Care of the Late Preterm Infant

Where Tradition Meets Innovation

Care of the Late Preterm Infant

Patricia A. Scott, MSN, APN, NNP-BC, C-NPTVanderbilt University School of Nursing, Neonatal Nurse

Practitioner FacultyPediatrix Medical Group of Tennessee at Centennial Medical

Center – The Women’s HospitalUniversity of Tennessee Health Science Center DNP Student


•Discuss the definition and incidence of late preterm birth.

•Discuss the incidence, risks for, and etiology ofrespiratory distress in the late preterm infant.

•Identify signs of hypo/hyperthermia.

•Describe the physiology, assessment, and managementof hyperbilirubinemia and why the late preterm infant isat increased risk.

•Discuss why this population is at increased risk forhypoglycemia and feeding difficulties.

Presentation Objectives


Definition of the Late Preterm Infant

Infants born between 34 and 36 completed weeks of gestation

“Near term” thought to imply that these babies are “near enough” term to be physiologically the same (Engle, 2009)


Distribution of Preterm Births (CDC)


•Morbidity: not fully known•Mortality: 3 X higher than the term infant

Morbidity and Mortality


•Vital period of maturationLung developmentBrain maturationLiver maturation

•Vital period of growthBody mass increasesFat stores increase

What does the Late Preterm Infant Miss?


Complications (Adamkin, 2009)

Complication Late Preterm Infant Term Infant

Feeding 32% 7%

Hypoglycemia 16% 5%

Jaundice 54% 38%

Temperature Instability 10% 0

Apnea 6% < 0.1%

Required IV Fluids 27% 5%

Septic Evaluation 37% 13%

Mechanical Ventilation 3.4% 0.9%


•Longer hospital stays•Higher rate of readmission •Increased nursing care•Location of care varies

Late Preterm Care Delivery Issues


•Respiratory distress•Temperature instability•Hyperbilirubinemia•Feeding challenges

Most Common Complications


Respiratory Distress


•35 to 36 week infants: 28.9% respiratory distress at birth compared to 4.2% of term infants

•35 to 36 week ventilated infants: RDS in 62%

Respiratory Distress: Incidence


•Delayed transition or respiratory distress?•Differential diagnosis includes:

TTN RDS Sepsis PPHN Congenital anomalies

Respiratory Distress


Risk Factors for Respiratory Distress

•Elective cesarean birth without the benefit of labor

•Maternal complications

•Fetal factors


•Delayed reabsorption of lung fluid•Onset: 2 to 6 hours of life•Risk factors for TTN

Cesarean delivery Precipitous delivery

Transient Tachypnea of the Newborn


• Clinical presentation Tachypnea Grunting / flaring / retractions

• Diagnostic studies Blood gases Chest x-ray Septic work-up

• Management / Outcome Supportive care

Transient Tachypnea of the Newborn


Chest X-Rays


•Immature lungs and surfactant deficiency •Onset: within minutes to hours of birth•Risk Factors PrematurityCesarean deliveryMaternal diabetesSecond born twinPerinatal asphyxiaMale gender

Respiratory Distress Syndrome


RDS: Clinical Presentation

•Tachypnea•Grunting•Flaring •Retractions•Pallor or cyanosis

•Decreased breathsounds/fine rales•Hypotension•Decreased perfusion•Tachycardia


•Arterial blood gasesHypoxemiaRespiratory acidosis

•Chest x-ray •Infection should be ruled out

• RDS: Diagnosis


Chest X-Rays


•Provide a NTE•Oxygen support, as needed•Ventilatory support, as needed•Surfactant replacement therapy

As early as possible

RDS: Management


•Fluid restriction•Monitor serum electrolytes•Minimal stimulation•Blood pressure support•Continued, comprehensive assessment

RDS: Management


Directly related to birth weight andgestational age Affected by prenatal glucocorticoid treatment and

surfactant replacement

RDS: Outcome


Thermoregulation


Non-Shivering Thermogenesis

Cold stress → hypothalamus → epinephrine →brown fat metabolism Function: heat production Location: axilla, nape of neck,

between scapulas, mediastinum, around the kidneys

Stores increase until 3-5 weeks postnatal life


•Conduction•Convection•Evaporation•Radiation

Heat Transfer Mechanisms


•Heat transfer by direct contact•Varies with exposed surface area

Decreased ability to flex extremitiesDecreased subcutaneous fat Limited ability to VC peripheral blood vessels

•Ways to minimize

Conduction


•Air currents move heat away from the body•Affected by ambient temperature, air flow

velocity, and relative humidity•Ways to minimize

Convection


•Liquid is converted into a vaporMajor source of heat loss at delivery/bathingLosses through skin and respiratory system

•Dependent upon air speed and relative humidity•Ways to minimize

Evaporation


•Transfer of radiant energy from the bodyto objects without direct contact

Radiant warmer – heat gain“Greenhouse effect”

•Ways to minimize

Radiation


•Axillary temperature Term: 97.9 – 99.5 F (36.5 – 37.5 C) ' 'Preterm: 97.5 – 98.5 F (36.3 – 36.9 C) ' '

•Skin temperatureTerm: 96.8 – 97.7 F (36 – 36.5 C) ' 'Preterm: 97.2 – 99 F (36.2 – 37.2 C) ' '

•Rectal/tympanic not recommended

Normal Temperature Ranges


Radiant Warmers versus Isolettes

•Advantages•Disadvantages•Wean to crib


Skin-To-Skin Care

•Can be close to thebreast for feeding

•Stable vital signs and oxygenation

•Improved sleepingpatterns and directsocial eye contact


•Pale, cool to touch•Acrocyanosis•Respiratory distress•Apnea, bradycardia, central cyanosis•Irritability → lethargy•Progressive or chronic cold stress

Hypothermia: Clinical Presentation


Free FattyFree FattyAcid ReleaseAcid Release

Brown Fat Brown Fat UtilizationUtilization

COOLINGCOOLING

Pulmonary VCPulmonary VC Peripheral VCPeripheral VC

Norepinephrine Norepinephrine ReleaseRelease

Metabolic Metabolic RateRate

OO22 ConsumptionConsumption

R to L ShuntingR to L Shunting

Dependence on Dependence on Anaerobic MetabolismAnaerobic Metabolism

Lactic Lactic AcidosisAcidosis

? DEATH? DEATH

HypoxemiaHypoxemiaHypoxiaHypoxia

OO22 Delivery to Tissues Delivery to Tissues


•Arterial blood gas•Septic workup•Blood glucose•Electrolytes

Temp Instability: Differential Diagnosis


•Gradual re-warming•Prevent further heat loss•Frequent evaluation of temperature•Potential complications

Hypothermia: Treatment


•Clinical presentation•Etiology•Treatment•Complications

Hyperthermia


Hyperbilirubinemia


•↑risk of significant hyperbilirubinemiaImmature liverHigher bilirubin levelsLater bilirubin peakLess vigorous feeding

•25% require phototherapy

Hyperbilirubinemia in the Late Preterm


Overview of Bilirubin Pathway


•Also called physiologic jaundice•Contributing factors: Increased bilirubin load Decreased hepatic uptake of bilirubin from plasma Decreased bilirubin conjugation Defective bilirubin excretion

Neonatal Jaundice


•Hemolytic disease ABO and/or Rh incompatibility

•RBC enzyme abnormalitiesGlucose-6-phosphate dehydrogenase deficiencyPyruvate Kinase Deficiency

•Polycythemia•Extravascular blood•↑ enterohepatic circulation

Overproduction


•↓ hepatic uptake of bilirubin•↓ bilirubin conjugation•Inadequate transport out of hepatocyte•Biliary obstruction

↓ Excretion


•Prematurity•Bacterial sepsis•Urinary tract infection•Intrauterine viral infections•Hypopituitarism•Hypothyroidism

Overproduction + ↓ Excretion


•Many advantages •Important to ensure good lactation support Inadequate lactation associated with increased TSB level Late preterm infant at risk for feeding problems

Less vigorous suck Less stamina with feedings Less coordination of suck and swallow Less alert-awake states

Breastfeeding and Jaundice


•May be prevented/reduced with frequent feedings in first days of life •Late onset or prolonged hyperbilirubinemia•Affects 10-30% in 2nd to 6th week of life•Screen for risk factors to plan F/U•Unconjugated bilirubin level > 12 mg/dl

Breastfeeding and Jaundice


•Family•Obstetric•Neonatal Decreasing gestational age Apgar scores LGA Elevated PCV Poor feeding

Hyperbilirubinemia: History


•Clinical presentation:Jaundice may be the only presentation

Hyperbilirubinemia: Clinical Presentation


•Maternal and infant blood types, Rh, and Coomb’s test•CBC/differential•Bilirubin levels

Hyperbilirubinemia: Laboratory Data


Hour-Specific Total Serum Bilirubin


•Develops subtly as the result of high bilirubinlevels causing neurological damage This damage may or may not be reversible with treatment. Prompt, aggressive treatment is more likely to reverse and

improve the outcome.

Acute Bilirubin Encephalopathy


•Permanent brain damage resulting •Clinical picture: Spasticity Deafness / decreased hearing Setting sun sign Dental enamel dysplasia Intellectual capacity is normal, but may not be evident

Chronic Bilirubin Encephalopathy


Feeding Difficulties


•Hypoglycemia•Hyperbilirubinemia•↑Increased weight loss initially•Slower return to birthweight•Readmission to the hospital

Why is adequate intake important?


•Decreased staminaLess effective sucklingDecreased transfer of milkSub-optimal breast stimulation

•Ability to suck-swallow-breathe

Feeding Concerns


•Poor muscle tone Leading to fatigue, latch difficulty, and suboptimal feeding

•Fewer alert-awake periods Not as likely to initiate feeds and may end them prematurely

Feeding Concerns


•Ensure adequate nutrition

Nursing Care


•How often does this happen in late preterm infant? 10-15% incidence 2/3 of late preterm infants will require intravenous

dextrose for a blood glucose level < 40 mg/dl

Hypoglycemia


•Inadequate substrate•Abnormal endocrine function•Increased glucose utilization

Hypoglycemia: Etiologies


Hypoglycemia: Risk Factors

•MaternalGlucose infusion in laborMaternal diabetesMaternal hypertensionTocolytic treatment

•Fetal/NeonatalIUGRPerinatal asphyxiaSepsisTemperature stabilityRespiratory distress


Hypoglycemia: Clinical Presentation

•Irritability, lethargy•Cyanosis, apnea•Poor feeding•Tachycardia

•Respiratory distress•Hypotonia•Tremors, jitters,

seizures•Hypothermia


•Assessment Lowest glucose level is 30 to 90 minutes after birth Frequent assessments are needed in this population Glucose levels associated with neurological injury not well-established

•Treatment Treat underlying problem Early feeding Glucose infusion as needed Other medications

Hypoglycemia: Treatment


•Knowledge of needs specific to this population

Significance and scope of the problem

•Care practices specific to this populationAssessmentAppropriate time for dischargeRisk for complications and readmission

•Continued research on best- and evidence-based practices in late preterm infant care

In Summary


•Adamkin, D.H. (2009). Late preterm infants: severe hyperbilirubinemiaand postnatal glucose homeostasis. Journal of Perinatology, 29, S12-S17.

•American Academy of Pediatrics Subcommittee on Hyperbilirubinemia(2004). Management of hyperbilirubinemia in the newborn infant 35 ormore weeks of gestation. Pediatrics, 114, 297-316.

•Askin, D.F. (2002). Complications in the transition from fetal to neonatallife. Journal of Obstetric, Gynecologic, and Neonatal Nursing, 31, 318-327.•Bhutani, V.K., & Johnson, L.H. (2001). Jaundice technologies: Prediction

ofhyperbilirubinemia in term and near-term newborns. Journal ofPerinatology, 21, S72-82.

•Bhutani, V.K., & Johnson, L.H. (2006). Kernicterus in late preterm infantscared for as term healthy infants. Seminars in Perinatology, 30, 89-97.

References


•Blackburn, S.T. (2003). Thermoregulation. In S.T. Blackburn (Ed.),Maternal, fetal, & neonatal physiology: A clinical perspective (2nd ed., pp. 77-730). St. Louis: Elsevier Saunders.

•Blackburn, S.T. (2003). Bilirubin metabolism. In S.T. Blackburn (Ed.),Maternal, fetal, & neonatal physiology (2nd ed., pp. 656-676). Philadelphia:Elsevier Saunders.

•Center for Disease Control and Prevention, National Center for Health Statistics Final Natality Data, 2005.

•Clark, R. (2005). The epidemiology of respiratory failure in neonates bornat an estimated gestational age of 34 weeks or more. Journal ofPerinatology, 25, 251-257.

•Engle, W.A. (2009). Infants born late preterm: Definition, physiologic and metabolic immaturity, and outcomes. NeoReviews, 10, e280-286.

References


•Escobar, G.J., Clark, R.H., & Green, J.D. (2006). Short-term outcomes ofinfants born at 35 and 36 weeks gestation: We need to ask morequestions. Seminars in Perinatology, 30, 28-33.•Maisels, M.J. (2005). Jaundice. In M.G. MacDonald, M.D. Mullett, &M.M.K. Seshia (Eds.), Avery’s neonatology: Pathophysiology &management of the newborn (6th ed., pp. 768-846). Philadelphia: Lippincott Williams & Wilkins.

•Shapiro-Mendoza, C.K. (2009). Infants born late preterm: Epidemiology,trends, and morbidity risk. NeoReviews, 10, e287-294.

•Wang, M.L., Dorer, D.J., Fleming, M.P., & Caitlin, E.A. (2004). Clinicaloutcomes of near-term infants. Pediatrics, 114, 372-376.

•Wight, N. (2003). Breastfeeding the borderline (near-term) preterm infant.

Pediatric Annals, 32(5), 329-336.

References

Documents

Care of the Late Preterm Infant