High Risk Newborn

High Risk Newborn

HIGH RISK NEWBORN LEVELS OF NICU National studies show: 30% survival rate for 23 wk preemies. 52 % for 24 wks. 76 % for 25 wks. African American women: twice as likely to deliver early, but babies more likely to survive. High risk newborns in NICU: Use cardiac & apnea monitors; radiant warmers; O2 sat, VS, BP monitoring. Assessed q 1-2 hrs. or continuously ^ risk of infections: GBS, septicemia, thrush

Moms encouraged to visit NICU daily Skin care to prevent breakdown. Good hand washing - parents/staff. RDS Pre-Term Resp.distress syndrome: aka hyaline membrane disease In preemie, insufficient surfactant in alveoli causing lungs to collapse; not enough O2. Most common disorder of preemies. ^ resistance causes fibrous tissue in bronchioles & alveoli poor O2/CO2 exchange. Self-limiting; ~ 72-96 hrs in most late preterm or full term.

VLBW (ELBW) - RDS can persist days/weeks. D/T immature lungs, non-compliance, and low surfactant levels. Causes of RDS - Term In term infant: Sepsis [GBS] Persistent Pulmonary Hypertension of Newborn (PPHN) ductus arteriosus does not close. Meconium aspiration r/t oligo, uteroplacental insufficiency, & fetal distress Infants of diabetic moms.

May need resuscitation @ birth. In Pre-term infant: Immature lungs, non-compliance, & low surfactant levels. S/S of RDS (In PRETERM) Retractions - drawing back of chest muscles with breathing. Infant works harder at lung expansion. SOB and expiratory grunting self-induced by infant maintains ^ pressure in lungs by causing expiratory braking using vocal cords (glottis partially closes

increasing alveolar surface tension) Nasal flaring; TTN [transient tachypnea = ^ 60 R/min.] Management: ABGs, O2 sats, CBC, bl.cx Skin/mouth care Suctioning (prn) Support for family Adequate fluids and electrolytes

Replace surfactant [Curasurf man made; ET tube] O2 therapy [Oxyhood; CPAP; ventilator] [CPAP= cont.+ airway pressure] helps keep small air sacs from collapsing; suction prn Terms AGA SGA LGA - Approp. for gestational age [5.7 9.1] - Small for gestational age. ~ < 5.7 lbs. - Large for gestational age. ~ > 9.1 lbs.

SGA: weight < 10th percentile compared to others of same gestational age. [38 wk. weighs 5 lbs.] Aka IUGR aka Failure to thrive. Most common cause: placental anomaly; placenta not receiving sufficient nutrition from uterine arteries or placenta. Severe DM, pre-eclampsia, poor nutrition, smoking, cocaine. Decreases blood flow to placenta. Fundal height lower than expected for gest.age. Bio Physical Profile: assesses placental function. If infant not thriving in utero, will do C/S; weigh pros/cons.

SGA infant: wasted look, dull hair, small liver [^^ bilis], poor skin turgor, low glucose, low temp. Mature neuro responses, sole creases, + ear cartilage. Lab findings: ^ HCT {low plasma levels} & ^ RBC {polycythemia} Causes thicker blood making heart work harder; ^ chance of thrombosis. Prolonged acrocyanosis. Manage: ^ fluids & freq.feedings. LGA: aka macrosomic infant. > 90% percentile. Appears healthy; may be gestationally immature {immature neuro responses & respiratory effort}.

Assess: larger than average uterine size for gestational age Do sono to estimate size. Check dates. C/S for CPD or shoulder dystocia. Causes: GDM, omphalocele, transposition great vessels. Appearance: possible fx clavicles; facial/head bruising, facial/neck palsy, caput, cephalohematoma. Observe: hypoglycemia, polycythemia, irregular HR, cyanosis [in transposition] Preterm Infant 90% term births [full-term] & 11% preterm [< 37 wks]

Calculated by gestational age; not weight. Maturity determined by physical findings: sole creases, skull firmness, ear cartilage, neurologic findings & pregnancy dates. SGA & Pre-terms: 2 different causes w. diff. problems. Preterm: fetus has been doing well in utero but trigger initiates labor & infant is born early. Problems: poor thermoregulation, hypoglycemia, intracranial bleed, RDS, NEC, immature kidney function, infection. 80-90% of infant mortality in 1st yr. life esp. VLBW infants Risk Factors of Preterm Delivery

Women of middle/upper socioeconomic: ~ 4-8% Lower socioeconomic levels: ~ 10-20% Inadequate nutrition; lack of money & knowledge about good nutrition; lack of support. American Academy of Pediatrics: live-born infant weighing 2500 g. or less. World Health Organization (WHO) & American College of Obstetricians and Gynecologists (ACOG) both define it as infant born prior to 37 wks. Appearance of Preterm Infant

24-36 weeks Small, underdeveloped, head disproportionately large; skin thin & ruddy [little subcut. fat]; veins noticeable; prolonged acrocyanosis. vernix depends on gest.age. < 24 wks.vernix not formed. None/few sole creases. Ear cartilage immature; no quick rebound of pinna. Extensive lanugo. Suck/swallow absent, weak cry < 33 wks. Ballard Gestational scale to estimate age. Infection decreased maternal antibodies Skin fragile; limit alcohol; rinse with water.

Adhesives cause skin tearing. Use skin barriers to protect skin. Tegaderm tape. Handwashing a **Former Extreme Premature Teen** 13 year old female Ex-24 week preemie BPD, trach/vent 15 mos in NICU G-tube 3 yrs Decannulated at age 4 Intensive learning support Eating age-typical diet Mild articulation errors Thermoregulation:

risk for hypothermia r/t large surface in relation to body weight. Limited stores of brown fat Decreased or absent reflex control of skin capillaries Immature temperature regulation in brain Kangaroo care [skin to skin contact] Assess Respiratory Effort May need intubation to maintain respirations. < 32 wks: irregular respiratory pattern normal Survanta in ET tube Urinary/Elimination Have high insensible water loss d/

t large body surface compared w/ total body weight. Lower GFR d/t immature kidneys. Fluid overload or dehydration. Strict I/O Immature kidneys secrete glucose slowly > hyperglycemia can result. Insensible Water Loss [Approx. water loss in body] Age group Premature infant

Newborn infant 12-24 months Adult Water 90% 70-80% 64% 60% Nutrition: promote normal growth & development Tries to maintain rapid rate of intrauterine growth. Lack of cough reflex: can aspirate formula.

Have weak sucking, swallowing, gag reflexes Weak abdominal muscles; weak gag reflex ^ aspiration risk ^ BMR - High caloric needs but small stomach capacity Limited store of nutrients Decreased ability to digest proteins and absorb nutrients, and immature enzyme systems. TPN, PPN, Gavage, or IV feedings Feeding Caloric requirement: PT: 95-130 kcal./kg/day. Term infant: 100-110. Smaller stomach capacity: sm.,freq. feedings

[q 2-3 hrs]. Formula: Calories for premie: 24 cal./oz. Term: 20 cal/oz. Breast milk good d/t immunologic properties. Gavage: nasogastric/orogastric. Gag reflex not intact til infant 32 wks; avoid over filling stomach; may cause respiratory distress. Use premie nipple. Developmentally Supportive Activities ** (new) Kangaroo Care/Skin to Skin Care Non Nutritive Sucking (Significantly reduced length of hospital stay for preterm infant)

Non Nutritive at the Breast (pacifer) Parent Education & Support Non-Nutritive Sucking at Breast ** Improved milk production Provides sucking experience Prepares infant for breastfeeding Long term effects: Increased length of exclusive breastfeeding Increased length of total breastfeeding

POTENTIAL COMPLICTATIONS of PT Infant Anemia of Prematurity: red blood cell life is short. Low bone marrow prod. until ~ 32 wks. Frequent blood testing. Kernicterus: destruction of brain cells by invasion of indirect bilirubin [bili ~20]. PT infants: low serum albumin available to bind indirect bili & excrete it. Persistent Patent Ductus Arteriosus: d/t hypoxia, lack of surfactant, lack of musculature. Lungs are noncompliant. ^ blood stays in pulmonary artery > pulmonary

artery HTN >persistent PDA. Indocin stimulates Bronchopulmonary Dysplasia. (Chronic Lung Disease) Results from long term O2 & being vented (PPV). Lungs immature; resp.infection, poor nutrition, Pressure damages & stretches lung tissue; results in airway edema & fibrotic buildup. Alveolar walls thicken; buildup of secretions; pneumonia & atelectasis possible. Decreased oxygenation results. S/S: tachypnea, tachycardia, hypoxia, grunting, retractions, feeding & activity intolerance. TX: prevent further disease; promote oxygenation,

promote lung healing. O2, nutrition, steriods, bronchodilators, diuretics, antibiotic tx; stop PPV; maintain venting @ lowest Neonatal Sepsis Premies more susceptible; immature immune sys. Transmission: viral, bacterial; transplacental (syphilis, toxoplasmosis) S/S: low temps, resp. distress, hypotension, ^HR, ^RR, lethargy, poor feeding, diarrhea, vomiting. Mortality: 5-20% CBC with diff (^bands, decreased neutrophils, decreased platelets), blood cx,

TX: broad spectrum antibiotics; VS, nutrition, fluids, O2. Parental support. ROP: Retinopathy of Pre-maturity. Caused by damage to immature blood vessels in retina. Results in scarring. Caused by high O2 levels. Blindness may result. 90% of cases no impairment. Occurs in VLBW <1500 g. TX: reattachment of retina; Frequent eye evals. Laser to reduce scarring. Nursing Care: routine high risk premie care; sepsis; VS; support groups & education

Intracranial Hemorrhage aka IVP germinal matrix made up of fragile & vascular capillaries. Grades 1-4 (3 & 4 worse) Bleeding into ventricles d/t hypoxia, ^ BP, ^ fluids. Dx with Cranial ultrasound Normal brain function assessed > bleed. IVH occurs in 20-25% of VLBW premies; suffer more severe grades of IVH IVH is an important predictor of adverse neurodevelopmental outcome -3/4 of infants with Grade 3-4 IVH develop CP & 75% in some type of special education

NEC NEC: necrotizing enterocolitis; common in PT baby; can result in ulcers/tissue necrosis in intestinal wall. Bacteria in bowel>infection>destroys bowel tissue> sepsis. Primary risk factor: prematurity & tube feedings; RDS, congenital heart defects. S/S abd. swelling, septic infant, emesis, blood in stool. Tx: stop tube feedings, start IVF & TPN, AB [sepsis],

ventilator, platelet transfusion [control bleeding] GDM Infants [GDM moms] macrosomic if not well controlled during pregnancy; lethargic d/t ^ glucose. Macrosomia: overstimulation of pituitary growth hormone in fetus in preg. d/t ^ maternal insulin. Mom insulin resistant; glucose x placenta; more insulin made by fetal pancreas. After delivery, glucose levels drop, but insulin remain ^ for several hours.

Infant jittery on admission. Glucose checked for 1st 4 hrs; Hypoglycemia = < 40 mg/100 ml whole blood. GDM Complications: Immature lungs d/t ^ fetal insulin which interferes with cortisol release; blocks formation of lecithin & prevents lung maturity. ^ chance of birth injury d/t ^ size; shoulder dystocia. Hypoglycemia: Check glucose on admission to NBN: 1, 1, 2, 4

hrs. of life. If < 40; stat serum glucose & feed formula [1/2 oz.] Repeat in - 1 hr. as protocol. Transient Tachypnea of Newborn: TTN Rapid, shallow RR 70-80/min. d/t slow absorption of lung fluid. Difficulty feeding; infant will not suck d/t rapid breathing. Chest x-ray shows fluid in lungs. Infant must ^ resp.depth to aerate effectively. Can signify obstruction. VS, O2 sat; give O2. Send to NICU for close observation if not resolved within 4-6 hrs.of life. Occurs more w. term C/S & preterm infants.

Meconium Aspiration Syndrome: Present in fetal bowel as early as 10 wks. Infant may aspirate meconium in utero or with 1st breath. Can cause severe respiratory distress, inflammation or blockage of small bronchioles by mechanical plugging Ductus arteriosus may remain open; causes blood to shunt from pulmonary artery to aorta instead of passing thru lungs [^ pulmonary resistance], causing ^ hypoxia. Symptoms

Tachypnea [RR>60] Retractions SOB and expiratory grunting Nasal flaring Periods of apnea Bluish color of skin and mucus membranes Arms or legs puffy or swollen Prevention Oropharyngeal suctioning of infant > delivery Laryngoscopic visualizaiton of vocal cords > intubation. Additional suctioning of trachea. Amnioinfusion: dilutes meconium. Thins out

particulate meconium. Do sepsis workup; CBC, bl.cx., chest x-ray. AB therapy to prevent pneumonia. SIDS: sudden infant death syndrome. Mainly in adolescent moms, closely spaced pregnancies, underweight, PT infants. 2nd hand smoke. Appear well nourished. ^ African American males. Silent death; poss.laryngospasm. Use of sleep apnea monitor for first few wks.-mos. Peak age: 2-4 mos. Cause unknown. Theories: HR abnormalities, decreased arousal [moro] responses, prone position, low surfactant, brain

stem abnorm. In 2000 Amer. Academy of Pediatrics recommended Hyperbilirubinemia ^ levels of unconjugated (indirect) bilirubin in blood. Breakdown of RBCs > Hgb > heme > Unconjugated bilirubin. Bilirubin binds with plasma protein (albumin) = bound goes to liver & converts to conjugated or H2O soluble where it s excreted via bile by feces. Immature livers which cannot convert indirect to direct; indirect bilirubin remains in bloodstream.

Unbound bilirubin = (indirect) jaundice. If indirect level rises > 7, yellow color results. Sclera, nail beds, then skin. Cephalocaudal progression: head to toe. Blanch skin Depends on hours/days of life. Younger infant (4-5 hrs.) high reading more significant; could rise steadily . Older infant (1-2 days), higher # less significant (more

mature liver). Pathologic [within 24 hrs.] Bili rises quickly. By 5-7 mg/dl/day or more. Blood type incompatibilities ; sepsis; birth trauma. Interventions: Early & frequent feedings to speed up excretion in stool. Phototherapy - bilirubin becomes water soluble to be excreted. Cover genitalia & eyes. Prevent organ damage. Single, double, triple phototherapy. Kernicterus: Indirect bilirubin of 20 > permanent brain damage; bilirubin encephalophathy.

Signs: hi-pitched cry, seizures, hypotonia Interventions: Immediate exchange transfusion; followed by phototherapy & frequent bili levels. Physiologic Jaundice: [> 24 hrs.] 2nd-3rd day. R/T low albumin (decreased binding sites for bilirubin). ^ levels of RBCs. Yellowing of skin caused by breakdown of fetal red blood cells which produces excessive amts. of bilirubin in blood stream. Excess bilirubin in blood causes jaundice. Management: frequent feedings, frequent bili levels. Bili declines within days. Teach parents to place near window to speed

up breakdown of bili. Sunlight will ^ breakdown. Gastroschisis: weakness in abdominal wall causing herniation of gut on umbilical cord during early development; most commonly on right side. Viscera lie outside abdominal cavity; not covered with sac. 1 in 4,000 live births Mortality: 10%-15%

Assoc.w.prematurity; malrotation of intestines; decreased abdominal capacity; other anomalies rare. TX: IV & NG tubes immediately; TPN; Silastic (synthetic covering) over viscera; surgical closure after contents returned to abd.cavity. If necrotic bowel Nursing Care: thermoregulation (monitor temps, radiant warmer); sterile technique (cover viscera warm, sterile, saline gauze & plastic); monitor VS, color, etc.) strict I&O, daily

weights, fontanels, pacifier, electrolytes. Minimize movement of area. encourage bonding asap; developmental stimulation for long term hosp; support group for parents; teach parents s/s bowel obstruction- ie. vomiting, pain, firm abdomen, anorexia, irritability. Omphalocele: large herniation of gut into umbilical cord. Viscera outside of abd.cavity & covered with peritoneal & amniotic membranes 1 in 5,000 to 10,000 live births Assoc.w.malrotation of intestines; decreased abdominal capacity.

Stenosis common; cardiac, genitourinary, or chromosomal anomalies common (1/3 to of cases) Mortality: 20-30%; sepsis & intestinal obstruction. TX: same as for gastroschisis Nursing Care: Same as for gastroschisis. Bladder Exstrophy: extrusion of urinary bladder to the outside of body through developmental defect in lower abdominal wall. Assoc.w.genital anomalies: wide symphysis pubis. Rare & congenital anomaly; bladder is

turned inside out TX: protect exposed bladder tissue; cover with saline gauze/plastic wrap til sugery. Prevent UTI. Reconstruction of bladder & genitalia. Provide support & education EA (esophageal atresia) TEF (tracheoesophageal fistula) Cause unknown. Congenital malformations esophagus ends before reaching stomach. (TEF) fistula may connect to trachea. 1 in 2,000 - 4,500 live births. 30-50% have

other anomalies (cardiac, GI, nervous sys). Premature or LBW common EA without TEF : Inability to pass suction or NG tube catheter @ delivery. Confirm with abd.x-ray; Excessive oral secretions; vomiting; risk of aspiration; Abdominal distention; Airless/sunken abdomen. Hx maternal polyhydramnios TEF without EA: food enters trachea; choking; cyanosis. Statistics Esophageal atresia with distal TEF 87% Isolated esophageal atresia without TEF 8%

Isolated TEF 4% Esophageal atresia with proximal TEF 1% Esophageal atresia with proximal and distal TEF 1% Management: infant supine w. HOB to decrease secretions. NG tube for frequent suctioning to prevent aspiration of gastric secretions; IVF; assess VS, resp.distress, measure abd.girth; provide education & support to family. Surgical repair: fistula ligation & end to end

anastomosis of atresia. Provide post op care. IVF, G-tube & foley care; pain; VS, I&O, skin care.

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