Failure of the placenta to deliver sufficient nutrients to the fetus during pregnancy From Wikipedia, the free encyclopedia
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]
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
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 the fetoplacental vascular bed, eventually leading to reduction in metabolically active mass of placenta in a type of vicious cycle.[citation needed]
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 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.[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.[citation needed]
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.[citation needed]
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]
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]
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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. PMID2536145.
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. PMID9396897.
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. PMID11641661.
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. PMID15167841.
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. PMID6386040. S2CID22642248.
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. PMID8058245.
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. PMID11876806.
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. PMID1951546.
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. PMID10221608.