This is a lecture note on Intrauterine Fetal death. It discusses about the causes, the management of future pregnancies. At the end of the lecture note are standard textbooks for further reading.
This is a lecture note on Intrauterine Fetal death. It discusses about the causes, the management of future pregnancies. At the end of the lecture note are standard textbooks for further reading.
IUGR
Intrauterine growth restriction is said to be present in those babies whose birth weight is below the tength percentile of the average for gestational age.
INCIDENCE
Dysmaturity comprised about one third of low birth weight babies.
In developed countries , its overall incidence is about
3-10%
Term babies (5%)
Post term babies (15%)
CAUSES OF IUGR
The causes of IUGR can be grouped as
Maternal causes
Fetal causes
Placental causes
Uterine and Environmental causes.
MATERNAL CAUSES
Pregnancy weight of mother influences the fetal size
Chronic maternal disease condition
Renal disease condition
Malnutrition
Multiple pregnancy
Hypertensive disorders of pregnancy
Severe anemia
Previous baby suffered iugr etc.
FETAL CAUSES
Chromosomal anomalies
Exposure to an infection
German measles (rubella), cytomegalovirus, herpes simplex, tuberculosis, syphilis, or toxoplasmosis, TB, Malaria, Parvo virus
Birth defects
(cardiovascular, renal, anencephally, limb defect, etc).
• Placenta or umbilical cord defects.
PLACENTAL FACTORS
Uteroplacental Insufficiency
Fetoplacetal Insufficiency
Abruptio placenta
Placenta previa
Post term pregnancy
UTERINE CAUSES
Septate uterus
Fibroid/ myoma uterus
ENVIRONMENTAL CAUSES
High altitude - lower environmental oxygen saturation
Toxins
PATHOPHYSIOLOGY
Due to maternal and placental causes
Decrease in placental transfer of nutrients and oxygen to the fetus
Resulting in reduced fetal body store of lipids, glycogen
Causes neonatal hypoglycemia
Lack of oxygen
Chronic hypoxia that leads to erythropoietin production
Polycythemia etc
CLASSIFICATION OF IUGR
Based On Pathological Processes
I)Type I- Symmetrical
II)Type II- Asymmetrical
SYMMETRICAL
Symmetric IUGR: (33 % of IUGR Infants)
height, weight, head circumference proportional
early pregnancy insult:
commonly due to congenital infection, genetic disorder, or intrinsic factors
reduced no of cells in fetus
normal ponderal index
low risk of perinatal asphyxia
low risk of hypoglycemia
ASYMMETRICAL
later in pregnancy:
commonly due to utero placental insufficiency, maternal malnutrition, hypoxia, or extrinsic factors
low ponderal index
cell number remains same but size is small
increased risk of asphyxia
increased risk of hypoglycemia
CLINICAL FEATURES OF BABY WITH IUGR AT BIRTH
Weight deficit
Large head circumference
Old man look
Cartilaginous ridges on pinna
Dry wrinkled skin
Length remain unaffected
Open eyes
Well defined creases
Alert and active
Normal reflexes Normal cry
Thin umbilical
Scaphoid abdomen
Signs of recent wasting - soft tissue wasting - diminished skin fold thickness - decrease breast tissue - reduced thigh circumference • Signs of long term growth failure - Widened skull sutures, large fontanelles - shortened crown – heel length - delayed development of epiphyses
Normal reflexes Normal cry
Thin umbilical
Scaphoid abdomen
Intrauterine growth restriction when to deliver by dr alka mukherjee & dr apu...alka mukherjee
Molecular basis of IUGR. –
1. Atypical expression of enzymes governed by TGFβ causes the placental apoptosis and altered expression of TGFβ due to hyper alimentation causes impairment of lung function.
2. Crosstalk of cAMP with protein kinases plays a prominent role in the regulation of cortisol levels.
3. Increasing levels of NOD1 proteins leads to development of IUGR by increasing the levels of inflammatory mediators.
4. Increase in leptin synthesis in placental trophoblast cells is associated with IUGR.
A positive history for risk factors of IUGR can raise the problem of an increased surveillance with the specific goal of an early detection of growth insufficiency [23]. Further diagnostic tests could have a better relevance in a selected high-risk population
Serum markers linked to IUGR
The placentation process starts with the migration of trophoblastic cells that invade the walls of spiral arteries and transform them from small caliber high resistant vessels into wide caliber low resistant vessels that deliver blood at low pressure to the intervillous space. Then, the utero-placental circulation develops in two stages: the first stage (until the 10th week of gestation) consists in endovascular plugging of the spiral arteries by trophoblastic cells, subsequently followed by invasion and destruction of the intradecidual spiral arteries; the second stage (between 14-16 weeks of gestation) consists in the invasion of the inner miometrial part of the spiral arteries [27]. The impaired spiral artery transformation is leading to weak development of the utero-placental circulation and is implied in the pathology of preeclampsia and IUGR
Pregnancy associated plasma protein A (PAPP-A), an Insulin–like Growth Factor Binding Protein Protease whose levels depend on placental volume and function, was assessed in several studies with congruent results. In 2000, Ong et al. evaluated 5584 singleton pregnancies at 10-14 weeks of gestation and measured maternal serum free beta human chorionic gonadotropin (β-hCG) and PAPP-A, concluding that low levels of maternal serum PAPP-A or β-hCG were associated with subsequent development of pregnancy
Seminar on critical Congenital heart disease Dr Habibur Rahim | Dr Faria YasminDr. Habibur Rahim
Seminar on critical Congenital heart disease Dr Habibur Rahim | Dr Faria Yasmin
Duct-dependent systemic circulations
Critical aortic stenosis
Coarctation of the aorta
Interruption of aortic arch
Hypoplastic left heart syndrome
Duct-dependent pulmonary circulations
Pulmonary atresia Critical pulmonary stenosis
Tricuspid atresia
Tetralogy of Fallot
Ebstein’s anomaly
Parallel non-mixing circulation
Transposition of great arteries
Other
Total anomalous pulmonary venous connection (TAPVC)
Double outlet right ventricle
Single ventricle
Truncus arteriosus
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
3. • A fetus with IUGR is one that has failed to achieve its
genetically determined growth potential, owing to one or more
pathological factors .
• SGA: when its estimated fetal weight is below a specific
percentile for its gestation (10th percentile) for a given
population.
Definition
WHO
4. • SGA baby having a higher rate of adverse outcome than
average for gestational age babies.
• up to 70% of fetuses identified as SGA are
‘constitutionally small.
• IUGR fetus has at least a 10-fold increased risk of
perinatal mortality
SGA vs IUGR
5. Epidemiology
• IUGR is the commonest cause of stillbirth.
• the second leading cause of perinatal mortality, after preterm
birth.
• recent reports shows undiagnosed IUGR associated with 50%
of stillbirths in the UK.
• 30% of babies born before 35 weeks have IUGR
• 4.5% of babies born at term have IUGR
• SGA is 6 times higher in babies born preterm than term
6. • At least 10% of singleton pregnancies are SGA.
• SGA is 20% in dichorionic and 30% of monochorionic twins.
• IUGR occurs in 30–40% of pregnancies affected by pre-
eclampsia.
• In women who had a previous IUGR pregnancy the recurrence
rate is about 20%
• This is increased to approximately 50% in women with
previous early IUGR
Incidence
7. • Nationwide data is not available.
• At NICU, BSMMU 2021
• SGA 11.8%
• IUGR 9.54%
• Symmetrical IUGR 7%
• Asymmetrical IUGR 2.54%
Many IUGR cases remain undetected.
Incidence at Bangladesh perspective
8. Classification
According to symmetry of growth:
1. Symmetrical IUGR
2. Asymmetrical IUGR
According to onset:
1. Early onset (onset before 32 weeks)
2. Late onset (onset after 32 weeks)
9. Symmetrical IUGR
• Head circumference, length, and weight are all proportionally
reduced for gestational age (below 10th percentile).
• When insufficiency appearing early in pregnancy.
• Fetal weight is reduced out of proportion to length and head
circumference .
• Head sparing IUGR.
When insufficiency appearing late in pregnancy.
Asymmetrical IUGR
10. Normal Fetal Growth
• upto 16 weeks = Cellular hyperplasia
• 16 to 32 weeks= Hyperplasia &
hypertrophy
• After 32 weeks = Hypertrophy
• Two third of fetal weight gain occurs
beyond 24 th week of pregnancy
17. Insulin
• Anabolic hormone
• It controls the cell number because of direct mitogenic
effects.
• It leads to glucose uptake and consumption by body
tissues and decreases protein breakdown.
• Fetal insulin acts as a signal of nutrient availability for
growth and insulin deficiency will lead to IUGR.
• In insulin deficiency, IUGR results because of reduced
uptake and utilization of nutrients.
18. IGF-I
• It has mitogenic properties inducing somatic cell growth and
proliferation.
• It influences the transport of glucose and amino acids across
the placenta.
• IGF-I also has positive effect on brain growth,
1. increase in oligodendrocytes
2. neuronal number and neuronal outgrowth,
3. increases dendritic branching
4. increases axon terminal fields.
19. Thyroid hormone
Thyroid hormone triggers discrete developmental events in the
fetal brain and somatic tissues from early in gestation.
Fetal hypothyroxinaemia leads to developmental abnormalities
such as-
• decreased oxygen consumption and
• decreased oxidation of glucose
• leading to decreased fetal energy supply for growth.
20. Others
• Glucocorticoid hormone- development and maturation of
fetal organs.
• Insulin-like growth factor-II (IGF-II) -intrauterine
programming of adipose tissue
• Insulin-like growth factor binding protein-2 (IGFBP-2)
developmental Neurotropic and Regenerative Functions IN
CNS - binds (IGFs)
• Insulin-like growth factor binding protein-3 (IGFBP-3)
• vasoactive intestinal polypeptide (VIP) signaling is critical
for the modulation of appetite/satiety and body mass
phenotype
21. Stress
Primary adaptive response
Secondary adaptive response
Progressive decompensation
Death
Chronic respiratory and nutritional insufficiency
Decrease fetal growth rate
• Fetal energy conservation
Decreased fetal movement
Decreased fetal heart rate reactivity
• Circular redistribution
Falling cerebral flow impedance
Rising umbilical and aortic impedence
• Fetal growth preferred over placental growth
• Increased efficiency of placental exchange
• Polycythemia- Greater O2 carrying capacity
• Hypoxia → metabolic acidosis
• High impedance in fetoplacental circulation → absent end diastolic flow in umbilical arteries
• Declining amniotic fluid volume → Oligohydroamnios
• Loss of fetal movement
• Loss of fetal heart rate activity
• Further detoriation
Pathophysiology
22. Adapted from Sharma D, Farahbakhsh N, Shastri S, Sharma P. Intrauterine growth restriction–part 2.
23. Diagnosis of IUGR
1. Proper history taking
2. Establishing gestational age
3. Fetal assessment
A) Clinical diagnosis
B) Ultrasonography
-Estimated fetal weight
-Ratio of head and abdominal circumference
-Femur length
-Placental morphology and amniotic fluid
-Placental volume measurements
C) Biophysical profile
D) Doppler study
24. Clinical Diagnosis
Symphysio Fundal height (SFH)
Closely correlates with gestational age after 24 weeks
Lag of 4 cm or more –IUGR
Sensitivity 21-27%
Specificity 80-90%
Serial measurement is important.
26. Biophysical profile score
• BPP <2 is 100% sensitive to
detect fetal acidemia
• However, BPP is less sensitive
to detect fetal detoriation
• Cardiotocography (CTG).
It is a component of BPP and
is limited when used alone.
27. USG of Pregnancy profile
• To assess for FGR, 4 biometric measures are commonly used:
1. abdominal circumference
2. biparietal diameter
3. head circumference
4. femur length
• The liver is the first organ suffers due to redistribution
of ductus venosus blood flow to the heart
• a decrease in glycogen deposition in the liver.
• Reduced abdominal circumference (<5 mm/wk) is the
earliest sign
28. • In the second trimester,
• the head circumference>abdominal circumference.
• 32 to 36 weeks =1:1
• after 36 weeks, the abdominal circumference ↑↑
• If the ration is <1 suggestive of IUGR.
• Femur length: Serial measurements of femur length are as
effective as head measurements for detecting early-onset FGR.
Ratio of head circumference to abdominal circumference
29. Placental morphology
• Placental morphology and amniotic fluid assessment
helps in differentiating a constitutional small fetus from
a growth-restricted fetus.
• Placental aging with oligohydramnios suggests FGR
• Placental volume measurements FGR with
decreased placental size is more likely to be associated
with fetal acidosis.
30. Doppler study
• used to detect, monitor, and optimize time of delivery
• Doppler studies are more helpful in diagnosing moderate to
severe FGR than mild FGR.
• The various groups of vessels used are as follows:
• Uterine artery Doppler
• Umbilical artery Doppler
• Middle cerebral artery Doppler
• Cerebro-placental ratio (CPR)
• Ductus venosus Doppler
• Aortic isthmus Doppler.
32. Quantitive analysis:
• Pulsatility index (PI)
• Resistance Index (RI)
• Systolic/diastolic ratio (SD ratio)
Qualitative analysis
• Uterine artery: presence or absence
of early diastolic notch
• Umbilical artery(UA): normal with
reduced diastolic flow
• Absent End diastolic flow
• Reversed EDF
35. • Uterine artery flow abnormalities
• Used to predict FGR as early as 12 to 14 weeks.
• A persistent abnormality at 23 to 24 weeks has an approximate
75% sensitivity in predicting early FGR.
36. Umbilical artery flow abnormalities
• Normally, the umbilical artery resistance declines with pregnancy.
• Increased pulsatility index (PI),
• decreased end-diastolic velocity (EDV)
• absent EDV (AEDV)
• reversed EDV (REDV)
• AEDV and REDV are associated with 20% to 68% mortality.
• Decreased EDV is seen when 30% of placental flow is attenuated
• AEDV/REDV is noted when 60% to 70% of placental flow is affected.
• AEDV and REDV are associated with a 4.0- and 10.6-fold increased
risk of mortality.
37. Fetal cerebaral arterial flow
• Usually studied in the MCA as a Pulsatility index and MCA peak
systolic velocity (MCA PSV).
• With worsening FGR, MCA PSV increases.
• decreased MCA resistance is associated with worse perinatal
outcomes.
• MCA Doppler changes better identify late-onset FGR
38. Cerebroplacental ratio
The CPR quantifies the redistribution of cardiac output by
dividing the Doppler PI of the MCA with that of the UA.
CPR = MCA PI/UA PI.
• Adverse outcomes = CPR ratio of <1 or <1.08.
• CPR can be affected in about 25% of term SGA fetuses.
A decrease in expected CPR measurement after 28 weeks
gestation is highly sensitive in diagnosing late onset FGR.
39. FREQUENCY OF MONITORING IN EARLY AND LATE FGR
BPP: biophysical profile; CPR, cerebroplacental ratio; CTG, cardiotocography; DV, ductus venosus; EDV, end-diastolic
flow; FGR, fetal growth restriction; FHR, fetal heart rate; MCA, middle cerebral artery; PI, pulsatility index;
40. Decreased amniotic fluid index
Increased uterine artery resistance with EDV
Decreased MCA resistance (brain sparing)
Absent UA EDV
Increased resistance in DV-reversed EDV in
UA
Reversed flow in DV and pulsatile flow in
Umbilical vein
Early Changes
(2-3 Weeks before
nonreactive FHR)
Initial changes
Late changes (6 days
before nonreactive FHR)
Very late changes (24
hours before changes in
BPP)
Sequential changes of doppler studies in decompensating
fetal growth restriction
52. International Archives of Integrated Medicine, 2019; 6(1): 118-127
In the present study, PIH was found to be the commonest
(50.9%) cause of IUGR. Abnormal Doppler Indices in Umbilical
and MCA correlated statistically with lower birth weight, higher
rates of caesarean delivery, oligohydramnios, lower Apgar
scores, perinatal death, and higher admissions to NICU.
AEDF/REDF was associated with highest perinatal loss, poor perinatal
outcome.
53. Ponderal index
• to diagnose impaired fetal growth
• to identify soft tissue mass is
below normal for skeletal
development.
• The higher the score, the higher
the level of body fat.
• Normal range: 2.2 to 3.0 g/cm3
.
• A ponderal index of <2 or <10%
is suggestive of asymmetrical FGR
54. Placental magnetic resonance
imaging
• severity of FGR can be assessed by
placental thickness-to volume ratio.
• Fetal demise can also be predicted
by a
• abnormal vasodilatation
• mesenteric vasoconstriction
• preferential shunting through the
foramen ovale etc
55. stages condition findings Intervention
Stage I mild placental
insufficiency
Abnormal
Doppler studies
Carefull monitoring
Stage II severe uteroplacental
insufficiency
There is absent
EDV in the UA
after 34 weeks
Stage III fetal deterioration, low
suspicion of fetal
acidosis
Risks of stillbirth
reversal of EDV in
the UA or DV PI
>95th percentile
around 32 weeks
Stage IV fetal acidosis
reversal of atrial flow on
DV
Imminent risk of
fetal demise
Deliver immediately
Timing of delivery
56. • Early Antenatal diagnosis
• Early admission of mother
• Mode of delivery
• Antenatal Corticosteroid
• Delivery and Resuscitation
• Prevention of heat loss
• Prevention of hypoglycemia
• Feeding protocol
• Infection control
• Management of complications
Management
57. Neonatal Assesment
Anthropometry
• Reduced birth weight for
gestational age.
• Appropriate growth charts
should be used.
• Ponderal index˂ 10th
percentile.
• Ballard scoring
58. • Heads are dis proportionately
large for their trunks and
extremities
• Facial appearance has been
likened to that of a “wizened
old man”.
• Thin loose, peeling skin
• Long nails.
• Scaphoid abdomen
Physical appearance
59. Gestation < 35 weeks
Gestation ≤ 29 weeks
If tolerating well
Start MEN * after 24 hours
if no contraindication
@10ml/kg/day
Birth weight ≥1250g
Birth weight <1250g
increase feeds @10-
20 ml/kg/day
increase feeds
@ 20-30 ml/kg/day
Start MEN on day 1 if no
contraindication
@10-20 ml/kg/day
Gestation ≥ 29 weeks
Continue MEN for 48
hours then increase feeds
@10ml/kg/day
Add fortification once baby tolerates 100ml/kg/day of feeds and increase
feeds till 150-180ml/kg/day AIIMS protocol 2019
Feeding algorithm
for absent or
reverse end
diastolic flow
*MEN minimal entral neutrition
61. Nine parameters (hair, cheeks, neck
and chin, arms, legs, back, buttocks,
chest, and abdomen)
The maximum score is 36
Each category ranges 1-4 marks
<25 is considered to be malnourished.
Clinical Assessment of Nutrition Score (CAN Score):
62. It is the ratio of the
head circumference
(HC) to body weight
• higher cephalization
index reflects greater
degree of brain
vulnerability and
• increased risk of
cerebral palsy and
severe psychomotor
retardation.
Cephalization Index
63. 1. Intrapartum:
• Fetal death
• Acute-on-chronic hypoxia
• Metabolic acidosis
• Meconium aspiration
Consequences of intrauterine growth restriction
67. They found that, despite a median difference of 3 weeks in
gestational age at birth between IUGR and AGA infants, neonatal
mortality was 35% higher in neonates who had experienced fetal
growth restriction, and that IUGR was five times more predictive
of CLD than was AGA.
Neonatology 2014;106:304–310
71. Thrifty Phenotype (Barker Hypothesis)
• This metabolic programming (epigenetic modification ie,
those molecular mechanisms affecting gene expression
patterns without causing alterations in DNA base sequence)
occurs at the critical time window of fetal development
• These epigenetic changes become permanent or
“programmed” in the genes of the fetus.
72. Antenatal epigenetic changes
•Postnatal mismatched (normal or excessive nutrition)
•Suboptimal environment (sedentary life, less physical activity,
and sedentary life habits)
•Child’s genetics
Developmental origin of health and diseases (DoHaD)
73. Prognosis
• Mortality decreases by 48% for each week that the fetus
remains in utero before 30 weeks’ gestation
• At 24 to 26 weeks gestation, survival is around 50%
• survival improves to >90% by 32 weeks.
• The total brain volume is also reduced by 10% particularly in
the hippocampal, parietal, and parietooccipital areas.
• Infants with congenital rubella or cytomegalovirus infection with
microcephaly have a poor outcome, with a disability rate >50%.
• increased prevalence of elevated fasting glucose and metabolic
syndrome in childhood and adolescence.
74. • Neurodevelopmental morbidities are 5 to 10 times more often
in FGR
• minimal brain dysfunction, including hyperactivity, short
attention span, and learning problems.
• shows early neurobehavioral functions, such as attention-
interaction capacity and cognitive and memory dysfunction.
• Increased risk of cerebral palsy, learning disabilities, mental
retardation, and neuropsychiatric disorders.
• Growth may be hampered, growth hormone therapy (started
before 8 years of age and continued for >7 years) can augment
growth parameters.
75. A higher incidence of almost 50% in poorer neurodevelopmental
scores during early childhood ages (from 15 to 24 months)
among infants born after a pregnancy complicated by IUGR.
results showed that the developmental outcome for children with
IUGR was not influenced by birth weight, GA, gender, or type of
IUGR, suggesting that IUGR is an independent variable for poor
neurodevelopmental outcome.
2018
76. Prevention of IUGR
• Prepregnancy counselling and proper health education
• Balanced protein energy and micronutrients supplementation
with healthy life style.
• Ensure planned pregnancy at right age
• Ensure regular antenatal check up
• Treating chronic disease and pregnancy-induced disorders
accordingly
• Development a strong surveillance system with skilled
manpower at all level
77. Key Messages
• IUGR is a major concern in worldwide.
• Proper history, antenatal, natal and postnatal assessment in
necessary for diagnosis.
• Better to follow up with Doppler study and ensure proper
mode and timing of delivery
• Early diagnosis and prompt management may reduce
complication and unexpected consequences
• These infants need to be monitored for long time with
appropriate intervention.