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 electronic monitoring, even if there is no other evidence of reduced blood flow to the placenta, normal uterine blood flow rate being 600mL/min.

Swelling (especially in the hands and face) was originally considered an important sign for a diagnosis of pre-eclampsia. However, because swelling is a common occurrence in pregnancy, its utility as a distinguishing factor in pre-eclampsia is not high. Pitting edema (unusual swelling, particularly of the hands, feet, or face, notable by leaving an indentation when pressed on) can be significant, and should be reported to a health care provider.

In general, none of the signs of pre-eclampsia are specific, and even convulsions in pregnancy are more likely to have causes other than eclampsia in modern practice. Further, a symptom such as epigastric pain may be misinterpreted as heartburn. Diagnosis, therefore, depends on finding a coincidence of several pre-eclamptic features, the final proof being their regression after delivery.

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)

- 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.

No single diagnostic test currently exists to predict the likelihood of developing gestational hypertension. High blood pressure is the major sign in diagnosing gestational hypertension. Protein in the urine, proteinuria, is a key indicator of the condition. Some women with gestational hypertension may present asymptomatic, but a number of symptoms are associated with the condition.

Symptoms

- Edema

- Sudden weight gain

- Blurred vision or sensitivity to light

- Nausea and vomiting

- Persistent headaches

- Increased blood pressure

Pre-eclampsia (PE) is a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine. The condition begins after 20 weeks of pregnancy. In severe disease there may be red blood cell breakdown, a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness of breath due to fluid in the lungs, or visual disturbances. Pre-eclampsia increases the risk of poor outcomes for both the mother and the baby. If left untreated, it may result in seizures at which point it is known as eclampsia.

Risk factors for pre-eclampsia include obesity, prior hypertension, older age, and diabetes mellitus. It is also more frequent in a woman's first pregnancy and if she is carrying twins. The underlying mechanism involves abnormal formation of blood vessels in the placenta amongst other factors. Most cases are diagnosed before delivery. Rarely, pre-eclampsia may begin in the period after delivery. While historically both high blood pressure and protein in the urine were required to make the diagnosis, some definitions also include those with hypertension and any associated organ dysfunction. Blood pressure is defined as high when it is greater than 140 mmHg systolic or 90 mmHg diastolic at two separate times, more than four hours apart in a woman after twenty weeks of pregnancy. Pre-eclampsia is routinely screened for during prenatal care.

Recommendations for prevention include: aspirin in those at high risk, calcium supplementation in areas with low intake, and treatment of prior hypertension with medications. In those with pre-eclampsia delivery of the baby and placenta is an effective treatment. When delivery becomes recommended depends on how severe the pre-eclampsia and how far along in pregnancy a person is. Blood pressure medication, such as labetalol and methyldopa, may be used to improve the mother's condition before delivery. Magnesium sulfate may be used to prevent eclampsia in those with severe disease. Bedrest and salt intake have not been found to be useful for either treatment or prevention.

Pre-eclampsia affects 2–8% of pregnancies worldwide. Hypertensive disorders of pregnancy (which include pre-eclampsia) are one of the most common causes of death due to pregnancy. They resulted in 46,900 deaths in 2015. Pre-eclampsia usually occurs after 32 weeks; however, if it occurs earlier it is associated with worse outcomes. Women who have had pre-eclampsia are at increased risk of heart disease and stroke later in life. The word eclampsia is from the Greek term for lightning. The first known description of the condition was by Hippocrates in the 5th century BC.

Gestational hypertension or pregnancy-induced hypertension (PIH) is the development of new hypertension in a pregnant woman after 20 weeks gestation without the presence of protein in the urine or other signs of preeclampsia. Hypertension is defined as having a blood pressure

greater than 140/90 mm Hg.

The seizures of eclampsia typically present during pregnancy and prior to delivery (the antepartum period), but may also occur during labor and delivery (the intrapartum period) or after the baby has been delivered (the postpartum period). If postpartum seizures develop, it is most likely to occur within the first 48 hours after delivery. However, late postpartum seizures of eclampsia may occur as late as 4 weeks after delivery.

There are 2 major categories of IUGR: symmetrical and asymmetrical. Some conditions are associated with both symmetrical and asymmetrical growth restriction.

In the early stages of placental abruption, there may be no symptoms. When symptoms develop, they tend to develop suddenly. Common symptoms include sudden-onset abdominal pain, contractions that seem continuous and do not stop, vaginal bleeding, enlarged uterus disproportionate to the gestational age of the fetus, decreased fetal movement, and decreased fetal heart rate.

Vaginal bleeding, if it occurs, may be bright red or dark.

A placental abruption caused by arterial bleeding at the center of the placenta leads to sudden development of severe symptoms and life-threatening conditions including fetal heart rate abnormalities, severe maternal hemorrhage, and disseminated intravascular coagulation (DIC). Those abruptions caused by venous bleeding at the periphery of the placenta develop more slowly and cause small amounts of bleeding, intrauterine growth restriction, and oligohydramnios (low levels of amniotic fluid).

Asymmetrical IUGR is more common (70%). In asymmetrical IUGR, there is restriction of weight followed by length. The head continues to grow at normal or near-normal rates (head sparing). A lack of subcutaneous fat leads to a thin and small body out of proportion with the liver. Normally at birth the brain of the fetus is 3 times the weight of its liver. In IUGR, It becomes 5-6 times. In these cases, the embryo/fetus has grown normally for the first two trimesters but encounters difficulties in the third, sometimes secondary to complications such as pre-eclampsia. Other symptoms than the disproportion include dry, peeling skin and an overly-thin umbilical cord. The baby is at increased risk of hypoxia and hypoglycaemia. This type of IUGR is most commonly caused by extrinsic factors that affect the fetus at later gestational ages. Specific causes include:

- Chronic high blood pressure

- Severe malnutrition

- Genetic mutations, Ehlers–Danlos syndrome

Eclampsia is a disorder of pregnancy characterized by seizures in the setting of pre-eclampsia. Typically the pregnant woman develops hypertension and proteinuria before the onset of a convulsion (seizure).

- Long-lasting (persistent) headaches

- Blurry vision

- Photophobia (i.e. bright light causes discomfort)

- Abdominal pain

- Either in the epigastric region (the center of the abdomen above the navel, or belly-button)

- And/or in the right upper quadrant of the abdomen (below the right side of the rib cage)

- Altered mental status (confusion)

Any of these symptoms may present before or after a seizure occurs. It is also possible that none of these symptoms will develop.

Other cerebral signs may immediately precede the convulsion, such as nausea, vomiting, headaches, and cortical blindness. If the complication of multi-organ failure ensues, signs and symptoms of those failing organs will appear, such as abdominal pain, jaundice, shortness of breath, and diminished urine output.

Based on severity:

- Class 0: Asymptomatic. Diagnosis is made retrospectively by finding an organized blood clot or a depressed area on a delivered placenta.

- Class 1: Mild and represents approximately 48% of all cases. Characteristics include the following:

- No vaginal bleeding to mild vaginal bleeding

- Slightly tender uterus

- Normal maternal blood pressure and heart rate

- No coagulopathy

- No fetal distress

- Class 2: Moderate and represents approximately 27% of all cases. Characteristics include the following:

- No vaginal bleeding to moderate vaginal bleeding

- Moderate-to-severe uterine tenderness with possible tetanic contractions

- Maternal tachycardia with orthostatic changes in blood pressure and heart rate

- Fetal distress

- Hypofibrinogenemia (i.e., 50–250 mg/dL)

- Class 3: Severe and represents approximately 24% of all cases. Characteristics include the following:

- No vaginal bleeding to heavy vaginal bleeding

- Very painful tetanic uterus

- Maternal shock

- Hypofibrinogenemia (i.e., <150 mg/dL)

- Coagulopathy

- Fetal death

The common clinical features are smaller symphysis fundal height, fetal malpresentation, undue prominence of fetal parts and reduced amount of amniotic fluid.

Women with placenta previa often present with painless, bright red vaginal bleeding. This commonly occurs around 32 weeks of gestation, but can be as early as late mid-trimester. 51.6% of women with placenta previa have antepartum haemorrhage. This bleeding often starts mildly and may increase as the area of placental separation increases. Previa should be suspected if there is bleeding after 24 weeks of gestation. Bleeding after delivery occurs in about 22% of those affected.

Women may also present as a case of failure of engagement of fetal head.

Intrauterine hypoxia occurs when the fetus is deprived of an adequate supply of oxygen. It may be due to a variety of reasons such as prolapse or occlusion of the umbilical cord, placental infarction and maternal smoking. Intrauterine growth restriction (IUGR) may cause or be the result of hypoxia. Intrauterine hypoxia can cause cellular damage that occurs within the central nervous system (the brain and spinal cord). This results in an increased mortality rate, including an increased risk of sudden infant death syndrome (SIDS). Oxygen deprivation in the fetus and neonate have been implicated as either a primary or as a contributing risk factor in numerous neurological and neuropsychiatric disorders such as epilepsy, ADHD, eating disorders and cerebral palsy.

Complications may include cord compression, musculoskeletal abnormalities such as facial distortion and clubfoot, pulmonary hypoplasia and intrauterine growth restriction. Amnion nodosum is frequently also present (nodules on the fetal surface of the amnion).

The use of oligohydramnios as a predictor of gestational complications is controversial.

Potter syndrome is a condition caused by oligohydramnios. Affected fetuses develop pulmonary hypoplasia, limb deformities, and characteristic facies. Bilateral agenesis of the fetal kidneys is the most common cause due to the lack of fetal urine.

A placental infarction results from the interruption of blood supply to a part of the placenta, causing its cells to die.

Small placental infarcts, especially at the edge of the placental disc, are considered to be normal at term. Large placental infarcts are associated with vascular abnormalities, e.g. hypertrophic decidual vasculopathy, as seen in hypertension. Very large infarcts lead to placental insufficiency and may result in fetal death.

Twin-to-twin transfusion syndrome (TTTS), also known as feto-fetal transfusion syndrome (FFTS) and twin oligohydramnios-polyhydramnios sequence (TOPS) is a complication of disproportionate blood supply, resulting in high morbidity and mortality. It can affect monochorionic multiples, that is, multiple pregnancies where two or more fetuses share a chorion and hence a single placenta. Severe TTTS has a 60–100% mortality rate.

It is associated with gestational diabetes, smoking and high altitude.

Premature rupture of membranes (PROM), or pre-labor rupture of membranes, is a condition that can occur in pregnancy. It is defined as rupture of membranes (breakage of the amniotic sac), commonly called breaking of the mother's water(s), more than 1 hour before the onset of labor. The sac (consisting of 2 membranes, the chorion and amnion) contains amniotic fluid, which surrounds and protects the fetus in the uterus (womb). After rupture, the amniotic fluid leaks out of the uterus, through the vagina.

Women with PROM usually experience a painless gush of fluid leaking out from the vagina, but sometimes a slow steady leakage occurs instead.

When premature rupture of membranes occurs at or after 37 weeks completed gestational age (full-term or term), there is minimal risk to the fetus and labor typically starts soon after.

If rupture occurs before 37 weeks, it is called preterm premature rupture of membranes (PPROM), and the fetus and mother are at greater risk for complications. PPROM causes one-third of all preterm births, and babies born preterm (before 37 weeks) can suffer from the complications of prematurity, including death.

Premature rupture of the membranes provides a path for bacteria to enter the womb and puts both the mother and fetus at risk for life-threatening infection. Low levels of fluid around the fetus also increase the risk of umbilical cord compression and can interfere with lung and body formation in early pregnancy.

Women who suspect they might have experienced premature rupture of membranes should be evaluated promptly in the hospital to determine whether a rupture of membranes has indeed occurred, and to be treated appropriately to avoid infection and other complications.

"Maternal floor infarcts" are "not" considered to be true placental infarcts, as they result from deposition of fibrin around the chorionic villi, i.e. perivillous fibrin deposition.

Uterine atony is a loss of tone in the uterine musculature. Normally, contraction of the uterine muscles during labor compresses the blood vessels and reduces flow, thereby increasing the likelihood of coagulation and preventing hemorrhage. A lack of uterine muscle contraction, however, can lead to an acute hemorrhage, as the uterine blood vessels are not sufficiently compressed. Clinically, 75-80% of postpartum hemorrhages are due to uterine atony.

A staging system proposed by fetal surgeon Dr. Ruben Quintero is commonly used to classify the severity of TTTS.

Stage I: A small amount of amniotic fluid (oligohydramnios) is found around the donor twin and a large amount of amniotic fluid (polyhydramnios) is found around the recipient twin.

Stage II: In addition to the description above, the ultrasound is not able to identify the bladder in the donor twin.

Stage III: In addition to the characteristics of Stages I and II, there is abnormal blood flow in the umbilical cords of the twins.

Stage IV: In addition to all of the above findings, the recipient twin has swelling under the skin and appears to be experiencing heart failure (fetal hydrops).

Stage V: In addition to all of the above findings, one of the twins has died. This can happen to either twin. The risk to either the donor or the recipient is roughly equal & is quite high in Stage II or higher TTTS.

The Quintero staging does not provide information about prognosis, and other staging systems have been proposed.

It is diagnosed by a microscopic examination of the placenta.

Commonly used criteria from Altshuler are: "a minimum of 10 villi, each with 10 or more vascular channels, in 10 or more areas of 3 or more random, non-infarcted placental areas when using a ×10 ocular." The Altshuler criteria are not theoretically rigorous, as they do not define the area. Normal villi have up to five vascular channels.

Placental villous immaturity, also villous immaturity and villous dysmaturity, is chorionic villous development that is inappropriate for the gestational age.

It is associated with diabetes mellitus

and fetal death near term, i.e. intrauterine demise close to the normal gestational period.