| Placental insufficiency |
| Classification and external resources |
| ICD-10 |
P02.2 |
| ICD-9 |
762.2 |
| DiseasesDB |
10107 |
| MedlinePlus |
001485 |
| MeSH |
D010927 |
Placental insufficiency or Utero-placental insufficiency is insufficient blood flow to the placenta during pregnancy. The term is also sometimes used to designate late decelerations of fetal heart rate as measured by electronic monitoring, even if there is no other evidence of reduced blood flow to the placenta, normal uterine blood flow rate being 600mL/min.
Contents
- 1 Causes
- 2 Pathophysiology
- 2.1 Maternal effects
- 2.2 Fetal effects
- 2.2.1 Fetal metabolic changes
- 2.2.2 Fetal hormonal changes
- 2.2.3 Fetal hematologic changes
- 2.2.4 Fetal immunological changes
- 2.2.5 Fetal cardiovascular changes
- 2.2.6 Fetal behavioral changes
- 2.2.7 Risk of later metabolic disease
- 3 Diagnosis
- 4 See also
- 5 References
Causes
Placental insufficiency can be induced experimentally by bilateral uterine artery ligation of the pregnant rat.
The following characteristics of placentas have been said to be associated with placental insufficiency, however all of them occur in normal healthy placentas and full term healthy births, so none of them can be used to accurately diagnose placental insufficiency:
- Abnormally thin placenta (less than 1 cm)[1]
- Circumvallate placenta (1% of normal placentas)
- Amnion cell metaplasia, (amnion nodosum) (present in 65% of normal placentas)
- Increased syncytial knots
- Calcifications
- Infarcts due to focal or diffuse thickening of blood vessels
- Villi capillaries occupying about 50% of the villi volume or when <40% of capillaries are on the villous periphery
Placental insufficiency should not be confused with complete placental abruption, in which the placenta separates off the uterine wall, which immediately results in no blood flow to the placenta, which leads to immediate fetal demise. In the case of a marginal, incomplete placental abruption of less than 50%, usually weeks of hospitalization precedes delivery and outcomes are not necessarily affected by the partial abruption.[2]
Pathophysiology
Maternal effects
Several aspects of maternal adaptation to pregnancy are affected by dysfunction of placenta. Maternal arteries fail to transform into low-resistance vessels (expected by 22–24 weeks of gestation).[3][4] This increases vascular resistance in fetoplacental vascular bed eventually leading to reduction in metabolically active mass of placenta like a vicious cycle.
Fetal effects
Placental insufficiency can affect the fetus, causing Fetal distress. Placental insufficiency may cause oligohydramnios, preeclampsia, miscarriage or stillbirth. Placental insufficiency is most frequent cause of asymmetric IUGR.[5]
Fetal metabolic changes
Metabolic changes occurring in uteroplacental insufficiency:[6]
| Substrate |
Change |
| Glucose |
Decreases in proportion to degree of fetal hypoxemia |
| Amino acids |
- Decrease in branched chain amino acids (valine, leucine, isoleucine), serine and lysine.
- Increase in hydroxyproline
- Glycine:Valine ratio increases in amniotic fluid
- Increase in ammonia in amniotic fluid (positive correlation with ponderal index)
|
| Fatty acids |
- Decrease in long-chain polyunsaturated fatty acids
- Decrease in overall fatty acid transport via umbilical cord
|
| Oxygen and Carbon dioxide |
- Degree of hypoxemia is proportional to villous damage
- Hypercapnia, acidemia, hypoglycemia and hyperlacticemia in proportion to hypoxemia
|
Fetal hormonal changes
Decrease in overall thyroid function is correlated with fetal hypoxemia.[7][8] Serum glucagon, adrenaline, noradrenaline levels increase, eventually causing peripheral glycogenolysis and mobilization of fetal hepatic glycogen stores.[9][10][11][12]
Fetal hematologic changes
Fetal hypoxemia triggers erythropoietin release. This stimulates RBC production from medullary and extramedullary sites and eventually results in polycythemia.[13][14][15][16] Oxygen carrying capacity of blood is thus increased. Prolonged tissue hypoxemia may cause early release of erythrocytes from maturation sites and thus count of nucleated RBCs in blood increases.[17][18][19][20] These factors, increase in blood viscosity, decrease in cell membrane fluidity and platelet aggregation are important precurosrs in accelerating placental vascular occlusion.
Fetal immunological changes
There is decrease in immunoglobulin, absolute B-cell counts[21] and total WBC count.[22] T-helper and cytotoxic T-cells are suppressed[23] in proportion of degree of acidemia. These conditions lead to higher infection susceptibility of infant after delivery.
Fetal cardiovascular changes
There is decrease in magnitude of umbilical venous volume flow.[24] In response to this, proportion of umbilical venous blood diverted to fetal heart increases.[25] This eventually leads to elevation of pulmonary vascular resistance and increased right ventricular afterload.[26][27][28] This redistribution of blood flow is early response to placental insufficiency. Blood flow is selectively redirected to myocardium, adrenal glands and, particularly, brain. The last phenomenon is called "brain-sparing effect".[29]
In late stage, the redistribution becomes ineffective, there is decrease in cardiac output, ineffective preload handling and elevation of central venous pressure.[30][31][32][33] This deterioration in cardiovascular state may ultimately lead to tricuspid insufficiency and fetal demise.[34][35] Peripheral circulatory disturbances also accompany these central circulatory changes.
Fetal behavioral changes
Chronic hypoxemia leads to delay in all aspects of CNS maturation.[36][37][38][39] With worsening fetal hypoxemia, there is decline in fetal activity.[40] With further hypoxemia, fetal breathing ceases. Gross body movements and tone decrease further.[41][42] Fetal heart rate decreases due to spontaneous deceleration due to direct depression of cardiac contractility. This leads to intrauterine fetal death.
Risk of later metabolic disease
According to the theory of thrifty phenotype, placental insufficiency triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment rich in food it may be more prone to metabolic disorders, such as obesity and type II diabetes.[43]
Diagnosis
The following tests have been promoted as supposedly diagnosing placental insufficiency, but all have been unsuccessful at predicting stillbirth due to placental insufficiency:[44][45]
- Placental grading
- Amniotic fluid index
- Fetal biophysical profile test scoring
- Doppler velocimetry
- Routine ultrasound scanning
- Detection and management of maternal diabetes mellitus
- Antenatal fetal heart rate monitoring using cardiotocography
- Vibroacoustic stimulation, fetal movement counting
- Home vs. hospital-based bed rest and monitoring in high-risk pregnancy
- In-hospital fetal surveillance unit
- Use of the partograph during labor
- Cardiotocography during labor with or without pulse oximetry
See also
- Small for gestational age
References
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- ^ Brosens, I; Dixon, HG; Robertson, WB (September 1977). "Fetal growth retardation and the arteries of the placental bed.". British journal of obstetrics and gynaecology 84 (9): 656–63. doi:10.1111/j.1471-0528.1977.tb12676.x. PMID 911717.
- ^ Meekins, JW; Pijnenborg, R; Hanssens, M; McFadyen, IR; van Asshe, A (August 1994). "A study of placental bed spiral arteries and trophoblast invasion in normal and severe pre-eclamptic pregnancies.". British journal of obstetrics and gynaecology 101 (8): 669–74. doi:10.1111/j.1471-0528.1994.tb13182.x. PMID 7947500.
- ^ Medical Physiology, 2e. Elsevier Health Sciences. ISBN 1455711810.
- ^ Gabbe, Steven G. (ed.). Obstetrics : normal and problem pregnancies (6th ed.). Philadelphia: Elsevier/Saunders. ISBN 978-1-4377-1935-2.
- ^ Thorpe-Beeston, JG; Nicolaides, KH; McGregor, AM (Fall 1992). "Fetal thyroid function.". Thyroid 2 (3): 207–17. doi:10.1089/thy.1992.2.207. PMID 1422233.
- ^ Thorpe-Beeston, JG; Nicolaides, KH; Snijders, RJ; Felton, CV; Vyas, S; Campbell, S (November 1991). "Relations between the fetal circulation and pituitary-thyroid function.". British journal of obstetrics and gynaecology 98 (11): 1163–7. doi:10.1111/j.1471-0528.1991.tb15371.x. PMID 1760429.
- ^ Hubinont, C; Nicolini, U; Fisk, NM; Tannirandorn, Y; Rodeck, CH (April 1991). "Endocrine pancreatic function in growth-retarded fetuses.". Obstetrics & Gynecology 77 (4): 541–4. PMID 2002976.
- ^ Weiner, CP; Robillard, JE (December 1988). "Atrial natriuretic factor, digoxin-like immunoreactive substance, norepinephrine, epinephrine, and plasma renin activity in human fetuses and their alteration by fetal disease.". American Journal of Obstetrics and Gynecology 159 (6): 1353–60. PMID 2974684.
- ^ Greenough, A; Nicolaides, KH; Lagercrantz, H (June 1990). "Human fetal sympathoadrenal responsiveness.". Early Human Development 23 (1): 9–13. doi:10.1016/0378-3782(90)90124-2. PMID 2120028.
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- ^ Thilaganathan, B; Athanasiou, S; Ozmen, S; Creighton, S; Watson, NR; Nicolaides, KH (May 1994). "Umbilical cord blood erythroblast count as an index of intrauterine hypoxia.". Archives of disease in childhood. Fetal and neonatal edition 70 (3): F192–4. doi:10.1136/fn.70.3.f192. PMC 1061039. PMID 8198413.
- ^ Franz, AR; Pohlandt, F (March 2001). "Red blood cell transfusions in very and extremely low birthweight infants under restrictive transfusion guidelines: is exogenous erythropoietin necessary?". Archives of disease in childhood. Fetal and neonatal edition 84 (2): F96–F100. doi:10.1136/fn.84.2.f96. PMC 1721217. PMID 11207224.
- ^ Snijders, RJ; Abbas, A; Melby, O; Ireland, RM; Nicolaides, KH (February 1993). "Fetal plasma erythropoietin concentration in severe growth retardation.". American journal of obstetrics and gynecology 168 (2): 615–9. doi:10.1016/0002-9378(93)90505-d. PMID 8438939.
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- ^ Bernstein, PS; Minior, VK; Divon, MY (November 1997). "Neonatal nucleated red blood cell counts in small-for-gestational age fetuses with abnormal umbilical artery Doppler studies.". American journal of obstetrics and gynecology 177 (5): 1079–84. doi:10.1016/s0002-9378(97)70018-8. PMID 9396897.
- ^ Baschat, AA; Gembruch, U; Reiss, I; Gortner, L; Harman, CR; Weiner, CP (July 1999). "Neonatal nucleated red blood cell counts in growth-restricted fetuses: relationship to arterial and venous Doppler studies.". American journal of obstetrics and gynecology 181 (1): 190–5. doi:10.1016/s0002-9378(99)70458-8. PMID 10411818.
- ^ Baschat, AA; Gembruch, U; Reiss, I; Gortner, L; Harman, CR (2003). "Neonatal nucleated red blood cell count and postpartum complications in growth restricted fetuses.". Journal of perinatal medicine 31 (4): 323–9. doi:10.1515/JPM.2003.046. PMID 12951889.
- ^ Singh, M; Manerikar, S; Malaviya, AN; Premawathi,; Gopalan, R; Kumar, R (July 1978). "Immune status of low birth weight babies.". Indian pediatrics 15 (7): 563–7. PMID 569131.
- ^ Davies, N; Snijders, R; Nicolaides, KH (1991). "Intra-uterine starvation and fetal leucocyte count". Fetal diagnosis and therapy 6 (3–4): 107–12. doi:10.1159/000263633. PMID 1789915.
- ^ Thilaganathan, B; Plachouras, N; Makrydimas, G; Nicolaides, KH (November 1993). "Fetal immunodeficiency: a consequence of placental insufficiency.". British journal of obstetrics and gynaecology 100 (11): 1000–4. doi:10.1111/j.1471-0528.1993.tb15141.x. PMID 8251449.
- ^ Rigano, S; Bozzo, M; Ferrazzi, E; Bellotti, M; Battaglia, FC; Galan, HL (October 2001). "Early and persistent reduction in umbilical vein blood flow in the growth-restricted fetus: a longitudinal study.". American journal of obstetrics and gynecology 185 (4): 834–8. doi:10.1067/mob.2001.117356. PMID 11641661.
- ^ Bellotti, M; Pennati, G; De Gasperi, C; Bozzo, M; Battaglia, FC; Ferrazzi, E (May 2004). "Simultaneous measurements of umbilical venous, fetal hepatic, and ductus venosus blood flow in growth-restricted human fetuses". American journal of obstetrics and gynecology 190 (5): 1347–58. doi:10.1016/j.ajog.2003.11.018. PMID 15167841.
- ^ Rizzo, G; Capponi, A; Chaoui, R; Taddei, F; Arduini, D; Romanini, C (August 1996). "Blood flow velocity waveforms from peripheral pulmonary arteries in normally grown and growth-retarded fetuses.". Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology 8 (2): 87–92. doi:10.1046/j.1469-0705.1996.08020087.x. PMID 8883309.
- ^ Griffin, D; Bilardo, K; Masini, L; Diaz-Recasens, J; Pearce, JM; Willson, K; Campbell, S (October 1984). "Doppler blood flow waveforms in the descending thoracic aorta of the human fetus.". British journal of obstetrics and gynaecology 91 (10): 997–1006. doi:10.1111/j.1471-0528.1984.tb03678.x. PMID 6386040.
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|
Certain conditions originating in the perinatal period / fetal disease (P, 760–779)
|
|
Maternal factors and
complications of pregnancy,
labour and delivery |
| placenta: |
- Placenta praevia
- Placental insufficiency
- Twin-to-twin transfusion syndrome
|
|
| chorion/amnion: |
|
|
| umbilical cord: |
- Umbilical cord prolapse
- Nuchal cord
- Single umbilical artery
|
|
|
Length of gestation
and fetal growth |
- Small for gestational age/Large for gestational age
- Preterm birth/Postmature birth
- Intrauterine growth restriction
|
|
| Birth trauma |
- scalp
- Cephalhematoma
- Chignon
- Caput succedaneum
- Subgaleal hemorrhage
- Brachial plexus lesion
- Erb's palsy
- Klumpke paralysis
|
|
| By system |
| Respiratory |
- Intrauterine hypoxia
- Infant respiratory distress syndrome
- Transient tachypnea of the newborn
- Meconium aspiration syndrome
- pleural disease
- Pneumothorax
- Pneumomediastinum
- Wilson–Mikity syndrome
- Bronchopulmonary dysplasia
|
|
| Cardiovascular |
- Pneumopericardium
- Persistent fetal circulation
|
|
Haemorrhagic and
hematologic disease |
- Vitamin K deficiency
- Haemorrhagic disease of the newborn
- HDN
- ABO
- Anti-Kell
- Rh c
- Rh D
- Rh E
- Hydrops fetalis
- Hyperbilirubinemia
- Kernicterus
- Neonatal jaundice
- Velamentous cord insertion
- Intraventricular hemorrhage
- Germinal matrix hemorrhage
- Anemia of prematurity
|
|
| Digestive |
- Ileus
- Necrotizing enterocolitis
- Meconium peritonitis
|
|
Integument and
thermoregulation |
- Erythema toxicum
- Sclerema neonatorum
|
|
| Nervous system |
- Periventricular leukomalacia
|
|
| Musculoskeletal |
- Gray baby syndrome
- muscle tone
- Congenital hypertonia
- Congenital hypotonia
|
|
|
| Infectious |
- Vertically transmitted infection
- Congenital rubella syndrome
- Neonatal herpes simplex
- Omphalitis
- Neonatal sepsis
- Group B streptococcal infection
- Neonatal conjunctivitis
|
|
| Other |
- Perinatal mortality
- Stillbirth
- Infant mortality
- Neonatal withdrawal
|
|
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Index of developmental medicine
|
|
| Description |
- Embryology
- Cell lines
- endoderm
- mesoderm
- ectoderm
|
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| Disease |
- Due to toxins
- Syndromes
- Chromosomal
- Neonate
- Twins
|
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Index of obstetrics
|
|
| Description |
- Pregnancy
- Development
- Anatomy
|
|
| Disease |
- Pregnancy and childbirth
- Placenta and neonate
- Infections
- Symptoms and signs
|
|
| Treatment |
- Procedures
- Drugs
- oxytocins
- labor repressants
|
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