"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.

Taking aspirin is associated with a 1% to 5% reduction in pre-eclampsia and a 1% to 5% reduction in premature births in women at high risk. The World Health Organization recommends low-dose aspirin for the prevention of pre-eclampsia in women at high risk and recommends it be started before 20 weeks of pregnancy. The United States Preventive Services Task Force recommends a low-dose regimen for women at high risk beginning in the 12th week. Benefits are less if started after 16 weeks.

Supplementation with a balanced protein and energy diet does not appear to reduce the risk of pre-eclampsia. Further, there is no evidence that changing salt intake has an effect.

Supplementation with antioxidants such as vitamin C, D and E has no effect on pre-eclampsia incidence; therefore, supplementation with vitamins C, E, and D is not recommended for reducing the risk of pre-eclampsia.

Calcium supplementation of at least 1 gram per day is recommended during pregnancy as it prevents preeclampsia where dietary calcium intake is low, especially for those at high risk. Low selenium status is associated with higher incidence of pre-eclampsia.

The four goals of the treatment of eclampsia are to stop and prevent further convulsions, to control the elevated blood pressure, to deliver the baby as promptly as possible, and to monitor closely for the onset of multi-organ failure.

Detection and management of pre-eclampsia is critical to reduce the risk of eclampsia. The USPSTF recommends regular checking of blood pressure through pregnancy in order to detect preeclampsia. Appropriate management of women with pre-eclampsia generally involves the use of magnesium sulphate to prevent convulsions.

Although the risk of placental abruption cannot be eliminated, it can be reduced. Avoiding tobacco, alcohol and cocaine during pregnancy decreases the risk. Staying away from activities which have a high risk of physical trauma is also important. Women who have high blood pressure or who have had a previous placental abruption and want to conceive must be closely supervised by a doctor.

The risk of placental abruption can be reduced by maintaining a good diet including taking folic acid, regular sleep patterns and correction of pregnancy-induced hypertension.

It is crucial for women to be made aware of the signs of placental abruption, such as vaginal bleeding, and that if they experience such symptoms they must get into contact with their health care provider/the hospital "without any delay".

The prognosis of this complication depends on whether treatment is received by the patient, on the quality of treatment, and on the severity of the abruption. Outcomes for the baby also depend on the gestational age.

In the Western world, maternal deaths due to placental abruption are rare. The fetal prognosis is worse than the maternal prognosis; approximately 12% of fetuses affected by placental abruption die. 77% of fetuses that die from placental abruption die before birth; the remainder die due to complications of preterm birth.

Without any form of medical intervention, as often happens in many parts of the world, placental abruption has a high maternal mortality rate.

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.

There is no effective pharmacological treatment for retained placenta. It is useful ensuring the bladder is empty. However, ergometrine should not be given as it causes tonic uterine contractions which may delay placental expulsion. Controlled cord traction has been recommended as a second alternative after more than 30 minutes have passed after stimulation of uterine contractions, provided the uterus is contracted. Manual extraction may be required if cord traction also fails, or if heavy ongoing bleeding occurs. Very rarely a curettage is necessary to ensure that no remnants of the placenta remain (in rare conditions with very adherent placenta such as a placenta accreta).

However, in birth centers and attended home birth environments, it is common for licensed care providers to wait for the placenta's birth up to 2 hours in some instances.

Some evidence suggests that magnesium sulfate administered to mothers prior to early preterm birth reduces the risk of cerebral palsy in surviving neonates. Due to the risk of adverse effects treatments may have, it is unlikely that treatments to prevent neonatal strokes or other hypoxic events would be given routinely to pregnant women without evidence that their fetus was at extreme risk or has already suffered an injury or stroke. This approach might be more acceptable if the pharmacologic agents were endogenously occurring substances (those that occur naturally in an organism), such as creatine or melatonin, with no adverse side-effects.

Because of the period of high neuronal plasticity in the months after birth, it may be possible to improve the neuronal environment immediately after birth in neonates considered to be at risk of neonatal stroke. This may be done by enhancing the growth of axons and dendrites, synaptogenesis and myelination of axons with systemic injections of neurotrophins or growth factors which can cross the blood–brain barrier.

It is the goal of evolutionary medicine to find treatments for diseases that are informed by the evolutionary history of a disease. It has been suggested that gestational hypertension is linked to insulin resistance during pregnancy. Both the increase in blood sugar that can lead to gestational diabetes and the increase in blood pressure that can lead to gestational hypertension are mechanisms that mean to optimize the amount of nutrients that can be passed from maternal tissue to fetal tissue. It has been suggested that techniques used to combat insulin insensitivity might also prove beneficial to those suffering from gestational hypertension. Measures to avoid insulin resistance include avoiding obesity before pregnancy, minimizing weight gain during pregnancy, eating foods with low glycemic indexes, and exercising.

Well-designed clinical trials for stroke treatment in neonates are lacking Recent clinical trials show that therapeutic intervention by brain cooling beginning up to 6 hours after perinatal asphyxia reduces cerebral injury and may improve outcome in term infants, indicating cell death is both delayed and preventable

Pancaspase inhibition and Casp3-selective inhibition have been found to be neuroprotective in neonatal rodents with models of neonatal brain injury, which may lead to pharmacological intervention In a study done by Chauvier, "et al.", it is suggested that a Caspase inhibitor, TRP601, is a candidate for neuroprotective strategy in prenatal brain injury conditions. They found a lack of detectable side effects in newborn rodents and dogs. This may be a useful treatment in combination with hypothermia.

MRI has proven valuable for defining brain injury in the neonate, but animal models are still needed to identify causative mechanisms and to develop neuroprotective therapies. In order to model human fetal or neonatal brain injury, one needs a species in which a similar proportion of brain development occurs in utero, the volume of white to grey matter is similar to the human brain, an insult can be delivered at an equivalent stage of development, the physiological outcome of the insult can be monitored, and neurobehavioral parameters can be tested. Some animals that meet these criteria are sheep, non-human primates, rabbits, spiny mice, and guinea pigs.

Transplantation of neural stem cells and umbilical cord stem cells is currently being trialed in neonatal brain injury, but it is not yet known if this therapy is likely to be successful.

Placental insufficiency can affect the fetus, causing Fetal distress. Placental insufficiency may cause oligohydramnios, preeclampsia, miscarriage or stillbirth. Placental insufficiency is most frequent cause of asymmetric IUGR.

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

It is recommended that women with vasa previa should deliver through elective cesarean prior to rupture of the membranes. Given the timing of membrane rupture is difficult to predict, elective cesarean delivery at 35–36 weeks is recommended. This gestational age gives a reasonable balance between the risk of death and that of prematurity. Several authorities have recommended hospital admission about 32 weeks. This is to give the patient proximity to the operating room for emergency delivery should the membranes rupture. Because these patients are at risk for preterm delivery, it is recommended that steroids should be given to promote fetal lung maturation. When bleeding occurs, the patient goes into labor, or if the membranes rupture, immediate treatment with an emergency caesarean delivery is usually indicated.

Gestational hypertension is one of the most common disorders seen in human pregnancies. Though relatively benign on its own, in roughly half of the cases of gestational hypertension the disorder progresses into preeclampsia, a dangerous condition that can prove fatal to expectant mothers. However, gestational hypertension is a condition that is fairly rare to see in other animals. For years, it has been the belief of the scientific community that gestational hypertension and preeclampsia were relatively unique to humans, although there has been some recent evidence that other primates can also suffer from similar conditions, albeit due to different underlying mechanisms. The underlying cause of gestational hypertension in humans is commonly believed to be an improperly implanted placenta. Humans have evolved to have a very invasive placenta to facilitate better oxygen transfer from the mother to the fetus, to support the growth of its large brain.

In last decade, similar to myocardial infarction treatment, thrombolytic drugs were introduced in the therapy of cerebral infarction. The use of intravenous rtPA therapy can be advocated in patients who arrive to stroke unit and can be fully evaluated within 3 h of the onset.

If cerebral infarction is caused by a thrombus occluding blood flow to an artery supplying the brain, definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die. In increasing numbers of primary stroke centers, pharmacologic thrombolysis with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery.

Another intervention for acute cerebral ischaemia is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective, though no differences have been found between newer and older versions of the devices. The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.

Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute cerebral ischaemia. In a systematic review of six uncontrolled, single-center trials, involving a total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90-98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable. This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.

If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after cerebral infarction. Carotid endarterectomy is also indicated to decrease the risk of cerebral infarction for symptomatic carotid stenosis (>70 to 80% reduction in diameter).

In tissue losses that are not immediately fatal, the best course of action is to make every effort to restore impairments through physical therapy, cognitive therapy, occupational therapy, speech therapy and exercise.

of fetal membranes (afterbirth) is observed more frequently in cattle than in other animals. In a normal condition, a cow’s placenta is expelled within a 12-hour period after calving.

Chorangiosis is a placental pathology characterized by an abundance of blood vessels within the chorionic villi.

The first step in management of uterine atony is uterine massage. The next step is pharmacological therapies, the first of which is oxytocin, used because it initiates rhythmic contractions of the uterus, compressing the spiral arteries which should reduce bleeding. The next step in the pharmacological management is the use of methylergometrine, which is an ergot derivative, much like that use in the abortive treatment of migraines. Its side effect of hypertension means its use should not be used in those with hypertension or pre-eclampsia. In those with hypertension, the use of prostaglandin F is indicated (but beware of its use in patients with asthma).

Another option Carbetocin and Carboprost where Oxytocin and ergometrin is inappropriate.

Typically, tissue plasminogen activator may be administered within three to four-and-a-half hours of stroke onset if the patient is without contraindications (i.e. a bleeding diathesis such as recent major surgery or cancer with brain metastases). High dose aspirin can be given within 48 hours. For long term prevention of recurrence, medical regimens are typically aimed towards correcting the underlying risk factors for lacunar infarcts such as hypertension, diabetes mellitus and cigarette smoking. Anticoagulants such as heparin and warfarin have shown no benefit over aspirin with regards to five year survival.

Patients who suffer lacunar strokes have a greater chance of surviving beyond thirty days (96%) than those with other types of stroke (85%), and better survival beyond a year (87% versus 65-70%). Between 70% and 80% are functionally independent at 1 year, compared with fewer than 50% otherwise.

Occupational Therapy and Physical Therapy interventions are used in the rehabilitation of lacunar stroke. A physiotherapy program will improve joint range of motion of the paretic limb using passive range of motion exercises. When increases in activity are tolerated, and stability improvements are made, patients will progress from rolling to side-lying, to standing (with progressions to prone, quadruped, bridging, long-sitting and kneeling for example) and learn to transfer safely (from their bed to a chair or from a wheel chair to a car for example). Assistance and ambulation aids are used as required as the patient begins walking and lessened as function increases. Furthermore, splints and braces can be used to support limbs and joints to prevent complications such as contractures and spasticity. The rehabilitation healthcare team should also educate the patient and their family on common stroke symptoms and how to manage an onset of stroke. Continuing follow-up with a physician is essential so that the physician may monitor medication dosage and risk factors.

In places where a Caesarean section could not be performed due to the lack of a surgeon or equipment, infant could be delivered vaginally. There were two ways of doing this with a placenta previa:

- The baby's head can be brought down to the placental site (if necessary with Willet's forceps or a vulsellum) and a weight attached to its scalp

- A leg can be brought down and the baby's buttocks used to compress the placental site

In rare cases, inherited bleeding disorders, like hemophilia, von Willebrand disease (vWD), or factor IX or XI deficiency, may cause severe postpartum hemorrhage, with an increased risk of death particularly in the postpartum period. The risk of postpartum hemorrhage in patients with vWD and carriers of hemophilia has been found to be 18.5% and 22% respectively. This pathology occurs due to the normal physiological drop in maternal clotting factors after delivery which greatly increases the risk of secondary postpartum hemorrhage.

Another bleeding risk factor is thrombocytopenia, or decreased platelet levels, which is the most common hematological change associated with pregnancy induced hypertension. If platelet counts drop less than 100,000 per microliter the patient will be at a severe risk for inability to clot during and after delivery.

Foetal demise occurs if the circulating blood volume is decreased significantly. The critical factor deciding the prognosis is the site of the hematoma and not the volume. If discovered antinatally, serial USG and/or Doppler scans is indicated to monitor the size of the hematoma and well-being of the foetus.