This document provides an overview of cardiotocography (CTG), which is the continuous monitoring of fetal heart rate and uterine contractions during pregnancy and labor. It discusses the history of CTG, indications for monitoring, CTG parameters including baseline heart rate, variability, accelerations, and decelerations. The different types of decelerations like early, late, variable and prolonged are defined. Interpretation of normal versus non-reassuring CTG tracings and management of non-reassuring tracings is covered. Supplementary procedures like fetal blood sampling that can further assess fetal wellbeing are also summarized.
CTG in simple methods in fetal assessment according to RCOG guidelines.
easy and concise
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by OSAMA AKL
MRCOG instructor
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CTG in simple methods in fetal assessment according to RCOG guidelines.
easy and concise
feel free to download
by OSAMA AKL
MRCOG instructor
contact me on WhatsApp 00201008067383
Intra Partum Cardiotocography - dr vivek patkardrvivekpatkar
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
CTG Interpretation, evidence based approach
Cardiotocography (CTG) or electronic fetal monitoring (EFM) is the most widely used technique for assessing fetal wellbeing in labour in the developed world. The primary purpose of fetal surveillance by CTG is to prevent adverse fetal outcomes. Continuous electronic foetal monitoring is recommended to assure fetal wellbeing in labour in high risk pregnant women. Understanding pathophysiology of fetal heart rate variation will help appropriate interpretation of the CTG.
Features & classification of CTG according to RCOG will be demonstrated in this presentation with sufficient trace demonstration.
Intra Partum Cardiotocography - dr vivek patkardrvivekpatkar
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
CTG Interpretation, evidence based approach
Cardiotocography (CTG) or electronic fetal monitoring (EFM) is the most widely used technique for assessing fetal wellbeing in labour in the developed world. The primary purpose of fetal surveillance by CTG is to prevent adverse fetal outcomes. Continuous electronic foetal monitoring is recommended to assure fetal wellbeing in labour in high risk pregnant women. Understanding pathophysiology of fetal heart rate variation will help appropriate interpretation of the CTG.
Features & classification of CTG according to RCOG will be demonstrated in this presentation with sufficient trace demonstration.
Undergraduate course lectuers in Obstetrics&Gynecology
Prepared by DR Manal Behery
Assistant Professor in OB&GYNE ,Faculty of medicine,Zagazig University
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
2. 15 September 2018 May All Be Happy & Healthy 2
Eye doesn’t see
what mind doesn’t know
-- Osler
3. History
1818-Francios Major in Geneva-DDx between FH and Maternal Pulse
1827- John C Ferguson –described FHR sounds.
1849-Killian indicated FHr parameters requiring interventions.
1876-Pinard produced his design for a fetal stethoscope.
1893-Winkel set normal FHR120-169 bpm.
1958-Hon in USA and Hammacher in Europe introduced first EFM.
1964- Doppler ultrasound scan replaced phonocord.
1966- Saling in Berlin introduced FBS.
1968-Hamacher and Hewitt-Packard developed first fetal monitor.
1985- Dublin RCT changed terminology for the CTG interpretation.
Pioneered in 1958 by Hon.in USA and Hammacher in Europe
Commercially available 1968
4. Timeline of FHM: Summery
15 September 2018 May All Be Happy & Healthy 4
Mayor described
hearing Fetal heart
sounds & association
of slow rate with SB &
NND
1818 1841
Kennedy described
association of
Meconium with SB &
NND
1958
Honn reported
EFM
1966
1966- Saling introduced
FBS
5. Why fetal assessment ?
The goal of fetal surveillance
is:
1. To detect fetal hypoxia at
early stage
2. To prevent CP & IUFD
15 September 2018 May All Be Happy & Healthy 5
6. Fetal heart monitoring
External fetal heart monitoring
Internal electronic FH monitoring- QRS wave
15 September 2018 6May All Be Happy & Healthy
10. Indications for Continuous Monitoring of Fetal Heart Rate:
Maternal medical illness:
-Gestational diabetes.
-Hypertension.
-Asthma.
Obstetric complications:
-Multiple gestation.
-Post-date gestation.
-Previous cesarean section.
-Intrauterine growth restriction.
-Oligohydramnios.
-Premature rupture of the membranes.
-Congenital malformations.
-Third-trimester bleeding- Antepartum hemorrhage.
-Oxytocin induction/augmentation of labor
-Preeclampsia.
-Meconium stained liquor.
11. 15 September 2018 May All Be Happy & Healthy 11
1. Baseline heart rate:
CTG parameters
12. Baseline FHR (110 – 160):
FHR occurs between contractions, regardless to
acceleration or deceleration.
Decrease gradually from 16 weeks gestation to
term as the parasympathetic system develops.
15 September 2018 May All Be Happy & Healthy 12
13. Fetal Bradycardia:
FHR between < 110 beats/min for a period of 10
min or more.
In the absence of other changes, is not considered
significant.
Causes
1. Hypoxia, Drugs (eg. Beta-blocker)
2. Autonomic effect (pressure on fetal head)
3. Fetal heart block
4. Severe Pyelonephritis
5. Hypothermia, Maternal hypotension
15 September 2018 May All Be Happy & Healthy 13
14.
15. FetalTachycardia (>160):
FHR > 160 bpm for a period of 10 min or more.
Causes:
1. Prematurity
2. Hypoxia
3. Maternal Fever, Maternal Hypotension
4. Maternal thyrotoxicosis
5. Chorioamnionitis
6. Fetal Cardiac arrhythmias
7. Drugs: Atropine, Ventolin, Hydralazine,
Nifedipine.
15 September 2018 May All Be Happy & Healthy 15
18. BaselineVariability:
Best indicators of intact integration between
fetal CNS & heart .
Normal BLV 5-25 bpm
Increased> 25 bpm.
Absent < 3bpm
15 September 2018 May All Be Happy & Healthy 18
• The oscillatory changes that occur during the
course of 1 min and result in the waviness of the
baseline (3 – 5 /min).
• Result from the continuous interaction between
symp & parasymp nervous system.
23. 15 September 2018 May All Be Happy & Healthy 23
3. Periodic Changes
• Acceleration
• Deceleration
CTG parameters
24. Accelerations:
Accelerations: Transient, abrupt, increase in FHR of
≥ 15 bpm lasting for ≥ 15 sec , return to baseline <
2 min.
Occurs with fetal activity.
Presence of FHR Accelerations have Good
outcome.
Absence of accelerations on an otherwise normal
CTG remains unclear.
25.
26. Causes of loss of Accelerations:
Sleeping fetus
CNS depressant drugs: Sedatives, Narcotic,
Analgesics
Hypertensive Crisis, Diabetic Keto Acidosis
Smoking
15 September 2018 May All Be Happy & Healthy 26
28. Decelerations:
Transient slowing of FHR ≥
15 bpm and lasting for ≥15
sec.
4 types are described:
1. Early
2. Late
3. Variable
4. Prolonged
15 September 2018 May All Be Happy & Healthy 28
29. Early Decelerations:
Begins with the onset of contraction and returns to
baseline as the contraction ends.
Mostly due to Head compression
Considered physiologic, not associated with fetal
acidosis.
Significant, if appear during early labor or
Antenatal.
15 September 2018 May All Be Happy & Healthy 29
32. Late decelerations:
Occurs after the peak and past the length of
uterine contraction, often with slow return to the
baseline.
Due to acute and chronic feto-placental
vascular insufficiency.
Associated with respiratory and metabolic
acidosis
Common in PIH, DM, IUGR, Post maturity,
abruption placenta, maternal anemia & sepsis
uterine hyperstimulation.
36. Deceleration occurs before, during, or after the
onset of uterine contraction.
Caused by umbilical cord compression between
fetal parts and uterine wall.
Common in oligohydramnios.
Variable Decelerations:
40. Recurrent Decelerations:
Decelerations occur with > 50% of uterine contractions in any 20
minute segment.
Recurrent variable decelerations (at least 3 in 20 minutes) may be
observed. However, close follow up is recommended because cord
accidents with subsequent fetal death may occur even in the
presence of normal amounts of amniotic fluid.
Recurrent late decelerations should lead to consideration of
cesarean delivery unless the abnormal results are believed to be the
result of a reversible maternal condition such as diabetic
ketoacidosis or pneumonia with hypoxemia.
41.
42. Prolonged decelerations:
15 September 2018 May All Be Happy & Healthy 42
• A deceleration of 30 bpm or more for 2-10 min.
• Reduced oxygen transfer to the placenta
• Associated with poor outcome
43.
44. Causes of Prolonged Deceleration:
1. Impending birth (head compression).
2. Fetal hypoxia:
Uterine hyperactivity- hypoperfusion/hypoxia
Placental abruption
Umbilical cord knots or prolapse.
Maternal hypotension
Maternal seizures including eclampsia and epilepsy.
Sympathetic blockade (regional anesthesia)
Maternal Valsalva maneuver.
15 September 2018 May All Be Happy & Healthy 44
45. The Contraction StressTest (CST):
The Contraction stress test is used by some antepartum testing
centers to evaluate placental function under stress. The test is
performed by placing transducers (ultrasound and toco), on patient's
abdomen as with the non-stress test.
The tracing is then observed for late decelerations.
The test requires three contractions in 10 minutes to be
present with the contractions lasting 40 to 60 seconds.
If uterine activity is absent then oxytocin is infused or nipple
stimulation is used.
46. CST:
The test is positive if late decelerations are consistent and present
with more than 50% of the contractions.
A positive CST has been associated with an increased incidence of
intrauterine death, late decelerations in labor, low 5-minute Apgar
scores, and intrauterine growth restriction.
The CST is equivocal or suspicious if there are intermittent late
decelerations
A suspicious or equivocal CST should be repeated in 24 hours
49. CTG Features:
Baseline(beats per minute)
Short term variability( beats per minute)
Phase rectified signal averaging (beats per minute)
Signal stability index
Number of decelerations in 15 min
Number of contractions in 15 min
Contraction duration (seconds)
Resting time between contractions (seconds)
50. CTG Interpretation:
Consider :
1. Intranatal or Antenatal
2. Stage of labour
3. Gestational Age
4. Fetal presentation ?Malpresentation
5. Induction or augmentation of labour
6. Medicines (especially OTC)
7. Maternal Vitals & medical disorders
51. CTG Interpretation:
It has to be taken into consideration the
following:
There are different differences in the way clinicians
interpret CTG tracings, depending on the guidelines they
use.
Differences in guideline structure as well as in clarity and
complexity of definitions, have a profound effect on inter-
observer agreement and reliability, as well as on the
sensitivity and specificity of CT classifications in
predicting acidemia.
53. Features of reassuring (Normal) CTG:
15 September 2018 May All Be Happy & Healthy 53
Normal Base line FHR (110 – 160)
Normal
BLV
(6 to 25)
≥ 2 Accelerations in 20 minutes
No
Significant
Deceleration
54.
55.
56. Non reassuring (Nonreactive) CTG:
Absence of one or more features of normal CTG
15 September 2018 May All Be Happy & Healthy 56
Normal Base line FHR
Normal
Base line
Variability
Presence of Acceleration
No
Significant
Deceleration
58. Sinusoidal pattern
Regular Oscillation of the Baseline long-term
Variability resembling a Sine wave ,with no B-b
Variability.
Has fixed cycle of 3-5 p min. with amplitude of 5-
15 bpm and above but not below the baseline.
Should be viewed with suspicion as poor outcome
has been seen (eg Feto-maternal hemorrhage)
60. DeadlyTrio:
Accelerations absent
Loss of BLV
Recurrent late decelerations at least for 20 minutes
15 September 2018 May All Be Happy & Healthy 60
61. Management of non reassuring CTG
Change maternal position.
Provide oxygen by face mask
Reversal of anesthetic effect.
Regulation of uterine activity:
Stop oxytocin
Good hydration
Correction of cord compression
Change maternal position
Amnioinfusion
62. Supplementary Procedures:
Allow further assessment of fetal wellbeing
Vibro acoustic stimulation (VAS)
Scalp Stimulation:
With Fingers
With Allis Forceps
If both negative: do Fetal blood sampling (FBS)
15 September 2018 May All Be Happy & Healthy 62
63.
64.
65. Fetal Blood Sampling:
Useful in the presence of a non reassuring CTG.
A scalp blood sample for pH or lactate
determination.
Specificity is high ( normal value rules out
asphyxia).
The sensitivity and positive predictive value of a
low scalp pH in identifying a newborn with
Hypoxic-ischemic encephalopathy is low.
66. FBS Contraindications
Premature –less than 34 weeks
Active Herpes
Known HIV, Hep B,C positive status.
Thrombocytopenia.
Maternal-
Unfavorable Cx
Mobile PP
Malpresentation(face etc.) uncertain??
Pl Praevia or APH
Sepsis
67. FBS-Sampling errors:
Between decelerations if possible
Avoid Excess pressure on PP reduces perfusion
Do not sample on the caput.
Failure of scalp to bleed –due to peripheral shut
down.
68. FBS:
• Normal pH 7.25—7.35
• If <7.20 – significant
acidosis/ immediate
delivery
Fetal blood oximetry
False positive diagnosis is reduced to 10 %
69. Problems with CTG:
1-Has a high sensitivity but with limited specificity
in the prediction of fetal hypoxia/acidosis.
2. Increases operative vaginal delivery
3. No change in incidence of CP
4. Reduction in Neonatal seizures rates only 0.51%
5. No significant difference in APGAR scores
6. ? About the efficacy
15 September 2018 May All Be Happy & Healthy 69