Placental insufficiency

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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.

Causes

Histopathology of placenta with increased syncytial knotting of chorionic villi, with two knots pointed out.

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]

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

vicious cycle.[citation needed
]

Fetal effects

Placental insufficiency can affect the fetus, causing

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 hypoglycemia
Amino acids
Fatty acids
  • Decrease in long-chain
    polyunsaturated fatty acids
  • Decrease in overall fatty acid transport via umbilical cord
Oxygen and Carbon dioxide

Fetal hormonal changes

Decrease in overall thyroid function is correlated with fetal hypoxemia.

noradrenaline levels increase, eventually causing peripheral glycogenolysis and mobilization of fetal hepatic glycogen stores.[9][10][11][12]

Fetal hematologic changes

Fetal hypoxemia triggers

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

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.[citation needed]

Fetal cardiovascular changes

There is decrease in magnitude of umbilical venous volume flow.

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

tricuspid insufficiency and death of the fetus.[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.

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

According to the theory of

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]

See also

References

  1. ISBN 9780683307337
    .
  2. PMID 18715242
    .
  3. S2CID 33620598
    .
  4. S2CID 22676459
    .
  5. ISBN 978-1455711819
    .
  6. ISBN 978-1-4377-1935-2
    .
  7. PMID 1422233
    .
  8. S2CID 2838294
    .
  9. PMID 2002976
    .
  10. PMID 2974684
    .
  11. PMID 2120028
    .
  12. PMID 8090385
    .
  13. PMID 2536145
    .
  14. PMID 8198413
    .
  15. PMID 11207224
    .
  16. PMID 8438939
    .
  17. S2CID 11457412
    .
  18. PMID 9396897
    .
  19. PMID 10411818
    .
  20. S2CID 608538
    .
  21. PMID 569131
    .
  22. PMID 1789915
    .
  23. S2CID 23159297
    .
  24. PMID 11641661
    .
  25. PMID 15167841
    .
  26. S2CID 8545352
    .
  27. S2CID 22642248
    .
  28. PMID 8058245
    .
  29. ISBN 978-1-4051-3216-9
    .
  30. PMID 11876806
    .
  31. PMID 1951546
    .
  32. PMID 7600206
    .
  33. PMID 8726878
    .
  34. PMID 7805194
    .
  35. S2CID 22358224
    .
  36. S2CID 21529722
    .
  37. PMID 2776681
    .
  38. PMID 10331150
    .
  39. PMID 10221608
    .
  40. S2CID 9439096
    .
  41. PMID 1822963
    .
  42. PMID 8238129
    .
  43. ISBN 978-0-7279-0743-1
    .
  44. PMID 19426468
    .
  45. S2CID 208788871
    .

External links

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