asfiksia neonatorum.ppt

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.”


•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



Asfiksia BBL ditandai dg keadaan : *hipoksemia *hiperkarbia *asidosis


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


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


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 ! ! !


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.



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)


Tindakan yang paling penting dan efektif pada resusitasi neonatus adalah pemberian ventilasi pada paru-paru bayi baru lahir dengan oksigen”



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

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 .


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


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 )


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 )


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


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


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 )


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 %)


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.


Patofisiologi ( lanj.)Patofisiologi ( lanj.)

Atelektasis hipoksia asidosis transudasi penurunan aliran darah paru hambatan pembentukan substansi surfaktan atelektasis. Hal ini berlangsung terus : penyembuhan / kematian


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.


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.


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


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


Pencegahan Pencegahan

Mencegah kelahiran bayi prematur Pemberian kortikosteroid ibu hamil

trimester III ( ? )


Penatalaksanaan Penatalaksanaan

Memberikan lingkungan yg optimal : suhu, humiditas

Oksigen Pemberian cairan, glukosa, elektrolit Antibiotika


Prognosis Prognosis

Tergantung tingkat prematuritas Terjadinya displasia bronkopulmoner

umumnya akibat tekanan positif terus menerus ( respirator )


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


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


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.


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 ?


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


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


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


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


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


erythema and edema of umbilical area

excellent medium for bacterial colonization

poor hygiene or hospital-acquired infection

Staphylococcus, Streptococcus, Gram (-) rods


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 %

15/06/1999 Dr.Bambang M104

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

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


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)


Failure to breath after birth

PO2 falls immediately to near zero

Acidosis

Biophysical stigmata of Asphyxia

Brain damage orAggravation of an existing CNS injury


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


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)


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)


“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)


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


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


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


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


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


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


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


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


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


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


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


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


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)


Positive Pressure Ventilation - Positive Pressure Ventilation - Correct Position & Size of Face MaskCorrect Position & Size of Face Mask



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


Correct Positioning of LaryngoscopeCorrect Positioning of Laryngoscope



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)


External Chest Compression

Technique of chest compression-Note the position of the thumbs on the midsternum,just below the nipples


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.)


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


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


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


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


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


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)


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


ABCD of Neonatal ABCD of Neonatal ResuscitationResuscitation

Drugs+


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


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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