoxin. Pulmonary banding is a surgical procedure that may be done to correct the defect if the diuretics and digoxin are not effective. Some will close spontaneously.
ASD is an opening between the right and left atria. These newborns may be asymptomatic or may develop congestive heart failure.
Hypoplastic left heart syndrome is an underdevelopment of the left side of the heart. The left ventricle is hypoplastic and there is aortic artresia. These newborns appear normal until the ductus arteriosus closes. The aorta in LHHS receives blood via the PDA which supplies systemic blood flow. When the ductus closes, the supply is cut off and cardiac abnormalities manifest themselves as cyanosis, decreased cardiac output, cardiovascular collapse and death within months if there is no intervention. The first step in intervening is to keep the ductus open, this is done with PGE1. Keeping the PDA allows for systemic perfusion. This is followed by a cardiac surgical procedure called the Norwood that allows another temporary fix. This is followed by a bi-directional Glenn shunt at 6-9 months and then the final repair is a modified Fontan.
Coarctation of the aorta should be suspected when there is marked difference in pulse intensity between the upper and lower extremities or if femoral pulses are absent. The body and lower extremities will have a weaker pulse compared to the head and upper extremities. Pulses will be bounding in the arms and weak in the femoral area. The lower extremities will be decidedly cooler and blood pressure will be lower. Correction is through cardiac surgery.
Transposition of the Great vessels (artery or vein) occurs when the pulmonary artery leaves the left ventricle, the aorta exits from the right ventricle and there is no communication between the systemic and pulmonary circulations. There MUST be another cardiac defect present in order for the newborn to survive until repair can be made surgically. Associated defects (compensatory defects) are PDA, PFO, VSD. In this newborn a pulse oximtery reading of 75% is optimal. PGE1 may have to be given to allow systemic and pulmonary blood mixing. A balloon atrial septostomy or Rashkind procedure is one step, followed by the Senning or Mustard procedures. The Senning using the baby’s atrial septum, the Mustard uses a prosthetic.
Tetralogy of Fallot involves 4 defects: VSD, pulmonic stenosis, over-riding aorta, and right ventricular hypertrophy. Acute episodes of cyanosis and hypoxia occur after crying or feeding and are termed Tet spells. The surgical procedure for this cardiac defect correction is called the Blalock. FYI An African American by the name of Viven Thomas, Blalock’s assistant was most instrumental in developing this procedure, see the movie Something the Lord made during your leisure.
VSD is an opening between the ventricles. Congestive heart failure is common. Management begins with diuretics and digoxin. Pulmonary banding is a surgical procedure that may be done to correct the defect if the diuretics and digoxin are not effective. Some will close spontaneously.
ASD is an opening between the right and left atria. These newborns may be asymptomatic or may develop congestive heart failure.
22. 22 Care of the Newborn with Congenital Heart Defect Notice the top diagram that looks like a Y, in the defect since there is left outflow obstruction between the atrium and ventricle, the valve has the look of a V
http://heart.health.ivillage.com/heartvalve/valvularstenosis.cfmNotice the top diagram that looks like a Y, in the defect since there is left outflow obstruction between the atrium and ventricle, the valve has the look of a V
http://heart.health.ivillage.com/heartvalve/valvularstenosis.cfm
23. 23 Care of the Newborn with an IEM Phenylketonuria (PKU)
Maple syrup urine disease (MSUD)
Homocystinuria
Galactosemia
Congenital Hypothyroidism
Congential Adrenal Hyperplasia
Sickle Cell Not all states tests for the same inborn errors of metabolism. If interested you can check out your state at http://genes-r-us.uthscsa.edu/nbsdisorders.htm Inborn errors of metabolism are detected on newborn metabolic screening tests, a mandatory test performed on all newborns prior to discharge. The newborn needs to have a good 24 hours of food to increase the reliability of the test. The more protein intake, the better. It is recommended to test the newborn 24 hours AFTER the first protein food is taken. Within 24-72 hours is suggested. Many newborns are discharged and/or tested prior this, so abnormal results may actually be a reflection of inopportune testing periods. Advise parents who are contacted by the state laboratory via their physician that the test needs to be repeated. The sooner the treatment, the less the sequelae, and the most prominent complication is that of mental retardation.
Phenylketonuria is one of the primary disorders tested for and so the battery of tests is commonly referred to as a PKU- however, the newborn screen test for more than just this one amino acid.
PKU is a treatable inborn error of metabolism, as are most IEM, a change in dietary habits is usually all that is needed to prevent mental retardation (the most common consequence of IEM’s). A newborn with PKU is unable to convert phenylalanine to tyrosine and so there is a build up of phenylalanine. Newborns with PKU have urine with a distinctive musty odor.
Maple syrup urine disease involves an error in the metabolism of leucine, isoleucine, and valine (amino acids). Is is common in groups that intermarry- Amenites of Pennsylvania. Pennsylvania screens all newborns for MSUD. The urine of these newborns smells like maple syrup. Testing the urine involves adding ferric chloride to the urine which turns the urine gray-green. Treatment must be started within 12 days to avoid mental retardation.
Homocystinuria is another amino acid disorder. This disorder is found mostly in persons of Irish descent. It is very rare. The disorder is caused by a deficiency of the enzyme cystathionine beta-synthase which is to metabolism methionine. Newborns are placed on a low methionine diet. If left untreated the newborn will die. Intravascular thromboses is the usual culprit.
Galactosemia is associated with newborn cataracts, anemia, sepsis, poor weight gain, jaundice, diarrhea, and mental retardation. All of these symptoms are reversible except the cataracts and MR. MR is preventable by removing galactose from the diet early on. Learning disabilities, speech problems, and ovarian failure. These children need to avoid milk and milk products and need to learn how to read nutrition labels very carefully. Nutramigen is one alternative to milk, another is the use of soy milk.
Congenital hypothyroidism also refered to cretinism is manifested by a large tongue, umbilical hernia, cool mottled skin, low hairline, hypotonia, and large fontanelles, especially the posterior fontanelle. Prolonged jaundice (more than 2 weeks), poor feeding, constipation, poor weight gain, low-pitched cry, poor weight gain, lethargy, delayed motor development are signs of congenital hypothyroidism. These newborns will be placed on thyroid medication. If untreated stunted growth occurs as well as mental retardation.
The results of the newborn metabolic screening test takes about 2 weeks from the state laboratory. The parents will not be contacted unless there is a problem. The problem could be an abnormal result, an improperly collected specimen, missing information on the Guthrie paper, a missed hearing screen. Not all states tests for the same inborn errors of metabolism. If interested you can check out your state at http://genes-r-us.uthscsa.edu/nbsdisorders.htm Inborn errors of metabolism are detected on newborn metabolic screening tests, a mandatory test performed on all newborns prior to discharge. The newborn needs to have a good 24 hours of food to increase the reliability of the test. The more protein intake, the better. It is recommended to test the newborn 24 hours AFTER the first protein food is taken. Within 24-72 hours is suggested. Many newborns are discharged and/or tested prior this, so abnormal results may actually be a reflection of inopportune testing periods. Advise parents who are contacted by the state laboratory via their physician that the test needs to be repeated. The sooner the treatment, the less the sequelae, and the most prominent complication is that of mental retardation.
Phenylketonuria is one of the primary disorders tested for and so the battery of tests is commonly referred to as a PKU- however, the newborn screen test for more than just this one amino acid.
PKU is a treatable inborn error of metabolism, as are most IEM, a change in dietary habits is usually all that is needed to prevent mental retardation (the most common consequence of IEM’s). A newborn with PKU is unable to convert phenylalanine to tyrosine and so there is a build up of phenylalanine. Newborns with PKU have urine with a distinctive musty odor.
Maple syrup urine disease involves an error in the metabolism of leucine, isoleucine, and valine (amino acids). Is is common in groups that intermarry- Amenites of Pennsylvania. Pennsylvania screens all newborns for MSUD. The urine of these newborns smells like maple syrup. Testing the urine involves adding ferric chloride to the urine which turns the urine gray-green. Treatment must be started within 12 days to avoid mental retardation.
Homocystinuria is another amino acid disorder. This disorder is found mostly in persons of Irish descent. It is very rare. The disorder is caused by a deficiency of the enzyme cystathionine beta-synthase which is to metabolism methionine. Newborns are placed on a low methionine diet. If left untreated the newborn will die. Intravascular thromboses is the usual culprit.
Galactosemia is associated with newborn cataracts, anemia, sepsis, poor weight gain, jaundice, diarrhea, and mental retardation. All of these symptoms are reversible except the cataracts and MR. MR is preventable by removing galactose from the diet early on. Learning disabilities, speech problems, and ovarian failure. These children need to avoid milk and milk products and need to learn how to read nutrition labels very carefully. Nutramigen is one alternative to milk, another is the use of soy milk.
Congenital hypothyroidism also refered to cretinism is manifested by a large tongue, umbilical hernia, cool mottled skin, low hairline, hypotonia, and large fontanelles, especially the posterior fontanelle. Prolonged jaundice (more than 2 weeks), poor feeding, constipation, poor weight gain, low-pitched cry, poor weight gain, lethargy, delayed motor development are signs of congenital hypothyroidism. These newborns will be placed on thyroid medication. If untreated stunted growth occurs as well as mental retardation.
The results of the newborn metabolic screening test takes about 2 weeks from the state laboratory. The parents will not be contacted unless there is a problem. The problem could be an abnormal result, an improperly collected specimen, missing information on the Guthrie paper, a missed hearing screen.
24. 24 Care of the Newborn with an IEM Congential Adrenal Hyperplasia
Sickle Cell The newborn metabolic screen also test for congenital adrenal hyperplasia-ambiguous genitalia and hemoglobinopathies which includes sickle cell anemia and thalassemia. The newborn metabolic screen also test for congenital adrenal hyperplasia-ambiguous genitalia and hemoglobinopathies which includes sickle cell anemia and thalassemia.
25. 25 The Newborn At-Risk: Birth-Related Stressors
26. 26 Care of the Newborn at Risk Due to Asphyxia Asphyxia
Cerbral palsy
Neonatal Resuscitation Program
S.T.A.B.L.E. Program Asphyxia should be considered when there is a non-reassuring fetal heart pattern, difficult delivery, meconium stained amniotic fluid, apneic episode unresponsive to tactile stimulation, male gender, prematurity, SGA, CHD, structural lung abnormality, inadequate ventilation.
A consequence of asphyxia is end organ damage. Remember when the newborn is placed in a fight or flight situation, blood shunts itself away from the less necessary organs. If this were to occur, the heart and brain would be the only organs to sustain an adequate perfusion. That means all the other organs are lacking- the kidneys, the stomach, the lungs for example are not as well perfused as the heart and brain. Any organ can take a direct hit in the course.
Cerebral palsy is one sequelae of asphyxia. It will be discussed in more detail in the following semesters.
In order to prevent bad outcomes, resuscitation programs have been formed. One of which is the Neonatal Resuscitation program (NRP) formerly known as Neonatal Advanced Life Support or NALS. These programs offer the practitioner who handles newborns a course that allows an increased recovery of compromised newborns. The STABLE (Sugar, Temperature, Airway, Blood Pressure, Labs, Emotions) program allows hospitals the information that allows the practitioner to prepare the compromised newborn for safe transport to a facility that manages a higher level of acuity. The higher the level, the more acute newborn can safely be recovered.
The first step of resuscitation of a newborn is the establishment of a patent airway. Suctioning is always provided before more involved resuscitation. After all, the newborn may have breathing difficulties simply because the airway is obstructed with amniotic fluid or thick secretions. The goals are to provide an adequate airway. Start simple. A flick of the heel, gentle rubbing of the back. Artificial breaths may need to be given via positive pressure ventilation also known as bag, mask, and valve since it involves the ambu bag.
FYI mmHg = 0.735 cmH2O.
Initial breaths may be around 30-40 mmHg compared to the 10-15 mmHg when the babe is breathing comfortably. Adequate respiration will be revealed by an easy rise and fall of the chest. If manual respirations need to be given it should be given at 40-60 bpm. Pay close attention to the pressure administered so as not to create an inadvertent pneumothorax.
If respirations have not been established soon after birth, the newborn will experience cardiac compromise. Bradycardia will ensue. If this occurs, if the heart rate is less than 60 after 30 seconds of effective respirations, compression are started. There are two methods to restore cardiac function. Two fingers are placed on the lower third of the sternum, just below the nipple line and compressions are given at a rate of 90 bpm. Another method is to place the thumbs in this position, the lower third of the sternum, letting the hands wrap around the back.
Remember the A, B, C, D, E: airway, breathing, circulation, drugs, and then emotions.
If cardiac compression AFTER effective ventilation has been established the next step is drug administration: 1:10,000 epinephrine. Be certain the concentration of epinephrine is for the neonate, not the 1:1000 concentration. If the resuscitation is prolonged metabolic acidosis is assumed- this is controversial. Sodium bicarb may be given at this point. Hopefully, the neonate is in an ICU by this time and a true assessment of respiratory and metabolic status via documented ABG results can be made. Sodium bicarbonate is usually given in the NICU rather than the delivery room. IF sodium bicarb is given, it should be given slowly because the vascular system is fragile and intraventricular hemorrhage will occur. Rather than giving sodium bicarb, normal saline may be given as a volume expander 10ml/kg.
If it is suspected that maternal narcotics are the source of the baby’s respiratory problem, Naloxone or narcan is given unless the mom is known to have consumed crack/cocaine or herionAsphyxia should be considered when there is a non-reassuring fetal heart pattern, difficult delivery, meconium stained amniotic fluid, apneic episode unresponsive to tactile stimulation, male gender, prematurity, SGA, CHD, structural lung abnormality, inadequate ventilation.
A consequence of asphyxia is end organ damage. Remember when the newborn is placed in a fight or flight situation, blood shunts itself away from the less necessary organs. If this were to occur, the heart and brain would be the only organs to sustain an adequate perfusion. That means all the other organs are lacking- the kidneys, the stomach, the lungs for example are not as well perfused as the heart and brain. Any organ can take a direct hit in the course.
Cerebral palsy is one sequelae of asphyxia. It will be discussed in more detail in the following semesters.
In order to prevent bad outcomes, resuscitation programs have been formed. One of which is the Neonatal Resuscitation program (NRP) formerly known as Neonatal Advanced Life Support or NALS. These programs offer the practitioner who handles newborns a course that allows an increased recovery of compromised newborns. The STABLE (Sugar, Temperature, Airway, Blood Pressure, Labs, Emotions) program allows hospitals the information that allows the practitioner to prepare the compromised newborn for safe transport to a facility that manages a higher level of acuity. The higher the level, the more acute newborn can safely be recovered.
The first step of resuscitation of a newborn is the establishment of a patent airway. Suctioning is always provided before more involved resuscitation. After all, the newborn may have breathing difficulties simply because the airway is obstructed with amniotic fluid or thick secretions. The goals are to provide an adequate airway. Start simple. A flick of the heel, gentle rubbing of the back. Artificial breaths may need to be given via positive pressure ventilation also known as bag, mask, and valve since it involves the ambu bag.
FYI mmHg = 0.735 cmH2O.
Initial breaths may be around 30-40 mmHg compared to the 10-15 mmHg when the babe is breathing comfortably. Adequate respiration will be revealed by an easy rise and fall of the chest. If manual respirations need to be given it should be given at 40-60 bpm. Pay close attention to the pressure administered so as not to create an inadvertent pneumothorax.
If respirations have not been established soon after birth, the newborn will experience cardiac compromise. Bradycardia will ensue. If this occurs, if the heart rate is less than 60 after 30 seconds of effective respirations, compression are started. There are two methods to restore cardiac function. Two fingers are placed on the lower third of the sternum, just below the nipple line and compressions are given at a rate of 90 bpm. Another method is to place the thumbs in this position, the lower third of the sternum, letting the hands wrap around the back.
Remember the A, B, C, D, E: airway, breathing, circulation, drugs, and then emotions.
If cardiac compression AFTER effective ventilation has been established the next step is drug administration: 1:10,000 epinephrine. Be certain the concentration of epinephrine is for the neonate, not the 1:1000 concentration. If the resuscitation is prolonged metabolic acidosis is assumed- this is controversial. Sodium bicarb may be given at this point. Hopefully, the neonate is in an ICU by this time and a true assessment of respiratory and metabolic status via documented ABG results can be made. Sodium bicarbonate is usually given in the NICU rather than the delivery room. IF sodium bicarb is given, it should be given slowly because the vascular system is fragile and intraventricular hemorrhage will occur. Rather than giving sodium bicarb, normal saline may be given as a volume expander 10ml/kg.
If it is suspected that maternal narcotics are the source of the baby’s respiratory problem, Naloxone or narcan is given unless the mom is known to have consumed crack/cocaine or herion
27. 27 Care of the Newborn at Risk with Neurological Insult Hydrocephalus Assessment
Frontal bossing
Bulging fontanels*
Setting-sun eyes*
Distended scalp veins*
High-pitched cry*
Irritability
Poor feeding
Change in level of consciousness
Neurological reflexes inappropriate
Late signs of hydrocephalus
Other signs of hydrocephalus include wide sutures- this is another late sign, the “cracked pot” sound or Macewen’s sign on percussion of the skull is another sign of hydrocephalus.
Serial head circumference measurements are important in the assessment of neonates at risk for hydrocephalus or progressive ventricular enlargement- the rate of growth is what’s important
Late signs of hydrocephalus
Other signs of hydrocephalus include wide sutures- this is another late sign, the “cracked pot” sound or Macewen’s sign on percussion of the skull is another sign of hydrocephalus.
Serial head circumference measurements are important in the assessment of neonates at risk for hydrocephalus or progressive ventricular enlargement- the rate of growth is what’s important
28. 28 Care of the Newborn with Respiratory Distress Respiratory distress syndrome (RDS)
Transient Tachypnea of the Newborn (TTN)
Meconium Aspiration Syndrome
Diaphragmatic hernia
PDA
PPHN Respiratory distress encompasses several different processes, this is a temporary diagnosis. Within 24 hours it should be established more definitively which type of respiratory distress the babe has succumbed to.
RDS is associated with a deficiency of surfactant as in prematurity or inactivation of surfactant as in MAS. Artificial surfactant is given. The newborn is intubated and placed on mechanical ventilation. Newborns on ventilators are at increased risk for pulmonary air leaks. Regardless of the reason the newborn is intubated and placed on a ventilator,the risk for air leak from barotrauma remains. As a nurse, your assessment skills are crucial. Noting decreased air entry or ‘wet” breath sounds should prompt suctioning of the ETT. In some ICU’s this is a respiratory therapist function, in most ICU’s this task is a collaboration of services. While performing ETT suctioning keep an eye on the oxygen levels by watching the pulse oximetry. If the newborn requires intermittent additional oxygen, provide it. Most facilities will increase the oxygen level prior to suctioning because this activity often wears on the newborn, and desaturation will occur. Anticipatory management is key. Since you know the oxygen demands increase with activity, increase the oxygen delivery prior to suctioning. It is important to note when the newborn needs oral suctioning as well because increased secretions may lead to an inadvertent extubation and require the newborn to be reintubated. The objective of mechanical ventilation is to assist the newborn from a respiratory standpoint for as little a time as possible. With that in mind, sometimes only one dose of surfactant is needed, others may need as many as 4 doses.The more preterm the newborn, the less surfactant the newborn has. Surfactant is required in order for alveoli to function. If there is not adequate surfactant the alveoli will collapse and gas exchange is impaired. The surfactant reduces the surface tension of the alveoli allowing them to be open and gas exchange to occur. A hallmark of RDS is increased respiratory effort, moderate to marked retractions, and of course the “ground glass appearance” on a chests radiograph. Artificial surfactant is administered via an endotracheal tube.
Transient tachypnea of the newborn is a condition in which the newborn has a respiratory rate over 70 after the 4-6 hour extrauterine transition mark. It is often found when the newborn has delivered via c-section and has not had the laboring experience to help the absorption of residual lung fluid. Clinically the infant may present with nasal flaring, grunting, mild cyanosis, and a mixed acidosis. The symptoms usually resolve spontaneously within about 72 hours. Chest radiograph initially will reveal fluid filled horizontal fissures. The picture looks like pneumonia and the newborn may be started on prophylactic antibiotics. This newborn cannot be fed because the risk of aspiration of formula or breastmilk is too high. If hypoxemia is severe and tachypnea continues PPHN should be considered.
MAS occurs when there has been stress in utero and meconium passage occurs. The fetus may aspirate the meconium in the womb or may aspirate the meconium after delivery. When meconium stained amniotic fluid is present, the newborn should have thorough suctioning. The most important point of suctioning is on the perineum. Then the newborn is placed on the radiant warmer and the mouth is suctioned, so that if contents are in the mouth the newborn will not gasp and inhale the secretions. The nose is then suctioned, after the mouth. The abdomen is then suctioned because the newborn may regurgitate meconium gastric content and aspirate meconium after the fact. Meconium may inactivate surfactant. It is not unusual to see a term newborn with MAS receive surfactant. The surfactant lowers surface tension so that the meconium is essentially washed away. Another example of surfactant is soap, when applied it helps release dirt from an object.
Diaphragmatic hernia is when there is another organ in the thoracic cavity. It can be intestines and/or liver. Either way, the crowding in the thoracic area places a burden on the respiratory system. The first step for the nurse is to decompress the abdomen so an NG/OG tube is place. If the bowels are full, they fill the thoracic cavity further. Surgical intervention is necessary for repair.
PDA as previously discussed may result in the newborn having pulmonary congestion, bradycardia, apnea, hypoxemia. The symptomatic PDA may require closure. This is accomplished by indomethacin (being careful to monitor electrolytes, especially creatinine and BUN; platelet count- thrombocytopenia may occur). If pharmalogical intervention does not close the symptomatic PDA, surgical ligation is the next step.
PPHN, persistent pulmonary hypertension may occur in response to respiratory distress that goes unresolved. It involves the newborn staying in fetal circulation. The most important part of PPHN treatment is maintaining adequate oxygenation and sedation.Respiratory distress encompasses several different processes, this is a temporary diagnosis. Within 24 hours it should be established more definitively which type of respiratory distress the babe has succumbed to.
RDS is associated with a deficiency of surfactant as in prematurity or inactivation of surfactant as in MAS. Artificial surfactant is given. The newborn is intubated and placed on mechanical ventilation. Newborns on ventilators are at increased risk for pulmonary air leaks. Regardless of the reason the newborn is intubated and placed on a ventilator,the risk for air leak from barotrauma remains. As a nurse, your assessment skills are crucial. Noting decreased air entry or ‘wet” breath sounds should prompt suctioning of the ETT. In some ICU’s this is a respiratory therapist function, in most ICU’s this task is a collaboration of services. While performing ETT suctioning keep an eye on the oxygen levels by watching the pulse oximetry. If the newborn requires intermittent additional oxygen, provide it. Most facilities will increase the oxygen level prior to suctioning because this activity often wears on the newborn, and desaturation will occur. Anticipatory management is key. Since you know the oxygen demands increase with activity, increase the oxygen delivery prior to suctioning. It is important to note when the newborn needs oral suctioning as well because increased secretions may lead to an inadvertent extubation and require the newborn to be reintubated. The objective of mechanical ventilation is to assist the newborn from a respiratory standpoint for as little a time as possible. With that in mind, sometimes only one dose of surfactant is needed, others may need as many as 4 doses.The more preterm the newborn, the less surfactant the newborn has. Surfactant is required in order for alveoli to function. If there is not adequate surfactant the alveoli will collapse and gas exchange is impaired. The surfactant reduces the surface tension of the alveoli allowing them to be open and gas exchange to occur. A hallmark of RDS is increased respiratory effort, moderate to marked retractions, and of course the “ground glass appearance” on a chests radiograph. Artificial surfactant is administered via an endotracheal tube.
Transient tachypnea of the newborn is a condition in which the newborn has a respiratory rate over 70 after the 4-6 hour extrauterine transition mark. It is often found when the newborn has delivered via c-section and has not had the laboring experience to help the absorption of residual lung fluid. Clinically the infant may present with nasal flaring, grunting, mild cyanosis, and a mixed acidosis. The symptoms usually resolve spontaneously within about 72 hours. Chest radiograph initially will reveal fluid filled horizontal fissures. The picture looks like pneumonia and the newborn may be started on prophylactic antibiotics. This newborn cannot be fed because the risk of aspiration of formula or breastmilk is too high. If hypoxemia is severe and tachypnea continues PPHN should be considered.
MAS occurs when there has been stress in utero and meconium passage occurs. The fetus may aspirate the meconium in the womb or may aspirate the meconium after delivery. When meconium stained amniotic fluid is present, the newborn should have thorough suctioning. The most important point of suctioning is on the perineum. Then the newborn is placed on the radiant warmer and the mouth is suctioned, so that if contents are in the mouth the newborn will not gasp and inhale the secretions. The nose is then suctioned, after the mouth. The abdomen is then suctioned because the newborn may regurgitate meconium gastric content and aspirate meconium after the fact. Meconium may inactivate surfactant. It is not unusual to see a term newborn with MAS receive surfactant. The surfactant lowers surface tension so that the meconium is essentially washed away. Another example of surfactant is soap, when applied it helps release dirt from an object.
Diaphragmatic hernia is when there is another organ in the thoracic cavity. It can be intestines and/or liver. Either way, the crowding in the thoracic area places a burden on the respiratory system. The first step for the nurse is to decompress the abdomen so an NG/OG tube is place. If the bowels are full, they fill the thoracic cavity further. Surgical intervention is necessary for repair.
PDA as previously discussed may result in the newborn having pulmonary congestion, bradycardia, apnea, hypoxemia. The symptomatic PDA may require closure. This is accomplished by indomethacin (being careful to monitor electrolytes, especially creatinine and BUN; platelet count- thrombocytopenia may occur). If pharmalogical intervention does not close the symptomatic PDA, surgical ligation is the next step.
PPHN, persistent pulmonary hypertension may occur in response to respiratory distress that goes unresolved. It involves the newborn staying in fetal circulation. The most important part of PPHN treatment is maintaining adequate oxygenation and sedation.
29. 29 Care of the Newborn with Respiratory Distress Syndrome http://www.uen.org/utahlink/tours/tourElement.cgi?element_id=28357&tour_id=15478&category_id=24288
Ground glass appearance is the hallmark of RDS. The air bronchograms of small areas of inflation give the appearance seen here, small areas of aerated alveoli interspersed with collapsed alveoli, which give the appearance of whitened lung field.
http://www.uen.org/utahlink/tours/tourElement.cgi?element_id=28357&tour_id=15478&category_id=24288
Ground glass appearance is the hallmark of RDS. The air bronchograms of small areas of inflation give the appearance seen here, small areas of aerated alveoli interspersed with collapsed alveoli, which give the appearance of whitened lung field.
30. 30 Care of Newborn with Cold Stress Apnea/Bradycardia
Hypoglycemia
Disseminated Intravascular Coagulation (DIC)
Shock
Death Cold stress is excessive heat loss to the point that the newborn starts to use compensatory mechanisms to bring his or her core temperature back to normal. The newborn will employ methods such as nonshivering thermogenesis- remember babies do not shiver. The newborn may also use increased respirations to increase his or her temperature. The newborn will use up his or her stores of brown fat in an effort to keep warm- this increased metabolic rate results in increased energy expenditure. That means the main energy source becomes depleted and the blood sugar starts to drop. Newborns who already have hypoglycemia (blood sugar less than 40 or 50 if the newborn is an at-risk newborn) or respiratory difficulties, including hypoxemia will not be able to respond to cold stress. Newborns in the transitional period are especially at risk for developing the consequences of cold stress: apnea and bradycardia, hypoglycemia, DIC, shock, and death.
The newborn with cold stress may be warmed no more than 1° C per hour, warming too fast can cause hypotension and apnea.
Keep the ambient temperature about 1-1.5° C (34-35 ° F) warmer than the newborn (the newborn should be under a radiant warmer, this statement refers to increasing heat in an auxiliary manner).
The room temperature should be 75 ° FCold stress is excessive heat loss to the point that the newborn starts to use compensatory mechanisms to bring his or her core temperature back to normal. The newborn will employ methods such as nonshivering thermogenesis- remember babies do not shiver. The newborn may also use increased respirations to increase his or her temperature. The newborn will use up his or her stores of brown fat in an effort to keep warm- this increased metabolic rate results in increased energy expenditure. That means the main energy source becomes depleted and the blood sugar starts to drop. Newborns who already have hypoglycemia (blood sugar less than 40 or 50 if the newborn is an at-risk newborn) or respiratory difficulties, including hypoxemia will not be able to respond to cold stress. Newborns in the transitional period are especially at risk for developing the consequences of cold stress: apnea and bradycardia, hypoglycemia, DIC, shock, and death.
The newborn with cold stress may be warmed no more than 1° C per hour, warming too fast can cause hypotension and apnea.
Keep the ambient temperature about 1-1.5° C (34-35 ° F) warmer than the newborn (the newborn should be under a radiant warmer, this statement refers to increasing heat in an auxiliary manner).
The room temperature should be 75 ° F
31. 31 Care of Newborn with Hypoglycemia Apnea/Bradycardia
Pallor
Hypotonia/Tremors
Exaggerated moro
Poor feeding
Seizures Hypoglycemia is a (beside measurement) blood sugar that is less than 40, if the newborn is at risk most institutions will intervene if the blood sugar is less than 50. Intervention will also occur if there is a drastic drop in the blood sugar, say from 80-60 in the first hour of life. Serum glucose levels are usually done to confirm a bedside blood sugar that is below the threshold mark BUT intervention is not delayed for the results. A serum glucose of 20-25 results in the newborn receiving parenteral dextrose (D10W). Administration may begin with a bolus of D10W at 2 ml/kg slow IVP and a couple attempts to bring up the blood sugar in this manner before a maintenance infusion is begun. If the newborn is otherwise clinically stable formula feeding will help to bring the blood sugar up. Newborn blood sugars for those at risk are taken every 30 minutes for the first couple of hours and then every 2 hours and then every 4 hours- depending on the facility.
Whole blood measurements- the bedside glucometer, are lower than serum or plasma glucose readings.
Consider hypoglycemia if the signs listed appear.Hypoglycemia is a (beside measurement) blood sugar that is less than 40, if the newborn is at risk most institutions will intervene if the blood sugar is less than 50. Intervention will also occur if there is a drastic drop in the blood sugar, say from 80-60 in the first hour of life. Serum glucose levels are usually done to confirm a bedside blood sugar that is below the threshold mark BUT intervention is not delayed for the results. A serum glucose of 20-25 results in the newborn receiving parenteral dextrose (D10W). Administration may begin with a bolus of D10W at 2 ml/kg slow IVP and a couple attempts to bring up the blood sugar in this manner before a maintenance infusion is begun. If the newborn is otherwise clinically stable formula feeding will help to bring the blood sugar up. Newborn blood sugars for those at risk are taken every 30 minutes for the first couple of hours and then every 2 hours and then every 4 hours- depending on the facility.
Whole blood measurements- the bedside glucometer, are lower than serum or plasma glucose readings.
Consider hypoglycemia if the signs listed appear.
32. 32 Care of the Newborn with Jaundice Physiologic
Pathologic
Erythroblastosis fetalis
Hemolytic disease of the newborn (HDN)
Hydrops fetalis Physiologic jaundice occurs after 24 hours of life. Pathologic jaundice appears within the first 24 hours. Bilirubin is a yellow pigmented waste product of rbc’s. Those newborns with hyperbilirubenemia or jaundice will have yellow-tinged skin and/or sclera. In newborns of ethnic descent, look at the mucous membrane and sclera for determination of jaundice. The degree of hyperbilirubinemia progresses from head to toe, when the trunk is jaundiced the newborn should have a detectable elevation in bilirubin.
Bilirubin is bound to albumin, conditions that cause disassociation of albumin and bilirubin cause the bilirubin to increase. Bilirubin that is excessive requires treatment with phototherapy. This can be in the form of a bili-blanket or overhead banks of phototherapy that resemble those seen in tanning salons. Aggressive treatment is needed to keep the bilirubin from reaching a level that will allow passage across the blood brain barrier. These levels differ, primarily based on the newborn’s birthweight and gestation. Most charts for guidance in treatment are based on newborns 35 weeks in gestation or greater. Increase in bilirubin level by more than 0.2mg/dl/hour indicate the need for intervention. Bronze babies are those with elevated direct bilirubin, these babies therapy does not include phototherapy as phototherapy may worsen the direct bilirubin elevation.
Potential causes of jaundice are listed above.Physiologic jaundice occurs after 24 hours of life. Pathologic jaundice appears within the first 24 hours. Bilirubin is a yellow pigmented waste product of rbc’s. Those newborns with hyperbilirubenemia or jaundice will have yellow-tinged skin and/or sclera. In newborns of ethnic descent, look at the mucous membrane and sclera for determination of jaundice. The degree of hyperbilirubinemia progresses from head to toe, when the trunk is jaundiced the newborn should have a detectable elevation in bilirubin.
Bilirubin is bound to albumin, conditions that cause disassociation of albumin and bilirubin cause the bilirubin to increase. Bilirubin that is excessive requires treatment with phototherapy. This can be in the form of a bili-blanket or overhead banks of phototherapy that resemble those seen in tanning salons. Aggressive treatment is needed to keep the bilirubin from reaching a level that will allow passage across the blood brain barrier. These levels differ, primarily based on the newborn’s birthweight and gestation. Most charts for guidance in treatment are based on newborns 35 weeks in gestation or greater. Increase in bilirubin level by more than 0.2mg/dl/hour indicate the need for intervention. Bronze babies are those with elevated direct bilirubin, these babies therapy does not include phototherapy as phototherapy may worsen the direct bilirubin elevation.
Potential causes of jaundice are listed above.
33. 33 Care of the Newborn with Jaundice http://aappolicy.aappublications.org/cgi/content/full/pediatrics;114/1/297#F1
Let’s talk about testing;
ABO- blood grouping is performed on all newborns whose mother is of the O blood group.
Blood type AND Rh type are determined by what antigens are on the rbc
The blood group O has antibodies toward blood types A and B, that is in the maternal serum of a mom who is O, the mom has anti-A and anti-B antibodies. That means her serum will recognize as foreign and attack blood cells that have the A or B antigen. If the O mom’s baby’s blood type is A or B, and there is a mixing of blood at any point, the newborn’s blood cells will be destroyed by mom’s serum. To find out if mom has sent her antibodies to attack her baby a blood test called a Direct Coombs or Direct Antiglobulin Test is performed. It tests for the presence of maternal antibodies DIRECTLY on the surface of the baby’s rbc’s.
FYI- A test for the presence of antibodies is done through Indirect Coombs aka Indirect Antiglobulin Testing. This is also called the antibody screen. It will detect all antibodies in the maternal serum or plasma. These antibodies when the come in contact with the corresponding antigen, will cause rbc destruction or hemolysis.
The same holds true for a mom who is Rh negative and has a Rh positive baby.
Because there is a potential for rbc destrction, babies born to O or Rh negative moms are at risk for hyperbilirubinemia. Add to that breastfeeding when there is a potential for dehydration while mom’s milk is yet coming in and you have an increased risk for jaundice.
Other tests that may be performed in the jaundiced newborn are
Hgb- to detect increased destruction of rbc’s- the newborn can become anemic and
Reticulocyte count will be increased as rbc’s are destroyed, this level reflects the baby’s attempt to reproduce rbc’s to replace the ones that were destroyed.http://aappolicy.aappublications.org/cgi/content/full/pediatrics;114/1/297#F1
Let’s talk about testing;
ABO- blood grouping is performed on all newborns whose mother is of the O blood group.
Blood type AND Rh type are determined by what antigens are on the rbc
The blood group O has antibodies toward blood types A and B, that is in the maternal serum of a mom who is O, the mom has anti-A and anti-B antibodies. That means her serum will recognize as foreign and attack blood cells that have the A or B antigen. If the O mom’s baby’s blood type is A or B, and there is a mixing of blood at any point, the newborn’s blood cells will be destroyed by mom’s serum. To find out if mom has sent her antibodies to attack her baby a blood test called a Direct Coombs or Direct Antiglobulin Test is performed. It tests for the presence of maternal antibodies DIRECTLY on the surface of the baby’s rbc’s.
FYI- A test for the presence of antibodies is done through Indirect Coombs aka Indirect Antiglobulin Testing. This is also called the antibody screen. It will detect all antibodies in the maternal serum or plasma. These antibodies when the come in contact with the corresponding antigen, will cause rbc destruction or hemolysis.
The same holds true for a mom who is Rh negative and has a Rh positive baby.
Because there is a potential for rbc destrction, babies born to O or Rh negative moms are at risk for hyperbilirubinemia. Add to that breastfeeding when there is a potential for dehydration while mom’s milk is yet coming in and you have an increased risk for jaundice.
Other tests that may be performed in the jaundiced newborn are
Hgb- to detect increased destruction of rbc’s- the newborn can become anemic and
Reticulocyte count will be increased as rbc’s are destroyed, this level reflects the baby’s attempt to reproduce rbc’s to replace the ones that were destroyed.
34. 34 Hydrops Fetalis www.motherbabyuniversity.com
HDN may result in jaundice, HDN refers to Rh or ABO incompatibility and does not occur very often since Rhogam is used.
Hydrops fetalis is an extreme case of HDN, this mismatch occurs in utero. It is very rare.
www.motherbabyuniversity.com
HDN may result in jaundice, HDN refers to Rh or ABO incompatibility and does not occur very often since Rhogam is used.
Hydrops fetalis is an extreme case of HDN, this mismatch occurs in utero. It is very rare.
35. 35 Care of the Newborn with Jaundice Phototherapy
Exchange transfusion
Partial
double Remember from a previous lecture a discussion of jaundice or hyperbilirubinemia. There are two types, essentially. One is pathologic jaundice which occurs prior to 24 hours of age. One is physiologic jaundice which occurs after 24 hours. Pathologic jaundice, of course, is the most worrisome.
Pathologic jaundice usually occurs either because of sepsis or blood incompatibility (ABO or Rh). Newborns who have acquired an infection in utero may show jaundice within the first 24 hours of life or may even be born with jaundice. Remember our discussion about immunity? The newborn who has been exposed to an intrauterine infection will have high levels of IgM (mine, all mine, the baby has developed increased IgM-greater than 20- in response to an intrauterine exposure). A test for IgG and IgM antibodies helps to determine when the baby acquired the infection. High IgM means the baby developed antibodies, had an immune response in utero- IgM does not cross the placenta, it is too large, so the baby with a high IgM has responded to his or her intrauterine environment.
Phototherapy is the least invasive. Phototherapy increases the excretion of unconjugated bilirubin. The baby should be exposed as much as possible and his or her eyes and gonads shielded from the UV light. These areas should be assessed however on a regular basis to allow for comparison of jaundice in the sclera, conjunctivitis, pupil reactivity, etc., The gonads need to be examined as well- skin integrity is a problem for newborn’s under phototherapy. Make sure the newborn gets turned every 2-4 hours. When completing an assessment on a newborn with jaundice, do so in a well lit area, and do so with the phototherapy turned off. Be sure to include an assessment of the newborn’s thermoregulation. Additional heat sources may be needed.
If this measure fails and the bilirubin level continues to rise at an unacceptable level, exchange transfusion is required.
In exchange transfusion, the baby’s blood is removed and donor blood given. A partial exchange may be performed or a double volume exchange. Usually a double volume exchange is performed. The exchange occurs through the umbilical vein and blood is pumped through a blood warmer and then transfused slowly into the baby. The baby’s calcium and glucose levels needs to be monitored diligently during this process.
After exchange transfusion or while the baby is undergoing phototherapy bilirubin measurements are made to monitor the effectiveness of the intervention. In order to get an accurate bilirubin level it is imperative that the phototherapy lights be discontinued while the sampling is done and the sample sent to the lab in a darkened container. If an amber tube is not available, cover the test bullet with a paper towel to keep the light out.
The goal of phototherapy is to prevent kernicturus, when the biirubin crosses the blood brain barrier. Bilirubin deposits on the brain result in seizures, mental retardation, and can be prevented.Remember from a previous lecture a discussion of jaundice or hyperbilirubinemia. There are two types, essentially. One is pathologic jaundice which occurs prior to 24 hours of age. One is physiologic jaundice which occurs after 24 hours. Pathologic jaundice, of course, is the most worrisome.
Pathologic jaundice usually occurs either because of sepsis or blood incompatibility (ABO or Rh). Newborns who have acquired an infection in utero may show jaundice within the first 24 hours of life or may even be born with jaundice. Remember our discussion about immunity? The newborn who has been exposed to an intrauterine infection will have high levels of IgM (mine, all mine, the baby has developed increased IgM-greater than 20- in response to an intrauterine exposure). A test for IgG and IgM antibodies helps to determine when the baby acquired the infection. High IgM means the baby developed antibodies, had an immune response in utero- IgM does not cross the placenta, it is too large, so the baby with a high IgM has responded to his or her intrauterine environment.
Phototherapy is the least invasive. Phototherapy increases the excretion of unconjugated bilirubin. The baby should be exposed as much as possible and his or her eyes and gonads shielded from the UV light. These areas should be assessed however on a regular basis to allow for comparison of jaundice in the sclera, conjunctivitis, pupil reactivity, etc., The gonads need to be examined as well- skin integrity is a problem for newborn’s under phototherapy. Make sure the newborn gets turned every 2-4 hours. When completing an assessment on a newborn with jaundice, do so in a well lit area, and do so with the phototherapy turned off. Be sure to include an assessment of the newborn’s thermoregulation. Additional heat sources may be needed.
If this measure fails and the bilirubin level continues to rise at an unacceptable level, exchange transfusion is required.
In exchange transfusion, the baby’s blood is removed and donor blood given. A partial exchange may be performed or a double volume exchange. Usually a double volume exchange is performed. The exchange occurs through the umbilical vein and blood is pumped through a blood warmer and then transfused slowly into the baby. The baby’s calcium and glucose levels needs to be monitored diligently during this process.
After exchange transfusion or while the baby is undergoing phototherapy bilirubin measurements are made to monitor the effectiveness of the intervention. In order to get an accurate bilirubin level it is imperative that the phototherapy lights be discontinued while the sampling is done and the sample sent to the lab in a darkened container. If an amber tube is not available, cover the test bullet with a paper towel to keep the light out.
The goal of phototherapy is to prevent kernicturus, when the biirubin crosses the blood brain barrier. Bilirubin deposits on the brain result in seizures, mental retardation, and can be prevented.
36. 36 Care of the Newborn with Anemia Hypovolemia
Glucose-6-phosphate dehydrogenase (G6PD)
Physiologic anemia Your text speaks of Hgb levels less than 14 in term babes and less than 13 in preterm babes as a definition of anemia. Practices in this area look upon a Hct of less than 40 as anemia.
Remember the rule of threes for rbc, Hgb, and Hct. The rbc x 3 should approximate the Hgb, and the Hgb x 3 should approximate the Hct.
Hypovolemia may occur from active blood loss in utero as in abruptio placentae, it may also occur from birth trauma to include cutting the umbilical cord below the clamp.
Another cause of anemia is decreased production of rbc’s secondary to a G6PD deficiency
.
Physiologic anemia is a benign condition and is seen as a progressive decrease in Hgb until about 2-3 months of age when the rbc nadir occurs. The blood volume should be stable over the next 3-6 months and then will approach adult values.Your text speaks of Hgb levels less than 14 in term babes and less than 13 in preterm babes as a definition of anemia. Practices in this area look upon a Hct of less than 40 as anemia.
Remember the rule of threes for rbc, Hgb, and Hct. The rbc x 3 should approximate the Hgb, and the Hgb x 3 should approximate the Hct.
Hypovolemia may occur from active blood loss in utero as in abruptio placentae, it may also occur from birth trauma to include cutting the umbilical cord below the clamp.
Another cause of anemia is decreased production of rbc’s secondary to a G6PD deficiency
.
Physiologic anemia is a benign condition and is seen as a progressive decrease in Hgb until about 2-3 months of age when the rbc nadir occurs. The blood volume should be stable over the next 3-6 months and then will approach adult values.
37. 37 Care of the Newborn with Polycythemia Cord-clamping
Trisomies
Twin-to-twin transfusion
Endocrine disorder Delayed cord clamping while the newborn is below the placenta can result in inadvertent transfusion from the placenta into the newborn.
Trisomies 5, 8, 9, 21, have been encountered with polycythemia.
Twin to twin transfusion usually occurs in discordant twins, one twin will take all the nutrients and the other twin is left with not as much to work with during development. One twin is decidedly larger than the other.
Endocrine disorders- pheochromcytoma for example can be the cause of polycythemia.
Delayed cord clamping and twin to twin transfusions are the most familiar causes of polycythemia.
Delayed cord clamping while the newborn is below the placenta can result in inadvertent transfusion from the placenta into the newborn.
Trisomies 5, 8, 9, 21, have been encountered with polycythemia.
Twin to twin transfusion usually occurs in discordant twins, one twin will take all the nutrients and the other twin is left with not as much to work with during development. One twin is decidedly larger than the other.
Endocrine disorders- pheochromcytoma for example can be the cause of polycythemia.
Delayed cord clamping and twin to twin transfusions are the most familiar causes of polycythemia.
38. 38 Care of the Newborn with Infection Sepsis neonatorum
Nosocomial infection Wash your hands. Tell the parents to wash their hands. Keep little people away from the newborn. Inform parents that the newborn should be in reduced crowds for at least the first six months.
Sepsis neonatorum can sneak up on you. Be mindful of subtle changes in the baby’s behavior. Notice increased irritability, temp instability (is a big clue), hypo or hyperglycemia, feeding intolerance, abdominal distention are all signs of sepsis and should be acted upon. The neonate has an immature immune system so it is imperative to act quickly and take heed to any signs or symptoms of sepsis.Wash your hands. Tell the parents to wash their hands. Keep little people away from the newborn. Inform parents that the newborn should be in reduced crowds for at least the first six months.
Sepsis neonatorum can sneak up on you. Be mindful of subtle changes in the baby’s behavior. Notice increased irritability, temp instability (is a big clue), hypo or hyperglycemia, feeding intolerance, abdominal distention are all signs of sepsis and should be acted upon. The neonate has an immature immune system so it is imperative to act quickly and take heed to any signs or symptoms of sepsis.
39. 39 Care of the Family with Birth of an At-Risk Newborn Grief
Support
Follow-up (continued monitoring)
Acknowledge the grief of parents who experience a loss, whether that is a loss of life or loss of expectations of a perfect baby.
The family should be allowed to grieve in whatever manner they choose as long as it does not interfere with the welfare of other families in the facility. If a babe has died or about to die, acknowledge the presence of all family members and offer them room- physical and mental to grieve.
Support groups are available for almost every condition recognized.
In the event of a neonatal demise, as sad as it may be, the occasion presents an opportunity for another baby to have a fuller life- explore organ procurement with the family. The family may not be ready to view the baby at first- whether the circumstance is a neonatal death or some other alteration of the typical pregnancy. Give the parents the power to make their own decisions.
Eventually the parents will elect to view the baby at other times the family may not be able to tolerate seeing the baby for several hours. Give them dignity and time. Some hospitals have designated grieving rooms or transition rooms for such an occurrence.
Also remember to offer professional support services of clergy, social work, and special support groups.
The family of a newborn at risk needs to have continued monitoring, early intervention is the key to the newborn’s well being.Acknowledge the grief of parents who experience a loss, whether that is a loss of life or loss of expectations of a perfect baby.
The family should be allowed to grieve in whatever manner they choose as long as it does not interfere with the welfare of other families in the facility. If a babe has died or about to die, acknowledge the presence of all family members and offer them room- physical and mental to grieve.
Support groups are available for almost every condition recognized.
In the event of a neonatal demise, as sad as it may be, the occasion presents an opportunity for another baby to have a fuller life- explore organ procurement with the family. The family may not be ready to view the baby at first- whether the circumstance is a neonatal death or some other alteration of the typical pregnancy. Give the parents the power to make their own decisions.
Eventually the parents will elect to view the baby at other times the family may not be able to tolerate seeing the baby for several hours. Give them dignity and time. Some hospitals have designated grieving rooms or transition rooms for such an occurrence.
Also remember to offer professional support services of clergy, social work, and special support groups.
The family of a newborn at risk needs to have continued monitoring, early intervention is the key to the newborn’s well being.
40. 40 That’s a wrap Please feel free to post any questions on the discussion board and anticipate a response within 24 hours. Please feel free to post any questions on the discussion board and anticipate a response within 24 hours.
