Placental insufficiency

From Wikipedia, the free encyclopedia
Jump to navigation Jump to search
Placental insufficiency
Other namesUtero-placental insufficiency
SpecialtyNeonatology, obstetrics, maternal–fetal medicine Edit this on Wikidata

Placental insufficiency or utero-placental insufficiency is the failure of the placenta to deliver sufficient nutrients to the fetus during pregnancy, and is often a result of insufficient blood flow to the placenta. The term is also sometimes used to designate late decelerations of fetal heart rate as measured by cardiotocography or an NST, even if there is no other evidence of reduced blood flow to the placenta, normal uterine blood flow rate being 600mL/min.


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:[citation needed]

  • 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]


Maternal effects[edit]

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.[citation needed]

Fetal effects[edit]

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[edit]

Metabolic changes occurring in uteroplacental insufficiency:[6]

Substrate Change
Glucose Decreases in proportion to degree of fetal hypoglycemia
Amino acids
Fatty acids
Oxygen and Carbon dioxide

Fetal hormonal changes[edit]

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[edit]

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 precursors in accelerating placental vascular occlusion.[citation needed]

Fetal immunological changes[edit]

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[edit]

There is decrease in magnitude of umbilical venous volume flow.[24] In response to this, the 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 fetal cerebral redistribution of blood flow is an early response to placental insufficiency. Blood flow is selectively redirected to the myocardium, adrenal glands, and in particular to the brain in a 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 circulation may ultimately lead to tricuspid insufficiency and death of the fetus.[34][35] Peripheral circulatory disturbances also accompany these central circulatory changes.

Fetal behavioral changes[edit]

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.[citation needed]

Risk of later metabolic disease[edit]

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]


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]

See also[edit]


  1. ^ Brant, William E. (2001). The core curriculum, ultrasound. Philadelphia: Lippincott Williams & Wilkins. p. 265. ISBN 9780683307337.
  2. ^ McCormack, RA; Doherty, DA; Magann, EF; Hutchinson, M; Newnham, JP (October 2008). "Antepartum bleeding of unknown origin in the second half of pregnancy and pregnancy outcomes". BJOG: An International Journal of Obstetrics and Gynaecology. 115 (11): 1451–7. doi:10.1111/j.1471-0528.2008.01856.x. PMID 18715242.
  3. ^ 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.
  4. ^ 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.
  5. ^ Medical Physiology, 2e. Elsevier Health Sciences. 2012-01-13. ISBN 978-1455711819.
  6. ^ Gabbe, Steven G., ed. (2012-01-01). Obstetrics : normal and problem pregnancies (6th ed.). Philadelphia: Elsevier/Saunders. ISBN 978-1-4377-1935-2.
  7. ^ 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.
  8. ^ 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.
  9. ^ 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.
  10. ^ 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. doi:10.1016/0002-9378(88)90555-8. PMID 2974684.
  11. ^ 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.
  12. ^ Ville, Y; Proudler, A; Kuhn, P; Nicolaides, KH (October 1994). "Aldosterone concentration in normal, growth-retarded, anemic, and hydropic fetuses". Obstetrics and Gynecology. 84 (4): 511–4. PMID 8090385.
  13. ^ Weiner, CP; Williamson, RA (February 1989). "Evaluation of severe growth retardation using cordocentesis--hematologic and metabolic alterations by etiology". Obstetrics and Gynecology. 73 (2): 225–9. PMID 2536145.
  14. ^ 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.
  15. ^ 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.
  16. ^ 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.
  17. ^ Thilaganathan, B.; Nicolaides, K. H. (1 January 1992). "Erythroblastosis in birth asphyxia". Ultrasound in Obstetrics and Gynecology. 2 (1): 15–17. doi:10.1046/j.1469-0705.1992.02010015.x. PMID 12797000.
  18. ^ 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.
  19. ^ 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.
  20. ^ 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. S2CID 608538.
  21. ^ 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.
  22. ^ 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.
  23. ^ 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.
  24. ^ 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.
  25. ^ 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.
  26. ^ 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. 8 (2): 87–92. doi:10.1046/j.1469-0705.1996.08020087.x. PMID 8883309.
  27. ^ 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.
  28. ^ Akalin-Sel, T; Nicolaides, KH; Peacock, J; Campbell, S (September 1994). "Doppler dynamics and their complex interrelation with fetal oxygen pressure, carbon dioxide pressure, and pH in growth-retarded fetuses". Obstetrics and Gynecology. 84 (3): 439–44. PMID 8058245.
  29. ^ Reece, E. Albert (2006). Clinical obstetrics : the fetus and mother (3rd ed.). Malden, MA: Blackwell Pub. p. 107. ISBN 978-1-4051-3216-9.
  30. ^ Mäkikallio, K; Jouppila, P; Räsänen, J (February 2002). "Retrograde net blood flow in the aortic isthmus in relation to human fetal arterial and venous circulations". Ultrasound in Obstetrics & Gynecology. 19 (2): 147–52. doi:10.1046/j.0960-7692.2001.00626.x. PMID 11876806.
  31. ^ Rizzo, G; Arduini, D (October 1991). "Fetal cardiac function in intrauterine growth retardation". American Journal of Obstetrics and Gynecology. 165 (4 Pt 1): 876–82. doi:10.1016/0002-9378(91)90431-p. PMID 1951546.
  32. ^ Rizzo, G; Capponi, A; Rinaldo, D; Arduini, D; Romanini, C (April 1995). "Ventricular ejection force in growth-retarded fetuses". Ultrasound in Obstetrics & Gynecology. 5 (4): 247–55. doi:10.1046/j.1469-0705.1995.05040247.x. PMID 7600206.
  33. ^ Gudmundsson, S; Tulzer, G; Huhta, JC; Marsal, K (April 1996). "Venous Doppler in the fetus with absent end-diastolic flow in the umbilical artery". Ultrasound in Obstetrics & Gynecology. 7 (4): 262–7. doi:10.1046/j.1469-0705.1996.07040262.x. PMID 8726878.
  34. ^ Hecher, K; Campbell, S; Doyle, P; Harrington, K; Nicolaides, K (Jan 1, 1995). "Assessment of fetal compromise by Doppler ultrasound investigation of the fetal circulation. Arterial, intracardiac, and venous blood flow velocity studies". Circulation. 91 (1): 129–38. doi:10.1161/01.cir.91.1.129. PMID 7805194.
  35. ^ Rizzo, G; Capponi, A; Pietropolli, A; Bufalino, LM; Arduini, D; Romanini, C (Mar 1, 1994). "Fetal cardiac and extracardiac flows preceding intrauterine death". Ultrasound in Obstetrics & Gynecology. 4 (2): 139–42. doi:10.1046/j.1469-0705.1994.04020139.x. PMID 12797208.
  36. ^ Arduini, D; Rizzo, G; Romanini, C; Mancuso, S (1988). "Computerized analysis of behavioural states in asymmetrical growth retarded fetuses". Journal of Perinatal Medicine. 16 (4): 357–63. doi:10.1515/jpme.1988.16.4.357. PMID 3221294. S2CID 21529722.
  37. ^ Arduini, D; Rizzo, G; Caforio, L; Boccolini, MR; Romanini, C; Mancuso, S (June 1989). "Behavioural state transitions in healthy and growth retarded fetuses". Early Human Development. 19 (3): 155–65. doi:10.1016/0378-3782(89)90076-5. PMID 2776681.
  38. ^ Nijhuis, IJ; ten Hof, J; Nijhuis, JG; Mulder, EJ; Narayan, H; Taylor, DJ; Visser, GH (May 1999). "Temporal organization of fetal behavior from 24-weeks gestation onwards in normal and complicated pregnancies". Developmental Psychobiology. 34 (4): 257–68. doi:10.1002/(sici)1098-2302(199905)34:2<257::aid-dev2>;2-v. PMID 10331150.
  39. ^ Vindla, S; James, D; Sahota, D (March 1999). "Computerised analysis of unstimulated and stimulated behaviour in fetuses with intrauterine growth restriction". European Journal of Obstetrics, Gynecology, and Reproductive Biology. 83 (1): 37–45. doi:10.1016/s0301-2115(98)00238-3. PMID 10221608.
  40. ^ Ribbert, LS; Nicolaides, KH; Visser, GH (July 1993). "Prediction of fetal acidaemia in intrauterine growth retardation: comparison of quantified fetal activity with biophysical profile score". British Journal of Obstetrics and Gynaecology. 100 (7): 653–6. doi:10.1111/j.1471-0528.1993.tb14233.x. PMID 8369249.
  41. ^ Vintzileos, AM; Fleming, AD; Scorza, WE; Wolf, EJ; Balducci, J; Campbell, WA; Rodis, JF (September 1991). "Relationship between fetal biophysical activities and umbilical cord blood gas values". American Journal of Obstetrics and Gynecology. 165 (3): 707–13. doi:10.1016/0002-9378(91)90314-h. PMID 1822963.
  42. ^ Manning, FA; Snijders, R; Harman, CR; Nicolaides, K; Menticoglou, S; Morrison, I (October 1993). "Fetal biophysical profile score. VI. Correlation with antepartum umbilical venous fetal pH". American Journal of Obstetrics and Gynecology. 169 (4): 755–63. doi:10.1016/0002-9378(93)90002-Z. PMID 8238129.
  43. ^ Barker, D. J. P., ed. (1992). Fetal and infant origins of adult disease. London: British Medical Journal. ISBN 978-0-7279-0743-1.
  44. ^ Haws, Rachel A; Yakoob, Mohammad; Soomro, Tanya; Menezes, Esme V; Darmstadt, Gary L; Bhutta, Zulfiqar A (1 January 2009). "Reducing stillbirths: screening and monitoring during pregnancy and labour". BMC Pregnancy and Childbirth. 9 (Suppl 1): S5. doi:10.1186/1471-2393-9-S1-S5. PMC 2679411. PMID 19426468.
  45. ^ Smith, GC; Fretts, RC (Nov 17, 2007). "Stillbirth". Lancet. 370 (9600): 1715–25. doi:10.1016/S0140-6736(07)61723-1. PMID 18022035. S2CID 208788871.

External links[edit]

External resources