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FETAL DISTRESS ( NEW ERA OF FHR TRACINGS – what is the difference ? ) Jaya Kusuma,dr,Obgyn Spec, MFM Subsepecialist Head Of MFM Division Obgyn Dept.Udayana Faculty of Med/Sanglah Hospital. dr. A.A.N Jaya Kusuma, SpOG(K), MARS Maternal fetal Medicine Division Obstetrics and Gynecology Department Faculty of medicine Udayana University Sanglah Hospital Bali KARDIOTOCOGRAPHY-interpretation and MANAGEMENT

Kardiotokografi Ppds (Dr.jks)

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FETAL DISTRESS( NEW ERA OF FHR TRACINGS –

what is the difference ? )

Jaya Kusuma,dr,Obgyn Spec, MFM SubsepecialistHead Of MFM Division Obgyn Dept.Udayana Faculty of

Med/Sanglah Hospital.

dr. A.A.N Jaya Kusuma, SpOG(K), MARSMaternal fetal Medicine Division

Obstetrics and Gynecology DepartmentFaculty of medicine Udayana University

Sanglah Hospital Bali

KARDIOTOCOGRAPHY-interpretation and MANAGEMENT

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INCREASINGLY DEFENSIVE

MEDICAL BEHAVIOURS ???

?

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Spilka, 2013

“.. Being born is one of the most crucial events in human life..After intra uterine growth and development a fetus, must adapt to a new environment and is going to estbalish itself with its own nutritional supply and pattern of reactions As an independent individuDuring pregnancy and labour..a fetus can suffer frOm oxygen insufficiency which is normal..But ---For fetuses with weakend defence mechanism ..a fetal distress and metabolic acidosis could be developed…Can lead neuro-developmental disability,cerebarl palsy,neonatal encephalopathy,and death…To cope this event fetuses are equipped with defence mechanism..That is why..we should know what is the signs and symptoms of defence meachanism failure..To react before the long term consequencies developed..

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Fetal Distress • Often used without evidence of Acidosis• Fetal distress. .” Pogressive fetal asphyxia that if

not corrected will result in decompensation of the physiological respones and can cause permanent nervous system,damage and death ..” ( Kither,2012)

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MATERNAL -FETAL OXYGEN PATHWAY

Lungs Heart

Vaculature Uterus

Umbilical Cord Placenta

FETUS( Fetal Circulation)

Hypoxemia Hypoxia

Metabolic Acidosis

Metabolic Acidemia

HYPOTENSION

DEATH

Fetal oxygenation involves the tansfer of oxygen from the environment to the fetus

along the “oxygen pathway

Fetal oxygenation also involves the fetal physiologic response to interruption of the

“oxygen pathway”

Clinical Signs/Symptomps- Organ dysfunction- Organ FailuredCourtesy by Jaya Kusuma,2015

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ACOG/AAP CRITERIA FOR DEFINING NEONATAL ENCEPHALOPATHY AND CEREBRAL PALSY(2003)

• Essensital criteria( must meet all 4) :1. Evidence of metabolic acidosis in intrapartum fetal,umb.cord arterial blood obtained at delivery pH

<7.00 and base deficit > 12 mmol/L2. Early onset of severe or moderat neonatal encephalopathy in infants born at >34 weeks3. Cerebral palsy of the spastic quadriplegia or dyskinetic type4. Exclusion of other identifiable etiologies, such as trauma,infections,genetic etc• Nonspecific criteria :1. A sentinel(signal) hypoxuc event occurring immediately before or during labor

2. A sudden and sustained fetal bradycardia or the absence of FHR variability in the presence of persistent,late or variable decelerations usually after a hypoxic sentinel event when pattern was previuosly normal

3. Apgar Score 0-3 beyond 5 minutes4. Onset of multisystems involvement withi 72 hours

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PHYSIOLOGY OF FETAL OXYGENATION• Aerobic metabolism required oxygen and glucosa

(main sources of energy) all cells need• Glucose usually be stored and mobilized when needed• Oxygen : if supplies is not enough cell at risk• Complication occurred in any levef of oxygen supply

may result decreased fetal oxygenation in fetal arterial blood(hypeoxemia) and fetal tissues hypoxia

• The severity of hypoxia depend on : intensity,duration,repetitive,and placental capacity

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FETAL HYPOXIA RESULT FROM :INTERRUPTED OXYGEN TRANSFER

Hypoxia may result from ( Miller, 2013)• (1) Reduced placental perfusion with maternal blood and consequent

decrease in fetal arterial blood oxygen content due to low pO2 (hypoxemic hypoxia);

• (2) Reduced arterial blood oxygen content due to low fetal hemoglobin concentration (anemic hypoxia);

• (3) Reduced blood flow to the fetal tissues (ischemic hypoxia).

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PLACENTA AS FETAL “GAS EXCHANGE” ORGAN ( HOW IMPORTANT) PLACENTA WORKS AS THE FETAL LUNG

• CO2 eleminate across the placenta diificulties in CO2 elimination increase CO2 concentration + H20 increase H2CO3 respiratory acidemia no injury because CO2 diffuses rapidly across the placenta

• When hyoxia occurred anaerobic metabolism to maintain cell energy production but 20 time less accumulation of lactic acid inside the cellfetal circulation and extra cellular fluid.

• H+ ion of lactic acidtransferred very slowly accros the placenta but they are buferred by circulating bases( bicarbonate) if buffering agents fail to neutralize H+ion( base deficit or base excess in nega number) tissue injury- cell death

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O2 is transferred to the fetus via passive diffusion

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FETAL PHYSIOLOGY : BLOOD SHORT CUTS

Oxygenated blood

De-oxygenated blood

Guyton & Hall,2005

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HEART RATE SENSITIVE TO

OXYGEN CONTENT

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FETAL RESPONSE TO INTERRUPTED OXYGEN TRANSFER ?

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FETAL RESPONSE TO INTERRUPTED OXYGEN TRANSFER(2)Fetus normally able to maintain aerobic metabolism until the avalaible oxygen in the intervillous space falls to 50% of normal levels- Compensatory mechanisme vasocnstriction + increase blood pressure ( Chemoreceptor) TACHYCARDA hypertension( barroreceptor) vagal stimulation fetal BRADICARDIAFETAL HEART TRACING/MONITORING ASSESS FETAL OXYGENATIONFETAL INJURY DUE TO INTERRUPTED OXYGENATION DOESN’T OCCUR UNLESS FETAL RESPONSE PROGRESS AT LEAST TO THE STAGE OF SIGNIFICANT MEATBOLIC ACIDEMIA ( UMBILICAL ARTERY pH < 7,0 and Base Deficit > 12 mmol/L) ( Miller,2013)

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FHR tracing as a tool to detection fetal hypoxia : what is the evidence ? ( ACOG,2012)

• Interpretation of FHR tracings has been difficult lack of agreement in definition,nomenclature and/or recommendations

• Abnormality of FHR tracing likely labelled as “foetal distress “

• Subjectivity when intepreted the pictures of tracings and implementation increasing SC rate/medical management of pregnancy

• Still leave some question how to definitely label each tracing ?

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The History of FHR Tracings• EFM > 50 years old USA > 4 million women giving birth have continous

EFM during labor CS rates higher than women who do not EFM• JA Le Jumeau,V de Kergaradecused Stethoscope to hear the noise of the

water in uterus and identified as the FHR• Evory Kennedy(1833) term of Fetal distress bardicardia as poor

prognosis of born baby due to fetal head compression• Head Fetoscope David Hillis (1917) and Joseph de Lee (1922)• Edward Hon,1958,Caldeyro Barcia,Hammacher FHR monitoring by

electronic devices Cardiotocography

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Research at the end of the 20th Century on EFM• The Issues : What went wrong with EFM ?• Fetal Heart rate patterns reflecting fetal distress varied among the different

sudies they used varied parameter to identified outcome of neonates who being asphyxia( Apgars,perinatal mortality,CP)

• 1996 National Institute of Child Health and Human development (NICHD) made recommendations three important aspects of FHR monitoring for research and clinical practice : 1) standard definitions of FHR pattern,2)absence of asphyxia described with normal baseline rate,moderate variability,presence of accelerations,and no decelerations, 3) predictive of current or impending asphyxia if we there are any recurrent late or varaible decelarations or substatial bradicardia with absent variability.

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Fetal Monitoring in the 21 th Century• 1997, NICHD defeinitions used in research

investigating the relationship between FHR and fetal acidemia and in 2008 new NICHD panel on FHR monitoring wa s convened ( as clarifications the old/tarditional terme” reassurung/non reassuring “)

• ACOG,AWHONN,ACNM endorsed NICHD for daily use of FHR monitoring

• The research still ongoing to predict abnoramlitiess of FHR with poor neonato outcame/fetal acidemia ( fetal scalp/pulsed oxymetry and ST segment analysies)

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Pattern Recognition and Interpretation

Clinical Aplication of e-FHR consists of three main component :1)Definition2)Interpretation3)Management

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Standar Interpretasi Garis Monitor Janin Pada kertas rekam KTG

• Kertas monitor KTG diatur dengan kecepatan 1 cm/menit (atau 3 cm/mt ) dan dapt merekam Djj interval 30-24 dpm

• Kertas KTG dibagi menjadi 2 bagian atas merekam grafik DJJ dan bagian bawah merekam kontraksi/aktiftas uterus

• Bagian atas (grafik Djj) dibagi garis horisontal tebal dan garis horisontal tipis, jarak antar dua garis tebal = 30-40 dpm dan jarak antar 2 garis tipis 2-5 dpm dan garis vertikal dibagi dalam garis tebal dan tipis, interval antara 2 garis tebal 1 menit dan antara dua garis tipis 10 detik.

• Bagian bawah (kontraksi uterus): interval dua grais tebal 1menit dan dua garis tipis 10 detik. Rentang nila 0-100 pd kolom horisontal mengukur intensitas kontraksi dg satuan mmHg

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GAMBARAN REKAMAN KTG BERDASARKAN KECEPATAN KERTAS KTG

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Definitions of fetal heart-rate patterns Pattern Definition Baseline

. The mean FHR rounded to increments of 5 bpm during a 10-min segment, excluding: Periodic or episode changes Periods of marked FHR variability Segments of baseline that differ by more than 25 bpm . The baseline must be for a minimum of 2 min in any 10-min segment

Baseline variability

. Fluctuations in the FHR of 2 cycles per min or greater . Variability is visually quantitated as the amplitude of peak-to-trough in bpm Absent – amplitude range undetectable Minimal – amplitude range detectable but 5 bpm or fewer Moderate (normal) – amplitude range 6–25 bpm Marked – amplitude range > 25 bpm

Acceleration

. A visually apparent increase (onset to peak in < 30 sec) in the FHR from the most recent calculated baseline . The duration of an acceleration is defined as the time from the initial change in FHR from the baseline to the return of the FHR to the baseline . At 32 wks of gestation and beyond, an acceleration has an acme of 15 bpm or more above baseline, with a duration of 15 sec or more, but < 2 min . Before 32 wks of gestation, an acceleration has an acme of 10 bpm or more above baseline, with a duration of 10 sec or more, but < 2mi . Prolonged acceleration lasts 2 min or more but < 10 min . If an acceleration lasts 10 min or longer, it is baseline change

Bradycardia . Baseline FHR < 110 bpm

Early deceleration . In association with a uterine contraction, a visually apparent, gradual (onset to nadir 30 sec or more) decrease in FHR with return to baseline

Tachycardia . Baseline FHR > 160 bpm Variable deceleration

. An abrupt (onset to nadir 30 sec or more), visually apparent decrease in the FHR below the baseline . The decrease in FHR is 15 bpm or more, with a duration of 15 sec or more, but < 2 min

Prolonged deceleration

. Visually apparent decrease in the FHR below the baseline . Deceleration is 15 bpm or more, lasting 2 min or more but less than 10 min from onset to return to baseline

FHR, fetal heart rate; bpm, beats per minute. Reprinted from the ACOG Practice Bulletin No. 70. American College of Obstetricians and Gynecologists. Obstet Gynecol 2005; 106: 1453–61.

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The Causes of Absent varibaility 1.Fetal metabolic acidosis2.Neurologic abnormality3.Marked prematuriity4.Drug effect5.Fetal quit sleep ( 15-30 mnt/ not more 60 mnts)6.Fetal inactvity

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1.Recurrent VD with atypia 2. Recurrent VD +Mixed featrures(Late/variable) associated with absent var-3. Prolonged dec without recovery/ recurrent with progresive depth,duration4. Checkmark pattern

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Atypia Var deceleration :1.Absent primary accl

2.Absent secundary accl3.Overshoot

4.Slow return to baseline5.Biphasic wave( W Shape with second componen

“late” )

- hati- hati..bila berulang dan persisten !!

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Hati- hati : electromechanical dissociation/ electrical activity of the heart might continue despite cessation of muscular cardiac activity : perhatikan variabilitas

Hati-hati : tidak ada akselerasi,menurunya variabilitas dan ada deselerasi,bedakan rebound tachycardia dengan ovrshoot (rebund accelerations )

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.

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The presence of moderate varibility is a signicant indicator of fetal oxygention,particularly when accompanied by accelerations, it reflects an intact autonomic nervous system

Hati-hati : bedakan dengan Sinusoidal pattern

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DESELERASI DINI

• Penurunan DJJ sesaat bersamaan dengan timbulnya kontraksi.

• Penurunan DJJ biasanya tidak mencapai 100 dpm.

• Penurunan DJJ merupakan ‘bayangan cermin’ dari kontraksi.

• Terjadi akibat kompresi kepaladi dasar pelvik.

» Tidak mempunyai arti patologis.

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DESELERASI DINI (HEAD COMPRESSION)

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DESELERASI LAMBAT

• Penurunan DJJ yang terjadi beberapa saat setelah kontraksi dimulai.

• Deselerasi lambat yang berulang merupakan keadaan patologis:

- insufisiensi plasenta- hipoksia/asfiksia janin.

.

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PROLONGED DECELERATION

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DESELERASI VARIABEL

• Deselerasi yang bervariasi dalam bentuk, lama, dan saat terjadinya.

• Jenis deselerasi yang paling sering dijumpai (terutama dalam partus kala II).

• Terjadi akibat kompresi tali pusat.• Kebanyakan tidak berbahaya bagi janin.• Beratnya derajat deselerasi variabel

berhubungan langsung dengan beratnya derajat hipoksia janin.

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KLASIFIKASI DESELERASI VARIABEL

• Deselerasi variabel ringan:- penurunan DJJ tidak mencapai 80 dpm.- lamanya kurang dari 30 detik.

• Deselerasi variabel sedang:- penurunan DJJ mencapai 70 - 80 dpm.- lamanya 30 – 60 detik.

• Deselerasi variabel berat:- penurunan DJJ sampai di bawah 70 dpm.- lamanya lebih dari 60 detik.

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DESELERASI VARIABEL

• Deselerasi variabel yg tidak patologis (tidak berbahaya bagi janin):- timbul dan menghilangnya berlangsung cepat.- variabilitas DJJ normal.- terdapat akselerasi pra- dan pasca-deselerasi (bahu deselerasi).

• Deselerasi variabel yg patologis (berbahaya bagi janin):- terjadinya lebih lambat dari saat timbulnya kontraksi.- menghilangnya deselerasi berlangsung lambat.- variabilits DJJ berkurang/hilang, atau meningkat secara berlebihan.- menghilangnya akselerasi pra- dan pasca-deselerasi.- semakin beratnya derajat deselerasi variabel.

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KONTRAKSI UTERUS

Komponen kontraksi uterus

• Frekuensi• Lama• Amplitudo• Tonus• Irama• Konfigurasi

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PATTERN RECOGNITION(nichd)--Note: patterns not defined by NICHD: Wandering baselien, lambda, overshoot, W Shape, etc.

Miller,2013

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The Management of (ACOG) : NEW THREE TIERED CLASSIFICATION OF FHR TARCINGS

• Category I : Normal Tracing which are not associated with fetal asphyxia ( Common in labor)

• Category II : Indeterminate tracing,including a wide variety of possible tracings that do not fit in

• Categogry I and IIICommon in labor)• Category III : Abnormal tracing and indicative of hypoxic

risk to the fetus and possible fetal acidemia.

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80% OF FHR TRACINGS FALL IN TO CATEGORY II CRITICISM TO THE

BROAD DEFINITION OF CATEGORY II

WHAT THE EXPERTS DO ?

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FHR SCORE VS 5-TIERS : LOOK SIMILAR ?

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NORMAL FETAL ACID BASE STATUS :Well Oxygenated Fetus

-Baseline rate :110-160pmBaseline var: moderateLate/Var desc : Absent

Early desc:+/-Accelreations :+/-

INDETERMINATECompensatory Response

-Moderate Var with recurent Late/Var Decel.

-Minimal Var without variable decl

-Absent Var without Recurrent Decel--Bradicardia with

Mod.var--Prolonged Decl-

Tachycardia

ABNORMAL FETAL ACID-BASE STATUS:

-absent Var with :-Recurrent late decl,or

-recurrent var,or -Bradicardia

ORSinusoidal pattern

DYNAMIC PHYSIOLOGIC RESPONSE MODEL

King T , Maternal Fetal neonatal Physiology, Blacburn 4th Ed, 2013

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STOPLIGHT ALGORITHM

Jaya Kusuma,2015

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TAKE HOME MESSAGES: We have to speaking a common language when descrbing FHR Tracing- Category I( Normal-well oxygenated fetus)-category II (Indeterminate )- category III (Abnormal )

E-FHR as a High FP for predicting adverse outcomeIncreased Operative Interventions, delivery or continue assesment cannot be directed by CTG alone

Knowing the limitations, Clinical Condition and Close Monitoring IMPROVED QUALITY OF CARE

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(Denpasar Society of MFM /HKFM Denpasar- Collaboration with Women N Children Harapan Kita Hospital, Prof Ananda/Singapore and Dr

Japaraj/Malaysia)