Complications during pregnancy: Pathology review

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Case Study0:00–2:04

26 year-old Effie is brought to the emergency department with severe lower abdominal pain and bloody vaginal discharge that began a few hours ago.
Her last menstrual period was 7 weeks ago. She has been sexually active with multiple partners and uses condoms on occasion.
Her past medical history is significant for pelvic inflammatory disease. On examination, her blood pressure is 80/40 mmHg and her pulse is 130 beats per minute.
She is pale and her extremities are cold and clammy. Next to her, there’s also 37-year-old Kate who came in noting an abrupt onset of abdominal pain and continuous vaginal bleeding.
She is going through week 28 of her fourth pregnancy and was involved in a car crash a couple of hours ago, but did not immediately seek medical care.
On presentation, fetal heart rate and movement are significantly diminished. Laboratory studies reveal low platelets, prolonged PT and PTT and elevated d-dimers.
Peripheral blood smear shows schistocytes.Based on their initial presentation, both Effie and Kate have a form of pregnancy complication.Now, the most common medical complication of pregnancy is hypertensive disorders of pregnancy.
These are diseases that cause high blood pressure during pregnancy, either a systolic blood pressure higher than 140 mmHg, or a diastolic blood pressure higher than 90 mmHg, or both.
So, when hypertension is diagnosed before 20 weeks gestation, it’s usually chronic hypertension, meaning that it’s not due to pregnancy.
After 20 weeks gestation, new onset hypertension without proteinuria or damage to other organs is gestational hypertension.
Now if hypertension gets severe, meaning systolic blood pressure of 160 mmHg or greater and/or diastolic blood pressure of 110 mmHg or greater, it can often lead to organ damage.

Hypertensive Pregnancy D2:04–9:15

One key thing to look out for is the presence of proteinuria, or excessive amounts of protein in the urine, which is a marker of kidney damage.
Other affected organs include the brain and liver. Now, if the hypertension coexists with proteinuria or other organ dysfunction, then it’s called preeclampsia.
Preeclampsia is more common during a person’s first pregnancy, in pregnancies with multiple gestations, or in mothers 35 years or older.
Other risk factors include having pre-existing hypertension, diabetes, chronic kidney disease or autoimmune disorders like the antiphospholipid syndrome.
The exact reason why preeclampsia develops is unclear, but a high yield pathophysiologic feature though is the development of an abnormal placenta.
Normally, during pregnancy, the spiral arteries dilate to 5-10 times their normal size and develop into large uteroplacental arteries that can deliver large quantities of blood to the developing fetus.
In preeclampsia, these uteroplacental arteries undergo fibrosis, causing them to narrow, which means less blood gets to the placenta.
This hypoperfused placenta starts releasing proinflammatory proteins. These then get into the mother’s circulation and cause the endothelial cells that line her blood vessels to become dysfunctional.
Endothelial cell dysfunction causes vasoconstriction or narrowing of the blood vessels and also affects the kidneys in a way that makes them retain more salt, both of which result in hypertension.
Vasoconstriction will also lead to reduced blood flow to the kidneys, which are particularly susceptible to ischemia and can cause glomerular damage leading to proteinuria.
The high blood pressure can also cause placental abruption, where the placenta detaches prematurely from the uterine wall.
Next, the increased pressure inside blood vessels can cause endothelial injury which leads to the formation of lots of tiny thrombi in the microvasculature.
This process uses up massive amounts of platelets so there’s an increased risk of bleeding. To make things worse, these tiny blood clots are like large rocks in a river and damages the red blood cells trying to move past them, so there’s extrinsic hemolytic anemia.
Specifically, red blood cells get split into smaller fragments called schistocytes. And bare in mind that these schistocytes are visible on peripheral blood smear.
If all this wasn’t bad enough, the thrombi can block blood flow to the liver, causing severe liver injury which can cause an elevation in liver enzymes.
Together all these make up HELLP syndrome, H for hemolysis, EL for elevated liver enzymes, and LP for low platelets. The damaged liver swells up and in some cases, as the condition worsens, the liver capsule may rupture leading to a subcapsular hematoma.
This can present as right upper quadrant or epigastric pain. But if a lot of blood is lost, it can also lead to severe hypotension.
Now, in other cases, HELLP syndrome can develop into disseminated intravascular coagulation, or DIC. That’s because damage to the endothelium can lead to the release of tissue factor, which triggers the coagulation cascade.
And this, except for platelets which are already low, also depletes coagulation factors, making it even harder to establish hemostasis.
This may present as bleeding from mucosal surfaces, intravenous lines or incision sites, if there are any. Now, what’s high-yield is that in terms of lab work, remember there’s decreased coagulation factors which means a prolonged prothrombin time, or PT, and prolonged partial thromboplastin time, or PTT.
Another important hint is elevated d-dimer levels which come from clot lysis. So an individual with ΗΕLLP plus prolonged PT and PTT and elevated d-dimers is having DIC!
Finally, endothelial injury in preeclampsia increases vascular permeability, which is when water is allowed to slip out of blood vessels between neighboring endothelial cells and get into the tissues.
Because there’s also a loss of protein from the blood due to the proteinuria, even more fluid moves from the blood vessels into the tissues.
And this causes generalized edema which is often seen in the legs, face and hands; pulmonary edema which can cause cough and shortness of breath; and cerebral edema which can cause headache, confusion, and seizures.
For your exams, what’s high-yield to remember is that when a female with preeclampsia develops seizures, we call it eclampsia.
Alright, now, let’s discuss treatment. The antihypertensive medications that can be used for chronic hypertension in pregnancy or gestational hypertension are hydralazine, methyldopa, labetalol, or nifedipine.
To remember this, you can use the mnemonic Hypertensive Moms Love Newborns. In preeclampsia and eclampsia, in addition to antihypertensives, IV magnesium sulfate is also given to prevent or treat seizures.
But since all of the problems of preeclampsia and eclampsia stem from placental dysfunction, it’s important to know that the definitive treatment is delivery of the fetus and placenta.
Especially in the case of eclampsia or HELLP syndrome, delivery has to be immediate.Okay, next, there is gestational trophoblastic disease, which includes both benign and malignant proliferations of placental or trophoblast cells.
At the benign end of the spectrum, there’s molar pregnancy, which is also called hydatidiform moles. At the malignant end, there’s invasive moles, which can arise from benign moles and choriocarcinoma, which is placental cancer that most frequently occurs in the absence of a molar pregnancy.

Gestational Trophoblasti9:15–17:31

Now, moles result from errors in normal fertilization. Normally, at fertilization, a single egg with 23 chromosomes fuses with a single sperm with 23 chromosomes, resulting in a new cell with 46 chromosomes.
This can go wrong in two ways, so we have two kinds of moles: complete, or classic, and incomplete, or partial mole. Both lead to an abnormal proliferation of placental or trophoblast cells.
The difference is that a complete mole appears when a chromosomally empty egg fuses with a normal sperm, and the sperm genetic material duplicates to form a 46 chromosome cell.
However, it doesn’t have both maternal and paternal chromosomes, so the mole develops into a mass rather than developing into a fetus.
An incomplete mole, on the other hand, appears when a normal egg is fertilized by two sperm - which forms an organism with 69 chromosomes, that usually develops into non-viable fetal parts.
What’s extremely high-yield is that with a complete mole, the placenta secretes a huge amount of hCG. So affected females initially present with signs of pregnancy, like missed periods.
Vaginal bleeding is another sign, which may range from light spotting to heavy bleeding, and parts of the mole may even be eliminated, and they look like grapes, or cherry-like clusters.
Additionally, for unclear reasons, this huge amount of hCG can lead to early preeclampsia, meaning hypertension and proteinuria before 20 weeks of gestation.
Don’t confuse that with chronic hypertension, which is hypertension without proteinuria before 20 weeks of gestation. At the same time, excess hCG can lead to hyperemesis gravidarum, which is extreme nausea and vomiting which can lead to severe dehydration.
Interestingly, hCG has a subunit that’s similar to TSH, so it can cause symptoms of hyperthyroidism, like insomnia, anxiety, tachycardia, and palpitations.
Too much hCG can also result in the growth of theca lutein cysts in the ovaries, which can cause symptoms like pelvic pain or pressure on the affected side.Finally, since the mole grows much faster than a normal pregnancy would, a physical examination shows a uterus that’s too big for gestational age.
Histologically, we’ll see fingerlike projections called chorionic villi which contain tiny arterioles and venules. Now, most villi will be hydropic, meaning swollen and edematous.
And all around the villi, there’ll be diffuse and circumferential proliferation of large trophoblast cells. These can be either cytotrophoblasts with central nuclei and pale cytoplasm, or syncytiotrophoblasts that have multiple nuclei and darker cytoplasm.
Another thing we can do is stain for the p57 protein. This is produced by a gene that’s only expressed on maternal cells.
So a complete mole will stain negative for p57. Now, a very high yield test result you must remember is that a transvaginal ultrasound will show no fetal parts.
Instead, there will be a diffuse echogenic pattern, called a “snowstorm” pattern, sometimes described as looking like a "clusters of grapes".
This results from the presence of abnormal placental villi and blood clots that accumulate in the uterus. An incomplete mole also secretes more hCG than normal, but not quite as much as a complete mole.
So while missed periods and vaginal bleeding are present, the uterus is not larger than expected for gestational age, and there are no symptoms of hCG hyperstimulation like early preeclampsia, hyperemesis gravidarum, hyperthyroidism, or ovarian cysts.
On histological examination, we’ll also see villi, but, unlike complete moles, only some of them will be hydropic. Another key distinction is that p57 staining will be positive.
On a transvaginal ultrasound, fetal parts will be visible. Treatment for both complete and incomplete moles is uterine evacuation through suction curettage and methotrexate.
Methotrexate is very frequently tested, so it’s important to know that it is an antimetabolite medication that is structurally similar to folic acid and is toxic to the rapidly dividing cells of the embryo.
For your test, remember that it’s essential to monitor the hCG levels afterwards until they go back to normal. If that doesn’t happen, we can suspect an invasive mole or choriocarcinoma.
Okay, so, a high-yield fact is that both complete and incomplete moles are benign conditions, but can develop into malignant tumors, like invasive moles or, in rare cases, choriocarcinomas.
In invasive moles, the villi invade deeper into the myometrium, which is the muscular wall of the uterus. In fact complete moles have a 15-20% risk of developing into invasive moles, whereas with incomplete moles, the risk is under 5%.
However, it’s high-yield to know that most choriocarcinomas develop during or after a non-molar pregnancy. Broadly speaking, choriocarcinomas are usually quite small but if they get large enough, they can present with lower abdominal pain or pressure.
They are also extremely aggressive, so they have a high chance of spreading via the circulation. A high-yield fact is that a very common location for metastasis is the lungs, causing shortness of breath and hemoptysis.
On a chest x-ray, this shows up with the characteristic “cannonball metastases”. These are multiple, large, well-circumscribed, and round metastatic masses.
Metastatic disease to the brain may also cause headache, dizziness, nausea, slurred speech or visual disturbances. Just like benign moles, choriocarcinomas also secrete hCG and this can cause symptoms of hyperthyroidism, as well as bilateral, multiple theca-lutein ovarian cysts.
For your test, remember that under the microscope, choriocarcinomas look very similar to moles, so they have cytotrophoblasts and syncytiotrophoblasts.
But the key distinction is that there are no villi. The main treatment is methotrexate.Alright, now let’s look at ectopic pregnancy.
Normally, a fertilized egg travels through the fallopian tube and implants in the uterus, but in an ectopic pregnancy, the fertilized egg ends up implanting somewhere else.

Ectopic Pregnancy17:31–26:25

For your exams, remember that the most common site is the ampulla of the fallopian tube, but it can also occur on various surfaces, like the ovaries.
The cause of an ectopic pregnancy is often unknown, but there are well known risk factors. A very high-yield one is pelvic inflammatory disease, since the inflammation results in scarring and adhesions, particularly in the fallopian tubes, thus, blocking the fertilized egg from traveling down into the uterus.
Scar tissue can also build up in the fallopian tubes as a result of previous surgery involving the fallopian tubes, endometriosis, advanced age, and smoking, which is thought to damage the epithelium lining the fallopian tubes.
The individual will frequently also have a history of prior ectopic pregnancy or infertility, which may indicate some anatomical abnormality of the fallopian tubes.
Okay, now, after implantation, the embryo begins developing and growing just like it would in a normal pregnancy. So, initial symptoms will include a missed menstrual period and other body changes like nausea and fullness of breasts, which are typically seen in early pregnancy.
What we fear the most though is that, if the ectopic pregnancy runs out of space in the fallopian tube, it may cause it to rupture.
A ruptured ectopic pregnancy will present with a sudden onset of severe lower abdominal pain which is occasionally accompanied with light vaginal bleeding.
If there’s massive hemorrhage into the abdominal cavity, there may also be hemodynamic instability or even hemorrhagic shock, meaning hypotension, tachycardia and even syncope or fainting.
So, if a test question describes a female of child bearing age with sudden, severe lower abdominal pain, vaginal bleeding and, in severe cases, signs of shock, as well as a history of missed menstrual periods, think of ruptured ectopic pregnancy at the top of your differentials!Diagnosis of an ectopic pregnancy can vary based on the hemodynamic status.
So, if the individual is hemodynamically unstable, then immediate surgery is needed to diagnose and treat the ectopic pregnancy.
If they are hemodynamically stable, then serial measurements of the serum levels of hCG can be done. For your exams, it’s high-yield to remember that in a normal intrauterine pregnancy, the hCG levels are doubling every 48 hours.
If this trend does not occur, then we can suspect an ectopic pregnancy. In addition, transvaginal ultrasound can detect the presence of an intrauterine pregnancy by week 5 or 6.
It’s also important to know that if uterine curettage or scraping of the uterus lining is performed, it would reveal changes in the endometrium due to progesterone secretion but no embryonic or trophoblastic tissue.Treatment, in a hemodynamically stable individual whose ectopic pregnancy is diagnosed early, meaning within the first 6 weeks of pregnancy, typically includes termination of the pregnancy with methotrexate.
In contrast, in a hemodynamically unstable individual, a salpingostomy can be done. That’s where the fallopian tube is opened up to remove the ectopic pregnancy, and then closed at the end of surgery.
Alternatively, a salpingectomy can be done, which is where the fallopian tube is completely removed.Okay, next, there’s placental abruption, also known as, “abruptio placentae”.
So, normally, the placenta has two layers. There’s the maternal layer, or decidua basalis, and the fetal layer, called the chorion.
Placental abruption happens when there is a partial or complete separation of the uterine wall and decidua basalis. Risk factors include acute blunt trauma, like from a car crash, fall, or domestic violence.
This can happen because the placenta is less elastic than the uterus, so the strong forces from traumatic events can cause the placenta to sheer away from the uterine wall.
Also commonly tested risk factors, which you should look for in a question stem, include smoking or chronic hypertension, which results in degeneration of the uterine arteries that supply the placenta.
Remember that severe preeclampsia can also cause placental abruption. Certain illicit drugs, like cocaine and methamphetamine can also cause significant vasoconstriction of the placental blood vessels and an abrupt increase in blood pressure, increasing the risk of an abruption.
Other risk factors include multiparity or multiple pregnancies and a maternal age over 35 years old. Symptoms of placental abruption include an abrupt onset of abdominal pain, which usually happens in the third trimester, meaning after about 20 weeks of pregnancy.
Now, if the separation is near the margin of the placenta, the individual might also have continuous vaginal bleeding, and this is called an apparent abruption.
But if the separation is more central, the abruption might be concealed, meaning there might be a pocket of blood that stays concealed between the decidua basalis and the uterine wall.
And in this case, it’s often identified later when it causes complications. So, placental abruption can lead to serious blood loss from large vessels, causing life threatening maternal and fetal complications.
Maternal complications include hypovolemic shock, presenting as hypotension, tachycardia or syncope, and Sheehan’s syndrome which is a type of perinatal pituitary necrosis that results from hypovolemia.
The telltale sign of Sheehan’s syndrome is agalactorrhea, where the individual is not able to produce enough or any breast milk, due to a lack of prolactin.
Another extremely popular concept among the examiners is that placental abruption is the most common cause of disseminated intravascular coagulation, or DIC.
That’s because the abruption causes the release of large quantities of tissue factor from the decidua basalis layer which results in extensive clotting in blood vessels throughout the body.
So what’s high-yield is that in terms of lab work, we’ll have low platelets, decreased coagulation factors leading to prolonged PT and PTT and elevated d-dimer levels from clot lysis.
So an individual with placental abruption, increased bleeding tendency and labs showing schistocytes, low platelets, prolonged PT and PTT and elevated d-dimers is having DIC!
On another note, fetal complications include intrauterine hypoxia and asphyxia because the fetus is no longer receiving adequate placental perfusion.
For your exams, a hint for that is fetal bradycardia or heart rate lower than 110 beats per minute and diminished or absent fetal movement.Diagnosis is made based on ultrasound, which can identify the position of the placenta.
For treatment, if the hemorrhage is severe or if there is evidence of fetal compromise, an emergency cesarean section is needed.Next, there’s vasa previa.
In this case, fetal blood vessels, meaning the two umbilical arteries and umbilical vein, run over or close to the cervical os.
For your exams, what’s high-yield is that it is commonly associated with velamentous umbilical cord insertion. Normally, the umbilical cord inserts into the middle of the placenta.
But in velamentous insertion, the umbilical cord inserts in the fetal or chorioamniotic membranes and then travels within the membranes to the placenta.

Vasa Previa26:25–28:12

The result is that umbilical vessels are exposed since they are not protected by Wharton's jelly, which is a yellow, gooey substance.
And when that’s combined with vasa previa, meaning that the vessels are near the cervical os, they are especially vulnerable to rupture.
So upon rupture of the membranes, these vessels rupture as well, causing massive, painless bleeding. Now, depending on the extent of blood loss, complications on the maternal end can be hypovolemic shock, with hypotension, tachycardia or syncope, and Sheehan syndrome with agalactorrhea, while fetal complications can include hypoxia, manifesting as bradycardia, or even fetal death.
So the classic triad for vasa previa is membrane rupture, painless vaginal bleeding and fetal bradycardia or fetal death.
Thanks to transvaginal ultrasound, diagnosis can now be made during pregnancy, before rupture of the membranes occurs. In this case, treatment consists of cesarean section.Moving on to placenta previa.
Normally the placenta implants in the upper uterus, but in placenta previa, it implants in the lower uterus. The reason why this happens is unclear but one hypothesis is that the placenta implants lower down when the endometrium in the upper uterus is not well vascularized.

Placenta Previa28:12–31:10

In fact, endometrial damage from things like a previous cesarean section, abortion, uterine surgery, multiparity, advanced maternal age or smoking can decrease vascularization and increase the risk of placenta previa.
In other cases, risk factors include having multiple placentas or a placenta with a larger than normal surface area, which can both happen with twins or triplets.
Now, for your exam, it’s high-yield to know that placenta previa is classified by how close the placenta is to the cervical os.
So, it can be complete where the placenta completely covers the cervical os; partial where the placenta partially covers the cervical os; or marginal where the edge of the placenta extends to within 2 cm of the cervical os.The classic presentation of placenta previa is a sudden onset of painless bright red bleeding that typically happens in the third trimester, meaning after 20 weeks gestation.
That’s because as the pregnancy progresses, the lower uterine segment grows, and if the placenta is in the lower uterus, this growth disrupts the placental blood vessels, which can cause bleeding.
The amount of bleeding can vary, and it can be intermittent or continuous, sometimes increasing during labor because of uterine contractions and cervical dilation.
Notice though that, unlike placental abruption, which causes painful third trimester bleeding, the bleeding here is painless.
Once again, based on the amount of blood loss, complications on the maternal end can be hypovolemic shock, with hypotension, tachycardia or syncope, and Sheehan syndrome with agalactorrhea, while fetal complications can include hypoxia, manifesting as bradycardia and decreased fetal movements.
Diagnosis is typically made during prenatal ultrasounds, but occasionally it’s not recognized until cervical changes during labor cause bleeding to happen.
For treatment, if the hemorrhage is severe or if there is evidence of fetal compromise, then an emergency cesarean section is required.Next is morbidly adherent placenta.
This means that there’s an abnormal attachment of the placenta to the uterine wall. Νormally, the placenta reaches the decidua basalis, which is basically endometrium that has been modified to accommodate pregnancy.
If it the decidua is too thin, the placenta may go further and attach to the myometrium, without penetrating it. That’s called placenta accreta and it’s actually the most common type of morbidly adherent placenta.

Morbidly Adherent Placen31:10–34:57

If it goes even deeper and penetrates the myometrium, but doesn’t go all the way through, it’s called placenta increta. And if it invades all the way through the myometrium, and into the uterine serosa and may even extend to neighboring organs, like the bladder or rectum, it’s called placenta percreta.
Now, the most important risk factor to remember here is prior Cesarean-section or uterine surgery, especially when the placenta implants itself near a scar from the previous surgery.
Advanced maternal age and multiparity are also risk factors. The way morbidly adherent placenta classically presents is with difficult delivery of the placenta.
You see, when the placenta is abnormally attached, it tears from the uterine wall and leaves a little bit of itself behind.
And that little bit still has placental vessels which can cause postpartum hemorrhage. While we’re on the topic, it’s necessary to know that there are 4 classic causes of postpartum hemorrhage, and you can remember them as the 4 “T”s.
So, first there’s uterine atony, or loss of uterine Tone, which is the most common cause, Trauma, like lacerations, incisions, or uterine rupture, Thrombin or clotting issues, such as various coagulopathies, and retained Tissue, which is the case in morbidly adherent placenta.
Remember that if the bleeding is severe, it can progress into hypovolemic shock, with hypotension, tachycardia or syncope, and Sheehan syndrome, with agalactorrhea.
Since the hemorrhage is postpartum, there are no fetal complications. Another high- yield piece of information is that, for unclear reasons, placenta accreta, increta and percreta are all associated with placenta previa.
So, if an exam question describes painless, bright red third-trimester bleeding pointing to placenta previa, keep in mind that the individual may also experience difficulty with separation of the placenta during delivery.
Diagnosis is typically made during prenatal ultrasound. Treatment depends on the severity of postpartum bleeding and can be an obstetrical emergency, so treatment begins immediately with uterine massage and uterotonic medications, like oxytocin, that help the uterus contract, and constricts its arteries.
If this doesn’t work, bilateral ligation of the internal iliac artery which supplies the uterus can be done. If that’s still unsuccessful, hysterectomy or surgical removal of the uterus is the only option.The last thing we’re going to discuss is amniotic fluid abnormalities.
Normally, there’s a certain volume of amniotic fluid within the amniotic sac that serves as a cushion for the growing fetus.
The volume of this fluid is determined by the volume of fluid flowing into and out of the amniotic sac. In the second half of the pregnancy, much of the amniotic fluid is made up of the fetus’ urine, with small contributions from the placenta.

Amniotic Fluid Abnormali34:57–37:35

And then it’s reabsorbed back as the fetus continually swallows it. Now, if the fetus can’t properly swallow amniotic fluid, excess fluid builds up in the amniotic sac.
This is known as polyhydramnios. For your exams, it’s important to know that an inability to swallow is typically a result of esophageal or duodenal atresia, but can be also due to anencephaly, where parts of the brain that’s responsible for controlling swallowing are absent.
Less commonly, polyhydramnios may result from increased urine production. This is the case in multiple gestation, where more fetuses produce more urine, fetal anemia, where increased cardiac output leads to increased urine production, and maternal diabetes, which causes fetal hyperglycemia and resulting polyuria.
The opposite of polyhydramnios is oligohydramnios where there’s too little amniotic fluid. This is usually due to inadequate urine excretion.
It can be caused by bilateral renal agenesis where there’s failure of both kidneys to develop, or posterior urethral valves in males, which block urine excretion.
Placental insufficiency or insufficient blood flow to the placenta can reduce blood flow to the kidneys of the fetus and thus decrease urine production.
For your exams you definitely need to know that any cause of oligohydramnios can result in Potter sequence. That’s because, with less amniotic fluid, there’s less space in the amniotic sac, and so the fetus is literally pressed up against the membrane of the sac.
This lack of room leads to developmental abnormalities like a flattened face, widely separated eyes with epicanthal folds, low-set ears, as well as limb abnormalities like clubbed feet.Alright, as a quick recap, gestational hypertension is hypertension that develops after 20 weeks gestation.
When there’s also proteinuria or other organ damage it’s preeclampsia. Preeclampsia with seizures is eclampsia.
Next, gestational trophoblastic disease refers to proliferation of trophoblastic cells. It can be benign, also called hydatidiform moles, which can be complete or partial, or malignant which include invasive moles and choriocarcinoma.
Ectopic pregnancy refers to the implantation of a fertilized egg outside the uterus and, most commonly, in the fallopian tubes.
It should be suspected when there’s a history of missed menstrual period and a slower-than-expected rise in hCG levels. If ruptured, it can manifest as sudden, severe lower abdominal pain, light vaginal bleeding and, in severe cases, shock.

Review37:35–40:42

Placental abruption is the premature, partial or complete separation of the placenta from the uterine wall, often as a result of trauma.
It classically presents with abrupt, painful third- trimester bleeding and can progress to DIC, maternal shock, and fetal distress.
Vasa previa occurs when fetal vessels run over, or is in close proximity to the cervical os. It is commonly associated with velamentous umbilical cord insertion and presents with the triad of membrane rupture, painless vaginal bleeding and fetal bradycardia or death.
Then, there’s placenta previa, where the attachment of the placenta is lower than normal in the uterus and manifests as painless, third - trimester bleeding.
Morbidly adherent placenta refers to invasion of the placenta deeper than normal into the uterine wall. The specific disorder depends on the depth of invasion: placenta accreta, which is the most common, reaches into the myometrium; increta goes through the myometrium but doesn’t penetrate the serosa; percreta penetrates the serosa and can reach other organs.
It causes difficult delivery of the placenta and postpartum hemorrhage. Finally, amniotic fluid abnormalities include polyhydramnios which is too much amniotic fluid and usually results from inability to swallow or excess urine production, while oligohydramnios, or too little amniotic fluid, is usually caused by reduced urine excretion like when there’s bilateral renal agenesis.Okay, let’s not forget about our cases.
Effie came in with severe lower abdominal pain, light vaginal bleeding, a missed menstrual period as well as hypotension and tachycardia.
This is a classic presentation of ruptured ectopic pregnancy. Another clue is the history of pelvic inflammatory disease, which is a major risk factor.
On the other hand, Kate presented with abrupt, painful and continuous vaginal bleeding in her third trimester after a traumatic event.
There were also signs of fetal distress so we are suspicious of placental abruption. The fact that she’s multiparous and over 35 are also risk factors for this condition.
Laboratory studies also showed low platelets, prolonged PT and PTT, elevated d-dimers and schistocytes, which point us towards DIC, a severe complication of placental abruption.

Summary40:42–41:47

vaginal bleeding. A missed menstrual.
As well as hypotension and tachycardia. This is a classic presentation of ruptured ectopic.
Pregnancy. Another clue is the history of pelvic inflammatory disease, which is a major risk factor.
On the other hand, Keith presented with abrupt painful and continuous vaginal bleeding, in her third trimester, after a traumatic event.
There was also signs of fetal distress. So we are suspicious of placental abruption.
The fact that she's multipurpose cleaner lips, prolonged, PT and PTT, elevated, D-dimer and schistocytes, which point us towards d?
I c a severe complication