Module 3: Sarah Flashcards

1
Q

What are some multi-system effects of prematurity?

A

Intraventricular Hemorrhage (IVH), Patent Ductus Arteriosus (PDA), Respiratory Distress Syndrome (RDS), Necrotizing Enterocolitis (NEC), Acute Kidney Injury (AKI), sepsis, hyperbilirubinemia, hypothermia, hypoglycemia, and apnea.

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2
Q

What is the most common cause of respiratory distress in preterm infants?

A

RDS

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3
Q

Give examples of why the respiratory system of the preterm newborn is immature using each of the following as a guide:

lung development

A

The respiratory system of the newborn develops relatively late in gestation compared with other systems. Therefore, anatomy compatible with life (i.e., capable of gas exchange at the alveolar level) must exist for the newborn to be viable.

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4
Q

respiratory muscles

A

The infant must have a way to move air in and out of the lungs (pumping system). Infants do this with their chest wall muscles, diaphragm, and accessory respiratory muscles. The neonate, full term and preterm, has a circular, compliant rib cage that makes the diaphragm less effective and generally achieves less negative pressure for indrawing air. The chest wall and respiratory accessory muscles are small and tire easily. This is even more so for premature infants.

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5
Q

surfactant

A

In addition to problems with lung anatomy (in prems) and an inefficient pumping system (in neonates), the newborn needs surfactant to keep the alveoli open. Surfactant works by reducing surface tension within alveoli and thereby making the lungs easier to inflate. Remember the balloon analogy …it’s easier to inflate a balloon that has a bit of air in it. If surfactant is not present in sufficient quantities, the infant’s alveoli collapse with every exhalation (atelectasis). This makes every breath as hard as the first.

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6
Q

surface tension

A

If surfactant is insufficient and the surface tension increases enough to cause atelectasis, then lung resistance is increased. This is because lung volume is decreased from the alveolar collapse. This means that for lung expansion to happen, increased pressure is needed. The neonate is ill equipped to do this due to some of the factors described above. Clinically, the result is signs and symptoms of respiratory distress.

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7
Q

resistance, compliance, elasticity

A

Resistance, compliance, and elasticity are all terms used to describe the ease of lung distensibility. Increased resistance, decreased compliance, and decreased elasticity would all make the lungs more difficult to inflate. All of this increases the work of breathing for the infant, who will surely soon tire.

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8
Q

Many neonatal diseases, including many with nonpulmonary origins, may manifest with signs of respiratory distress. What does this statement mean?

A

This statement means that, even if you have a 12-hour old prem, you can’t just assume RDS from a respiratory distress picture. Respiratory distress is a set of symptoms from an underlying problem or disorder which requires investigation. There are many causes of respiratory distress. Respiratory Distress Syndrome is just one of the common causes of respiratory distress for premature infants.

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9
Q

Name other pulmonary disorders that may present with respiratory distress in preterm infants.

A
pneumonia
transient tachypnea of the newborn
air leak
pulmonary edema
hemorrhage
hypoplastic lung
congenital diaphragmatic hernia (CDH)
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10
Q

Name other non-pulmonary disorders that may present with respiratory distress in preterm infants.

A
necrotizing enterocolitis
other abdominal conditions
sepsis
CNS depression
congenital heart disease (CHD)
anemia
shock
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11
Q

Describe and explain the pathophysiology of Respiratory Distress Syndrome (RDS). How is RDS different from respiratory distress.

A

Lack of type II alveolar cells in the premature infant and the corresponding lack of surfactant is the major cause of RDS. Other contributing factors are poorly developed/few units of gas exchange and increased distance between alveolar-capillary units due to immature pulmonary vasculature. In term infants, asphyxia and maternal diabetes can cause decreased surfactant production. The infant’s “limited” respiratory system discussed in question 1 means that compensation for this problem is often inadequate.

Alveoli collapse due to increased surface tension. Hypercarbia, hypoxia, and respiratory acidosis result. Pulmonary vasoconstriction and worsening mixed acidosis occur. Intervention is aimed at improving oxygenation/ventilation through mechanical ventilation and artificial surfactant. Recovery is usually seen at around 72 hours when type II cells are regenerated and surfactant produced. This is the clinical picture of RDS. The clinical picture of RDS will include respiratory distress, which is a response to a variety of causative factors, as outlined in the above questions.

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12
Q

Based on what you have learned about respiratory distress and RDS, and what you know about Sarah so far, what further assessment data would you collect?

A

The missing data could be obtained by asking the following questions:

Is Sarah AGA, SGA, or LGA?
What is her HR? Her pulses? Blood pressure?
What is her temperature?
What are her blood gases? (We only know her oxygen saturation.)
What is her blood sugar?
Is there a history of infection? What is Brooke’s temperature?
Are there other pieces of information from the pregnancy history that might be relevant?
Is the gestational age accurate? Could Sarah be more preterm than 34 weeks?

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13
Q

What are your priorities regarding nursing care at this point?

A
  • maintain airway and breathing
  • closely monitor FiO2, SpO2, HR, RR, and BP using appropriate monitor
  • maintain oxygen saturation 88–95%
  • provide warmth
  • provide glucose and fluid. Will you feed Sarah? If not, how will you provide glucose and fluid?
  • provide developmentally supportive care
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14
Q

What about developmentally supportive care? Is it a priority? Should Selina incorporate developmentally supportive care principles into her care of Sarah?

A

Developmentally supportive care is always a priority. Every intervention should be conducted with the principles of developmentally supportive care in mind. Developmentally supportive care is not done in addition to other care; rather, it is an integral part of all care.

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15
Q

What about family-centered care? How might Brooke and Matt be feeling? What do you think about the way that Selina and Terry interacted with Matt and Brooke in the delivery room?

A

Family­centered care is not about using a set of pre-established rules to provide care. It is about putting Brooke and Matt in the center of the picture, working to establish a partnership with them, and providing care and making decisions which reflect their individual needs.

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16
Q

Hypoxia

A

a deficiency in the amount of oxygen reaching the tissues

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17
Q

Hypoxemia

A

a deficiency in the amount of oxygen in the blood

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18
Q

Early Responses to Hypoxia

A

tachypnea
tachycardia
pallor and mottling
air hunger

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19
Q

Late Responses to Hypoxia

A

apnea
bradycardia
cyanosis
lethargy

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20
Q

Early responses to hypoxia suggest efforts to compensate. Specifically:

A
  • tachypnea reflects an infant’s efforts to increase oxygen intake
  • tachycardia reflects efforts to increase cardiac output, thereby increasing delivery of oxygen to cells
  • pallor and mottling reflect redistribution of blood away from non-vital organ such as skin, toward vital organs such as the heart and brain. Other organs that receive less blood are: skin, skeletal muscles, liver, lungs, kidneys, and gut (often referred to as the “diving reflex”)
  • air hunger reflects efforts to increase oxygen intake
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21
Q

Infants, unlike adults and older children, do not often demonstrate early responses to hypoxia for very long before they begin to decompensate and show late responses. Specifically:

A

-apnea reflects central nervous system hypoxia and depression
-bradycardia reflects cardiac hypoxia
-cyanosis reflects increased amounts of deoxygenated hemoglobin reaching the cells
l-ethargy reflects generalized hypoxia, central nervous system depression, and tiring
-Understanding early signs of hypoxia and respiratory distress are the key to preventing respiratory failure.

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22
Q

Assessment of Hypoxia

A

Assessment of oxygenation includes monitoring for early and late signs of hypoxia. Respiratory rates, heart rates, skin color, and level of consciousness and activity all reflect how well an infant is oxygenated.

Hypoxemia (low blood oxygen) can be assessed by looking at pO2 and SaO2 saturation. Oxygen is carried in blood in two ways:

-dissolved

accounts for only 2–3% of the total oxygen content of blood
It is measured by pO2
pO2 values, arterial = 50–80, capillary = 40–60
Arterial pO2 values are more accurate than capillary pO2 values

-attached to hemoglobin

accounts for 97–98% of the total oxygen content of blood
is measured by SaO2 via pulse oximetry

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23
Q

Assessment

A

Pulse oximetry

a way of assessing oxygenation
non-invasive, continuous, reliable, and easy to use
a mainstay in the management of respiratory distress
tells us about the oxygen attached to hemoglobin which is the bulk of the oxygen available
measures the extent to which hemoglobin is saturated with oxygen molecules

pO2 (partial pressure of oxygen)

is a measurement of the amount of oxygen dissolved in the blood done by a capillary or arterial blood sample

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24
Q

Hemoglobin

A

Anemia (decreased hemoglobin) and polycythemia (excess hemoglobin) affect oxygen saturation interpretation.

Consider this:
There are two infants:

one is anemic (Hgb = 100)
one is polycythemic (Hgb = 200)
both infants are showing oxygen saturations of 90%
What the 90% saturation value means is that of the hemoglobin that each infant has, 90% of it is saturated with oxygen.

Is 90% of a hemoglobin of 100 the same as 90% of a hemoglobin of 200?
Clearly the infant who is polycythemic is carrying more oxygen than the infant who is anemic, even though both show pulse oximeter readings of 90%.

What this means is that whenever you are using pulse oximetry to assess oxygenation, you need to be aware of an infant’s hemoglobin. If it is normal, your oximeter readings are valid. If the hemoglobin is elevated, oximeter readings are falsely low. If the hemoglobin is low, oximeter readings are falsely high.

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25
Q

Describe the two ways that oxygen is transported in the blood and how each is measured.

A

Oxygen is transported in the blood in two ways:

dissolved in plasma — measured as pO2, by blood gas analysis, 2–3% of O2 is carried this way
bound to hemoglobin — measured as oxygen saturation, by pulse oximetry, 97–98% of O2 is carried this way

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26
Q

Where can you not place a saturation probe on an infant?

A

The ear of an infant is too small to give an accurate saturation reading.

27
Q

What are the normal SaO2 ranges for an infant who is receiving oxygen?

A

88-95

This range will help to prevent secondary complications related to hyperoxia and hypoxia

28
Q

How nurturing do you think Sarah’s environment is at this time and how might this be affecting her vulnerability?

A

Sarah is experiencing extreme physiological, motor, and state instability and disorganization in response to handling. Sarah has experienced one procedure after another without any time to recover. These procedures involve multiple caregivers as well as invasive procedures which put her at risk for infection as well as difficulty transitioning due to stress and hypoxia.

When you stop and list what has happened to Sarah since her arrival in the nursery, it is quite significant. She was transferred to an incubator, unbundled, ECG patches applied, oximeter probe applied, multiple assessments, temperature and BP taken, unsuccessful venous puncture attempts, heel warmed, repositioned on side, slipped onto back again, x-ray taken, and heel puncture. In reality, Sarah would have most likely had erythromycin eye drops instilled, intramuscular vitamin K, and a few other things done to her.

Sarah desperately needs pacing and time out based on her behavioral cues.

29
Q

normal blood gas values:

A
pH: 7.35-7.45
pCO2: 35-45
paO2: 50-80
pcO2: 40-60
HCO3-: 20-26
BE: -4 - +4
30
Q

What is Sarah’s blood pH? Is it normal? Acidotic? or Alkalotic?

A

A pH of 7.22 is low, indicating acidosis.

31
Q

Is Sarah’s blood pCO2 normal, elevated or decreased?

A

A pCO2 of 60 is elevated.

32
Q

Are the base excess and bicarbonate levels normal, elevated or decreased?

A

A base excess of -10 and bicarbonate of 18 are both decreased.

33
Q

Is the pO2 of any clinical value?

A

The pO2 is 35: this is borderline low. However, pcapO2 is of little value clinically. Remember that pO2 values in capillary blood are unreliable indicators of oxygenation. A pulse oximeter would be a better way to assess Sarah’s oxygen status.

34
Q

Now try to put these four assessments together by thinking about the following questions.

What is causing the decreased (acidotic) pH?

What effect would an elevated pCO2 have on the pH?

What effect would a decreased base excess and bicarbonate have on the pH?

A

A high pCO2 would lead to acidosis, as would a decreased HCO3- and decreased base excess. All of these values are contributing to Sarah’s low pH. Therefore, her acidosis is mixed.

35
Q

Why is the HC3- low?

A

The low HCO3- is a reflection of excess lactic acid that has combined with HCO3-. This buildup of lactic acid is due to anaerobic metabolism, which is the result of hypoxia. This lactic acidosis is contributing to the metabolic component of Sarah’s mixed acidosis.

36
Q

Quick overview of Sarah’s condition:

A

Sarah’s blood gas is a serious concern. Normal body functioning depends on a normal range of pH, adequate amounts of oxygen, and elimination of carbon dioxide. In addition, prolonged hypoxia puts Sarah at risk for Patent Ductus Arteriosus (PDA). During the transition to extrauterine life the ductus arteriosus normally closes. Hypoxia can either prevent it from closing or can cause it to reopen after it has closed.

In addition, her poor blood gases compromise her gastrointestinal functioning, putting her at risk for necrotizing enterocolitis. Hypoxia initially increases cerebral blood flow, which can lead to intraventricular hemorrhage in a preterm infant. Reduced renal blood flow will disrupt urine output, and fluid and electrolyte imbalance. Renal damage may occur. Reduced blood flow to the lungs interferes with surfactant production.

At 34 weeks gestation, Sarah is likely experiencing Respiratory Distress Syndrome (RDS), a problem largely related to lack of adequate pulmonary surfactant and structural immaturity of the lung.

37
Q

Other possible causes of Sarah’s respiratory distress need to be ruled out and include:

A
  • transient tachypnea of the newborn (TTN)
  • pneumonia
  • sepsis depletes an infant’s energy reserves and can result in increased O2 needs (this will be discussed in more detail later in this module)
  • abdominal distention secondary to bag and mask ventilation. The distended abdomen puts pressure on the diaphragm
  • Sarah may be tiring. Any disease which leads to tiring will tend to increase or cause respiratory distress
  • hypothermia
38
Q

How are infants immune systems described as?

A

immature and inexperienced

39
Q

Nursing care of infants should include monitoring for signs and symptoms of sepsis as well as prevention of sepsis:

A

-Monitor CBC and differential, CRP, pH, blood cultures, temperature, work of breathing, color, respiratory rate as well as apnea, bradycardia and desaturations.
-Administer IV antibiotics as required to manage risk factors
prematurity, premature rupture of membranes (PROM), maternal signs of infection, maternal infection, unknown or positive group B strep status, invasive procedures
-Maintain incubator isolation and clean and aseptic techniques
-Limit handling and procedures, especially invasive procedures

40
Q

Why is Sarah at risk for developing an infection and/or sepsis? List as many risk factors as you can think of, including those that arise from her environment.

A

At 34 weeks gestation, Sarah’s immune system is both immature and inexperienced, putting her at risk for infection, in particular, for sepsis. Other risk factors for infection are: Brooke’s temperature, her concern about a possible urinary tract infection, and the fact that she is not feeling well. She may have passed microorganisms on to Sarah prior to or during delivery. Other factors which increase the risk of infection for Sarah relate to the handling she has experienced since birth. Health care professionals’ hands, equipment, and invasive procedures all increase the risk of introducing microorganisms into Sarah’s environment.

41
Q

What are the main signs of infection in an infant? Is Sarah demonstrating any of these signs? If so, which ones?

A

Hypothermia, or temperature instability, is one of the main signs of sepsis. Sarah’s temperature is normal. Lethargy is another main sign. Sarah looked “exhausted” shortly after admission, but seems to be irritable as opposed to lethargic with handling. Her tone is not suggestive of lethargy. Poor feeding is not in evidence, as feeds have not begun. Abdominal distention is not evident (again, feeds have not yet begun). Hyper and hypoglycemia are associated with sepsis. Sarah’s blood glucose is normal. Apnea is a major sign of sepsis Sarah is not showing. Unexplained bradycardia is another sign not shown by Sarah. She has no rashes or petechiae. Labored respirations and tachypnea are both signs of infection. Sarah is experiencing both of these.

42
Q

Is Sarah on prophylactic antibiotics? Should she be? Why or why not?

A

Sarah has not been started on antibiotics. She should be due to maternal history, her prematurity, her clinical picture, and her laboratory findings. Infection (maternal and fetal) is a known cause of premature labor so a high level of suspicion is warranted.

43
Q

mmediately after birth, infants must adapt to the loss of a constant supply of maternal glucose. What is this often called?

A

Often called the postnatal energy crunch

44
Q

What are the signs and symptoms of neonatal hypoglycaemia?

A
  • abnormal cry
  • apnea
  • cardiac arrest
  • coma
  • convulsions
  • cyanosis
  • hypothermia
  • hypotonia
  • jitteriness
  • lethargy
  • tachypena
  • tremors
45
Q

What are causes of neonatal hypoglycaemia?

A

1) conditions associated with diminished hepatic glucose production
2) conditions associated with hyperinsulinism or excessive insulin production

46
Q

What are conditions associated with diminished hepatic glucose production?

A
  • cold stress
  • congenital heart disease/congestive heart failure
  • Inborn errors of metabolism: defective gluconeogenesis/glucogenolysis
  • intrauterine growth retardation
  • prematurity
  • perinatal stress/hypoxia
  • sepsis
47
Q

What are conditions associated with hyperinsulinism?

A
  • infant of a diabetic mother
  • rh incompatibility
  • beckwith-wiedemann syndrome
  • nesidioblastosis, islet cell adenomas, adenomatosis
  • adrenal insufficiency
  • Latrogenic causes
    • sympathomimetic exposure
    • exchange transfusion
    • high umbilical artery catheter
48
Q

Name the two ways glycolysis occurs.

A

aerobic and anaerobic metabolism

49
Q

How does each of these processes differ in terms of how much glucose they use and how much energy they produce and of the by-products produced?

A

Energy

Aerobic metabolism yields 36 moles of ATP per mole of glucose.
Anaerobic metabolism yields 2 moles of ATP per mole of glucose.
While both aerobic and anaerobic metabolism burn the same major intermediary substrate (pyruvic acid), anaerobic metabolism converts pyruvic acid to lactic acid. Aerobic metabolism further metabolizes pyruvic acid for extra energy (hence the 38 moles of ATP).

By products

The aerobic by-products are CO2 and H2O as opposed to the anaerobic by-product of lactic acid.

50
Q

What does this mean for Sarah, given her current respiratory problems?

A

Preterm infants have diminished glycogen stores. If Sarah has an infection, there is increased glucose consumption for the infectious process. Respiratory distress, handling, and the work of breathing also increases her metabolic demands, further compromising Sarah’s limited glucose stores.

51
Q

How will you assess for neonatal hypoglycemia? In particular, how will you distinguish between hypoglycemia and other neonatal health problems that produce similar signs?

A

Symptoms of neonatal hypoglycemia are often subtle, non­specific, and variable; this is why it is important to know who is at risk. The responses are non-specific because they may also be found in a number of other conditions. They are considered variable because some infants will be asymptomatic while others present with responses. This highlights the importance of knowing the infant, and in the case of an unstable infant, knowing the serum glucose level.

Jitteriness and/or seizures are often due to hypoglycemia. Serum glucose should be monitored closely for all jittery or seizing infants.

52
Q

Nursing care and monitoring for hypoglycemia should include:

A

Monitor serum glucose for all at-risk infants who:
are small for gestational age (SGA)
have experienced perinatal asphyxia
have RDS
are experiencing hypoxia or have been hypoxic
have a diabetic mother (IDM)
feed or start IV glucose shortly after birth
minimize glucose utilization by minimizing pain, stress, and handling

53
Q

Describe what “stability” might look like for Sarah.

A

Your responses will vary. In general, “stability” means that Sarah would be:

pink
Well oxygenated — normal heart rate, pink color, satisfactory pulse oximeter readings, good tone.
Breathing easily — normal heart rate, no indrawing, no grunting, no nasal flaring.

warm

Warm — normal temperature.

sweet

Not hypoglycemic — receiving IV dextrose.
Well hydrated — receiving IV fluid.

clean

Not infected — receiving antibiotics.

organized

Neurodevelopmentally supported by a quiet environment, eyes shaded from excess light, care is being paced, body supported by linen rolls, etc.

attached

Supported by her family, who are well informed of her condition and participating in her care.

54
Q

Respiratory distress syndrome (RDS) is caused by an excess of alveolar type II cells

A

False

55
Q

Normal pH range is

A

7.35-7.45

56
Q

Infants at risk for sepsis are

A
  • preterm infants
  • term infants
  • infants in the NICU environment
57
Q

Neonatal conditions that place an infant at risk for hypoglycaemia are:

A
  • prematurity
  • sepsis
  • hypothermia
  • hypoxia
58
Q

The “diving reflex” refers to the the shunting of blood away from non-vital organs to vital organs in response to hypoxia.

A

True

59
Q

Preterm infants are unable to localize an infection

A

True

60
Q

A premature infants respiratory muscles are small and tire easily

A

True

61
Q

Hypoventilation leads to

A
  • Hypoxia

- Hypercapnia

62
Q

Possible causes of Respiratory distress are:

A
  • Respiratory Distress syndrome
  • Transient Tachypnea of the newborn
  • spesis
63
Q

Decompensatory respinse to hypoxia are:

A
  • Apnea
  • Bradycardia
  • Cyanosis