This document provides an overview of neonatal respiratory care training. It covers topics like primary team roles and responsibilities, neonatal disorders/conditions like transient tachypnea of the newborn and respiratory distress syndrome, changes to the NICU respiratory therapy department effective July 1st, and procedures like surfactant administration and meconium suctioning. Key expectations and next steps in training are also outlined.

1. SCN TRAINING, PHASE 1
• PRIMARY TEAM ROLES & RESPONSIBILITES
• REPORT SHEET
• EXPECTATIONS
• NEONATAL DISORDERS/
CONDITIONS
• NEXT STEPS

2. JULY 1ST CHANGES IN NICU RT
• 7/1- GOAL IS TO HAVE DEDICATED THERAPIST
WHO IS A PRIMARY TEAM MEMBER
• ALL BACKUP STAFF HAVE BASIC KNOWLEDGE AND
COMPETENCY
• THE NICU THERAPIST WILL HELP IN THE MAIN
HOSPITAL IF NO BABIES ARE IN NEED
• THIS THERAPIST WILL NOT TAKE CARE OF PATIENTS IN
ISOLATION
• THEY WILL START THEIR SHIFT IN NICU, GIVE
REPORT IN NICU AND BE AVAILABLE FOR ANY
DELIVERY NNP IS CALLED TO, AND ANY NICU
BABY ON O2.

3. JULY 1ST CHANGES
• THE NICU THERAPIST WILL BE RESPONSIBLE
FOR MAINTAINING THE AIRWAY BOXES WITH
PROPER AND AVAILABLE EQUIPMENT
• TIME AND TASKS WILL CONTINUE TO BE
LOGGED FOR NOW

4. FETAL TRANSISTION PROCESS
• The transition from a fetus to a newborn is the most
complex adaptation that occurs in human experience.
• Lung adaptation requires the coordinated clearance of
fetal lung fluid, surfactant secretion, and the onset of
consistent breathing. With the removal of the low-
pressure placenta, the cardiovascular response requires
striking changes in blood flow, pressures and pulmonary
vasodilation. The newborn must also quickly control its
energy metabolism and thermoregulation.
• Abnormalities in adaptation are frequently found following
preterm birth or delivery by cesarean section at term, and
many of these infants will need delivery room resuscitation
to assist in this transition

6. EXTRAUTERINE TRANSITION
• At birth, the clamping of the umbilical
cord eliminates the placenta as a
reservoir for blood, triggering an
increase in systemic vascular resistance
(SVR), an increase in blood pressure,
and increased pressures in the left side
of the heart.

7. DELAYED CORD CLAMPING
• DELAYING THE CORD CLAMPING AT DELIVERY
ALLOWS BABY TO RETAIN A GREATER
AMOUNT OF THE FETAL BLOOD VOLUME.
– COMMON PRACTICE IS 30 SECONDS
• POSSIBLE COMPICATIONS
– INCREASED INCIDINCE OF HYPERBILIRUBINEMIA
THIS IS NOT USUALLY DONE IN EARLY PRETERMS
OR BABIES EXPERIENCING DISTRESS AT
DELIVERY

8. EXRTAUTERINE TRANSITION
• Umbilical cord clamping decreases O2 concentration,
increases CO2 concentration, and decreases the blood
pH. This stimulates the fetal respiratory center in the
medulla to initiate respiration.
• Mechanical compression of the chest during the
vaginal birth forces approximately 1/3 of the fluid out
of the fetal lungs. As the chest is delivered, it re-
expands, generating a negative pressure and drawing
air into the lungs. Passive inspiration of air replaces
fluid. As the infant cries, a positive intrathoracic
pressure is established which keeps the alveoli open,
forcing the remaining fetal lung fluid out.

10. TERM NEWBORN DELIVERY
• WHAT DOES A NEONATE LOOK LIKE AT BIRTH WHEN
NOT DISTRESSED

11. PRETERM DELIVERY
WHAT ARE THE INDICATIONS A NEONATE
REQUIRES PPV?
– HR LESS THAN 100
– INEFFECTIVE RESPIRATIONS- APNEA, GASPING
HOW CAN WE PROVIDE PPV?
T PIECE RESUSCITATOR ( NEOPUFF)
FLOW INFLATING BAG
SELF INFLATING BAG
STARTING PRESSURES= 20/5

12. RESPIRATORY DISTRESS
• WHAT DOES IT LOOK LIKE IN A NEONATE
–GASPING
–NASAL FLARING
–RETRACTIONS
–GRUNTING
–APNEA

13. RESPIRATORY DISTRESS
• RDS SUBCOSTAL RETRACTIONS

14. RECOGNIZING RESPIRATORY DISTRESS

15. GRUNTING

16. RESPIRATORY DISTRESS
• DEPENDING ON SEVERITY, WE CAN TREAT THIS
WITH
– LOW FLOW NC
– HHFNC
– RAM CANNULA
– CPAP
– MECHANICAL VENTILATION
TREAT UNDERLYING CAUSES OF THE RESP
DISTRESS

17. SPO2 MONITORING
• NEONATAL SATS ARE MEASURED IN 2 WAYS
– PRE DUCTAL
– POST DUCTAL
THE DIFFERENCE BETWEEN PRE AND POST
DUCTAL SATS CAN REFLECT THE DEGREE OF
RIGHT TO LEFT SHUNTING

18. SPO2 MONITORING
• PRE DUCTAL SATS ARE TAKEN ON THE RIGHT
WRIST OR HAND
• REFLECTS THE BLOOD STATE BEFORE THE DUCTUS
ARTERIOSUS & BEFORE IT MIXES WITH
DEOXYGENATED BLOOD
• POST DUCTAL SATS ARE TAKEN ON THE LEFT ARM
AND LOWER EXTREMITIES
– TAKEN AFTER THE DUCTUS ARERIOSUS WHEN BLOOD
HAS BEEN MIXED, DEOXYGENATED FROM THE
PULMONARY CIRCULATION

20. NEONATAL ABNORMALITIES AND
CONDITIONS
• TTN- RDS TYPE 2
• RDS- TYPE 1
• MECONIUM/ MECONIUM ASPIRATION
SYNDROME
• CHD
• PPHN
• BPD

21. TRANSIENT TACHYPNEA OF THE
NEWBORN
• TTN- RDS TYPE 2
• GENERALLY TERM OR NEAR TERM INFANTS
• OCCURANCE: ABOUT 5 OUT OF 1000
• MOST COMMON IN 37-42 WEEK INFANTS
• MOST COMMON AFTER ELECTIVE C SECTION
WITHOUT LABOR
– IN BABIES WHO DON’T GET THE THORACIC
SQUEEZE THROUGH NORMAL VAGINAL BIRTH

22. TRANSIENT TACHYPNEA OF THE
NEWBORN
• KNOWN RISK FACTORS
– MOM WITH ASHTMA
– MALE GENDER
– MACROSOMIA
– MULTIPLES
– GESTATIONAL DIABETES IN MOM
– PROLONGED LABOR
– PERINATAL ASPHYXIA
– FLUID OVERLOADED MOM

23. TRANSIENT TACHYPNEA OF THE
NEWBORN
• CLINICAL PRESENTATION– FIRST FEW HOURS
AFTER BIRTH
– TACHYPNEA( UP TO 100-120 BPM )
– CYANOSIS
– BARREL CHEST ( HYPERINFLATION)
• CHEST X RAY
– PULMONARY VASCULAR CONGESTION
– PERIHILAR STREAKING
– HYPEREXPANSION/ FLAT DIAPHRAGM
– FLUID IN FISSURES

24. TRANSIENT TACHYPNEA OF THE
NEWBORN
• TREATMENT
– SUPPORTIVE
• MAINTAIN ADEQUATE OXYGENATION AND
VENTILATION
• CPAP FOR DISTRESS
• NEUTRAL THERMAL ENVIRONMENT
THE RESPIRATORY DISTRESS, HYPOXEMIA, MILD
RESPIRATORY ACIDOSIS USUALLY RESOLVES
WITHIN 48 HOURS
COMPLICATIONS FROM JUST TTN ARE RARE

25. TRANSIENT TACHYPNEA OF THE
NEWBORN
• TTN IS A CLINICAL DIAGNOSIS OF EXCLUSION
• IT CAN LOOK LIKE OTHER CONDITIONS
– RDS
– SEPSIS
– PNEUMONIA
– PPHN

26. TTNB

27. RESPIRATORY DISTRESS SYNDROME
• HMD
– HYALINE MEMBRANE DISEASE
• SDD
– SURFACTANT DEFECIENCY DISORDER
• MOST COMMONLY OCCURING IN PRETERM
INFANTS, LESS THAN 35 WEEKS GESTATION

28. RESPIRATORY DISTRESS SYNDROME
• SURFACTANT THERAPY
– VERY EFFECTIVE
• PROPHYLACTIC TREATMENT
WITHIN 15-30 MINUTES OF BIRTH
RESCUE TREATMENT
GIVEN WITH CLINICAL EVIDENCE OF RDS
MOST COMMONLY GIVEN AS A BOLUS VIA
ETT

29. SURFACTANT ADMINISTRATION

30. SURFACTANT REPLACEMENT
• IN OUR FACILITY, SURFACTANT IS A RESCUE
THERAPY, NOT PROPHYLACTIC
• WE USE CUROSURF, 4 DOSES ARE KEPT IN THE
PYXIS
DOSE IS 2.5 MG/KG INITIAL
1.25 MG/KG SUBSEQUENT

31. CUROSURF
Before use, the vial should be slowly warmed
to room temperature and gently turned upside
down, in order to obtain a uniform suspension
Visually inspect suspension for discoloration
prior to administration. Suspension should be
white to creamy white. Discard if suspension is
discolored
DO NOT SHAKE

32. MECOMIUM
• MAS- MECONIUM ASPIRATION SYNDROME
– AFFECTS 5% OF INFANTS BORN IN MECONIUM
STAINED FLUID
• MECONIUM ASPIRATION
– INHALATION OF FETAL FECAL DISCHARGE INTO
THE FETAL LUNGS IN UETERO
• OFTEN ASSOCIATED WITH POST TERM BABIES
» RARELY BEFORE 34 WEEKS
• SIGN OF FETAL DISTRESS

33. MECOMIUM
• IN THE PAST, MECOMIUM WAS ALWAYS
SUCTIONED BY INTUBATING BABY AND THEN
SUCTIONING THE AIRWAY WHILE
EXTUBATING. THIS IS NO LONGER THE
RECOMMENDED/ COMMON PRACTICE

34. MECONIUM
• TODAY, CURRENT PRACTICE STATES THAT
ATTEMPTS TO SUCTION MECONIUM FROM
THE PHARYNX OR TRACHEA BEFORE, DURING
OR AFTER BIRTH CAN INCREASE THE
LIKLIEHOOD OF SEVERE ASPIRATION
PNEUMONIA
– NO INTRAPARTUM SUCTIONING
– INFANTS THAT ARE VIGOROUS AT BIRTH SHOULD
NOT BE TRACHEALLY SUCTIONED

35. MECONIUM
– INFANTS THAT ARE NOT VIGOROUS MAY NEED
DIRECT LAYRNGEAL SUCTIONING
– HR LESS THAN 100
– NO OR POOR RESPIRATORY EFFORT
– POOR TONE
• CLEARING THE AIRWAY AT DELIVERY:
– AIRWAY OBSTRUCTION SHOULD BE SUSPECTED IF
BABY RESPIRATORY EFFORTS ARE NOT EFFECTIVE.
– IMMEDIATELY POSITION HEAD
– SUCTION BULB OR CATHETER MOUTH FIRST, THEN NOSE

36. MECONIUM
• MECONIUM ASPIRATOR

37. CONGENITAL HEART DEFECTS
• DURING FETAL DEVELOPMENT, GAS EXCHANGE TAKES
PLACE THROUGH THE PLACENTA ( THE LUNGS ARE
FLUID FILLED & HAVE HIGH RESISTANCE)
– THE SYSTEMIC CIRCULATION INCLUDES THE PLACENTA &
HAS LOW RESISTANCE
• THE PDA ( PATENT DUCTUS ARTERIOSUS) CONNECTS
THE PULMONARY AND SYSTEMIC CIRCULATION.
• MOST BLOOD PASSING INTO THE PA SHUNTS FROM PA
INTO DESCENDING AORTA
• 90% OF BLOOD BYPASSES THE LUNGS, ONLY ABOUT
10% OF NORMAL BLOOD FLOW IS DELIVERED TO THE
LUNGS TO PROVIDE NOURISHMENT FOR GROWTH

38. CHD
• DURING THE FIRST BREATH:
– MOST AIR SPACES FILL WITH AIR
• THIS REDUCES PVR DRASTICALLY
» ALSO CONTINUES TO OCCUR OVER THE FIRST FEW DAYS
– INCREASES IN PaO2 LEAD TO DECREASES IN PVR
AND CLOSURE OF THE PDA
» REDUCED RIGHT VENTRICULAR PRESSURE & INCREASED
PULMONARY BLOOD FLOW

39. CHD
• IN NORMAL TERM KIDS, THE PDA USUALLY
CLOSES 24 TO 48 HOURS AFTER BIRTH
• MANY FACTORS CAN LEAD TO DELAYED
CLOSURE AND THERE ARE CASES WHERE WE
WOULD WORK TO KEEP THE DUCTUS
ARTERIOSUS PATENT ON PURPOSE

40. CHD
• CONGENTIAL HEART ANOMOLIES CAN BE
CLASSIFIED AS EITHER CYANOTIC OR
ACYANOTIC
CYANOTIC—THESE CAUSE A DECREASE IN
SYSTEMIC OXYGENATION
ACYANOTIC– THESE DO NOT CAUSE A
DECREASE IN SYSTEMIC OXYGENATION

41. CHD
• CYANOTIC CONDITIONS
– TETROLOGY OF FALLOT
– AORTIC STENOSIS
– COARCTATION OF THE AORTA
– TRANSPOSITION OF THE GREAT VESSELS
– PERSISTENT TRUNCUS ARTERIOSIS
– TOTAL ANOMOLOUS PULMONARY VENOUS
RETURN

42. CHD
• ACYANOTIC CONDITIONS
– VSD -VENTRICULAR SEPTAL DEFECT
– ASD -ATRIAL SEPTAL DEFECT
– PDA- PATENT DUCTUS ARTERIOSUS
– AORTIC COARCTATION
– HYPOPLASTIC LEFT HEART SYNDROME

43. CHD
FOR OUR PURPOSES AND PATIENT POPULATION:
WE NEED TO BE ABLE TO RECOGNIZE THE SIGNS
AND SYMPTOMS OF THE COMMON CARDIAC
ANOMOLIES. THE FOLLOWING THINGS MIGHT
TRIGGER FUTHER INVESTIGATION

44. CHD
FINDINGS THAT MIGHT SUGGEST CARDIAC
ANOMOLIES OR DISEASE
– COMFORTABLY TACHYPNIC , LOW SaO2 WITHOUT
DISTRESS
– CARDIOMEGALY
– WEAK PULSES
– PULSE DIFFERENTIAL BETWEEN UPPER AND
LOWER EXTREMETIES
– PULMONARY EDEMA

45. CHD
• MORE THAN 40,000 KIDS EVERY
YEAR ARE BORN WITH
CONGENITAL HEART DISEASE
• THE MOST COMMON BIRTH
DEFECT IN THE US

46. PPHN
• PERSISTENT PULMONARY HYPERTENSION IN
THE NEWBORN
• OCCURS AS A RESULT OF A DISRUPTION IN
THE NORMAL FETAL-NEONATAL CIRCULATORY
TRANISITON
– SUSTAINED ELEVATED PVR
– RT TO LEFT SHUNTING OF BLOOD ACROSS THE
PDA OR PFO

47. PPHN
• PPHN IS PRESENT WHEN A BABY HAS A
STRUCTURALLY NORMAL ( CONFIRMED WITH
ECHO) HEART BUT HAS:
– HYPOXEMIA DISPROPORTIONATE TO THE DEGREE
OF SUSPECTED LUNG DISEASE
– EVIDENCE OF RT TO LEFT DUCTAL SHUNT
– PaO2 GRADIENT B/W PRE AND POST DUCTAL SAMPLE MORE
THAN 20 MMHG ( OR SPO2 DIFFERENCE OF 10%)

48. PPHN
• PPHN RISK FACTORS
– LATE PRETERM BABIES 34-37 WEEKS
– BLACK RACE
– MALE
– LGA BABIES
– DIABETIC MOMS
– OBESE MOMS
– LUNG DISEASE ( MAS, RDS….)
– FETAL ASPHYXIA

49. PPHN
• PPHN CAN BE IDIOPATHIC OR SECONDARY
• REMEMBER THAT AT BIRTH, THE UMBILICAL
CORD IS CUT AND THE LUNGS TRANSITION TO
BECOME THE ORGAN FOR GAS EXCHANGE
– DURING THE 1ST POSTNATAL BREATHS, PVR
DECREASES IN RESPONSE TO THE INCREASE IN
PAO2 AND PH, AIR EXPANDING THE LUNGS, AND
THE RELEASE OF VASOACTIVE SUBSTANCES

50. PPHN
• IF THE DECREASE IN PVR FAILS TO OCCUR
ADEQUATELY OR IS REVERSED AS A RESULT OF
STRESS FOR ANY REASON
– IT’S THE FAILRURE OF THE PULMONARY
VASCULATURE TO RELAX
– THERE IS AN INITIAL DROP IN PRESSURE BUT IT TAKES SEVERAL
WEEKS TO FULLY RELAX
PPHN SHOULD BE SUSPECTED IN TERM INFANTS
WHO ARE CYANOTIC DESPITE ADEQUATE
VENTILATION

51. PPHN
• CLINICAL PRESENTATION
– USUALLY IN THE FIRST 12 HOURS OF LIFE
• CYANOSIS
• TACHYPNEA REFRACTORY TO O2 THERPAY
• HYPOXIA
• DISTRESS
» RETRACTIONS, GRUNTING, NASAL FLARING

52. PPHN
• CLINICAL PRESENTATION
• CHEST X RAY
– OFTEN CLEAR EARLY ON
– MAYBE EVIDENCE OF ABNORMAL PULMONARY
FINDINGS AS A RESULT OF MAS, RDS, TTN WHICH
MAY HAVE BEEN PRIMARY CONDITION
– MAY SHOW CARDIOMEGALY

53. PPHN
• CLINICAL PRESENTATION
• ABG
– REVEAL HYPOXEMIA
– BABY MAY HYPERVENTILATE DUE TO PERSISTENT
HYPOXEMIA
A NUMBER OF DISORDERS OR CONDITIONS CAN
BE MISDIAGNOSED AS PPHN

54. PPHN
• TREATMENT
• RESPIRATORY SUPPORT TO ACHIEVE NORMAL
OXYGENATION & VENTILATION
– CPAP/MECHANICAL VENT
• NUETRAL THERMAL ENVIRONMENT
ACIDOSES WORSENS PVR

55. PPHN
• TREATMENT
• MINIMAL HANDLING IS IMPORTANT!
– THESE INFANTS ARE LABILE & CAN
DECOMPENSATE QUICKLY
– REDUCE NOISE
– REDUCE TOUCHING
– REDUCE STIMULI
– SUCTION ONLY WHEN INDICATED

56. PPHN
• TREATMENT
• O2 HYPOXIA IS A POTENT PULMONARY
VASONCONSTRICTOR, O2 THERPY IS VERY IMPORTANT
TO DECREASE THE PVR
– GOAL SATS GREATER THAN OR EQUAL TO 95%
• CLOSELEY MONITOR YOUR PRE & POST DUCTAL SATS
– VENTILATION MAY BE REQUIRED

57. PPHN
• OTHER THERAPIES THAT MAY BE REQUIRED, BUT
THAT WE DON’T DO
– NO NITRIC OXIDE GIVEN BY INOVENT
– RELAXES VASCULAR SMOOTH MUSCLE
– ECMO
– WHEN USED FOR PPHN, 93% OF KIDS SURVIVE
• MORTALITY RATES IN PPHN ARE AS HIGH AS 5%
• HFV, NO & ECMO IMPROVED RATES FROM THE
PAST

58. RETINOPATHY OF PREMATURITY
• KNOWN AS ROP
• ABNORMAL BLOOD VESSEL GROWTH IN THE
RETINA POTENTIALLY CAUSING BLINDNESS
DUE TO RETINAL DETACHMENT

59. ROP
FACTORS IN THE DEVELOPMENT OF ROP:
-HYPEROXIA ( EXCESSIVE OXYGEN DELIVERY) PLAYS A BIG
ROLE IN THE DEVELOPMENT OF ROP
-GESTATIONAL AGE/ LOW BIRTH WEIGHT
GENERALLY LESS THAN 32 WEEKS
-SWINGS IN OXYGENATION
REPEATED CYCLES OF HYPEROXIA & HYPOXIA
FAVOR DEVELOPMENT
-SWINGS IN BLOOD PRESSURE
-SEPSIS

60. ROP
• ROP CAN RESOLVE SPONTANEOUSLY OR
CAUSE PERMANENT VISUAL IMPAIRMENT UP
TO AND INCLUDING COMPLETE BLINDNESS
• ROP WAS AN EPIDEMIC IN THE 1940’S AND
1950’S DUE TO WHEN OXYGEN WAS
ADMINISTERED LIBERALLY
• CURRENT PRACTICE SUPPORTS O2 THERAPY
TARGETING SPO2 LEVELS TO REDUCE RISK IN
EXTREMELY PREMATURE BABIES

61. BRONCHOPULMONARY DYSPLASIA
• BPD
• AKA CLD ( NEONATAL CHRONIC LUNG
DISEASE)
• THIS IS THE MOST COMMON LONG TERM
COMPLICATION OF PREMATURITY
THERE IS SIGNIFICANT MORTALITY
ATTACHED TO BPD

62. BPD
• BPD IS A CHRONIC SEVERE LUNG INJURY IN
PREMATURE INFANTS WHO SURVIVED
HYALINE MEMBRANE DISEASE WITH
MECHANICAL VENTILATION AND OXYGEN
THERAPY
• THERE IS (OLD) BPD AND (NEW) BPD
• THE INCIDENCE DECREASES AS GESTATIONAL
AGE INCREASES, IT BECOMES RARE AFTER 32
WEEKS

63. BPD
• How are the lungs different with BPD?
The lungs move oxygen from the air into the
blood through tiny sacs called alveoli. Babies
with BPD have fewer, larger alveoli with thicker
walls. As a result, the baby must work harder
to get enough oxygen.

64. BPD
• 4 MAJOR FACTORS IN BPD
– LUNG INMATURITY
– RESPIRATORY FAILURE
– OXYGEN SUPPLEMENTATION
– PPV ( BAROTRAUMA AND VOLUTRAUMA)
• THERE ARE OTHER COMPLEX FACTORS WE
WON’T GET INTO
THE CHALLENGE IN BPD IS THAT WHILE PPV AND
O2 ARE NEEDED FOR GAS EXCHANGE, THOSE SAME
THINGS ARE CAUSING THE LUNG DAMAGE

65. BPD
• BAROTRAUMA CAN HAPPEN IMMEDIATELY
AFTER BIRTH, AT THE START OF PPV
• ALWAYS BE VIGILIANT WITH MAINTAINING
APPROPRIATE PIP AND PEEP
• MINIMIZE THE POTENTIAL TO DO DAMAGE
WHILE AVOIDING HYPOXIA

66. BPD
• BOTH HYPEROXIA AND HYPOXIA WILL
EXACERBATE BPD
– PROVIDERS MUST WALK A FINE LINE WITH O2
• PRETERM INFANTS WITH GROWTH
RESTRICTION ARE AT INCREASED RISK
• SOME GENETIC FACTORS INCREASE RISK AS
WELL

67. BPD
• CLINICAL PRESENTATION:
– BPD FOLLOWS THE USE OF MECHANICAL
VENTILATION, USUALLY WHEN USED GREATER
THAN 10 TO 14 DAYS, IN THE FIRST WEEKS OF LIFE
CHEST XRAY:
DIFFUSE HAZINESS
PREVENTION IS THE KEY CONCEPT IN BPD

68. BPD
• LUNG PROTECTIVE STRATEGIES SHOULD BE
USED
– HFV HAS BEEN SHOWN NOT TO PROTECT FROM
BPD AS WAS PREVIOUSLY THOUGHT
– NCPAP IN THE DELIVERY ROOM ( TO ESTABLISH
FRC & STABALIZE RESPIRATORY STATUS) IS THE
MOST RECENT WIDELY ACCEPTED PRACTICE
– WHEN CMV IS REQUIRED, USE GENTLE
VENTIALTION ( LOW VT, PERMISSIVE
HYPERCAPNIA)

69. BPD—PREVENTION!

70. MATERNAL STEROIDS
• CORTICOSTEROIDS
ANTENATAL STEROIDS TO ACCELERATE FETAL LUNG
MATURATION IS KNOWN TO BE A SUCCESSFUL
PRACTICE
THEY ARE NOT WIDELY USED POSTNATAL IN
THE BABY DUE TO NUEROLOGIC DEVELOPMENT
CONCERNS
INHALED STEROIDS ARE NOT ROUTINELY USED AS
TRIALS FAILED TO SHOW EFFECTIVENESS IN
NEONATES ( BUDESONIDE W/IN 24 HOURS BPD
BUT MORTALITLY)

71. MATERNAL STEROIDS
BETAMETHASONE
• FOR THE REDUCTION OF NEONATAL
RESPIRATORY COMPLICATIONS DUE TO
PREMATURITY
• 2 DOSES GIVEN 24 HOURS APART FOR
MOTHERS LESS THAN 37 WEEKS GESTATION
• ACCELERATES FETAL LUNG MATURITY TO
IMPROVE GAS EXCHANGE ( SURFACTANT
PRODUCTION)

73. THE DRAEGER BABYLOG 8000 PLUS