

MINISTRY OF PUBLIC HEALTH OF UKRAINE

DEPARTMENT OF PEDIATRICS

IRYNA LEMBRYK
SPECIFIC ADAPTATION, CARE AND FEEDING
OF PREMATURE NEWBORNS. RESPIRATORY
DISTRESS SYNDROME OF THE NEWBORNS
 
PREMATURE AND LOW-BIRTH-WEIGHT
INFANTS: DEFINITIONS

 Based on the WHO’s definition preterm gestation

and prematurity refer to delivery at less than 38
weeks gestation (complete 37 weeks) or less than
259 days, calculating from the first day of the last
menstrual period.
 Preterm newborns usually represent the category
of so called LOW-BIRTH-WEIGHT infants (BW <
2500 g). Important to remember that growth-
retarded newborns may have BW < 2500 g as well.
 CLINICAL CLASSIFICATION OF NEWBORNS 
BASED ON THE BIRTH WEIGHT

 Low-birth-weight (LBW) infants

< 2500 g
 Very-low-birth-weight (VLBW) infants

 < 1500 g
 Extremely low-birth-weight (ELBW) infants

 < 1000 g
 
SURVIVAL RATES, CANADA

94% 98%
90%
78% 82%

60%
40%

< 600 600-699 700-799 800-899 900-999 1000-1100 1300-1399

BW, g
 
Survival rates, Japan

100 96
90 85
80
70
1980
60
1985
50
37 1990
40
1995
30 2000
20
10
0
<500 g 500-999 g 1000-1499 g
 GESTATIONAL CHART

Large for gestational age

Adequate

2,500 g

Small for gestational age

 
Appearance of Prematurity and Asymmetric IUGR
Prematurity Asymmetric IUGR
 Abundant lanugo  Thin and wafted, little subcutaneous
tissue
 Visible blood  Loose, dry, scaling skin
vessels  Thin musculature; length and head size
may be normal
 Edema  Sparse bead hair
 Alert, active, seems hungry
 Decreased breast  Possibly won't void until 24 hours of age
tissue  Cord dries more rapidly
 Appears old for size
 Ears soft and
 Possible anomalies, e.g., unilateral or
pliable (slow
bilateral single palmar creases, single
recoil) umbilical artery, and peculiarities of the
ears
 Immature genitalia
 
Extremely preterm newborns
 
Main causes of preterm birth
 
Background
 Only one of every 20 deliveries in average is
preterm but every 2 of 3 cases of neonatal death
are connected with prematurity.
 Among preterm infants who survived there are
higher incidences of acute and chronic morbidity
including severe disability.
 Newborns with birth weight less than 1500 gm
(VLBW infants) represent up to 1,5% of all live-
born infants, but their mortality determines more
than 50% of total infant mortality rate.
 
Background

VLBW infants are 200 times more likely to die

than the infants of normal birth weight.
That is why costs of their medical care are very
high and disproportional.
VLBW and preterm infants in general represent
today the larger group of patients at the modern
neonatal intensive care units.
 Clinical problems

of prematurity
 Associated with low birth weight

 Determined by immaturity of the all organs and systems

 Low tissue fat content, relatively high water content, and a

high area to weight ratio characterize LBW premature
newborns
 These peculiarities of premature newborns determine the
problems of extrauterine growth (nutrition) and
thermoregulation
 Immediate clinical issues, related 
to
prematurity
 Caused by functional immaturity
 Appeared within the first 72 hours of infants’ life:
 Asphyxia, intraventricular hemmorhage (IVH)
 RDS
 Infections
 Apnea
 Patent ductus arteriosus (PDA)
 Metabolic disturbances
 Hyperbilirubinemia
 
Morphological data of IVH
 
Chronic clinical problems

 May be connected to specific therapeutic measures or

represent the delayed outcomes of immediate
problems, metabolic and functional immaturity
 CNS pathology (PVL, hydrocephaly, CP);
 Sepsis and congenital infections, NEC
 Metabolic bone diseases (rickets,
osteopathy of prematurity);
 Retinopathy of premature babies
 Anemia of premature infants
 Social problems
 Clinical Problems and Causes 
 Hypocalcemia
 Respiratory Distress Transient hypoparathyroidism
Syndrome (RDS) Transient bypercalcitoninemia
 Lack of surfactant Asphyxia
 Weaker respiratory
muscle activities  Bleeding
 Less rigid thoracic cage Increased capillary fragility
Decreased synthesis of
 Hypothermia clotting factors in liver
 Smaller supplies of Delayed bacterial coloniz. of
brown fat gut (interferes with ability to
 Large surface area produce Vit. K)
Poor fat absorption (Vitamin
 Hypoglycemia K is a fat soluble vitamin)
 Fewer glycogen stores
 Few fat stores
 CLINICAL PROBLEMS AND CAUSES OF
PREMATURITY
 Hyperbilirubinemia
 Poor clearance of billirubin
 Hypoproteinemia
 Acidosis
 Edema
 Decreased synthesis of proteins
 Decreased glomerular nitration
rates
 Decreased tubular reabsorption
of amino acids
 Drug accumulation
 Decreased glomerular filtration
rates
 Decreased tubular secretion
drugs
 Apnea
 Decreased ability to maintain
threshold activity level of
respiratory center neurons
 Metabolic acidosis
 Decreased tubular
reabsorption of HCO,
 Decreased tubular secretion of
fixed acids
 Abdominal distension
 Decreased secretion of gastric
acid and digestive enzymes
 Weak suck and swallow
 Delayed stomach emptying
 Necrotizing enterocolitis
 Clinical Problems and Causes
 Sepsis  Necrotinng enterocolitis
 Low levels of alpha and beta Thin walled gut
globulins Low Secretory IgA
 Fewer specific antibodies from Primed by asphyxia
mother (IgG)
 Decreased WBC bacteria-killing  Metabolic bone disease
ability
Low calcium and phosphorus
 Lower complement intakes
 Inability to keep infection Decreased absorption of
localized vitamin D secondary to
cholestasis
 
Thermal protection in the delivery room
 Care of the ‘Small Baby‘ at birth(1)

 Implement Universal Precautions (nosocomial infection

prevention)
 Prevent hypothermia
 Delivery or operation room not < 25° C
 Careful drying with warm towels, remove wet towels;
 Put the baby immediately on mother chest;
 Assess breathing and heart beat on mother chest ;
 Cover the baby’s head and feet with warm cap and socks
 Cover baby and mother with warm blanket
 Support early breastfeeding/feeding within 1-2 hour
 Monitor baby’s temperature each 30 min during the 2 first
hours of life
 
Care of the ‘Small Baby‘ at birth (2)
 Prevent hypoglycemia

- Initiate breastfeeding/feeding within 1-2 hours after birth

to insure adequate calories intake
 Monitor breathing each 30 min during the first 2 hours in
delivery room
- Listen for grunting
- Count breathing rate, recount if <30 or > 60 min
- Look - for chest intradrawing
- for nasal flaring
 Care for ‘Small baby’ until discharge (1) 

 Keeping warm and rooming-in:

 Do not separate mother and baby (strict rooming-in)
 Post partum room very warm 25 °C – 28 °C, no
draught, cradle far from cold wall/window.
 Teach the mother to control the temperature each 4
hours and to provide skin to skin if baby’s temperature
is less 36.5°C or baby has cold feet
 Keep baby dry (use appropriate nappy)
 Baby warmly clothed (hat, socks, warm clothes)
 Provide extra blankets for baby and mother
 Do not bath ‘small baby’ . Wash as needed
 Do not swaddle. Tight swaddling makes baby cold.
 Prevent hypoglycemia & insure

adequate calories intake

 Early and frequent feedings

- Encourage mother to breastfeed to each 2-3 hours
- Assess breastfeeding daily:
- Correct attachment,
- Effective suckling,
- Duration and frequency of feeds,
- Baby satisfaction.
- Weigh daily and assess weight gain
- If alternative feeding methods used:
- Assess the daily quantity of milk given and taken
 Implement Universal Precautions and

Respect good hygiene procedure

 Insist on mother taking care by herself

of ‘Small Baby’: changing, cleaning,
checking temperature
 Teach and monitor good hand washing
for mother and medical staff
 Use open cord care management
 Definition of RDS
 Respiratory distress syndrome, also known
as hyaline membrane disease, occurs
almost exclusively in premature infants.
 The incidence and severity of respiratory
distress syndrome are related inversely
to the gestational age of the newborn
infant
 Epidemiology of RDS
 In the United States, respiratory distress syndrome has been
estimated to occur in 20,000-30,000 newborn infants each year and
is a complication in about 1% pregnancies. Approximately 50% of
the neonates born at 26-28 weeks' gestation develop respiratory
distress syndrome, whereas less than 30% of premature neonates
born at 30-31 weeks' gestation develop the condition.
 International data. Respiratory distress syndrome is encountered
less frequently in developing countries than elsewhere, primarily
because most premature infants who are small for their gestation
are stressed in utero because of malnutrition or pregnancy-induced
hypertension.
 ARDS
Definition
 Severe, acute lung injury involving diffuse
alveolar damage, increased microvascular
permeability and non cardiogenic pulmonary
edema
 Acute refractory hypoxemia
 Annual incidence 75/100,000 in the US
 High mortality- 40%-60%

 First described in 1967

 ARDS
Criteria
 Acute onset of respiratory failure

 Bilateral infiltrate on CXR(some cases

do present unilaterally or with pleural
effusion
 PCWP <18 or absence of left atrial htn,

 PaO2/FiO2 < 200

 ARDS 
mechanism of lung injury
 Activation of inflammatory mediators and
cellular components resulting in damage to
capillary endothelial and alveolar epithelial cells
 Increased permeability of alveolar capillary
membrane
 Influx of protein rich edema fluid and
inflammatory cells into air spaces
 Dysfunction of surfactant
 Pathophysiology of RDS
 In premature infants, respiratory distress syndrome develops
because of impaired surfactant synthesis and secretion leading
to atelectasis, ventilation-perfusion (V/Q) inequality, and
hypoventilation with resultant hypoxemia and hypercarbia. Blood
gases show respiratory and metabolic acidosis that cause
pulmonary vasoconstriction, resulting in impaired endothelial and
epithelial integrity with leakage of proteinaceous exudate and
formation of hyaline membranes.
 The deficiency of surfactant decreases lung compliance and
functional residual capacity, with increased dead space. The
resulting large V/Q mismatch and right-to-left shunt may involve
as much as 80% of the cardiac output.

 Risk factors of RDS
 A brother or sister who had RDS.

 Diabetes in the mother.

 Cesarean delivery or induction of labor before

the baby is full-term.
 Problems with delivery that reduce blood flow
to the baby.
 Multiple pregnancy (twins or more)

 Rapid labor.
 
ARDS causes
 Direct Lung Injury:

a) PNA and aspiration of gastric contents

or other causes of chemical pneumonitis

b) pulmonary contusion, penetrating lung injury

c) fat emboli

d) near drowning

e) inhalation injury

f) reperfusion pulmonary edema after lung transplant

 
ARDS causes

 Indirect lung injury

a) sepsis

b) severe trauma w/ shock hypo perfusion

c) drug over dose

d) cardiopulmonary bypass

e) acute pancreatitis

f) transfusion of multp blood products

 
Stages of ARDS

 1.Exudative (acute) phase - 0- 4

days
 2. Proliferative phase - 4- 8 days

 3. Fibrotic phase - >8 days

 4. Recovery
 
ARDS exudative and fibrotic phases
 Clinics of RDS
 Respiratory distress syndrome frequently occurs in the
following individuals:
 White male infants

 Infants born to mothers with diabetes

 Infants born by means of cesarean delivery

 Second-born twins

 Infants with a family history of respiratory distress syndrome

 Secondary surfactant deficiency may
occur in infants with the following:
 Intrapartum asphyxia

 Pulmonary infections (eg, group B beta-hemolytic

streptococcal pneumonia)
 Pulmonary hemorrhage

 Meconium aspiration pneumonia

 Oxygen toxicity along with barotrauma or volutrauma to the

lungs
 Congenital diaphragmatic hernia and pulmonary hypoplasia
 Clinics of RDS (cont.)
 the incidence of RDS decreases with the
following:
 Use of antenatal steroids
 Pregnancy-induced or chronic maternal
hypertension
 Prolonged rupture of membranes
 Maternal narcotic addiction
 Physical findings in RDS
 They are consistent with the infant's maturity assessed by
using the Dubowitz examination or its modification by Ballard.
 Progressive signs of respiratory distress are noted soon after
birth and include the following:
 Tachypnea

 Expiratory grunting (from partial closure of glottis)


 Physical findings in RDS (cont.)
 Subcostal and intercostal retractions
 Cyanosis
 Nasal flaring
 Extremely immature in neonates may
develop apnea and/or hypothermia
 
Predictors of outcome

 Factors whose presence can be used to predict the

risk of death at the time of diagnosis of acute lung
injury and the acute respiratory distress syndrome
include

a) chronic liver disease

b) non-pulmonary organ dysfunction,

c) sepsis,

d) advanced age.
 Diagnostic Considerations due to RDS

 Conditions to consider in the differential

diagnosis of respiratory distress
syndrome include the following:
 Metabolic problems

 Hematologic problems

 Pulmonary air leaks

 Congenital anomalies of the lungs

 Approach considerations in RDS

 Several diagnoses may coexist with and complicate the

course of respiratory distress syndrome, including the
following:
 Pneumonia - Usually secondary to group B beta-
hemolytic streptococci and often coexists with
respiratory distress syndrome
 Metabolic problems - Eg, hypothermia, hypoglycemia

 Hematologic problems - Eg, anemia, polycythemia,

jaundice
 Approach considerations in RDS

 Transient tachypnea of the newborn - Usually occurs in term or near-

term neonates, often after cesarean delivery; the chest radiograph of
an infant with transient tachypnea shows good lung expansion and,
often, fluid in the horizontal fissure

 Aspiration syndromes - May result from aspiration of amniotic fluid,

blood, or meconium; aspiration syndrome is observed in more mature
infants and is differentiated by obtaining a history and by viewing the
chest radiographs.

 Pulmonary air leaks - Eg, pneumothorax, interstitial emphysema,

pneumomediastinum, pneumopericardium; in premature infants, these
complications may be due to excessive positive-pressure ventilation
(in rare cases, spontaneous pneumothorax may occur in large infants)
 Approach considerations in RDS

 Congenital anomalies of the lungs - Eg,

diaphragmatic hernia, chylothorax, congenital
cystic adenomatoid malformation of the lung,
lobar emphysema, bronchogenic cyst,
pulmonary sequestration
 Congenital anomalies of the heart
 Work up in RDS
 Fetal lung maturity tests

 Prediction of fetal lung maturity is derived by estimating the

lecithin-to-sphingomyelin ratio and/or by testing for the
presence of phosphatidylglycerol in the amniotic fluid obtained
with amniocentesis.
 Procedures in RDS

 Vascular access procedures

 Vascular access procedures used in infants with respiratory

distress syndrome include:
 Intravenous (IV) line placement

 Umbilical arterial catheterization

 Umbilical artery cut down

 Peripheral artery cannulation

 Umbilical venous catheterization

 Other procedures in RDS

 Sedation, analgesia, or anesthesia whenever feasible

 Arterial puncture, venous puncture, and capillary blood

sampling
 Tracheal intubation or tracheostomy

 Bronchoscopy

 Placement of thoracotomy tubes

 Placement of pericardial tubes

 Placement of gastric tubes

 Work up in RDS

 Transfusion of blood, blood products, and

exchange transfusion
 Lumbar puncture

 Suprapubic bladder aspiration and bladder

catheterization
 Blood gases are usually obtained in respiratory
distress syndrome, as clinically indicated, from
an indwelling peripheral or central (umbilical)
arterial catheter or by means of arterial puncture.
 Work up in RDS
 Pulse oximetry is used as a noninvasive tool to
monitor oxygen saturation, which should be
maintained at 90-95%.
 However, it is unreliable for determining hyperoxia
because of the flat-top portion of the S -shaped
oxygen-hemoglobin dissociation curve.

 Transcutaneous CO2 monitors should be used in

infants with ongoing respiratory distress to monitor
ventilation if it correlates with PaCO2.
 Work up in RDS
 Chest radiographs reveal bilateral, diffuse, reticular
granular or ground-glass appearances; air bronchograms;
and poor lung expansion. The prominent air bronchograms
represent aerated bronchioles superimposed on a
background of collapsed alveoli.
 The cardiac silhouette may be normal or enlarged.
Cardiomegaly may be the result of prenatal asphyxia,
maternal diabetes, patent ductus arteriosus (PDA), an
associated congenital heart anomaly, or simply poor lung
expansion. These findings may be altered with early
surfactant therapy and adequate mechanical ventilation
 Work up in RDS
 Echocardiographic evaluation is performed in
selected infants to assist in diagnosing PDA
and in determining the direction and degree
of shunting on Doppler study.
 It is also useful in diagnosing pulmonary
hypertension, assessing cardiac function,
and excluding structural heart disease.
 Pulmonary Mechanics Testing

 Although pulmonary mechanics testing (PMT) has

primarily been used as a research tool in the past, newer
ventilators are equipped with PMT capabilities to assist the
neonatologist in adequately managing the changing
pulmonary course of premature newborn infants with
respiratory distress syndrome.
 Constant PMT may be helpful in preventing volutrauma due
to alveolar and airway overdistension. Monitoring may also
facilitate weaning the infant from the ventilator after
surfactant therapy or in determining if the infant can be
extubated.
 Pulmonary mechanical testing
 Infants with respiratory distress syndrome have substantially decreased lung
compliance, with a range of 0.0005-0.0001 L/cm water. For the same pressure
gradient, the delivered tidal volume is reduced in premature infants with RDS.

 Pulmonary compliance may improve after surfactant administration. Hence, the

patient's lung compliance and end-expiratory tidal volume should be monitored
closely after surfactant therapy, and the peak inspiratory pressure should be
adjusted accordingly.

 The resistance (airway and tissues) may be normal or increased. The time
constant and the corresponding pressure and volume equilibration are shortened.

 The anatomic dead space and the functional residual capacity are increased.


 Management and treatment of RDS
 A neonatologist experienced in the resuscitation and care of
premature infants should attend the deliveries of fetuses born
at less than 28 weeks' gestation. These neonates are at a high
risk for maladaptation, which further inhibits surfactant
production.
 In the delivery room, nasal continuous positive airway pressure
(CPAP) is often used in spontaneously breathing premature
infants immediately after birth as a potential alternative to
immediate intubation and surfactant replacement to minimize
the severity of bronchopulmonary dysplasia (BPD).
 Management of RDS
 Transfer the following patients to a tertiary care center:

 Mothers with high-risk pregnancy

 Mothers in premature labor

 Newborn infants with respiratory failure

 Corticosteroids in RDS
 Obstetricians with experience in fetal medicine
should care for mothers whose infants are at an
increased risk for respiratory distress syndrome,
preferably at a tertiary perinatal center.
 Strategies to prevent premature birth include
bed rest, tocolytics, antibiotics, and antenatal
steroids
 Corticosteroids in RDS
 Corticosteroid treatment at recognition of a risk of preterm
delivery is indicated. If the mother does not deliver within 1 week,
retreatment may be considered; most perinatologists administer a
single, 12-mg dose of betamethasone, rather than 2 doses.
 Clinical judgment should be used about the risk for preterm
delivery before any repeat dose is administered. If cervical
dilation or signs of labor persist, a repeat dose may help. If the
pregnancy appears to be at lower risk, retreatment may be
deferred. Multiple retreatment (>4 times) may increase risk;
however, the effect of corticosteroid retreatment for the risk of
preterm delivery remains unclear.
 Surfactant Replacement Therapy

 The advent of surfactant therapy has reduced the mortality rate

from respiratory distress syndrome by approximately 50%
 Early surfactant therapy in tiny neonates followed by rapid
extubation to nasal continuous positive airway pressure (CPAP)
decreased the need for and duration of mechanical ventilation
and decreased the rate of pulmonary air leakage and 28-day
mortality compared with selective surfactant therapy in
respiratory distress syndrome followed by ventilation. Extremely
premature neonates administered surfactant in the delivery
room may have improvement in short-term outcomes and
milder BPD.
 Management of RDS
 Neonates with respiratory distress syndrome who
require assisted ventilation with a fraction of
inspiratory oxygen (FIO2) of more than 0.40 should
receive intratracheal surfactant as soon as possible,
preferably within 2 hours after birth.
 Because surfactant protects the immature lungs,
several investigators have recommended its
prophylactic use after resuscitation in extremely
premature neonates (< 27 weeks' gestation).
 Premature neonates with surfactant deficiency and respiratory
distress syndrome have an alveolar pool of about 5mg/kg.
Recommended dosages of clinically available surfactant preparations
are 50-200mg/kg, approximately the surfactant pool of term newborn
lungs. Rapid bolus administration of surfactant after adequate lung
recruitment with 3-4cm of positive end-expiratory pressure (PEEP)
and adequate positive pressure may improve its homogeneous
distribution. Most neonates require 2 doses; however, as many as
4 doses, given at 6-hour to 12-hour intervals, were used in
several clinical trials. If the patient rapidly improves after 1 dose,
respiratory distress syndrome is unlikely.
 Types of surfactant medications
Type Source Composition Dosing Comments

Dipalmitoyl
phosphatid
Beractant ylcholine
4mL/kg
(Survanta) (DPPC),
Bovine lung (100mg/kg),
Surfactant- tripalmitin, Refrigerate
mince 1-4 doses
TA SP-B <
every 6h
(Surfacten) 0.5%, SP-C
99% of TP
wt/wt

From the
99% PL, 1%
Bovactant Bovine lung Federal
SP-B and 45mg/mL
(Alveofact) lavage Republic of
SP-C
Germany
 Types of surfactant medications

Type Source Composition Dosing Comments

75%
135mg/kg/
Bovine lipid phosphatidy
dose
extract Bovine lung lcholine
(5mL/kg), 1- Canadian
surfactant lavage (PC) and 1%
4 doses
(bLES) SP-B and
every 12h
SP-C

DPPC,
Infasurf
tripalmitin, 3mL/kg
Calf lung
Calf lung SP-B (105mg/kg), 6mL vials,
surfactant
lavage 290g/mL, 1-4 doses refrigerate
extract
SP-C every 6-12h
(CLSE)
360g/mL
 Types of surfactant medications
Type Source Composition Dosing Comments

Phospholipids
(DPPC,
phosphatidylgl
ycerol [PG]),
neutral lipids,
fatty acids; Initially
SP-B and SP- 2.5mL/kg
Poractant alpha Minced pig C; 80mg/mL (200mg/kg),
1.5 and 3mL
(Curosurf) lung of PL/mL followed by
[54mg PC 1.25mL
(30.5mg (100mg)/kg
DPPC and
1mg protein
includes
0.3mg of SP-
B)]
 Types of surfactant medications
Type Source Composition Dosing Comments

Protein: KL4
(sinapultide)
resembles SP-
B;
175 FDA
Phospholipids
Lucinactant Synthetic mg/kg/dose approved at
: DPPC,
phospholipid Mach 2012
palmitoyloleo
yl
phosphatidylc
holine (POPG)

No longer
85% DPPC, 5mL/kg
Colfosceril available;
9% (67.5mg/kg),
palmitate Synthetic lyophilized,
hexadecanol, 1-4 doses
(Exosurf) dissolve in
6% tyloxapol every 12h
8mL
 Oxygenation in RDS
 Continuous positive airway pressure (CPAP) was introduced as
the primary therapeutic modality when Gregory et al
demonstrated a marked reduction in respiratory distress
syndrome mortality.
 Oxygen is administered via a hood or nasal canula or in the
isolette to treat infants with mild respiratory distress syndrome
or after discontinuation of CPAP or assisted ventilation.
 CPAP keeps the alveoli open at the end of expiration,
decreasing the right-to-left pulmonary shunt.
 Oxygenation in RDS

 CPAP is often administered using nasal prongs. 

 In a Cochrane database review in which devices and pressure

 

sources for administration of nasal CPAP were assessed, short,

binasal prong devices were found to be more effective than
single prongs and also reduced the rate of reintubation

 CPAP is an adjunct therapy given after surfactant if prolonged

assisted ventilation is not required.

 Use of nasal CPAP after initial surfactant therapy has been

successful in some infants. In a retrospective study, bubble
nasal CPAP was successful in 76% of infants who weighed less
than 1250 g and in 50% of infants who weighed less than 750 g
 Vapotherm in RDS

 Vapotherm with heated and humidified, high-flow nasal

canula (>2 L/min) has been used for respiratory support
of neonates and to facilitate early extubation. 
 Neonatal units in the United States and the United
Kingdom use Vapotherm as a means of providing
respiratory support. This device allows the delivery of
high flows of gas at body temperature with close to
100% relative humidity
 Advantages of vapotherm in RDS

 Evidence suggests that Vapotherm may be an

effective and well-tolerated method of providing
babies with respiratory support.
 Advantages over therapies such as CPAP, include:
a reduction in the number of ventilator days and
reduced nasal trauma. It may be better tolerated
than other forms of noninvasive respiratory
therapy; weight gain is improved using Vapotherm
and that oral feeding can be introduced earlier.
 Assisted ventilation of the lungs

 Kirby and deLemos introduced assisted ventilation several

decades ago. 
  Assisted ventilation further decreased respiratory distress
syndrome–related morbidity and mortality; however, early
ventilators were associated with complications, such as air
leaks, bronchopulmonary dysplasia (BPD; secondary to
barotrauma or volutrauma), airway damage, and
intraventricular hemorrhage.
 Assisted ventilation of the lungs

 Advances in microprocessor-based technology,

transducers, and real-time monitoring have enabled
patient-driven ventilator control and synchronization of
mechanical ventilation with patient effort.
 The novelty of the newer ventilation techniques has
generated controversies that remain to be resolved.
Among these are signal detection and transduction,
optimal volume delivery (ventilation modes), and weaning
from mechanical ventilation.
 Synchronous intermittent mandatory
ventilation
 Synchronous intermittent mandatory ventilation is a
technique in which some of the patient's respirations are
synchronized with breaths the ventilator delivers.
 In a randomized, controlled trial, the incidence of BPD
(defined as oxygen requirement at a corrected
gestational age of 36 wk) was significantly reduced with
this therapy compared with standard intermittent
mandatory ventilation (47% vs 72%, respectively).
 High-Frequency Ventilation

 With high-frequency ventilation (HFV), small tidal volumes (less

than anatomic dead space) are usually delivered at rapid
frequencies, thus eliminating the wide pressure swings seen
with conventional ventilators. Conventional ventilators may
deliver high or low tidal volumes (barotrauma or volutrauma),
cause wide pressure swings, or cause cardiovascular
compromise.
 HFV was originally designed to treat patients with air leak.

 HFV techniques involve a learning curve, and optimal ventilator

strategies vary with the stage of respiratory distress syndrome.
 Types of high-frequency ventilation
 High-frequency oscillatory ventilation (HFOV) has a frequency
range of 10-15Hz. Early in its use, high-HFOV was found to be
clearly superior to conventional ventilation. In one clinical trial,
prophylactic HFOV reduced chronic lung disease.
 High-frequency jet ventilation. The frequency range of this modality
is 4-11Hz (usually 7Hz). High-frequency jet ventilation has to be
used in tandem with conventional ventilation to provide positive
end-expiratory pressure (PEEP) and sigh breaths. It decreases air
leaks.
 Some neonatologists prefer to use high-frequency jet ventilation to
treat infants with pulmonary air leaks
 Treatment of RDS(cont.)

 High-frequency flow interrupter. The frequency range of this

modality is 6-15Hz, with the advantages of a built-in
conventional ventilator and an ability to provide sigh breaths. Its
use is also associated with a decreased incidence of air leaks
in infants with respiratory distress syndrome
 Inhaled NO has selective pulmonary vasodilation and, in
premature infants, it may have a role in decreasing
inflammation, reducing oxidative stress, and enhancing
alveolarization and lung growth. The effects of iNO may be
dependent on the timing, dose, and duration of iNO therapy
and on the extent of the infant's lung disease
 Nitric oxide therapy :precautions
 In selected premature neonates born at less than 32
weeks' gestation with respiratory distress syndrome and
hypoxic respiratory failure, low pulmonary blood flow, as
determined with Doppler echocardiography, may be
helpful in determining which patients are likely to benefit
from iNO therapy.
 For better understanding the issue, please read the NIH
Consensus Development Conference on “Inhaled Nitric Oxide
Therapy for Premature Infants” held October 27-29, 2010
 Supportive therapy in RDS
 Temperature regulation. Prevent hypothermia in neonates with
respiratory distress syndrome during delivery, resuscitation, and
transport. Care for these patients in a neutral thermal environment
with the use of a double-walled incubator or radiant warmer.
 Fluid, metabolic, and nutritional support. In infants with respiratory
distress syndrome, initially administer 5% or 10% dextrose
intravenously at a rate of 60-80 mL/kg/d.
 Closely monitor blood glucose (with Dextrostix testing), electrolytes,
calcium, and phosphorous levels, as well as renal function and
hydration (as determined by body weight and urine output), to
prevent any imbalance.
 Supportive therapy in RDS
 Add calcium at birth to the initial IV fluid. IV sodium
bicarbonate is often misused and is considered to be an
unproven therapy.
 Electrolytes should be added as soon as the patient
voids and as indicated by estimated serum electrolyte
levels.
 Gradually increase fluid intake to 120-140 mL/kg/d.
Extremely premature infants occasionally require fluid
intake of 200-300mL/kg or more because of insensible
water loss occurring from their large body surfaces.
 Supportive therapy in RDS

 After the neonate is stable, IV nutrition with amino

acids and lipid are commenced within 24-48
hours of birth. As soon as the patient can tolerate
oral feedings, trophic feeding with small volumes
(preferably breast milk) is commenced by using
the orogastric tube to stimulate gut development.
Gastric feedings are increased as tolerated, and
IV nutritional support is decreased proportionately
to maintain adequate fluid and calorie intake.
 Supportive therapies in RDS
 Circulation and anemia. Assess the baby's circulatory status by
monitoring his or her heart rate, peripheral perfusion, and blood
pressure. Administer blood or volume expanders, and use appropriate
vasopressors to support circulation. Closely monitor blood withdrawn
for laboratory tests in tiny patients and replace the blood with packed-
cell transfusion when it reaches 10% of the patient's estimated blood
volume or if the hematocrit level is less than 40-45%.
 Anemia and blood loss can be minimized by using placental
transfusion at delivery, by limiting blood loss with in vivo blood gas and
electrolyte estimations, and by using erythropoietin with iron in
extremely premature neonates.
Thank You …