Dr. Shivaprasad

Mehta hospital

• Effect on neonatal mortality and the development of long-term morbidity.

• Placental examination- means of investigating the intrauterine past.

• Timely examination of the placenta.

• Specific patterns of placental pathological findings.

Placental examination Description of the disk shape, surface, and

thickness. Placental weight The distance from the cord insertion to the nearest

margin should be measured Meconium staining should be noted Cord attachment and cord characteristics.

Pathological features

1. Ischemic changes such as hemorrhagic endovasculitis (HEV), perivillous fibrin deposition, villous ischemia.;

2. Villous infarction and decidual necrosis;

3. Chronic villitis;

4. Abnormal villus maturity

5. Placental abruption;

6. Meconium staining; and

7. Others , such as villous edema, intervillous thrombosis, amnion nodosum, and congested villi,

Placental findings indicating acute in utero compromise

Normal placental weight or weight appropriate for fetal weight

Acute villous oedema Intravillous haemorrhage Acute retroplacental haemorrhage Acute meconium staining

Placental findings indicating chronic in utero compromise

Abnormal placental weight in relation to fetal weight Chorangiosis Fetal normoblastaemia Chronic meconium staining Meconium-associated myonecrosis of cord vessel(s) Acute or necrotising funisitis Significant chronic villitis Amnion nodosum Significant placental ischaemia or infarction Decidual vasculopathy Maternal floor infarction/massive perivillous fibrinoid deposition Chronic fetal vascular obstruction/fetal thrombotic vasculopathy

Gross placental lesions and neonatal outcome

Lesion Possible neonatal outcome

Intervillous thrombosis Fetomaternal hemorrhage

Massive perivillous fibrin deposition

IUGR, Asphyxia

Infarcts IUGR , Asphyxia

Stem villous arterial thrombosis- induced infarction

Fetal thrombophilia and sequelae

Avery’s diseases of newborn, 8th edition

Microscopic pathologic findings

Finding Neonatal outcome

Funisitis Fetal inflammation, CP

Villitis Transplacental infection (CMV)

Chorangiosis Fetal stress or a non-specific finding

Stem villous thrombosis Fetal thrombophilia, cerebral disease

Listeria abscesses Preterm labor, fetal demise

Abnormal villous maturation ? IUGR

Maternal vascular disease(decidua)

IUGR

Avery’s diseases of newborn, 8th edition

Pregnancy conditions diagnosable at birth by placental examination and associated neonatal outcomes

Monochorionic twinning TTTS, Pump twin in trap, survivor status after fetal demise, growth discordance without TTT.

Acute chorioamnionitis Fetal sepsis, fetal inflammatory response syndrome, CP

Chorioangioma Hydrops, cardiac failure, consumptive coagulopathy.

Maternal floor infarction IUGR, Cerebral disease

Abruption Asphyxial brain disease

Chronic abruption oligohydromnios sy IUGR

Amnion nodosum Severe oligohydromnios leading to pulmonary hypoplasia

Meconium staining Possible asphyxia, aspiration lung disease

Pregnancy conditions diagnosable at birth by placental examination and associated neonatal outcomes

Chorionic plate vascular thrombosis

Asphyxia , possible thrombophilia

Amniotic bands Fetal limb reduction abnormalities

Breus mole Asphyxia , IUGR

Abnormal cord coiling IUGR, possible asphyxia

Velamentous cord IUGR , vasa previa

Cord knot Asphyxia

Umbilical vein thrombosis Asphyxia

Single umbilical artery IUGR, associated malformations

Avery’s diseases of newborn, 8th edition

Placental Pathology and IUGR Two pathologic developmental pathways leading to

IUGR, presumably through placental insufficiency.

One of these pathways probably involves placental ischemia and placental infarction, leading to decreased placental perfusion.

An alternative path to placental insufficiency and IUGR may involve chronic villous inflammation.

In general, 5% of cases of villitis can be attributed to intrauterine infection, whereas the great majority are classified as villitis of unknown etiology (VUE)

Problems of IUGR• Maternal complications due to underlying disease

risk of CS• Fetal complications Stillbirth, hypoxia/acidosis,

malformations • Neonatal complications Hypoglycemia,

hypocalcemia,Hypoxia & acidosis, hypothermia, meconium aspiration , Polycythemia, hyperbilirubinemia, sepsis, low APGAR score , congenital malformations, apneic spells, intubation, sudden infant death syndrome

• Long term complications Lower IQ, learning & behavior Problems, major neurological handicap seizures, cerebral Palsy, mental retardation.

• Perinatal mortalility 1.5-2X

Abruptio placentae: Perinatal outcome

Perinatal mortality – 20-40%

Fetal death 25% among perinatal mortality.

50-70% preterm deliveries.

If a/w PPROM – mean gestational age is 28 weeks.

Amnion nodosum Almost 20-fold increase in the odds of dying when

amnion nodosum is present & is more strongly predictive than extreme prematurity.

Amnion nodosum tends to be associated with oligohydramnios arising from various causes.

Villous edema Neonatal complications such as death, CLD, and

IVH (Redline et al.,) grade 3 villous edema was associated with long-term

neurological impairment in low birth weight neonates (OR 5.7; 95% CI, 1.5–21.0).

It is linked to placental ischemia on the fetal side is probably associated with impaired placental function, as emphasized by its correlation with SGA.

Disorders of Placental Circulation and the Fetal Brain

The placenta is the sole provider of nutrients and oxygen to the developing fetus.

Serves a significant protective function, buffering the effects of teratogenic exposures, such as infection, trauma, and various toxins during pregnancy.

Raymond W. Redline, MD. Clin Perinatol 36 (2009) 549–559

Proper functioning of the placenta depends on the

Patency and integrity of the maternal arteries, Proper conductance of maternal blood through the

intervillous space,

Exposure of maternal blood to the villous trophoblastic epithelium,

Maintenance of a normal diffusion distance between maternal and fetal blood at the interhemal membrane,

Patency and integrity of larger vessels in the villous tree, and

Unobstructed flow in the umbilical cord

Maternal circulatory lesionsreduced flow,large vessels (mechanisms of brain injury) Generalized hypoperfusion or repeated episodes of ischemia and

reperfusion- increased syncytial knots and intervillous fibrin, villous agglutination, and laminar necrosis of the placental membrane .

decreased functional reserve to withstand periods of acute hypoxia which can cause fetal metabolic abnormalities affecting short- and long-term responses to stress.

Large villous infarcts have been associated with ischemic CNS lesions.

Decreased Conductance, Intervillous Space (mechanisms of brain injury) Excessive fibrin or fibrinoid deposition on the

trophoblast surface and surrounding intervillous space interferes with conductance and can have profound effects on fetal growth and circulatory physiology.

It is a/w numerous adverse perinatal outcomes including miscarriage, stillbirth, intrauterine growth restriction, indicated preterm delivery, and long-term neurodisability

Adams-Chapman I, Vaucher YE, Bejar RF, et al. Maternal floor infarction of the placenta:association with central nervous system injury and adverse neurodevelopmentaloutcome. J Perinatol 2002;22(3):236–41.

Umbilical cord obstruction (mechanisms of brain injury)

Significant deformational forces including extrinsic compression, hypercoiling, or torsion of unprotected vessels at the insertion site may retard or prevent flow, particularly in the less well protected umbilical vein.

Thromboinflammatory Lesions, Large Vessels (mechanisms of brain injury)• Prolonged meconium exposure - significant

vasospasm of large fetal vessels.

• Chorioamnionitis with intense chorionic vasculitis - the most frequent risk factor for CNS injury in VLBW.

• Fetal inflammatory responses(chorionic vasculitis), a/w with increased levels of circulating cytokines and chemokines in the neonatal circulation.

• Chorionic vasculitis may also lead to nonocclusive chorionic vessel thrombi.

Altshuler G, Hyde S. Meconium-induced vasocontraction: a potential cause of cerebral and other fetal hypoperfusion and of poor pregnancy outcome. J Child Neurol 1989;4:137–42

Microcirculatory abnormalities (mechanisms of brain injury)

Diffuse villous edema affecting immature intermediate villi is a placental risk factor for later CP and abnormal neurocognitive performance at school age in premature infants.

Diffuse villous edema has also been a/w an increased incidence of respiratory distress syndrome and neonatal death.

Altshuler G. Chorangiosis: an important placental sign of neonatal morbidity and mortality. Arch Pathol Lab Med 1984;108(1):71–4.

Fetal hemorrhage (mechanisms of brain injury)

• Long-standing FMHs show increased circulating nucleated RBCs and villous hydrops related to high-output CCF.

• Increased circulating NRBCs, also serves as an indicator of protracted (6–12 hours or more) significant fetal hypoxia of any etiology and can be helpful in the evaluation of infants presenting with severe neurologic problems.

Redline RW. Elevated circulating fetal nucleated red blood cells and placental pathology in term infants who develop cerebral palsy. Hum Pathol 2008;39(9): 1378–84

Cerebral infarction (mechanisms of brain injury)

Thrombosis on the maternal side may contribute to hypertensive disorders (eg, preëclampsia), IUGR miscarriage, or fetal death from hypoperfusion with or without hypercoagulability.

Thrombosis on the fetal side will predispose the infant to emboli that bypasses the pulmonary and hepatic circulations to lodge in the fetal cerebral vasculature.

CP and monochorionicity

Single fetal demise Brain damage in the survivor after single fetal

demise is exclusively seen in MC twins. Embolic theory – discarded Recently “ischemic” theory A cohort study by Pharaoh and Adi – of the 241

survivors( twin preg) 23 had CP and 28 had other cerebral impairment.

Survivor co-twin is at 20% increased risk of cerebral impairment.

Isaac Blickstein, Clin perinatol 31 2004, 395-408

Thank you