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HIGH RISK NEONATES
Presented by Ann Hearn RNC, MSN
CLASSIFICATION OF HIGH RISK NEWBORNS
 Gestational Age
 Preterm
 (Late Preterm)
 Term
 Postterm
 Gestational Age & Birth
Weight
 SGA
 AGA
 LGA
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
 Respiratory and Cardiac
 Thermoregulation
 Digestive
 Renal
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
 Respiratory and Cardiac
 Lack of surfactant
 Pulmonary blood vessels
 Ductus arteriosus
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
 Respiratory - Nursing Interventions
 Maintain airway
 Administer O2
 Monitor O2 saturation
 Monitor heart/respiratory rates
 S/S respiratory distress
 Cyanosis
 Tachicardia
 Retractions
 Expiratory grunting
 Nasal flaring
 Apnic episodes
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
 Thermoregulation
 Increased body surface
 Decreased brown fat
 Thin Skin
 Lack of flexion
 Decrease sub-q fat
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
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
 Digestive
 Poor gag reflex
 Small stomach capacity
 Relaxed cardiac sphincter
 Poor suck and swallow reflex
 Difficult fat, protein and lactose digestion
 Absorption
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
 Nutrition and Hydration – Nursing Interventions
 Daily weights
 Monitor I&O
 Accurate IV rates
 Accurate OGT feedings
 Monitor urine pH and specific gravity
 Signs of dehydration
 Weight loss
 Poor skin turgor
 Dry oral mucus membranes
 Decreased urinary output
 Increased specific gravity
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
 Pre-feeding assessment
 Measure abdominal girth
 Bowel sounds
 Gastric residual
 Sucking and gag reflexes
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
 Renal
 Decreased glomerular filtration rate
 Inability to concentrate urine or excrete excess
 Decreased ability of kidneys to buffer
 Decreased drug excretion time
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
PHYSIOLOGIC CHALLENGES OF THE
PREMATURE INFANT
 Facilitating Parent-Infant Attachment
 Prepare parents for first visit
 Establish safe/trusting environment
 Encourage visitation
 Involved in care taking
 Repeat explanations
 Promote touching, talking, rocking, cuddling
 Refer to infant by name
 Allow parents to phone as desired
DISORDERS OF INFANTS IN NICU
 SGA and IUGR
 Infants of Diabetic Mothers
 Postmature Infant
 Infants of Addicted Mothers
 Respiratory Distress Syndrome
 Meconium Aspiration Syndrome
 Hyperbilirubinemia
 Retinopathy of Prematurity
 Necrotizing Entercolitis
 Infectious Diseases - TORCH
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.
INFANTS OF DIABETIC MOTHERS
INFANTS OF DIABETIC MOTHERS
 Clinical manifestations IDM
 Ruddy color
 Macrosomia
 Excessive adipose tissue
 Hypoglycemia
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
INFANTS OF DIABETIC MOTHERS
 Nursing Interventions for Hypoglycemia
 Assess for signs/symptoms
 Tremors
 Cyanosis
 Apnea
 Temperature instability
 Poor feeding
 Hypertonia / Lethargy
 Assess blood glucose
 Intervene if < 40mg/dl:
 Feed infant
 If no improvement:
 IV of D10W
POST MATURE INFANT
 Post term: infant born after __?__ wks
 Physical manifestations:
 Dry, cracking, parchment-like skin
 Loose appearing skin
 No vernix or lanugo
 Long fingernails
 Profuse scalp hair
 Long, thin body appearance
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.
INFANTS OF ADDICTED MOTHERS
 Clinical Manifestations of Infant Withdrawal:
 IRRITABILITY
 Hyperactivity
 Shrill cry
 Exaggerated reflexes
 Facial scratches
 Short non-quiet sleep
 Sneezing, coughing, yawning
 Poor feeding
 Disorganized vigorous suck
 Vomiting
 Diarrhea
 Tachypnea
 Sweating
 Excoriated skin
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
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
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 - RDS
 Nursing Care Plan
 Page 826-828
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)
 If THICK meconium, 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.
 If THIN meconium, no visualization performed.
MECONIUM ASPIRATION SYNDROME
Intubation 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
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
 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
 Additional assessments:
 Maternal, paternal, and fetal blood type and Rh factor
 Newborn
 Skin color, sclera, oral mucosa
 Hypotonia, diminished reflexes, lethary and seizures
HYPERBILIRUBINEMIA
 Positive Coombs Test
 Direct coombs test reveals antibody-coated Rh positive
RBCs in the newborn
 Nursing Interventions for Phototherapy
 Exposure of skin
 Cover eyes (remove for feeding/parent visit)
 Monitor temperature
 Increase fluids
 Assess for dehydration
 Perform 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
 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
RETINOPATHY OF PREMATURITY
 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
 NEC - Inflammatory disease of the intestinal tract
caused by ischemia, infection, and/or prematurity of
the gut.
 Preterm infant at increased risk
 undeveloped protective intestinal mucin layer
 slow careful introduction to oral feedings
 Early detection:
 Measure abdominal girth daily
 Assess color of abdomen
 Assess residual feeding
 Assess bowel sounds
 Assess S/S sepsis
INFECTIOUS DISEASES: TORCH
 Toxoplasmosis
 Other
 Syphillis
 Hepititis B
 Rubella
 Cytomegalovirus
 Herpes Simplex II
 HIV
TOXOPLASMOSIS
 Protozoan infection in the pregnant woman
 Raw or under cooked meats
 Cat feces
 Affects on the fetus
 Blindness
 Deafness
 Convulsions
 Microcephaly
 Hydrocephaly
 Severe mental impairment
OTHER
 Syphilis
 Hepatitis B
OTHER
 Syphillis
 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
RUBELLA
 S/S of Newborn
 Congenital cataracts
 Deafness
 Congenital heart defects
 Sometimes fatal
 MMR Immunization of mother
 Give when not pregnant
CYTOMEGALOVIRUS
 Herpatic virus
 Crosses placental barrier
 Direct contact at birth
 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
HIV/AIDS
 Transmission: < 2%
 Transplacentally
 Exposure at birth
 Breast milk
 Nursing Interventions
 Protect self from body fluids
 Labs - + antibody titer
 Administer AZT
 Provide care like that of any other newborn

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HighRisk Neonates for undergraduates.pptx

  • 1. HIGH RISK NEONATES Presented by Ann Hearn RNC, MSN
  • 2. CLASSIFICATION OF HIGH RISK NEWBORNS  Gestational Age  Preterm  (Late Preterm)  Term  Postterm  Gestational Age & Birth Weight  SGA  AGA  LGA
  • 3. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT
  • 4. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT  Respiratory and Cardiac  Thermoregulation  Digestive  Renal
  • 5. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT  Respiratory and Cardiac  Lack of surfactant  Pulmonary blood vessels  Ductus arteriosus
  • 6.
  • 7. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT  Respiratory - Nursing Interventions  Maintain airway  Administer O2  Monitor O2 saturation  Monitor heart/respiratory rates  S/S respiratory distress  Cyanosis  Tachicardia  Retractions  Expiratory grunting  Nasal flaring  Apnic episodes
  • 8. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT  Thermoregulation  Increased body surface  Decreased brown fat  Thin Skin  Lack of flexion  Decrease sub-q fat
  • 9. 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
  • 11. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT  Digestive  Poor gag reflex  Small stomach capacity  Relaxed cardiac sphincter  Poor suck and swallow reflex  Difficult fat, protein and lactose digestion  Absorption
  • 12. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT  Nutrition and Hydration – Nursing Interventions  Daily weights  Monitor I&O  Accurate IV rates  Accurate OGT feedings  Monitor urine pH and specific gravity  Signs of dehydration  Weight loss  Poor skin turgor  Dry oral mucus membranes  Decreased urinary output  Increased specific gravity
  • 13. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT  Pre-feeding assessment  Measure abdominal girth  Bowel sounds  Gastric residual  Sucking and gag reflexes
  • 14. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT  Renal  Decreased glomerular filtration rate  Inability to concentrate urine or excrete excess  Decreased ability of kidneys to buffer  Decreased drug excretion time
  • 15. 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
  • 16. 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
  • 17. PHYSIOLOGIC CHALLENGES OF THE PREMATURE INFANT  Facilitating Parent-Infant Attachment  Prepare parents for first visit  Establish safe/trusting environment  Encourage visitation  Involved in care taking  Repeat explanations  Promote touching, talking, rocking, cuddling  Refer to infant by name  Allow parents to phone as desired
  • 18.
  • 19. DISORDERS OF INFANTS IN NICU  SGA and IUGR  Infants of Diabetic Mothers  Postmature Infant  Infants of Addicted Mothers  Respiratory Distress Syndrome  Meconium Aspiration Syndrome  Hyperbilirubinemia  Retinopathy of Prematurity  Necrotizing Entercolitis  Infectious Diseases - TORCH
  • 20. 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.
  • 22. INFANTS OF DIABETIC MOTHERS  Clinical manifestations IDM  Ruddy color  Macrosomia  Excessive adipose tissue  Hypoglycemia Increase risk of birth injuries.
  • 23. 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
  • 24. INFANTS OF DIABETIC MOTHERS  Nursing Interventions for Hypoglycemia  Assess for signs/symptoms  Tremors  Cyanosis  Apnea  Temperature instability  Poor feeding  Hypertonia / Lethargy  Assess blood glucose  Intervene if < 40mg/dl:  Feed infant  If no improvement:  IV of D10W
  • 25. POST MATURE INFANT  Post term: infant born after __?__ wks  Physical manifestations:  Dry, cracking, parchment-like skin  Loose appearing skin  No vernix or lanugo  Long fingernails  Profuse scalp hair  Long, thin body appearance
  • 26. 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.
  • 27. INFANTS OF ADDICTED MOTHERS  Clinical Manifestations of Infant Withdrawal:  IRRITABILITY  Hyperactivity  Shrill cry  Exaggerated reflexes  Facial scratches  Short non-quiet sleep  Sneezing, coughing, yawning  Poor feeding  Disorganized vigorous suck  Vomiting  Diarrhea  Tachypnea  Sweating  Excoriated skin
  • 28. 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
  • 30. 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
  • 31. 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
  • 32. RESPIRATORY DISTRESS SYNDROME - RDS  Nursing Care Plan  Page 826-828
  • 33. 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.
  • 34. 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)  If THICK meconium, 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.  If THIN meconium, no visualization performed.
  • 36. 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
  • 37. 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.
  • 38. 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
  • 39.
  • 40. HYPERBILIRUBINEMIA  Additional assessments:  Maternal, paternal, and fetal blood type and Rh factor  Newborn  Skin color, sclera, oral mucosa  Hypotonia, diminished reflexes, lethary and seizures
  • 41. HYPERBILIRUBINEMIA  Positive Coombs Test  Direct coombs test reveals antibody-coated Rh positive RBCs in the newborn
  • 42.  Nursing Interventions for Phototherapy  Exposure of skin  Cover eyes (remove for feeding/parent visit)  Monitor temperature  Increase fluids  Assess for dehydration  Perform T-Bili q 12 – 24 hr as ordered HYPERBILIRUBINEMIA
  • 43.  Exchange Transfusion  Treat anemia  Remove sensitized RBCs that will soon lyse  Remove serum bilirubin  Provides albumin to increase bilirubin binding sites HYPERBILIRUBINEMIA
  • 44.  Rhogam  Provides temporary passive immunity which prevents permanent active immunity (antibody formation)  Given within 72 hours of delivery  Prevents production of maternal antibodies HYPERBILIRUBINEMIA
  • 45.  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
  • 46.  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
  • 47. RETINOPATHY OF PREMATURITY  Formation of immature blood vessels in the retina constrict and become necrotic  Most common in infants < 28 weeks gestation  Also associated with O2 therapy
  • 48. RETINOPATHY OF PREMATURITY  Nursing Interventions to Prevent ROP  Administer O2 in concentration ordered  Ensure proper ventilatory settings
  • 49. NECROTIZING ENTEROCOLITIS  NEC - Inflammatory disease of the intestinal tract caused by ischemia, infection, and/or prematurity of the gut.  Preterm infant at increased risk  undeveloped protective intestinal mucin layer  slow careful introduction to oral feedings  Early detection:  Measure abdominal girth daily  Assess color of abdomen  Assess residual feeding  Assess bowel sounds  Assess S/S sepsis
  • 50. INFECTIOUS DISEASES: TORCH  Toxoplasmosis  Other  Syphillis  Hepititis B  Rubella  Cytomegalovirus  Herpes Simplex II  HIV
  • 51. TOXOPLASMOSIS  Protozoan infection in the pregnant woman  Raw or under cooked meats  Cat feces  Affects on the fetus  Blindness  Deafness  Convulsions  Microcephaly  Hydrocephaly  Severe mental impairment
  • 53. OTHER  Syphillis  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
  • 54. OTHER  Hepatitis B  Transmission  Placental  Birth  Breast milk  Treatment  If mother + HbSAG administer to newborn  Hepitisis B vaccine  HBIG
  • 55. RUBELLA  S/S of Newborn  Congenital cataracts  Deafness  Congenital heart defects  Sometimes fatal  MMR Immunization of mother  Give when not pregnant
  • 56. CYTOMEGALOVIRUS  Herpatic virus  Crosses placental barrier  Direct contact at birth  S/S of Newborn  Severe neurological problems  Eye abnormalities  Hearing loss  Microcephaly  Hydrocephaly  Cerebral palsy  Mental delays
  • 57. HERPES SIMPLEX II  Transmission:  Direct contact at birth  S/S of Newborn  Microcephaly  Mental delays  Seizures  Retinal dysplasia  Apnea  Coma
  • 58. HIV/AIDS  Transmission: < 2%  Transplacentally  Exposure at birth  Breast milk  Nursing Interventions  Protect self from body fluids  Labs - + antibody titer  Administer AZT  Provide care like that of any other newborn

Editor's Notes

  1. Preterm < 37 wks SGA – below 10th percentile Late preterm 34.0 – 36.6 wks AGA – Between 10th & 90th percentile Term 37-42 wks LGA - > 90th percentile Post term >42 wks IUGR – pregnancy circumstances that contribute to growth restriction. May be maternal, placental or fetal. Gestational age and birth weight are criteria used to measure neonatal maturity and mortality risks. As weight and gestation increase, neonatal mortality risks decrease.