Placenta and amniotic fluid


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Placenta and amniotic fluid

  1. 1. Placenta and amniotic fluid
  2. 2. Embryogenesis
  3. 3. Fertilization
  4. 4. The Nuclei Fuse Together
  5. 5. What happens now?  Development of the zygote, the study of which is known as embryology or developmental biology.  The zygote undergoes a series of mitotic cell divisions called cleavage.  The stages of development are: Fertilized ovum (zygote)  2-cell stage  4-cell stage  8-cell stage  Morula  Blastula  Early Gastrula  Late Gastrula
  6. 6. Cleavage (divide via mitosis) forms the 2 cell stage
  7. 7. They split again to form the 4 cell stage
  8. 8. And again to form the 8 cell stage…
  9. 9. And eventually form a Morula
  10. 10. Next it becomes a blastula  58 cell stage  5 embryo producing cells+53 cells form trophoblast  107 cell blastocyst (8+99)  no larger  Released from zona pellucida
  11. 11. And next, a gastrula
  12. 12. The Regents Diagram… 1. Sperm and ovum 2. Zygote (fertilized ovum) 3. 2-cell stage 4. 4-cell stage 5. Morula 6. Blastula 7. Gastrula
  13. 13. Differentiation (Organogenesis)  Organogenesis is the formation of the organs (Organo = organs, genesis = creation)  Arises from the layering of cells that occurs during gastrula stage  The layers are germ layers; they have specific fates in the developing embryo:
  14. 14. Differentiation (Organogenesis)  Endoderm  The innermost layer  Goes on to form the gut  Mesoderm  In the middle  Goes on to form the muscles, circulatory system, blood and many different organs  Ectoderm  The outermost  Goes on to form the skin and nervous system
  15. 15. Late Gastrula Ectoderm Endoderm Mesoderm
  16. 16. Where does this all take place?
  17. 17. Decidual structure Decidua is an analogy to deciduous leaves (to indicate that it is shed after childbirth)  Decidua basalis  Decidua capsularis  decidua parietalis or vera
  18. 18. Fusion of capsularis and parietalis at 14-16wks causes functional obliteration of the uterine cavity
  19. 19. 8th week 1. Decidua parietalis 2. Decidua capsularis 3. Decidua basalis 4. Uterine cavity  The decidua consists of various parts, depending on its relationship with the embryo:  Decidua basalis, where the implantation takes place and the basal plate is formed. This can be subdivided into a zona compacta and a zona spongiosa (where the detachment of the placenta takes place following birth).  Decidua capsularis, lies like a capsule around the chorion  Decidua parietalis, on the opposite uterus wall
  20. 20. 5. Smooth chorion (laeve) 6. Chorionic villi 7. Amniotic cavity 8. Decidua capsularis and parietalis, grown together
  21. 21. Decidual reaction  polygonal or round  Round and vesicular nucleus  Cytoplasm clear, basophilic  Pericellular membrane Walls around themselves and around the fetus
  22. 22. Decidual blood supply  Spiral arteries in the parietalis retain smooth muscle wall and epithelium  Cytotrophoblast invasion of spiral arteries and arterioles -vessel wall in the basalis destroyed-not responsive to vasoconstrictors
  23. 23. Decidual histology  True decidual cells  Maternal bone marrow derived cells  Decidual NK cells  Secrete cytokines  Express angiogenic factors  Basalis-mainly arteries and widely dilated veins(glands virtually disapperared)  Invasion by trophoblasts
  24. 24. Decidual prolactin  Paracrine between maternal and fetal tissues  Amnionic 10,000ng/ml  Maternal 150-200ng/ml  Fetal 350ng/ml  Role ?  Transmembrane solute and water transport  Stimulate T-cells  Regulates angiogenesis
  25. 25. Implantation  The embryo implants in the wall of the uterus on about the 7th day of development
  26. 26. Blastocyst implantation  Apposition- days 20-24 of cycle endometrium primed by E&P  Adhesion modification in expression of cellular adhesion molecules (integrins)  Invasion
  27. 27. 12-day Human Embryo
  28. 28. Gas and nutrient exchange system  Embryo is nourished in the first weeks through simple diffusion  Utero-placental circulation system in which the circulation systems of the mother and of the embryo get closer together, thus allowing an exchange of gases and metabolites via diffusion.  Maternal and fetal blood never come into direct contact with each other.
  29. 29. Trophoblast differentiation  cytotrophoblast inner layer well demarcated  Syncytiotrophoblast outer layer multinucleated
  30. 30. After implantation  Villous trophoblast • chorionic villi  Extra-villous trophoblast • interstitial • endovascular
  31. 31. Lacunar stage  Through the lytic activity of the syncytiotrophoblast the maternal capillaries are eroded and anastomose with the trophoblast lacunae, forming the sinusoids.  Lacunae communicate with each other and form a single, connected system that is delimited by the syncytiotrophoblast and is termed the intervillous space.
  32. 32. Lacunar stage
  33. 33. primary villi  D11-13  Syncytiotrophoblast penetrated by cords of cytotrophoblast
  34. 34. primary villi
  35. 35. Secondary villi After the 16th day The extra-embryonic mesoblast also grows into this primary trophoblast villus, which is now called a secondary villus and expands into the lacunae that are filled with maternal blood. The ST forms the outermost layer of every villus.
  36. 36. Secondary villi
  37. 37. Tertiary villi  At the end of the 3rd week the villus mesoblast differentiates into connective tissue and blood vessels.  Villi that contain differentiated blood vessels are called tertiary villi  The EEM remains in this stage, still surrounded by cytotrophoblast.The outer envelope of the villus is still formed by the ST
  38. 38. Tertiary villi
  39. 39. Free villi  After 4th month the cytotrophoblast in the tertiary villi disappear slowly  the villi divide further and become very thin.
  40. 40. 1. Anchoring villus 2. Septum 3. Syncytiotrophoblast (ST) 4. Cytotrophoblast (CT) 5. Remainder of the cytotrophoblast layer 6. CT in the spiral artery wall A-Basal plate and myometrium B-Chorionic plate
  41. 41. Ageing of the placenta A. Langhans' fibrinoid layer B. Rohr's fibrinoid layer C. Nitabuch's fibrinoid layer
  42. 42. Cytotrophoblastic invasion  destruction of the smooth muscle layer  partial replacement of the endothelial cells  change in elasticity of the spiral arteries,  Absent in preecclampsia and intra-uterine growth retardation.  excessive proliferation of the cytotrophoblast can lead to tumor formation, especially to a chorion carcinoma.
  43. 43. Development of the Placenta
  44. 44. Placental tissue structure Chorionic plate Basal plate 1 Amnion 2 Extra-embryonic mesoblast 3 Cytotrophoblast 4 Syncytiotrophoblast 5 Zona compacta 6 Zona spongiosa 7 Decidua basalis 8 Myometrium
  45. 45. Fetal circulation system 1. Umbilical arteries 2. Umbilical vein 3. Fetal capillaries A network of fetal capillaries (2 to 8) is found in each villus; 20 to 40 first order stem villi exist from each one of which 20 to 50 second and third order daughter villi arise.
  46. 46. Maternal circulation system 1. Spiral arteries 2. Uterine veins 3. Intervillous spaces Spiral arteries (branches of the uterine arteries) High pressure At the level of the placenta (intervillous spaces), therefore, maternal blood is to be found at times outside the vessel network.
  47. 47. Blood pressure values and oxygen distribution in the intervillous spaces Maternal blood is pumped with high pressure and leaves via the uterine veins. At the level of the placenta (intervillous spaces), therefore, maternal blood is to be found at times outside the vessel network.
  48. 48. Development of the placenta (> 4th month) 1. Decidual tissue 2. Syncytiotrophoblast 3. Cytotrophoblast islands 4. Septum The cytotrophoblast islands move into the periphery of the cotyledons and, together with the decidual tissue, are involved with formation of the placental inter- cotyledon septa.
  49. 49. Fibrinoid degradation  The villus stems of the placenta lengthen considerably towards the end of the pregnancy and the fibrinoid deposits (extra- cellular substance made up of fibrin, placental secretions and dead trophoblast cells), accumulate in the placenta
  50. 50. Fibrinoid degradation structurally and chemically closely related to fibrin can take up a maximum of 30% of the placental volume without affecting its function. When these deposits are massive and block one or more vessels to the villi, they form white infarcts, Functional importance  sealing effects,  Immunologic "barrier“  anchoring of the placenta. A. Subchorial Langhans' layer B. Rohr's layer C. Nitabuch's layer
  51. 51. Placental barrier  First trimester 1. Intervillous space 2. Syncytiotrophoblast 3. Cytotrophoblast 4. Villus mesenchyma 5. Fetal capillaries 6. Hofbauer macrophages
  52. 52. Placental barrier  2nd trimester 1. Intervillous space 2. Syncytiotrophoblast 3. Cytotrophoblast 4. Villus mesenchyma 5. Fetal capillaries 6. Hofbauer macrophages
  53. 53. Placental barrier  3rd trimester 1. Intervillous space 2. Placental barrier of a terminal villus 3. Fetal capillaries 4. Merged basal membranes 5. Endothelial cells 6. Rare cytotrophoblast cells 7. Basal membrane of the capillaries 8. Basal membrane of the trophoblast portion 9. Syncytiotrophoblast with proliferation knots (nuclei rich region)
  54. 54. Placenta
  55. 55. Placental transport  Passive transport  Simple diffusion:  non-polar molecules  fat-dissolvable substances (e.g., diffusion of oxygen, carbon dioxide, fats and alcohol).Water enters the placenta through specialized pores (see osmosis).  Osmosis: theaquaporines or water channels, proteins localized within the plasma membrane.  Simplified transport: transition from the side with higher concentration to the one with lower concentration with the help of transport molecules (e.g., glucose).
  56. 56. Placental transport  Active transport:Transport through the cellular membrane against a concentration gradient using energy (Na+/K+ or Ca++)  Vesicular transport (Endocytosis / Exocytosis): Macro-molecules are captured by microvilli and absorbed in the cells or repelled (immunoglobulin).
  57. 57.  averages 22 cm (9 inch) in length  2–2.5 cm (0.8–1 inch) in thickness  weighs approximately 500 grams  dark reddish-blue or crimson color  Umbilical cord of approximately 55–60 cm, which contains two umbilicalAs and one umbilicalV and has an eccentric attachment.  On the maternal side, these villous tree structures are grouped into lobules called cotyledons
  58. 58. Placental functions The placental exchange surface is enlarged from 5 m2 at 28 weeks to roughly 12 m2 shortly before delivery!
  59. 59. Placental functions  Breathing function  Nutritive and excretory functions  Placenta and the immunological barrier  Protein transfer  Protective function  Endocrinal function
  60. 60. Breathing function The placenta, which plays the role of "fetal lungs", is 15 times less efficient (with equivalent weight of tissue) than the real lungs. The supply of the fetus with oxygen is facilitated by three factors:  difference of oxygen concentration and partial pressure within the feto-maternal circulation system  higher affinity of fetal hemoglobin (HbF) for oxygen  Bohr effect
  61. 61. Nutritive and excretory functions  Water diffuses into the placenta along an osmolar gradient.The water exchange increases during the pregnancy up to the 35th week (3.5 liter / day).  The electrolytes follow the water, whereby iron and calcium only go from mother to child.  Glucose is the fetus' main source of energy and passes the placenta via simplified transport. At the level of the trophoblast the placenta can synthesize and store glycogen in order to satisfy local glucose requirements through glycogenolysis.
  62. 62. Nutritive and excretory functions  Peptides and amino acids via active transport and thus insure the fetus' own protein synthesis.  Amino acids, precursors of fetal protein synthesis, stem from the metabolism of the maternal proteins.The placental transport is facilitated by the influence of hormones, e.g., GH (growth hormone) andTSH (thyroid stimulating hormone) against a concentration gradient (2-3 times higher in the fetus as in the mother).  Lipids and triglycerides are decomposed in the placenta, where new lipid molecules are synthesized.  Cholesterol passes through the placental membrane easily, just like its derivates: e.g., steroid hormones.
  63. 63. Nutritive and excretory functions  Water-soluble vitamins easily pass through the placental membrane.The amount of the fat soluble vitamins (A,D,E and K) in the fetal circulation is, on the other hand, quite low.Vitamin K plays an important role in blood coagulation and is applied to the child immediately after birth, in order to prevent hemorrhages.  Placental exchange processes are also involved in the removal of waste products from the fetal metabolism. They cross over into the maternal blood in order to be excreted by the mother (urea, creatinine, ureic acid).
  64. 64. Placenta and the immunological barrier  The fetus is not rejected even though its set of chromosomes differs from that of its mother and halfway represents an allogenic transplantation  Fetal tissue and especially that of the placenta that stand in direct contact to the maternal organismproduce no tissue antigens  HLA -G antigens, which do not distinguish between individuals, occurs through the extravillous cytothrophoblast.The HLA-G antigen takes over anti- viral and immunosuppressive functions as well as non- immunologic tasks.
  65. 65. Placenta and the immunological barrier  In addition, the placenta blocks cytotoxic maternal cell effects by secreting various factors.The insufficiency of these mechanisms may be responsible for immune- dependent miscarriages.  some steroid hormones (e.g., progesterone) have an immunosuppressive effect on the lymphocytes of the pregnant woman. Progesterone (the concentration of which is especially elevated during pregnancy) seems to play an important immunosuppressive role that is mediated by the PBIF protein (Progesterone Induced Blocking Factor).
  66. 66. Protein transfer  The maternal proteins do not traverse the placental barrier, with the exception of immunoglobulin (IgG).Through pinocytosis of syncitiothrophoblast cells the mother thus transfers to the fetus the variety of IgG that she has synthesized during her life.This transfer occurs mainly towards the end of pregnancy.Thereby the fetus obtains a passive immunity that protects it against various infectious diseases in the first six months of its life.The other immunglobulins, mainly IgM proteins, do not pass through the placental barrier. 
  67. 67. Protein transfer  Other proteins: Transferrin is another important maternal protein that, as the name indicates, transports iron. On the surface of the placenta specific receptors exist for this protein, which, by means of active transport, enters into fetal tissue.  Protein can also be transferred from the fetus to the mother; alpha-fetoprotein (the concentration of which is elevated in several fetal abnormalities) can be detected in the maternal circulation system.  Maternal or placental polypeptide hormones do not enter the fetal circulation system.
  68. 68. Protective function Sexually transmitted diseases:  After the 5th month of pregnancy treponema pallidum bacteria, the syphilis pathogen, can pass through the placental barrier.  HIV transmission from the mother to the fetus amounts to roughly 15 to 25%. It depends on the viremia status of the mother.  Anti-HIV treatment during the pregnancy and birth as well as further treatment of the newborn during the first few weeks.  Birth via caesarian section  No breastfeeding of the child When all of these measures have been carried out the risk of infection for the baby can be reduced to below 1%.
  69. 69. Protective function Fetotoxic infections:  The rubella virus may be responsible for a miscarriage during pregnancy (before the first month), for embryopathies (when the virus invades between the 1rst and 3rd month) or for fetopathies (after the 3rd month).  Toxoplasmosis is harmless for the mother, but can cause severe anomalies in the fetus.  Listeriosis can be responsible for miscarriages, intrauterine death or neonatal sepsis due to transplacental infection or for secondary late meningitis due to a contaminated birth passage.
  70. 70. Protective function Fetotoxic infections:  The cytomegalovirus is generally the cause of infections that remain subclinical. It can also be responsible for miscarriages as well as for microcephaly and growth retardation.The infection happens transplacental or during birth.  The parvovirus B19 is responsible for aplastic crises in utero (marked decrease of blood cells).
  71. 71. Protective function  In addition, the placenta also presents an incomplete barrier against certain injurious effects of drugs: Antibiotics and corticoids can pass through the placental barrier. Depending on their size, certain steroid hormones get through as well.
  72. 72. Endocrinal function The placenta and especially the syncytiotrophoblast can be seen as a large endocrine gland. Before implantation hormone production is ensured through ovarian and hypophysial hormones. At the beginning of the pregnancy the synthesis of estrogen and progesterone is ensured by the corpus luteum graviditatis that is maintained by the human chorion-gonadotropin (HCG), a product of the trophoblast.The activity of the corpus luteum decreases progressively with the beginning of the 8th week in order to be entirely replaced by the placenta at the end of the 1st trimester During the pregnancy the hormone concentration in the maternal blood is regulated by the cooperation of the placental, hypophysial and fetal suprarenal hormones as well as hormones from the gonads 
  73. 73. Endocrinal function a Placenta b Fetal suprarenal glands c corpus luteum graviditatis
  74. 74. Implantation and form anomalies  placenta previa
  75. 75. Implantation and form anomalies  Ectopic, i.e., extra-uterine pregnancies
  76. 76. Implantation and form anomalies
  77. 77. Implantation and form anomalies  Velamentous insertion
  78. 78. Implantation and form anomalies  marginal
  79. 79. Implantation and form anomalies  Eccentric insertion
  80. 80. Implantation and form anomalies • Placenta multilobata
  81. 81. CLINICAL BIOCHEMISTRY AMNIOTIC FLUID Implantation and form anomalies
  82. 82. Implantation and form anomalies  placenta succenturia
  83. 83. Implantation and form anomalies  bilobate when both segments of the placenta are almost equal in size (right on the figure) and succenturiate when there is a greater difference (left on the figure).When there is not such a connection, the placenta is called placenta spuria.
  84. 84. CLINICAL BIOCHEMISTRY AMNIOTIC FLUID Implantation and form anomalies
  85. 85. Implantation and form anomalies •Circumvalate placenta
  86. 86. Implantation and form anomalies
  87. 87. CLINICAL BIOCHEMISTRY AMNIOTIC FLUID Implantation and form anomalies  fenestrated placenta
  88. 88. CLINICAL BIOCHEMISTRY AMNIOTIC FLUID Implantation and form anomalies  Membranaceous placenta
  89. 89. Implantation and form anomalies  Disc shaped placenta
  90. 90. Toxemia of pregnancy
  91. 91. Fetal erythroblastosis  anemia (due to the hemolysis)  splenomegaly (location of the macrophages that destroy the erythrocytes)  hepatomegaly (intensive hematopoesis in order to compensate the hemolysis)  icterus (transformation of hemoglobin of the destroyed erythrocytes into bilirubin)
  92. 92. Inflammation of the placenta  Bacterial infections can also strike the placenta (placentitis) or the fetal membranes (chorioamnionitis). Normally, these infections are transmitted vaginally in the case of an early rupture of the amnion. An infection rarely occurs via the blood, i.e., when the fetal membrane is still intact. Syphilis was earlier a frequent cause for placentitis, also for placental tuberculosis, whereby here the placenta was infected via the blood
  93. 93. Hydatid mole The hydatid mole pregnancy corresponds to a cystic chorion villus degeneration Macroscopically, the mole looks like a heap of transparent bubbles, held together by filaments, and supported by a central core.
  94. 94. Hydatid mole  Microscopically, the villus degeneration exhibits no vascularization, a proliferation of trophoblasts (from cytotrophoblasts – Langhans' cells and from syncytiotrophoblasts) and dystrophic alterations of the connective tissue with stroma edema.
  95. 95. The chorion and amnion enclose the embryo The chorion surrounds the entire embryo The amnion encloses the embryo and forms an open volume between the embryo & the amnion called the amniotic cavity Amnion provides almost all tensile strength
  97. 97. CLINICAL BIOCHEMISTRY AMNIOTIC FLUID Development  Amniogenic cells line the inner surface of trophoblast  Derived from fetal ectoderm of the embryonic disc
  98. 98. Amnion & Amniotic Fluid  Composition of Amniotic Fluid  99% H2O  Un-disolved material  Organic & inorganic salts  Pregnancy advancement changes its composition  Meconium & urine
  99. 99. Amniotic Fluid  Before 20 weeks gestation –  AF is an ultrafiltrate of maternal serum  Maternal & AF osmolality, sodium, urea, and creatinine are roughly equal.  At term  Volume = 900cc  Reflective of fetal renal function.  Progressively hypotonic.  Contains fetal debris: squamous cells, mucin, lanugo.
  100. 100. Amniotic Fluid  Amniotic fluid surrounds the fetus during intrauterine development.  This fluid cushions the fetus against trauma,  Has antibacterial properties to lessen infections,  Reservoir that may provide a short-term source of fluid and nutrients to the fetus.
  101. 101. Amniotic Fluid  Amniotic fluid are required for the fetal musculoskeletal system to develop normally, for gastrointestinal system development, and for the fetal lungs to develop.  It is not surprising to find that oligohydramnios and polyhydramnios are associated with increased rates of perinatal morbidity and mortality.
  102. 102. Sources of amniotic fluid  The two primary sources of amniotic fluid are fetal urine and lung liquid, with an additional small contribution due to secretions from the fetal oral-nasal cavities.  Fetal urine is a major source of amniotic fluid in the second half of pregnancy.
  103. 103. Sources of amniotic fluid  Urine production Approximately 110/ml/kg every 24 hours at 25 weeks to approximately 190 ml/kg every 24 hours at 39 weeks  At term, the current best estimate of fetal urine flow rate may average 700-900 ml/day.
  104. 104. Sources of amniotic fluid  The fetal lungs are the second major source of amniotic fluid during the second half of gestation.  Studies in near-term fetal sheep have shown that there is an outflow from the lungs of 200- 400 ml/day
  105. 105. Sources of amniotic fluid  The inward transfer of solute across the amnion with water following passively is the most likely source of amniotic fluid very early in gestation  Part of AFV may be derived from water transport across the highly permeable skin of the fetus during the first half of gestation, at least until keratinization of the skin occurs around 22-25 weeks.
  106. 106. Routes of amniotic fluid removal  The two primary routes of amniotic fluid removal are fetal swallowing and absorption into fetal blood perfusing the fetal surface of the placenta.  Fetal swallowing plays an important role in determining AFV during the last half of gestation.
  107. 107. Routes of amniotic fluid removal  The fetus begins swallowing at the same gestational age when urine first enters the amniotic space, that is around 8-11 weeks.  It is estimated that the volume of amniotic fluid swallowed in late gestation averages 210-760 ml/day
  108. 108. Intermembranous & transmembranous pathways  As a further pathway, rapid movements of both water and solute occur between amniotic fluid and fetal blood within the placenta and membranes; this is referred to as the intramembranous pathway.  Movement of water and solute between amniotic fluid and maternal blood within the wall of the uterus is an exchange through the transmembranous pathway
  109. 109. Amniotic fluid volume
  110. 110. Amniotic fluid volume
  111. 111. Amniotic fluid volume  The rate of change in AFV is a strong function of gestational age.  There is a progressive AFV increase from 30 ml at 10 weeks’ gestation to 190 ml at 16 weeks and to a mean of 780 ml at 32- 35 weeks, after which a decrease occurs  The decrease in post-term pregnancies has been found to be as high as 150 ml/week from 38 to 43 weeks
  112. 112. Individual amniotic fluid volumes from a collection of 705 measurements in patients with a normal pregnancy outcome
  113. 113. Regulatory mechanisms act at three levels:  Placental control of water and solute transfer.  Regulation of inflows and outflows from the fetus: fetal urine flow and composition are modulated by vasopressin, aldosterone, and angiotensin II in much the same way as they in adults.  Maternal effect on fetal fluid balance: during pregnancy, there is a strong relationship between maternal plasma volume and AFV,
  114. 114. Measurement of amniotic fluid volume  Single vertical pocket  Amniotic fluid index
  115. 115. Oligohydramnios  Diminished amniotic fluid volume (AFV)  Amniotic fluid volume of less than 500 mL at 32-36 weeks' gestation - Amniotic fluid volume depends on the gestational age; therefore, the best definition may be AFI less than the fifth percentile.  Single deepest pocket (SDP) of less than 2 cm  Amniotic fluid index (AFI) of less than 5 cm or less than the fifth percentile
  116. 116. Oligohydramnios-causes  Fetal  Chromosomal anomalies  Congenital abnormalities  Growth restriction  Demise  Post-term pregnancy  Ruptured membranes  Placental  Abruption  TTTS  Maternal  Uteroplacental insufficiency  Hypertension  Pre-ecclampsia  Diabetes  Iatrogenic  PG synthesis inhibitors  ACE inhibitors  Idiopathic
  117. 117. Congenital anomalies associated with oligohydramnios  Amnionic band syndrome  Cardiac  Fallots tetralogy  Septal defects  CNS  Holoprosencephaly  Meningocele  Encephalocele  microcephaly  Cloacal dysgenesis  Chromosomal  Triploidy  Trisomy 18  Turner syndrome  Cystic hygroma  Diaphragmatic hernia  Genitourinary  Renal dysgenesis/aplasia  Urethral obstruction  Bladder exystrophy  Meckel gruber syndrome  Uretro-pelvic junction obstruction  Prune belly syndrome  Hypothyroidism  Skeletal  TRAP sequence  TTTS  VACTERL association
  118. 118. Oligohydramnios  Fetal mortality rates as high as 80-90% have been reported with oligohydramnios diagnosed in the second trimester.  Midtrimester PROM often leads to pulmonary hypoplasia, fetal compression syndrome, and amniotic band syndrome.  Oligohydramnios is a frequent finding in pregnancies involving IUGR and is most likely secondary to decreased fetal blood volume, renal blood flow, and, subsequently, fetal urine output.  AFV is an important predictor of fetal well-being in pregnancies beyond 40 weeks' gestation  AFV is a predictor of the fetal tolerance of labor,
  119. 119. Oligohydramnios  Ultrasonography  diagnosis is confirmed  ultrasonography of the fetal anatomy  Sterile speculum examination  Pooling in posterior fornix  Nitrazine paper turns blue  arborization or ferning pattern  amnioinfusion
  120. 120. Polyhydramnios  Polyhydramnios is the presence of excess amniotic fluid in the uterus.  Deepest vertical pool is more than 8 cm  AFI is more than 95th percentile for the corresponding gestational age.  The incidence is 1-3% of all pregnancies.  About 20% are associated with fetal anomalies.  The diagnostic approach to polyhydramnios consists of (1) physical examination of the mother with an investigation for diabetes mellitus, diabetes insipidus, and Rh isoimmunization; (2) sonographic confirmation of polyhydramnios and assessment of the fetus; (3) fetal karyotyping; and (4) maternal serologic testing for syphilis.
  121. 121. polyhydramnios  Maternal hyperglycemia  GIT anomalies(obstructive)  Esophageal atresia  Tracheoesophageal fistula  Duodenal atresia  Nonimmune hydrops  CNS anomalies  Anencephaly  Open spina bifida  Thoracic malformations  Diaphragmatic hernia  Congenital infections  Syphilis, hepatitis  Chromosomal anomalies  High output Cardiac failure  Fetal anemia  Sacrococcygeal teratoma  chorioangioma  Fetal polyuria  Fetal pseudohyperaldosteronism  Fetal bartter  Nephrogenic diabetes insipidus  Placental chorioangioma  Maternal substance abuse
  122. 122. Amniotic fluid testing Chromosome and DNA analysis Biochemistry Fetal infections Rh disease and other alloimmunisation Lung maturity Chorioamnionitis Obstetric cholestasis Fetal therapy- decompression severe oligohydramnios multifetal pregnancy reduction throxine therapy
  123. 123. Prenatal diagnosis
  124. 124. Alpha fetoprotein  Measurement of AFP in maternal serum and amniotic fluid is used extensively for the prenatal detection of some serious fetal anomalies.
  125. 125. AFP Biochemistry  AFP is produced initially by the fetal yolk sac in small quantities and then in larger quantities by fetal liver as the yolk sac degenerates.  Trace amounts are also produced in the fetal gut and kidneys.
  126. 126. AFP Biochemistry  Concentrations of AFP in fetal serum  Early in embryonic life:1/10 the concentration of albumin in fetal serum  16 weeks gestation:3,000,000 ng/ml  At term:declines steadily to 5000 to 120,000 ng/ml
  127. 127. AFP Biochemistry  The rise and fall in concentration of AFP in the amniotic fluid roughly parallels that in the fetal serum but lower in concentration  20,000 ng/ml at 16 weeks gestation
  128. 128. Clinical significance of AFP  Maternal serum and amniotic fluid AFP are useful tests for detecting some serious fetal anomalies  Maternal serum AFP is elevated in 85% to 95% of cases of fetal open neural tube defect and is low in about 30% of cases of fetal Down’s syndrome.
  129. 129. Acetyl cholinesterase  A useful adjunct in the diagnosis of neural tube defects is the measurment of acetylcholinesterase (AChE,EC in amniotic fluid  The usual technique for identification of AChE is polyacrylamide gel electrophoresis.
  130. 130. Acetyl cholinesterase test sensitivity  A study of more than 5000 patients reported that determination of AChE by electrophoresis had specificity of 99.76% and following sensitivities:
  131. 131. Anencephaly,97%
  132. 132. Open spina bifida,99%
  133. 133. Abdominal wall defects,94%
  134. 134. Amniotic fluid testing  Testing amniotic fluid for AFP and AChE can predict open neural tube defects more accurately than maternal serum screening.  Patient with unexplained high maternal serum AFP levels and normal ultrasonography findings should be offered amniotic fluid testing.  Any patient who has had a child with a neural tube defect has 3% to5% risk for recurrence and also should be offered amniotic fluid AFP testing  Any elevation of AFP in amniotic fluid should lead to AChE analysis
  135. 135. Amniotic fluid testing  Testing should be performed at or before 16 weeks gestation.  Determination of fetal karyotype is also reasonable.
  136. 136. AF and Respiratory distress syndrome (RDS)
  137. 137. AF and Respiratory distress syndrome (RDS)  Respiratory distress syndrome (RDS) was associated with a significant mortality rate approaching approximately 30%.  In the 1950s, it was discovered that the resistance of pulmonary alveoli to collapse during expiration was mainly caused by the presence of a surface tension-lowering material lining the alveolus (surfactant).  As the lungs develop, significant quantities of surfactant are washed out of the fetal lung and accumulate in the amniotic fluid.
  138. 138. AF and Respiratory distress syndrome (RDS)  all of the available biochemical tests for fetal lung maturity rely on the amniotic fluid content of surfactant  adult mature surfactant is approximately 80% phospholipids, about 10% protein, and about 10% neutral lipids (primarily cholesterol).  The major species of phospholipid in surfactant is phosphatidylcholine (also referred to as lecithin), which accounts for 80% of the total phospholipid
  139. 139. Surfactant lipid Composition
  140. 140. L/S ratio test  The L/S ratio test remains one of the most commonly used tests, and one of the standardized tests against which all other tests are compared.  With a L/S ratio of 1.5-1.9, approximately 50% of infants will develop RDS. Below a ratio of 1.5, the risk of subsequent RDS increases to 73%.  One of the major disadvantages of the L/S ratio is the inability to use this test in the setting of contaminated amniotic fluid. Both blood and meconium staining of amniotic fluid have been found to interfere with L/S ratio determinations.
  141. 141. PG determinations:  It is found that the false-positive rate for PG determination was 1.8%. This rate is significantly lower than the false-positive rate they found for the L/S ratio(5%)  PG performs much better than the L/S ratio in predicting babies who will develop RDS. Finally, PG determinations accurately predict pulmonary maturity and give a better indication of pulmonary immaturity than does the L/S ratio
  142. 142. Saturated Phosphatidylcholine  Saturated Phosphatidylcholine has been found to predict pulmonary maturity  Respiratory distress syndrome was correctly predicted 55.5% of the time by L/S ratio and 82% of the time by SPC.  Pulmonary immaturity = an SPC <500 μg/dl  In addition, the SPC was found to be valid in the presence of blood and meconium, whereas the L/S ratio was not.
  143. 143.  The lung profile includes the L/S ratio, desaturated lecithin, PG and PI concentrations.  lung profile help to form a clearer picture of fetal lung development  The L/S ratio had a false-positive rate of 3%-5%, which was reduced to less than 1% with the combined lung profile test Lung Profile
  144. 144. Microviscosimeter  Microviscosimeter testing measures surfactant associated with a phospholipid membrane using fluorescent dye techniques.  The microviscosimeter commonly used in the fetal lung maturity analyzer or FELMA machine.
  145. 145. Surfactant/Albumin Ratio  A recently introduced TDx FLM assay is an automated fetal lung maturity test based on the principle of fluorescent polarization used previously with the microviscosimeter.  A surfactant albumin ratio of 50-70 mg surfactant/g of albumin has been considered mature in most studies  The TDx test correlates well with the L/S ratio and has few false-immature results, making it an excellent screening test  It only requires approximately 1 ml of amniotic fluid and the test can be performed in less than an hour,
  146. 146. Shake test  this test use the principle that when ethanol is added to amniotic fluid, the nonsurfactant foam causing substances in amniotic fluid are removed.  any stable foam layer that persists after shaking is due to the presence of surfactant in a critical concentration.  when serial dilutions of ethanol are used, the surfactant can be quantified.  it is found that the shake test was comparable to the L/S ratio and had a high predictive value for RDS when applied to uncontaminated amniotic fluid.
  147. 147. Tap Test  the tap test examines the ability of surfactant within amniotic fluid to break down bubbles within an ether layer.  the test is performed on 1 ml of amniotic fluid mixed with a drop of 6N hydrochloric acid and 1.5 ml of diethylether  the tube is tapped 4 times and examined for the presence of bubbles within the ether layer.  in mature samples, the bubbles quickly breakdown, whereas in immature amniotic fluid specimens more than 5 bubbles persist in the ether layer.  this rapid test was comparable with the phospholipid profile
  148. 148. Visual Inspection  The basis is whether or not newspaper could be read through the amniotic fluid sample, that is, was the fluid too turbid to read text through.  with clear fluid (readable newsprint) the sensitivity of an immature result is 98%.
  149. 149. Optical Density at 650 nm with a OD 650 value of 0.15 or greater, the L/S ratio was always greater than 2.0 when the OD 650 was less than 0.15, only 6% of L/S ratios were greater than 2
  150. 150. Diabetes and pulmonary maturity
  151. 151. Amniotic fluid and renal maturity
  152. 152. AF assesment and Renal maturity  The fetal kidneys start to develop during the 4th and 5th weeks of gestation and begin to excrete urine into the amniotic fluid at the 8th to 11th week  At the 20th week the fetal kidneys produce most of the amniotic fluid  Renal maturity is defined by the increase in glomerular filtration and by the maturity of renal tubular cells that begin to express various tubular transporters over the months of gestation
  153. 153. AF assesment and Renal maturity  Glomerular filtration in the fetal kidney can be assessed by the concentrations of creatinine and urea in the amniotic fluid  Creatinine concentrations of 2 mg/dl represent an age of at least 37 weeks of gestation  The function of the renal tubule system, specifically proximal tubules, can also be assessed by the concentrations of ß2- microglobulin and NAG in the third trimester of gestation
  154. 154. AF assesment and Renal maturity  ß2-Microglobulin produced by the fetus is filtered and reabsorbed by proximal tubules, with an expected reduction in its concentrations at week 36 in normal pregnancies.  This reduction can be considered as an index of renal tubular maturation
  155. 155. AF assesment and Renal maturity  Analysis of creatinine and urea in amniotic fluid permits an evaluation of renal maturation.  Creatinine values in the amniotic fluid that best represent fetal maturity are 1.5 to 2.0 mg/dl
  156. 156. AF and Bone Healing
  157. 157. AF and Bone Healing  Hyaluronic acid (HA) is a linear polysaccharide with a high molecular weight.  It is found in all extracellular matrices and has the same structure in all species.  If HA is administered during surgery, scar formation is prevented.  HA is known to reduce scar formation by inhibiting lymphocyte migration, proliferation and chemotaxis, granulocyte phagocytosis , degranulation, and macrophage motility
  158. 158. AF and Bone Healing  HA influences and enhances tissue regeneration through its ability to retain large amounts of water.  HA has been reported to increase osteoblastic bone formation in vitro through increased mesenchymal cell differentiation and migration.
  159. 159. AF and Bone Healing  Human amniotic fluid (HAF), obtained by amniocentesis during the second trimester of gestation, contains high molecular weight HA in high concentrations.  It has been showed that HASA (HA- stimulating activator) which is present in HAF, stimulates the wound to increase the production of endogenous HA.  HAF may increase both endogenous and exogenous HA in the application region.  HAF has been reported to enhance new cartilage formation.
  160. 160. CLINICAL BIOCHEMISTRY AMNIOTIC FLUID Risk and complications  Pain  Leakage  Hemorrhage  Abortion  Fetal injury  Orthopaedic abnormalities  alloimmunisation