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The Late Preterm Infant (34 0/7 to 36 6/7 weeks)

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Presentation on theme: "The Late Preterm Infant (34 0/7 to 36 6/7 weeks)"— Presentation transcript:

1 The Late Preterm Infant (34 0/7 to 36 6/7 weeks)
Physical Exam & Physiologic Challenges EB

2 Why is this a problem? The Late Preterm Infant (LPTI) population has increased by 30% since the 1980’s and accounts for as much as 75% of all preterm births in the US. Possibly due to increasing maternal age, increased use of fertility treatments, multiple gestation, increasing obesity rates, maternal morbidity. One study reports that a cost of $51,600 is associated with each late preterm birth. EB

3 Physical Exam Findings
LPTI should essentially have a normal exam, but may have some of these variations: Increased lanugo, increased vernix, thin appearing skin, more visible veins Boys may have high rising testes and a smoother appearing scrotum Girls may have more prominent labia minora EB

4 Physical Exam Findings
Decreased creases on soles of feet Lack of fully developed cartilage in ear Decreased subcutaneous fat May have decreased tone, with resting tone not in flexed position Most of the differences between a full term and late preterm infant are things you can’t see during a routine physical exam! EB

5 Risks to the Late Preterm Infant
Excessive sleepiness Excessive weight loss Feeding problems Hyperbilirubinemia Hypoglycemia Respiratory distress Sepsis Hypothermia and temp instability ED visits and readmissions Development delay Increased medical costs EB

6 Physiologic Challenges: Thermoregulation
Increased risk for COLD STRESS: Less subQ fat to insulate and less brown fat/adipose tissue to generate heat Immature skin does not function well as a barrier for evaporative heat loss High surface area to body mass ratio Higher metabolic rate and little reserve Less muscle tone and activity EB

7 Cold Stress Can lead to metabolic acidosis, increased metabolic rate, pulmonary vasoconstriction Signs and symptoms may include: apnea, bradycardia, lethargy, poor tone, mottled or pale skin. May contribute to poor transitioning and lead to unnecessary sepsis work ups. EB

8 Minimizing Cold Stress
Goal: neutral thermal environment in which infant maintains temp without increased O2 or glucose/energy demand. Drying skin and hair with warm blankets after delivery and placing skin to skin Swaddle in 2-3 blankets Use of hats Use radiant warmer as needed EB

9 Thermoregulation: Clinical Pathway Interventions
Increased frequency of VS and temp checks Ensure neutral thermal environment Frequent skin to skin If not skin to skin, keep infant dressed with hat on and wrapped in 1-2 blankets Continue delayed 1st bath Hypothermia: slow rewarming with radiant warmer, check blood sugar. EB

10 Physiologic Challenges: Breathing
Development of terminal air sacs in the lungs continues in utero during weeks /7. Alveoli are maturing and becoming lined with Type 1 epithelial cells. These cells are closer in proximity to capillaries to help with gas exchange. Type 2 cells develop during this time also to secrete surfactant. Immaturity can lead to poor lung compliance and increased pulmonary resistance. EB

11 Physiologic Challenges: Breathing
Less effective clearance of amniotic fluid Difficult to maintain alveolar expansion More likely to experience RDS, TTN, even respiratory failure. Other risks include apnea, bradycardia, ALTE’s, SIDS EB

12 Respiratory Distress Usually manifests in first hours after birth with grunting, flaring, tachypnea, retractions. Risk increases if c-section delivery with no labor. During labor, catecholamines are released which help with absorption of lung fluid and surfactant release helping to improve lung compliance. EB

13 Breathing: Clinical Pathway Interventions
More frequent VS and respiratory assessments Pulse ox screenings with VS Parent education regarding respiratory distress If RR >60 breathes per minute, consider holding feeding temporarily EB

14 Physiologic Challenges: Energy and Metabolism
Regulation of temperature helps minimize risk of hypoglycemia All babies have physiologic nadir of blood sugar between 1-2 hours of life. This decrease in blood sugar is more pronounced in the late preterm than full term infant. Should have blood sugars monitored and have first feeding within 1 hour of life (if stable) and no less than every 3 hours after EB

15 Physiologic Challenges: Hypoglycemia
LPTI 3x more likely to suffer from hypoglycemia than term infants. Decreased glycogen stores and adipose tissue Immature liver enzymes less able to increase glucose production through gluconeogenesis Immature pancreatic beta cells may secrete more insulin than necessary Medical complications increasing demand. EB

16 Hypoglycemia Sources vary as to what is a ‘normal’ glucose in infants. Reported ranges: to 80% of total glucose is consumed by the brain LPTIs cannot effectively use other forms of fuel such as ketones, amino acids, and glycerol to raise blood sugar. This, combined with immature protective systems in the brain, make the LPTI more at risk for adverse neurologic outcomes related to hypoglycemia. LPTIs can use lactate as an alternate source. EB

17 Energy and Metabolism: Clinical Pathway Interventions
Hypoglycemia protocol Assess weight loss daily Assess ability to eat safely: coordination of suck, swallow, breathe. Early and effective feedings EB

18 Physiologic Challenges: Feeding & Nutrition
Risk for poor feeding & inadequate caloric intake Mom at risk for delayed/low milk production, weak suck, small mouth, high energy demand with low stores, sleepy, uncoordinated suck/swallow/breathe, lack of hunger cues, ineffective milk transfer. These mother baby dyads need extra help: Assistance with latch, education on frequency of feeding and hunger cues, use of nipple shield, pumping, supplementing. EB

19 Feeding and Nutrition: Clinical Pathway Interventions
Early and effective feedings with assessment of milk transfer Initiate feeding plan based on infants method of feeding. Feeding plan for discharge. Assist mother with learning to pump. Early supplementation or increased caloric formula for excessive weight loss as indicated in feeding plan Feeding cues: rapid eye movements, wipe open eyes looking all around, arms and legs wiggle, head moves back and forth, mouth opens/rooting, sucking, crying (late cue that may lead to difficulty feeding) EB

20 Physiologic Challenges: Hyperbilirubinemia
LPTIs have a later peak (day 5-7) and prolonged phase of elevated bilirubin. Low milk intake and transient slower intestinal motility leads to slowing passage of meconium This increases enterohepatic circulation and reuptake of bilirubin Bilirubin conjugating enzyme activity is lower Increased risk of readmission for jaundice. Risk of kernicterus is higher US Pilot Kernicterus Registry: most LPTIs with kernitcterus noted to have suboptimal breastfeeding documented as dominant cause for disease. Bilirubin enzyme: diphosphate glucoronyltransferase EB

21 Minimizing Hyperbilirubinemia
Optimize feeding with increased milk intake Consider early supplementation Assist with meconium clearance Prevent excessive weight loss Keep moms and babies together and maximize stay in hospital Monitor with TC or serum bilirubin checks Start phototherapy at a lower threshhold. EB

22 Hyperbilirubinemia: Clinical Pathway Interventions
Serum bilirubin at 24 hours of life (obtain with newborn screen). Early and effective feedings Daily assessment of jaundice with clinical assessment and TC/serum checks Maximize length of hospital stay EB

23 Physiologic Challenges: Immature Nervous System
Significant brain growth and maturation occurs in last 6-8 weeks of pregnancy 34 weeker has 50% less brain volume than term infant LPTI less able to control state regulation and regulate internal processes. Decreased tone, positional apnea, disorganized suck/swallow/breathe, frequent startling, more spitting up, unpredictable response to stimuli (even when attempting to soothe) Minimizing or clustering stimulation is helpful EB

24 Physiologic Challenges: Immature Nervous System
Because of the significant amount of brain growth, neuronal connections to be made, and overall nervous system development that still is occuring, the LTPI is at a higher risk for long term neurodevelopmental delays. In severe cases, IVH and PVL, although this is not common EB

25 Immature Nervous System: Clinical Pathway Interventions
Encourage skin to skin Minimize unnecessary stimulation Allow uninterrupted periods of rest Parent education of behavioral states, infant soothing techniques, developmental milestones, etc. EB

26 Physiologic Challenges: Immature Immune System
Less maternal antibody transfer across placenta as compared to full term infant. Other risk factors are common to all infants, although preterm infants more susceptible. Chorioamnionitis, ROM >18h, maternal fever. Signs and symptoms can be vague. Temp instability, respiratory distress, hypoglycemia, lethargy, jaundice, irritability, feeding difficulties. EB

27 Immature Immune System: Clinical Pathway Interventions
Handwashing! GBS protocol Evaluate maternal and infant risk factors that may predispose infant to infection No sick contacts EB

28 LPTI Discharge Considerations: Suggestions from the AAP
Demonstrate weight gain Competent feeding by parents preferred method Able to maintain body temperature while dressed in open crib with normal room temp Stable cardiorespiratory function Parents educated on special needs of LPTI and competent in all care PCP identified and close follow up arranged EB

29 Additional UNC LPTI Discharge Considerations
Discourage any discharge prior to 48 hours of age. Feeding plan in place prior to going home Late preterm specific parent education PCP follow up within 24 (or 48) hours of discharge required. Consider outpatient follow up with LC hours after discharge. EB

30 References Darcy, A. (2009). Complications of the Late Preterm Infant. Journal of Perinatal Neonatal Nursing , 23 (1), Hubbard, E., Stellwagen, L., & Wolf, A. (2007). The Late Preterm Infant: A Little Baby with Big Needs. Contemporary Pediatrics . Mally, P., Bailey, S., & Hendricks-Munoz, K. (2010). Clinical Issues in the Management of Late Preterm Infants. Current Problems in Pediatric and Adolescent Healthcare , 40 (21), National Guideline Clearinghouse. (2010). Assessment and Care of the Late Preterm Infant. Evidence-based clinical practice guideline. Oklahoma Infant Alliance. (2010, September). Caring for the Late Preterm Infant. A Clinical Practice Guideline. EB

31 References University of California, San Diego Medical Center. (2006, October). Late Preterm Infant Policy Statement. Raju, T., Higgins, R., Stark, A., & Leveno, K. (2006). Optimizing Care and Outcome for Late-Preterm (Near Term) Infants: A Summary of the Workshop Sponsored by the National Institute of Child Health and Human Development. Pediatrics (118), Ramachandrappa, A., & Jain, L. (2009). Health Issues of the Late Preterm Infant. Pediatric Clinics of North America (56), Verklan, M. T. (2009). So, He's a Little Premature...What's the Big Deal? Critical Care Nursing Clinics of North America , 21, EB

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