Respiratory Problems in Neonates

Magdalena Sidhartani
DEPARTMENT OF CHILD HEALTH
FACULTY OF MEDICINE DIPONEGORO UNIVERSITY

Respiratory Distress Syndrome

Also called as hyaline membrane disease
Most common cause of respiratory distress in

premature infants, correlating with structural &

functional lung immaturity.

1/3 infants born between 28 to 34 weeks, but

less than 5% of those born after 34 weeks.

Pathophysiology- surfactant deficiency-

increase in alveolar surface tension- decrease in

compliance.

RDS
Hyaline membrane- combination of sloughed

epithelium, protein & edema.

Diagnosis of respiratory distress should be

suspected when grunting, retraction or other

typical distress symptoms occur in premature
infant.
CXR- homogenous opaque infiltrates & air

bronchograms.

APGAR Score
0

Appeatance

Body and
extremities
blue, pale

Body pink,
extremities
blue

Completetly
pink

Pulse Rate

Absent

Below
100/min

100/min or
above

Grimace

No Response

Grimace

Cough,
sneeze, cry

Activity

Limp

Some flexion
of extremities

Active motion

Respiratory
Effort

Absent

Slow &
irreguler

Strong Cry
Total Score

1 Minute
Score

5 Minute
Score

10 Minute
Score

APGAR Score
Scores of 0 3 = Severly depressed and require
immediate ventilatory and circulatory support.

Scores of 4 6 = moderately depressed and require

oxygen and stimulation to breath.
Scores of 7 10 = generaly healthy newborn and require
supportive measures only.

HYALINE MEMBRANE DISEASE

Predisposed
-premature infants < 34 weeks
-caesarian section
- infants of diabetic mother
-decreased L/S ratio in amniotic fluid

Hyaline membrane disease

IMAGING FINDINGS:
=Granularity is the interplay of
-air distended in bronchioles and ducts

-background of atelectasis of alveoli

May change from film to film if there is
-expiration (air disappears)
-Better aeration (small bubble formation)

Supine chest radiograph

demonstrates a bell shaped
thorax with diffuse and
symmetrical ground glass
infiltrates

Supine chest radiograph

from day one of life
demonstrates bilateral,
irregular coarse infiltrates

Supine chest radiograph

demonstrates diffuse and
symmetrical ground glass
infiltrates

Supine
chest
radiograph of a newborn
demonstrating
mild
cardiomegaly
and
bilateral reticulonodular
densities that radiate
from the hila. There is
atelectasis in the upper
lobes

Supine chest
radiograph in the same
patient taken one day later
showing interval clearance of
the reticulonodular densities

Supine chest radiograph at five

hours of life demonstrates
diffusae bilateral granular
infiltrates

HMD

Classic respiratory distress syndrome (RDS). Bell-shaped thorax is due

to generalized underaeration. Lung volume is reduced, the lung
parenchyma has a diffused reticulogranular pattern, and peripherally
extending air bronchograms are present.

HMD

Moderate-severe RDS The

reticulogranular pattern is
more
prominent
and
uniformly
distributed
than usual. The lungs are
hypoaerated.
Increased
air bronchograms are
observed.

Hyaline membrane disease

Treatment:

- PEEP, CPAP
- surfactant administration

- oxygen and diuretics

Prenatal administration of corticosteroids between 24-

34 wks gestation reduces risk of respiratory distress

when risk of preterm delivery is high.
Post natal steroids may decrease mortality but may

increase risk of cerebral palsy.

Hyaline Membrane Disease

COMPLICATIONS:

1.PULMONARY INTERSTITIAL EMPHYSEMA

- Usually on day 2 or 3: small bubbles, streaky appearance
- frequent recurrence of pneumothorax
2. Chronic complication:

-Lobar emphysema, Localized interstitial

emphysema,
Retrolental fibroplasia,
Subglottic stenosis d/t intubation

Respiratory distress Syndrome

Prognosis:
In the past, almost all infants died of HMD by 72H
-With assisted ventilation, recovery is more than 90%.

Meconium Aspiration Syndrome

Incidence- 1.5- 2 % in term or post term

infants.
Meconium is locally irritative, obstructive &

medium for for bacterial culture

Meconium aspiration causes significant

respiratory distress. Hypoxia occurs because

aspiration occurs in utero.
CXR- Patchy atelectasis or consolidation.

Meconium Aspiration Syndrome

Clinical Presentation:
Tachypnea and
Grunting respirations in a meconium stained infant.
Intubation showed meconium noted below the
vocal cords

Meconium Aspiration Syndrome

Meconium Aspiration Syndrome

IMAGING FINDINGS:
diffuse ropey densities (similar to BPD)
Patchy areas of atelectasis from air trapping
Hyperinflation of the lung
spontaneous pneumothorax and pneumonia
no air bronchogram

25% usually require no therapy, clearing usually quick if mostly watery,

days to weeks if mostly meconium

Algorithm

Meconium Aspiration Syndrome

TREATMENT:

Supportive
-antibiotics and O2
-ECMO can be used
COMPLICATIONS:

1. Pulm Hypertension- RL shunting-cyanosis

2. Anoxic brain damage

Algorithm

Bronchopulmonary Dysplasia (BPD)

Clinical Presentation:
Premature infant who had severe lung disease (usually
hyaline membrane disease) and was treated with ventilatory
and oxygen therapy.

Bronchopulmonary dysplasia
Chronic respiratory insufficiency of the premature
is the consequence of early acute lung disease.
frequently complicate HMD also MAP and

pneumonia

Imaging Findings:

Initially the typical "ground glass" pattern of hyaline

membrane
At 1-2 weeks complete opacification of the lungs
"white lung.
At 2-3 weeks multiple small cystic lucencies of
relatively uniform size and distribution bubbly
appearance.
By several months of age: lung volume is increased,
and the small cystic lucencies have coalesced into
larger ones surrounded by fibrotic stranding.
In most survivors, clinical and radiologic signs of BPD
clear within 2-3 years.

Supine and lateral chest

radiographs obtained in the
same patient at 20 days of age
show the development of
small cystic lucencies in the
lungs and increased lung
volume

Supine chest radiograph

obtained in the same
patient at 5 months of age
shows the small cystic
lucencies
to
have
coaelesced into larger
lucencies
with
interspersed
fibrotic
stranding

Supine chest radiograph

obtained at 1 day of age
reveals a ground glass
appearance to the lungs

Supine chest radiograph

obtained in the same
patient at 10 days of age
reveals
complete
opacification of the lungs

Supine chest radiograph

obtained at 1 week of age reveals
a ground glass appearance to the
lungs

Supine chest radiograph obtained

in the same patient at 1 month of
age shows the development of
small cystic lucencies in the lungs.

BPD
DDX:
1.Pneumonia Interstitial Emphysema

smaller air-containing spaces in PIE (bubbly appearance)

2. Meconium Aspiration Syndrome
3. Shunts- such as PDA
4. Infection- esp. with Grp. A Beta strep
5. CHF and pulm. Edema

BPD

Complications:
1. Sudden infant death
2. Increased risk for pulm. Infection
4. Development of asthma?

Evaluation
Detailed history
Differential diagnosis changes with EGA, GBS status

& prophylaxis, duration of rupture of membrane,

color of amniotic fluid, maternal temperature,
maternal tachycardia, fetal heart tracing

Physical signs: look for apnea, tachypnea or

cyanosis, cardiac auscultation for murmur.

Lung auscultation (asymmetrical chest movements

in pneumothorax ,crackles in pneumonia, clear in

TTN, & persistent pulmonary hypertension of the
newborn)

NEONATAL PNEUMONIA

Introduction
Pneumonia
is an important cause of neonatal infection
Accounts morbidity and mortality aspecialy in

developing country

Pathogenesis
Routes of acquisition: Varies in part with
the time of onset of pneumonia

Early onset pneumonia

Late - onset pneumonia

 Early onset pneumonia

Generally within three days of birth
Aquired from the mother by one of three routes
Intra uteri aspiration of infected amniotic fluid
Transplacental tranmision of organisms from the mother to the

fetus
Aspiration during or after birth of infected amniotic fluid or
vaginal organisms

 Late - onset pneumonia

Occures during hospitalization or after discharge
Nosocomial acquired from
Infected individuals
Contaminated equipment

Microorganisms can invide through

injury tracheal

bronchoia mucosa
bloodstream

Mechanisms of injury in GBS pneumonia

In GBS pneumonia,
the level of beta hemolysin expression
correlate directly with the abilility of the
organism to injure of epithelial cell
Hemolysin act as pore forming cytolysis
alveolar edema and hemorrhage
Surfactant phospholipid inhibits betahemolysis- associated lung epithelial cell injury
premature infants more severelly affected

Pathology
(The patologic changes very with type of organisms)
Bacteria :
Inflammation of pleura
infiltration / distruction of brochopulmonary tissue
leukocyte and fibrious exudate within alveoli and

bronchi/ bronchioles
Bacteria are seen within interstitial spaces,

alveoli,bronci/bronchioles

 Virus
Cause an interstitial pneumonia
Infiltration of mononuclear cell and lympocytes hyalin

membrane formation - interstitial fibrosis and scarring

Microbiology
Cause :
Bacterial
Viral
Spirochetal
Protozoan
Fungal pathogens

Early- onset pneumonia

1.

Bacterial infections
1.
2.
3.

4.
5.
6.

Escherichia coli
Group B streptococcus
Kleibsiella spp
Staphylococcus aureus
Streptococcus pneumonia
Mycobacterium tuberculosis
transplacentally

7.

Listeria monocytogenes

2.

Viral infections
1.
2.

3.
4.
5.
6.

3.

Fungal infections
1.

4.

Herpes simplex virus ( HSV)

Adenovirus
Enteroviruses
Mumps
Rubella
Cytomegalovirus
Candida sp

Other patogens
1.
2.

Toxoplasma
Syphilis

Late onset pneumonia

1.

Bacterial infections
1.
2.
3.
4.
5.
6.
7.

Staphylococcus
Kleibsiella
Escheichia coli
Enterobacter cloacae
Streptococcus pneumoniae
Pseuodomonas aeroginosa
Serratia marcescens

2.

Viral infections
1.

2.
3.
4.
5.

6.

3.

Adenovirus
Parainfluenza virus
Rhinovirus
Enteroviruses
Influenza
RSV

Fungal infections
1.

Candida sp

Risk factors
Early onset pneumonia
PRM > 18 hours
Maternal amnionitis
Premature delevery
Fetal tachycardia
Maternal intrapartum fever
Late onset pneumonia
Assisted ventilation

 Other factors
Anomaly of the airway (choanal atresia, tracheoesophageal

fistule)
Severe underlying disease
Prolonge hospitalization
Neurologic empairment aspiration gastroentestinal
contents
Poor hand washing
Overcrowding

Clinical manifestation
Early- onset pneumonia

Respiratory distress beginning at / soon after birth

May have associated

Lethagy
Apnea
Tachycardia
Poor perfusion
Septic
Shock

Other sign

Temperature instability
Metabolic acidosis
Abdominal distentions

Late onset pneumonia

Respiratory distress
Apnea

Tachypnea
Tachycardia
Poor feeding
Abdominal distention

Jaundice
Emesis
Circulatory collapse

Diagnosis
Sudden onset of respiratory distress or

other sign of illness should be evaluated for

pneumonia / sepsis
culture: Blood,cerebrospinal fluid, pleural

fluid
Chest radiography
Bilaterall alveolar densities + air bronchograms
Irregular patchy infiltrates
Normal pattern

Treatment
Early- onset pneumonia

Ampicillin + gentamycin
Cephalosphorin
Late - onset pneumonia
Vancomycin + aminoglycoside

viral infection
Acylovir

Outcome
Predicted
Severity disease
Gestational age
Underlying medical conditions
Infecting organism
Increased mortality :
preterm birth
chronic lung disease
immune deficiencies

Thank You

Question
A male infant weighing 3000 g (6 lb 10 oz)

is born at 36 weeks' gestation, with normal

Apgar scores and an unremarkable initial
examination. At 48 hours of age he is noted
to have dusky episodes while feeding, and
does not feed well. On repeat examination
the child is tachypneic, with subcostal
retractions. Lung sounds are clear and
there is no heart murmur.

What Next ?

Tests & labs

Pulse oximetry on room air is 82%.

Arterial blood gases on 100% oxygen show a pCO2

of 26 mm Hg (N 27-40), a pO2 of 66 mm Hg (N 83108),

blood pH of 7.50 mg/dL (N 7.35-7.45), and a base

excess of -2 mmol/L (N -10 to -2).

Labs

Hemoglobin- 22.0g/dl (N13.020.0)

Hematocrit- 66 % (N 42- 66)

WBC- 19,000/mm3 (N900030,000)

Blood cultures- Pending.

Chest X-ray- Increased vascular

marking, Large thymus.

Most likely diagnosis

1- Transient tachypnea of newborn
2- Congenital heart disease
3- Hyaline membrane disease
4- Neonatal sepsis
5- Hyperviscosity syndrome

Answer
Cyanotic congenital heart disease can appear at the time

of ductus closure. A heart murmur is not usually audible,

and murmurs heard this early are usually not due to
heart disease. The failure to correct hypoxemia with
100% oxygen is diagnostic for abnormal mixing of blood
from the right and left circulations.

Transient tachypnea presents earlier, and the hypoxia

corrects with supplemental oxygen.

Hyaline membrane disease can occur at 36 weeks, but

would cause problems in the first hours of life. It can
make oxygenation difficult, but would cause extreme
distress with CO2 retention in such cases.

Answer
This patient has the energy to hyperventilate and has

slight respiratory alkalosis as a result. Neonatal sepsis

can cause V/Q mismatching and hypoxia, and can have a
delayed presentation. Concern would be high enough in
this case that the patient would probably receive broadspectrum antibiotics while awaiting culture results. On
the other hand, the clinician would not want to be
distracted from the evidence for congenital heart
disease.

The baby is polycythemic from poor intake in the first 2

days of life. The hyperviscosity syndrome can occur
when the hematocrit is over 65%. It can cause poor
feeding, tachypnea, and sluggishness, but does not
cause hypoxia.


Kasus
Neonatus dengan Aspirasi Susu

Magdalena Sidhartani, Adelina Prajitno

Departemen Ilmu Kesehatan Anak
FK UNDIP

Identitas pasien
Nama

: An.

Usia / tgl lahir

: 27 hari/ 8 September 2009

Jenis kelamin

: Perempuan

Alamat

: Ringin Jajar RT1, RW2

TK

Mranggen,Demak
No. CM

: C 248002

Masuk RSDK

: 3-10-2010

Alloanamnesis :

Kel. Utama: sesak nafas

Riwayat Penyakit Sekarang :

Batuk (-), Pilek (-),
Panas(-), Sesak (-),
Kejang(-), berobat bidan
1x, minum/menetek mau,
Batukmuntah

1 minggu SMRS

SMRS

Batuk makin bertambah,

Pilek(-), Panas (-), Sesak(-),
Kejang (-), Muntah tiap kali
minum,
Menetek/minum
Tampak lemas, mata
cekung

3 hari

Alloanamnesis

Muntah tiap kali

menetek/minum,
Sesak (+), lemah,
menangis terus, mata
cekung
Kencing

1 hari SMRS
jam SMRS

Muntah setelah menetek,

susu keluar dari mulut &
hidung, biru-biru di mulut, bibir
dan tangan, sesak nafas
bertambah,
Dibawa ke RS swasta
dirujuk ke RSDK

CM

UGD : Sianosis(+), Tanda

dehidrasi (+)
Laringoskopaspirat
susu 2-3cc Intubasi
Infus RL30cc/kgBB/jam
(2x) 200cc/kgBB/5jam
Dilakukan pemeriksan
Lab dan X-Foto thorax.

UGD RSDK
PBRT HP1

Ku: apatis, dispneu, nafas

spontan inadekuat, retraksi(+)
HR 140-150x/mnt,
RR=42x/mnt, t= 370 C
O2 VTP 100% 10 lt/mnt
RL 40 tpm 2jam D5% 8tpm
(mikro),
Inj.Ampicillin 2X125mg IV,
inj.Gentamicin 2x12,5mg IV,
Diet ditunda.

CM
Ku: sadar, kurang aktif
Dispneu,nafas spontan inadekuat,retraksi,
HR 140x/mnt, RR=40/mnt,t= 36,80 C
O2 VTP 100% 10 lt/mnt
D10% 240/10/10tpm
+NaCl 5% (2mEq) 11cc
Dalam 500cc D10%
+ KCl otsu (2mEq)13cc
inj.Ampicillin 2X125mg IV, inj.Gentamicin 2x12,5mg IV,
inj.Ca Gluconas 2x1,5cc ,
diet ditunda.

PBRT HP2

Alloanamnesis
Riwayat kelahiran
Antenatal:

G1P0A0, ANC(+) di bidan, penyakit

kehamilan (-)
Lahir : cukup bulan, KPD 24 jam, spontan di RS
swasta, BBL=2900gr, PBL=47cm, langsung menangis,
biru(-), AS tidak tahu.
Post natal: bayi sehat, gerak aktif.
Riwayat imunisasi: Hepatitis B & Polio.

Alloanamnesis
Riwayat makan dan minum : ASI tidak eksklusif

(sejak usia 2 hari diberi tambahan SGM 1 30 cc

3 - 4x/hari)

Riwayat pertumbuhan:
BBL=2900gr, PBL= 47cm, LK lahir tidak tahu.

BBS= 2830, PB=48,5cm, LK=35cm

Riwayat perkembangan:

Dalam batas normal

Pemeriksaan Fisik (5-10-2010)

Bayi , 27hari, BB=2830gr, PB= 48,5cm

KU

: sadar, kurang aktif, dispneu(+), terpasang

bubble CPAP.

TV

: N: 150x/m RR: 40x/m t: 38,90C

Kepala: LK 35cm, mesosefal,UUB datar

Mata, hidung, mulut dan telinga dalam batas normal.

 Paru

Vesikuler,
Ronki basah
halus(+)
hantaran(+),
wheezing(-)

Vesikuler, ronki
basah halus (+),
hantaran(+),
wheezing (-)

Vesikuler, ronki
basah halus(+),
hantaran(+),
wheezing(-)

Jantung, abdomen, genitalia dan ekstremitas dalam

batas normal.
Status Gizi : gizi baik

Pemeriksaan Penunjang: Foto baby gram

Tampak terpasang ETT dengan ujung distal setinggi
V.Th 4
COR: CTR = 47%
PULMO : Corakan vaskuler meningkat. Tampak bercak di
perihiler dan parakardial kanan
Diafragma kanan setinggi kosta 8 posterior.
Sinus kostofrenikus kanan kiri lancip
ABDOMEN : Pre peritoneal kanan kiri baik. Psoas line dan
kontur kedua ginjal tak jelas. Jumlah udara usus banyak.
Tampak sebagian dilatasi usus di abdomen disertai
adanya fekal material di dalamnya. Tak tampak udara
usus di cavum pelvis. Tak tampak gambaran pneumatosis
intestinalis. Tak tampak free air.
Kesan :

Kedudukan ETT VTH.4

Cor tidak membesar
Gambaran neonatal pneumonia
Gambaran
meteorismusGambaran
belum dapat disingkirkan.

NEC

Assessment
1. Pasca gagal nafas

DD/:

Ekstrapulmonal
Intrapulmonal

2. Neonatal pneumonia
DD/ :

Pneumonia aspirasi
Pneumonia infeksi

3. Neonatal infeksi
DD/:

Early onset

Late onset

Rencana Pemecahan Masalah

1. Pasca gagal nafas
Diagnosa S : O: Terapi
: Bubble CPAP FiO2 40% O2 5lt/mnt
Monitoring
: Pengawasan keadaan umum, tanda
vital, pengawasan jalan nafas dan tanda distres respirasi
Edukasi
:
- Menjelaskan kepada orangtua tentang penyakit yang
diderita dan menjelaskan tindakan yang akan dilakukan.
- Memotivasi orang tua penderita agar tetap memberikan
ASI peras per NGT

2. Neonatal pneumonia
Diagnosa : S : dispneu
O: suhu, tanda-tanda distres respirasi, ronkhi.
Terapi
: Inj.Cefotaxime 2 x 125 mg IV
Inj Gentamisin 1 x 12,5 mg IV
Inj Ca Glukonas 2 x 1,5 cc ad aqua IV pelan
Ambroxol 3 x 1,5 mg p.o
Program rehabilitasi medik
Pemberian diet melalui NGT:8 x 5 cc ASI peras
Monitoring : suhu, ronkhi, tanda distress respirasi
Edukasi : menjelaskan kepada ibu bahwa anak masih
sesak dan saat ini diet harus diberikan melalui NGT

3. Neonatal infeksi
Diagnosa :S : O: suhu, preparat darah apus, hitung jenis,
kultur darah
Terapi
: Inj.Cefotaxime 2 x 125 mg IV (1)
Inj Gentamisin 1 x 12,5 mg IV (3)
Inj Ca Glukonas 2 x 1,5 cc ad aqua IV pelan
Monitoring : tanda vital,darah rutin, kultur darah.
Edukasi :
- Memberi pengertian kepada orang tua tentang manfaat
ASI eksklusif dan kerugian ASI tidak eksklusif
- Motivasi untuk relaktasi
- Menjaga kebersihan ketika berkontak dengan bayi.

Perjalanan Penyakit
41

70

40

60

39

50

38
40

37

30

36
35

20

= CPAP ganti head box

= Head box lepas

6
Hari
Perawatan

10
Suhu

RR

Perjalanan Penyakit

3-10-2010 tiba di UGD RSDK bayi sianosis, nafas

hilang timbul, dehidrasi berat.

Dilakukan:
Laringoskopiaspirat susu 2-3cc

Intubasi, VTP 100% O2 10 l/mnt

Rehidrasi
inj.Ampicillin 2X125mg IV, inj.Gentamicin 2x12,5mg

IV
Evaluasi KU, tanda vital, tanda dehidrasi , tanda
DOPE
Kirim PBRT.

Perjalanan Penyakit
5-10-2010 nafas spontan tidak adekuat, lemas, kurang aktif,

dispneu +, suhu 38,9C retraksi+, ronki basah halus +, hantaran

+
Dilakukan:
Bubble CPAP FiO2 5 lt/mnt
Diet 8x5cc ASI peras per NGT
Terapi ganti inj. Cefotaxime 2X125mg IV & Inj.Gentamicin

1X12,5mg IV karena tidak ada perbaikan klinis

Program rehabilitasi medik
6-10-2010

nafas spontan cukup adekuat sehingga dipakai

O2 head box 5 lt/menit

7-10-2010 hasil kultur darah : Enterobacter aerogenes,

sensitif terhadap Cefotaxime dan Gentamicin sehingga terapi

BAGAN PERMASALAHAN
Kondisi rumah
kurang sehat

Ketidaktahuan orang
tua tentang manfaat
ASI eksklusif

Ayah perokok

Masalah ekonomi

Bayi perempuan, umur 27 hari, BB 2830 gr

Pasca gagal nafas

Aneonatal pneumonia
Neonatal infeksi

Terapi medikamentosa dan

suportif, serta rehabilitasi
medik

TUMBUH KEMBANG
OPTIMAL

Pendekatan sosial,
behavioral.
Monitoring: Edukasi
ASI eksklusif,
perilaku hidup sehat,
perbaikan ekonomi

Program Rehabilitasi Medik

1. Fisioterapi

Assesment:
Anak usia 27 hari, panas, batuk(+), pilek (-) dan sesak,
terpasang CPAP
PF : pulmo vesikuler, ronkhi basah halus (+/+), wheezing (-/-),
hantaran (+/+).
Ekstremitas : kekuatan : sulit dinilai,, tonus normal, RF + /+ ,
klonus -/ Program:
Proper bed positioning tiap 2 jam
Postural drainage dan tapotage

2. Sosial Medik
Assesment:

- Sosial ekonomi kurang

- Penderita tinggal serumah bersama 5 orang dewasa.
Ukuran rumah 3,5 m x 7 m. Dinding rumah papan, lantai
semen, tidak ada jendela.
- Ayah penderita mempunyai kebiasaan merokok setelah
makan ( 3 batang/hari) di dalam rumah, namun tidak
seruangan dengan pasien
- Biaya pengobatan ditanggung pribadi, karena tidak
memiliki JAMKESMAS.

 Program:
- Edukasi bahwa ASI merupakan sumber makanan yang terbaik
bagi pasien, manfaat ASI ekslusif.
- Motivasi untuk relaktasi
- Edukasi kepada ayah untuk tidak merokok di dalam rumah,
- Membuat rumah menjadi lebih sehat.

- Mengusahakan JAMKESMAS/ JAMKESDA

Pembahasan
Pneumonia neonatus sering disebabkan:

transmisi vertikal ibu-anak yang berhubungan dengan

proses persalinan
hospital-aquired pneumonia
Neonatus : paling sering Streptococcus Grup B dan

bakteri enterik gram negatif dari transmisi vertikal pada

proses persalinan. Juga organisme anaerob dari
chorioamnionitis.

Sumber : Opstapchuk M, Roberts DM, Haddy R. Community acquired pneumonia in children. Am Fam Physician 2004; 70 : 899-908

Sumber : Opstapchuk M, Roberts DM, Haddy R. Community acquired pneumonia in children. Am Fam Physician 2004; 70 : 899-908

Rehabilitasi Medik
Fisioterapi membantu transportasi lendir cegah obstruksi

jalan nafas.

Pada penderita ini dilakukan postural drainage atas

pertimbangan:
- suara hantaran+, bed rest dengan memakai head box, sehingga
memungkinkan terkumpulnya sekret pada saluran nafas .
- tidak ada kontra indikasi: hemoptisis, edema paru, gagal
jantung kongestif, efusi pleura masif, emboli paru,
pneumothorak, instabilitas kardiovaskular,TIK yang meningkat.

Rehabilitasi Medik
Cara:
Postural Drainage
Tapotage

Terima Kasih