Asfiksia Neonatorum
Fakultas Kedokteran Universitas Muhammadiyah Malang
Pendahuluan (1)
Asfiksia Bayi Baru Lahir Asfiksia Lahir (BBL) : 15% kematian kematian BBL (5 juta) /tahun
Angka kejadian kejadian asfiksia di di RS Propinsi Propinsi : 25,2% (Jawa Barat)
Angka kematian 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
Pendahuluan (1)
Asfiksia Bayi Baru Lahir Asfiksia Lahir (BBL) : 15% kematian kematian BBL (5 juta) /tahun
Angka kejadian kejadian asfiksia di di RS Propinsi Propinsi : 25,2% (Jawa Barat)
Angka kematian 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
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.”
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
Definisi (2) Asfiksia
BBL ditandai dg keadaan : *hipoksemia *hiperkarbia *asidosis
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)
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-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.
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 tinggi aliran 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 relatif ekspansi par < gagal nafas ! ! !
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 brain’s 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 depression of cold stress
Patofisiologi (1-d)
Onset of respiration stimulates cardiovascular cardiovascul ar changes – As – As air enter the lungs, 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 “inter organs 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
Etiologi / Faktor resiko (1)
Matern al facto r :
hypoxia, anemia, diabetes, hypertension, smoking, nephritis, heart disease, too old or too young,etc D el i v er y c o n d i t i o n : Abruption of placenta, placenta previa, prolapsed cord, premature rupture of membranes,etc
Fetal fact or :
Multiple birth, congenital or malformed fetus,etc
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)
Fetal asphyxia
fetal heart rate: tachycardia fetal movement: increase
bradycardia decrease
amniotic fluid: meconium-stained
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) 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)
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
0
1
2
Heart Rate
Absent
<100
>100
Respiratory Effort
Absent, irregular
Slow, crying
Good
Muscle Tone
Limp
Some flexion of extremities
Reflex irritability (nose suctioning)
No response
Grimace
Cough or sneeze
Color
Blue, pale
Acrocyanosis
Completely pink
Active motion
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) 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) Tujuan : 1 Expansion of lungs(b y c l e ar i n g u p p e r a ir w a y s & e n s u r i n g p a t en t r o u t e t o t h e t r ac h ea )
2 Increasing the arterial PO2 (b y p r o v i d i n g a d e q u a t e al v e o l a r v e n t i l a t i o n , w i t h O 2 i f n e ed e d )
3 Supporting adequate cardiac output 4 Ensuring that O2 consumption by newborn is minimized (b y r ed u c i n g h eat l o s s e s i n t h e i m m ed i a t e p o s t p a r t u m p e r i o d )
Resusitasi BBL (2) Tindakan yang paling penting dan efektif pada resusitasi neonatus adalah pemberian ventilasi pada paru-paru bayi baru lahir dengan oksigen”
Resusitasi BBL (2)
1)Basic Resuscitation 2)Advanced Resuscitation
ABC’s 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
Resusitasi BBL (2-a)
Neonatal Resuscitation Program
BASIC RESUSCITATION
Basic Resuscitation
Initial steps: – Thermal management – Positioning – Suctioning – Tactile stimulation
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
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 meconium
If there is no cry, assess breathing: if the chest is rising symmetrically with frequency >30/minute, no immediate action is needed
If the newborn is not breathing or gasping: immediately start resuscitation.
Occasional gasps are not considered breathing.
Open the airway Put the baby on its back Position the head so that it
is slightly extended
.
Position of Newborn for Resuscitation
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)
•P l ac e U n d e r w a r m e r •D r y t h o r o u g h l y •R e m o v e w e t l i n e n •P o s i t i o n •S u c t i o n m o u t h t h e n n o s e •Tactile stim ulation
Evaluate Respirations
Spontaneous
None Inj. Narcan
Evaluate HR
Overview of Resuscitation
Yes Drug Depressed
No
HR
PPV
<100
15-30 sec
>100 HR <60 Ct Ventilation + Chest compression
HR 60-100 -HR increasing Ct ventilation
-HR not increasing (<80)
HR >100 look for spont. Resp DC ventilation
Evaluate color
Ct chest compression
Drugs if: HR <80,after 30 secs PPV +100% O2 +chest compression
Observe Monitor
Pink
Blue Oxygen
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
Least common treatment
Drugs
Gangguan napas pada bayi baru lahir Apnea attack attack Respiratory Distress Syndrome Hyaline Membrane Disease
Apnea attack ( serangan apnu, episode apnu )
Keadaan bayi tidak bernafas untuk beberapa saat
Abnormal
: > 20 detik, disertai disertai sianosis, sianosis,
bradikardi
Pada hari-hari I kelahiran, biasanya berulang-ulang
Sering pada bayi prematur ( berat lahir < 1.500 gr, kehamilan < 32 minggu )
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 keseimbang an asam-basa cairan dan elektrolit )
Sikap dan tindakan
Lakukan rangsangan mekanis ( mengubah letak bayi, memukul telapak kaki )
Bersihkan saluran nafas
Berikan O2 dg sedikit tekanan
Mencari dasar etiologinya
Sikap selanjutnya sesuai dengan etiologi
Respiratory Distress Syndrome
Sindroma Gangguan Nafas / SGN
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 / 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 disease Penyakit membran hialin Sindroma gangguan pernafasan idiopatik
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 surfactant
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
，
PS
，
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 %)
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.
Patofisiologi
( lanj.)
hipoksia asidosis transudasi penurunan aliran darah paru hambatan pembentukan substansi surfaktan atelektasis. Hal ini berlangsung terus :
Atelektasis
penyembuhan / kematian
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.
Gambaran radiologis
Gambaran klasik foto rontgen paru : bercak difus infiltrat retikulogranuler
Untuk diagnosis dini, walaupun klinis belum jelas
Untuk menyingkirkan DD : pneumotoraks, hernia diafragma.
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
Gambaran patologi dan histopatologi
Otopsi : atelektasis, membran hialin dlm alveolus atau duktus alveolaris, emfisema. Membran hialin : febrin, sel eosinofilik, dari darah atau sel epitel alveolus yg rusak
Pencegahan
Mencegah kelahiran bayi prematur
Pemberian kortikosteroid ibu hamil trimester III ( ? )
Penatalaksanaan
Memberikan lingkungan yg optimal : suhu, humiditas
Oksigen
Pemberian cairan, glukosa, elektrolit
Antibiotika
Prognosis
Tergantung tingkat prematuritas
Terjadinya displasia bronkopulmoner umumnya akibat tekanan positif terus menerus ( respirator )
SEPSIS PADA BAYI BARU LAHIR
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
Neonatal Infections Sepsis Meningitis Pneumonia Otitis Media Diarrheal Disease UTI Osteomyelitis Suppurative Arthritis Conjunctivitis Orbital Cellulitis Cellulitis - - Omphalitis
Bacterial / Viral / Fungal
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 System • All neonates relatively immunocompromised • Immature and Ineffective: – Antibodies – Complement – Neutrophils – Skin / mucosal barriers
Neonatal Bacterial Sepsis: Disease Patterns
Early Onset Neonatal Sepsis (EONS) – Fulminant, multisystem 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 Neonatal 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: Signs/Symptoms Strongly suggestive hypoglycemia / hyperglycemia hypotension metabolic acidosis apnea shock DIC hepatosplenomegaly bulging fontanelle seizures petechiae hematochezia respiratory distress
Early Onset Neonatal Sepsis: Signs/Symptoms Nonspecific lethargy, irritability temperature instability -- hypothermia or fever poor feeding cyanosis tachycardia abdominal distention jaundice tachypnea
Early Onset Neonatal Sepsis: Summary
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 Sepsis
Perinatal acquisition with later onset – – – –
Term or preterm Bacterial: GBS, Chlamydia Viral: HSV, CMV, HepB, HIV Fungal: C a n d i d a
Nosocomial acquisition – Health care associated infections – Preterm or sick term infant
Late 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 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: Incidence
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
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.)
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.)
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 Sepsis Frequency(%) Group B Streptococci Escherichia coli
Streptococcus viridans Staphylococcus aureus Enterococcus spp Coagulase-negative staphylococci Klebsiella pneumoniae Pseudomonas spp Serratia marcescans Others
*Schuchat et al,
40 17 7 6 6 5 4 3 2 10
Congenital nasolacrimal 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)
Conjunctivitis
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
Eye Care To Prevent or Manage Ophthalmia Neonatorum
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
Eye Care To Prevent or Manage Ophthalmia 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
Summary The essential components of normal newborn care include:
Clean delivery and cord care
Thermal protection
Early and exclusive breastfeeding
Monitoring
Eye care
Immunization
Dacryocystitis Bacterial infection of nasolacrimal gland with duct obstruction Mgt: – Swab C+S – Topical + systemic antibiotics
Gonorrheal 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 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
Herpetic conjunctivitis
Day 2-16 Flourescein stain: dendritic ulcer
Do FSW
Rx: IV acyclovir, topical vidarabine 30-50% of cases recur w/i 2 years
Omphalitis
When should the umbilical cord separate?
Usually w/i 2 weeks
Delayed separation: think of possible leukocyte adhesion defect
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
Necrotizing fasciitis
Sepsis
Portal vein thrombosis
Hepatic abscesses
Treatment
IV Antibiotics
Local cleaning
Can rapidly progress to Necrotizing fasciitis (16%)
Usually polymicrobial
Rapidly fatal (50%)
Surgical debridement necessary
10
Apshyxi Contrl
75 % n o i t a50 r u t a S 25 0 0123456 78910
mniutesafr bith Rao,Smji: IndaPeitrcs201;38:762-
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)
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)
Asphyxia development:
a.
Primary apnea breathing stop but normal muscular tone or hypertonia, tachycardia(quick heart rate), and hypertension Happens early and shortly, selfdefended 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)
Other damages:
a.
Persistent pulmonary hypertension (PPHN)
b.
Hyper/hypoglycemia
c.
Hyperbilirubinemia
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
Neonatal Resuscitation Program
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 Transition to Neonatal
Circulation ( with
closure of Foramen Ovale and Ductus Arteriosis)
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
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
Failure to breath after birth PO2 falls immediately to near zero Acidosis Biophysical stigmata of Asphyxia
Brain damage or Aggravation of an existing CNS injury
Effects of Asphyxia on Body Systems
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 After Delivery As
quickly after delivery as possible
Record the response to resuscitation as a narrative in babies notes
Methods of assessment •Traditional way- Apgar score •Cord blood analysis •Other biochemical methods •Clinical examination
Apgar scores for different signs in Newborns Sign
Heart rate Respiratory
Score
0
1
Nil
<100
Absent
effort Muscle tone
Gasping or irregular
Flaccid
Some tone
2 >100 Regular or crying Active
Response to None stimulation
Grimace
Cry or cough
Color
Blue
Pink centrally
White
Factors Affecting Apgar Score False positive score
F al s e n e g a t i v e s c o r e
Prematurity
Maternal acidosis
Drugssedatives,narcotics,mgso4
High fetal catecholamine levels
A/c cerebral trauma
Some full term infants
Precipitate labor
Cong. Myopathy
Cong. Neuropathy
Spinal cord trauma
CNS anomaly
Lungs-diaphragmatic hernia
Airway-choanal atresia
Cong. Pneumonia (GBS)
Limitations of Apgar Score
Affected by many factors, so low apgar score do not necessarily signify fetal asphyxia
1 min. Apgar scorestrongly correlated with cord pH & an index of intrapartum 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..)
Apgar score beyond 1 min. (5,10,15 & 20min)reflective of child’s changing condition & indicative of adequacy of resuscitative efforts
Sco re 0-3 at 20 Mts.i n d i c a t e h i g h m o r t a li t y & morbidity
Cord 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: -P o o r r e la t io n s h i p w i t h A p g a r s c o r e -2 % b a b i e s w i t h n o r m a l A p g a r s c o r e h a s p H < 7 .1 -M o s t b a b i e s w i t h p H < 7 .1 h a v e n o r m a l A p g a r
If both Apgar & pH abnormal & no other cause detected, strongly s/o recent Asphyxia
Other biochemical indicesLactate,hypoxanthine,CPK
Examination of the Newborn A r e a Ex a m i n a t io n 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
Conditions to Exclude in Initial External Examination of Newborns 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
Labor Ward Management of 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
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
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 Assessment Most infants fall into four groups
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%)
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
Group 2-Primary Apnea
Prems <32 weeks – all with no respiration & fail to turn pinkintubate & 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
Resuscitation With Bag & 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)
Positive Pressure Ventilation - Correct 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)
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 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)
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
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 Admit
10 cc/kg
in NICU
Further management as terminal apnea
Drugs for use in neonatal resuscitation Adrenaline Preparation 1 in 10 000 dilution (100 µg/ml) D o s e 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 D o s e 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 D o s e 10-20 ml/kg via umbilical venous catheter over 5-10 minutes (may be repeated)
Naloxone hydrochloride* D o s e 100 µg/kg (0.25 ml/kg) intramuscularly
*Never give to the baby of an opiate dependent mother
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
B.Infants who do not start to breathe Pink,good cardiac output,but by 20 min. No
spont.respiration despite empirical drugsdelay 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
Infants Who Do Not Respond to 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 Resuscitation
+
D rugs
Begin
Medications •Adrenaline
•HR- Zero or •HR <80/Mt after 30 sec PPV +chest compression
•Volume expander
Can be repeated every 5 Minutes
Adrenaline
•Sodium Bicarbonate
HR>100
Metabolic Acidosis
No
Yes DC drugs
A/c bleeding + Hypovolemia
Volume expanders
Soda Bicarbonate ? Shock
Resp. depression & H/o Narcotics given to Mother <4hr
Dopamine Narcan
