Module 5: Respiratory Distress Syndrome Flashcards

1
Q

What is a key aspect of early intervention for infants at risk for RDS?

A
  • stabilization
  • early intervention can prevent the downward spiral described above in which surfactant deficiency leads to respiratory distress and respiratory distress interferes with surfactant production.
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2
Q

Describe what Wendy should check and prepare for this admission. Use the ACoRN Primary Survey of the six main areas of potential concern to guide your response.

A

Respiratory:
- check for functioning blended gas source with a bag with manometer/neopuff and appropriate size masks
- Make sure a transcutaneous C02 monitor is ready for use.
- gather an oxygen saturation monitor and probe, and ECG leads.
- Suction catheters and functional suctioning set up would need to be present.
- Monitors and alarms should be set per unit policy.
- Assessment of rate and respiratory effort would be ongoing.

Cardiovascular:
- Initial vital signs will include blood pressures to monitor for hypotension
- The appropriate sized B/P cuff will be needed- having a few sizes on hand is prudent.
- ensure that the equipment needed for insertion of an UAC is available (sterile line tray and supplies, fluids, infusion pump).
- Ongoing assessment of HR, color, pulses, perfusion and blood pressure will be incorporated into care.

Surgical Conditions:
- There is no history in this case to suggest that surgical intervention will be anticipated imminently.

neurology:
- Flexing of infant’s limbs to midline, providing containment and tucking, and trying to facilitate a quiet environment to support and facilitate infant organization and transition.
- have a warm, nest prepared for baby.
- Assessment of tone and monitoring for abnormal movements and jitteriness will be performed.

fluid and glucose:
- provide IV glucose for metabolic functioning.
- An IV pump will be needed.
- Equipment for insertion of a peripheral line should also be assembled. I
- have a glucometer available to monitor sugars and sample from either capillary or umbilical arterial route.
- Other labs to consider would include complete blood count with differential, possibly blood cultures and blood gas.
- Feeds are usually started in small volumes, after stabilization.

thermoregulation:
- It is of utmost importance that we keep Robyn in a neutral thermal environment in which she uses the least energy, oxygen and calories to maintain a normal temperature.
- a preheated radiant warmer and warm linen is needed in both the operating room and nursery.
- At birth, NRP guides practitioners to place the infant (for infants < 35 weeks) wet-in-bag at birth to decrease convective heat loss.
- Once stabilized in the unit, I would transfer the baby to a prewarmed, humidified incubator, and remove the bag.
- Careful temperature control is imperative in all VLBW infants and is especially important in infants with RDS to minimize metabolic demands and oxygen consumption.
- RDS can limit oxygen uptake leading to hypoxia which limits the ability of an infant to increase their metabolic rate when cold stressed, resulting in a fall in body temperature.
- Skin probe temperature monitoring should be applied to follow trending of temperature and decrease need to disturb the baby with axillary checks.

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3
Q

Interpret this gas:
pH: 7.26
PaCO2: 54
PaO2: 56
HCO3: 23
BE: 21

A

pH 7.26 acidosis
PaCO2 54 high normal (hypoventilation)
PaO2 56 low normal (poor diffusion of O2)
HCO3 23 normal

  • respiratory acidosis
  • this is what I would expect of an infant with RDS.
  • The elevated pCO2 reflects hypoventilation. In RDS, hypoventilation is largely due to atelectasis.
  • The low pO2 reflects both hypoventilation and poor diffusion of oxygen across the alveolar-capillary membrane.
  • Poor diffusion may be due to edema and the large distance between alveoli and capillaries.
  • The low pH is due to the effects of respiratory acidosis (pCO2).
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4
Q

Why are preterm infants prone to respiratory distress?

A

surfactant deficiency

  • RDS is a condition caused by lack of pulmonary surfactant … (which) results in decreased lung volume and increased work of breathing

**This is why infants with RDS often require respiratory support to provide oxygenation and ventilation to achieve adequate respiration and ease their work of breathing.

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5
Q

What are some other reasons (aside from prematurity and surfactant deficiency) cause of respiratory distress (3)?

A
  • Transient Tachypnea of the Newborn TTNB
  • Pneumonia
  • Pneumothorax
  • Neuromuscular disorders
  • Congenital abnormalities of the lung, chest wall or diaphragm
  • Congestive Heart Failure
  • Persistent Pulmonary Hypertension PPHN
  • Meconium Aspiration Syndrome MAS
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6
Q

Is the 28-week gestation infant in the case at risk for any respiratory distress? If so, why?

A
  • This infant is at risk for Respiratory Distress Syndrome.
  • At 28 weeks gestation, the Type II surfactant cells, responsible for the production and secretion of surfactant, are not fully developed.
  • This lack of surfactant causes the infant’s alveoli to collapse therefore their functional residual capacity (FRC) is not established.
  • This all causes increased energy output in an already compromised infant.
  • Merenstein and Gardner (2011) further explain that, “this infant’s immature lungs cannot support oxygenation and ventilation because her alveolar saccules are insufficiently developed, causing a deficient surface area for gas exchange. (Further), the pulmonary capillary bed is deficient and the interstitial mesenchyme is present to a greater extent, increasing the distance between the alveolar and the endothelial cell membranes” (p. 636).
  • There is also a lack of development of the pulmonary capillary bed, compliant rib cage, stiff lungs and weak respiratory muscles.
  • In addition, this infant has also experienced acute stress due to maternal bleeding.
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7
Q

What other potential health challenges leading to respiratory distress could this infant experience?

A

One health challenge I would want to rule out is sepsis or pneumonia.
- Although membranes have only been ruptured for 10 hours, there may be bacterial colonization which is not creating any maternal problems.
- There is also the factor that premature infants are at greater risk to a sepsis/pneumonia due to immaturity of the lungs and immune system.
- I remember a 28week gestation infant that I looked after just recently. She presented very similar to Robyn, minus maternal bleeding, and was found to have pneumonia secondary to H. influenza which had been contracted via the birth canal. Mother was asymptomatic.

A second health challenge I would anticipate this infant experiencing is TTN (transient tachypnea of the newborn) due to a cesarean birth.
- There may be some retained fetal lung fluid.
- However, this generally affects term or near to term infants’ more than preterm infants.

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8
Q

What other information would you like to have to assist you in anticipating this infant’s respiratory status?

A

I would like to gather several pieces of information:
- First, has this mother received any corticosteroids, such as Dexamethasone? If so, how many doses and when in relation to the planned delivery? If corticosteroids have been given, this infant may have less of a problem with RDS.
- Secondly, does mom have any history of infection (urinary tract, Group B streptococcus)? If so, is she being treated with antibiotics?
- Thirdly, how long has she been bleeding, and how much blood has she lost? With large blood losses, I would be anticipating problems with shock in this infant.

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9
Q

What does RDS stand for?

A

Respiratory Distress Syndrome (RDS)

once referred to as Hyaline Membrane Disease (HMD), is the most common respiratory disorder associated with preterm birth.

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10
Q

RDS occur as a result of what 2 things?

A

As a result of:
- pulmonary hypoperfusion and
- ischemia

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11
Q

What kind of trajectory does RDS follow?

A

Decreased lung volume due to surfactant deficiency.
- Decreased lung compliance
- Atelectasis
- Hypoxemia (oxygenation) and acidosis (ventilation)

Ventilation/Perfusion (V/Q) mismatch and hypoventilation.
- Increased pulmonary vascular resistance (PVR)
- Decreased pulmonary perfusion

Increased capillary permeability
- Pulmonary edema

Formation of hyaline membrane
- Increased diffusion gradient

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12
Q

Is the incidence of RDS inversely proportional to GA?

A

yes
- the incidence of RDS is inversely proportional to gestational age and
- occurs most frequently in infants of less than 1200g and 30 weeks gestation

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13
Q

What is the difference between respiratory distress and RDS?

A
  • Respiratory distress refers to the way that infants respond to a variety of health challenges that interfere with gas exchange.
  • There are several causes of respiratory distress, including TTN, meconium aspiration, infection, and RDS. RDS is a particular syndrome which occurs as a result of surfactant insufficiency and leads to respiratory distress.
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14
Q

Respiratory distress due associated with RDS is due to what 3 pulmonary challenges?

A
  • immature lung structures,
  • small and few alveoli, and
  • surfactant deficiency.
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15
Q

What is surfactant?

A

a biochemical substance that lines the walls of the alveoli

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16
Q

What are 2 role of surfactant?

A
  • to lower alveolar surface tension,
  • helping to prevent alveolar collapse (atelectasis) at the end of an exhaled breath.
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17
Q

What are 3 things surfactant deficiency leads to?

A
  • leads to increased alveolar surface tension and
  • decreased lung compliance,
  • therefore resulting in a tendency toward atelectasis.
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18
Q

What is functional residual capacity (FRC)?

A
  • when infants exhale, some air is left in the alveoli at the end of the exhaled breath.
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19
Q

What is the purpose of FRC?

A
  • to make the subsequent breath easier by allowing inflation to occur from a position of partial rather than complete collapse of the alveoli
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20
Q

What is the balloon analogy?

A
  • It is easier to inflate a balloon if you inflate it once and, rather than letting all of the air out, you keep some air in the balloon (FRC) by pinching with your fingers and then re-inflate the balloon.
  • Infants’ alveoli work the same way. It is easier for an infant to take a breath if some air remains in the alveoli at the end of the previous breath.

**Surfactant is a substance that allows this to happen by preventing alveolar collapse

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21
Q

What is the trajectory is theres inadequate surfactant?

A

With inadequate surfactant
- the FRC decreases,
- the alveoli become more atelectatic and,
- as a result, more effort is required for inhalation.
- In this way, the work of breathing increases for infants with surfactant deficiency.
- Breathing at a rate > 60 breaths per minute, with few and undeveloped alveoli, a compliant chest wall, inadequate surfactant, worsening atelectasis and weak respiratory muscles
- means that preterm infants with RDS tire very easily!

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22
Q

What are the five cardinal signs of respiratory distress?

A
  • Indrawing
  • Tachypnea
  • Nasal flaring
  • Grunting
  • Cyanosis
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23
Q

What are the responses to inadequate gas exchange: O2 level?CO2 level? pH?

A
  • Hypoxia: low O2
  • hypercapnia: high CO2
  • acidosis: low pH
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24
Q

Tachypnea is an attempt for?

A
  • to compensate for hypoxia and hypercapnia by increasing minute ventilation
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25
Q

Indrawing occurs as a result?

A
  • as a result of a compliant chest wall.
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26
Q

Nasal flaring is an attempt for?

A
  • an attempt to decrease the work of breathing by decreasing airway resistance.
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27
Q

Grunting reflects what?

A
  • an infant’s attempt to prematurely close his/her glottis in order to prevent alveolar collapse by keeping some air in the alveoli at the end of a breath.
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28
Q

Cyanosis reflects what?

A
  • reflects (indirectly) hypoxia in that cyanosis results from hemoglobin that is not saturated with oxygen.
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29
Q

Why is cyanosis an unreliable assessment of oxygenation?

A
  • because cyanosis may be due to either too little oxygen or increased circulating fetal hemoglobin.

**fetal hemoglobin has a high affinity for oxygen, making it less available to the tissues

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30
Q

Why are early responses to RDS compensatory (tachypnea, grunting, nasal flaring)?

A
  • are aimed at overcoming hypoxia, hypercapnia, acidosis, and the increased work of breathing.
  • Over time, these compensatory responses (particularly tachypnea) fail to adequately compensate and the result is worsening hypoxia, hypercapnia, and acidosis.
  • Hypoxia, hypercapnia, and acidosis, in turn, interfere with surfactant production, making the problem all the worse.
  • This is often referred to as the downward spiral or vicious cycle of RDS.
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31
Q

Use your own words to describe the pathophysiology of RDS. You may want to use a diagram format with key words and arrows joining the key words.

A

There are numerous ways to use a diagram format. Does yours include some of the key words that I have used?

Atelectasis → hypercapnia, hypoxia, hypoxemia and respiratory acidosis → increased pulmonary vascular resistance → right-left shunting via foramen ovale and ductus arteriosus → damage to alveoli → hyaline membranes form → impairment of gas exchange → decreased pulmonary vascular resistance → left-right shunting via foramen ovale and ductus arteriosus → pulmonary edema, further damage to alveoli and leaky capillaries.

Cycle begins again.

32
Q

Critique the case in relation to developmentally supportive care

A

All of you will have different perspectives. My sense is that we don’t have a lot of information about how this infant is responding to her environment, including the care giving activities. Is this because the nurses caring for her are not tuned in to her cues?

I also get a sense that she is being handled a lot. Is all of the handling necessary? How is she responding? How urgent are her physiologic needs - necessitating handling and how do her physiologic needs impact her developmental needs? Where is the balance? These are questions I’d be asking myself if I was the nurse caring for this infant all the while aware of Robyn’s vulnerabilities. It is also important to consider Elaine who may not have been able to see Robyn. Consider having Dad take a quick picture before intubation if she is stable.

33
Q

What assessment data, provided in this case, help you generate hypotheses for explaining Robyn’s respiratory distress?

A
  • Her gestational age! At 28 weeks I would anticipate some degree of respiratory distress, either due to RDS and/or tiring.
  • Her birth history also suggests the potential for respiratory distress.
  • Cesarean birth often means that less lung fluid gets reabsorbed, leading to “wet lungs.”
  • The Apgar scores, particularly the one minute score, suggest some hypoxia at birth and this may interfere with transition, leading to persistent hypoxia and, potentially, to reduced surfactant production.
  • Only one dose of antenatal steroids means that the infant will not get the full benefit of antenatal steroid therapy, which is aimed at increasing surfactant production and increasing lung maturity.
  • The initial respiratory status of the infant indicates early respiratory distress. Grunting, nasal flaring, and indrawing all suggest poor compliance and alveolar collapse. Decreased air entry and moist crackles indicate atelectasis and fluid respectively. Tachypnea (50-70) suggests the infant is attempting to compensate for hypoxia and/or hypercapnia. Peripheral cyanosis may be a benign sign, particularly in the first few hours after birth as it may only be a function of vasomotor instability during transition to extrauterine life. Persistent peripheral cyanosis indicates poor perfusion and would need to be investigated.
  • In summary, this infant is demonstrating both risk factors for and early responses to respiratory distress.
34
Q

Based on this data and the information in the article by Hermansen & Lorah (2007), what (in addition to RDS) could be causing the infant’s respiratory problems?

A
  • RDS is the most likely cause of this infant’s respiratory distress.
  • Wet lung could be contributing but is unlikely as a major cause considering her gestational age.
  • Pneumonia is a possibility as the infant is preterm and, therefore, at high risk for infection.
  • The clinical and radiographic features of pneumonia may be indistinguishable from RDS at birth.
  • As a result, all infants with RDS should have blood cultures and CBC drawn, and should receive empiric antibiotic therapy.
35
Q

In order to rule in more likely hypotheses and rule out less likely hypotheses, what other information would be helpful?

A
  • Chest x-ray results would help rule in/rule out both RDS, TTN and pneumonia.
  • CBC results with WBC differential would help rule in/rule out infection/pneumonia.
  • Wet lung is generally diagnosed on the basis of history, symptoms and chest x-ray.
  • In the short term, while you are certainly aiming your assessment at ruling in/ruling out causes, my view is that all possible causes of respiratory distress should be kept in mind - some on the front burner and some on the back!
36
Q

What are 4 goals of management of infant with RDS?

A
  • Avoid hypoxemia and acidosis
  • Optimize fluid management: avoid fluid overload and resultant body and pulmonary edema while averting hypovolemia and hypotension
  • Reduce metabolic demands and maximize nutrition
  • Minimize lung injury secondary due to barotrauma, volutrauma and oxygen toxicity
37
Q

What are the three most important advancement in prevention/treatment of RDS?

A
  • Antenatal steroids
  • Surfactant replacement therapy
  • Continuous positive airway pressure (CPAP) and Positive End Expiratory Pressure (PEEP)
38
Q

How does antenatal steroid administration help with RDS prevention?

A
  • Antenatal corticosteroids accelerate fetal lung maturity by increasing formation and release of surfactant.
  • Administration of antenatal steroids at least 24-48 hours (and no more than 7 days) before preterm delivery decreases both the incidence and severity of RDS.
  • Administering two doses of a steroid, at 12-hour intervals, to a mother in preterm labor in conjunction with delaying delivery for a minimum of 24 hours past the initial dose has been shown to be the most effective in reducing RDS in premature infants
39
Q

What does giving a single course of corticosteroids (Betamethasone or Dexamethasone) to pregnant mom as risk for preterm birth reduce risks of (3)?

A

Reduces risk:
- death
- RDS
- IVH in their preterm newborn

40
Q

How can surfactant deficiency be treated postnatally?

A

with the administration of an exogenous surfactant product

41
Q

What are 4 things does the use of exogenous surfactant in preterm improves?

A
  • improves oxygenation,
  • decreases air leaks,
  • reduces mortality due to RDS, and
  • decreases overall mortality.
42
Q

What does exogenous surfactant do?

A

decrease alveolar surface tension, thereby
- increasing lung compliance,
- improving alveolar stability,
- increasing FRC, and
- decreasing the work of breathing.

43
Q

How is exogenous surfactant administered?

A

directly into the lungs via an endotracheal tube.

44
Q

What are the two approaches used for surfactant delivery?

A
  • prophylactic therapy: give exogenous surfactant immediately following birth to infants at risk for RDS
  • rescue therapy: wait for the appearance of clinical signs of RDS
45
Q

What are infants exhibiting signs of respiratory distress treated with?

A
  • CPAP (Continuous Positive Airway Pressure) or with
  • mechanical ventilation
46
Q

What is the first-line method of respiratory support for preterm infants?

A

cpap

47
Q

What are the functions of CPAP?

A
  • to maintain FRC by keeping the alveoli open at the end of expiration,
  • preventing alveolar collapse, and
  • making the work of breathing easier.
48
Q

If conventional mechanical ventilation is used, what are the settings aimed at?

A
  • normalizing blood gases and
  • preventing barotrauma and volutrauma.
49
Q

What does pressure (PIP) cause? using high tidal volume?

A
  • Pressure, particularly PIP, causes trauma to the developing lung tissue (barotrauma).
  • Overinflation, using high tidal volumes, can lead to volutrauma.
    **This trauma, in conjunction with other etiologic factors, can lead to the development of bronchopulmonary dysplasia (BPD).
50
Q

What is the recommendations when considering surfactant and CPAP?

A
  • Treatment with surfactant is often given if the FiO2 requirements exceed 0.3.
  • Preterm neonates who receive treatment with nasal CPAP as their initial method of respiratory support should be provided with exogenous surfactant treatment (via ETT) if exhibiting clinical signs of RDS with a demonstrated need for escalating or sustained levels of supplemental oxygen to maintain adequate arterial oxygen saturation.
51
Q

Prior to administering surfactant, what needs to be consider in regards to suctioning?

A
  • Ensure that you suction the infant’s ETT prior to administering surfactant.
  • Suctioning post-surfactant administration will remove the surfactant from the lungs.
  • Ideally, you should wait approximately 2 hours post-surfactant administration to suction.
52
Q

What are some less invasive methods to administer surfactant?

A
  • LISA method (Less Invasive Surfactant Administration) using a thin catheter and McGill forceps to assist with placement has been well received in recent studies
  • MIST (Minimally Invasive Surfactant Treatment) method which uses a more rigid catheter is currently being tested
53
Q

What are the recommendations for which patients qualify for surfactant administration?

A

In neonatal care settings where continuous positive airway pressure (CPAP) is routinely used to stabilize preterm infants, and when the rate of antenatal corticosteroid administration has been high (>50%), prophylactic surfactant is no longer recommended (Grade A).

Non-invasive respiratory support (e.g., CPAP) should be provided to preterm infants with respiratory distress syndrome (RDS) from birth. Early surfactant should be provided for newborns with increasing severity of RDS, demonstrated by escalating or sustained levels of oxygen requirement and other clinical or radiological indications (Grade B).

Infants with RDS whose oxygen requirements exceed FiO2 of 0.5 should receive surfactant replacement therapy (Grade A).

54
Q

What are some complications of surfactant therapy?

A
  • obstruction of the endotracheal tube
  • bradycardia and hypoxemia during instillation
  • transient increases in O2 requirement and ventilatory settings
  • pulmonary hemorrhage (an infrequent adverse effect reported in 2-6% of infants given surfactant)
  • Complications resulting from intubation or difficulties with intubation procedure.
55
Q

What can be done to minimize complications of additional stress and handling to infant with surfactant therapy?

A

Complications are minimized by
- adjusting ventilation and oxygenation
- continuous oximeter and CO2 monitoring,
- blood gases,
- chest x-rays, and
- careful physical assessment of an infant’s respiratory system.

56
Q

Why is it important to monitor infant temperature and surfactant is warmed?

A
  • in order to decrease the risk of it thickening and obstructing the ETT
57
Q

What does administration of surfactant improves?

A
  • improves lung mechanics (↑ lung compliance) and
  • increases oxygenation by reducing atelectasis and
  • increasing FRC.
58
Q

What should HCP pay close attention to after surfactant administration?

A
  • Close attention must be paid to tidal volume, pressures, blood gases, transcutaneous CO2 and pulse oximetry values in order to avoid inadvertent hyperventilation, hyperoxia and overdistension of the lung - all of which can result in lung injury.
59
Q

What other system complications are associated with hypoxia and hypoventilation?

A
  • PDA,
  • oliguria,
  • renal failure,
  • metabolic acidosis,
  • hypo/hypernatremia,
  • hypoglycemia,
  • IVH, and
  • retinopathy of prematurity
60
Q

Why is it that premature infants with RDS often develop symptoms of PDA once their lung disease resolve?

A
  • While infants are experiencing RDS, extensive atelectasis can result in hypoventilation with subsequent hypoxia creating a high pulmonary vascular resistance (PVR).
  • This causes a right to left shunt of blood flow through the ductus arteriosus.
  • As infants recover from RDS, oxygenation improves and PVR begins to decrease.
  • Because the ductus arteriosus is muscle tissue and premature infants have decreased constriction value, their ductus is not as responsive to increased oxygen as full-term infants.
  • Therefore, the ductus does not necessarily close and blood starts to shunt from left to right through the ductus arteriosus, re-entering the pulmonary circulation.
  • This can cause increased pulmonary venous congestion and decreased lung compliance.
  • With a large shunt, symptoms of congestive heart failure and an inability to wean off ventilator support may occur.
  • Increasing inspiratory ventilatory pressures and increasing oxygen requirements may occur as lung compliance decreases.
61
Q

What are some responses of infant to PDA include?

A
  • pallor and mottling,
  • apnea, bradycardia, and desaturations (ABDs)
  • murmur,
  • widened pulse pressure (the difference between systolic and diastolic pressures),
  • bounding pulses,
  • labile saturations and an
  • active precordium.
62
Q

How is surgical ligation of a PDA done?

A
  • Surgical ligation of a PDA is done through a left thoracotomy incision
  • The ductus is then closed. Surgical ligation produces definitive ductus arteriosus closure
63
Q

What are some complications of surgical ligation?

A
  • thoracotomy,
  • pneumothorax,
  • chylothorax,
  • post-operative hypotension,
  • vocal cord paralysis,
  • infection, and
  • scoliosis”
64
Q

What kind of adverse physiological effect does pain-induced stress have on critically ill infants?

A
  • hyperglycemia,
  • acidosis, and
  • protein catabolism
65
Q

What other measures would you like to see implemented to decrease stress and pain responses for Robyn as she recovers from her PDA ligation?

A
  • I would ensure Robyn is receiving adequate pain medication post-operatively.
  • I would also ensure that Robyn is well nested, with limbs flexed and midline.
  • If possible, I would like to have only a bedside light on with the overhead lighting off.
  • While in the admission room, I would probably have the door partially closed, if not all the way closed.
  • What I would be doing is trying to decrease noxious stimuli and decrease stress levels for Robyn.
  • I do find that when lights are dimmed, other people in the room automatically tend to talk in lower tones.
  • With the door to the admission room shut, external noises are immensely decreased.
  • I would encourage Robyn’s mom to talk softly to her.
  • As soon as Robyn is stable, I would encourage kangaroo care.
66
Q

With the knowledge that you have regarding prematurity, RDS, and surfactant replacement therapy, what complications would you be anticipating for Robyn? What does this mean for you regarding nursing care and planning? Think of what you have learned in the previous courses regarding hypoxia, cold stress, PDA, etc.

A

In examining the problems of prematurity, the pathophysiology of RDS and potential problems with surfactant replacement therapy, several common denominators come up. They all involve some degree of hypoxia and change in blood flow. I think of IVH, PDA, NEC, and renal shutdown as the main problems I would be anticipating and providing nursing care to minimize.

By making use of ACoRN and what I know about neonatal pathophysiology, I would plan around maintaining thermoregulation, minimizing hypoxic episodes, monitoring for and correcting any hypotension, and maintaining fluid balance.

I would also be clustering Robyn’s care based upon her individual cues of tolerance of handling. Involving the family at every step is also important. I would make sure this family was aware of and involved in decisions made and as soon as Robyn is stable, I would encourage kangaroo care.

The main problem definitely seemed to be her PDA. This has been proved by several echocardiograms, blood gases, and Robin’s clinical presentation - hence she had her PDA ligated. I would be very conscious about Robyn’s pain control both before and after ligation.

67
Q

What are some health challenges being born prematurely?

A
  • could develop necrotizing enterocolitis,
  • intraventricular hemorrhage,
  • sepsis,
  • hypothermia,
  • apnea, bradycardia, and
  • dehydration
68
Q

What is the best infant transport?

A
  • the uterus is the natural and best means of transport for the fetus
  • infants at high risk for requiring tertiary care must be identified in the antepartum period
  • maternal stabilization and consideration of transport so that delivery of premature infants occurs in the appropriate setting is inherent to achieving optimal neonatal outcomes
69
Q

Treatment with surfactant is often given if the FiO2 requirements exceed?

A

0.3 = 30%

70
Q

According to Perinatal Services BC (PSBC, 2005), all pregnant women between _____ and ______ weeks gestation who are at risk of preterm delivery within seven days should be administered a single course of corticosteroids.

A

23+0 and 33+6

71
Q

How long does the ductus arteriousus usually closes after birth?

A

full term infants within 72hours

72
Q

what position has been shown to improve ventilation and oxygenation?

A

prone

73
Q

What are 2 pharmaceuticals used to treat PDA?

A
  • acetaminophen
  • ibuprofen
74
Q

What test should all infants with RDS also have done? why?

A

to r/o pneumonia or infection:
- have blood cultures and CBC drawn, and should receive empiric antibiotic therapy.

75
Q

What does decreased air entry may indicate?

A

atelectasis