PRETERM NEONATE

WHAT ARE THE PHYSIOLOGIC CHARACTERISTICS OF RESPIRATORY DISTRESS SYNDROME (RDS)

and risk factors

Insufficient surfactant producstion

-birth prior to 34-36 weeks

-results in impaired alveolar function

Risk Factors

prematurity

diabetic mother

hypoxia/asphyxia

(resultant of acidosis)

Respiratory function / RDS

Thermoregulation

Gastrointestinal immaturity / NEC

Neurologic immaturity

(weak reflexes, impaired regulation of behavioral states)

Nursing Management 

RDS

(Assessments)

close, careful monitoring

Increase risk of patent ductus arteriosus (PDA)

Signs a few hours after birth:

tachypnea

tachycardia

GFR

(grunting, flaring, retracting)

Transient tachypnea of neonate (TTN)

Meconium aspiration syndrome (MAS)

Respiratory distress syndrome (RDS)

Transient Tachypnea of the neonate

DEF: tachypnea clinically evident by six hours of age, caused by excessive fluid or mucous in lungs

-commonly seen early in transition to extrauterine life

-as aveoli open some absorbed

meconium aspiration syndrom (MAS)

Inhilation of meconium or meconium-stained fluid, characterized by respiratory distress

respiratory distress syndrom (RDS)

impaired ventilation at the alveolar level:formally called hyaline membrane disease

lack of breathing lasting more than 20 seconds or accompanied by cyanosis and a drop in HR and O2 sat.

they occur along with periodic breathing, mayrequire gentle stimulation, bag and mask ventilation, or medication

Nutritional deficiencies of iron, vitamin E, vitamin B-12, and folate may exaggerate the degree of anemia, as may blood loss and/or a reduced red cell life span.

AOP spontaneously resolves in many premature infants within 3-6 months of birth. In others, however, medical intervention is required.

failure of the ductus arteriosus to close after birth

Blood flows from the higher pressure of the aorta to the pumonary artery and the lungs (left to right shunt). It is common in pretirm infant.SYMPTOMS: vary from non to early congestive heart failure. Prostaglandins cause vasodilation and may interfere with closure of the duct. SOLUTION: indomethacin, may effectifly close, or surgical ligation. 

RDS

Retinopathy of prematurity ROP

necrotizing enterocolitis (NEC)

Describe retinopathy of prematurity

(ROP)

retinal damage by immature blood vessels in the eye

CAUSE: oxygen therapy (high levels of O2), prolonged ventilatory assistance, sepsis, acidosis

Monitor oxygen levels frequently

facilitate opthalmix exams -watch for htn, bradycardia, apnea

explain tests to parents

have them swaddle and give rest after exams(very stressful)

Necrotizing Enterocolitis (NEC)

Define/Causes

DEF: serious inflammatory condition of the intestinal tract that can lead to cellular death of intestinal mucosa

Pathophys: immaturity of the neonatal gut (intestines)

perinatal asphyxia (previous hypoxia of intestines)

mothers should breast feed or provide colostrum

abdominal girth measurements

(worried about perforation-distention-infection)

IVF/parenteral nutrition

(allows intestines to rests)

Side-lying position

(facilitates gastric emtpying, keeps pressure off diaphragm)

Intrapartal Hypoxia

-from decreased placental function

-from diminished fetal reserves

Hypoglycemia

-from depleted glycogen stores

Hypothermia/Cold Stress

-from depleted brown fat reserves

Prematurity

Fetal hypoxia

hypothermia

maternal diabetes

Betamethasone

classification, action, S/E, TNI's

classification: corticosteroid

action: acceleration of fetal lung maturity to reduce the incidence and severity of repiratory distress syndrome (RDS)

Side Effect: precaution to pregnancies complicated by diabetes. Contraindicated in those with chorioamnionitis

TNI: explain benefits to woman, can not prevent or lessen severity of premature complications, assess lung sounds, report chest pain, heaviness or dyspnea

hemolytic disease of the newborn characterized by anemia, jaundice, hepatomegaly (enlarged liver), and generalized edema

agglutination and hemolysis of fetal erythrocytes caused by incompatibility between the maternal and fetal blood types, such as when the fetus is Rh+ and the mother is Rh-

Pathologic Jaundice

primary cause

Erythroblastosis Fetalis-transplantal passage of maternal antibodies

-hemolysis of fetal RBC

Hydrops Fetalis-most sever form of E.F. 

-severe anemia and multiorgan system failure

State the purpose of phototherapy lights

Treatment of pathologic jaundice

Bilirubin in the skin absorbs the llight and changes into water-soluble products that can be excreted in bile and urine.

Have infant wear only a diaper and eye patches

check bilirubin levels frequently to determine effectiveness

Assess for side effects as frequent loose stools, that damage the skinand result in fluid loss

Increase fluid intake

Infant may need lactose free formula

Skin rash normal and will disappear

TURN THE INFANT q2hrs

Eye protection: pssible retina damage, avoid abrasions of cornea, and conjunctivitis

Tactile: Monitor reflexes, lethargy and inc/dec in muscle tone that are signs of encephalopathy

some of the side effects are frequent, loose, green stool from increased bile flow and peristalsis

RAPID excretion of bilirubin can damage skin and result in fluid loss

Jaundice in face=5-7mg/dl serum bilirubin

Jaundice moves down the body as the bil. levels rise

seen in the first 24 hours of life

Nursing Assessment and Interventions 

with Pathologic Jaundice

Identify Risk Factors

maternal blood type and Rh

Prenatal care and screening

perinatal course

gestational age 

Determine blood type, Rh, direct Coombs'

Draw bilirubin levels per protocol/order

Initiate phototherapy protocol per order

Unconjugated (fat Soluble) bilirubin attaches to binding sites on albumin in plasma

Unconjugated bilirubin is carried to the liver and converted to conjugated (water soluble)bilirubin

-glucuronyl transferase

conjugated

doesn't harm the body

Unconjugated

can't excrete unless converted by liver

Assessments of Infant of diabetic mother

IDM

Congenital anomalies

-cardiac, renal, gi

Hypoglycemia

-increased pancreatic size and function

Respiratory Distress Syndrom (RDS)

-hyperinsulinemia impairs surfactant production

Macrosomia

-insulin acts as growth hormone 

-birth trauma

Assess glucose according to protocol

Report under 40 (40-60 mg/dl normal)

feed

reassess BG in 30-45 min

keep hydrated

be alert for other complications (RDS-cold stress-need for more O2)

support parents

generalized infection that spreads rapidly through the bloodstream during the neonatal period(first 28 days of life)

immature immune system

-anybaby who becomes stressed

maternal infection

PROM

prematurity and low birthweight

early onset occurs during first week after birth-sepsis, pneumonia, and maningitis are primary infections

late-onset after the first week and meningitis is most common

reported substance use/abuse

absence of prenatal care

mothers behavior during labor

• prenatal opiate, codeine, tranquilizer, sedative exposure
• Onset ETOH - 3-12 hours seen right away, OPTIATES 48-72 hours
• SIGNS AND SYMPTOMS
• Irritability/high-pitched cry
• tremors/hypertonicity
• excessive sucking
• poor suck/swallow reflexes

NAS Nursing Resposibilities

(special care needed by drug exposed infant)

collect uring for chimical dependency

admin medical withdrawal regimen

(NAS scoring)

Feeding

(minimize distractions, guard against aspiration)

Environment

(containment-swaddle tightly, snuggle)

Parent/child attachement

its a genetic disorder that causes central nervous system damage from toxic levels of the amino acid phenylaline in the blood. 

-Severe intellectual disability occurs in untreated infants

deficiency of the liver enzyme phenylalanine hydrolase, which is needed to convert phen. to tyrosine for use (breaks up protein)

its an autosomal recessive disorder

facilitate mandated NYS screening

parent education

MANAGEMENT

LIFELONG LOW-PHEN DIET