Lapkas Anak Rds

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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.
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 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
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 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.
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
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)
(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)
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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
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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.
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
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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.
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.
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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.
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
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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
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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.
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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
: IVFD D5% NaCl 0.225%
History of family
None
History of parents medication
None
History of pregnancy
: The age of the patients mother was 17

during pregancy. The gestation age was 7
months.
History of birth
: Birth was assisted by traditional midwife.

The patient was born pervaginam and
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doesnt cry immediately after birth. Body

weight at birth was 1400 gram, body length
at birth was unclear and head circumference
was unclear. Cyanosis (-), Jaundice (-).
History of feeding
: Breast feeding
Physical Examination:
Present status:
Sensorium : compos mentis
Body temperature: 36.9C
HR: 98 bpm
RR: 22 bpm
BW: 21 kg
BL: 39 cm
Chest circumference (CC): 21cm
Head circumference (HC) : 25cm
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
: 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: 135 bpm, regular, murmur (-/-)
RR: 35 bpm, regular, ronchi (-/-)
Abdomen :
Soepel, normal peristaltic, liver and spleen
unpalpable, icteric (+)
Extremities
:
adequate p/v, felt warm, CRT < 3, pitting oedema
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(-/-), icteric (+)
Anogenital
: Male
Differential diagnosis :1) Respiratory distress

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

- Hyalin Membrane
Disease
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
GIR: 7,3 kg/kgBW/minute (D8%)
20
- 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/substitute of breast feeding: 3cc/2jam/orogastric tube
- Ceftazidime injection 55mg/12 hour/iv (Day 1)
- Gentamicin injection 5mg/24 hour/iv (Day 1)
- Aminofilin loading injection with dosage 6mg/kgBW = 6,5 mg/iv
FOLLOW UP
S
May 24th 2016

Difficulity in breathing (+) become lesser; icteric (+); fever (-); cry out
loud; active movement; sucking refleks seen weak

Sens: CM; temperature: 36.5o C BW: 1.1 kg, BH: 39 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 : limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (+), icteric (+)
HR : 150 bpm, reguler, murmur(-)
21
RR : 42 bpm, reguler, rhonchi (-)

Abdomen : peristaltic (+) normal, hepar/ lien, icteric (+)
Extremities : pulse : 150 bpm, regular, adequate p/v, warm, CRT < 3,
BP : 100/50 mmHg, muscular rigidity (+)
Systemic Infection: still not stable, fever (-), temperature: 36.5
23/5 : Leu: 15.64 10/L
Systemic Hematologic: still not stable, pale and bleeding not found
23/5: Hb/Ht/Tr: 13.7?40/100.000
Systemic musculoskeletal: Stable
A
Systemic urogenital: Stable, enough urine output

1. Respiratory distress ec DD/ - Neonatal Pneumonia
- Hyaine Membrane Disease
2. Apnoe of Prematurity
3. Suspect of sepsis
4. Icteric Neonatorum
5. Baby born with less weight

Infant Radiant Warmer Theraphy with target skin temperature 36,537,5.
Nasal CPAP with FiO2: 30% , PEEP: 5, Flow: 9 liter per minute.
Oxygen saturation: 90%.
Total fluid requirement: 150 cc/kgBW/day = 210cc/ day
IVFD D5% NaCl 0,225% (500cc) + D40% (50cc) + KCl 10 mEq + Ca
GIR: 4,8 kg/kgBW/minute (D8%)
Aminosteril 6% 2,5gr/kgBW/day = 3,5 gr/day = 58cc/day =

2,4cc/hour/iv
Ivelip 20% 1gr/kgBW/day = 1,4 gr/day = 7cc/day = 0,3cc/hour/iv
Enteral: Tropic Feeding 40cc/kgBW/day = 56cc/day
Breast feeding diet/substitute of breast feeding: 5cc/2jam/orogastric
tube
Ceftazidime injection 55mg/12 hour/iv (Day 2)
22
Gentamicin injection 5mg/24 hour/iv (Day 2)

Aminofilin maintanance dosage 4,4mg/12 hour/iv (Day 2)
Neo-K Injection 1mg/iv still waiting for family past 3 days
Recomemded: - konsul to Pediatric Neurology division
- If patient getting worse, repeated apnoe
Intubation plan: ventilator standby
May 25th 2016

Difficulity in breathing (+) become lesser; icteric (+); fever (-); cry out

Head :
Eye

Face : icteric (+)

Ear
Thorax : symmetric fusiform, retraction (+), icteric (+)
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
System Infection: still not stable, fever (-), temperature: 36.7
23
23/5 : Leu: 15.64 10/L

25/5: IT Ratio: 0.06, CRP kuantitatif: <0.7, Procalcitonin:0.62
System Hematologic: still not stable, pale and bleeding not found
23/5: Hb/Ht/Tr: 13.7?40/100.000
System musculoskeletal: Stable
System urogenital: Stable, enough urine output
1. Respiratory distress ec Neonatal Pneumonia

4. Hiperbilirubinemia unconjugated

Nasal CPAP with FiO2: 23% , PEEP: 5, Flow: 9 liter per minute.
Oxygen saturation: 90%.
Aminosteril 6% 3gr/kgBW/day = 4.2 gr/day = 70cc/day =
2,9cc/hour/iv
Ivelip 20% 1gr/kgBW/day = 1,4 gr/day = 7cc/day = 0,3cc/hour/iv
tube
24
Neo-K Injection 1mg/iv (Day 2) for 3 days

Light terapi 1x24 hour untill 25/5/16, time: 22.00
Recommended: - Hipocalemic correction
0.5cc/kgBW = 0.55cc in D5% (1:5) = 2.75cc
= 3cc finish in 20 minutes
May 26th 2016

Difficulity in breathing (+) become lesser; icteric (+) become lesser; fever
(-); cry out loud; active movement; sucking refleks seen weak
Head :
Eye

Face : icteric (+) become lesser

Ear
Thorax : symmetric fusiform, retraction (+), icteric (-)
Abdomen : peristaltic (+) normal, hepar/ lien, icteric (-)
Extremities :icteric (-) adequate p/v, warm, CRT < 3,
System Metabolic: icteric (+) bocome lesser
ALP/OT/PT: 135/42/20
Ca: 7.7
Ca ion: 0.98

23/5 : Leu: 15.64 10/L
25

26/5: Blood glucose level: 104 mg/dL
23/5: Hb/Ht/Tr: 13.7?40/100.000


Nasal CPAP with FiO2: 21% , PEEP: 5, Flow: 7,95 liter per minute.
Oxygen saturation: 90-95%.
Aminosteril 6% 3gr/kgBW/day = 4.2 gr/day = 70cc/day =
2,9cc/hour/iv
Ivelip 20%
aff

Breast feeding diet/substitute of breastfeeding: 6cc/2jam/orogastric
tube
26
Neo-K Injection 1mg/iv (Day 3) for 3 days

Nyastatin drop 4x0,5cc
May 27-29th 2016

Difficulity in breathing (-) ; icteric (+) become lesser; fever (-); cry out

Head :
Eye

Face : icteric (+) become lesser

Ear
Thorax : symmetric fusiform, retraction (-), icteric (-)
ALP/OT/PT: 135/42/20
Ca: 7.7
Ca ion: 0.98

23/5 : Leu: 15.64 10/L
27/5: Blood Culture: No Growth
23/5: Hb/Ht/Tr: 13.7?40/100.000
27

3. Unproven sepsis

Nasal CPAP with FiO2: 21% , PEEP: 5, Flow: 7,95 liter per minute.
Oxygen saturation: 90-95%.
tube
Ceftazidime injection 55mg/12 hour/iv (Day 5-7)
Gentamicin injection 5mg/24 hour/iv (Day 5-7)
Aminofilin maintanance dosage 4,4mg/12 hour/iv (Day 5-7)
May 30th 2016
28
Difficulity in breathing (-) ; icteric (+) found minimal on face; fever (-); cry
out loud; active movement; sucking refleks seen weak

Head :
Eye

Face : icteric (+) found minimal

Ear
ALP/OT/PT: 135/42/20
Ca: 7.7
Ca ion: 0.98

23/5 : Leu: 15.64 10/L
23/5: Hb/Ht/Tr: 13.7?40/100.000
A

29
3. Unproven sepsis
P

Parenteral 70cc/kgBW/day
Enteral: Tropic Feeding 80cc/kgBW/day
Breast feeding diet/substitute of breastfeeding: 9cc/2jam/orogastric
tube
May 31th 2016

Difficulity in breathing (-) ; icteric (+) found minimal ; fever (-); cry out

Head :
Eye

Face : icteric (+)

Ear
30

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
31/5: Leukosit: 14,200
A

3. Unproven sepsis

Parenteral 60cc/kgBW/day = 79,8cc/day
Enteral: Tropic Feeding 90cc/kgBW/day = 119,7cc/day
tube
31
June 1-3th 2016

Difficulity in breathing (-) ; icteric (-); fever (-); cry out loud; active
movement; sucking refleks seen weak

Head :
Eye

Face : icteric (-)

Ear
System Metabolic: icteric (-)
30/5:Ca ion/Ca/Na/K/Cl: 1,05/8,1/135/3,3/105
31/5: Leukosit: 14,200
A

32
3. Unproven sepsis
P

tube
June 4-7th 2016

Difficulity in breathing (-) ; icteric (-); fever (-); cry out loud; active
movement; sucking refleks seen weak

Head :
Eye

Face : icteric (-)

Ear
33

System Metabolic: icteric (-)
30/5:Ca ion/Ca/Na/K/Cl: 1,05/8,1/135/3,3/105
31/5: Leukosit: 14,200
A

3. Unproven sepsis

tube
34

Zamel drop 1x0,3cc
Fevriz drop 1x0,3cc
Congural method theraphy
35
CHAPTER IV
DISCUSSION
Theory
Definition
Case
Baby SP is a preterm baby with
Neonatal respiratory distress syndrome gestational age 30 - 32 weeks who

(RDS) is a condition of pulmonary suffered with main complain difficulity
insufficiency that in its natural course in breathing and turning blue one day
commences at or shortly after birth and before admitted in HAM hospital.
increases in severity over the first 2
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 SP suffered from chief
Signs of RDS appear immediately after

birth
or
within
characterized
by
h.
RDS
tachypnea
complaint difficulity in breathing.
is History of milk feeding which is
(>60
breaths/min), intercostal and subcostal
incontinuous
and sweathing is
found when milk feeding failed.
retractions, nasal flaring, grunting, and History of turning blue found one
cyanosis in room air. Tachypnea is due
day before admitted and according
to an attempt to increase minute
to parents, blue has been found in
36
ventilation
to
compensate
for
lips, fingers and toes.
decreased tidal volume and increased Through the confession of parents,

dead space. Retractions occur as the
tiredness in drinking is found since
infant is forced to generate a high
2 days before admitted.
intrathoracic pressure to expand the Through

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
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
physical
examination
found retraction in epigastrial and

suprasternal.
37
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 difficulity in
- Rapid breathing
breathing known as apnea.
- Shallow breathing
- One day before admitted in HAM
- Shortness of breath and grunting

sounds while breathing
hospital,
according
to
patients
parents, patients mouth, toe and
- Increased oxygen requirement
fingers turn blue which is known as
- Paradoxical chest wall movement
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.
Theraphy that used in this case is:

- Nasal CPAP with PEEP: 5-6 cmH2O,
Flow 8-10 liter per minute, FiO2:
30% Target of oxygen saturation: 9296%.
- Gentamicin injection 5mg/24 hour/iv
- Infant Radiant Warmer Theraphy with
target skin temperature 36,5-37,5.
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:
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

Fortunately, the natural course of the disease in many low-birthweight infants

American babies than in Caucasian babies, although Caucasian babies are at a

3. Persistent pulmonary hypertension

adenosine, serotonin, prostaglandins,

Diagram 1 Patofisiology of RDS

2.5 Risk Factors

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

Table 1 : Downes Score

avoiding mechanical ventilation and volutrauma. The current approach to the

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

C. Criteria for rescue treatment

Table 2: Indications for intubation of preterm infant during

no growth after 48 hours, unless prenatal history or clinical scenario warrants

: IVFD D5% NaCl 0.225%

History of parents medication

: The age of the patients mother was 17

: Birth was assisted by traditional midwife.

doesnt cry immediately after birth. Body

Body temperature: 36.9C

Chest circumference (CC): 21cm

Head circumference (HC) : 25cm

: both ear lobe in normal morphologic

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

RR: 35 bpm, regular, ronchi (-/-)

(-/-), icteric (+)

Differential diagnosis :1) Respiratory distress

: 1) Respiratory Distress ec DD/ - Neonatal Pneumonia

GIR: 7,3 kg/kgBW/minute (D8%)

- Aminosteril 6% 2gr/kgBW/day = 2,8 gr/day = 47cc/day = 1,9cc/hour/iv

May 24th 2016

loud; active movement; sucking refleks seen weak

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

Face : icteric (+)

: both ear lobe in normal morphologic

RR : 42 bpm, reguler, rhonchi (-)

Systemic urogenital: Stable, enough urine output

5. Baby born with less weight

GIR: 4,8 kg/kgBW/minute (D8%)

Aminosteril 6% 2,5gr/kgBW/day = 3,5 gr/day = 58cc/day =

Gentamicin injection 5mg/24 hour/iv (Day 2)

May 25th 2016

loud; active movement; sucking refleks seen weak

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

Face : icteric (+)

: both ear lobe in normal morphologic

System Infection: still not stable, fever (-), temperature: 36.7

23/5 : Leu: 15.64 10/L

1. Respiratory distress ec Neonatal Pneumonia

5. Baby born with less weight

Neo-K Injection 1mg/iv (Day 2) for 3 days

May 26th 2016