asfiksia neonatorum.ppt
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Asfiksia Asfiksia NeonatorumNeonatorum
Asfiksia Asfiksia NeonatorumNeonatorum
Dr.Bambang Mulyawan SpADr.Bambang Mulyawan SpA
Fakultas KedokteranFakultas Kedokteran
Universitas MuhammadiyahUniversitas Muhammadiyah
M a l a n gM a l a n g
Pendahuluan (1)Pendahuluan (1) Asfiksia Bayi Baru Lahir (BBL) : 15% kematian BBL
(5 juta) /tahun Angka kejadian asfiksia di RS Propinsi : 25,2% (Jawa
Barat) Angka kematian asfiksia di RS Pusat Rujukan
Propinsi di Indonesia : 41% 10% BBL membutuhkan bantuan untuk mulai
bernafas ( bantuan ringan res.lanjut yg ekstensif) 5% BBL membutuhkan tindakan resusitasi ringan 1% - 10% BBL di RS perlu bantuan ventilasi, hanya
sedikit yg perlu intubasi dan kompresi dada
15/06/1999 Dr.Bambang M2
Pendahuluan (2)Pendahuluan (2)
“Sebagian besar bayi yaitu sekitar 90% tidak membutuhkan atau hanya sedikit memerlukan bantuan untuk memantap-kan pernafasannya setelah lahir dan akan melalui masa transisi dari kehidup-an intrauterin ke ekstrauturin tanpa ma-salah.”
15/06/1999 Dr.Bambang M3
•6-10 out of 130 mill newborns need intervention at birth
Pendahuluan (3) Pendahuluan (3)
•Most newborn infantsare born outsidehospitals withouthealth personelattending
•1 mill die and a similar numberdevelop sequels due to birthasphyxia (CP, Epilepsia)
•4 mill birth asphyxia
PePendahuluan (4)ndahuluan (4)
Infant resuscitation required in 6% of all births.
Asphyxia usually not anticipated. All labor and delivery units required to be
skilled in neonatal resuscitation (Standard of Practice)
NALS (Neonatal Advanced Life Support)
Definisi (1)Definisi (1)
Asfiksia neonatorum : BBL yang tidak dapat bernafas secara spontan dan teratur pada saat lahir atau beberapa saat setelah lahir.
BBL : Bayi Baru Lahir pada menit-menit pertama sp beberapa jam selanjutnya
Periode neonatal : lahir 28 hari
15/06/1999 Dr.Bambang M6
Definisi (2)Definisi (2)
Asfiksia BBL ditandai dg keadaan : *hipoksemia *hiperkarbia *asidosis
15/06/1999 Dr.Bambang M7
Definisi (3)Definisi (3) Karakteristik asfiksia BBL /Perinatal (menurut AAP
dan ACOG -2004 ) : 1. asidemia metabolik atau campuran (metabolik dan respiratorik) yang jelas, yaitu ph<7, pada sampel darah yang diambil dari a.umbilikal 2. nilai Apgar 0-3 pada menit ke 5 3. manifestasi neurologi pd periode BBL segera, termasuk kejang,hipotonia,koma atau ensefalopati hipoksisk isemik 4. terjadi disfungsi sistem multiorgan segera pada periode BBL
15/06/1999 Dr.Bambang M8
Definisi (3-a)Definisi (3-a)
Inconsistent Definitions Criteria for Neonatal Asphyxia (APA and ACOG,
1992)– Profound metabolic (or mixed) acidosis (ph <
7.0)– Persistence of Apgar score 0 - 3 for > 5
minutes– Clinical neurological sequelae– Evidence of multi-organ system dysfunction
Definisi (4)Definisi (4)
This is pathologic condition referred to neonate who have no spontaneous breathing or represented irregular breathing movement after birth. Usually caused by perinatal hypoxia. It is emergency condition and need quickly treatment (resuscitation).
birth asphyxia is defined simply as the failure to initiate and sustain
breathing at birth
The common worry of health professionals and parents is the permanent brain damage that
birth asphyxia can cause.
Definisi (4-a)
Patofisiologi asfiksia (1)Patofisiologi asfiksia (1) BBL mempunyai karakteristik yg unik. Alveoli paru janin dalam rahim berisi cairan paru
lahir nafas pertama udara masuk alveolicairan paru diabsorpsi oleh jaringan paru dstseluruh alveoli berisi udara oksigen. Paru membutuhkan tek.puncak inspirasi dan tek.akhir ekspirasi yg tinggialiran darah paru meningkat.
Kegagalan penurunan resistensi vaskuler paru hipertensi pulmonal persisten pada BBL (Persisten pulmonary Hypertension of the neonate ) aliran drh paru inadekuat dan hipoksemia relatifekspansi par < gagal nafas ! ! !
15/06/1999 Dr.Bambang M12
Patofisiologi (1-a)Patofisiologi (1-a)
Production of lung fluid diminishes 2-4 days before delivery
80-100 ml remain in the passageway of a full term infant
during the birth, fetal chest is compressed and squeezes fluid
Patofisiologi (1-b)Patofisiologi (1-b)
First breath is inspiratory gasp Changes trigger aortic and caratoid
chemo receptors that trigger brain’s respiratory center
Natural result of a normal vaginal delivery
Patofisiologi (1-c)Patofisiologi (1-c)
Significant decrease in environmental temperature after birth
– Stimulates skin nerve endings
– Newborn responds with rhythmic respirations
– Excessive cooling may lead to profound depression of cold stress
Patofisiologi (1-d)Patofisiologi (1-d)
Onset of respiration stimulates cardiovascular changes
– As air enter the lungs, oxygen content rises in alveoli and stimulates relaxation of pulmonary arteries
Patent ductus arteriosus closes
– With increased oxygenated pulmonary blood flow and loss of placenta, systemic blood flow increases, foreaman ovale closes, and PDA begins to close
– Leads to decrease in pulmonary vascular resistance-allows complete vascular flow to the lungs
Patofisiologi (1-e)
Patofisiologi (2)Patofisiologi (2)
When fetal asphyxia happens, the body will show a self-defended mechanism which redistribute blood flow to different organs called “inter-organs shunt” in order to prevent some important organs including brain, heart and adrenal from hypoxic damage.
Patofisiologi (3)Patofisiologi (3) Hypoxic cellular damage :
_reversible ( early stage ) _unreversible damage
Primary apnea Secondary apnea Other damage :
persisten pulmonary hypertension, hypo/hyperglicemia, hyperbilirubinemia
15/06/1999 Dr.Bambang M.19
Etiologi / Faktor resiko (1)Etiologi / Faktor resiko (1)
Maternal factor: hypoxia, anemia, diabetes, hypertension, smoking,
nephritis, heart disease, too old or too young,etc Delivery condition:Abruption of placenta, placenta previa, prolapsed
cord, premature rupture of membranes,etc Fetal factor:Multiple birth, congenital or malformed fetus,etc
Etiologi / faktor resiko (2)Etiologi / faktor resiko (2) Anticipate Asphyxia
–Preterm delivery–Thick meconium–Acute fetal or placental hemorrhage–Use of narcotics in labor–Maternal infection–Polyhydramnios: GI obstruction–Oligohydramnios: Hypoplastic lungs
Manifestasi klinis (1)Manifestasi klinis (1)
Fetal asphyxia
fetal heart rate: tachycardia bradycardia
fetal movement: increase decrease
amniotic fluid: meconium-stained
Manifestasi klinis (2)Manifestasi klinis (2)
Apgar score:
A: appearance(skin color)
P: pulse(heart rate)
G: grimace(reactive ability)
A: activity(muscular tension)
R: respiration
manifestasi klinis (2-a)manifestasi klinis (2-a)
Assign Apgar Score at 1, 5, and 10 Minutes. Apgar Score more useful in Term than
Preterm Infant, but not specific for diagnosis of neonatal asphyxia.
Cord Arterial Blood Gases: Ph (< 7) and Base Deficit ( > - 4 ).
Manifestasi klinis (2-b)Manifestasi klinis (2-b)
Degree of asphyxia:
Apgar score 8~10: no asphyxia
Apgar score 4~8: mild/cyanosis asphyxia
Apgar score 0~3: severe/pale asphyxia
Apgar Score Apgar Score ScoreScore 00 11 22
Heart RateHeart Rate AbsentAbsent <100<100 >100>100
Respiratory EffortRespiratory Effort Absent, irregularAbsent, irregular Slow, cryingSlow, crying GoodGood
Muscle ToneMuscle Tone LimpLimp Some flexion of Some flexion of extremitiesextremities
Active motionActive motion
Reflex irritability Reflex irritability (nose suctioning)(nose suctioning)
No responseNo response GrimaceGrimace Cough or sneezeCough or sneeze
ColorColor Blue, paleBlue, pale AcrocyanosisAcrocyanosis Completely pinkCompletely pink
Apgar V. Anesth Analg 1953; 32:260.Scoring at 1 and 5 minutes of age
Additional scoring could be continued at 5 minute intervals
if needed.
Resusitasi BBL (1)Resusitasi BBL (1)
Tujuan resusitasi BBL adalah untuk memperbaiki fungsi pernafasan dan jantung bayi yang tidak bernafas.
Penilaian pada bayi yang terkait dengan penatalaksanaan resusitasi dibuat berdasarkan keadaan klinis.
15/06/1999 Dr.Bambang M27
15/06/1999 Dr.Bambang M28
Resusitasi BBL (1-a)Resusitasi BBL (1-a)Tujuan :Tujuan :
1 Expansion of lungs(by clearing upper airways & ensuring patent route to the trachea)
2 Increasing the arterial PO2 (by providing adequate alveolar ventilation,with O2 if needed)
3 Supporting adequate cardiac output4 Ensuring that O2 consumption by newborn is
minimized (by reducing heat losses in the immediate postpartum period)
Resusitasi BBL (2)Resusitasi BBL (2)
Tindakan yang paling penting dan efektif pada resusitasi neonatus adalah pemberian ventilasi pada paru-paru bayi baru lahir dengan oksigen”
15/06/1999 Dr.Bambang M29
Resusitasi BBL (2)Resusitasi BBL (2)
1)1) Basic ResuscitationBasic Resuscitation
2)Advanced Resuscitation2)Advanced Resuscitation
ABC’s of ResuscitationABC’s of Resuscitation
A - establish open airwayPosition, suction
B - initiate breathingTactile stimulationOxygen
C - maintain circulationChest compressionsMedicationsD. DrugE. Evaluation
A B C (A: Airway, B: Breathing, C: Circulation)
Neonatal Resuscitation Program
Johns Hopkins: The Harriet Lane Handbook: A Manual for Pediatric House Officers, 16th ed., Copyright © 2002 Mosby, Inc.
Resusitasi BBL (2-a)
BASIC BASIC RESUSCITATIONRESUSCITATION
Basic ResuscitationBasic Resuscitation
Initial steps:– Thermal management– Positioning– Suctioning– Tactile stimulation
15/06/1999 Dr.Bambang M35
1.Prevention of heat loss, 2.Opening the airway and 3.Positive pressure ventilation that starts within the first minute of life
The important steps in The important steps in resuscitation are:resuscitation are:
The surface on which the baby is placed should always be warm as well as flat, firm and clean
This consists of :This consists of :drying, positioning the neonate under radiant warmer to minimize heat loss and suctioning of mouth and nose (Tracheal suctioning if meconium present).
This should only take approximately 20 seconds
provides sufficient stimulation of breathing in mildly depressed newborns and no further stimulation is appropriate
DryingDrying
The second step (within 20-30 seconds of birth)
is assessment of neonatal respiration
If the newborn is crying and breathing is normal,
no resuscitation is needed
The upper airway (the mouth then the nose) should be
suctioned to remove fluid if stained with blood or meconiumblood or meconium
if the chest is rising symmetrically with frequency
>30/minute,
no immediate action is needed
If there is no cry, assess If there is no cry, assess breathing:breathing:
If the newborn is not breathing or gasping:
immediately start resuscitation.
Occasional gasps are not Occasional gasps are not considered breathing.considered breathing.
Open the airwayOpen the airway
Put the baby on its backPosition the head so that it
is slightly extended .
15/06/1999 Dr.Bambang M45
Position of Newborn for Position of Newborn for ResuscitationResuscitation
Illustrations courtesy to Resuscitation of Babies at Birth (Royal College of Paediatrics and Child Health and Royal College of Obstetricians and Gynaecologists. London: BMJ Publishing, 1997)
15/06/1999 Dr.Said Alavi46
•Place Under warmer•Dry thoroughly•Remove wet linen•Position•Suction mouth then nose•Tactile stimulation
Evaluate Respirations
None Spontaneous
PPV HR<100
EvaluateHR
Inj.Narcan
Drug Depressed
Yes
No
HR <60Ct Ventilation +
Chest compression
Drugs if:HR <80,after 30 secs PPV
+100% O2+chest compression
HR 60-100-HR increasing Ct ventilation-HR not increasing (<80) Ct chest compression
HR >100look for spont. RespDC ventilation
Evaluate color
>100
ObserveMonitor Oxygen
PinkBlue
15-30 sec
Overview of ResuscitationOverview of Resuscitation
American Heart Association
15/06/1999 Dr.Bambang M47
Hubungan antara prosedur resusitasi Hubungan antara prosedur resusitasi dan jumlah bayi yang perlu prosedur dan jumlah bayi yang perlu prosedur
tsb.tsb.
Most common treatment
Least common treatment
Keep dry & warmSuction & stimulation
Oxygen
Establish effective ventilation Bag &mask
Tracheal Intubation
Chest compressions
Drugs
Gangguan napas pada Gangguan napas pada bayi baru lahirbayi baru lahir
Apnea attack
Respiratory Distress Syndrome
Hyaline Membrane Disease
Apnea attack ( serangan Apnea attack ( serangan apnu, episode apnu )apnu, episode apnu )
Keadaan bayi tidak bernafas untuk beberapa saat
Abnormal : > 20 detik, disertai sianosis, bradikardi
Pada hari-hari I kelahiran, biasanya berulang-ulang
Sering pada bayi prematur ( berat lahir < 1.500 gr, kehamilan < 32 minggu )
15/06/1999 Dr.Bambang M49
Etiologi Etiologi
Imaturitas pusat pernafasan Obstruksi jalan nafas oleh lendir / susu Pada bbrp kelainan paru berat ( peny. hialin
membran, pneumonia, perdarahan paru ) Gangguan SSP ( perdarahan intrakaranial, “Kern
icterus”) Gangguan metabolik ( hipoglikemi, perubahan
keseimbangan asam-basa cairan dan elektrolit )
15/06/1999 Dr.Bambang M50
Sikap dan tindakanSikap dan tindakan
Lakukan rangsangan mekanis ( mengu-bah letak bayi, memukul telapak kaki )
Bersihkan saluran nafas Berikan O2 dg sedikit tekanan Mencari dasar etiologinya Sikap selanjutnya sesuai dengan
etiologi
15/06/1999 Dr.Bambang M51
Respiratory Distress Respiratory Distress SyndromeSyndrome
Sindroma Gangguan Nafas / SGN
Pendahuluan Pendahuluan
Merupakan masalah yg sering dijumpai pd hari I kehidupan Bayi Baru Lahir
Ditandai : takipnea, napas cuping hidung (NCH), retraksi interkostal, sianosis dan apnu
Penyebab : - di dalam paru ( pneumotoraks/mediastinum, penyakit membran hialin, pneumonia aspirasi sindroma Wilson Mikity ) - di luar paru
15/06/1999 Dr.Bambang M53
Definisi / pengertianDefinisi / pengertian
Definisi Gangguan Napas adl. suatu keadaan meningkatnya kerja pernafasan yg ditandai dengan :
Takipnea : > 60 - 80 kali/menit Retraksi interkostal dan atau substernal slm inspirasi Napas Cuping Hidung ( NCH ) Merintih/ grunting saat inspirasi Sianosis ( sentral/bibir : jantung, hematologik, nafas ) Apnu atau henti napas ( dalam jam2 I : takipnea, retraksi, NCH, grunting, kadang
dijumpai pd BBL normal. Jika menetap bbrp jam, waspada adanya ggn nafas/RDS )
15/06/1999 Dr.Bambang M54
Hyaline membrane diseaseHyaline membrane disease
Penyakit membran hialin
Sindroma gangguan pernafasan idiopatik
Brief IntroductionBrief Introduction
Neonatal Hyaline Membrane Disease,almost exclusively occurred in premature infants, with
progressive dyspnea-respiratory distress: expiratory
grunting, cyanosis and the vicious cycle of hypoxia if not be
hindered. Respiratory distress defined as respiratory rate >
60, some grunting, retraction, flaring, and cyanosis in room
air. Expiratory grunting is due to partial closure of the glottis,
why?
Why?Deficiency-pulmonary surfactant
Symmetric alveolar atelectasis
HMD-CHEST X-RAY
DefinitionDefinition Hyaline membrane disease , HMD Deficiency of pulmonary surfactant , PS Pulmonary alveoli collapse at the end of expiration Progressively aggravated respiratory distress shortly
after birth Mainly in preterm infant Higher incidence rate with smaller gestational age Infant of DM mother, cesarean section, the second
baby of twins
Etiologi Etiologi
Belum sepenuhnya jelas Pematangan paru yg belum sempurna Berkaitan dg faktor pertumbuhan sal. nafas/paru Sering pd bayi prematur Pd ibu pend.gangguan perfusi darah uterus slm
kehamilan : DM, toksemia grav.,hipotensi, SC, perdarahan
Penyebab utama kematian prematur ( 50 – 70 %)
15/06/1999 Dr.Bambang M59
patofisiologipatofisiologi
Pembentukan substansi surfaktan paru tidak sempurna alveoli kolaps pd akhir ekspirasi utk nafas berikut perlu tek.negatif> dan usaha inspirasi yg kuat hipoksia, retensi CO2 dan asidosis. Asidosis : oksigenasi jaringan <, kerusakan endotel terbentuk fibrin, jar.epitel rusak lapisan/membran hialin.
15/06/1999 Dr.Bambang M60
Patofisiologi ( lanj.)Patofisiologi ( lanj.)
Atelektasis hipoksia asidosis transudasi penurunan aliran darah paru hambatan pembentukan substansi surfaktan atelektasis. Hal ini berlangsung terus : penyembuhan / kematian
15/06/1999 Dr.Bambang M61
Gambaran klinisGambaran klinis
Pada bayi BB 1.000 – 2.000 gram / masa gestasi 30 – 36 minggu, riwayat asfiksia atau gawat janin.
Tanda gg pernafasan dlm 6 – 8 jam I, karakteristik pd 24 jam – 72 jam
Gejala gg nafas ok. atelektasis dan perfusi yg menurun : dispneu/hiperpnu, sianosis, retraksi suprasternal, epigrastium, interkostal, ekspiratory grunting. Bradikardi, hipotensi, kardiomegali, edema, hipotermi, tonus menurun.
15/06/1999 Dr.Bambang M62
Gambaran radiologisGambaran radiologis
Gambaran klasik foto rontgen paru : bercak difus infiltrat retikulogranuler
Untuk diagnosis dini, walaupun klinis belum jelas
Untuk menyingkirkan DD : pneumotoraks, hernia diafragma.
15/06/1999 Dr.Bambang M63
Gambaran laboratoriumGambaran laboratorium
Darah : asam laktat >, bilirubin >, kadar PaO2 <, kadar PaO2 > o.k.atelektasis dan pH < : asidosis metabolik dan respiratorik
Funsi paru : frek.nafas >, tidal vol <, lung compliance <, fungsi ventilasi dan perfusi terganggu, dll
15/06/1999 Dr.Bambang M64
Gambaran patologi dan Gambaran patologi dan histopatologihistopatologi
Otopsi : atelektasis, membran hialin dlm alveolus atau duktus alveolaris, emfisema. Membran hialin : febrin, sel eosinofilik, dari darah atau sel epitel alveolus yg rusak
15/06/1999 Dr.Bambang M65
Pencegahan Pencegahan
Mencegah kelahiran bayi prematur Pemberian kortikosteroid ibu hamil
trimester III ( ? )
15/06/1999 Dr.Bambang M66
Penatalaksanaan Penatalaksanaan
Memberikan lingkungan yg optimal : suhu, humiditas
Oksigen Pemberian cairan, glukosa, elektrolit Antibiotika
15/06/1999 Dr.Bambang M67
Prognosis Prognosis
Tergantung tingkat prematuritas Terjadinya displasia bronkopulmoner
umumnya akibat tekanan positif terus menerus ( respirator )
15/06/1999 Dr.Bambang M68
SEPSIS PADA BAYI BARU LAHIRSEPSIS PADA BAYI BARU LAHIR
DEFINISIDEFINISI
Sepsis adalah infeksi aliran darah yang bersifat invasif dan ditandai dengan ditemukannya bakteri dalam cairan tubuh seperti darah, cairan sumsum tulang atau air kemih
Sering terjadi pd bayi resiko : BKB, BBLR, Sindroma Ggn Nafas, lahir dari ibu berisiko
15/06/1999 Dr.Bambang M70
Neonatal InfectionsNeonatal Infections
Sepsis Meningitis
PneumoniaOtitis Media
Diarrheal DiseaseUTI
OsteomyelitisSuppurative Arthritis
ConjunctivitisOrbital Cellulitis
Cellulitis - - Omphalitis
Bacterial / Viral / Fungal
Definisi (lanj.)Definisi (lanj.)
Pembagian : - sepsis awitan dini - sepsis awitan lambat
Sepsis awitan dini : di bawah 3 hari. Terjadi secara vertikal dari ibu hamil, selama persalinan/ kelahiran
Sepsis awitan lambat : > 3 hari, kuman dari lingkungan, horizontal, nosokomial
15/06/1999 Dr.Bambang M72
Neonatal Immune SystemNeonatal Immune System
• All neonates relatively immunocompromised
• Immature and Ineffective:
– Antibodies
– Complement
– Neutrophils
– Skin / mucosal barriers
Neonatal Bacterial Sepsis:Neonatal Bacterial Sepsis:Disease PatternsDisease Patterns
Early Onset Neonatal Sepsis (EONS)– Fulminant, multi-
system illness– < 5 days old– Obstetrical
complications– Prematurity– Perinatal acquisition– High mortality, 5-50%
Late Onset Neonatal Sepsis (LONS)– Sepsis or meningitis– 5 days to 3 months old– Perinatal or postnatal
acquisition– Lower mortality, 2-6%
Risk Factors for Early Onset Risk Factors for Early Onset Neonatal SepsisNeonatal Sepsis
Primary (significant) Prematurity or low birth weight– Preterm labor– Premature or prolonged rupture of membranes Maternal fever / chorioamnionitis– Fetal hypoxia– Traumatic delivery
Secondary– Male– Lower socioeconomic status– African-American race
Remington and Klein, Sixth Edition, 2006
Early Onset Neonatal Sepsis:Early Onset Neonatal Sepsis:Signs/SymptomsSigns/Symptoms
Strongly suggestivehypoglycemia / hyperglycemia
hypotensionmetabolic acidosis
apneashockDIC
hepatosplenomegalybulging fontanelle
seizurespetechiae
hematocheziarespiratory distress
Early Onset Neonatal Sepsis:Early Onset Neonatal Sepsis:Signs/SymptomsSigns/Symptoms
Nonspecificlethargy, irritability
temperature instability -- hypothermia or fever
poor feeding
cyanosis
tachycardia
abdominal distention
jaundice
tachypnea
Early Onset Neonatal Sepsis:Early Onset Neonatal Sepsis:SummarySummary
GBS is still the predominant organism isolated in EONS
Our efforts at IAP have reduced, but not eliminated, early onset GBS sepsis
Obstetrical risk factors, including premature/near-term delivery and maternal intrapartum fever, help to identify the infants at highest risk for EONS
Ancillary laboratory evaluations, including the CRP value, may assist in determination of the most appropriate length of therapy
Late Onset Neonatal SepsisLate Onset Neonatal Sepsis
Perinatal acquisition with later onset– Term or preterm– Bacterial: GBS, Chlamydia– Viral: HSV, CMV, HepB, HIV– Fungal: Candida
Nosocomial acquisition– Health care associated infections– Preterm or sick term infant
Late Onset GBSLate Onset GBS
Transmission - Perinatally or postnatally -- intrapartum prophylaxis or neonatal treatment of early onset disease does not decrease risk of late onset disease
Symptoms - 7days - 3 months. Typically 3-4 weeks old.
Occult bacteremia or meningitis most common. However, focal infections (pneumonia, UTI, cellulitis, osteomylelitis, septic arthritis) may occur.
Diagnosis - Culture of blood, sputum, urine, abscess or other body fluid.
Treatment - Penicillin, as with early onset disease.
Beberapa istilahBeberapa istilah
Sepsis sindroma respon inflamasi sistemik (Systemic Inflamatory Respons Syndrome – SIRS) yg terjadi akibat infeksi bakteri, virus, jamur, parasit.
Sepsis berat : disertai disfungsi organ kardiovaskuler dan ggn nafas akut atau terdapat ggn dua organ lain ( neurologi, hematologi, urogenital, dan hepatologi )
Syok sepsis terjadi bila masih dlm keadaan hipotensi walau telah mendapatkan cairan adekuat/cukup )
Sindroma disfungsi multi organ : bayi tidak mampu lagi mempertahankan homeostasis tubuh terjadi perubahan fungsi dua atau lebih organ tubuh.
15/06/1999 Dr.Bambang M81
Neonatal Sepsis: Neonatal Sepsis: IncidenceIncidence
2/1000 live births with culture proven sepsis
– Bacterial / Viral / Fungal
– 80% infants develop bacterial sepsis
– 20% infants perinatally acquired viral infections
– ~ 25% of infected infants have meningitis
Higher rate with preterm birth
– 26/1000 preterm infants with BW < 1000g
– 8-9/1000 preterm infants with BW 1000-2000g
Remington and Klein, Sixth Edition, 2006
Diagnosis Diagnosis
Masalah : gambaran klinis tidak spesifik tanda/gejala = peny.non infeksi ( sin. gn nafas, perdarahan intrakranial, gjl sepsis klasik ( pd anak besar) jarang pd bayi
Baku emas : biakan darah Pemeriksaan penunjang : C reactive protein,
biomolekuler, respon imun/sitokin ?
15/06/1999 Dr.Bambang M83
Diagnosis ( lanj.)Diagnosis ( lanj.)
Beberapa informasi yg diperlukan : - faktor resiko ( pd awitan dini/ lambat) - gambaran klinik - pemeriksaan penunjang
Faktor resiko awitan dini : - faktor ibu : persalinan dan kelahiran kurang bulan, ketuban pecah lebih dari 18-24 jam, chorioamnionitis, persalinan dg tindakan, demam pd ibu (> 38.4 C ), infeksi sal.kencing ibu, faktor sosial dan gizi ibu. - faktor bayi : asfiksia perinatal, lahir rendah, kurang bulan, prosedur infasif, cacac bawaan
15/06/1999 Dr.Bambang M84
Diagnosis ( lanj.)Diagnosis ( lanj.)
Faktor resiko sepsis awitan lambat : - dirawat di ruang intensif, perawatan lama, nutrisi parenteral lama, dari alat perawatan bayi, infeksi nosokomial dari bayi lain/ perawat
15/06/1999 Dr.Bambang M85
Etiologic Agents of Neonatal SepsisEtiologic Agents of Neonatal Sepsis
Frequency(%) Group B Streptococci 40 Escherichia coli 17Streptococcus viridans 7Staphylococcus aureus 6Enterococcus spp 6
Coagulase-negative staphylococci 5Klebsiella pneumoniae 4Pseudomonas spp 3Serratia marcescans 2Others 10
*Schuchat et al, Pediatrics 105: 21-26, 2000
Congenital nasolacrimalCongenital nasolacrimal duct obstruction duct obstruction
5% of all newborns
*absence of conjunctival injection!
Warm compresses, gentle massage, watchful waiting
95% resolve by 6 months; if not, refer for probing (earlier if multiple episodes of dacryocystitis)
ConjunctivitisConjunctivitis
Close contacts affected Unilateral bilateral Sticky discharge Diffuse redness Cornea and pupil normal Chloramphenicol
Cellulitis- Refer urgently
Neonatal conjunctivitis: refer urgently– Risk of corneal perforation from n.
gonorrhoea
89 Normal Newborn Care
Eye Care To Prevent or Eye Care To Prevent or Manage Ophthalmia Manage Ophthalmia
NeonatorumNeonatorum Ophthalmia neonatorum
– Conjunctivitis with discharge during first 2 weeks of life
– Appears usually 2–5 days after birth
– Corneal damage if untreated
– Systemic progression if not managed Etiology
– N. gonorrhea More severe and rapid development of complications 30–50% mother-newborn transmission rate
– C. trachomatis
90 Normal Newborn Care
Eye Care To Prevent or Eye Care To Prevent or Manage Ophthalmia Manage Ophthalmia
Neonatorum (continued)Neonatorum (continued) Prophylaxis
– Clean eyes immediately– 1% Silver nitrate solution
Not effective for chlamydia– 2.5% Povidone-iodine solution– 1% Tetracycline ointment
Not effective vs. some N. gonorrhea strains Common causes of prophylaxis failure
– Giving prophylaxis after first hour– Flushing of eyes after silver nitrate application– Using old prophylactic solutions
91 Normal Newborn Care
SummarySummary
The essential components of normal newborn care include:
Clean delivery and cord care Thermal protection Early and exclusive breastfeeding Monitoring Eye care Immunization
Dacryocystitis Dacryocystitis
Bacterial infection of nasolacrimal gland with duct obstruction
Mgt:
– Swab C+S
– Topical + systemic antibiotics
Gonorrheal conjunctivitisGonorrheal conjunctivitis
Hyperpurulent discharge at day 2-4
Potentially a disaster!! Mgt?
– Need FSW– Admit for antibiotics, eye irrigation, mgt of
complications: corneal ulceration, scarring, synechiae formation
– Rx concomitantly for Chlamydia– Rx mom and her partner
Chlamydial conjunctivitisChlamydial conjunctivitis
C. trachomatis : presents on day 3-10 (but may be up to 6 weeks)
Mom with active untreated chlamydia: babe has 40% chance of infection
What’s the real worry here?
10-20% have associated pneumonia – untreated can lead to chronic cough and pulmonary impairment
“well” with pneumonia and staccato cough Creps/wheezes; patchy infiltrates w/ hyperinflation CBC: eosinophilia Rx: systemic erythro x 14 days Treat mom and her partner,
Herpetic conjunctivitisHerpetic conjunctivitis
Day 2-16 Flourescein stain: dendritic ulcer
Do FSW
Rx: IV acyclovir, topical vidarabine 30-50% of cases recur w/i 2 years
OmphalitisOmphalitis
When should the umbilical When should the umbilical cord separate?cord separate?
Usually w/i 2 weeks
Delayed separation: think of possible leukocyte adhesion defect
OmphalitisOmphalitis
erythema and edema of umbilical area
excellent medium for bacterial colonization
poor hygiene or hospital-acquired infection
Staphylococcus, Streptococcus, Gram (-) rods
OmphalitisOmphalitis
Purulent, foul-smelling discharge with erythema of surrounding skin
Secondary to poor cord hygiene
S. aureus/Group A Strep/Gm –’s
Tx; topical care and systemic antibiotics (
Omphalitis: complicationsOmphalitis: complications
Necrotizing fasciitis Sepsis Portal vein
thrombosis Hepatic abscesses
TreatmentTreatment
IV Antibiotics Local cleaning Can rapidly progress to Necrotizing
fasciitis (16%) Usually polymicrobial Rapidly fatal (50%) Surgical debridement necessary
T e r i m a k a s i h
T e r i m a k a s i h
Virginia Apgar
0 1 2 3 4 5 6 7 8 9 100
25
50
75
100AsphyxiaControls
R Rao, S Ramji: Indian Pediatrics 2001;38:762-766
minutes after birth
Saturation %
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Physical EaminationPhysical Eamination
Vital signs
– RR 40-60
– HR 120-160
– Temperature axilary 35.5-37.5 Over bundling Heater
EtiologyEtiology
Pathologically, any factors which interfere with the circulation between maternal and fetal blood exchange could result in the happens of perinatal asphyxia. These factors can be maternal factor, delivery factor and fetal factor.
Pathophysiology(I) Pathophysiology(I)
Hypoxic cellular damages:
a. Reversible damage(early stage):
Hypoxia may decrease the production of ATP, and result in the cellular functions . But these change can be reversible if hypoxia is reversed in short time.
b. Unreversible damage:
If hypoxia exist in long time enough, the cellular damage will become unreversible that means even if hypoxia disappear but the cellular damages are not recovers. In other words, the complications will happen.
Pathophysiology(II)Pathophysiology(II)
Asphyxia development:
a. Primary apnea
breathing stop but normal muscular tone or hypertonia, tachycardia(quick heart rate), and hypertension
Happens early and shortly, self-defended mechanism , could not be damage to organ functions if corrected quickly
b. Secondary apnea
features of severe asphyxia or unsuccessful resuscitation, usually result in damage of organs function.
Pathophysiology(III)Pathophysiology(III)
Other damages:
a. Persistent pulmonary hypertension (PPHN)
b. Hyper/hypoglycemia
c. Hyperbilirubinemia
Clinic manifestationsClinic manifestations
Complications:
CNS: HIE, ICH
RS: MAS, RDS, pulmonary hemorrhage
CVS: heart failure, cardiac shock
GIS: NEC, stress gastric ulcer
Others: hypoglycemia, hypocalcemia, hyponatremia
Management Management
ABCDE resuscitation
A (air way)
B (breathing)
C (circulation)
D (drug)
E (evaluation)
1.Anticipation. 2.Adequate preparation. 3.Timely recognition. 4.Quick and correct action are critical for the success of resuscitation
Resuscitation must be anticipated at every birth. Every birth attendant should be prepared and able to resuscitate
Good management of pregnancy and labour/delivery complications is the best means of preventing birth asphyxia
For resuscitation:For resuscitation:1. A self-inflating Ambou bag (newborn size) 2. Two infant masks (for normal and small newborn), 3. A suction device (mucus extractor),4. A radiant heater (if available), warm towels, a blanket
and 5. A clock are needed
Neonatal Resuscitation Program
Johns Hopkins: The Harriet Lane Handbook: A Manual for Pediatric House Officers, 16th ed., Copyright © 2002 Mosby, Inc.
Perinatal AsphyxiaPerinatal Asphyxia
Normal Birth Transition:– Lung Expansion (after negative intrathoracic pressure)– Cry (expiration against a partially closed glotis)– Umbilical Cord Clamping
BP Increases Massive Stimulation of Sympathetic Nervous
System Pulmonary Vascular Resistance Falls Gradual Transition to Neonatal Circulation ( with
closure of Foramen Ovale and Ductus Arteriosis)
Perinatal AsphyxiaPerinatal Asphyxia
Transition in the Asphyxiated Neonate– Primary Apnea:
Spontaneous respiration can be induced with stimulation. May require Narcan
– Secondary Apnea: Following 1 minute of apnea 4 - 5 minutes of deep gasping “Last gasp” Requires vigorous ventilatory support within a few minutes
or death will occur.
Apgar ScoreApgar Score
Originally proposed as a predictor for newborns at risk for complications for bad outcomes (cerebral palsy)
Outcomes– If the Apgar score at twenty minutes after
delivery is less than five, there is still only a 20% chance of a handicapping condition. Level of evidence (LOE) 5
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Causes of Delayed Onset of Regular Respiration After Delivery
Acute asphyxia Chronic partial asphyxia Pre existing brain diseases Depression of respiratory center-drugs Trauma to CNS Prematurity Sepsis (GBS) Primary maternal diseases Anemia
(several of this may be present in a single baby)
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Failure to breath after birth
PO2 falls immediately to near zero
Acidosis
Biophysical stigmata of Asphyxia
Brain damage orAggravation of an existing CNS injury
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Effects of Asphyxia on Body Effects of Asphyxia on Body SystemsSystems
CNS-most serious impact,neurologic sequelae CVS-heart failure, myocardial ischaemia,
necrosis, cardiac dilatation,TR Lungs-RDS,massive pulmonary hemorrhage,
pul.edema,suppression of surfactant production Kidneys-ATN,renal failure,myoglobinuria Temp. homeostasis-hypothermia,hyperthermia Others-NEC,SIADH,GH deficiency,liver
necrosis, jaundice,coagulation defects, DIC
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One out of 50 requires active resuscitation in labor ward 5.7% of all deliveries found to be apneic & 25% of them
need intubation 70% of infants that require resuscitation come from
predictably high-risk situations 30% infants who need active resuscitation are born
after an apparently normal labor, in which no e/o fetal compromise
At every delivery someone capable of resuscitating the newborn baby needed -midwife
-anesthetist -pediatrician
-obstetrician (Gupta & Tizard 1967,Primhak 1984, Milner & Vyas-1985)
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Perinatal Complications Requiring a Pediatrician at Delivery
CS (6.2% will need intubation & ppv) Forceps Ventouse Breech (8% will need intubation & PPV) Malpresentations Multiple pregnancy Thick meconium staining of amniotic fluid Gestational age <36 weeks Fetal distress(sustained bradycardia,scalp pH <7.1) Fetal complications:
– Rh disease & Hydrops– Serious congenital malformations (by antenatal USG)
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“At every delivery, wherever it takes place, there should be at least one person who is responsible for giving basic care to the baby, initiating resuscitation if necessary, and summoning more help if needed”
(British Pediatric Association,1993)
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Assessment of Newborn Assessment of Newborn After DeliveryAfter Delivery
As quickly after delivery as possible Record the response to resuscitation as a narrative in
babies notes
•Traditional way-Apgar score•Cord blood analysis•Other biochemical methods•Clinical examination
Methods of assessment
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Apgar scores for different signs in NewbornsSign Score
0 1 2
Heart rate Nil <100 >100
Respiratory Absent Gasping or Regular or
effort irregular crying
Muscle tone Flaccid Some tone Active
Response to None Grimace Cry or coughstimulation
Color White Blue Pink centrally
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Factors Affecting Apgar Factors Affecting Apgar ScoreScore
Prematurity Drugs-
sedatives,narcotics,mgso4 A/c cerebral trauma Precipitate labor Cong. Myopathy Cong. Neuropathy Spinal cord trauma CNS anomaly Lungs-diaphragmatic hernia Airway-choanal atresia Cong. Pneumonia (GBS)
Maternal acidosis High fetal
catecholamine levels Some full term infants
False positive score False negative score
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Limitations of Apgar Limitations of Apgar ScoreScore
Affected by many factors, so low apgar score do not necessarily signify fetal asphyxia
Do not predict neonatal mortality or subsequent development of CP
(score normal in most cases with CP & incidence of CP is very low in those with apgar score 0-3 at 5 Mts..)
1 min. Apgar score-strongly correlated with cord pH & an index of intrapartum asphyxia
Apgar score beyond 1 min. (5,10,15 & 20min)-reflective of child’s changing condition & indicative of adequacy of resuscitative efforts
Score 0-3 at 20 Mts.- indicate high mortality & morbidity
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Cord Blood AnalysisCord Blood Analysis Objective way to assess asphyxia Collection from a double clamped segment of umbilical
artery Ideally should be done in all deliveries- at least in all
high-risk cases Help to diagnose the neonates failure to breathe other
than asphyxia
Limitations: -Poor relationship with Apgar score
-2% babies with normal Apgar score has pH<7.1
-Most babies with pH<7.1 have normal Apgar
If both Apgar & pH abnormal & no other cause detected, strongly s/o recent Asphyxia
Other biochemical indices- Lactate,hypoxanthine,CPK
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Area Examination
Head-Fontanelle, sutures, ears, eyes,face, lip, and palate
Arms-Numbers of fingers, palmar creases
Chest-Listen to heart and lungs
Abdomen-Umbilicus, groins, anus, genitalia
Back-Skin, spine
Legs -Toes, ankles, hips
Examination of the Newborn
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Birth injuries
Abnormalities of limbs or digits
Cyanosis, tachypnoea, or grunting
Imperforate anus
Cleft lip or palate
Significant naevi
Ambiguous genitalia
Esophageal atresia (if polyhydramnios)
Other obvious congenital abnormality
Conditions to Exclude in Initial External Examination of Newborns
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Labor Ward Management Labor Ward Management of Resuscitationof Resuscitation Preparation
history equipment & drugs equipment check on arrival
Initial care of baby after delivery (60-90 sec) start clock & note gestational age assess HR,RR,tone,reflexes dry,cover with warm blanket traditional apgar score at 1 minute if baby did not breathe quick assessment
whether apnea primary or terminal
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ApneaApneaPRIMARY APNEA HR>80,good peripheral perfusion,tone & reflexes Apgar score usually 4-7 The onset of gasping & regular respiration can be
established by peripheral(tactile) stimulation
TERMINAL (SECONDARY) APNEA HR<60, pale,apneic,poor tone & reflexes, Apgar score usually 1-3 Spontaneous respiration is never established
unless actively resuscitated by intubation & PPV
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Care After Initial Care After Initial AssessmentAssessment
Group 1. Fit & healthy,crying well (90-95%) Group 2. (primary apnea) (5-6%)
Not breathing well,blue,
Group 3. (terminal apnea) (0.2-0.5%) Pale,limp, apneic, HR<60
Group 4. Dead but resuscitatable (<0.1%)
Most infants fall into four groups
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Management(contd.)Management(contd.)
Leave this baby alone ! No vigorous suction Dry & wrap in warm blanket Inj.Vitamin K Give to mother for breast feeding
Group 1-Fit & healthy
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Prems <32 weeks– all with no respiration & fail to turn pink-
intubate & IPPV Full term
– peripheral stimulation – small percentage need bag & mask – if no resp.By 1-3 min. Intubation & IPPV – majority extubated & given to mother by 2-3
min.
– If still no respiration, consider terminal apnea, drug depression, neurologic illness or
congenital defects
Group 2-Primary Apnea
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Resuscitation With Bag & Resuscitation With Bag & MaskMask
Illustrations courtesy to Resuscitation of Babies at Birth (Royal College of Pediatrics and Child Health and Royal College of Obstetricians and Gynecologists. London: BMJ Publishing, 1997)
15/06/1999 Dr.Said Alavi141
Positive Pressure Ventilation - Positive Pressure Ventilation - Correct Position & Size of Face MaskCorrect Position & Size of Face Mask
Illustrations courtesy to Resuscitation of Babies at Birth (Royal College of Pediatrics and Child Health and Royal College of Obstetricians and Gynecologists. London: BMJ Publishing, 1997)
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Group 3-Terminal Apnea 5-10% of all apneic infants at 2 min Severely asphyxiated,never spontaneous
respiration Intuabtion & IPPV,O2-most respond If HR<60-ECM & soda bicarb- majority
improve,breathe & turn pink by 4-5 min If still no respiration, s/o-
drug depression-naloxone severe asphyxia & acidemia- soda bicarbonate
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Correct Positioning of LaryngoscopeCorrect Positioning of Laryngoscope
Illustrations courtesy to Resuscitation of Babies at Birth (Royal College of Pediatrics and Child Health and Royal College of Obstetricians and Gynecologists. London: BMJ Publishing, 1997)
15/06/1999 Dr.Said Alavi144
Group 4-Dead but resuscitatable ECM Laryngoscopy,clear airways Intubation & IPPV(some respond & vigorous cry by 5-10
min) Endotracheal adrenaline UVC insertion & sodabicarb ECG monitoring Still no cardiac activity-sodabicarb,10%
dextrose,ca.Gluconate,adrenaline Repeat adrenaline-still no response by 10 min-abandon
resuscitation except in acute episode of asphyxia like shoulder dystocia or difficult breech (in these try resuscitation for 10 min more)
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External Chest Compression
Technique of chest compression-Note the position of the thumbs on the midsternum,just below the nipples
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Heart beat returns but cardiac output low or bradycardic-atropine 0.1 mg iv
Lignocaine 1-2 mg/kg for V-tach or fibrillation
Ca.gluconate 1-2 mmol 0f 10% soln. Albumin/plasma 10 cc/kg Admit in NICU Further management as terminal apnea
Group 4 (contd.)
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Drugs for use in neonatal resuscitation Adrenaline
Preparation 1 in 10 000 dilution (100 µg/ml) Dose 1st and 2nd dose 10 µg/kg (0.1 ml/kg); 3rd dose 100 µg/kg ,(1 ml/kg) Route 1st dose, tracheal tube (provided that lungs are inflated); 2nd and 3rd doses, umbilical venous catheter
Sodium bicarbonate
Preparation 4.2% (0.5 mmol/ml) or 8.4% (1 mmol/ml) solution with equal volume of dextrose Dose 1-2 mmol/kg (2-4 ml/kg of 4.2% solution) via umbilical venous catheter; 2 doses may be given
Volume expanders
Preparations Plasma, or group O Rh negative blood that is not cross matched; 4-5% human albumin Dose 10-20 ml/kg via umbilical venous catheter over 5-10 minutes (may be repeated)
Naloxone hydrochloride*
Dose 100 µg/kg (0.25 ml/kg) intramuscularly
*Never give to the baby of an opiate dependent mother
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Continuing Therapy After Terminal Continuing Therapy After Terminal ApneaApnea
If not pink by 5-10 min admit in NICU Monitor BP,PCV,hypocount,blood gases,
CXR (in most all WNL, no further treatment, transfer to mother by 24-36hrs)
Symptomatic >24-48 hrs-problems HIE Renal failure Myocardial damage
A.Infants with regular respiration
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Pink,good cardiac output,but by 20 min. No spont.respiration despite empirical drugs-delay further treatment until blood gas,glucose & CXR results
Then treat according to results If all investigations WNL & apnea persists-
s/o profound neurologic problem with bad prognosis or underlying neurologic disorder or intractable cerebral edema
Those fulfill criteria of brain death-discontinue from IPPV with parental consent
B.Infants who do not start to breathe
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Infants Who Do Not Respond Infants Who Do Not Respond to IPPV & Resuscitationto IPPV & Resuscitation
A Babies clinically assessed as asphyxiated, but despite all procedures still cyanosed & bradycardic at 5-10 min.
B Vigorous & active babies with good respiratory efforts,yet cyanosed & fail to go pink- s/o unasphyxiated baby with serious malformations of CVS or RS
C Babies born apneic with feeble efforts,needed intubation,goes pink but remain hypotonic with no or poor respiratory efforts - s/o primary neurologic or muscle diseases
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A.Asphyxiated Baby Not Responding to Resuscitation
Technical error in procedure(commonest) -disconnection of equipment,tube in esophagus or in right main bronchus, insufficient inflation pressure,tubal block
Very ill infant with serious underlying lung disease-RDS,MAS,congenital pneumonia, anemia
Pneumothorax Profound & severe asphyxial insult Congenital structural anomalies preventing
oxygenation
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B.Vigorous but Persistently Cyanosed
•URT-choanal atresia,Pierre-Robin syndrome, laryngeal webs & cleft
•Lung-hypoplasia(PPROM,Potters syndrome), pleural effusion,cong.cystic adenomatiod malformation,cong.lobar emphysema
•Extra pulmonary-diaphragmatic hernia (commonest), eventration,intrathoracic tumors, gross abdominal distention (ascitis, tumor, hepatosplenomegaly), small chest(asphyxiating thoracic dystrophy, thanatophoric dwarfism)
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C.Persistent Apnea,Hypotonia,good Cardiovascular Response
•Severe terminal apnea
•Structural CNS or muscle disorder•Severe antenatal brain damage
•Fracture cervical spine or cord
•Dystropia myotonica
•Congenital myopathies
•Werdnig-Hoffman disease
•Brain tumor
•Degenerative brain disorder
•Ondine’s curse
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ABCD of Neonatal ABCD of Neonatal ResuscitationResuscitation
Drugs+
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Medications•Adrenaline
•Volume expander
•Sodium Bicarbonate
Begin •HR- Zero or•HR <80/Mt after 30 sec PPV +chest compression
Adrenaline
HR>100
A/c bleeding +Hypovolemia
Volume expanders
MetabolicAcidosis
Soda Bicarbonate
? Shock
DopamineResp. depression &
H/o Narcotics given to Mother <4hr
Narcan
Can be repeated every 5 Minutes
DC drugsYes
No
American Heart Association
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ReferencesReferences American Academy of Pediatrics Committee on Drugs.Emergency Drug Doses
for Infants & Children.Pediatrics.1988;81:462
American Academy of Pediatrics.Use & Abuse of the Apgar Score.Pediatrics.1996;98:141-142
Apgar,V.A Proposal for New Method for Evaluation of the Newborn Infant.Anesth.Analg.1953:32:260-267
Ballard R.A.Schaffer & Avery's Diseases of the Newborn-6th Ed.1991; 193-206
British Pediatric Association. Neonatal Resuscitation. London: BPA, 1993
Bloom R.S, Cropley C.S. Textbook of Neonatal Resuscitation. American Heart Association, American Academy of Pediatrics,1987;1-37
Hamilton P.Care of the Newborn in the Delivery Room.BMJ 1999;318:1403-1406
Royal College of Obstetricians and Gynecologists. Working Party Report on Maternity Care in Obstetrics and Gynecology. London: Royal College of Obstetricians and Gynecologists, 1990
Roberton N.R.C.Resuscitation of the Newborn.Textbook of Neonatology 2nd Edn.Churchill Livingstone.1992;173-198
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