Intra Partum Cardiotocography - dr vivek patkar

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Cardiotocography ( CTG ) is a procedure of graphically ( graph) recording fetal heart activity and uterine contractions ( Toco ) – both recorded in the same time scale simultaneously and continuously through uterine quiscience and contractions

Transcript of Intra Partum Cardiotocography - dr vivek patkar

Intra Partum Cardiotocography

Dr. Vivek D. Patkar Ex. Hon. Prof.

LTMGH & LTMMC, SionV.D.P.

Definition

Cardiotocography ( CTG )

is a procedure of graphically ( graph) recording fetal heart activity and uterine contractions ( Toco ) – both recorded in the same time scale simultaneously and continuously through uterine quiscience and contractions

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Importance of Cardiotocography

• Scientific

• Social

• Medico legal

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Pioneers

The main credit for CTGs goes to the following

1. Prof. E. H. Hon California

2. Prof. Caldeyro Barcia Uruguay

3. Prof. G. S. Dawes U.K.

4. Prof. C. Redman U.K.

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Specifications of an Intrapartum Monitor

• Reliable• FHR by external doppler ultrasound ( US ) with

auto co – relation • FHR by fetal electrode ( ECG )• Twin monitoring US & ECG • External & Internal tocography• Maternal Heart Rate & Event Marker • Mode, Date & Time printout• No machine or printing errors

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Control of the Fetal Heart Rate

1. Activity of the sino atrial node ( fast )

2. Atrio ventricular node ( slow )

3. C.N.S – cortical & sub cortical influence

4. Cardioregulatory centre in brain stem

5. Baro & chemo receptors & catecholamines

6. Autonomic Nervous System Sympathetic ↑ Parasympathetic ↓

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Terminology• Baseline Heart Rate ( BHR ) – 110 – 150 bpm• Bradycardia – BHR < 110 bpm

» Mod – 100 – 110 bpm

• Tachycardia - BHR > 150 bpm » Mod – 150 – 170 bpm

• Acceleration / Deceleration - > 15 bpm for 15 sec. • Baseline Variability - 10 – 25 bpms

» Silent - 0 – 5 bpm

» Reduced - 5 – 10 bpm

» Saltatory - > 25 bpm

(Sleep or Quiet phase, Prematurity, Anaemia, Infection, Anaesthetics, Sedatives, Anti hypertensive all ↓ variablity )

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Terminology ( contd.)• Deceleration

– Early – Synchronous with uterine contractions. ( Head compression, ARM, PV exam)

– Late – Onset, nadir, recovery out of phase with ut. Ctr. ( Pathological )

– Variable – shape, size & timing ( Cord compression )• Deceleration > 60 bpm and > 60 sec – hypoxia• Biphasic Deceleration ~ ~ Late deceleration

• Shouldering – Acceleration before / after deceleration ( good ANS response )– Exaggeration – Pre pathological– Loss - Pathological

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Late deceleration

• Late deceleration followed by normal baseline – mild compromise

• Late deceleration followed by reduced baseline variability and tachycardia – severe compromise

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Interpretation – FIGO Normal Pattern

• BHR – 110 – 150 bpm• Baseline variability – 5 – 25 bpm

FIGO does not refer to accelerations but must be present

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Interpretation – FIGO Suspicious Pattern

• BHR – 150 – 170 bpm

• Baseline variability 5 – 10 bpm for 40 min

• Increased variability > 25 bpm

• Variable decelerations

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Interpretation – FIGO Pathological Pattern

• BHR < 100 bpm or > 170 bpm

• Baseline variability < 5 bpm for > 40 min.

• Severe variable decelerations

• Severe repetitive decelerations

• Prolonged decelerations.

• Late decelerations w/o baseline variability

• Sinusoidal pattern

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Cardiotocography

• Antenatal

• Admission Test

• Intrapartum

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Proper Assessment

• In order to interpret and logically conclude findings in an intrapartum strip, it is preferable to have an antenatal or an admission test strip, though not absolutely mandatory.

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Admission test • It is a dynamic screening method of the state

of oxygenation of the fetus on admission.• Importance:

1. Low risk or normal trace – clinical monitoring

2. High risk –

suspicious : intermittent monitoring

gross : continuous monitoring or unsafe for labour

( Arulkumaran)

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Indications for intrapartum monitoring

• All cases of BOH ( previous still birth, asphyxia, low Apgar, recurrent abortion, neonatal death)

• High premium babies ( elderly, diabetic, infertility, IVF )

• All cases where fetus can be hypoxic ( IUGR, postdatism, hypertension, MSAF, induction of labour, prolonged labour)

• Patients with epidural.V.D.P.

CLINICAL SCENARIOS

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• SECOND STAGE OF LABOUR: mechanical effects resulting from descent of fetus causing head compression, resulting in early decelerations returning to normal in between contractions ,

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SECOND STAGE OF LABOUR

• SECOND STAGE OF LABOUR

Delivery Within 15 Minutes

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• Obstructed Labour – gradual tachycardia, reduced variability and late decelerations- deliver in 15 mins, or irreversible hypoxia

contd.

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Obstructed LabourLost baby, multi-para with macrosomic baby sudden hypoxia

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TWINS- require a three channel trace or a two channel trace

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TWINS

• BREECH: look for cord compression and relative IUGR, compression of skull above orbits causing variable deceleration

Patient had cord prolapse, lost baby before LSCS

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• BROW PRESENTATION: head compression and variable deceleration

LSCS done baby healthy

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• PREVIOUS SCAR: prolonged bradycardia – indicative of scar dehiscence or rupture possible

Transferred case of previous LSCS. Ruptured, baby lost.

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PREVIOUS SCARScar dehiscence recognized on CTG, immediate section, baby salvaged, AS-8

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• HYPERTENSIVE DISORDERS: IUGR causes baseline bradycardia , antihypetensive drugs like methyldopa, B blockers causes baseline variability and accelerations

V.D.P.Patient on alhpamethyldopa normal delivery

• ECLAMPSIA: prolonged deceleration during a fit

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Patient on Magsulf and occ nefidenpene1.8 KGs Baby, Baby depressed, but made good recovery

• PLACENTAL ABRUPTION – Frequent low amplitude contractions – irritable UTERUS, Fetal Tachycardia with no acceleration, reduced base line variability with deceleration and bradychardia contd.

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• PLACENTAL ABRUPTION – Frequent low amplitude contractions – irritable UTERUS, Fetal Tachycardia with no acceleration, reduced base line variability with deceleration and bradychardia

Baby Lost, retro placental clot of 600 gms

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EPIDURAL ANESTHESIA

EPIDURAL ANESTHESIA: short tachycardia, deep deceleration, loss of beat to beat variabilityt/t: Ringer’s, oxygen, change of position

Immediately after epidural contd. V.D.P.

• EPIDURAL ANESTHESIA: short tachycardia, deep deceleration, loss of beat to beat variability

• t/t: Ringer’s, oxygen, change of position

After Ringer’s and Oxygen

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• NARCOTIC DRUGS: pethidine, diazepam- cause decreased beat to beat variability, decreased baseline FHR, reduced amplitude of acceleration

• t/t: naloxone

Case of toxaemia of pregnancy, forceps applied good AS

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• OXYTOCIN DRIP : regular dose- type 1 deceleration, excessive dose- sustained / hypertonic contraction with bradycardia. 45 mins for effect to go and blood pH to return to normal.

• t/t: tocolytics, if no change in 45 mins5 units drip for augmentation at 30 drops PM contd. V.D.P.

OXYTOCIN DRIPDrip reduced to 20 drops and then stopped all together contd.

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OXYTOCIN DRIP

Normal delivery after 8 hours

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• SINUSOIDAL PATTERN : amplitude and period of variation remains constant , trace is smooth regular and wavy , 5 – 10 bpm- in fetal anemia, Rh, fetal hhage, cordocentesis, vasa previa, anticoag therapy.

Vasa Previa, Baby lost

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SINUSOIDAL PATTERNRH –ve, IUGR COOMBS +ve,1:64, 34 weeks LSCS, died after 5 days

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PROLONGED BRADYCARDIA - r. acidosis- m. acidosis, can be a signal for cord prolapse, abruptio, scar dehiscence, extreme uterine hyperstimulation

• 3 mins - attention!• 6 mins – expect recovery LSCS baby fine• 9 mins – prepare for operative delivery• 12 -15 mins – deliver baby

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PROLONGED BRADYCARDIA

Immediate LSCS, AS-8 on birth

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• TERMINAL BRADYCARDIA: after prolonged bradycardia or tachycardia, random uncontrolled undulatory pattern with no baseline variability, suggests a CNS damage, mostly irreversible

Severe IUGR due to high BP, AFI 2, baby lost

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TERMINAL BRADYCARDIASevere IUGR , viral encephalitis at 8 months, baby could not be salvaged

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Tracing character sequence and degree of hypoxia

Normal trace

• Early hypoxia- Disappearance of acceleration with FM and then uterine contraction

- Further hypoxia- Rising baseline FHR- baseline tachycardia

- Further hypoxia- Reduction in baseline variability <5 bpm (straight line)

- Further hypoxia- Late deceleration

( Arulkumaran, Gibbs, Debdas)

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Abnormal tracing- acidosis interval

• With repeated late decelerations – 2 hours

• With repeated variable decelerations – 2 1/2 hours

• With flat trace ( baseline variability < 5 bpm) – 3 hours

( Fleischer et al)

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Interpretation of IPCTG

Integrated approach :

1. Antepartum strip , USG

2. Biophysical profile ( esp. AFI)

3. Doppler of vessels

4. Fetal pH , if possible

5. Sudden intrapartum event ( cord prolapse , acci hhage, rupture, oxytocin drip, AFE)

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Alternative Methods of Intrapartum Surveillance

• Fetal ECG waveform analysis• Time intervals of fetal cardiac cycles• Pulse oximetry• Doppler ultrasound• Continuous pH measurements

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Computers and Cardiotocography

• Data management• Storage • Archiving and Retrieval • Teleconferencing and sharing• Interpretation and decision making

The best computer is the human BRAIN !

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Medicolegal issues• Use of modern generation CTG machines • Rechecking an abnormal tracing by added

biophysical profile, Doppler velocimetry and fetal blood pH

• Minute analysis of all tracings• CTG tracings to be kept for 25 years (Carter

and Steer, 1993)• A high standard of note keeping, good

practice, good care and good communication

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Cardiotocography is useful if :

1. Adequate knowledge is available to interpret the trace.

2. Its limitations are known.

3. It is used appropriately.

4. The clinical picture is incorporated.

5. Additional tests are used when in doubt.

6. Common sense prevails!

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THANK YOU !!!

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