TO UPDATE NURSES KNOWLEDGE ON RESPIRATORY DISTRESS IN NEWBORN

1. RESPIRATORY DISTRESS IN NEWBORN
PRESENTED BY :GILY JACOB
NICU CRN

2. INTRODUCTION TO RESPIRATORY
SYSTEM

3. LUNG DEVELOPMENT

4. RESPIRATORY DISTRESS
• RESPIRATORY DISTRESS IN THE NEWBORN IS RECOGNIZED
AS ONE OR MORE SIGNS OF INCREASED WORK OF BREATHING,
SUCH AS TACHYPNEA, NASAL FLARING, CHEST RETRACTIONS,
OR GRUNTING.

5. SIGNS AND SYMPTOMS
TACHYPNOEA
CHEST
RETRACTION
HEAD
BOBBING
NASAL
FLARING
AND
GRUNTING
CYANOSIS

6. DIFFERENTIAL
DIAGNOSIS
TTN
(TRANSIENT
TACHYPNOEA
OF
NEWBORN)
CONGENITAL
PNEUMONIA
RESPIRATORY
DISTRESS
SYNDROME
MECONIUM
ASPIRATION
SYNDROME
PPHN
PNEUMOTHORAX
OTHERS
CONGENITAL
HEART DISAESE
,PERINATAL
ASPHYXIA,SEPSIS
,METABOLIC DIS
ORDERS
CONGENITAL
DIAPHRAMATIC
HERNIA
OBSTRUCTIVE
CHOANAL
ATRESIA,LARYNG
OMALASIA, TOF

7. TRANSIENT TACHYPNOEA OF NEWBORN
• TRANSIENT TACHYPNEA OF THE NEWBORN
(TTN) is a parenchymal lung disorder
characterized by pulmonary edema resulting
from delayed resorption and clearance of fetal
alveolar fluid
• TTN is a common cause of respiratory distress in
the immediate newborn period.
INCIDENCE
• TTN was 5.7 per 1000 births .

8. RISK FACTORS
TTN develops in infants born prematurely or after
cesarean delivery without labor because mechanisms
to reabsorb alveolar fluid have not been initiated
Diabetic mothers (IDM)
Maternal asthma
DIAGNOSIS
Auscultation-crackles
Chest radiograph-perihilar streaky markings.
MANAGEMENT
 SUPPORTIVE THERAPY
OXYGEN ADMINISTRATION
VENTILATOR SUPPORT

9. RESPIRATORY DISTRESS SYNDROME
• RESPIRATORY DISTRESS SYNDROME FORMERLY
KNOWN AS HYALINE MEMBRANE DISEASE ,IS A
COMMON PROBLEM IN PRETERM NEWBORN DUE
TO DEFICIENCY OF SURFACTANT ,THAT
CHARACTERISED BY PROGRESSIVE AND USUALLY
FATAL RESPIRATORY FAILURE RESULTING FROM
ATELECTASIS AND IMMATURITY OF LUNG .

10. PULMONARY SURFACTANT
• THE PRIMARY CAUSE OF RDS IS DEFICIENCY OF SURFACTANT.
• SURFACTANT IS PRODUCED FROM TYPE II ALVEOLAR CELLS COMPOSED OF 90% LIPIDS
AND 10% PROTEINS .SURFACTANT PRODUCTION STARTS AT 20TH WEEK OF
GESTATION PEAKS AT 35 WEEKS OF GEATATION.SURFACTANT REDUCES THE
ALVEOLAR SURFACE TENSION, THEREBY FACILITATING ALVEOLAR EXPANSION AND
REDUCING THE LIKELIHOOD OF ALVEOLAR COLLAPSE( ATELECTASIS).

11. ETIOLOGY
PREMATURITY- In preterm infants, surfactant deficiency is the
primary cause of RDS
CONTRIBUTING FACTORS (ANY FACTORS WHICH DECREASE THE
PRODUCTION OF SURFACTANT )
ACIDOSIS
HYPOTHERMIA
ASPHYXIATED NEWBORN
INFANT WITH DIABETIC MOTHER
MECONIUM ASPIRATION

12. PATHOPHYSIOLOGY
PREMATURITY
DECREASED
SURFACTANT
INCREASED ALVEOLI
SURFACE
TENSION(UNEQUAL
INFLATION ON
INSPIRATION)
ATLECTASIS
CO2
RETENSION
HYPOXEMIA
ACIDOSIS

13. PULMONARY
VASOCONSTRICTION AND
HYPOPERFUSION
CAPILLARY
DAMAGE
PLASMA LEAK
FIBRIN(DECREAS
ED LUNG
COMPLAINCE)

14. DIAGNOSIS
1.PHYSICAL EXAMINATION-ONSET OF PROGRESIVE
RESPIRATORY FAILURE
2.BLOOD GAS EXAMINATION-RESPIRATORY AND METABOLIC
ACIDOSIS(MIXED ACIDOSIS)
3.CHEST RADIOGRAPH-GROUND GLASS APPEARANCE OR
WHITE WASH LUNG
SEVERE RDS MODERATE
RDS

15. PREVENTION AND TREATMENT OF RDS
SPECIFIC INTERVENTIONS ARE FOCUSED ON PREVENTING OR
DECREASING THE SEVERITY OF RDS.
THEY INCLUDE THE FOLLOWING:
●Administration of antenatal corticosteroids-acs (antenatal corticosteroids) helps
in maturational development of lung with increased production and release of
surfactant
●EXOGENOUS SURFACTANT THERAPY

16. SURFACTANT ORIGIN PHOSPHOLIPIDS PROTEIN INITIAL
DOSE
REPEAT
DOSING
Calfactant
(Infasurf)
Calf lung
lavage, lipid
extraction
35 mg PL per mL 0.7 mg per
mL (contains
0.26 mg/mL
of SP-B and
0.44 mg/mL
of SP-C)
3 mL/kg
(contains
105 mg/kg
PL)
3 mL/kg
(105 mg/kg
PL) every
12 hours as
needed up
to three
total doses.
Beractant
(Survanta)
Bovine lung
minces, lipid
extraction.
25 mg PL per mL <1 mg per
mL (contains
both SP-B
and SP-C)
4 mL/kg
(contains
100 mg/kg
PL)
Repeat
same dose
every six
hours as
needed for
total of four
doses.
TYPES OF SURFACTANT

17. SURFACTANT ADMINISTRATION TECHNIQUE
THE STANDARD TECHNIQUE OF SURFACTANT ADMINISTRATION IS
ENDOTRACHEAL ADMINISTRATION

19. RECENT ADVANCES
INSURE –Intubation surfactant and extubation to CPAP
MINIMALLY INVASIVE SURFACTANT THERAPY (MIST)OR LESS INVASIVE
SURFACTANT THERAPY (LISA) -is a new mode of surfactant administration
without intubation to spontaneously breathing preterm infants with respiratory
distress syndrome (RDS)
DIFFERENT METHODS
 Tracheal Catheterization-size 5 or6 fr feeding tube or by using size 16G
angiogram catheter.
 Aerosolized Surfactant-As nebulization
 Surfactant Deposition Using a Laryngeal Mask Airway
LARYNGEAL
MASK

20. STUDY ON MINIMAL INVASIVE SURFACTANT THERAPY AND
INTUBATION OF THE BABAY TO ADMINISTER SURFACTANT
In total, 53 VLBW infants who were born before 32 gestational weeks with
spontaneous breathing, respiratory distress, and requiring surfactant therapy
were divided into two groups. The infants in group A (n = 29) were intubated and
received surfactant replacement therapy via endotracheal tube, followed by mechanical
ventilation (MV). The infants in group B (n = 24) received tracheal instillation of
surfactant via a semi rigid vascular catheter during spontaneous breathing under nasal
continuous positive airway pressure (nCPAP). After surfactant instillation, the infants in
group B were still placed on nCPAP.
Results
Our data showed that infants in group B (MIST group) had significantly lower rate
(P < 0.05) of composite outcome of death or bronchopulmonary dysplasia (BPD),
duration of intermittent positive airway pressure ventilation (IPPV) or MV, drug
treatment of patent ductus arteriosus (PDA), and surgical ligation of PDA than group A
.
CONCLUSION
MIST IS FEASIBLE, SAFE AND IT MAY REDUCE THE COMPOSITE OUTCOME OF
DEATH OR BPD FOR VLBW INFANTS WITH RDS REQUIRING SURFACTANT
REPLACEMENT THERAPY.

21.  Maintaince of respiration with ventilatory support
 Maintance of normal body temperature
 Maintance of nutrition
 Antibiotics as needed
 Prevent hypotension

22. CONGENITAL PNEUMONIA
INTRODUCTION
pneumonia refers to inflammatory changes of
the respiratory system caused by infection.
Pneumonia is an important cause of neonatal
infection and accounts for significant morbidity
and mortality, especially in developing countries
Neonatal pneumonia accounts for 10% of global
child mortalites .

23. PATHOGENESIS
• PNEUMONIA THAT PRESENT WITHIN 24
HRS KNOWN AS CONGENITAL PNEUMONIA
3 CATEGORIES OF CONGENITAL PNEUMONIA
 True congenital pneumonia-Already
established at birth infection occurs by
haematogenous , ascending or aspiration
Intrapartum –Acquired during passage through
the birth canal
Post natal -originates after the infant out from
the birth canal

24. CAUSATIVE ORGANISAM
• Bacterial Escherichia coli, GBS, Klebsiella ,
Staphylococcus aureus, and Streptococcus
pneumoniae.
• Viral infections — Herpes simplex virus (HSV)
,corona virus ,adeno virus ,entero virus
• Fungal infections -Candida

25. DIAGNOSIS
• The diagnosis of neonatal pneumonia is based
on a clinical, radiographic, and microbiologic
findings
• Cultures — Cultures of blood and cerebrospinal
fluid should be obtained. In infants who are
intubated, Gram stain and culture of tracheal
aspirates may help identify the pathogen
• Chest radiograph-Diffuse infiltrates

26. MANAGEMENT
• General supportive management
• Oxygen administration
• Ventilator support
• Antibiotic or antiviral medication according to
the identified causative pathogen

27. NURSING ASSESSMENT
• Review the birth history
• Medications or anesthesia administered to the mother during
delivery
• Type of resuscitation required
• Estimated gestational age
• Maternal history – contributing factors or complications
2.CAREFULLY ASSESS THE INFANTS RESPIRATORY STATUS TO
DETERMINE THE DEGREE OF RESPIRATORY DISTRESS
• Determine the degree and severity of retraction
• Count respiratory rate for full one minute
• Identify the periods of apnoea,length and type of stimulation
necessary
• Note nasal flaring
• Note cyanosis
3.OBSERVE INFANTS GENERAL ACTIVITY
• Lethargic or listless
• Active and responds to stimuli
4.Assess the skin for cyanosis,jaundice ,mottling
,paleness or greyness
NURSING MANAGEMENT

28. NURSING DIAGNOSIS
1.IMPAIRED GAS EXCHANGE RELATED TO DISEASE PROCESS
2.IMBALANCED NUTRITION LESS THAN BODY REQUIREMENT REALTED
TO PREMATURITY AND INCREASED ENERGY EXPENDITURE ON
BREATHING
3.INEFFECTIVE THERMOREGULATION RELATED TO PREMATURITY

29. NURSING INTERVENTION
• HAVE EMERGENCY EQUIPMENT READILY AVAILABLE FOR
USE IN THE EVENT OF CARDIAC OR RESPIRATORY
ARREST.
• INSTITUTE CARDIORESPIRATORY MONITORING TO
CONTINUOUSLY MONITOR HEART AND RESPIRATORY
RATES.
• ADMINISTER SUPPLEMENTAL OXYGEN
• ASSIST WITH ET INTUBATION AND MAINTAIN
MECHANICAL VENTILATION ,AS INDICATED
• MEASURE OXYGEN CONCENTRATION EVERY HOUR AND
RECORD
• MONITOR ABGS LEVELS AS APPROPRIATE .
• STIMULATE INFANT IF APNOEA OCCURS
• POSITION THE INFANT TO ALLOW FOR MAXIMAL LUNG
EXPANSION.
• SUCTION AS NEEDED OBSERVE THE PATIENT DURING
THE PROCEDURE AVIOD HYPOXEM IA
• PROVIDE A THERMO NEUTRAL ENVIRONMENT

30.  START AND MONITOR IV FLUIDS AS PER DOCTORS ORDER
MONITOR FOR HYPOGLYCEMIA
PROVIDE A THERMO NEUTRAL ENVIRONMENT

32. Case 1: Transient tachypnea of the newborn is characterized by
streaky, pulmonary interstitial markings and fluid in the fissure
apparent on chest radiograph.
Case 2: Neonatal pneumonia with bilateral opacities, air
bronchograms, and pleural effusions is apparent.
Case 3: Respiratory distress syndrome is characterized by
diffuse, bilateral, ground glass fields with air bronchograms
secondary to diffuse atelectasis.
Case 4: Meconium aspiration syndrome causes a chemical
pneumonitis, partial airway obstruction, and a localized
surfactant inactivation that leads to areas of hyperinflation
mixed with diffuse, patchy infiltrates radiographically.

33. • UPTODATE
• LIPPINCOTT MANNUAL OF NURSING PRACTICE