HIGH RISK NEWBORN 13 student version.ppt

7/28/2019 HIGH RISK NEWBORN 13 student version.ppt

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HIGH RISK NEWBORN

Lecture 13


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LEVELS OF NICULevel I

Basic neonatal care; minimum requirement for afacility that provides inpatient maternity care. Able to perform neonatal resuscitation. Evaluate healthy newborns; provide standard care. Stabilize newborns til transfer to intensive care

Level II AKA Special Care Nurseries Basic care to moderately ill infants; ~ 32 42 wks. Step down from level III NICU; infants recover

Level III Newborns


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National studies show: 30% survival rate for 23 wk preemies.

52 % for 24 wks. 76 % for 25 wks. African American women: twice as likely todeliver 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.


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RDS Pre-Term Resp.distress syndrome: aka hyaline membrane disease

In preemie, insufficient surfactant in alveoli causing lungs tocollapse; 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 immaturelungs, non-compliance, and low surfactant levels.


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Causes ofRDS - Term

In term infant: Sepsis [GBS] Persistent Pulmonary Hypertension of

Newborn (PPHN) ductus arteriosus doesnot 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.


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S/S of RDS (In PRETERM)

Retractions - drawing back of chest muscles with breathing.Infant works harder at lung expansion. SOB and expiratory gruntingself-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


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Terms

AGA - Approp. for gestational age [5.7 9.1]SGA - Small for gestational age. ~ < 5.7 lbs.

LGA - Large for gestational age. ~ > 9.1 lbs.


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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; weighpros/cons.


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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.


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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]


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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 triggerinitiates 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


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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 infantweighing 2500 g. or less.

World Health Organization (WHO) & American College ofObstetricians and Gynecologists (ACOG) both define itas infant born prior to 37 wks.


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Appearance of Preterm Infant24-36 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. BallardGestational 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 must !


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13 year old femaleEx-24 week preemie

BPD, trach/vent

15 mos in NICUG-tube 3 yrs

Decannulated at age 4

Intensive learning support

Eating age-typical diet

Mild articulation errors

**Former Extreme Premature Teen**


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Thermoregulation:

risk for hypothermia r/t large surface in relation to

body weight.Limited stores of brown fatDecreased or absent reflex control of skin capillariesImmature temperature regulation in brainKangaroo care [skin to skin contact]Assess Respiratory EffortMay need intubation to maintain respirations. < 32 wks: irregular respiratory pattern normalSurvanta in ET tube


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Urinary/Elimination

Have high insensible water loss d/tlarge body surface compared w/ totalbody weight. Lower GFR d/t immature

kidneys. Fluid overload or dehydration. Strict I/O

Immature kidneys secrete glucose

slowly > hyperglycemia can result.


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Insensible Water Loss[Approx. water loss in body]

Age group Water

Premature infant 90%

Newborn infant 70-80%

12-24 months 64%

Adult 60%


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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 stomachcapacity

Limited store of nutrients

Decreased ability to digest proteins and absorb

nutrients, and immature enzyme systems. TPN, PPN, Gavage, or IV feedings


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Feeding

Caloric requirement: PT: 95-130 kcal./kg/day. Term infant: 100-110.

Smaller stomach capacity: sm.,freq. feedings [q 2-3hrs].

Formula: Calories for premie: 24 cal./oz. Term: 20cal/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.


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Developmentally SupportiveActivities ** (new) Kangaroo Care/Skin to Skin Care

Non Nutritive Sucking (Significantlyreduced length of hospital stay for

preterm infant)

Non Nutritive at the Breast (pacifer) Parent Education & Support


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Non-Nutritive Sucking atBreast ** Improved milk production

Provides sucking experience

Prepares infant for breastfeeding Long term effects:

Increased length of exclusive breastfeeding

Increased length of total breastfeeding


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POTENTIAL COMPLICTATIONS of PT InfantAnemia 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 PDA closure.


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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, promotelung healing.

O2, nutrition, steriods, bronchodilators, diuretics, antibiotic tx;stop PPV; maintain venting @ lowest pressure.

Nitric oxide;Vitamin A


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ROP: Retinopathy of Pre-maturity.

Caused by damage to immature blood vessels inretina. Results in scarring. Caused by high O2 levels.Blindness may result. 90% of cases no impairment.Occurs in VLBW


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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 adverseneurodevelopmental outcome

-3/4 of infants with Grade 3-4 IVH develop CP &75% in some type of special education


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NECNEC: 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]

Prevention: Delayed /Slow feedings: advance < 20ml/kg/day; Enteral Antibiotics; Antenatal Steroids;enteral IgG, IgA; Human Milk Feedings.


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GDM

Infants [GDM moms] macrosomic if not wellcontrolled during pregnancy; lethargic d/t ^ glucose. Macrosomia: overstimulation of pituitary growthhormone 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.


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GDM

Complications:Immature lungs d/t ^ fetal insulin which interfereswith 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, 4hrs. of life. If < 40; stat serum glucose & feedformula [1/2 oz.] Repeat in - 1 hr. as protocol.


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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 resolvedwithin 4-6 hrs.of life.

Occurs more w. term C/S & preterm infants.


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Meconium Aspiration Syndrome:

Present in fetal bowel as early as 10 wks. Infantmay aspirate meconium in utero or with 1stbreath.

Can cause severe respiratory distress,inflammation or blockage of small bronchioles bymechanical plugging

Ductus arteriosus may remain open; causes

blood to shunt from pulmonary artery to aortainstead of passing thru lungs [^ pulmonaryresistance], causing ^ hypoxia.


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SymptomsTachypnea [RR>60]

RetractionsSOB and expiratory gruntingNasal flaringPeriods of apneaBluish color of skin and mucus membranes

Arms or legs puffy or swollen

PreventionOropharyngeal suctioning of infant > delivery

Laryngoscopic visualizaiton of vocal cords > intubation.Additional suctioning of trachea.Amnioinfusion: dilutes meconium. Thins out particulatemeconium. Do sepsis workup; CBC, bl.cx., chest x-ray. ABtherapy to prevent pneumonia.


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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 recommendedback or side position; not prone. Incidence declined 50%

since then. New data: use of pacifier for 2-4 mos.


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Hyperbilirubinemia ^ levels of unconjugated (indirect) bilirubin in blood.

Breakdown of RBCs > Hgb > heme > Unconjugated bilirubin.

Bilirubin binds with plasma protein (albumin) = bound goesto liver & converts to conjugated or H2O soluble where it sexcreted 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).


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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 upexcretion in stool.

Phototherapy - bilirubin becomes water soluble to beexcreted.

Cover genitalia & eyes. Prevent organ damage. Single,double, triple phototherapy.

Kernicterus: Indirect bilirubin of 20 > permanent braindamage; bilirubin encephalophathy.

Signs: hi-pitched cry, seizures, hypotonia Interventions: Immediate exchange transfusion;

followed by phototherapy & frequent bili levels.


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Physiologic Jaundice: [> 24 hrs.] 2nd-3rd day.

R/T low albumin (decreased binding sites forbilirubin). ^ levels of RBCs. Yellowing of skincaused by breakdown of fetal red blood cells whichproduces excessive amts. of bilirubin in bloodstream. 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.


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Gastroschisis:weakness in abdominal wallcausing herniation of gut on umbilical cordduring 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; surgicalclosure after contents returned to abd.cavity.If necrotic bowel present, remove.


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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; developmentalstimulation for long term hosp; support group forparents; teach parents s/s bowel obstruction- ie.vomiting, pain, firm abdomen, anorexia, irritability.


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Omphalocele:large herniation of gut intoumbilical cord. Viscera outside of abd.cavity& covered with peritoneal & amnioticmembranes

1 in 5,000 to 10,000 live birthsAssoc.w.malrotation of intestines; decreased

abdominal capacity. Stenosis common;cardiac, genitourinary, or chromosomalanomalies common (1/3 to of cases)

Mortality: 20-30%; sepsis & intestinal

obstruction. TX: same as for gastroschisis Nursing Care: Same as for gastroschisis.


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Bladder Exstrophy:extrusion of urinarybladder to the outside of body through

developmental defect in lower abdominalwall. Assoc.w.genital anomalies: widesymphysis pubis.

Rare & congenital anomaly; bladder is turned

inside out

TX: protect exposed bladder tissue; cover withsaline gauze/plastic wrap til sugery. Prevent

UTI. Reconstruction of bladder & genitalia.Provide support & education


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EA (esophageal atresia) TEF (tracheo-esophageal fistula)

Cause unknown. Congenital malformations esophagus ends before

reaching stomach. (TEF) fistula may connect totrachea.

1 in 2,000 - 4,500 live births. 30-50% have otheranomalies (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 ofaspiration; Abdominal distention; Airless/sunken

abdomen. Hx maternal polyhydramnios TEF without EA: food enters trachea; choking;

cyanosis.


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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 distalTEF 1%


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Management: infant supinew. HOB to decreasesecretions. NG tube for frequent suctioning toprevent aspiration of gastric secretions; IVF; assessVS, resp.distress, measure abd.girth; provideeducation & support to family.

Surgical repair: fistula ligation & end to endanastomosis of atresia.

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

HIGH RISK NEWBORN 13 student version.ppt

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