Maternal & Newborn Lecture 11 Flashcards

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1
Q

Maternal NEW born Cherie.

A
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2
Q

AT RISK NEWBORNS

A

The most importnat when giving birth for a mom is to at a place where she can be given care

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3
Q

Classification According to Size

A
  • Classification of At-Risk
    Newborns Based on Size:
    • Low-birth-weight (LBW) infant: We consider infants weighing less than 2500 grams (5.5 pounds) as LBW, regardless of gestational age. This is a straightforward guideline.
    • Very low-birth-weight (VLBW) infant: Infants weighing less than 1500 grams (3.3 pounds) are classified as VLBW.
    • Extremely low-birth-weight (ELBW) infant: Infants weighing less than 1000 grams (2.2 pounds) fall into the ELBW category.
  • Appropriate for Gestational Age (AGA): Babies with birth weights that fall between the 10th and 90th percentiles on intrauterine growth curves. This is the most common category for newborns.
  • Small for Date (SFD) or Small for Gestational Age (SGA): Infants whose birth weights fall below the 10th percentile on intrauterine growth curves.
  • Large for Gestational Age (LGA): Infants whose birth weights exceed the 90th percentile on intrauterine growth curves.
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4
Q

Ballard
Gestational
Scoring Tool

Maybe watch a youtube video. Min 7 cherie.

A

It was used before we could use ultrasounds to determine the gestation age. This test was done on every infant that was born.

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5
Q

SMALL/LARGE FOR GESTATIONAL AGE.

A
  • Example: If a baby is born at 38 weeks but weighs 2100 grams, it falls below the 10th percentile on the intrauterine growth curve, classifying it as Small for Gestational Age (SGA).
  • Another example: If a baby is born at 30 weeks and weighs 2100 grams, it exceeds the 90th percentile on the intrauterine growth curve, categorizing it as Large for Gestational Age (LGA).
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6
Q

7

A
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7
Q

SMALL FOR GESTATIONAL AGE.

A
  • Reasons for Assessing Newborns and Associated Concerns:
    • Asphyxia: This can result from breathing difficulties at birth.
    • Aspiration: Coordination issues between sucking and breathing can lead to aspiration. The sucking reflex typically develops around 32 weeks, but full development occurs at 36 weeks. Infants born between 32-36 weeks require close monitoring of their feeding ability.
    • Hypoglycemia: Babies born small for gestational age may not have received enough glucose in the womb and can be at risk for low blood sugar levels. They may also be insulin resistant.
    • Temperature instability: Newborns in this category struggle to regulate their body temperature due to the absence of a shivering reflex and limited fat stores. Skin-to-skin contact and warm clothing are essential to prevent rapid temperature loss.
    • Polycythemia: These infants can have abnormally high red blood cell (RBC) counts, increasing the risk of blood clots. Hemoglobin (hgb) levels exceeding 20 and hematocrit levels greater than 65% are common. Their skin may appear maroon or reddish due to the excess RBCs.
    • Small for Gestational Age (SGA): SGA is not necessarily pathological, but Intrauterine Growth Restriction (IUGR) can lead to SGA. IUGR may present with asymmetrical growth, such as variations in head and abdominal measurements and long bone lengths. An association exists between SGA and maternal factors like smoking, poor nutrition, alcohol or drug use, uterine infections, chronic maternal diseases (e.g., thyroid issues, diabetes, chronic hypertension), and multiple gestations. Identifying SGA early allows for intervention and support for the mother before delivery.
    • Note: SGA refers to birth weight below the 10th percentile for gestational age.
  1. Less Glucose in the Womb: Babies born small for gestational age (SGA) often receive less glucose and other nutrients in the womb due to various factors, such as placental insufficiency or maternal conditions. This limited nutrient supply can result in slower growth and development during fetal development.
  2. Reduced Insulin Production: In response to the lower glucose levels in the womb, the developing baby’s pancreas may produce less insulin. Insulin is a hormone that helps regulate blood sugar by facilitating the uptake of glucose into cells. If there is less glucose available during fetal development, the baby’s pancreas may produce less insulin.
  3. Insulin Resistance: After birth, when the baby begins to receive regular feedings, their body may not be accustomed to handling the sudden increase in glucose intake. This relative lack of exposure to high glucose levels during fetal development, combined with potential alterations in insulin sensitivity, can contribute to insulin resistance.
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8
Q

LARGE FOR GESTATIONAL AGE

A
  • Large for Gestational Age (LGA):
    • Refers to babies born with a birth weight above the 90th percentile for their gestational age.
    • Often called “macrosomic,” indicating excessive fetal growth.
  • Causes:
    • Multiple factors contribute to LGA, including genetics, maternal conditions, and maternal health.
    • Common causes include maternal diabetes (especially poorly controlled during pregnancy), excessive maternal weight gain, and genetic factors.
  • Health Implications:
    • LGA itself is not a medical condition but can lead to birth complications.
    • Risks include shoulder dystocia (difficulty delivering the baby’s shoulders), birth injuries, and potential need for a cesarean section (C-section).
    • Some LGA babies may experience hypoglycemia (low blood sugar) and other health issues.
  • Monitoring and Management:
    • Healthcare providers closely monitor pregnancies with LGA babies to assess fetal well-being.
    • Interventions may include better management of maternal diabetes, birth plan adjustments, or induction of labor if fetal size becomes a concern.
  • Postnatal Care:
    • After birth, LGA babies are at risk of certain issues due to their size, such as hypoglycemia and jaundice.
    • Healthcare providers monitor these infants and provide necessary care.
  • Long-Term Outlook:
    • The long-term outlook for LGA babies depends on factors like the cause of their size and any associated health problems.
    • With proper care and monitoring, most LGA babies lead healthy lives.
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9
Q

LARGE FOR GESTATIONAL AGE

A
  • Birth Trauma: Birth trauma can occur when the baby is too large and may result in:
    • Brachial plexus injury
    • Facial palsy, typically caused by prolonged pressure on the baby’s face during a long second stage of labor, leading to temporary nerve damage.
  • Hypoglycemia: Babies born to mothers with gestational diabetes or those who produced excessive glucose in the womb may experience hypoglycemia due to an abundance of insulin and insufficient glucose at birth.
  • Asphyxia: Asphyxia during birth can lead to acidosis. Increased variability on monitoring graphs indicates a well-oxygenated baby. Decreased variability, unless caused by baby’s sleep or medication, can be an early sign of fetal distress, which may progress to late decelerations.
  • Cardiac Anomalies
  • Large for Gestational Age (LGA): LGA infants are often associated with diabetic mothers, particularly those who are insulin-dependent or have gestational diabetes. Multiparity, having multiple pregnancies, can also contribute to LGA. Incorrect gestational age assessment may be a factor.
  • Polycythemia and hyperviscosity can be associated with fine and gross motor skill delays and speech delays. Polycythemia may require increased fluid intake to alleviate viscosity. Excess glucose in the blood can lead to stickiness, impairing blood circulation and causing neuropathies in the extremities, leading to infections and tissue damage.
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10
Q

A term newborn was born 30 minutes ago. The newborn required positive pressure ventilation but responded quickly to resuscitation. Apgar Scores were 1 and 7. The newborn’s birth weight is 4250 grams. Vital signs now are: T 35.6C (96F), P158 and RR 56. Based only on this information, which of the following nursing diagnoses would have the highest priority for this newborn?

Risk for altered parenting
Risk for alteration in nutrition, < body requirements
Risk for injury, CNS
Risk for ineffective tissue perfusion

A

C

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11
Q

Classification According to Gestational Age

A
  1. Preterm (premature): These are babies who are born before 37 weeks of pregnancy are completed. They are born early.
  2. Late preterm: These babies are born between 34 weeks and 36 weeks and 6 days of pregnancy. They are a bit closer to full term but still born a little early.
  3. Early term: Babies born between 37 weeks and 38 weeks and 6 days of pregnancy are considered early term. They are almost at full term but not quite.
  4. Full term: Babies born between 39 weeks and 40 weeks and 6 days of pregnancy are considered full term. This is when most babies are born.
  5. Late term: Babies born between 41 weeks and 41 weeks and 6 days of pregnancy are considered late term. They are born a bit after the usual due date.
  6. Post term (postmature): These are babies born after 42 weeks of pregnancy. They are born later than expected and are considered overdue.

*Preterm (premature):born before completion of 37 weeks of gestation
*Late preterm:from 34 0/7 through 36 6/7 weeks of gestation
*Early term:from 37 0/7 through 38 6/7 weeks of gestation
*Full term:from 39 0/7 weeks through 40 6/7 weeks of gestation
*Late term:from 41 0/7 through 41 6/7 weeks of gestation
*Post term (postmature):born after 42 weeks of gestation,

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12
Q

PRETERM

A
  • Brain Development: A baby’s brain at 35 weeks weighs only about 2/3 of what it will weigh at 39 to 40 weeks of gestation.
  • Four Main Suggested Etiologies for Preterm Deliveries:
    1. Infection and Inflammation
    2. Maternal or Fetal Stress
    3. Bleeding
    4. Stretching of Uterine Cells: The uterus doesn’t gain more cells but stretches and enlarges to accommodate fetal growth. Excessive stretching, especially in the early stages, is believed to potentially trigger labor.
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13
Q

PRETERMRisks of

A
  • Risks Associated with Preterm Birth:
    1. Respiratory Distress Syndrome: The respiratory system is one of the last systems to develop in a fetus, leading to respiratory problems in premature infants. This is often due to a lack of surfactant, a substance that prevents the collapse of the lungs between breaths. Insufficient surfactant forces premature babies to take deep breaths to keep their lungs open, sometimes resulting in grunting sounds during respiration.
    2. Temperature Regulation: Premature infants may struggle to regulate their body temperature due to limited fat stores and an underdeveloped ability to generate heat.
    3. Intraventricular Hemorrhage: Preterm infants have fragile veins, and any increased pressure in the brain can lead to vein rupture and bleeding within the brain.
    4. Jaundice: Premature infants often experience jaundice because their livers are not yet fully functional, and they receive limited nutrition.
    5. Sepsis: The immature immune system of preterm infants leaves them vulnerable to infections.
    6. Feeding Problems: Coordination issues with sucking reflex, which starts developing around week 32 and fully matures at week 36, can cause feeding difficulties. Their underdeveloped bowels can also rupture if fed too early, leading to necrotizing enterocolitis.
    7. Retinopathy of Prematurity: Excessive oxygen administration to preterm babies can result in retinopathy of prematurity, a condition where the retina detaches due to the accumulation of oxygen in the blood vessels, potentially leading to blindness. This phenomenon occurs exclusively in preterm infants.
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14
Q

The neonate was born 2 hours ago, birth weight is 2475 grams. By Ballard exam, the gestational age is 41 weeks. Which of the following nursing diagnoses has the HIGHEST priority for this neonate?

A. Ineffective thermoregulation related to decreased brown fat reserves
B. Ineffective breathing pattern related to surfactant deficiency
C. Risk for infection, related to immature white blood cells
D. Risk for injury, related to fragile cerebral blood vessels

A

A

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15
Q

The nurse is caring for a late preterm infant (LPI). The infant was born by Cesarean Birth 15 minutes ago. Which of the following assessment findings would alert the nurse to possible complications associated with late preterm infants?
A. Irregular respirations.
B. Acrocyanosis.
C. Tachypnea.
D. Coarse breath sounds.

A

C

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16
Q

The nurse is preparing to care for a neonate soon to be born at 26 weeks gestation. The nurse anticipates which of the following medications may be given to this neonate as soon as possible following birth?
A. Betamethasone (Celestone)
B. Surfactant (Exosurf)
C. Nifedipine (Procardia)
D. Brethine (Terbutaline)

A

B

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16
Q

The nurse is caring for an infant 2 hours of age. By Ballard exam, the gestational age is 29 weeks. The nurse will incorporate the parents in this infant’s care by;
A. encouraging Kangaroo care.
B. limiting visiting in the NICU to only the infant’s
mother and father.
C. allowing the parents to hold their infant after the
first crucial 48 hours of life
D. making a social work consult.

A

A

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17
Q

Blood Glucose

A
  • Blood Glucose:
    • Post-term infants are at as much risk as preterm infants for various complications.
    • Post-term infants may exhibit dry skin, and if they remain in utero for too long with a deteriorating placenta, they can develop emaciated extremities. The body might begin breaking down its own tissues, primarily muscle, for sustenance.
    • Prolonged gestation can lead to thinning of the umbilical cord, meconium staining, and the possibility of polycythemia (abnormally high red blood cell count) once again.
    • Neonatal hypoglycemia is the major cause of brain injury
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18
Q

The newborn is an infant of a diabetic mother at 36 weeks gestation. The newborn was born 15 minutes ago, birth weight of 4200 grams (9#5oz). Which of the following nursing actions will be included in the plan of care for this infant?
A. Begin an IV of dextrose per MD order stat
B. Delay first feeding until respiratory distress syndrome is ruled out
C. Immediately obtain a heel stick blood sample to screen for polycythemia
D. Assess infant for jitteriness and lethargy

A

D

This action is important because infants born to diabetic mothers are at risk of hypoglycemia (low blood sugar), which can manifest as symptoms such as jitteriness and lethargy

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19
Q

ASSESSMENT OF INFANT OF DIABETIC MOTHER.

A
  • Macrosomia:
    • Macrosomia increases the risk of anomalies, particularly in the heart, brain, and neural tube. Possible anomalies include spina bifida, congenital heart disease, and cognitive disorders that may manifest later in life.
  • Additional Risks for Infants of Diabetic Mothers (IDM):
    • Respiratory Distress Syndrome (RDS)
    • Hypoglycemia: IDM infants are prone to low blood sugar levels due to their exposure to high blood glucose levels in the womb, which stimulates their pancreas to produce excess insulin.
    • Hypocalcemia: Abnormal intracellular calcium regulation affects insulin sensitivity and, therefore, insulin release. Consequently, IDM infants with hypoglycemia may also experience hypocalcemia because these conditions are interrelated.
    • Hyperbilirubinemia: IDM babies are susceptible to hyperbilirubinemia due to polycythemia, an increase in red blood cell count. The breakdown of excess red blood cells can lead to elevated bilirubin levels, causing jaundice.
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20
Q

HYPOGLYCEMIARisk Factors

A

Risk Factors for Hypoglycemic Infants:
1. Late Preterm Infants (LPI): Babies born between 34 to 36 6/7 weeks of gestation may have limited glycogen reserves, making it challenging to maintain normal blood glucose levels.
2. Intrauterine Growth Restriction (IUGR): Infants with growth restriction in the womb may have underdeveloped pancreases, which can affect their glucose regulation.
3. Small for Gestational Age (SGA) or Large for Gestational Age (LGA): Babies significantly smaller or larger than expected for their gestational age may have increased energy demands, affecting glucose homeostasis.
4. Birth weight less than 2500 grams: Low birth weight babies may be at risk of hypoglycemia due to limited energy stores.
5. Infants of Diabetic Mothers (IDM): Babies born to mothers with insulin-dependent diabetes or gestational diabetes are at risk due to potential glucose level fluctuations.

Screening Protocol for Hypoglycemic Infants:
1. Symptomatic Infants: If symptomatic and less than 40 weeks gestation, initiate IV glucose.
2. Initial Feeding: The first feeding is important, with glucose levels checked 30 minutes later to ensure proper digestion and glucose distribution.
3. Initial Screening: If the initial screen is less than 25 mg/dL, a repeat screen is done in 1 hour. If still under 25 mg/dL, IV glucose is administered.
4. Glucose Levels Between 25 and 40 mg/dL: If glucose levels fall within this range, a repeat check is performed, and the need for IV glucose is considered within the first 4 hours.
5. Monitoring After 24 Hours: After 24 hours, feeds continue, and glucose levels are screened before each feed.
6. Glucose Levels Less Than 35 mg/dL: If the screen is less than 35 mg/dL, feeding is initiated, and glucose levels are checked after 1 hour.
7. Glucose Levels Between 35 and 45 mg/dL: Consideration is given to providing glucose supplementation if blood sugar cannot be adequately raised, possibly using glucose gel based on the baby’s weight.
8. Target Glucose Level Before Routine Feeding: The target glucose level before routine feeding is greater than or equal to 45 mg/dL. However, levels down to 35 mg/dL may be tolerated with close monitoring.

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21
Q

HYPOGLYCEMIA: Symptomatic

A
  • To assess blood glucose levels in symptomatic hypoglycemia, obtain a blood drop from the heel tip and measure it using a glucometer.
  • Concerning Symptoms in Hypoglycemic Infants:
    • Seizures (no glucose = no energy to brain)
    • Lethargy or decreased responsiveness
    • Hypotonia: Infants may exhibit weak muscle tone, causing their arms to fall when picked up.
    • Apnea: A temporary pause in breathing. (brainstem controls breathing= no glucose = brainstem can’t work properly)
    • Cyanosis: A bluish discoloration of the skin, indicative of poor perfusion and oxygenation.
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22
Q

HYPOGLYCEMIA: Symptomatic

A

“Possible” meaning not always.
Jitteriness
Irritability
Exaggerated Moro reflex
High Pitched Cry
Poor feeding
Excessive sleepiness and drowsiness

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23
Q

Administration guidlines of glucose in infants

A
  • Administration Guidelines for Oral Glucose in Infants:
    • Dose: Administer 0.2 grams of glucose per kilogram of the infant’s body weight per dose.
    • Administration Method: Use an orange syringe specifically designed for oral medication delivery.
    • After administering the glucose, monitor the infant’s condition and check their glucose levels 30 minutes later to assess the response and effectiveness of the treatment.
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24
Q

HYPOGLYCEMIAInterventions: Symptomatic. Iv guidlines.

A
  • Hypoglycemia Interventions: Symptomatic. Follow IV guidelines.
  • IV Dextrose Administration in Infants:
    • Initial Bolus: Administer 0.2 grams of dextrose per kilogram (0.2 g/kg) over 5 to 15 minutes. This is typically done with 2 milliliters per kilogram (2 mL/kg) of 10% dextrose in water (D10W).
    • Continuous Infusion: Following the initial bolus, initiate a continuous infusion at an initial rate of 5 to 8 milligrams per kilogram per minute (5-8 mg/kg/min).
    • Adjustment: If hypoglycemia persists, increase the infusion rate as necessary.
  • Note: The dextrose concentration used in infants is 10%, which is more concentrated than the 5% typically used in adults. It’s administered as a titratable medication, starting at a low rate and increasing as necessary for each infant. The feet are a preferred site for IV access.
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25
Q

HYPOGLYCEMIAInterventions: Asymptomatic.

A
  1. “They have low blood sugar readings but they look fine and they don’t have any other symptoms. So we are just gonna keep with Early Frequent Feedings.”
  2. “Thermoregulation: make sure that they stay nice and warm. Not too much cause that would cause a fever, remember that they can’t regulate their temp and they won’t be able to get rid of that heat. In this case, the body is going to think that they have a fever.”
  3. “Assess all newborns for signs and symptoms of hypoglycemia.”
  4. “Follow unit protocol for high-risk newborns.”
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26
Q

HYPERBILIRUBINEMIA OF THE NEWBORN

A
  • Hyperbilirubinemia (Jaundice) Types:
  1. Pathologic Jaundice:
    • Onset: Occurs within the first 24 hours of age.
    • Causes: Typically attributed to conditions such as polycythemia (an abnormally high red blood cell count), ABO incompatibility, systemic acidosis, or the presence of the Rh factor.
  2. Physiologic Jaundice:
    • Onset: Develops after 24 hours of age.
    • Prevalence: Approximately 60% of newborns will exhibit physiologic jaundice within the first few weeks of life. It often becomes noticeable on the third or fourth day after birth.
    • Causes: Physiologic jaundice can result from factors such as dehydration, inadequate feeding, or delayed passage of meconium (the baby’s first stool). (indicate a slower transition to normal digestive processes.)
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27
Q

Pathologic Jaundice. Means that there something wrong in the body.

A
  • Serum bilirubin concentrations greater than 5 mg/dL in cord blood.
  • Clinical jaundice evident within 24 hours of birth.
  • Total serum bilirubin levels increasing by more than 5 mg/dL in 24 hours or increasing at a rate of 0.5 mg/dL per hour.
  • A serum bilirubin level in a term newborn that exceeds 12.9 mg/dL at any time.
  • A serum bilirubin level in a preterm newborn that exceeds 15 mg/dL at any time. Preterm infants may have slightly higher acceptable levels due to their expected differences.
  • Any case of visible jaundice that persists for more than 14 days of life in a term infant.
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28
Q

Which of the following newborns is at the HIGHEST risk for pathological jaundice?
A. A newborn @ 16 hours of life and breastfeeding with a LATCH score of 5
B. A post-term newborn at 8 hours of life with a caput succedaneum
C. A newborn @ 20 hours of life with a heel stick hematocrit of 56%
D. A preterm newborn at 4 hours of life with an initial Apgar score of 3, 7.

A

D

The risk factors for pathological jaundice include prematurity, a low Apgar score, and other factors that may indicate an underlying medical condition. Here’s why Option D represents the highest risk:

Preterm newborn: Preterm infants have an underdeveloped liver, which may not be able to process bilirubin as efficiently as full-term infants. This makes them more susceptible to jaundice.

Initial Apgar score of 3: An Apgar score is a quick assessment of a newborn’s overall health immediately after birth, with scores typically ranging from 0 to 10. A score of 3 at 4 hours of life indicates a significant compromise in the newborn’s condition at birth. This could be due to a variety of factors, including respiratory distress, birth trauma, or other medical conditions, which can increase the risk of pathological jaundice.

While the other options (A, B, and C) involve various factors like breastfeeding, caput succedaneum, and hematocrit levels, they do not present as high a risk for pathological jaundice as the preterm newborn with a low initial Apgar score. Prematurity and a low Apgar score are strong indicators of increased susceptibility to pathological jaundice, which requires careful monitoring and management to prevent complications associated with high bilirubin levels.

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29
Q

ConjugationofBilirubin

A

RBC have hemoglobin and hemoglobin is made of: heme and globin.
The heme in turn is made of iron and billirunin. The billiruben portion hooks onto a plasma protein which transports it to the liver. In the liver the glucoronly transferase conjugates the billiruben by adding glucorionic acid. Now the conjugated billiruben glucuronite becomes water soluble and it can be excreted through feces.

And this is why if the liver is not working you can’t get rid of the billiruben.

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30
Q

The baby’s mother is blood type O, Rh positive, indirect Coomb’s positive. The nurse understands that the baby is at risk for pathological jaundice if the baby’s tests results are;
A) O negative
B) A positive
C) Direct Coombs negative.
B) RhoGAM positive

A

B

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31
Q

JAUNDICE RISK FACTORS

A

These are various factors and conditions that can contribute to elevated bilirubin levels and jaundice in newborns:

  1. ABO Incompatibility: Incompatibility between the blood types of the mother and baby can lead to increased breakdown of red blood cells and subsequent bilirubin production.
  2. Sepsis: Infection in the newborn can cause the breakdown of red blood cells, leading to higher bilirubin levels.
  3. Delayed Meconium Passage: Delayed passage of meconium, the baby’s first stool, can hinder normal bowel movements and the excretion of bilirubin.
  4. Bruising: Trauma or bruising during birth can cause the breakdown of red blood cells, contributing to bilirubin buildup.
  5. Asphyxia/Hypoxia: Oxygen deprivation during birth, known as asphyxia or hypoxia, can affect various body processes, including the metabolism of bilirubin.
  6. Hypothermia: Low body temperature can slow down metabolic processes, potentially affecting bilirubin clearance.
  7. Hypoglycemia: Low blood sugar levels may impact bilirubin metabolism.
  8. Prematurity/Small for Gestational Age (SGA): Premature infants and those born with a lower birth weight may have underdeveloped liver function, leading to difficulties in processing bilirubin.
  9. Hepatitis: inflammation of the liver (not hepatitis A, B, or C), can impair liver function and bilirubin processing.
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32
Q

NURSING CAREFOR NEONATAL JAUNDICE

A
  • When assessing and managing newborns for risk factors and jaundice:
    • Obtain Maternal and Delivery History: Gather information on the mother’s medical history, the delivery process, and any factors that could contribute to jaundice.
    • Promote Frequent Breastfeeding: Encourage frequent breastfeeding to help expel meconium and promote intestinal function.
    • Prevent Kernicterus: Be vigilant in monitoring for signs of severe jaundice, as bilirubin can potentially cross the blood-brain barrier in the first few days of life, leading to cognitive brain damage.
    • Assess Visual Jaundice: Examine the baby for visible jaundice, which often starts at the head and progresses downward.
    • Monitor Bilirubin Levels: Use transcutaneous monitors and/or serum bilirubin tests to assess bilirubin levels before discharge from the hospital. This helps determine if further intervention is needed.
    • Communication: Notify the primary caregiver of any findings related to jaundice and bilirubin levels. Early detection and management are key to preventing complications.
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33
Q
  • Kernicterus:
    • Kernicterus is a severe consequence of untreated or inadequately treated jaundice in newborns, especially those with additional risk factors for jaundice.
    • It occurs when excessive bilirubin crosses a barrier and enters the brain tissue, where it is highly toxic.
    • Bilirubin permanently stains the gray matter in the brain, which is essential for functions such as hearing, eye movement, balance, and coordination.
    • Kernicterus often leads to cerebral palsy, with two common types being athetoid cerebral palsy (“without smooth or coordinated movements,) and dystonic cerebral palsy (abnormal muscle contractions)
  • The Grading System for Jaundice Severity (Modified Kramer’s Scale):
    • Level 1: Jaundice is noticeable from the top of the head to the neck.
    • Level 2: Jaundice is observed from the neck to the belly button.
    • Level 3: Jaundice extends from the belly button to the knees.
    • Level 4: Jaundice covers the area from the knees to the ankles.
    • Level 5: The entire body appears yellow due to severe jaundice.
A

.

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34
Q

TRANSCUTANEOUS BILIRUBIN MONITOR

A

we use it with 3 taps to the sternem.

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35
Q
  • When obtaining a blood sample from a newborn:
    • Use a heel warmer, as it promotes vasodilation, making it easier to obtain blood.
  • The heel warmer should reach a maximum temperature of 105°F/40.5°C.
  • Additionally, a convenient ankle strap can hold the warmer in place, eliminating the need for the clinician to hold it during the procedure.
A
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36
Q

Serum Bilirubin (TSB)

A

When collecting a blood sample, particularly for serum bilirubin (TSB) testing, it’s important to choose specific locations on the baby’s heel to avoid harming the sensitive nerves. These locations are typically slightly to the side of the center of each heel. Careful and precise collection ensures that the baby is not injured during the process.

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37
Q

The “Butani Nomogram” is a graphical tool used to assess the risk of severe hyperbilirubinemia (high levels of bilirubin) in newborns based on their total bilirubin levels and age in hours. It helps healthcare providers determine whether phototherapy or other interventions are necessary.

The nomogram typically includes different zones, which are defined based on bilirubin levels and the baby’s age in hours. These zones help categorize the risk as low, moderate, or high. The specific values for these zones can vary slightly between different nomograms, but the general concept remains the same.

Here is a simplified explanation of the zones:

  1. Low-Risk Zone: Newborns falling in this zone have bilirubin levels and age combinations that are considered low risk. No immediate intervention is typically required, and close monitoring may suffice.
  2. Intermediate-Risk Zone: Newborns in this zone have bilirubin levels and age combinations that are of moderate concern. Additional monitoring or phototherapy may be considered based on individual factors.
  3. High-Risk Zone: Newborns in this zone have bilirubin levels and age combinations that indicate a high risk of severe hyperbilirubinemia. Phototherapy or other interventions are often recommended.

The Butani Nomogram is a valuable tool to guide clinical decision-making and ensure timely intervention when necessary, helping to prevent complications associated with severe jaundice. Healthcare providers can use it to assess the risk and provide appropriate care for newborns.

A
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38
Q

51 msut learn how to interpret that graph

A
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39
Q

https://bilitool.org/ you can play and learn with it

A
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40
Q

PHOTOTHERAPY

A
  • Goal: Reduce unconjugated bilirubin levels inside an incubator.
  • Blue fluorescent spectrum used; Ultraviolet no longer employed due to reduced effectiveness.
  • Equipment options: Lamp, fiberoptic pad, or LED mattress.
  • Expected outcome: Bilirubin levels SHOULD decrease within 4 to 6 hours.

I

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41
Q

Phototherapy is the use of visible light for the treatment of hyperbilirubinemia in the newborn. This relatively common therapy lowers the serum bilirubin level by transforming bilirubin into water-soluble isomers that can be eliminated without conjugation in the liver.Then it gets to the intestine to be pooped out or peed out.

A
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42
Q

PHOTOTHERAPYNURSING CARE

A
  • Ensure safety, including eye protection to prevent harm to the retina.
  • Cover the baby’s genitals during phototherapy.
  • Assess for signs of dehydration, weigh the baby before and after feeding, and after they defecate.
  • Monitor the baby’s temperature.
  • Track intake and output (I & O).
  • Weigh diapers to assess fluid output.
  • Limit the baby’s exposure time While phototherapy is essential for treating conditions like jaundice, prolonged exposure can lead to potential risks such as overheating or dehydration
  • Monitor for signs of skin breakdown.
  • Ensure regular feeding.
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43
Q

Birth Injuries section begins here

A

.

44
Q

Molding

A
  • Molding refers to the changing shape of the baby’s head during birth due to the unfused skull bones.
  • Suture lines remain open, allowing the skull bones to overlap, making the head smaller to facilitate passage through the birth canal.
45
Q

On assessment the nurse finds a caput succedaneum. The parents ask the nurse how long it will take for the head to return to normal. Which of the following would be the best responses?
A. “It depends how long it takes for all the blood to re-absorb, probably 5-7 days.”
B. “You will need to position the newborn on the left or right side, then it will disappear in about 48 hours.”
C. “This is a common occurrence with first born babies, it only lasts about 24 hours.”
D. “This is swelling on your baby’s head, it will go away without any treatment in 3-4 days.”

A

D

46
Q

BIRTH INJURIES

A

Molding
Caput Succedaneum
Cephalhematoma they don’t cross the suture line.

Google

47
Q

Cephalohematoma

A
  • Collection of blood between skull bone and periosteum
  • Does NOT cross suture lines
  • Firmer and more well-defined than caput
  • Resolves in 2 – 8 weeks
48
Q

The nurse is assessing a newborn following a difficult vaginal forceps birth. Which of the following would be indicative of a complication of a difficult forceps birth?
A. Absent rooting reflex on the left cheek
B. Overlapping cranial sutures
C. Caput succedaneum
D. Transient tachycardia of the newborn

A

A

49
Q

BIRTH INJURIES

A
  • Facial Paralysis:
    • Large for gestational age (LGA) babies at higher risk.
    • May occur due to forceps delivery.
    • Can result from prolonged second stage of labor and pressure on the baby’s head.
    • Typically resolves within hours to days.
50
Q

BIRTH INJURIES

A

Brachial Palsy
Clavicle Fractures

51
Q

Sepsis

A
52
Q

The mother had ruptured membranes for 36 hours prior to giving birth. The newborn is 39 weeks gestation. Which of the following newborn assessments would alert the nurse to a possible complication based only on this information?
A. Hyperactive Moro reflex and frequent sucking
B. Hyper-tonicity of the arms and the legs
C. Heart rate of 170 while crying and capillary refill of 3 seconds
D. Axillary temperature of 36.1C (96.9F) and mottling

A

D

Here’s why:

The mother had ruptured membranes for 36 hours prior to giving birth. Prolonged rupture of membranes can increase the risk of infection for the newborn.

An axillary temperature of 36.1°C (96.9°F) is below the normal range for a newborn. Normal axillary temperature for a newborn is usually around 36.5°C to 37.2°C (97.7°F to 99.0°F). A temperature below this range can be a sign of hypothermia, which is a potential complication in newborns, especially if there was prolonged rupture of membranes, as it can lead to heat loss.

53
Q

NEONATAL SEPSIS

A
  • Neonatal Sepsis:
    • Risk due to an immature immune system.
    • Can be acquired:
      • In utero, such as through chorioamnionitis.
      • During labor and delivery (L&D).
      • During resuscitation, including potential exposure during IV placement.
      • During the hospital stay, emphasizing the importance of hand hygiene.
54
Q

NEONATAL SEPSIS SIGNS/SYMPTOMS

A
  • Signs/Symptoms of Neonatal Sepsis:
    • Typically generalized and nonspecific.
    • Fever may be present but not always very high, making it an unreliable indicator of the severity of illness.
    • More concerning is mottling, which can indicate inadequate perfusion due to the infection. However, it’s important to note that mottling can also result from factors other than infection.

Vasodilation: In response to infection, the body’s immune system releases various chemicals and signaling molecules, such as cytokines, to combat the infection. These substances can cause blood vessels to dilate (expand), leading to a drop in systemic vascular resistance. When blood vessels dilate excessively, it can result in a decrease in blood pressure and reduced perfusion to vital organs and tissues. This is often seen in septic shock, a severe and life-threatening form of infection.

55
Q

NEONATAL SEPSIS SIGNS/SYMPTOMS

A

Apnea
Bradycardia
Tachypnea
GFR
Decreased 02
Tachycardia
Hypotension
Decreased perfusion

Temperature instability
Lethargy
Hypotonic
Seizures
Feeding intolerance
Abdominal distention
Vomiting, Diarrhea
Hyperglycemia

56
Q

Neonatal SepsisNursing Care

A

Good hand hygine 10 min scrub

57
Q

Neonatal SepsisNursing Care

A
  • Neonatal Sepsis Nursing Care:
    • Maintain strict asepsis in care practices.
    • Review the prenatal and intrapartum records to determine if the mother had chorioamnionitis and the duration of ruptured membranes.
    • Conduct close monitoring and assessments of the newborn.
    • Perform necessary laboratory tests to confirm and monitor the infection.
    • Encourage breastfeeding to enhance the baby’s immune response.
    • Administer antibiotics, typically via IV, as prescribed by the healthcare provider.
  • Newborn Infections:
    • Common pathogens causing illness in newborns include Staphylococcus aureus and Staphylococcus epidermidis, often acquired at birth due to their presence as normal flora on the baby’s skin.
    • Streptococcus B (Strep B), Neisseria, and E. coli can be transmitted during labor and delivery, originating from the mother’s vagina and rectum.
58
Q

Neonatal Abstinence Syndrome section starts here

A

.

59
Q

The newborn was born to a mother that had positive urine toxicology screens during pregnancy for OxyContin. Based on this information, the nurse will carefully assess this newborn for;
A. transient bradycardia and absent babinski reflex.
B. poor feeding and frequent yawning.
C. hypotension and decreased sucking reflex.
D. constipation and fever.

A

B

60
Q

79

A
61
Q

80

A
62
Q

Goals of Nursing Care for NAS

A
  • Goals of Nursing Care for Neonatal Abstinence Syndrome (NAS):
    • Reduce the signs and symptoms of withdrawal in the newborn.
    • Increase feeding frequency and promote weight gain, as NAS infants are often in a hyperactive state that can lead to diarrhea.
    • Prevent seizures, which can be a complication of NAS.
    • Decrease mortality by providing appropriate medical care and monitoring.
    • Support normal neurological development to ensure the best long-term outcomes for the baby.
63
Q

82 Must min 1;48

A
64
Q

83

A
65
Q

NEONATAL WITHDRAWALNURSING CARE

A
  • Neonatal Withdrawal Nursing Care:
    • Perform a urine toxicology screen to identify substances present in the newborn’s system.
    • Continuously assess for signs of worsening withdrawal symptoms.
    • Administer medications as prescribed by the MD based on withdrawal symptom scores and monitor respiratory status.
    • Create a quiet environment with reduced stimuli to help soothe the baby.
    • Offer a pacifier to satisfy the sucking reflex, as the infant may not be able to nurse on the mother for a while.
    • Provide swaddling and gentle rocking to aid in relaxation.
    • Promote proper nutrition for the newborn to support their recovery and growth.
66
Q

FETAL ALCOHOL SYNDROME/FASFETAL ALCOHOL EFFECTS/FAE

A

It’s highly underrated. Because there is a stigma and the mom won’t admit to drinking during pregnancy.

67
Q

The mother of a newborn has a history of regular alcohol consumption during the pregnancy. Based on this information, the nurse will carefully assess this newborn for;
A. macrosomia.
B. cleft palate.
C. polycythemia.
D. simian crease.

A

B

68
Q

88 must picture and

A
69
Q

FETAL ALCOHOL SYNDROME

A
  • Fetal Alcohol Syndrome (FAS) Risks:
    • Increased risk for cleft lip and palate.
    • Co-occurrence of cervical vertebrae malformation is common with cleft lip and palate.
    • Elevated risk of spinal bifida.
    • Potential for congenital heart and kidney defects.
    • The possibility of extra digits (polydactyly) as an associated condition.
70
Q

FETAL ALCOHOL SYNDROME/ It is the main causes of non-genetic intellectual disabilities.

A
  1. Prenatal/Postnatal Growth Deficiency:
    • Refers to inadequate growth both before and after birth, resulting in below-average size and weight for the baby’s age.
  2. CNS Involvement:
    • Involvement of the central nervous system (CNS), which can lead to a range of neurological issues and developmental challenges.
  3. Characteristic Facial Features:
    • Distinctive facial features associated with certain conditions, which may include:
      • Low-set ears compared to the eyes.
      • A low nasal bridge.
      • Extra eye folds (epicanthal folds).
      • Thin upper lip.
      • Small head circumference.
      • Short nose.
71
Q

Congenital Conditions starts now. A partir de aqui.

A
  1. Fetal Circulation Pathway:
    • Oxygenated blood is received from the placenta through the umbilical vein.
    • Some of this blood passes through the liver via the portal vein, but the majority bypasses the liver through the ductus venosus.
    • The blood then enters the right atrium of the heart.
    • In the fetal heart, there is an opening known as the foramen ovale that allows blood to pass directly from the right atrium to the left atrium, bypassing the lungs.
    • From the left atrium, blood enters the left ventricle and is pumped out to the body via the aorta.
    • A small portion of the blood does flow into the right ventricle and is pumped into the pulmonary artery. However, the majority of this blood bypasses the fetal lungs through a vessel called the ductus arteriosus (not the PDA, which stands for Patent Ductus Arteriosus) and joins the aorta, mixing with oxygenated blood and then going to the body.
  2. Difference Between Venous and Arterial Blood:
    • In fetal circulation, the umbilical vein carries oxygenated blood from the placenta to the fetus.
    • In contrast, the umbilical arteries carry deoxygenated blood (waste products) from the fetus to the placenta for oxygen and nutrient exchange.

It’s important to note that fetal circulation is different from postnatal (adult) circulation, where oxygen exchange occurs in the lungs rather than bypassing them, and the foramen ovale and ductus arteriosus typically close shortly after birth as the baby begins to breathe and the heart adapts to the new oxygen-rich environment.

Your description provides an overview of the transition from fetal to neonatal circulation and the closure of certain fetal cardiovascular structures. Here’s a summary with a few clarifications:

  1. Transition from Fetal to Neonatal Circulation:
    • Blood from the venae cavae enters the right atrium.
    • It passes through the tricuspid valve into the right ventricle.
    • From there, it goes through the pulmonary valve into the pulmonary arteries.
    • In the fetus, a significant portion of this blood bypasses the fetal lungs through the ductus arteriosus, joining the aorta.
    • The blood in the aorta then goes to the rest of the body.
    • After birth, as the baby starts breathing and oxygenating blood in the lungs, the ductus arteriosus begins to close off and eventually becomes the ligamentum arteriosum.
  2. Closure of Ductus Arteriosus and Foramen Ovale:
    • The ductus arteriosus typically starts closing shortly after birth and usually seals off completely within a few days to weeks. It eventually becomes the ligamentum arteriosum, as you mentioned.
    • The foramen ovale, which allowed blood to bypass the fetal lungs, typically closes as well, and the two atria become separate chambers.
  3. Murmurs and Monitoring:
    • It’s common to hear murmurs when these structures are closing. The “whooshing” sound occurs as blood flows through the narrowing ductus arteriosus or as pressure changes within the heart during the transition.
    • The healthcare team monitors these closures and any associated murmurs during neonatal assessments. If a murmur persists or is concerning, further evaluation and follow-up may be required.
  4. Congenital Heart Screening:
    • Congenital heart screening is an important part of newborn care. Healthcare providers check for any congenital heart defects, including assessing for murmurs or other signs of abnormal heart function.

Your explanation helps clarify the process of cardiovascular changes that occur as a newborn transitions from fetal to neonatal circulation, including the closure of key structures.

72
Q

Congenital Heart Disease

A

Septal Wall defects
Obstruction defects
Cyanotic heart lesions
Defects of the great vessels

73
Q

Screening for Critical Congenital Heart Disease

A
74
Q

Septal Wall Defect (ASD,PSD, & PDA)

Atrial Septal Defect (ASD), Ventricular Septal Defect (VSD), Patent Ductus Arteriosus (PDA):

A

Septal Wall Defects (ASD, VSD, PDA):
- These are congenital heart defects involving openings or holes in the septal walls of the heart chambers.
- They often result in increased pulmonary blood flow, as oxygenated blood can flow from the left side of the heart (higher pressure) to the right side (lower pressure).

Common Clinical Features:
- Left-to-right shunting of blood, meaning oxygenated blood flows from the left side of the heart to the right side.
- Asymptomatic: Some individuals with small defects may not exhibit symptoms and may go undiagnosed for a while.
- Murmur: A heart murmur may be heard during a physical examination due to the turbulent blood flow through the defect.
- Congestive Heart Failure (CHF) Symptoms: In larger defects, individuals may experience symptoms of congestive heart failure, such as breathing difficulties, rapid heartbeat, and fluid retention.
- Feeding Difficulties: Infants with significant septal defects may have difficulty feeding, tire easily, or exhibit poor weight gain due to increased work on the heart and respiratory system.

Ibuprofen, which is a nonsteroidal anti-inflammatory drug (NSAID), is sometimes used in the management of certain congenital heart defects, such as a patent ductus arteriosus (PDA) in premature infants. The PDA is a normal fetal blood vessel that should close shortly after birth but may remain open in some cases. Ibuprofen can be used to help close the PDA by reducing blood flow through it.
These defects can vary in size and severity, and treatment may involve observation, medication, or surgical repair, depending on the individual case. Early detection and appropriate management are essential for optimizing outcomes for individuals with septal wall defects.

75
Q

Cyanotic Heart Lesions (Tetralogy of Fallot & Tricuspid Atresia: means that the tricuspid valve doesn’t work at all, it’s totally closed off, so the r atrium can’t empty into the r ventricle)

A

Tetralogy of Fallot (TOF):
- Four heart abnormalities: VSD, pulmonary stenosis, right ventricular hypertrophy, overriding aorta.
- Results in cyanosis due to mixing of oxygenated and unoxygenated blood.
- Surgical intervention required for correction, typically with a “total repair” procedure.

Tricuspid Atresia:
- Characterized by the absence or severe underdevelopment of the tricuspid valve.
- Blocks blood flow from the right atrium to the right ventricle.
- Often accompanied by an atrial or ventricular septal defect (ASD or VSD).
- Requires complex surgical procedures to create alternate blood flow pathways.

In summary, Tetralogy of Fallot involves four specific heart defects and causes cyanosis, while Tricuspid Atresia involves the absence of the tricuspid valve and necessitates surgical interventions to redirect blood flow.

Common Clinical Features:
- Anatomical Defect: Atrial Septal Defect (ASD) or Ventricular Septal Defect (VSD) may be present in these conditions.
- Mild to Severe Desaturation: Insufficient oxygenated blood is pumped into the systemic circulation, resulting in low oxygen levels in the body.
- Polycythemia: Chronic hypoxemia can stimulate the body to produce more red blood cells, leading to polycythemia (increased red blood cell count).
- Murmur: A heart murmur is often present due to turbulent blood flow through the septal defect or other structural abnormalities.
- Hypoxemia: Inadequate oxygen levels in the blood, leading to cyanosis.
- Dyspnea: Shortness of breath and respiratory distress may occur due to reduced oxygenation.
- Increased Cardiac Workload: The heart must work harder to compensate for the limited oxygen supply, potentially leading to cardiac hypertrophy (enlargement of the heart muscle).

Management of these cyanotic heart lesions typically involves surgical correction or palliative procedures to improve oxygenation and reduce the workload on the heart. Timely intervention is crucial to address these congenital heart defects effectively.

You’re describing a congenital heart defect known as Tetralogy of Fallot, which is one of the cyanotic heart lesions. Here’s a breakdown of the key features of Tetralogy of Fallot:

  1. Aorta Override: In Tetralogy of Fallot, the aorta is positioned in such a way that it receives blood from both the right and left ventricles, leading to mixing of oxygen-poor (deoxygenated) and oxygen-rich (oxygenated) blood. This means that some oxygen-poor blood is pumped into the systemic circulation, causing cyanosis (blueness) due to reduced oxygen levels in the body.
  2. Pulmonary Bypass: Because of the aorta’s overriding position and the presence of a ventricular septal defect (VSD), deoxygenated blood can bypass the lungs and be circulated throughout the body without receiving adequate oxygenation.
  3. Right Ventricular Hypertrophy: The right ventricle has to work harder to pump blood into the aorta against resistance, leading to hypertrophy (enlargement) of the right ventricle over time.

Tetralogy of Fallot is typically treated surgically to correct the structural defects and improve oxygenation. Surgical repair aims to close the VSD, reposition the aorta, and alleviate the right ventricular outflow obstruction to ensure proper oxygenation of blood and reduce the workload on the right ventricle. Timely intervention is essential to manage this congenital heart condition effectively.

76
Q

Obstructive Defects (Pulmonary Stenosis, Aortic Stenosis, & Coarctaction of the Aorta, meaning that it goes backwards so it just keeps feeding itself )

A
  • Obstructive Defects: Pulmonary Stenosis, Aortic Stenosis, and Coarctation of the Aorta
    • Pulmonary arteries are narrowed or obstructed.
    • The aortic valve is too small or narrow, leading to increased workload on the left ventricle and resulting in left ventricular hypertrophy.
    • Coarctation of the aorta causes narrowing of the aorta, reducing the delivery of oxygen-rich blood to the body.
    • Aortic stenosis slows down blood flow, leading to symptoms such as congestive heart failure and, eventually, heart failure.
    • Blood flow exiting the heart is obstructed due to these conditions.
  • Narrowing or constriction of anatomical openings.
  • Increased pressure occurs behind the constriction.
  • Decrease in the volume of systemic blood flow.
  • Symptoms of Congestive Heart Failure (CHF) may include:
    • Decreased cardiac output.
    • Pump failure.
77
Q

Defects of the Great Vessels

A
  • Defects of the Great Vessels
    • Transposition of the Great Vessels: The great vessels connected to the right ventricle instead of the left.
      • The pulmonary artery is connected to the left ventricle, causing a circulation loop where the left ventricle pumps to the pulmonary veins and then to the pulmonary artery, creating two separate circulating systems.
      • In this condition, rich oxygenated blood is not effectively delivered to the body.
    • Truncus Arteriosus: Only one vessel leaves the heart instead of two.
      • During development, these two vessels fail to separate, resulting in a single vessel that doesn’t deliver oxygenated blood where it’s needed.
      • This leads to the mixing of saturated blood with unsaturated blood.
    • Symptoms and Consequences:
      • Pulmonary congestion, resulting in inadequate oxygen delivery.
      • Decreased cardiac output.
      • Symptoms of Congestive Heart Failure (CHF):
        • Ruddiness of the skin.
        • Dusky or gray skin color.
        • Dyspnea (difficulty breathing).
78
Q

Neural Tube Defects

A

Anencephaly
Spina Bifida

79
Q

Anencephaly which means without brain. The chances of survival after birth are 0.

A
  • Anencephaly: A condition characterized by the absence of the brain.
    • Survival chances after birth are virtually nonexistent.
    • Considered the most severe Neural Tube Defect (NTD).
    • Approximately 1,000-2,000 infants are born with this condition.
    • Both genetic and environmental factors can contribute to its development.
    • Anencephaly is mostly incompatible with life.
80
Q

Spina Bifida.

A
  • Spina Bifida: A condition characterized by caudal defects, resulting in the failure to close the spinal column in a specific area.
    • There are different types:
      • Spina Bifida Occulta: A rare cause of disability, often not easily visible. It’s typically detected by checking for a dimple or the end of the hair column during a newborn assessment.
      • Meningocele: Involves a bony defect with the protrusion of the meninges (membranes surrounding the spinal cord) and spinal fluid, without nerve involvement. It appears as a small bulge, with no major spinal nerves passing through.
      • Myelomeningocele: Involves the herniation of the spinal cord and root nerves into a sac through the bony defect. Disabilities occur below the protrusion.
    • Prevention efforts, such as advocating for the use of folic acid, have been significant because it’s an easy intervention for women to reduce the risk of spina bifida in their offspring.
81
Q

Other Congenital Anomalies

A
82
Q

Microcephaly we heard about it in the news due to zika virus

A
  • Microcephaly: A condition where a small brain forms within a normal-sized cranium.
    • Various factors can contribute to its development, including genetics, alcohol use, drug abuse, low maternal BMI (Body Mass Index), NSAID (Nonsteroidal Anti-Inflammatory Drug) use, Zika virus infection, and exposure to toxins, especially in areas with high industrial activity.
    • Microcephaly typically becomes evident by age 2.
    • Due to the small brain size, individuals with microcephaly often experience cognitive impairments.
    • Education and awareness efforts are essential to inform people about the cognitive deficiencies associated with microcephaly and its potential causes.
83
Q

Hydrocephalus

A
  • Hydrocephalus: An increase in cerebrospinal fluid (CSF) in the brain’s ventricles.
    • This can occur due to overproduction, obstruction, or impaired circulation or absorption of CSF.
    • Individuals with hydrocephalus often have another congenital defect as well.
    • The pressure of excess CSF can disrupt normal brain growth.
    • Treatment often involves the surgical placement of a valve and tube into the abdomen to drain the excess CSF. These may need to be replaced as the child grows to accommodate their changing size.
84
Q

Choanal Atresia

A
  • Nasal Airway Narrowing or Occlusion: A condition characterized by the narrowing or blockage of the nasal airway.
    • The first sign often includes difficulty with breastfeeding, as the infant struggles to simultaneously suck and breathe.
    • Symptoms may include dyspnea (difficulty breathing) related to the nasal airway.
    • This is a rare condition.
    • Diagnosis may involve the inability to pass a suction catheter through the nasal airway.
    • The neonate may exhibit cyanosis (bluish discoloration) and become pink with crying, indicating potential respiratory distress.
85
Q

Congenital Diaphragmatic Hernia.

A
  • Congenital Diaphragmatic Hernia: A condition characterized by the severe development of the diaphragm into the thoracic cavity.
    • One of the first noticeable signs in affected infants is a concave abdomen due to the absence of abdominal organs in the appropriate position.
    • This condition is often associated with other congenital anomalies.
    • Complications may include pulmonary hypoplasia (underdeveloped lungs) and decreased pulmonary vasculature.
    • To support respiratory effort, surgical intervention is typically required to correct the diaphragmatic hernia and reposition the abdominal organs into the abdominal cavity.
86
Q

Cleft Lip & Palate.

A
  • Cleft Lip and Palate: The most common congenital malformation of the head and neck.
    • It can manifest as a fissure of the lip or a fissure of both the lip and palate.
    • Surgical repair is typically performed between 6-12 weeks of age.
    • Cleft lip and palate can be unilateral (affecting one side) or bilateral (affecting both sides).
    • Infants with this condition may experience immediate feeding problems because they can’t create a proper seal while breastfeeding due to the lip or palate fissure.
    • To facilitate feeding, milk can be provided in bottles designed to bypass the palate and reach the back of the mouth, allowing the baby to swallow without risking aspiration into the lungs.
    • Long-term considerations include dentition and language acquisition.
87
Q

Esophageal Atresia & Tracheoesophageal Fistula

A
  • Tracheoesophageal Fistula (TEF): An abnormal connection between the esophagus and the trachea during the 3-6 weeks of embryonic development.
    • The esophagus may not be patent, meaning it closes off, preventing the passage of fluids and food.
    • The esophagus communicates with the trachea at its distal end, causing a direct connection.
    • Infants with TEF often have continuous saliva production but are unable to swallow their own saliva due to the lack of a functional esophagus.
    • Aspiration occurs because the saliva has no proper pathway.
    • Feeding-related symptoms are known as the “3 C’s”: coughing, choking, and cyanosis.
    • Orogastric tubes are placed for suctioning saliva to prevent aspiration.
    • TEF can manifest as just an issue with the esophagus or as tracheoesophageal fistula, involving both the trachea and the esophagus.
    • Surgical intervention is typically required to correct this condition.
88
Q

Omphalocele & Gastroschisis

A
  • Omphalocele: It results from a weakened area of the umbilical ring, allowing the peritoneal membrane to protrude, followed by abdominal organs.
    • During treatment, caution is exercised to avoid introducing infection by not inserting the first clamp into the baby’s exposed tissue.
    • Detectable by the presence of a bulging mass around the umbilical site.
  • Gastroschisis: Involves a full abdominal wall opening with abdominal organs protruding, without the protection of a peritoneal sac.
    • Both omphalocele and gastroschisis require surgical intervention.
    • Gastroschisis is associated with a higher morbidity and mortality rate.

Common care considerations for both conditions include:
- Insertion of an orogastric tube for suctioning.
- Maintaining thermal regulation, as the exposure of abdominal organs outside the body can lead to decreased body temperature. Keeping the baby warm is crucial.
- Strict infection precautions to prevent contamination and ensure aseptic conditions during treatment.

89
Q

Imperforate Anus

A
  • Anorectal Malformation: A congenital malformation affecting the anorectal area.
    • It may present with a pouch that doesn’t connect to the colon.
    • Fistulas may also be present, with openings into either the vagina or the urinary tract.
    • These malformations are classified as low or high, depending on their location.
    • Surgical repair is typically required, and in some cases, a colostomy may be necessary.
    • Gastric decompression may also be performed as part of the treatment plan.
90
Q

Hypospadias & Epispadias

A
  • Hypospadias: A congenital condition where the urethral opening is not at the tip of the penis but rather on the top or bottom, in a location other than where it is supposed to be.
    • Epispadias is a related condition that occurs more commonly in men but can also be found in females, often in conjunction with bladder exstrophy.
    • Hypospadias might be associated with abnormalities of the testicles and scrotum.
    • Surgical repair is typically performed and is associated with good outcomes.
    • Repair is usually recommended to be done within the first 6 months of life to achieve the best results.
91
Q

Bladder Exstrophy

A
  • Bladder Exstrophy: A congenital condition where the bladder is located outside the abdominal wall due to a failure to close properly during the embryonic stage.
    • This condition is characterized by wide spacing of the rectal muscles and the symphysis pubis.
    • Surgical repair is necessary to correct the anatomical defect.
    • In some cases, cosmetic surgery may be required to correct genitalia, particularly in females, where it is more common.
    • A suprapubic catheter is often needed before surgery to manage urine drainage.
    • Strict infection precautions are essential in the care of individuals with bladder exstrophy to prevent complications and maintain aseptic conditions. I mean the organ is sitting outside where all the germs and microbes are so …
92
Q

Congenital Clubfoot

A
  • Congenital Clubfoot: A condition characterized by an extremely turned-in foot that is difficult to straighten due to its formation.
    • Limited normal range of motion (ROM) in the affected foot.
    • Treatment typically involves serial casting, often using the Ponseti method.
    • Surgical intervention may be necessary between 4 to 9 months of age in some cases.
    • Priorities in care include addressing bathing, diapering, and developmental goals to ensure the well-being and proper development of the affected child.

There are 2 types one is called positioning and the other is called intrensic : Congenital clubfoot is a congenital musculoskeletal deformity that affects the foot and ankle. It is characterized by an abnormal positioning of the foot, making it difficult to place the foot in a normal position. However, the terms you mentioned, “positioning” and “intrinsic” or “extrinsic,” are not typically used to describe the two main types of congenital clubfoot.

The two primary types of congenital clubfoot are:

  1. Idiopathic or Isolated Clubfoot: This is the most common type of congenital clubfoot, and the exact cause is not known. It is not typically associated with any other underlying medical condition. Idiopathic clubfoot can often be corrected with non-surgical methods like casting, stretching, and bracing, and sometimes it may require surgical intervention.
  2. Non-Idiopathic or Syndromic Clubfoot: This type of clubfoot is associated with other congenital conditions or syndromes. In these cases, the clubfoot is just one component of a broader medical condition, and treatment may involve addressing the underlying syndrome in addition to correcting the clubfoot deformity.

The terms “intrinsic” and “extrinsic” are not commonly used to classify clubfoot, and they do not describe the two main types of clubfoot. Clubfoot is primarily classified based on its underlying cause, as mentioned above. Treatment options depend on the severity of the clubfoot and whether it is idiopathic or associated with another syndrome.

If you have specific concerns about clubfoot, I would recommend consulting with a medical professional or orthopedic specialist who can provide you with accurate information and guidance based on the individual case.

93
Q

Developmental Dysplasia of the Hips

A
  • Developmental Dysplasia of the Hips (DDH): A condition characterized by subluxation, dislocation (luxation), or malformation of the acetabulum (hip socket).
    • Treatment often involves the use of a Pavlik harness to help improve hip joint alignment.
    • Early detection and intervention are crucial to achieve the best outcomes.
    • In the care of infants with DDH, priorities include addressing bathing, diapering, and developmental goals to ensure their well-being and healthy hip development.
94
Q

Inborn Errors of Metabolism

A
  • Inborn Errors of Metabolism: Genetic disorders that disrupt the normal metabolism of carbohydrates, proteins, fatty acid oxidation, or glucose.
    • Early detection is essential for achieving the best outcomes.
    • Newborn screening is a critical tool for identifying these conditions shortly after birth, allowing for timely intervention and management.
95
Q

Screenings

A

This is where we do some of the newborn assessments

96
Q

The nurse is teaching the new parents about newborn screening tests, including PKU. The nurse knows the teaching has been effective when the new mom states:
A. “Testing my baby is optional at this point, I will wait until the baby is about 6 months old.”
B. “You will wait to test my baby’s blood until after the first 24 hours of life.”
C. “I know that my baby will need to have a venous sample of blood for these tests.”
D. “I understand you will test my baby’s cord blood to diagnose any of these diseases.”

A

B

97
Q
  • Newborn Screening Categories:
    • Metabolic: These tests check for inborn errors of metabolism, where the baby might be missing a crucial enzyme or protein required for digestion. Early detection can lead to dietary adjustments and prevent potential health issues.
    • Endocrine: Screening for endocrine disorders that can affect hormone production and regulation.
    • Hemoglobin: Includes tests related to blood disorders, such as sickle cell disease.
    • Other: This category may include tests for various conditions, including immune disorders and cystic fibrosis.

Newborn screening, often referred to as the PKU (phenylketonuria) test, is a crucial step in identifying and addressing these conditions early in life, helping to prevent complications and ensure the child’s well-being.

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98
Q

Propionic Acidemia X Methylmalonic Acidemia (methylmalonyl-CoA mutase) X Methylmalonic Acidemia (Cobalamin disorders) X Isovaleric Acidemia X 3-Methylcrotonyl-CoA Carboxylase Deficiency X 3-Hydroxy-3-Methyglutaric Aciduria X Holocarboxylase Synthase Deficiency X ß-Ketothiolase Deficiency X Glutaric Acidemia Type I X Carnitine Uptake Defect/Carnitine Transport Defect X Medium-chain Acyl-CoA Dehydrogenase Deficiency X Very Long-chain Acyl-CoA Dehydrogenase Deficiency X Long-chain L-3 Hydroxyacyl-CoA Dehydrogenase Deficiency X Trifunctional Protein Deficiency X Argininosuccinic Aciduria X Citrullinemia, Type I X Maple Syrup Urine Disease X Homocystinuria X Classic Phenylketonuria X Tyrosinemia, Type I X Primary Congenital Hypothyroidism X Congenital adrenal hyperplasia X S,S Disease (Sickle Cell Anemia) X S, βeta-Thalassemia X S,C Disease X Biotinidase Deficiency X Critical Congenital Heart Disease X Cystic Fibrosis X Classic Galactosemia X Glycogen Storage Disease Type II (Pompe) X Hearing Loss X Severe Combined Immunodeficiencies X Mucopolysaccharidosis Type 1 X X-linked Adrenoleukodystrophy X Spinal Muscular Atrophy due to homozygous deletion of exon 7 in SMN1 X Recommended Uniform Screening Panel1 SECONDARY2 CONDITIONS 3 (As of July 2018) Secondary Condition Metabolic Disorder Hemoglobin Disorder Other Disorder Organic acid condition Fatty acid oxidation disorders Amino acid disorders Methylmalonic acidemia with homocystinuria X Malonic acidemia X Isobutyrylglycinuria X 2-Methylbutyrylglycinuria X 3-Methylglutaconic aciduria X 2-Methyl-3-hydroxybutyric aciduria X Short-chain acyl-CoA dehydrogenase deficiency X Medium/short-chain L-3-hydroxyacylCoA dehydrogenase deficiency X Glutaric acidemia type II X Medium-chain ketoacyl-CoA thiolase deficiency X 2,4 Dienoyl-CoA reductase deficiency X Carnitine palmitoyltransferase type I deficiency X Carnitine palmitoyltransferase type II deficiency X Carnitine acylcarnitine translocase deficiency X Argininemia X Citrullinemia, type II X Hypermethioninemia X Benign hyperphenylalaninemia X Biopterin defect in cofactor biosynthesis X Biopterin defect in cofactor regeneration X Tyrosinemia, type II X Tyrosinemia, type III X Various other hemoglobinopathies X Galactoepimerase deficiency X Galactokinase deficiency X T-cell related lymphocyte deficiencies

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99
Q

Hearing screening can indeed involve different methods:

  1. Otoacoustic Emissions (OAE) Test: In this test, a small probe is placed in the baby’s ear canal, which emits sounds or clicks. The ear’s response is measured, specifically the otoacoustic emissions generated by the inner ear. A lack of response may indicate a hearing problem.
  2. Auditory Brainstem Response (ABR) Test: This test involves placing electrodes on the baby’s head and soft earphones or inserts in the ears. Sounds or clicks are presented through the earphones, and the brain’s electrical activity in response to these sounds is recorded. This helps assess the auditory nerve and brainstem’s function.

Both tests aim to identify hearing issues in newborns, and the choice of test may depend on various factors, including the baby’s age, medical condition, and the availability of equipment.

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100
Q

Screening for Critical Congenital Heart Disease. We put the o2 sat on thier right hand and then on either foot. This is to look for huge diffrences. Too much differnce is not good. It would mean that the oxygenated blood is not getting to the lower extremites and this might indicate heart disease or something going on

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101
Q

It seems like you’re describing an algorithm or protocol for newborn health screening related to cardiac health. Here’s a simplified breakdown:

  1. Age Requirement: The baby should be at least 24 hours old.
  2. Initial Screening:
    • Check the oxygen saturation (SpO2) levels.
    • Screen the right foot, aiming for a minimum of 90% SpO2.
    • Screen the left foot and compare the SpO2 to the right foot. Ideally, it should be 95% or higher.
  3. Follow-up if Needed: If there’s a significant difference in SpO2 levels between the right and left foot or if the SpO2 levels are below the specified thresholds, the baby should be referred to a cardiologist for further evaluation.
  4. Cardiologist Assessment: The cardiologist will assess various cardiac parameters, including ejection fraction and other relevant factors to determine if there are any cardiac issues that require attention or intervention.

This algorithm appears to be a guideline for screening newborns for potential cardiac issues, with specific thresholds for oxygen saturation levels and a referral process for further evaluation by a cardiologist when necessary.

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102
Q

Pathologic jaundice in newborns is a condition characterized by the yellowing of the skin and the whites of the eyes (jaundice) that occurs within the first 24 hours of life. This early onset of jaundice is concerning because it may be indicative of an underlying medical problem. Pathologic jaundice is distinct from physiological jaundice, which typically appears after the first 24 hours of life and is a normal physiological response to the breakdown of fetal red blood cells.

The causes of pathologic jaundice in newborns can include:

  1. Hemolytic Disease of the Newborn (HDN): This condition occurs when there is a blood group incompatibility between the mother and the baby, most commonly due to the ABO or Rh factor. For example, if the mother is Rh-negative and the baby is Rh-positive, the mother’s antibodies may attack the baby’s red blood cells, leading to their destruction and the release of bilirubin, which causes jaundice.
  2. Polycythemia: Polycythemia refers to an abnormally high red blood cell count in the newborn. When there is an excessive breakdown of red blood cells, it can lead to increased bilirubin production and subsequent jaundice.
  3. Hemorrhage: Bleeding within the baby’s body, such as from a traumatic delivery or internal bleeding, can lead to the release of bilirubin into the bloodstream, causing jaundice.
  4. Infections: Certain infections, such as sepsis, can affect the baby’s liver’s ability to process bilirubin, resulting in jaundice.
  5. Metabolic Disorders: In rare cases, metabolic disorders like galactosemia or Gilbert syndrome can lead to elevated bilirubin levels and jaundice in newborns.
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103
Q

The provided information appears to be related to the assessment and management of newborn infants based on certain criteria, particularly in relation to bilirubin levels and risk factors. Here’s an explanation of the key points:

  1. Grading: The initial section shows numerical values (25, 20, 15, 10) which could represent some sort of grading or scoring system. However, without additional context, it’s unclear what these numbers specifically refer to.
  2. SmartArt: “Convert to SmartArt” likely suggests converting this data into a visual representation using SmartArt graphics in programs like Microsoft Office. This can help make complex information more visually understandable.
  3. Picture A: This may refer to an image or diagram associated with the information, but the specific content of Picture A is not provided.
  4. Infants’ Risk Categories: The text discusses different risk categories for newborn infants based on their gestational age and certain risk factors. These categories include:
    • Infants at lower risk (≥ 38 weeks gestation and well)
    • Infants at medium risk (≥ 38 weeks gestation with risk factors or 35-37 6/7 weeks gestation and well)
    • Infants at higher risk (35-37 6/7 weeks gestation with risk factors)
  5. Timeframes: The information mentions various timeframes (24 hours, 48 hours, 72 hours, 96 hours) and “Days.” These might be related to monitoring or intervention intervals for newborns.
  6. Bilirubin Levels: It advises the use of total bilirubin levels for assessment and recommends not subtracting direct reacting or conjugated bilirubin. Bilirubin is a substance related to jaundice in newborns.
  7. Risk Factors: The text lists various risk factors that could influence the risk category of newborns. These include isoimmune hemolytic disease, G6PD deficiency, asphyxia, lethargy, temperature instability, sepsis, acidosis, or low albumin levels (< 3.0g/dL).
  8. Adjustment for TSB Levels: It suggests that for well infants between 35 and 37 6/7 weeks, the total serum bilirubin (TSB) levels could be adjusted for intervention. This adjustment likely depends on the specific risk factors and gestational age.
  9. Phototherapy: The information mentions the use of phototherapy to treat high bilirubin levels. It indicates that phototherapy can be considered in the hospital or at home when TSB levels are between 2-3 mg/dL (35-50 mmol/L), but not for infants with risk factors.
  10. Investigate and Notes: These headings suggest there might be more detailed information or comments related to the subject, but the content under these headings is not provided.

If you have specific questions or need further clarification on any of these points, please let me know, and I’ll be happy to assist you further.

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104
Q

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A

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105
Q

Certainly, let’s delve deeper into how an infection, particularly one leading to neonatal sepsis, can affect each of the points you mentioned:

  1. Apnea: Infections can affect the respiratory center in the brain by causing inflammation. Inflammatory substances released in response to the infection can reach the brain and irritate or disrupt the neural pathways responsible for controlling breathing. This irritation can lead to a disruption in the normal rhythm of breathing, resulting in apnea (temporary cessation of breathing).
  2. Bradycardia: Infections can influence heart rate by affecting the autonomic nervous system. Inflammatory signals from the infection can disrupt the normal balance between sympathetic and parasympathetic nerves that control heart rate. This disruption can cause bradycardia (slow heart rate) as the parasympathetic system becomes more dominant.
  3. Tachypnea: To combat the infection, the body often needs more oxygen. In response, the respiratory center in the brain can increase the respiratory rate (tachypnea) to deliver more oxygen to the bloodstream. This is a protective mechanism to meet the increased oxygen demand.
  4. GFR (Glomerular Filtration Rate): Infections can affect the kidneys by impairing blood flow to these organs. Reduced blood flow can disrupt the delicate filtration process in the glomeruli, leading to a decrease in the glomerular filtration rate. This can result in impaired waste removal and electrolyte balance.
  5. Decreased Oxygen (O2): Infections can cause respiratory distress or pneumonia, which can reduce the exchange of oxygen in the lungs. Additionally, inflammation caused by infection can impair the ability of red blood cells to carry oxygen effectively, leading to decreased oxygen levels in the bloodstream.
  6. Tachycardia: Infections often trigger an immune response that releases cytokines and other signaling molecules. These molecules can reach the heart and stimulate an increase in heart rate (tachycardia) as part of the body’s efforts to pump more blood and immune cells to the infection site.
  7. Hypotension: Infections can lead to vasodilation, a widening of blood vessels. This can result from the release of inflammatory mediators and toxins. Vasodilation reduces blood pressure, causing hypotension, as the heart struggles to maintain adequate blood flow to vital organs.
  8. Decreased Perfusion: Reduced blood pressure and impaired cardiovascular function can result in inadequate perfusion, meaning that tissues and organs receive less blood and oxygen than they require. This can lead to organ dysfunction and damage.
  9. Temperature Instability: The body’s temperature regulation is influenced by the hypothalamus in the brain. Infections can disrupt the normal functioning of the hypothalamus, causing fluctuations in body temperature as the body attempts to fight the infection.
  10. Lethargy: Infections can lead to fatigue and lethargy due to the diversion of energy resources to support the immune response. Additionally, fever and inflammation can directly affect brain function, leading to reduced alertness and activity.
  11. Hypotonic: Infections can impact the nervous system, including motor neurons responsible for muscle tone. This can lead to hypotonia, characterized by reduced muscle tone and weakness, affecting the baby’s ability to move and control their muscles.
  12. Seizures: Infections can directly affect brain tissue, leading to irritability and increased electrical activity in the brain. This heightened activity can result in seizures as the brain struggles to maintain normal neural functioning.
  13. Feeding Intolerance: Infections can disrupt gastrointestinal motility and function. The inflammation and metabolic demands placed on the body during an infection can lead to feeding intolerance, making it difficult for the baby to tolerate or digest feedings.
  14. Abdominal Distention: Gastrointestinal complications of infection, such as inflammation and slowed motility, can lead to a buildup of gas and fluids in the digestive tract, causing abdominal distention.
  15. Vomiting and Diarrhea: Infections can directly affect the gastrointestinal lining, leading to increased secretion of fluids, irritation, and inflammation. These factors can result in vomiting and diarrhea as the body tries to expel pathogens and toxins.
  16. Hyperglycemia: Stress responses triggered by infections, including the release of stress hormones like cortisol, can lead to an increase in blood sugar levels (hyperglycemia). The body releases glucose into the bloodstream to provide energy for the immune response and to support vital functions during infection.

In summary, infections can have a wide-ranging impact on the body, from directly affecting specific organs and tissues to triggering systemic responses such as inflammation and changes in heart rate and blood pressure. These effects can collectively result in the observed signs and symptoms associated with neonatal sepsis. Early recognition and treatment of the infection are crucial to mitigate these effects and improve the baby’s chances of recovery.

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106
Q

Differences:

  • Cause:
    • Physiologic Jaundice: This is a normal and common occurrence in newborns, resulting from the increased breakdown of fetal red blood cells and the immature liver’s slower processing of bilirubin.
    • Pathologic Jaundice: It is caused by an underlying medical condition or abnormality that either increases bilirubin production (as in hemolytic disease) or impairs bilirubin excretion (as in liver or metabolic disorders).
  • Onset:
    • Physiologic Jaundice: Typically appears after the first 24 hours of life, peaking around the third to fourth day.
    • Pathologic Jaundice: Appears within the first 24 hours of life or persists beyond the first week.
  • Bilirubin Levels:
    • Physiologic Jaundice: Bilirubin levels are usually below 15 mg/dL and rarely exceed 20 mg/dL.
    • Pathologic Jaundice: Bilirubin levels are typically higher than 20 mg/dL and may rapidly rise.
  • Clinical Presentation:
    • Physiologic Jaundice: Often presents as mild and benign yellowing of the skin and eyes. The baby is usually well and feeds adequately.
    • Pathologic Jaundice: Clinical presentation can be more severe, with signs of systemic illness such as poor feeding, lethargy, and abnormal physical findings. The baby may appear very jaundiced and may have other concerning symptoms depending on the underlying cause.
  • Management:
    • Physiologic Jaundice: Typically resolves on its own without the need for medical intervention. It can be managed by ensuring adequate feeding and monitoring bilirubin levels if they become significantly elevated.
    • Pathologic Jaundice: Requires identification and treatment of the underlying cause. This may involve diagnostic tests, phototherapy, and, in severe cases, exchange transfusions to reduce bilirubin levels.
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107
Q

It seems like you’ve listed some signs and symptoms of Neonatal Abstinence Syndrome (NAS) categorized by different systems. NAS occurs in newborns who were exposed to drugs in the womb. The signs you’ve mentioned can include:

Gastrointestinal signs: Poor feeding, vomiting, regurgitation, diarrhea, excessive sucking.

Central nervous signs: Irritability, tremors, shrill cry, incessant crying, hyperactivity, little sleep, excoriations on the face, and possibly convulsions.

Metabolic, vasomotor, respiratory signs: Nasal congestion, tachypnea (increased breathing rate), sweating, frequent yawning, increased respiratory rate (60 breaths/min), and fever (37.2° C).

These signs and symptoms can vary in severity depending on the substance the baby was exposed to and the duration of exposure. NAS often requires medical attention and management in a neonatal intensive care unit (NICU). If you suspect a baby may be experiencing NAS, it’s crucial to seek immediate medical care for proper evaluation and treatment.

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