High Risk Neonates

HIGH RISK NEONATESPresented by Ann Hearn RNC, MSN

A High-Risk Newborn is one who is susceptible to illness (morbidity) or even death (mortality) due to: dysmaturity immaturity physical disorders complications of birth

In most cases, the infant is the product of a pregnancy involving one or more predictable risk factors, including the following:◦ Low socioeconomic level of the mother, poor nutrition◦ Exposure to environmental dangers such as toxic chemicals◦ Preexisting maternal conditions such as heart disease,

diabetes◦ Obstetric factors such as age or parity, other premature births◦ Medical conditions related to pregnancy such as hypertension,

Premature rupture of membranes, infection, etc.

THE HIGH RISK NEWBORN

CLASSIFICATION OF HIGH RISK NEWBORNS

Gestational Age

Preterm (Late Preterm) Term Postterm

Gestational Age & Birth Weight

SGA AGA LGA

Ballard Scale or Dubowitz scale Neuromuscular characteristics Physical Characteristics

Scoring of all characteristics determines the gestational age

ASSESSMENT OF GESTATIONAL AGE

ASSOCIATED COMPLICATIONS OF:

Asphyxia Aspiration syndrome Hypothermia Hypoglycemia Polycythemia

Congenital malformations

Intrauterine infections

Continued growth difficulties

Cognitive difficulties

SGA IUGR

Nursing Interventions: Monitor heart rate, respiratory rate, temperature and blood glucose.

Born before 37 weeks gestation

The Premature Infant

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT

Respiratory Thermoregulation Digestive Renal (fluid & electrolyte) Infection Pain

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Respiratory

Insufficient production of surfactant Immaturity of alveolar system Immaturity of musculature Respirations 40-60, shallow, irregular, usually

diaphragmatic

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Respiratory Nursing Interventions

Assess for S/S respiratory distress Cyanosis Retractions Expiratory grunting Nasal flaring Apnic episodes

Maintain airway Administer O2 Monitor O2 saturation Monitor heart/respiratory rates

o Positioning◦ Position with head slightly elevated and neck slightly extended

◦ Side-lying or prone

SuctioningOnly use when necessaryBe gentle so as not to damage fragile mucus membranes

NURSING CARE

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Thermoregulation

Increased body surface area compared to body mass

Decreased brown fat Thin skin Vessels close to skin Decrease sub-q fat Lack of flexion

Axillary temperature <36.3 or >36.9 degrees C

Abdominal skin temperature <36 or >36.5 degrees C

Poor feeding or feeding intolerance Irritability Lethargy Weak cry or suck Decreased muscle tone Cool skin temperature Skin pale, mottled, or acrocyanotic Signs of hypoglycemia Signs of respiratory difficulty Poor weight gain

SIGNS OF INADEQUATE THERMOREGULATION

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT

Thermal Neutrality – Nursing Interventions Incubator or radian warmer Warm surfaces Warm humidified oxygen Warm ambient humidity Warm feedings Keep skin dry and head covered

ISOLETTE/ RADIANT or INCUBATOR OPEN WARMER

FLUID AND ELECTROLYTE BALANCEDehydration Urine output <2 ml/kg/hour Urine specific gravity >1.01 Weight loss greater than

expected Dry skin and mucous

membranes Sunken anterior fontanel Poor tissue turgor Blood: Elevated sodium,

protein, and hematocrit levels

Overhydration Urine output >5 ml/kg/hour Urine specific gravity

<1.002 Edema Weight gain greater than

expected Bulging fontanels Moist breath sounds Difficulty breathing Blood: Decreased sodium,

protein, and hematocrit levels

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Hydration – Nursing Interventions

Daily weights Monitor I&O

Parental fluids Feedings Oral medications 1gm = 1ml urine Regurgitation/emesis Stool

Accurate IV rates, assess site Accurate OGT feedings Monitor urine pH & specific gravity

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Renal

Decreased glomerular filtration rate Inability to concentrate urine or dilute

urinePoor electrolyte regulation

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Skin

Fragile Permeable Easily damaged

Nursing interventions Little use of tape and back with cotton Rinse disinfectants off with water Assess skin for infection Avoid pressure points Reposition frequently as tolerated

Lack of passive immunity from mother; deficient placental transmission.

Inability to produce own antibodies - immature system.

Exposure to procedures and prolonged hospital stay.

Skin is thin and offers little protection from disease causing organisms.

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT - IMMUNE SYSTEM

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Prevention of Infection – Nursing

Interventions Initial scrub / strict hand washing

Visitors & staff Reverse isolation Single infant equipment Short / no artificial nails Maintain sterile technique

IV start and dressing changes Procedures

Clean incubators weekly Position changes; use of sheepskin Judicious use of tape on skin

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Signs and Symptoms of Infection

Behavioral changes Physiological changes

Tonus Color Temperature Skin Feeding Hyperbilirubinemia Heart rate Respiratory rate

??? WHAT ARE THE SIGNS AND SYMPTOMS OF PAIN IN A PREMATURE INFANT??? High-pitched, intense, harsh cry Whimpering, moaning “Cry face”, grimacing, furrowing of brow Eyes squeezed shut Mouth open Tense, rigid muscles or flaccid muscle tone Rigidity or flailing of extremities Color changes: Red, dusky, pale Increased or decreased heart rate and

respirations, apnea Decreased oxygen saturation Increased blood pressure Sleep-wake pattern changes

NURSING CARESwadd

lePacife

rMedications

Changes in Oxygenation: Respirations Pulse Blood pressure Oxygen saturation levels Color Sneezing, coughing, hiccupping

Behavior changes Posture Facial expression Gaze Regurgitation Yawning Fatigue

SIGNS OF OVERSTIMULATION IN PRETERM INFANTS

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Nutrition

Poor suck and swallow reflex Decreased gag reflex Relaxed cardiac sphincter Small stomach capacity Intolerance of fats Immature absorption of nutrients

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Pre-feeding assessment:

Measure abdominal girth Bowel sounds Gastric residual Sucking and gag reflexes

NUTRITION Feeding methods:

Parenteral PO NGT Direct Breastfeeding

PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT Facilitating Parent-Infant Attachment

Prepare parents for first visit Establish safe/trusting environment Encourage visitation Involve in care taking Repeat explanations Promote touching, talking, rocking, cuddling Refer to infant by name Allow parents to phone as desired

COMMON COMPLICATIONS OF PRETERM INFANTS

RESPIRATORY DISTRESS SYNDROME

RESPIRATORY DISTRESS SYNDROME - RDS Pathophysiology

Primary absence, deficiency or alteration in the production of surfactant

Surfactant, atelectasis = lack of gas exchange

Leads to hypoxia and acidosis which further inhibit surfactant production and causes pulmonary vasoconstriction.

Clinical manifestations: Cyanosis Tachypnea Nasal flaring Retracting Apnea

RESPIRATORY DISTRESS SYNDROME-SURFACTANT REPLACEMENT THERAPY Surfactant preparation can be lifesaving and

reduces complications, such as pneumothorax.

Administered through an endotracheal tube

Surfactant treatments may be repeated several times during the first days until respiratory distress syndrome resolves.

RESPIRATORY DISTRESS SYNDROME-NURSING INTERVENTIONS Maintain airway, oxygenation,

ventilation Supplemental oxygen:

Nasal prongsOxyhood

Continuous positive airway pressure (CPAP)

Intubation with endotracheal tube Maintain thermoregulation

RESPIRATORY DISTRESS SYNDROME-NURSING INTERVENTIONSNutrition Support Newborns with RDS may fed by the following

means: Tube feeding—a tube is inserted through

the baby's mouth and into the stomach Parenteral feeding—nutrients are delivered

directly into a veinSupport to Parents

Allow parents to hold and feed when possible.

Assist to decrease their fears

PERIVENTRICULAR-INTRAVENTRICULARHEMORRHAGE (PIVH)

PERIVENTRICULAR-INTRAVENTRICULARHEMORRHAGE Rupture of fragile blood vessels around the

ventricles of the brain Usually associated with hypoxia

Diagnosed via cranial ultrasound

Signs – lethargy, poor muscle tone, decreased reflexes, seizures, apnea or cyanosis, full or bulging fontanels

Nursing Care – daily measure FOC, observe for changes in LOC

RETINOPATHY OF PREMATURITY

RETINOPATHY OF PREMATURITY Contributing factors:

Formation of immature blood vessels in the retina constrict and become necrotic

Most common in infants < 28 weeks gestation Also associated with O2 therapy

RETINOPATHY OF PREMATURITY Nursing Interventions to Prevent ROP

Administer O2 in concentration ordered Ensure proper ventilatory settings

NECROTIZING ENTEROCOLITIS

NECROTIZING ENTEROCOLITIS NEC - Inflammatory disease of the

intestinal tract caused by ischemia, infection, and/or prematurity of the gut. NEC develops when there is asphyxia or hypoxia in

which cardiac output tends to be directed more toward the heart and brain and away from the abdominal organs.

The intestinal cells become ischemic and damaged and stop secreting protective mucus infection occurs.

Perforation may occur with overwhelming sepsis.

NECROTIZING ENTEROCOLITISSIGNS AND SYMPTOMS Early:

Increase in gastric aspirate - >5-25 ml. Increase in abdominal girth Decrease bowel sounds, abdominal

tenderness or rigidity of abdominal wall. Subtle:

Lethargy, sudden listlessness, temperature instability, decrease urine output, occult blood in stools, poor color, and apneic periods.

Dramatic: Massive abdominal distention, vasomotor

collapse.

NECROTIZING ENTEROCOLITISTREATMENT AND NURSING CARE Surgery: Resection of necrotic sections

and possible temporary colostomy. This allows bowel to recover.

Medical: NPO with NG tube. Peripheral or central hyperalimentation Antibiotic therapy. Continue to monitor for changes in condition. Gradually introduce oral feedings

POST-TERM NEWBORNGREATER THAN 42 WEEKS GESTATION

POST MATURE INFANTo Physical

manifestations: Dry, cracking,

parchment-like skin

Reduced subq tissue – Skin appears loose

No vernix or lanugos Long fingernails Profuse scalp hair Long, thin body appearance Often meconium stained

skin, cord and nails

POST MATURE INFANT Complications of post term:

Hypoglycemia Meconium aspiration Congenital anomalies Seizure activity Cold stress

Nursing considerations Monitor blood sugars per protocol Evaluate respiratory status Assess for seizure activity Treat cold stress.

SMALL FOR GESTATIONAL AGEBELOW THE 10TH PERCENTILE

SGA - RISK FACTORS: Maternal factors:

◦ High blood pressure. ◦ Chronic kidney disease. ◦ Advanced diabetes. ◦ Heart or respiratory disease. ◦ Malnutrition, anemia. ◦ Infection. ◦ Substance use (alcohol, drugs); Cigarette smoking.

Factors involving the uterus and placenta: ◦ Decreased blood flow in the uterus and placenta. ◦ Placental abruption (placenta detaches from the uterus). ◦ Placenta previa (placenta attaches low in the uterus). ◦ Infection in the tissues around the fetus.

Factors related to the developing baby (fetus): ◦ Multiple gestation (twins, triplets, etc.). ◦ Infection. ◦ Birth defects. ◦ Chromosomal abnormality.

COMPLICATIONS OF THE SGA NEWBORN Asphyxia

Aspiration syndrome

Hypothermia

Hypoglycemia

Polycythemia

LARGE FOR GESTATIONAL AGEGREATER THAN 90TH PERCENTILE

What condition is associated with the newborn being LGA?

COMPLICATIONS OF THE LGA NEWBORN Birth Trauma

Increase of Cesarean births

Hypoglycemia

Polycythemia

Hyperviscosity

ASPHYXIA Lack of oxygen and increase of carbon

dioxide in the bloodOccurs in utero or after birth

S/S asphyxia after birth:Cessation of respirations and rapid fall in

heart rate Interventions:

Primary apnea: stimulation and O2Secondary apnea: positive pressure

ventilation &/or chest compressionsNaloxone 0.1mg/kg IM (if narcotics given to

expectant mother shortly before birth)

MECONIUM ASPIRATION SYNDROME

MECONIUM ASPIRATION SYNDROME Meconium stained amniotic fluid

Aspirated into the trachobronchial tree Occurs either in utero or after birth with the first

breaths.

Meconium in the lungs causes air to become trapped and results in alveoli over-distension and rupture.

MECONIUM ASPIRATION SYNDROME Measures for Prevention of Meconium Aspiration

After delivery of the infant’s head but before shoulders Suction oropharynx and nasopharynx (no longer

recommended)

After delivery of the infant’s body

Crying Not crying

- Stimulate - Do not stimulate- Suction with - Visualize the vocal cords and bulb syringe provide direct suction with

endotracheal tube, then stimulate.

MECONIUM ASPIRATION SYNDROMEIntubation Suction

MECONIUM ASPIRATION SYNDROME Nursing Interventions:

Maintain adequate oxygenation and ventilation Regulate temperature Accurate IV fluid administration Assess for hypoglycemia Administer antibiotics Provide caloric requirements Provide support care if on ECMO

Nursing Interventions: Maintain adequate oxygenation and ventilation Regulate temperature Accurate IV fluid administration Assess for hypoglycemia Administer antibiotics Prevent caloric requirements Provide support care if on ECMO

MECONIUM ASPIRATION SYNDROME

HYPERBILIRUBINEMIA

HYPERBILIRUBINEMIA Pathophysiology

Bilirubin is released in serum when RBC lyse Conjugation in liver = water soluble & excretable Rate & amount of conjugation dependent upon:

Rate of hemolysis Bilirubin load Maturity of liver Presence of albumin-binding sites

Hyperbilirubinemia occurs when the body cannot conjugate the bilirubin released into the serum.

Results in jaundice where the unconjucated bilirubin is deposited in the tissue.

HYPERBILIRUBINEMIA Pathophysiology

Unconjugated bilirubin is produced by the break-down destroyed RBC’s.

Unconjugated bilirubin is normally transferred in the plasma firmly bound to albumin to the liver where conjugation occurs.

Conjugated bilirubin is water soluble and can then be excreted into the bile and eliminated with the feces.

Unconjugated bilirubin is not in excretable form and remains in the circulation causing problems.

Hyperbilirubinemia occurs when the body cannot conjugate the bilirubin released into the serum.

CAUSES OF HYPERBILIRUBINEMIA Hemolytic disease (Rh and ABO

incompatibility) Extravascular bleed (cephalhematoma) Bilirubin conjugation defects (breastmilk

jaundice, asphyxia) Hypoalbumin Physiologic jaundice (occurs after the

first 24 hours of birth. Mainly due to immature liver and lack of glucoronyl transferase).

HYPERBILIRUBINEMIA Hemolytic Disease (Pathologic

Hyperbilirubinemia) Results from incompatibility between mother’s

blood type or Rh factor and that of the fetus Maternal antibodies develop from + fetal antigen Antibodies cross placental into fetal circulation Antibodies attach to and destroy fetal RBCs. Fetal RBCs lyse & release bilirubin into fetal

circulation

HYPERBILIRUBINEMIA Clinical Manifestations:

Sclerae appearing yellow before skin appears yellow – usually in the first 24 hours after delivery

Skin appearing light to bright yellow – advances from head to toe

Lethargy Dark, amber concentrated urine Poor feeding Dark stools

HYPERBILIRUBINEMIA Diagnosis:

Bilirubin levels on Cord BloodAverage level of unconjugated bilirubin is 2 mg/dl at birth

Bilirubin levels should NOT exceed 5 mg/dl

Coombs Test may be done on the fetal cord blood (direct Coombs test) or on the maternal blood (indirect Coombs test).

Detects the presence of maternal antibodies attached on the infant’s red blood cells.

The test is positive if there are maternal antibodies.

HYPERBILIRUBINEMIA NURSING CARE Careful observation of infant for signs of

increased jaundice Careful observation for and prevention

of acidosis/hypoxia and hypoglycemia, which decrease binding of bilirubin to albumin and contribute to jaundice.

Maintain adequate hydration Avoid cold stress Phototherapy – use of “bili” lights,

special fluorescent Exchange Transfusion

Nursing Interventions for PhototherapyExposure of skin to UV lights

Reposition q 2 hrRemove from lights only for feedings

Cover eyes (remove for feeding/parent visit)

Monitor temperatureMonitor hydration status

Increase fluidsAssess for dehydrationPerform T-Bili q 12 – 24 hr as ordered

HYPERBILIRUBINEMIA

Exchange Transfusion Treat anemia Remove sensitized RBCs that will soon lyse Remove serum bilirubin Provides albumin to increase bilirubin binding

sites

HYPERBILIRUBINEMIA

Rhogam – Given to postpartum woman Provides temporary passive immunity which

prevents permanent active immunity (antibody formation)

Given within 72 hours of delivery Prevents production of maternal antibodies

HYPERBILIRUBINEMIA

ABO incompatibility Occurs when type O pregnant woman with A, B

or AB blood type fetus If woman has anti A or anti B antibodies, these

antibodies cross the placental barrier Results in hemolysis of fetal RBCs

HYPERBILIRUBINEMIA

Complications of Hemolytic Disease Kernicterus – Deposits of conjugated and

unconjugated bilirubin in the basal ganglia of the brain Neurologic damage

Hydrops fetalis – severe anemia Marked edema Cardiac decompensation Multiple organ failure Possible death

HYPERBILIRUBINEMIA

TORCH INFECTIONS

INFECTIOUS DISEASES: TORCH Toxoplasmosis Other

Syphillis Hepititis B

Rubella Cytomegalovirus Herpes Simplex II HIV -AIDs

TOXOPLASMOSIS Protozoan infection in the pregnant woman

Raw or under cooked meats Cat feces

Transmission: Transplacental Affects on the fetus

Blindness Deafness Convulsions Microcephaly Hydrocephaly Severe mental impairment

OTHER - SYPHILLIS Transmission: Transplacental Clinical Manifestations:

S/S of Newborn: Rhinitis Excoriated upper lip Red rash around mouth and anus Copper colored rash of face, palms and soles Irritability Edema Cataracts.

Treatment: Culture orifices Isolation Penicillin

OTHER – Hepatitis B Transmission

Placental Birth Breast milk

Treatment If mother + HbSAG administer to newborn

Hepitisis B vaccine HBIG (Administer within 12 hrs of birth)

Transmission: transplacental S/S of Newborn

Congenital cataracts Deafness Congenital heart defects Sometimes fatal Intellectual disability(Affects are greatest if infected in 1st trimester)

MMR Immunization of motherGive when not pregnant – usually in immediate

postpartum period. Newborns are infectious:

CONTACT ISOLATION

RUBELLA

CYTOMEGALOVIRUS –(HERPATIC VIRUS) Transmission

Crosses placental barrier Direct contact at birth Breast milk

S/S of Newborn Severe neurological problems Eye abnormalities Hearing loss Microcephaly Hydrocephaly Cerebral palsy Mental delays

HERPES SIMPLEX II Transmission:

Direct contact at birth S/S of Newborn

Microcephaly Mental delays Seizures Retinal dysplasia Apnea Coma

Contact Isolation – Culture vesicles Treatment: Antivial Drugs

Transmission:TransplacentallyExposure at birthBreast milk

Diagnosis:Serology tests are performed within 48

hours of birth; repeated at 3 and 6 monthsHIV antibodyELISACD4 + T-cell

HIV/AIDS

HIV infected (two or more positive tests for HIV)

Perinatally exposed (born to a mother know to be infected with HIV)

Seroconverter (born to a mother known to be infected with HIV but has had two negative HIV tests

HIV/ AIDSDIAGNOSIS:

Nursing Interventions HIV infected mothers should be identified and

begin treatment with AZT during pregnancy and in labor

All infants born to an infected mother should be treated prophylactically◦ 6 weeks of AZT orally after birth◦ Bactrim and Septra

Provide care like that of any other newborn Protect against opportunistic infections

HIV / AIDS

INFANTS OF DIABETIC MOTHERS

What causes the

Excessive fetal growth?

INFANTS OF DIABETIC MOTHERS Clinical manifestations IDM

Hypoglycemia Hypocalcemia Polycythemia Macrosomic Excessive adipose tissue RDS

Increase risk of birth injuries.

INFANTS OF DIABETIC MOTHERS Why Hypoglycemia?

High levels of glucose cross the placenta In response, fetus produces high levels of insulin High levels of insulin production continues after

cord cut Depletes the infant’s blood glucose

Clinical Manifestations:Large size – Macrosomia; enlarged spleen, heart,

liverTremorsCyanosisApneaTemperature instabilityPoor sucking and feedingHypotonic muscle tone / Lethargy

Nursing Interventions Assess blood glucose

Intervene if < 45mg/dl: Feed infant

Revaluate blood sugar 30-45 minutes pc If no improvement: IV of D10W

INFANTS OF DIABETIC MOTHERS

NEWBORN OF SUBSTANCE ABUSE MOTHER

FETAL ALCOHOL SYNDROME - FAS

FETAL ALCOHOL SYNDROME - FAS Clinical Manifestations:

Jitteriness Abdominal distention Exaggerated rooting and sucking reflexes

Affected body systems: CNS

GI system

Long-term psychosocial implications: Feeding difficulties Mental retardation

Central Nervous Systemo IRRITABILITY

• Hyperactivity• Shrill cry• Exaggerated reflexes• Facial scratches• Short non-quiet sleep

Sneezing, coughing, yawning Gastroinestional System

o Poor feedingo Disorganized vigorous sucko Vomiting and/or Diarrhea

Vasomotor and Cutaneous Signso Tachypneao Sweatingo Excoriated skin

INFANTS OF ADDICTED MOTHERSCLINICAL MANIFESTATIONS OF INFANT WITHDRAWAL

INFANTS OF ADDICTED MOTHERS Nursing Interventions for Infant Withdrawal:

Swaddle with hands near mouth Offer pacifier Place in quiet dimly lit area of the nursery Protect skin from excoriation Monitor V/S Provide small frequent feedings Position with HOB elevated Weigh every 8 hours (if vomiting & diarrhea) Assess with Finnegan Abstinence Scale Administer morphine, phenobarbitol, methadone

AFFECTS OF SMOKING ON THE FETUS DURING PREGNANCY

Nicotine Causes vasoconstriction Reduces placental blood circulation

Carbon Monoxide Inactivates fetal and maternal hemaglobin

Reduced amount of oxygen to fetus results in prematurity or low birth weight

THE END !