Makalah Lapkas

1
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.
Fortunately, the natural course of the disease in many low-birthweight infants
has been altered by the introduction of exogenous surfactant. The management of
these infants is complex and requires a multidisciplinary team approach to obtain
best outcomes. The application of the basic principles of neonatal care, such as
thermoregulation, cardiovascular and nutritional support, treatment of early
neonatal infection, and prevention of nosocomial infection, is crucial to achieve
the therapeutic goals. Clearly, surfactant replacement therapy, continuous positive
airway pressure (CPAP), and mechanical ventilation in its different modalities are
the mainstay for the respiratory support of these patients.
CHAPTER 2
LITERATURE REVIEW
2.1 Definition 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 Epidemiology 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
American babies than in Caucasian babies, although Caucasian babies are at a
higher risk to develop the condition. In Indonesia, out of 950.000 newborn with
low-weight, approximately 150.000 newborn suffers from RDS and most of the
case is hyalin membrane disease.
2.3 Patogenesis
1. Transient tachypnea of the newborn
TTN is a parenchymal lung disorder characterized by pulmonary edema that
results from delayed resorption and clearance of fetal alveolar fluid in term
infants). The excess fluid in the lungs in TTN results in decreased pulmonary
compliance and increased airway resistance The mechanism causing changes in
pulmonary function are primarily associated with the extrinsic compression of
small airways by fluid in the extra-alveolar interstitium. Tachypnea develops to
compensate for the increased work of breathing associated with reduced
compliance and increased airway resistance. (Avery ME, 2004)
2. Respiratory distress syndrome
RDS is also known as hyaline membrane disease; it is the major cause of
neonatal respiratory distress, especially in preterm infants. RDS is caused by a
deficiency of surfactant. Surfactant is a phospholipid mixture that is responsible
for stabilizing distal alveoli, at low end-expiratory lung volumes, by reducing
surface tension). When surfactant is deficient, the infant may not be able to
generate the increased inspiratory pressure required to inflate alveolar units,
resulting in the development of progressive atelectasis. Diffuse atelectasis results
in low compliance, high resistance in small airways, and low functional residual
capacity. Hypoxemia results primarily from mismatching of ventilation and
perfusion as blood bypasses the atelectatic air spaces. Right-to-left shunting then
occurs through the ductus arteriosus and foramen ovale because of increased
pulmonary vascular resistance (PVR) and contributes to the decreased
oxygenation.
3. Persistent pulmonary hypertension
PPHN is caused by persistently elevated PVR that leads to right-to-left
shunting through the foramen ovale and the ductus arteriosus, resulting in
hypoxemia). PPHN occurs primarily in term or late preterm infants (34 weeks
gestation). The high pulmonary resistance is secondary to a number of factors,
including: low arteriolar and alveolar oxygen levels; hypercarbia; acidosis;
alveolar fluid pressure; lack of mechanical, rhythmic distention of the lung; and
the net vasoconstricting action of a number of humoral agents. Catecholamines,
histamine, bradykinin, angiotensin, adenosine, serotonin, prostaglandins,
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 oxygenation 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.
Diagram 1 Patofisiology of RDS

2.5 Risk Factors
Prematurity
Male gender
Familial predisposition
Cesarean section without labor
Perinatal asphysia
Cancasian race
Infant of diabetic mother
Chorioamnonitis
Non-Immune hydrops fetalis
2.6 Clinical Manifestation

Signs of RDS appear immediately after birth or within 4 h. RDS is
characterized by tachypnea (>60 breaths/min), intercostal and subcostal
retractions, nasal flaring, grunting, and cyanosis in room air. Tachypnea is due to
an attempt to increase minute ventilation to compensate for a decreased tidal
volume and increased dead space. Retractions occur as the infant is forced to
generate a high intrathoracic pressure to expand the poorly compliant lungs.
Grunting results from the partial closure of the glottis during forced expiration in
an effort to maintain FRC. After an initial improvement with resuscitation and
stabilization, an uncomplicated course is often characterized by a progressive
worsening for 48 to 72 h. Recovery usually coincides with a diuresis after an
initial period of oliguria. Other clinical features may include hypotension,
acidosis and hyperkalemia. The typical chest radiograph shows low lung volumes
and a bilateral, reticular granular pattern (ground glass appearance) with
superimposed air bronchograms. In more severe cases, there is complete white
out of the lung fields. Application of positive airway pressure may minimize or
even eliminate these radiographic findings. Acute complications include air leaks
and intracranial hemorrhage. Long-term, RDS has been associated with an
increased incidence of chronic lung disease, ROP, and neurologic impairment.
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
Decreased urine output
Nasal flaring
Puffy or swollen arms and legs
Rapid breathing
Shallow breathing
Shortness of breath and grunting sounds while breathing
Increased oxygen requirement
Paradoxical chest wall movement with breathing
Breath sounds that include rales
Poor lung aeration
Accessory muscle usage
Chest x-ray showing atelectasis, air bronchograms, and granular
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
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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.
Table 1 : 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)
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(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)
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
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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
avoiding mechanical ventilation and volutrauma. The current approach to the
timing of surfactant therapy at UCSF is summarized in Table 1.
Table 1: Guidelines for intubation and timing of surfactant administration in

preterm infants.
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B. Administration and dose of surfactant

For prophylactic administration, the position of the endotracheal (ET) tube
should be verified by two people before surfactant is given. Attach the surfactant
syringe to the side port of the ET tube, occlude end of ET tube, and administer
surfactant as a single aliquot over 5 sec. For rescue therapy, obtain chest
radiograph to confirm tube position. Administer surfactant through a feeding tube
inserted to (but not past) the end of the ET tube. Administer in same manner as
with prophylactic treatment. Slower administration may interfere with its
efficacy. After administration, the infant should be hand ventilated and may
transiently require higher ventilatory support. Several studies have shown that
two doses, 12 h apart, may be more effective than single dose therapy. More than
2 doses is rarely required and is rarely effective. The dose of surfactant is:
Infasurf 3mL/kg
Survanta 4 mL/kg
C. Criteria for rescue treatment

Rescue treatment with surfactant should be given to preterm infants who have:
Respiratory distress, necessitating intubation and assisted ventilation,
No radiological evidence of another disease process, and require either
FIO2 > 0.3 or a mean airway pressure 7 cmH2O
D. Complications
Although surfactant administration is relatively safe, complications include
obstruction of the endotracheal tube, transient increases in O2 requirement and
ventilatory settings, and pulmonary hemorrhage, an infrequent adverse effect
reported in 2-6% of infants given surfactant.
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3. Oxygen
Oxygen should be administered to preterm infants in concentrations sufficient
to maintain PaO2 between 50-70 mmHg or saturation (by pulse oximetry)
between 85-92%. Higher O2 concentrations may exacerbate lung injury and will
increase the risk of retinopathy of prematurity.
4. Respiratory Management
The initial decision in respiratory management of an infant with RDS is
whether the infant can be adequately managed with nasal CPAP (i.e., no treatment
with surfactant) or should receive endotracheal intubation, surfactant therapy and
mechanical ventilation. Endotraheal intubation should be performed in infants
that require prophylactic surfactant administration or who meet the criteria.
Table 2: Indications for intubation of preterm infant during

resuscitation.
The goals of ventilatory management in the intubated infant are to maintain
adequate oxygenation and ventilation while minimizing ventilator induced lung
injury. To achieve these aims, utilize a strategy of permissive hypercarbia,
maintaining PaCO2 between 45- 55 mmHg, theoretically reducing volutrauma
and preventing deleterious effects of hypocarbia. To reduce further the risk of
volutrauma, adjust ventilatory pressures to maintain tidal volume between 4-5
mL/kg. Administration of surfactant improves lung mechanics ( lung
compliance) and increases oxygenation by reducing atelectasis and increasing
FRC. It is extremely important to recognize the time frame of these changes.
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After surfactant administration, there may be very rapid improvements in

pulmonary function that necessitate rapid weaning of ventilator settings.
Close attention must be paid to tidal volume, blood gas tensions, transcutaneous
CO2 and pulse oximetry values in order to avoid inadvertent hyperventilation,
hyperoxia and overdistension of the lung, all of which can result in lung injury.
Although it may be necessary to wean FIO2, inspiratory pressure and ventilator
rate, one should decrease PEEP with extreme caution. Infants in the early phases
of RDS will rarely maintain adequate lung inflation if PEEP is <5 cmH2O, even
after administration of surfactant. Recently, much effort has been directed
towards other, less invasive modalities of respiratory support to prevent lung
injury, specifically nasal CPAP. CPAP, as treatment for RDS, was first described
in 1971 by George Gregory at UCSF. Modifications in the nasal CPAP delivery
system have generated renewed interest in nasal CPAP for the ventilatory
management of RDS. Randomized controlled trials have shown a decreased need
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,
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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
no growth after 48 hours, unless prenatal history or clinical scenario warrants
extended treatment.
6. Thermoregulation
Careful temperature control is imperative in all VLBW infants and is especially
important in infants with RDS to minimize metabolic demands and oxygen
consumption. RDS can limit oxygen uptake leading to hypoxia which limits the
ability of an infant to increase their metabolic rate when cold stressed, resulting in
a fall in body temperature. An incubator or radiant warmer must be utilized to
maintain a neutral thermal environment for the infant.
CHAPTER III
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CASE REPORT
3.1 Objective
The objective of this paper is to report a case of a 11 days old girl with a
diagnosis of respiratory distress.
3.2 Case
Baby PR, a girl 11 days old, with 1.49 kg of body weight and 41 cm of body
height, consulted to perinatology in RSUP Haji Adam Malik Medan as soon as
she was born on 18th July at 11:36 AM. Her main complaint was difficulty in
breathing.
3.3 History of disease:
Baby PR, a girl, 11 days old, with 1.49 kg of BW and 41 cm of BH, consulted
to perinatalogy in RSUP Haji Adam Malik Medan on 18th July at 11:36 AM with
difficulty in breathing as a chief complaint. It has been experienced by patient
two hours after she was born in HAM hospital. The patient was born by sectio
cesarean and doesnt cry immediately after birth. History of milk feeding which is
incontinuous when milk feeding. History of turning blue found two hours after
born according to doctor, blue has been found in lips, arm n shoulder. Theres no
fever, vomiting or diarrhea found.
History of medication
: None
History of family
None
History of parents medication
None
History of pregnancy
: The age of the patients mother was 41

during pregnancy. The gestation age was 28
weeks.
History of birth
: Birth was assisted by doctor in HAM

hospital. The patient was born sectio
cesarean and doesnt cry immediately after
birth. Body weight at birth was 1490 gram,
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body length at birth was 41cm and head

circumference was 28cm. Cyanosis (+),
Jaundice (-).
History of feeding
: Breast feeding (-)
Physical Examination:
Present status:
Sensorium: compos mentis
Body temperature: 37.2C
HR: 142 bpm
RR: 56 bpm
BW: 14.9 kg
BL: 41 cm
Chest circumference (CC): 26cm
Head circumference (HC): 28 cm
Downe score: 4
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
: both ear lobe in normal morphologic
Nose : septum deviation (-), nasal CPAP (-), NGT (-)

Mouth : normal
Neck
Thorax
: Lymph node enlargement (-), neck stiffness (-)

: Symmetrical fusiform, retraction (+) epigastrial,
Intercostalis, suprasternal, icteric (-)
HR: 134 bpm, regular, murmur (-/-)
RR: 38 bpm, regular, ronchi (-/-)
Abdomen : Soepel, normal peristaltic, liver and spleen

unpalpable, icteric (-)
Extremities
: adequate p/v, felt warm, CRT < 3, pitting
oedema
(-/-), icteric (-)
Anogenital
: Female
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Differential diagnosis :1) Respiratory distress

2) Transient tachypnea of the newborn
3) Meconium aspiration syndrome
Working diagnosis
: 1) Respiratory Distress ec DD/ - Hyalin Membrane

Disease
2) Apnoe of Prematurity
3) Suspect of sepsis
4) Baby born with less weight
Laboratory finding:
Complete blood analysis (July 18th 2016 / 15:54)
Test
Hemoglobin
Erythrocyte
Leucocyte
Thrombocyte
Hematocrite
Eosinophil
Basophil
Neutrophil
Lymphocyte
Monocyte
Neutrophil absolute
Lymphocyte absolute
Monocyte absolute
Eosinophil absolute
Basophil absolute
MCV
MCH
MCHC
Clinical Chemistry
Blood Gas Analysis
Result
11.0
3.05
13.440
144000
34
0.70
0.60
57.00
27.80
13.90
7.65
3.74
1.87
0.10
0.08
111
36.1
32.4
Unit
g/dL
106/L
103/L
103/L
%
%
%
%
%
%
103/L
103/L
103/L
103/L
103/L
fL
pg
g/dL
References
17-22
4.50-6.50
10.000-30.000
150000-350000
31-59
1.00-3.00
0.00-1.00
50.00-70.00
20.00-40.00
2.00-8.00
5.5-18.3
2.8-9.3
0.5-1.7
0.02-0.70
0.1-0.2
80-97
26.5-33.5
31.5-36.0
20
Test
pH
pCO2
pO2
HCO3
Total CO2
BE
Saturasi O2
Electrolyte
Natrium (Na)
Potassium(K)
Chloride (Cl)
Kalsium (Ca)
Result
7.270
27.0
172.0
12.4
13.2
-13.0
99.0
Unit
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
134
5.6
107
7.90
mEq/L
mEq/L
mEq/L
mEq/L
135-155
3.6-5.5
96106
8.410.2
16.20
ng/mL
< 0.05
Test Lain
Procalcitonin
Radiology :
21
Theraphy :
- Recommended: Infant Radiant Warmer Theraphy with target skin temperature
36,5-37,5.
- Nasal CPAP with PEEP: 5-6 cmH2O, Flow 8 liter per minute, FiO2: 35%
Target of oxygen saturation: 92-96%.
- Total fluid requirement: 80 cc/kgBW/day = 120cc/ day
Parenteral 80cc/kgBW/day = 120cc/day
- IVFD Dex 10% 5cc/hour
- Ceftazidime injection 75mg/12 hour/iv (Day 1)
- Gentamicin injection 8mg/36 hour/iv (Day 1)
- Vitamin K Injection 0.5mg/IM
- Gentamicin eye drops 1gtt (ED)
FOLLOW UP
July 19th 2016

Difficulity in breathing (+); icteric (-); fever (-); inactive movement;
sucking refleks seen weak

Sens: CM; temperature: 37.0o C BW: 1.49 kg, BH: 41 cm
Head :
Head : Frontal within normal limit.
Eye
: light reflex (+/+); isochoric pupil (+/+), pale conjungtiva

palpebral inferior (-/-)
Face : icteric (-)

Ear
Nose : within normal range, O2 via nasal CPAP (+), NGT (-)
Mouth : using NGT (-), dysphagia (-)
Neck : lymph node enlargement (-), neck stiffness (-)
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Thorax : symmetric fusiform, retraction (+), icteric (-)

HR : 145 bpm, reguler, murmur(-)
RR : 50 bpm, reguler, rhonchi (-)
Abdomen : peristaltic (+) normal, hepar/ lien, icteric (-)
Extremities : pulse : 145 bpm, regular, adequate p/v, warm, CRT < 3,
BP : 100/50 mmHg, muscular rigidity (+)
Systemic Infection: stable, fever (-), temperature: 37.0
18/7 : Leu: 13.440 10/L
Systemic Hematologic: stable, pale and bleeding not found
18/7: Hb/Ht/Tr: 11/34/144.000
Systemic musculoskeletal: Still not stable. extremital cyanosis (+), from left
arm to left shoulder
A
Systemic urogenital: Stable, enough urine output

1. Respiratory distress ec DD/ - Hyaline Membrane Disease
2. Apnoe of Prematurity
3. Suspect of sepsis
4. Baby born with less weight

Infant Radiant Warmer Theraphy with target skin temperature 36,537,5.
Nasal CPAP with FiO2: 30%, PEEP: 4-5, Flow: 8 liter per minute.
Oxygen saturation: 94-95%.
Total fluid requirement: 80 cc/kgBW/day = 120cc/ day
IVFD D 12,5% + Ca Gluconas 10cc 4cc/hour
Aminosteril 6% 2,0gr/kgBW/day = 2,58 gr/day = 49,6cc/day =
2,0cc/hour/iv
Ivelip 20% 0.5gr/kgBW/day = 1,24 gr/day = 6.2cc/day = 0,2cc/hour/iv
Enteral: Tropic Feeding 20cc/kgBW/day = 29.8cc/day = 2,5cc/2hour
Ceftazidime injection 75mg/12 hour/iv (Day 2)
Gentamicin injection 8mg/36 hour/iv (Day 2)
Heparin Injection 0.3cc/hour
23
July 20th 25th 2016

Difficulity in breathing (+) become lesser; icteric (-); fever (-); inactive
movement; sucking refleks seen weak; vomiting (+),4x

Head :
Eye

Face : icteric (-)

Ear
Mouth : using NGT (-), dysphagia (-)
Neck : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (+), icteric (+)
Extremities : icteric (-), adequate p/v, warm, CRT < 3,
System Metabolic: stable, Abdomen: distension (-)
18/7 : pH:7.270/ pCO2:27/ pO2:172/ HCO3:12.4/ Total CO2:13.2/
BE:-23/ Sat O2:99%
System Infection: stable, fever (-), temperature: 36.9
18/7 : Leu: 13.440 10/L, Procalcitonin:16.2
System Hematologic: stable, pale and bleeding not found
18/7: Hb/Ht/Tr: 11/34/144.000
System musculoskeletal: Still not stable, extremital cyanosis (+), from left
A
System urogenital: Stable, enough urine output

1. Respiratory distress ec Hyaline Membrane Disease
24
P

Nasal CPAP with FiO2: 30% , PEEP: 4-5, Flow: 8 liter per minute.
Oxygen saturation: 94-95%.
IVFD D12,5% + Ca Gluconas 10cc 91,9cc/day 5cc/hour
Aminosteril 6% 2gr/kgBW/day = 12.98 gr/day = 49,7cc/day =
2,0cc/hour/iv
Ivelip 20% 1gr/kgBW/day = 1,49 gr/day = 7.4cc/day = 0,3cc/hour/iv
Enteral: fasting
Ceftazidime injection 75mg/12 hour/iv (Day 3-8)
Gentamicin injection 8mg/36 hour/iv (Day 3-8)
Heparin Injection 0.3cc/hour
Recommended: - Light therapy 1x24 hour
-
S
O
Observe work of breathing
July 26 - 28th 2016

Difficulity in breathing (+) become lesser; inactive movement
Head :
Eye

Face : icteric (-)

Ear
Mouth : using OGT (+), dysphagia (-)
25
Neck : lymph node enlargement (-), neck stiffness (-)

Thorax : symmetric fusiform, retraction (+), icteric (-)
Extremities :icteric (-) adequate p/v, warm, CRT < 3,
System Metabolic: stable, icteric (-)
25/7: kolesterol total : 123
Trigliserida : 105
Ca/Na/K : 8.2/137/4.7
GDS : 59
HDL/LDL : 34 / 79
P:3.3/ Cl:109/Mg:1.95
Ca ion:1.2
System Infection: still not stable, fever (-), temperature: 36.9
25/7 : Leu: 14.490 10/L
25/7: Procalcitonin:0.45
System Hematologic: stable, pale and bleeding not found
25/7: Hb/Ht/Tr: 9.1/28/490.000
CRP: <0.7
System musculoskeletal: Still not stable, extremital cyanosis (+) from left
A
System urogenital: Stable, enough urine output


Nasal CPAP with 1/2 liter per minute.
Total fluid requirement: 150 cc/kgBW/day
Parenteral 50cc/kgBW/day
IVFD D5% NaCl 0,225% (430cc) + D40% (70cc) + KCl 10 mEq + Ca
Gluconas 10cc 2cc/hour
26
Aminosteril 6% 3gr/kgBW/day = 4.97 gr/day = 3cc/hour

Ivelip 20%
3gr/kgBB/day 2.98gr/day 9.6cc/hour
Enteral: 100cc/kgBW/day = 149cc/day

Breast feeding diet/substitute of breastfeeding: 12cc/2jam/orogastric
tube
Heparin Injection 0.3cc/jam (Day 9-11)
S
O
July 29th - August 1st 2016

Cry out loud; active movement; sucking refleks seen weak
Head :
Eye

Face : normal
Ear
Nose : within normal range, O2 via nasal CPAP (-), NGT (-)
Thorax : symmetric fusiform, retraction (-), icteric (-)
A
Extremities : HR:142bpm, icteric (-) adequate p/v, warm, CRT < 3,

27

IVFD D5% NaCl 0,225% (430cc) + D40% (70cc) + KCl 10 mEq + Ca
Gluconas 10cc 3cc/hour
Enteral: 110cc/kgBW/day = 162cc/day
Breast feeding diet/substitute of breast feeding: 14cc/2jam/orogastric
tube
S
O
August 2nd 2016

Head :
Eye

Face : Normal
Ear
A

28
P

Parenteral threeway
Enteral: 160cc/kgBW/day
tube
Aminofilin injection 4mg/12 hour/iv (Day 16)
Ferris drop 1 x 0.3cc
Zamel drop 1 x 0.3cc
Nyastatin drop 4x0,5cc
Recommended : vitamin E 100 IU 1 x 0.25cc
S
O
August 3rd 2016

Head :
Eye

Face : Normal
Ear
29

A

3. Unproven sepsis

Parenteral : threeway
Enteral: 160cc/kgBW/day
tube
Vitamin E 100 IU 1 x 0.3cc
S
O
August 4th 2016

Cry out loud; active movement; sucking refleks seen good; fever (-)
Head :
Eye

Face : Normal
Ear
30


3. Unproven sepsis

Parenteral : Enteral: 160cc/kgBW/day
tube
S
O
August 5th 13th 2016

Cry out loud; active movement; sucking refleks seen weak; fever (-)
Head :
31

Eye

Face : Normal
Ear
A

3. Unproven sepsis

tube
Recommended : Observe temperature
Vitamin K injection 1g/ IM per week
32
S
O
August 14 - 17th 2016

Cry out loud; active movement; sucking refleks seen weak; fever (-)
Head :
Eye

Face : Normal
Ear
A

3. Unproven sepsis

tube
33

Recommeded : tranfuse PRC III 11 cc
S
O
August 18 - 26th 2016

Cry out loud; active movement; sucking refleks seen good; fever (-)
Head :
Eye

Face : Normal
Ear
Nose : within normal range, O2 via nasal CPAP (-), NGT (-),
Left anterior nasal cavum closed.
A

3. Unproven sepsis
5. Sinekia cavum sinistra dextra
34

Breast feeding diet/substitute of breastfeeding: 30cc/2jam/oral
Recommeded : tranfuse PRC III 11 cc
35
CHAPTER IV
DISCUSSION
Theory
Definition
Case
Baby PR is a preterm baby with
Neonatal respiratory distress syndrome gestational age 32 - 34 weeks who

(RDS) is a condition of pulmonary suffered with main complain difficulty
insufficiency that in its natural course in breathing. It has been experienced by
commences at or shortly after birth and patient two hours after she was born in
increases in severity over the first 2 HAM hospital.
days of life. Clinically, RDS presents
with
early
comprising
respiratory
cyanosis,
distress
grunting,
retractions and tachypnea. RDS is due

to a deficiency of alveolar surfactant
along with structural immaturity of the
lung
and
it
exclusively, a
is
mainly, but
disease
of
not
preterm
babies. However, defining RDS is

difficult when prophylactic surfactant
and very early continuous positive
airway pressure (CPAP) are used.
Clinical Manifestation
Baby PR suffered from chief
36
Signs of RDS appear immediately after

birth
or
within
characterized
by
h.
RDS
tachypnea
complaint difficulty in breathing.
is History of milk feeding which is
(>60
breaths/min), intercostal and subcostal

retractions, nasal flaring, grunting, and
incontinous when milk feeding.

History of turning blue found two
hours after born according to
cyanosis in room air. Tachypnea is due
doctor, blue has been found in lips,
to an attempt to increase minute

ventilation
to
compensate
for
decreased tidal volume and increased

dead space. Retractions occur as the
infant is forced to generate a high
intrathoracic pressure to expand the
poorly
compliant
lungs.
Grunting
results from the partial closure of the

glottis during forced expiration in an
effort to maintain FRC. After an initial
improvement with resuscitation and
stabilization, an uncomplicated course
is often characterized by a progressive
worsening for 48 to 72 h. Recovery
usually coincides with a diuresis after
an initial period of oliguria. Other
clinical
features
hypotension,
hyperkalemia.
may
include
acidosis
and
The
typical
chest
radiograph shows low lung volumes

and a bilateral, reticular granular
pattern (ground glass appearance) with
superimposed air bronchograms. In
more severe cases, there is complete
white
out
of
the
lung
arm and shoulder.
fields.
Theres no fever, vomiting or

diarrhea found.
Through
physical
examination
found retraction in epigastrial and

intercostal.
37
Application of positive airway pressure

may minimize or even eliminate these
radiographic
findings.
Acute
complications include air leaks and

intracranial hemorrhage. Long-term,
RDS has been associated with an
increased incidence of chronic lung
disease,
ROP,
and
neurologic
impairment.
Diagnosis
Clinical criteria:
Based on the theory, this patient also
- Cyanosis
fulfilled some of the clinical and
- Apnea
laboratory criteria to be diagnosed as
- Decreased urine output
respiratory distress:
- Nasal flaring
a) Cinical manifestation
- Puffy or swollen arms and legs
- Patient suffers from difficulty in
- Rapid breathing
- Shallow breathing
- Shortness of breath and grunting
sounds while breathing
- Increased oxygen requirement
- Paradoxical chest wall movement
with breathing
- Breath sounds that include rales
breathing known as apnea.

- It has been experienced by patient
two hours after she was born in
HAM hospital.
- History of turning blue found two
hours after born according to doctor,
blue has been found in lips, arm n
shoulder.
- Poor lung aeration

- Accessory muscle usage
- Chest x-ray showing atelectasis, air
bronchograms, and granular
infiltrates
Theraphy
Theraphy that used in this case is:

- Nasal CPAP with PEEP: 4-5 cmH2O,
38
Theraphy which is given for RDS is:
Flow 8-10 liter per minute, FiO2:
-Respiratory
30% Target of oxygen saturation: 94-
management
through
CPAP
- Antibiotic theraphy such as ampicilin
and gentamicin.
- Thermoregulation such as radiant
warmer.
95%.
- Gentamicin injection 8mg/36 hour/iv
- Infant Radiant Warmer Theraphy with
target skin temperature 36,5-37,5.
39
CHAPTER 5
SUMMARY
Baby PR, a girl 11 days old, with 1.49 kg of body weight and 41 cm of body
height, consulted to perinatology in RSUP Haji Adam Malik Medan as soon as
she was born on 18th July at 11:36 AM. Her main complaint was difficulty in
breathing. It has been experienced by patient two hours after she was born in
HAM hospital. The patient was born by sectio cesarean and doesnt cry
immediately after birth. History of milk feeding which is incontinous when milk
feeding. History of turning blue found two hours after born according to doctor,
blue has been found in lips, arm n shoulder. Theres no fever, vomiting or
diarrhea found. Patient was diagnosed with Respiratory Distress ec Hyalin
Membran Diseases. Patient was treated with Infant Radiant Warmer Theraphy
with target skin temperature 36,5-37,5, nasal CPAP with PEEP: 4-5 cmH2O,
Flow 8-10 liter per minute, FiO2: 30% Target of oxygen saturation: 94-95%, total
fluid requirement: 80 cc/kgBW/day = 120 cc/ day, parenteral 80 cc/kgBW/day =
120 cc/day, IVFD D 12,5% + Ca Gluconas 10cc: 4cc/hour, Aminosteril 6%
2gr/kgBW/day = 2,58 gr/day = 49,6cc/day = 2cc/hour/iv, Ivelip 20%
0,5gr/kgBW/day = 1,24 gr/day = 6,2cc/day = 0,2cc/hour/iv, Enteral: Tropic
Feeding 20cc/kgBW/day = 29,8cc/day = 2,5cc/2hour, Ceftazidime injection
75mg/12 hour/iv, Gentamicin injection 8mg/36 hour/iv, Aminofilin injection
4mg/12 hour/iv.
40
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
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:
http://www.marchofdimes.com/ 21209_11560.asp. Accessed January 21, 2010.

9. Respiratory distress syndrome of the newborn fact sheet. American Lung
Association,
2006.
Accessed
May
7,
http://www.lungusa.org/site/pp.asp? c=dvLUK9O0E&b=35693.
2007,
at:

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1

oxide in preterm infants when hypoxemia is unresponsive to adequate support

2.1 Definition RDS

may further impair oxygenation by causing pulmonary vasoconstriction, resulting

Diagram 1 Patofisiology of RDS

Cesarean section without labor

Infant of diabetic mother

Non-Immune hydrops fetalis

2.6 Clinical Manifestation

Decreased urine output

Puffy or swollen arms and legs

Shortness of breath and grunting sounds while breathing

Increased oxygen requirement

Paradoxical chest wall movement with breathing

Breath sounds that include rales

Poor lung aeration

Accessory muscle usage

Chest x-ray showing atelectasis, air bronchograms, and granular

(c) surfactant replacement therapy. These have dramatically decreased

Table 1: Guidelines for intubation and timing of surfactant administration in

B. Administration and dose of surfactant

C. Criteria for rescue treatment

Table 2: Indications for intubation of preterm infant during

After surfactant administration, there may be very rapid improvements in

History of parents medication

: The age of the patients mother was 41

: Birth was assisted by doctor in HAM

body length at birth was 41cm and head

: Breast feeding (-)

Body temperature: 37.2C

HR: 142 bpm

Chest circumference (CC): 26cm

Head circumference (HC): 28 cm

: both ear lobe in normal morphologic

Nose : septum deviation (-), nasal CPAP (-), NGT (-)

: Lymph node enlargement (-), neck stiffness (-)

RR: 38 bpm, regular, ronchi (-/-)

Abdomen : Soepel, normal peristaltic, liver and spleen

Differential diagnosis :1) Respiratory distress

: 1) Respiratory Distress ec DD/ - Hyalin Membrane

July 19th 2016

sucking refleks seen weak

: light reflex (+/+); isochoric pupil (+/+), pale conjungtiva

Face : icteric (-)

: both ear lobe in normal morphologic

Thorax : symmetric fusiform, retraction (+), icteric (-)

Systemic urogenital: Stable, enough urine output

4. Baby born with less weight

July 20th 25th 2016

movement; sucking refleks seen weak; vomiting (+),4x

: light reflex (+/+); isochoric pupil (+/+), pale conjungtiva

Face : icteric (-)

: both ear lobe in normal morphologic

System urogenital: Stable, enough urine output

4. Baby born with less weight

Observe work of breathing

July 26 - 28th 2016

: light reflex (+/+); isochoric pupil (+/+), pale conjungtiva

Face : icteric (-)

: both ear lobe in normal morphologic

Neck : lymph node enlargement (-), neck stiffness (-)

System urogenital: Stable, enough urine output

4. Baby born with less weight