Final: Neonatal Complications Flashcards

1
Q

Infants having thin skin, less subcutaneous fat and a greater body surface, are factors that affect what complication?

A

Hypothermia.

This causes them to lose body heat faster.

  • Preterm babies lose heat even faster.

** Infants have poor compensatory mechanisms.

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2
Q

Ways of losing heat: conduction, convection, evaporation, and radiation

A

Convection: flow of warmer heat rising and cooler falling. Like in a convection oven.

Conduction: direct transfer of heat through touch.

Radiation is the transfer of heat by means of electromagnetic waves. To radiate means to send out or spread from a central location

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3
Q

What is “cold stress” in a newborn?

A

Hypothermia.

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4
Q

What happens to the newborn if they are not receiving adequate heat? (On a physiological level)

A

They begin to burn their brown fat stores. Brown fat is more vascular and easy to burn; it surrounds their internal organs.

The metabolic waste byproduct of this exchange leads to metabolic acidosis.

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5
Q

What causes a newborn to experience respiratory distress (secondary to hypothermia)?

A

By burning their brown fat stores increases their need for oxygen. (and can result in hypoxemia)

This leads to increased respiratory rate and the need for more calories.

This also hampers their surfactant production, leading to respiratory distress.

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6
Q

Why does a hypothermic baby experience hypoglycemia?

A

Because they are burning more calories due to needing to breath faster to keep up with their oxygen demand needed while they are burning their brown fat.

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7
Q

Explain the process of the hypothermic baby experiencing hyperbilirubinemia:

A
  • Increased acid production as a byproduct of the brown fat being metabolized.
  • This leads to metabolic acidosis.
  • Metabolic acidosis leads to hyperbilirubinemia (jaundice). This is toxic to the nervous system and can lead to brain damage.
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8
Q

Why is hypoglycemia so dangerous for a newborn?

What are some common risk factors for it to occur?

A

It can cause brain damage.

Risk factors:
* Pre/Post Maturity

  • LGA / SGA
  • Asphyxia (lack of oxygen, d/t working harder to breath)
  • Hypothermia
  • Maternal DM
  • Maternal terbutaline (tachycardia = increased work)
  • Infection (increased metabolic workload)
  • Drug withdrawal
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9
Q

Signs and Symptoms for newborn hypoglycemia:

A

– Jitteriness

– Poor muscle tone

– Diaphoresis (babies don’t normally sweat)

– Poor suck/ feeding

– Dyspnea/ Apnea

– Cyanosis/ pallor

– Tachycardia

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10
Q

MORE signs and symptoms of hypoglycemia in the newborn:

A
  • Low temperature
  • High pitched cry
  • Exaggerated moro
  • Lethargy
  • Seizures (because it’s hard on the CNS)
  • May NOT have any signs and symptoms… so watch ALL babies!
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11
Q

What is the weight, in grams, of a LBW baby?

A

Anything under 2,500 g

About 5.5 pounds.

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12
Q

This baby is at or below the 10th percentile of normal weight for gestational age:

A

SGA

Can be preterm, at term, or post-term.

Babies who are SGA AND premature are at greatest risk for problems.

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13
Q

This rate of growth is a reflection of something else going on… the rate of growth doesn’t fit the usual pattern:

A

IUGR

Implies that the placenta is not working well (usually not genetic)… may be from drugs/tobacco/ alcohol or sickle cell anemia, infection, or high blood pressure.

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14
Q

What are the populations at risk for having an SGA baby?

A
  • Ages <16 or greater than 40 (not able to create as good of a placenta, too young = immature, AMA = decreased circulation)
  • Preeclampsia, HTN, chronic renal or heart disease, DM
  • Women who abuse substances
  • Infants with intrauterine infection (maternal body fighting the infection = leaves less calories for fetus)
  • Placental insufficiency
  • Genetic conditions
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15
Q

What is diagnostic for SGA?

A

Decreased fundal height for gestational age.

Ultrasound. Can check size, development, blood flow and circulation, and any placental calcifications.

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16
Q

What is the appearance of an SGA baby?

A
  • Wasted appearance w/loose skin folds (decreased or zero SQ fat)
  • Poor skin turgor, dry skin
  • Increased Hct = d/t polycythemia bc decreased O2 supply from poor placental perfusion so they’re trying to compensate.
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17
Q

MORE regarding SGA appearance:

A
  • Relatively thin arms
  • Sunken abdomen
  • Thin, yellow, dry umbilical cord
  • Sparse hair (including lanugo bc using glucose for other things).
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18
Q

What are the most common problems associated with SGA?

A

Hypothermia: d/t less SQ fat

Hypoglycemia: d/t less glycogen stores.

Plycythemia: r/t chronic hypoxia.

May have impaired mental development.

Greater incidence of heart disease later in life.

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19
Q

MORE problems associated with SGA:

A
  • Poor catch-up ability. Tend to follow the growth curve.
  • Increased risk for congenital malformations: cardiac being the biggest.
  • Increased morbidity/ mortality
  • Often won’t void for up to 24 hours after birth: bc of their dehydration.
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20
Q

Nursing care for SGA:

A
  • May need resuscitation at birth (decreased O2, dehydration, energy spent on RBC production, low glycogen levels all lead to possible difficulty with respirations). Watch for meconium aspiration (when baby is stressed, their anal sphincter relaxes=meconium released.
  • Accu checks, gavage for hypoglycemia; need early and frequent feedings
  • Temperature regulation
  • Parents need support to provide a supportive environment. They don’t realize the possible implications involved with an SGA baby.
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21
Q

At or above 90th percentile of normal weight for gestational age:

A

LGA - Large for Gestational Age

May be deceptive at birth by appearing to be full term when they may not be.

  • Gestational test (“cricket test”)
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22
Q

What is the normal BG level?

A

Above 40

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23
Q

What population is at risk for LGAs?

A
  • Women with DM
  • Multiparas: babies tend to get bigger w/each pregnancy
  • Women who gain more than 35 pounds during pregnancy or are large before pregnancy.
  • Genetic conditions
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24
Q

Respiratory Distress Syndrome, birth injuries / trauma, and asphyxia all are possible problems with what type of baby?

A

LGA

If mom has DM, can interfere with surfactant production (d/t the increased insulin from the increased glucose environment).

Asphyxia - if baby gets stuck, lower O2.

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25
Q

CNS injury: Brachial-plexus palsy, facial palsy, Intracranial hemorrhage, and other risks are problems associated with what type of baby?

A

LGA

Intracranial hemorrhage d/t prolonged labor.

Other risks:
Hypoglycemia
Polycythemia and hyperviscosity
Hyperbilirubinemia (which leads to brain damage)

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26
Q

At this week of gestation, this Syndrome implies that the placenta is deteriorating and may not be able to sustain fetus or function adequately through labor:

A

42 weeks gestation.

Postmaturity Syndrome.

Leads to hypoxia and malnutrition of the baby. Very rarely will they let someone carry to 42 weeks.

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27
Q

How postmaturity syndrome diagnosed?

A

Ultrasound measurements of fetal size and placental grade.

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28
Q

How is the appearance of a postmature infant?

A
  • Absence of vernix
  • Dry, cracked, leathery skin (dehydrated d/t placental deterioration).
  • Increased level of alertness: this is a symptom of chronic intrauterine hypoxia.
  • Longer fingernails
  • Decreased weight: d/t decreased perfusion and the malnutrition d/t placental deterioration.
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29
Q

These are potential problems from Postmaturity Syndrome:

A
  • Increased fetal distress: d/t hypoxia. This can lead to meconium in the amniotic fluid and risk of aspiration.
  • Hypoglycemia from depleted glycogen stores.
  • Oversize baby. This can lead to risk of birth trauma, prolonged labor, hemorrhage, and uterine atony.
  • Cold stress: d/t decreased SQ fat.
  • Polycythemia: d/t hypoxia. Leading to viscous blood.
  • Seizure: d/t hypoxia
  • Mother often fatiqued, frustrated, angered over the prolonged pregnancy.
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30
Q

What gestation is considered preterm?

A

Between 20 weeks and 36 weeks 6 days.

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31
Q

This type of baby has a 3-4 times mortality rate of other infants of the same weight:

A

Preterm.

Immaturity of physiologic function.

32
Q

Babies who have problems with initiating and maintaining respirations, maintaining body temperature, maintaining adequate nutrition and maintaining CNS function are showing signs of problems associated with why kind of birth?

A

Preterm.

They also have a hard time maintaining renal function (renal system is one of the last to mature) and may experience necrotizing enterocolitis.

Necrotizing enterocolitis is from the body shunting the oxygenated blood to the brain… causing necrosis of the GI. Great mortality.

The lung tissue is the greatest issue. It continues to grow all through term.

The lack of maintaining adequate nutrition is d/t suck-swallow not intact, and GI not mature enough… so give TPN through the central line (the umbilical cord)

33
Q

What are health problems are preemie’s at risk for?

A
  • Inability to resist infection
  • Resisting hematologic problems
  • Maintaining musculoskeletal integrity (they were supposed to be in mom, swimming around, making long bones, etc.
  • Chronic, long term problems.
34
Q

What is the treatment for a premature infant?

A

To simulate the environment of a healthy, well-nourished uterus.

Plan of care is aimed at conserving energy for repair, maintenance, and growth.

35
Q

What are some actions nurses may do for support of a premature infant?

A
  • Control the body temp via incubator
  • O2
  • Electronic cardiac monitoring
  • IV fluids (many times D 10 WNS fluid)
  • Oral or gavage feedings q 2-3 h (if GI is mature enough, determined by gas, vomiting, etc.)
  • GENTLE handling/ padding (fragile and don’t want to stress them.
  • Conserve energy (cluster care)
  • Careful swaddling = neurological organization.
36
Q

What are some indicators that we are stressing the baby?

A

HR
Breathing
Yawning
Hiccuping

37
Q

Nursing support for the parents of a preemie may be focused on what?

A
  • Anticipatory grieving
  • Grief/ Guilt
  • Altered bonding (can’t have as much skin to skin)
  • Balancing home/ NICU/ Other children

They will typically stay in the NICU the same amount of time they should have been in utero.

38
Q

Gestational age for “late” Preterm Infants:

A

34-37 weeks.

39
Q

More than 1/3 of the brain volume at term is acquired during which weeks gestation?

A

The last 6-8 weeks of gestation

There have been some developmental problems as late as 39 weeks.

Immaturity of brain structures may cause baby to respond negatively to stimuli. May manifest as tachycardia/ bradycardia/ abnormal breathing/ skin mottling/ frequent startling/ vomiting (more difficulty with GERD too)

40
Q

How long is the mandatory hospital stay for late preterm infants?

A

48 hours.

41
Q

What risks are late preterm infants exposed to?

A

Apnea

Bradycardia

Excessive sleepiness

Dehydration

Excessive weight loss

Feeding difficulties (suck/swallow/breath)

Weak suck

42
Q

What other risks are late preterm infants at risk for?

A

Jaundice

Hypoglycemia

Hypothermia

Respiratory distress

Sepsis

Hospital readmit (from jaundice/ respiratory/ feeding)

Breast feeding failure: these are the babies that REALLY need breast milk. Formula causes other problems.

43
Q

What weeks’ gestation is considered term?

Post term?

A

37 - 42 weeks = term

42 + = post term

44
Q

What sort of things need to be considered and done before a late preterm infant is able to be discharged?

A
  • There will be a 12 hour transition and a 48 hour minimum hospital stay.
  • There is a tiered checklist of milestones that they will need to accomplish.
  • Need to check VS every 3 hr
  • May need to assist with feeding (mom should pump if she plans to BF bc their such may not be hard enough).
  • Need to pass the car seat challenge test (cardiac monitor and pulseox: looking for periods of apnea).
  • Parent teaching, resources, follow up plans.
45
Q

What is Hemolytic Disease of the Newborn (HDN)?

A

During pregnancy, red blood cells from the unborn baby can cross into the mother’s blood through the placenta. HDN occurs when the immune system of the mother sees a baby’s red blood cells as foreign. Antibodies then develop against the baby’s red blood cells. These antibodies attack the red blood cells in the baby’s blood and cause them to break down too early.

HDN may develop when a mother and her unborn baby have different blood types

46
Q

What does hemolytic disease put a baby at a higher risk for?

A

Hyperbilirubinemia.

This occurs bc the baby’s body is trying to compensate for the hemolysis of its RBCs from the mother’s antibodies by making more RBCs but are still young erythroblasts (causing erythroblastosis fetalis too).

This is in combination with an immature liver, and perhaps not expelling meconium… all leading to increased bilirubin.

47
Q

This blood disease occurs when Rh negative mother and an Rh positive father produce an Rh positive fetus, if the mother has been already exposed to positive antigens then her body will begin to make antibodies that will travel through the placenta and attach the baby’s RBCs:

A

Erythroblastosis Fetalis.

This may not be an issue with the first baby but the risk increases with each subsequent pregnancy.

48
Q

What is isoimmunization?

A

Development of a significant titer of specific antibody as a result of antigenic stimulation with material contained on or in the red blood cells of another individual—called also alloimmunization.

49
Q

What is hydrops?

A

Gross edema of the entire body of the newborn infant, in erythroblastosis fetalis.

50
Q

What happens to the Rh positive fetus if the Rh negative mother begins making antibodies?

A

FETAL:
- Anemia

  • Jaundice
  • hydrops
  • death
51
Q

What are some ways the Rh neg mother could have been exposed to Rh pos blood?

A
  • Previous transfusion
  • Placenta abruptio
  • Placenta previa
  • Trauma
  • Birth (through tears)
  • SAB
  • Amniocentesis
52
Q

What test will we generally see given in the first trimester to Dx hemolytic disease of the newborn?

A

Indirect Coomb’s test.

This checks level of antibodies in the mother’s blood.

53
Q

What test will give the baby after being born to test for hymolytic disease?

A

Direct Coomb’s test.

Checks cord blood for antibodies that are attached to infant’s RBCs.

54
Q

What is the treatment for erythroblastosis fetalis?

A

Rhogam.

Given (deep IM) to mother at 28 weeks and within 72 hours of birth (ONLY if baby is Rh +) or other events such as amniocentesis, SAB, etc. to PREVENT antibodies from forming.

Rhogam is created from donated Rh antibodies. We can give up to 5 vials. This prevents MORE antibodies from forming.

55
Q

What do we do for an infant that has an Indirect Coomb’s test that reveals a high level of antibodies present?

A

Before delivery: intrauterine transfusion of O neg PRBCs every 2 weeks. This “washes out” the RBCs that are being attacked and gives the body the oxygen carrying RBCs needed for life. Eventually this wears off so another transfusion is needed. Since the RBCs are negative, the mother’s antibodies do not attack.

56
Q

What do we do for an infant that has a Direct Coomb’s test come back that reveals a high level of antibodies present?

A

After delivery: exchange transfusion of 75-85% of blood volume with Rh- blood. This is done a little at a time, over a couple of hours period of time. This method is taking out and “washing out” with replacement O- blood.

This corrects:
Anemia
Prevents kernicterus

57
Q

Which is more dangerous, Rh factor or ABO incompatibility?

A

Rh Factor is more dangerous.

Fetus just inherits a different blood type than mom.

This is less predictable than Rh, but Rhogam is NOT needed and usually is not problematic. Just need to WATCH the baby for jaundice.

58
Q

What are the most common blood difference of inheritance?

A

Mother is O = baby has A or AB

Mother is A = baby has AB or B

59
Q

This occurs in 50% of full term newborns d/t the increased production of RBC that don’t live as long as normal RBCs do:

A

Jaundice.

(80% of FT newborns in Colorado)

This results in an increase in bilirubin production. Bili is an orange-yellow pigment formed in the liver by the breakdown of hemoglobin and excreted in bile. The combo of increased amount and the subsequent increase of reabsorption in the newborn gut… will continue to rise until frequent stooling.

60
Q

What organ is responsible for the issue of jaundice in the newborn? When does it peak?

A

Due to their immature liver.

Peaks in 4-5 days.

Not physiologic if occurs before 24 hours (if jaundiced w/in the first 24 hours, worrisome. If after 24 hours, less worrisome).

Age/level relationship.

61
Q

Common causes of pathological jaundice:

A

Common causes of pathological jaundice include:

  1. Hemolysis: blood group incompatibility such as those of ABO, Rh and minor groups, enzyme
    deficiencies such as G6PD deficiency, autoimmune hemolytic anemia
  2. Decreased conjugation such as prematurity
  3. Increased enterohepatic circulation such as lack of adequate enteral feeding that includes
    insufficient breastfeeding or the infant not being fed because of illness, GI obstruction
  4. Extravasated blood: cephalhematoma, extensive bruising etc
62
Q

What does TORCH stand for regarding infections?

A

T - Toxoplasmosis

O - Other: syphilis, varicella zoster, parvovirus…

R - Rubella

C - Cytomegalovirus (CMV)

H - Herpes

63
Q

This type of jaundice develops in the first 24 hours or level is really high:

A

Pathological. The cause is more than usual physiologic issues…

Can cause damage to:

  • Brain
  • Kidneys
  • Intestines
  • Pancreas
64
Q

High levels of serum bilirubin can cause what results, regarding neurotoxicity?

A

Bilirubin encephalopathy AKA Kernicterus.

Can cause Cerebral Palsy or Mental Retardation.

Circulating bilirubin crosses the blood-brain barrier and, because it is lipid soluble, it penetrates neuronal and glial membranes… collecting in the brain tissue if it is not bound to albumin (protein) in the blood.

65
Q

What are the MATERNAL risk factors that may cause hyperbilirubinemia in newborns?

A
  • Blood type ABO or Rh incompatibility.
  • Breastfeeding (maybe bc milk not in yet so not moving food through much).
  • Drugs: oxytocin (Pitocin)
  • Ethnicity: Asian, Native American
  • Maternal illness: gestational DM
66
Q

What are the NEONATAL risk factors that may cause hyperbilirubinemia in newborns?

A

– Birth trauma (cephalohematoma, bruising, instrumental delivery)

– Excessive weight loss after birth: d/t not eating well… if they’re not eating well, they’re not having bm’s either.

– Infections: TORCH

– Infrequent feedings (sets up cycle to make jaundice worse)

– Male

– Polycythemia: any baby with this is at greater risk bc more RBCs to have to breakdown.

– Premature

– Sibling with hyperbilirubinemia

67
Q

Jaundice treatment:

A

First is early and frequent feedings. This increases intestinal activity and stooling and provides protein.

Second is phototherapy: decomposes bili by photooxidation in the skin. This helps it to be excreted in the urine and feces. It also allows unconjugated bili to be excreted.

Third is Albumin (protein in general) bind with the bilirubin. Can give this IV if serious.

68
Q

What sort of Nursing Care is involved with Phototherapy?

A
  • Monitor temp (naked increases hypothermic risk)
  • Evaluate stools and urine (green, watery, orange-red)
  • Watch for dehydration, replace fluids
  • No lotions, etc. (rash, block photo treatment)
  • Monitor and graph serum levels of bilirubin.
69
Q

Babies of diabetic mothers can be LGA or small and scrawny… it depends on the health of her placenta.

What are some other risks they may encounter?

A

LGA from the increased stimulation of the pituitary growth hormone which leads to an increase of fat deposits.

Polycythemia leads to a rosy-looking baby.

Risks:
- Birth trauma/ dystocia (fractured clavicle: limited ROM, crepitus, absent moro on affected side). Treatment: gentle handling, pain meds, can pin shirt.

  • Hyperbilirubinemia from the polycythemia.
  • Respiratory Distress Syndrome: the increased state of insulin blocks surfactant production.
  • Congenital defects: especially heart defects.
70
Q

What is the window of time that is the most important for assessing s/s of hypoglycemia and other risk factors?

A

The first 6-24 hours.

  • Accucheck @ birth and frequently per protocol. Normal glucose is greater than 40.
  • IV glucose (titrated) or formula PO feedings for low glucose.
  • Steroids in an emergency. They break up glucose.
  • Minimize energy expenditure
  • Watch for dehydration
71
Q

What is the major cause of mortality, especially in 1000-1500 gram babies?

A

Respiratory Distress Syndrome

Causes 20% of all neonatal deaths in the US

Deliver high flow nasal cannula: upward of 3,000 puffs in a minute to keep alveoli open.

Can give surfactant several times by squirting down their airway and ventilating.

72
Q

What is hypercapnia?

A

AKA hypercarbia

Abnormally high levels of carbon dioxide in the blood.

73
Q

This syndrome is when air is able to get into the alveoli but is not able to escape:

A

Meconium aspiration syndrome (MAS): this leads to overdistention of the alveoli, they rupture and then they experience a pneumothorax (collapsed lung).

The meconium inactivates the surfactant.

Also may develop secondary bacterial infection pneumonia from the meconium.

The severity of MAS depends on the amount of mec aspirated.

There is an increased mortality rate d/t hypoxemia and acidosis.

74
Q

When is Meconium Aspiration Syndrome most common? During which gestation/stage?

A

It is most common in term, SGA, LGA, post-term and stressed babies.

Prematurity is NOT a risk factor.

75
Q

Dx and Tx of Meconium Aspiration Syndrome:

A

Dx:
– Respiratory distress

– Tachycardia

– Overdistended chest w/ decreased lung sounds or course crackles.

Tx:
* If low respirations/ HR/ or tone: intubate, suction and check below cords?

  • Mechanical ventilator
  • Monitor ABG’s
  • Antibiotics: broadrange
  • Bicarb (if needed for acid/ base balance)
  • Conserve energy
76
Q

When is a newborn the most susceptible for infection?

Who is at most risk for infection?

A

For one month.

Premature and LBW