kuliah abd-rab 2013

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Respiratory Problems in Neonates

Magdalena Sidhartani

DEPARTMENT OF CHILD HEALTH

FACULTY OF MEDICINE DIPONEGORO UNIVERSITY

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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, butless than 5% of those born after 34 weeks.

Pathophysiology- surfactant deficiency-increase in alveolar surface tension- decrease incompliance.

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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.

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APGAR Score

0 1 2 1 Minute

Score

5 Minute

Score

10 Minute

Score

 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 flexionof extremities

 Active motion

Respiratory

Effort

 Absent Slow &

irreguler

Strong Cry

Total Score

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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.

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HYALINE MEMBRANE DISEASE

Predisposed

-premature infants < 34 weeks

-caesarian section

- infants of diabetic mother

-decreased L/S ratio in amniotic fluid

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 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)

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Supine chest radiographdemonstrates a bell shapedthorax with diffuse andsymmetrical ground glassinfiltrates

Supine chest radiographdemonstrates diffuse and

symmetrical ground glassinfiltrates

Supine chest radiographfrom day one of lifedemonstrates bilateral,irregular coarse infiltrates

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Supine chestradiograph of a newborndemonstrating mildcardiomegaly andbilateral reticulonodular

densities that radiatefrom the hila. There isatelectasis in the upperlobes

Supine chestradiograph in the samepatient taken one day latershowing interval clearance of

the reticulonodular densities

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Supine chest radiograph at fivehours of life demonstratesdiffusae bilateral granularinfiltrates

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 HMD

Classic respiratory distress syndrome (RDS). Bell-shaped thorax is dueto generalized underaeration. Lung volume is reduced, the lungparenchyma has a diffused reticulogranular pattern, and peripherallyextending air bronchograms are present.

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 HMD

Moderate-severe RDS Thereticulogranular pattern ismore prominent and

uniformly distributedthan usual. The lungs arehypoaerated. Increasedair bronchograms areobserved.

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 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 mayincrease risk of cerebral palsy. 

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 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

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 Respiratory distress Syndrome

Prognosis:

In the past, almost all infants died of HMD by 72H

-With assisted ventilation, recovery is more than 90%.

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Meconium Aspiration Syndrome

Incidence- 1.5- 2 % in term or post terminfants.

Meconium is locally irritative, obstructive &medium for for bacterial culture

Meconium aspiration causes significant

respiratory distress. Hypoxia occurs becauseaspiration occurs in utero.

CXR- Patchy atelectasis or consolidation.

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Clinical Presentation: 

• Tachypnea and• Grunting respirations in a meconium stained infant.

• Intubation showed meconium noted below the

vocal cords

Meconium Aspiration Syndrome

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 Meconium Aspiration Syndrome

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  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

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Algorithm

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  Meconium Aspiration Syndrome

TREATMENT:

Supportive

-antibiotics and O2

-ECMO can be used

COMPLICATIONS:

1. Pulm Hypertension- R—L shunting-cyanosis

2. Anoxic brain damage

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Algorithm

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Bronchopulmonary Dysplasia (BPD)

Clinical Presentation: Premature infant who had severe lung disease (usually

hyaline membrane disease) and was treated with ventilatory

and oxygen therapy.

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Bronchopulmonary dysplasia 

Chronic respiratory insufficiency of the premature

is the consequence of early acute lung disease.

frequently complicate HMD also MAP andpneumonia

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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 ofrelatively uniform size and distribution  bubbly

appearance.• By several months of age: lung volume is increased,and the small cystic lucencies have coalesced intolarger ones surrounded by fibrotic stranding.

• In most survivors, clinical and radiologic signs of BPD

clear within 2-3 years. 

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Supine and lateral chestradiographs obtained in the

same patient at 20 days of ageshow the development ofsmall cystic lucencies in thelungs and increased lung

 volume

Supine chest radiographobtained in the same

patient at 5 months of ageshows the small cysticlucencies to havecoaelesced into largerlucencies withinterspersed fibrotic

stranding

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Supine chest radiographobtained at 1 day of agereveals a ground glassappearance to the lungs

Supine chest radiographobtained in the samepatient at 10 days of agereveals completeopacification of the lungs

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Supine chest radiographobtained at 1 week of age revealsa ground glass appearance to thelungs

Supine chest radiograph obtainedin the same patient at 1 month of

age shows the development ofsmall cystic lucencies in the lungs.

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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

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BPD

Complications:

1. Sudden infant death

2. Increased risk for pulm. Infection

4. Development of asthma?

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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 orcyanosis, cardiac auscultation for murmur.

Lung auscultation (asymmetrical chest movementsin pneumothorax ,crackles in pneumonia, clear inTTN, & persistent pulmonary hypertension of thenewborn)

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 NEONATAL PNEUMONIA

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Introduction 

Pneumonia

is an important cause of neonatal infection

Accounts morbidity and mortality aspecialy in

developing country

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Pathogenesis

Routes of acquisition: Varies in part with

the time of onset of pneumonia

Early – onset pneumonia

Late - onset pneumonia

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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 orvaginal organisms

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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

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Mechanisms of injury in GBS pneumonia

In GBS pneumonia,

the level of beta – hemolysin expression

correlate directly with the abilility of theorganism to injure of epithelial cell

Hemolysin act as pore forming cytolysis 

alveolar edema and hemorrhage

Surfactant phospholipid inhibits beta-hemolysis- associated lung epithelial cell injury

 premature infants more severelly affected

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Pathology

(The patologic changes very with type of organisms) 

Bacteria :

Inflammation of pleura

infiltration / distruction of brochopulmonary tissue

leukocyte and fibrious exudate within alveoli andbronchi/ bronchioles

Bacteria are seen within interstitial spaces,alveoli,bronci/bronchioles

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Virus

Cause an interstitial pneumonia

Infiltration of mononuclear cell and lympocytes hyalin

membrane formation - interstitial fibrosis and scarring

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Microbiology

Cause :

Bacterial

Viral Spirochetal

Protozoan

Fungal pathogens

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Early- onset pneumonia

1. Bacterial infections

1. Escherichia coli

2. Group B streptococcus

3. Kleibsiella spp4. Staphylococcus aureus

5. Streptococcus pneumonia

6. Mycobacterium tuberculosis

transplacentally7. Listeria monocytogenes

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2. Viral infections

1. Herpes simplex virus ( HSV)

2. Adenovirus

3. Enteroviruses

4. Mumps

5. Rubella

6. Cytomegalovirus

3. Fungal infections

1. Candida sp

4. Other patogens

1. Toxoplasma

2. Syphilis

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Late – onset pneumonia

1. Bacterial infections

1. Staphylococcus

2. Kleibsiella

3. Escheichia coli

4. Enterobacter cloacae

5. Streptococcus pneumoniae

6. Pseuodomonas aeroginosa

7. Serratia marcescens

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2. Viral infections

1. Adenovirus

2. Parainfluenza virus

3. Rhinovirus

4. Enteroviruses

5. Influenza6. RSV

3. Fungal infections

1. Candida sp

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Risk factors

Early – onset pneumonia

PRM > 18 hours

Maternal amnionitis

Premature delevery

Fetal tachycardia

Maternal intrapartum fever

Late – onset pneumonia Assisted ventilation

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Other factors

Anomaly of the airway (choanal atresia, tracheoesophageal

fistule) Severe underlying disease

Prolonge hospitalization

Neurologic empairment aspiration gastroentestinal

contents Poor hand washing

Overcrowding

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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

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Late – onset pneumonia

Respiratory distress

Apnea

Tachypnea

Tachycardia

Poor feeding

Abdominal distention Jaundice

Emesis

Circulatory collapse

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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

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Treatment

Early- onset pneumonia

Ampicillin + gentamycin

Cephalosphorin

Late - onset pneumonia

Vancomycin + aminoglycoside

 viral infection

Acylovir

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Outcome

Predicted

Severity disease

Gestational age

Underlying medical conditions

Infecting organism

Increased mortality :

preterm birth

chronic lung disease

immune deficiencies

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Thank You … 

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Question

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

is born at 36 weeks' gestation, with normal

Apgar scores and an unremarkable initialexamination. 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 subcostalretractions. Lung sounds are clear and

there is no heart murmur.

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What Next ?

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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 83-108),

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

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

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Labs… 

Hemoglobin- 22.0g/dl (N13.0-20.0)

Hematocrit- 66 % (N 42- 66)

WBC- 19,000/mm3 (N9000-30,000)

Blood cultures- Pending.

Chest X-ray- Increased vascularmarking, Large thymus.

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Most likely diagnosis

1- Transient tachypnea of newborn

2- Congenital heart disease

3- Hyaline membrane disease

4- Neonatal sepsis

5- Hyperviscosity syndrome

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Answer

Cyanotic congenital heart disease can appear at the timeof ductus closure. A heart murmur is not usually audible,and murmurs heard this early are usually not due toheart disease. The failure to correct hypoxemia with

100% oxygen is diagnostic for abnormal mixing of bloodfrom the right and left circulations.

 Transient tachypnea presents earlier, and the hypoxiacorrects with supplemental oxygen.

 Hyaline membrane disease can occur at 36 weeks, butwould cause problems in the first hours of life. It canmake oxygenation difficult, but would cause extremedistress with CO2 retention in such cases.

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Answer

This patient has the energy to hyperventilate and hasslight respiratory alkalosis as a result. Neonatal sepsiscan cause V/Q mismatching and hypoxia, and can have adelayed presentation. Concern would be high enough in

this case that the patient would probably receive broad-spectrum antibiotics while awaiting culture results. Onthe other hand, the clinician would not want to bedistracted from the evidence for congenital heartdisease.

 The baby is polycythemic from poor intake in the first 2

days of life. The hyperviscosity syndrome can occurwhen the hematocrit is over 65%. It can cause poorfeeding, tachypnea, and sluggishness, but does notcause hypoxia.

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Kasus

Neonatus dengan Aspirasi Susu 

Magdalena Sidhartani, Adelina Prajitno

Departemen Ilmu Kesehatan Anak

FK UNDIP

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Identitas pasien

Nama : An. TK

Usia / tgl lahir : 27 hari/ 8 September 2009

Jenis kelamin : Perempuan

 Alamat : Ringin Jajar RT1, RW2

Mranggen,Demak

No. CM : C 248002

Masuk RSDK : 3-10-2010

All i

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Alloanamnesis :

Kel. Utama: sesak nafas

Riwayat Penyakit Sekarang :

Batuk (-), Pilek (-),

Panas(-), Sesak (-),Kejang(-), berobat bidan

1x, minum/menetek mau,

Batukmuntah

Batuk makin bertambah,

Pilek(-), Panas (-), Sesak(-),

Kejang (-), Muntah tiap kali

minum,

Menetek/minum  

Tampak lemas, mata

cekung

1 minggu SMRS 3 hari

SMRS

All i

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Alloanamnesis

Muntah tiap kali

menetek/minum,

Sesak (+), lemah,menangis terus, mata

cekung

Kencing ↓ 

1 hari SMRS 4 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

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CM

UGD : Sianosis(+), Tanda

dehidrasi (+) 

Laringoskopaspirat

susu 2-3cc  IntubasiInfus RL30cc/kgBB/jam

(2x) 200cc/kgBB/5jam

Dilakukan pemeriksan

Lab dan X-Foto thorax.

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.

UGD RSDK

PBRT HP1

C

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CM

Ku: sadar, kurang aktifDispneu,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

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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.

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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

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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.

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Paru 

Vesikuler,Ronki basah

halus(+)

hantaran(+),

wheezing(-)

Vesikuler, ronkibasah 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

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Pemeriksaan Penunjang: Foto baby gram

Tampak terpasang ETT dengan ujung distal setinggiV.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 disertaiadanya 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 membesarGambaran neonatal pneumonia

Gambaran meteorismusGambaran NEC

belum dapat disingkirkan.

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Assessment 

1. Pasca gagal nafas

DD/: Ekstrapulmonal

Intrapulmonal

2. Neonatal pneumonia

DD/ : Pneumonia aspirasi

Pneumonia infeksi

3. Neonatal infeksi

DD/: Early onset

Late onset

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Rencana Pemecahan Masalah

1. Pasca gagal nafas 

Diagnosa S : -

O: -

Terapi : Bubble CPAP FiO2 40% O2 5lt/mnt

Monitoring : Pengawasan keadaan umum, tandavital, 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

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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

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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.

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  erjalanan enyakit

20

30

40

50

60

70

35

36

37

38

39

40

41

1 2 3 4 5 6 7 8 9 10

Suhu RR  Hari

Perawatan= CPAP ganti head box

= Head box lepas

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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 2x12,5mgIV

Evaluasi KU, tanda vital, tanda dehidrasi , tanda

DOPE

Kirim PBRT.

erjalanan enyakit

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

dispneu +, suhu 38,9◦C 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

erjalanan enyakit

BAGAN PERMASALAHAN

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BAGAN PERMASALAHAN

Kondisi rumah

kurang sehat Masalah ekonomi

Bayi perempuan, umur 27 hari, BB 2830 gr

Pasca gagal nafas

Aneonatal pneumonia

Neonatal infeksi

Terapi medikamentosa dan

suportif, serta rehabilitasimedik

TUMBUH KEMBANG

OPTIMAL

Pendekatan sosial,

behavioral.

Monitoring: Edukasi

ASI eksklusif,

perilaku hidup sehat,

perbaikan ekonomi

Ketidaktahuan orang

tua tentang manfaatASI eksklusif

Ayah perokok

P R h bilit i M dik

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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

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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 setelahmakan (±  3 batang/hari) di dalam rumah, namun tidak

seruangan dengan pasien

- Biaya pengobatan ditanggung pribadi, karena tidak

memiliki JAMKESMAS.

2. Sosial Medik 

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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

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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 padaproses persalinan. Juga organisme anaerob dari

chorioamnionitis.

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

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Sumber : Opstapchuk M, Roberts DM, Haddy R. Community –

 acquired pneumonia in children. Am Fam Physician 2004; 70 : 899-908 

R h bili i M dik

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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.

R h bili i M dik

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Cara:

Postural Drainage

Tapotage

Rehabilitasi Medik

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