kuliah abd-rab 2013
TRANSCRIPT
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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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Terima asih