Professional Documents
Culture Documents
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 M
Pendahuluan (2)
Sebagian besar bayi yaitu sekitar 90% tidak membutuhkan atau hanya sedikit memerlukan bantuan untuk memantapkan pernafasannya setelah lahir dan akan melalui masa transisi dari kehidupan intrauterin ke ekstrauturin tanpa masalah.
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Dr.Bambang M
Pendahuluan (3)
6-10 out of 130 mill newborns need intervention at birth 4 mill birth asphyxia 1 mill die and a similar number develop sequels due to birth asphyxia (CP, Epilepsia)
Most newborn infants are born outside hospitals without health personel attending
Pendahuluan (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)
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
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Dr.Bambang M
Definisi (2)
Asfiksia
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Dr.Bambang M
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
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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)
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).
Definisi (4-a) 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.
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 ! ! !
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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)
First breath is inspiratory gasp Changes trigger aortic and caratoid chemo receptors that trigger brains respiratory center Natural result of a normal vaginal delivery
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)
Onset of respiration stimulates cardiovascular changes As air enter the lungs, oxygen content rises in alveoli and stimulates relaxation of pulmonary arteries
Patofisiologi (1-e)
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 (2)
When fetal asphyxia happens, the body will show a self-defended mechanism which redistribute blood flow to different organs called interorgans shunt in order to prevent some important organs including brain, heart and adrenal from hypoxic damage.
Patofisiologi (3)
Hypoxic cellular damage : _reversible ( early stage ) _unreversible damage Primary apnea Secondary apnea Other damage : persisten pulmonary hypertension, hypo/hyperglicemia, hyperbilirubinemia
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Anticipate Asphyxia Preterm delivery Thick meconium Acute fetal or placental hemorrhage Use of narcotics in labor Maternal infection Polyhydramnios: GI obstruction Oligohydramnios: Hypoplastic lungs
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
Score Heart Rate Respiratory Effort 0 Absent Absent, irregular 1 <100 Slow, crying 2 >100 Good
Muscle Tone
Reflex irritability (nose suctioning) Color
Limp
No response Blue, pale
Active motion
Cough or sneeze Completely 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
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Tindakan yang paling penting dan efektif pada resusitasi neonatus adalah pemberian ventilasi pada paru-paru bayi baru lahir dengan oksigen
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1) Basic Resuscitation
2)Advanced Resuscitation
ABCs of Resuscitation
A B C (A: Airway, B: Breathing, C: Circulation)
A - establish open airway Position, suction B - initiate breathing Tactile stimulation Oxygen C - maintain circulation Chest compressions Medications D. Drug E. Evaluation
Johns Hopkins: The Harriet Lane Handbook: A Manual for Pediatric House Officers, 16th ed., Copyright 2002 Mosby, Inc.
BASIC RESUSCITATION
Basic Resuscitation
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The important steps in resuscitation are: 1.Prevention of heat loss, 2.Opening the airway and 3.Positive pressure ventilation that starts within the first minute of life
The surface on which the baby is placed should always be warm as well as flat, firm and clean
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
Drying provides sufficient stimulation of breathing in mildly depressed newborns and no further stimulation is appropriate
The second step (within 20-30 seconds of birth) is assessment of neonatal respiration
The upper airway (the mouth then the nose) should be suctioned to remove fluid if stained with blood or meconium
If there is no cry, assess breathing: if the chest is rising symmetrically with frequency >30/minute, no immediate action is needed
Open the airway Put the baby on its back Position the head so that it is slightly extended .
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)
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Place Under warmer Dry thoroughly Remove wet linen Position Suction mouth then nose Tactile stimulation
Evaluate Respirations
Overview of Resuscitation
None
Inj. Narcan
Spontaneous
Yes
Drug Depressed
Evaluate HR No
HR <60 Ct Ventilation + Chest compression
PPV
15-30 sec
HR
<100
>100
HR 60-100
-HR increasing Ct ventilation -HR not increasing (<80) Ct chest compression
Evaluate color
Blue Oxygen Dr.Said Alavi
Observe Monitor
Pink
Hubungan antara prosedur resusitasi dan jumlah bayi yang perlu prosedur tsb.
Most common treatment
Keep dry & warm Suction & stimulation
Oxygen
Establish effective ventilation Bag &mask Tracheal Intubation Chest compressions
Drugs
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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 )
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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
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Definisi / 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 )
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Brief 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
Definition
Hyaline membrane disease HMD Deficiency of pulmonary surfactantPS 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
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 %)
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patofisiologi
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.
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Patofisiologi
( lanj.)
Atelektasis hipoksia asidosis transudasi penurunan aliran darah paru hambatan pembentukan substansi surfaktan atelektasis. Hal ini berlangsung terus : penyembuhan / kematian
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Gambaran 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.
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Gambaran radiologis
Gambaran klasik foto rontgen paru : bercak difus infiltrat retikulogranuler Untuk diagnosis dini, walaupun klinis belum jelas Untuk menyingkirkan DD : pneumotoraks, hernia diafragma.
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Gambaran 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
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Otopsi : atelektasis, membran hialin dlm alveolus atau duktus alveolaris, emfisema. Membran hialin : febrin, sel eosinofilik, dari darah atau sel epitel alveolus yg rusak
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Pencegahan
Mencegah kelahiran bayi prematur Pemberian kortikosteroid ibu hamil trimester III ( ? )
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Penatalaksanaan
Memberikan lingkungan yg optimal : suhu, humiditas Oksigen Pemberian cairan, glukosa, elektrolit Antibiotika
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Prognosis
Tergantung tingkat prematuritas Terjadinya displasia bronkopulmoner umumnya akibat tekanan positif terus menerus ( respirator )
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DEFINISI
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
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Neonatal Infections
Sepsis Meningitis Pneumonia
Otitis Media Diarrheal Disease UTI Osteomyelitis Suppurative Arthritis Conjunctivitis Orbital Cellulitis Cellulitis - - Omphalitis
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
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Late Onset Neonatal Sepsis (LONS) Sepsis or meningitis 5 days to 3 months old Perinatal or postnatal acquisition Lower mortality, 2-6%
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
Nonspecific
lethargy, irritability temperature instability -- hypothermia or fever poor feeding cyanosis tachycardia abdominal distention jaundice tachypnea
Nosocomial acquisition
Health care associated infections Preterm or sick term infant
Symptoms -
Occult bacteremia or meningitis most common. However, focal infections (pneumonia, UTI, cellulitis, osteomylelitis, septic arthritis) may occur.
Beberapa 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.
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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 ?
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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
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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
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Group B Streptococci Escherichia coli Streptococcus viridans Staphylococcus aureus Enterococcus spp Coagulase-negative staphylococci Klebsiella pneumoniae Pseudomonas spp Serratia marcescans Others
40 17 7 6 6
5 4 3 2 10
Conjunctivitis
Close contacts affected Unilateral bilateral Sticky discharge Diffuse redness Cornea and pupil normal Chloramphenicol
Cellulitis- Refer urgently Neonatal conjunctivitis: refer urgently
Summary
The essential components of normal newborn care include: Clean delivery and cord care Thermal protection Early and exclusive breastfeeding Monitoring Eye care Immunization
91 Normal Newborn Care
Dacryocystitis
Bacterial infection of nasolacrimal gland with duct obstruction Mgt:
Swab C+S
Gonorrheal conjunctivitis
Hyperpurulent discharge at day 2-4
Chlamydial 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 Whats 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 conjunctivitis
Omphalitis
Omphalitis
erythema
and edema of umbilical area excellent medium for bacterial colonization poor hygiene or hospitalacquired infection Staphylococcus, Streptococcus, Gram (-) rods
Omphalitis
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: complications
Treatment
IV
Antibiotics Local cleaning Can rapidly progress to Necrotizing fasciitis (16%) Usually polymicrobial Rapidly fatal (50%) Surgical debridement necessary
10
%
75 50 25 0 0 1 2 3 4 5 6 7 8 9 10
minutesafrbih
Asphyxia Contrls
t a S
r u
t a
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Rao,Smji:IndaPeitrcs201;38:76-
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Physical Eamination
Vital signs RR 40-60 HR 120-160 Temperature axilary 35.5-37.5 Over bundling Heater
Etiology
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)
a.
Hypoxic cellular damages: 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)
Asphyxia development: a. Primary apnea breathing stop but normal muscular tone or hypertonia, tachycardia(quick heart rate), and hypertension Happens early and shortly, selfdefended mechanismcould 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)
a.
b.
c.
Clinic 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
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: 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
Johns Hopkins: The Harriet Lane Handbook: A Manual for Pediatric House Officers, 16th ed., Copyright 2002 Mosby, Inc.
Perinatal 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
Perinatal 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 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
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) 122
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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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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
Methods of assessment
Traditional way-Apgar score Cord blood analysis Other biochemical methods Clinical examination
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0
Heart rate Nil
1
<100
2
>100
Respiratory
effort Muscle tone
Absent
Flaccid
Gasping or
irregular Some tone Grimace Blue
Regular or
crying Active Cry or cough Pink centrally
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Prematurity Drugssedatives,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)
130
Maternal acidosis High fetal catecholamine levels Some full term infants
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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 scorestrongly correlated with cord pH & an index of intrapartum asphyxia Apgar score beyond 1 min. (5,10,15 & 20min)reflective of childs changing condition & indicative of adequacy of resuscitative efforts Score 0-3 at 20 Mts.indicate high mortality & morbidity
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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
If both Apgar & pH abnormal & no other cause detected, strongly s/o recent Asphyxia
Back-Skin, spine
Legs -Toes, ankles, hips
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Apnea
PRIMARY 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 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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Management(contd.)
Group 1-Fit & healthy
Leave
this baby alone ! No vigorous suction Dry & wrap in warm blanket Inj.Vitamin K Give to mother for breast feeding
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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
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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 140 Dr.Said Alavi
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) Dr.Said Alavi
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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 143 Dr.Said Alavi
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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Group 4 (contd.)
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
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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 g/kg (0.25 ml/kg) intramuscularly
*Never give to the baby of an opiate dependent mother
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Continuing Therapy After Terminal Apnea A.Infants with regular respiration 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
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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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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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Drugs
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Begin
Medications
Adrenaline Volume expander Sodium Bicarbonate
Adrenaline
HR>100
Yes DC drugs
No
? Shock
Dopamine Narcan
Dr.Said Alavi
References
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
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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