"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.

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.

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.

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.

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.

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.

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.

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.

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

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).

HELLP syndrome is defined as hemolysis (microangiopathic), elevated liver enzymes (liver dysfunction), and low platelets (thrombocytopenia). This condition may occur in 10–20% of patients with severe pre-eclampsia and eclampsia and is associated with increased maternal and fetal morbidity and mortality. In 50% of instances, HELLP syndrome develops preterm, while 20% of cases develop in late gestation and 30% during the post-partum period.

Symptoms of cerebral infarction are determined by the parts of the brain affected. If the infarct is located in primary motor cortex, contralateral hemiparesis is said to occur. With brainstem localization, brainstem syndromes are typical: Wallenberg's syndrome, Weber's syndrome, Millard-Gubler syndrome, Benedikt syndrome or others.

Infarctions will result in weakness and loss of sensation on the opposite side of the body. Physical examination of the head area will reveal abnormal pupil dilation, light reaction and lack of eye movement on opposite side. If the infarction occurs on the left side brain, speech will be slurred. Reflexes may be aggravated as well.

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

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.

There are various classification systems for a cerebral infarction.

- The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms. Based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.

- The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).

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

Breus' mole (Ova tuberculosa, massive mole) is a massive, subchorionic, tuberous hematoma, formed out of maternal blood in the uterus in pregnancy. It was first described by Karl Breus in 1892.

Besides placenta previa and placental abruption, uterine rupture can occur, which is a very serious condition leading to internal or external bleeding. Bleeding from the fetus is rare, but may occur with two conditions called vasa previa and velamentous umbilical cord insertion where the fetal blood vessels lie near the placental insertion site unprotected by Wharton's jelly of the cord. Occasionally this condition can be diagnosed by ultrasound. There are also tests to differentiate maternal blood from fetal blood which can help in determining the source of the bleed.

Abnormal bleeding after delivery, or postpartum hemorrhage, is the loss of greater than 500 ml of blood following vaginal delivery, or 1000 ml of blood following cesarean section. Other definitions of excessive postpartum bleeding are hemodynamic instability, drop of hemoglobin of more than 10%, or requiring blood transfusion. In the literature, primary postpartum hemorrhage is defined as uncontrolled bleeding that occurs in the first 24 hours after delivery while secondary hemorrhage occurs between 24 hours and six weeks.

Clinically, Breus' mole may be asymptomatic, or may present with signs of decreased blood flow to the foetus such as growth restriction and foetal distress. Postnatally, Breus' mole is found in placental examination following live birth or spontaneous abortion. Breus' mole is diagnosed antinatally by ultrasound, where a thick multilobulated hematoma can be seen beneath the chorion. Occasionally, subchorial thrombohematoma may later become intraplacental, making its diagnosis difficult. The mole may be echogenic or hypoechoic depending upon the amount of fresh blood present in it. Breus' mole should be differentiated from vesicular mole and missed abortion in an ultrasound examination.

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.

Each of the 5 classical lacunar syndromes has a relatively distinct symptom complex. Symptoms may occur suddenly, progressively, or in a fluctuating (e.g., the capsular warning syndrome) manner. Occasionally, cortical infarcts and intracranial hemorrhages can mimic lacunar infarcts, but true cortical infarct signs (aphasia, visuospatial neglect, gaze deviation, and visual field defects) are always absent. The 5 classic syndromes are as follows:

A silent lacunar infarction (SLI) is one type of silent stroke which usually shows no identifiable outward symptoms thus the term "silent". Individuals who suffer a SLI are often completely unaware they have suffered a stroke. This type of stroke often causes lesions in the surrounding brain tissue that are visibly detected via neuroimaging techniques such as MRI and computerized axial tomography (CT scan). Silent strokes, including silent lacunar infarctions, have been shown to be much more common than previously thought, with an estimated prevalence rate of eleven million per year in the United States. Approximately 10% of these silent strokes are silent lacunar infarctions. While dubbed "silent" due to the immediate lack of classic stroke symptoms, SLIs can cause damage to the surrounding brain tissue (lesions) and can affect various aspects of a persons mood, personality, and cognitive functioning. A SLI or any type of silent stroke places an individual at greater risk for future major stroke.

A neonatal stroke is one that occurs in the first 28 days of life, though a late presentation is not uncommon (as contrasted with perinatal stroke, which occurs from 28 weeks gestation through the first 7 days of life). 80% of neonatal strokes are ischemic, and their presentation is varied, making diagnosis very difficult. The most common manifestation of neonatal strokes are seizures, but other manifestations include lethargy, hypotonia, apnoea, and hemiparesis. Seizures can be focal or generalized in nature. Stroke accounts for about 10% of seizures in term neonates.

Neonatal strokes occur in approximately 1 in 4000 births, but this number is likely much higher due to lack of noticeable symptoms at time of birth. They generally present with seizures, but only half to three quarters of cases have identifiable causes. Diagnosis often occurs around 36 hours after onset of neonatal stroke due to the interval between stroke and clinical presentation, if any occurs at all. Neonatal strokes can be confirmed with neuroimaging or neuropathalogical studies, and other various imaging techniques can be used to diagnose neonatal strokes, such as ultrasound, Doppler sonography, computerized tomography (CT) scan, CT angiography, and multimodal MR.