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CHAPTER 1
INTRODUCTION
1.1 Background
Neonatal respiratory distress syndrome (RDS) is a condition of pulmonary
insufficiency that in its natural course commences at or shortly after birth and
increases in severity over the first 2 days of life. Clinically, RDS presents with
early respiratory distress comprising cyanosis, grunting, retractions and
tachypnea. Respiratory failure may develop, indicated by blood gas analysis, and
the diagnosis can be confirmed on chest X-ray with a classical ground glass
appearance and air bronchograms. If left untreated death may occur from
progressive hypoxia and respiratory failure.
In survivors resolution begins between 2 and 4 days. RDS is due to a deficiency
of alveolar surfactant along with structural immaturity of the lung and it is
mainly, but not exclusively, a disease of preterm babies. However, defining RDS
is difficult when prophylactic surfactant and very early continuous positive
airway pressure (CPAP) are used. The Vermont Oxford Neonatal Network
definition requires that babies have a PaO 2 <50 mm Hg (<6.6 kPa) in room air,
central cyanosis in room air or need for supplemental oxygen to maintain PaO 2
>50 mm Hg (>6.6 kPa), as well as the classical chest X-ray appearances.
The pathophysiology of this disorder has been clearly elucidated. Briefly, the
structurally immature and surfactant- deficient lung has a tendency to collapse.
The presence of relatively well perfused but poorly ventilated areas of the lung
results in ventilation/perfusion mismatch, with hypoxemia and hypercarbia. In
some patients, pulmonary vasoconstriction leads to persistence of pulmonary
hypertension and right-to-left shunts (via the patent ductus arteriosus and/or the
foramen ovale), resulting in more severe hypoxemia. This phenomenon, once
thought to be patrimony of the full term infant, is frequently observed in preterm
babies with RDS and has led some clinicians to consider the use of inhaled nitric
oxide in preterm infants when hypoxemia is unresponsive to adequate support
with mechanical ventilation.
CHAPTER 2
LITERATURE REVIEW
2.1 Defenition RDS
Neonatal respiratory distress syndrome (RDS) is a condition of pulmonary
insufficiency that in its natural course commences at or shortly after birth and
increases in severity over the first 2 days of life. Clinically, RDS presents with
early respiratory distress comprising cyanosis, grunting, retractions and
tachypnea. Respiratory failure may develop, indicated by blood gas analysis, and
the diagnosis can be confirmed on chest X-ray with a classical ground glass
appearance and air bronchograms. If left untreated death may occur from
progressive hypoxia and respiratory failure. In survivors resolution begins
between 2 and 4 days. RDS is due to a deficiency of alveolar surfactant along
with structural immaturity of the lung and it is mainly, but not exclusively, a
disease of preterm babies. However, defining RDS is difficult when prophylactic
surfactant and very early continuous positive airway pressure (CPAP) are used.
2.2 Epidiemology RDS
About 12 percent of babies born in the United States are preterm, which is
higher than in other developed countries. About 10 percent of premature babies in
the United States develop RDS each year. The risk of RDS rises with increasing
prematurity. In 2003, the total number of live births in the United States for all
races was 4,089,950; about 0.6 percent of newborns had RDS (about 24,000 or 6
per 1,000 live births). In 2005, there were 4,138,000 live births in the United
States, and a slightly larger number of babies were affected with RDS because the
rate of premature births had increased from 11.6 percent to 12.7 percent, mainly
due to a rise in late preterm births (34 to 36 weeks of gestation).
Even though the number of RDS cases in the United States is growing, the
infant mortality rate from RDS has dramatically declined from about 25,000
deaths per year in the 1960s to 860 deaths in 2005 because of surfactant
replacement therapy. Infant deaths from RDS were 2.6 times greater in African
thromboxane, atrial natriuretic peptide, endothelin, and nitric oxide (NO) are
involved in the regulation of pulmonary vascular tone in the fetus). Newborns
with PPHN are at risk of severe asphyxia and its complications including death,
neurologic injury and other problems. Studies over the past two decades have
clearly shown the critical role of NO-cGMP signaling in the regulation of the
fetal and neonatal pulmonary circulation, and that disruption of the NO-cGMP
cascade during the perinatal period leads to PPHN.
2.4 Patofisiology
The primary cause of RDS is inadequate pulmonary surfactant. The structurally
immature and surfactant-deficient lung has compliance and a tendency to
atelectasis; other factors in preterm infants that the risk of atelectasis are
decreased alveolar radius and weak chest wall. With atelectasis, well perfused but
poorly ventilated areas of lung lead to V/Q mismatch (with intra-pulmonary
shunting) and alveolar hypoventilation with resultant hypoxemia and hypercarbia.
Severe hypoxemia and systemic hypoperfusion result in decreased O2 delivery,
anaerobic metabolism and subsequent lactic acidosis. Hypoxemia and acidosis
may further impair oxygenatiob by causing pulmonary vasoconstriction, resulting
in right-to-left shunting at the levels of the foramen ovale and ductus arteriosus.
(Hermencan C,2007)
Other factors, such as baro/volutrauma and high FiO2, may initiate release of
inflammatory cytokines abd chemokines causing more endothelial and epithelial
cell injury. The injury results in reduced surfactant synthesis and function as well
as increased endothelial permeability leading to pulmonary edema. Leakage of
proteins into the alveolar space further exacerbates surfactant deficiency by
causing surfactant inactivation. Macroscopically, the lungs appear congested,
atelectatic and solid. Microscopically, diffuse alveolar atelectasis and pulmonary
edema are seen. An eosinophilic membrane composed of a fibrinous matrix of
materials from the blood and cellular debris (the hyaline membrane) lines the
visible airspaces that usually constitute dilated terminal bronchioles and alveolar
ducts.
Prematurity
Male gender
Familial predisposition
Perinatal asphysia
Cancasian race
Chorioamnonitis
2.7 Diagnosis
RDS diagnosis can be enforced through clinical manisfestation and can be
confirmed with gas blood analysis. Clinical manisfestation that happen to
neonatal baby is:
Cyanosis
Apnea
Nasal flaring
Rapid breathing
Shallow breathing
infiltrates
Blood gas analysis is a defenite indicator from exchange of gas to measure
acute respiratory failure. Eventhough the clinical manifestation need intubation
action and use of mechanical ventilation, the sampling of atrial blood is needed to
analys blood gas pressure ( PaO2, PaCO2 and pH) while monitoring with pulse
oxymetry. Heavy hypocxemia is marked with PaO2 < 50-60 mmHg with FiO2
60% or PaO2 <60 mmHg with FiO2 > 40% for babies < 1250 g, heavy
hipercapnea with PaCO2 > 55-60 mmHg with pH < 7,2 -7,25. Severity level of
respiratory distress can be evaluated through Silverman-Anderson score or
Downes score.
2.8 Management
The goals of management of an infant with RDS are to (Halliday, 2010)
Avoid hypoxemia and acidosis
Optimize fluid management which is avoid fluid overload and resultant body
and pulmonary edema while averting hypovolemia and hypotension
Reduce metabolic demands and maximize nutrition
Minimize lung injury secondary due to volutrauma and oxygen toxicity
The three most important advances in prevention and treatment of RDS have
been:
(a) antenatal glucocorticoids
(b) continuous positive airway pressure (CPAP) and positive end-expiratory
pressure (PEEP)
(c) surfactant replacement therapy. These have dramatically decreased
morbidity and mortality from RDS.
1. Antenatal glucocorticoids
Antenatal administration of corticosteroids that pass through the placenta to the
foetus (betamethasone 24 mg; or dexamethasone 24 mg; or 2 g. hydrocortisone)
10
has been shown to decrease the incidence of RDS. Best results are obtained if
more than 24 hours and less than 7 days have elapsed between commencement of
treatment and delivery.
2. Exogenous surfactant
It has been shown in multiple randomized controlled trials that the use of
exogenous surfactant in preterm infants improves oxygenation, decreases air
leaks, reduces mortality due to RDS, and decreases overall mortality.
A. Timing of surfactant administration:
Two approaches have been used for surfactant delivery which is prophylactic
and rescue treatment.
Prophylactic administration
Involves giving surfactant soon after birth, as soon as the infant has been
stabilized. The theoretical benefit of this approach is that replacement of
surfactant before RDS develops will avoid or ameliorate lung injury. Animal
studies have shown that the lung epithelium of very premature subjects can be
damaged within minutes of onset of ventilation. The damage can result in protein
leak which subsequently interferes with surfactant function.
Rescue administration
Involves giving surfactant to infants who have established RDS and require
mechanical ventilation and supplemental O2. The advantage of this approach is
that patients are not treated unnecessarily. Because surfactant currently can only
be given via an endotracheal tube, this would prevent intubation and mechanical
ventilation of infants who would do well without surfactant and avoid
unnecessary baro/volutrauma, adverse physiological effects of laryngoscopy, and
possible inadvertent hyperventilation. Past studies have shown greater reduction
in neonatal mortality with prophylactic administration versus rescue, especially in
infants greatest at risk for RDS (i.e., <27 weeks GA). However, with the use of
nasal CPAP in VLBW infants and higher rates of antenatal steroid administration,
there exists controversy on the optimal timing of surfactant administration,
balancing the benefits of early surfactant administration with the advantages of
11
Infasurf 3mL/kg
Survanta 4 mL/kg
12
13
14
for mechanical ventilation in VLBW infants treated with nasal CPAP, although
the impact on mortality and chronic lung disease have not been defined.
Furthermore, recent reports indicate that approximately 70% of infants with
birth weight <1,000 g will not be adequately managed with nasal CPAP and will
require intubation and mechanical ventilation. Nevertheless, in order to minimize
ventilator-induced lung injury, early extubation to nasal CPAP is a reasonable
strategy. Criteria for extubation to nasal CPAP in the first week of life are:
Adequate respiratory drive, and
Mean airway pressure 7 cmH2O, and
FIO2 0.35
Nasal CPAP is delivered via a specialized nasal mask or prongs, utilizing a
patient demand flow system. CPAP is administered between 4 and 6 cmH2O.
Lower pressures do not maintain lung inflation and higher pressures often cause
gastric distension. Limitations to the use of nasal CPAP include hypercarbia,
frequent episodes of apnea, gastric distension and breakdown of nasal skin and
mucosa from the mask/prongs. The method and timing of further weaning, from
nasal CPAP to supplemental O2 via nasal cannula, varies with gestational age,
post-natal age, weight and stability of the individual patient. Some infants require
a gradual transition to nasal cannula through sprinting, a process in which
infants are trialed on nasal cannula for a portion of the day and then returned to
nasal CPAP. As the infant demonstrates increased tolerance of these trials, the
length of these trials is slowly extended.. The time of these trials often coincides
with feeds, in order to minimize handling of VLBW infants (e.g., if feedings are
q3 hours, trials of nasal cannula are usually increased in 3 hour intervals).
5. Antibiotic therapy
The clinical and radiographic features of pneumonia may be indistinguishable
from RDS at birth. As a result, all infants with RDS should have blood cultures
and CBC drawn, and should receive empiric antibiotic therapy (Ampicillin and
Gentamicin). Generally, antibiotics may be discontinued if the blood culture has
15
16
CHAPTER III
CASE REPORT
3.1 Objective
The objective of this paper is to report a case of a 15 days old boy with a
diagnosis of respiratory distress.
3.2 Case
Baby SP, a 15 days old boy, with 1.1 kg of body weight and 29 cm of body
height, came to RSUP Haji Adam Malik Medan on 23th May at 12:00 AM. His
main complaint was difficulity in breathing
3.3 History of disease:
Baby SP, a boy, 15 days old, with 1.1 kg of BW and 29 cm of BH, came to
RSUP Haji Adam Malik Medan on 23th May at 12:00 AM with difficulity in
breathing as a chief complaint. It has been experienced by patient one day before
being admitted to the HAM hospital and this happened during milk feeding.
History of milk feeding which is incontinuous and sweathing is found when milk
feeding failed. History of turning blue found one day before admitted and
according to parents, blue has been found in lips, fingers and toes. Theres no
fever and history of fever also not found. Vomiting and diarrhea also not found.
Through the confession of parents, tiredness in drinking is found since 2 days
before admitted.
History of medication
History of family
None
None
History of pregnancy
History of birth
17
: Breast feeding
Physical Examination:
Present status:
Sensorium : compos mentis
HR: 98 bpm
RR: 22 bpm
BW: 21 kg
BL: 39 cm
Downe score: 5
anemic (-), icteric (+), dyspnea (+), cyanosis (-), edema (-).
Localized status:
Head
:
Head : frontal within normal limit
Face : edema (-), icteric (+)
Eye : light reflex (+/+), isochoric pupil, palpebral
conjunctiva pale (-/-), icteric (-)
Ears
Neck
Thorax
:
Lymph node enlargement (-), neck stiffness (-)
:
Symmetrical fusiform, retraction (+) epigastrial,
Intercostalis, suprasternal, icteric (+)
HR: 135 bpm, regular, murmur (-/-)
Abdomen :
Soepel, normal peristaltic, liver and spleen
unpalpable, icteric (+)
Extremities
:
adequate p/v, felt warm, CRT < 3, pitting oedema
18
Anogenital
: Male
2) Apnoe of Prematurity
3) Suspect of sepsis
4) Icteric Neonatorum
5) Baby born with less weight
Laboratory finding:
Complete blood analysis (May 23th 2015 / 02:41)
Test
Hemoglobin
Erythrocyte
Leucocyte
Thrombocyte
Hematocrite
Eosinophil
Basophil
Neutrophil
Lymphocyte
Monocyte
Neutrophil absolute
Lymphocyte absolute
Monocyte absolute
Eosinophil absolute
Basophil absolute
MCV
Result
16.7
4.53
21.74
435
47
0.30
0.30
64.20
24.20
11.00
13.96
5.26
2.39
0.06
0.07
104
Unit
g/dL
106/L
103/L
103/L
%
%
%
%
%
%
103/L
103/L
103/L
103/L
103/L
fL
References
10.3-17.9
3.20-5.60
5.0-19.5
229-553
31-59
1.0-5.0
0.00-1.00
17.00-60.00
20.00-70.00
1.00-11.00
5.5-18.3
2.8-9.3
0.5-1.7
0.02-0.70
0.1-0.2
82-126
19
MCH
MCHC
36.9
35.3
pg
g/dL
26-38
25-37
Clinical Chemistry
Blood Gas Analysis
Test
pH
pCO2
pO2
HCO3
Total CO2
BE
Saturasi O2
Result
7.390
17.0
192.0
10.3
10.8
-12.2
100.0
mmHg
mmHg
mmol/L
mmol/L
mmol/L
%
References
7.35-7.45
38-42
85-100
22-26
19-25
(-2) - (+2)
95-100
Carbohydrate Metabolism
Blood Glucose
74
mg/dL
40-60
Electrolyte
Natrium (Na)
Potassium(K)
Chloride (Cl)
135
3.5
107
Unit
mEq/L
mEq/L
mEq/L
135-155
3.6-5.5
96106
Theraphy :
- Recommended: Infant Radiant Warmer Theraphy with target skin temperature
36,5-37,5.
- Nasal CPAP with PEEP: 5-6 cmH2O, Flow 8-10 liter per minute, FiO2: 30%
Target of oxygen saturation: 92-96%.
- Total fluid requirement: 150 cc/kgBW/day = 210cc/ day
Parenteral 150cc/kgBW/day = 210cc/day
- IVFD D5% NaCl 0,225% (500cc) + D40% (50cc) + KCl 10 mEq + Ca
Gluconas 10cc 6cc/hour
20
FOLLOW UP
S
Nose : within normal range, O2 via nasal CPAP (+), NGT (-)
Mouth : using NGT (-), dysphagia (-)
Neck : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (+), icteric (+)
HR : 150 bpm, reguler, murmur(-)
21
22
Nose : within normal range, O2 via nasal CPAP (+), NGT (-)
Mouth : using NGT (-), dysphagia (-)
Neck : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (+), icteric (+)
HR : 150 bpm, reguler, murmur(-)
RR : 42 bpm, reguler, rhonchi (-)
Abdomen : peristaltic (+) normal, hepar/ lien, icteric (+)
Extremities : icteric (+), adequate p/v, warm, CRT < 3,
System Metabolic: icteric (+)
24/5: Bil.total/direk: 19.6/0.7
ALP/OT/PT: 135/42/20
Ca: 7.7
Ca ion: 0.98
23
24
(-); cry out loud; active movement; sucking refleks seen weak
Sens: CM; temperature: 36.7o C BW: 1.1 kg, BH: 39 cm
Head :
Head : Frontal within normal limit.
Eye
Nose : within normal range, O2 via nasal CPAP (+), NGT (-)
Mouth : using NGT (-), dysphagia (-)
Neck : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (+), icteric (-)
HR : 143 bpm, reguler, murmur(-)
RR : 40 bpm, reguler, rhonchi (-)
Abdomen : peristaltic (+) normal, hepar/ lien, icteric (-)
Extremities :icteric (-) adequate p/v, warm, CRT < 3,
System Metabolic: icteric (+) bocome lesser
24/5: Bil.total/direk: 19.6/0.7
ALP/OT/PT: 135/42/20
Ca: 7.7
Ca ion: 0.98
25
aff
26
Nose : within normal range, O2 via nasal CPAP (+), NGT (-)
Mouth : using NGT (-), dysphagia (-)
Neck : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (-), icteric (-)
HR : 145 bpm, reguler, murmur(-)
RR : 50 bpm, reguler, rhonchi (-)
Abdomen : peristaltic (+) normal, hepar/ lien, icteric (-)
Extremities :icteric (-) adequate p/v, warm, CRT < 3,
System Metabolic: icteric (+) bocome lesser
24/5: Bil.total/direk: 19.6/0.7
ALP/OT/PT: 135/42/20
Ca: 7.7
Ca ion: 0.98
27
28
Difficulity in breathing (-) ; icteric (+) found minimal on face; fever (-); cry
Nose : within normal range, O2 via nasal CPAP (+), NGT (-)
Mouth : using NGT (-), dysphagia (-)
Neck : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (-), icteric (-)
HR : 132 bpm, reguler, murmur(-)
RR : 48 bpm, reguler, rhonchi (-)
Abdomen : peristaltic (+) normal, hepar/ lien, icteric (-)
Extremities :icteric (-) adequate p/v, warm, CRT < 3,
System Metabolic: icteric (+) bocome lesser
24/5: Bil.total/direk: 19.6/0.7
ALP/OT/PT: 135/42/20
Ca: 7.7
Ca ion: 0.98
29
3. Unproven sepsis
4. Hiperbilirubinemia unconjugated
P
Nose : within normal range, O2 via nasal CPAP (+), NGT (-)
Mouth : using NGT (-), dysphagia (-)
Neck : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (-), icteric (-)
30
31
Nose : within normal range, O2 via nasal CPAP (+), NGT (-)
Mouth : using NGT (-), dysphagia (-)
Neck : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (-), icteric (-)
HR : 140 bpm, reguler, murmur(-)
RR : 48 bpm, reguler, rhonchi (-)
Abdomen : peristaltic (+) normal, hepar/ lien, icteric (-)
Extremities :icteric (-) adequate p/v, warm, CRT < 3,
System Metabolic: icteric (-)
30/5: Bil. total/direk: 4/0,3
30/5:Ca ion/Ca/Na/K/Cl: 1,05/8,1/135/3,3/105
ALP/SGOT/SGPT: 135/42/20
System Infection: still not stable, fever (-), temperature: 36.7
27/5: Blood Culture: No Growth
31/5: Leukosit: 14,200
System Hematologic: still not stable, pale and bleeding not found
System musculoskeletal: Stable
A
32
3. Unproven sepsis
4. Hiperbilirubinemia unconjugated
P
Nose : within normal range, O2 via nasal CPAP (+), NGT (-)
Mouth : using NGT (-), dysphagia (-)
Neck : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (-), icteric (-)
33
34
35
CHAPTER IV
DISCUSSION
Theory
Definition
Case
Baby SP is a preterm baby with
early
comprising
respiratory
cyanosis,
distress
grunting,
and
it
exclusively, a
is
mainly, but
disease
of
not
preterm
or
within
characterized
by
h.
RDS
tachypnea
(>60
incontinuous
and sweathing is
retractions, nasal flaring, grunting, and History of turning blue found one
cyanosis in room air. Tachypnea is due
36
ventilation
to
compensate
for
compliant
lungs.
Grunting
features
hypotension,
hyperkalemia.
may
include
acidosis
and
The
typical
chest
out
of
the
lung
fields.
findings.
Acute
physical
examination
37
disease,
ROP,
and
neurologic
impairment.
Diagnosis
Clinical criteria:
- Cyanosis
- Apnea
respiratory distress:
- Nasal flaring
a) Cinical manifestation
- Rapid breathing
- Shallow breathing
hospital,
according
to
patients
cyanosis.
with breathing
- Breath sounds that include rales
- Poor lung aeration
- Accessory muscle usage
- Chest x-ray showing atelectasis, air
bronchograms, and granular
infiltrates
Theraphy
Theraphy which is given for RDS is:
-Respiratory
management
through
CPAP
- Antibiotic theraphy such as ampicilin
and gentamicin.
- Thermoregulation such as radiant
warmer.
38
CHAPTER 4
SUMMARY
Baby SP, a boy, 15 days old, with 1.1 kg of BW and 29 cm of BH, came to
RSUP Haji Adam Malik Medan on 23th May at 12:00 AM with difficulity in
breathing as a chief complaint. It has been experienced by patient one day
before being admitted to the HAM hospital and this happened during milk
feeding. History of milk feeding which is incontinuous and sweathing is found
when milk feeding failed. History of turning blue found one day before
admitted and according to parents, blue has been found in lips, fingers and toes.
39
Theres no fever and history of fever also not found. Vomiting and diarrhea also
not found. Through the confession of parents, tiredness in drinking is found
since 2 days before admitted. Patient was diagnosed with Respiratory Distress
ec
Neonatal
Pneumonia,
apnoe
of
prematurity,
unproven
sepsis,
Hiperbilirubinemia unconjugated and baby born with less weight. Patient was
treated with Infant Radiant Warmer Theraphy with target skin temperature
36,5-37,5, nasal CPAP with PEEP: 5-6 cmH2O, Flow 8-10 liter per minute,
FiO2: 30% Target of oxygen saturation: 92-96%, total fluid requirement: 150
cc/kgBW/day = 210cc/ day, parenteral 150cc/kgBW/day = 210cc/day, IVFD
D5% NaCl 0,225% (500cc) + D40% (50cc) + KCl 10 mEq + Ca Gluconas
10cc: 6cc/hour ;GIR: 7,3 kg/kgBW/minute (D8%), Aminosteril 6%
2gr/kgBW/day = 2,8 gr/day = 47cc/day = 1,9cc/hour/iv, Ivelip 20%
1gr/kgBW/day = 1,4 gr/day = 7cc/day = 0,3cc/hour/iv, Enteral: Tropic Feeding
30cc/kgBW/day = 42cc/day, breast feeding diet/PASI: 3cc/2jam/orogastric
tube, Ceftazidime injection 55mg/12 hour/iv, Gentamicin injection 5mg/24
hour/iv, Aminofilin loading injection with dosage 6mg/kgBW = 6,5 mg/iv.
REFERENCE
1. Kasap B, Duman N, Ozer E, Tatli M, Kumral A, Ozkan H.Transient tachypnea of
the newborn: predictive factor for prolonged tachypnea. Pediatr Int
2008;501:81-4.
2. Avery ME, Gatewood OB, Brumley G. Transient tachypnea of newborn.
Possible delayed resorption of fluid at birth. Am J Dis Child 2004;111:380-5.
3. The Reagent Of University of California, 2004
40
4. Halliday HL, Ehrenkranz RA, Doyle LW: Early (<8 days) postnatal
corticosteroids for preventing chronic lung disease in preterm infants. Cochrane
Database Syst Rev 2010:CD001146.
5. Hermansen C, Lorah K. Respiratory distress in the newborn. Am Fam Physician.
2007;76:987-94.
6. Eichenwald E. Mechanical ventilation. Dalam: Cloherty J, Eichenwald E, Stark
A, penyunting. Manual of neonatal care. Edisi 6. Philadelphia: Lippincott
Williams & Wilkins; 2008. h. 331-42.
7. Rennie JM, Bokhari SA. Recent advances in neonatology. Arch. Dis. Child.
Fetal Neonatal ed. 1999;81:F1-F4
8. March
of
Dimes
Web
site.
Premature
birth.
Available
at:
2006.
Accessed
May
7,
http://www.lungusa.org/site/pp.asp? c=dvLUK9O0E&b=35693.
2007,
at: