What happens if there is a blood incompatibility during pregnancy?

What happens if there is a blood incompatibility during pregnancy?

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There are possible combinations of blood types with the rH factors:

Rh factors are genetically determined. A baby may have the blood type and Rh factor of either parent, or a combination of both parents. Rh factors follow a common pattern of genetic inheritance. The Rh-positive gene is dominant (stronger) and even when paired with an Rh-negative gene, the positive gene takes over.

If a person has the genes + +, the Rh factor in the blood will be positive.

If a person has the genes + -, the Rh factor will also be positive.

If a person has the genes - -, the Rh factor will be negative.

I am aware that an infant receives one gene from the father and one from the mother, but what happens when the mother's Rh factor is negative and the newborn's is positive? What happens if the mother is O and the infant is A or B?

What happens within the placenta and to the maternal blood poles which are connected by open ended arterioles into intervillous spaces? Will the chorionic villi be "demolished" and exchange of materials isn't as possible?

Little harm comes from ABO incompatibility (that would have been a major problem with reproduction.) Rh incompatibility is more dangerous, though.

If a fetus is Rh+ and the mother is Rh-, when there is mixing of maternal-fetal blood (at birth, but sometimes before that), the mother will form antibodies to the blood cell surface antigen. It doesn't usually affect the first baby (not sufficient antibodies), but if a subsequent baby is Rh+, there can be major consequences, which are multiplied with repeated exposure. Those maternal antibodies - which cross the placenta - can attack the fetal red blood cells and cause destruction of many of them (called hemolytic anemia) which, if severe enough, can be fatal to the fetus. It was a not-uncommon cause of fetal demise before Rhogam (Rh immune globulin) injections.

The immune globulin shots are given to women who are Rh- with Rh+ mates at a period before birth (before blood mixing), and immediately after birth if the child is Rh+. The antibodies bind with Rh+ antigens and "mask" the antigen from the mother's immune detection, so to speak, preventing the mother from making antibodies that can be used against subsequent pregnancies.

The major risk is to the fetal blood cells, not the placenta. The placenta isn't attacked. But with anemia, the fetus struggles, for example, without enough blood, the fetus can go into congestive heart failure and die.

It's also possible to form anti-Rh antibodies from blood transfusions. If an Rh- female has had a blood transfusion prior to her first pregnancy, maternal antibody levels will be drawn earlier during the pregnancy.

What Is Rh Incompatibility?

Rhesus Factor And Pregnancy: A Must Read If You Have Rh- Blood

Human blood is grouped into four types: A, B, AB, or O. Each letter refers to a type of antigen found on the surface of red blood cells. For example, Type A blood has antigens known as A-antigens. Each blood type is also grouped by its Rhesus factor (Rh).

Rhesus is another type of antigen on the surface of red blood cells.

Blood is either Rh positive (Rh+) or Rh negative (Rh-).

Most people who have the Rhesus factor are Rh positive and those who don’t have the Rhesus factor are Rh negative.

How Do I Know My Blood Type?

If you don’t know your blood type you can ask your care provider to refer you for a blood typing test. Globally, the most common blood types are O+ and A+. Approximately 85% of the population has the Rh factor and the remaining 15% is Rh negative.

The Rh factor is passed down from parents’ genes to their children. If a mother is Rh negative and the father is Rh positive, their baby can inherit the Rh gene from the father and be either Rh positive or Rh negative. The Rh positive gene tends to be stronger and will take over, even when paired with a Rh negative gene. So if the mother is Rh negative and the father is Rh positive, the baby is likely to be Rh positive. If the mother and father are both Rh negative, the baby will also be Rh negative.

How Can The Rhesus Factor / A Negative Blood Group Be A Problem?

Problems with the Rhesus factor occur when the mother’s Rh factor is negative and the baby’s Rh factor is positive. This is called Rh incompatibility. These problems usually don’t occur in first pregnancies but will arise in subsequent pregnancies.

If the baby’s Rh positive blood manages to mix with the mother’s Rh negative blood during pregnancy or labour, the mother’s blood will create antibodies against the Rh factor, as though it were a harmful substance. This means the mother becomes ‘Rh sensitised’.

The Rh antibodies can cross the placenta and attack the baby’s blood, destroying the red blood cells. This causes hemolytic anaemia, which is when the red blood cells are destroyed faster than they can be replaced. If this occurs, bilirubin (a by-product of red blood cell breakdown) builds up in the baby’s bloodstream. After birth, the baby can appear lethargic, have low muscle tone, and yellowing of skin and eyes (jaundice).

Red blood cells carry oxygen to all parts of the body. If there aren’t enough red blood cells, the baby might not receive enough oxygen. Fetal hemolytic anemia can lead to serious illness and potentially death.

How Does Rh Sensitising Happen During Pregnancy

During pregnancy, the mother’s and baby’s blood systems are separate. However, during pregnancy, labour or birth, a small number of red blood cells from the baby can cross the placenta and enter the mother’s blood. This can also happen if the mother experiences:

  • Amniocentesis (sampling of amniotic fluid via a needle inserted through the abdomen)
  • Chorionic villus sampling (sample from the placenta via needle inserted into the abdomen or through the cervix)
  • Any bleeding during pregnancy
  • Any blunt trauma to the abdomen during pregnancy
  • A pregnancy that ends in miscarriage, termination or is ectopic (implanted in the fallopian tube instead of the uterus), or
  • If baby is breech and manual rotation is attempted before labour

This Is My First Pregnancy With Rh Factor – Are There Any Concerns?

In most situations it takes time for a woman’s body to produce antibodies once sensitisation has occurred. This means in the first pregnancy with an Rh positive baby there are rarely serious problems, as the baby is born before many antibodies are developed.

However, during the first pregnancy with Rh factor, it is necessary for a mother to have treatment, if she intends to have more children. Any future pregnancies with a Rh positive baby are at risk, if the mother’s antibodies cross the placenta and attack the baby’s blood cells.

How Can This Be Prevented?

Nothing can be done about the Rhesus factor of your blood, or your partner’s. If your blood test comes back with a Rh negative result, your care provider will request that your partner’s blood type be tested. If your partner is also Rh negative, there’s nothing to be concerned about. If your partner’s results are Rh positive, further testing might be needed.

Your care provider can organise several blood tests during your pregnancy, to monitor the antibody levels in your blood. After birth, your baby’s blood will be tested for its type. If your baby has Rh positive blood, you will be offered an Anti-D injection within a few days of the birth. This will prevent antibodies from forming in your bloodstream. When given to a non-sensitised Rh negative person, the Anti-D targets any Rh positive cells in the bloodstream and prevents the production of Rh antibodies. Anti-D isn’t useful if you have already become Rh sensitised.

If you experience any bleeding during pregnancy, or if you have an amniocentesis, miscarriage, ectopic pregnancy or termination, make sure your care provider is aware as soon as possible. All of these might present opportunities for the blood of the fetus to mix with yours, and it will be unclear in most of those cases as to which blood type the baby has.

Some care providers recommend giving Rh negative women Anti-D injections without doing blood tests to detect antibodies. This might prevent antibodies from forming but it’s not without risks. The Anti-D is a blood product (which has its own risks), and in rare cases can cause allergic reactions.

If your pregnancy is normal and healthy you might opt not to have Anti-D injections until after the birth, when your baby’s Rh factor is known. The chances of blood mixing in a normal, healthy pregnancy are very slim, and if your blood tests show no antibodies present, you might prefer to find out whether it’s necessary before having the injections.

I Have Already Formed Antibodies Against The Rhesus Factor

If your blood has already formed antibodies you’ll need to be closely monitored for any signs your baby is anaemic. If your baby has mild anaemia and it’s safe to do so, your baby should be able to go full term. If the anaemia is severe, your baby might need to be born early or, in rare cases, be given a blood transfusion through the umbilical cord while still in your uterus.

If Rh incompatibility occurs, specialist care your baby might require after birth includes:

  • Blood transfusions
  • Hydrating fluids
  • Electrolytes to regulate metabolism
  • Phototherapy

The risk of antibodies forming exists with every pregnancy, even if you have been given the Anti-D injection in your previous pregnancy. It’s important to make sure, with any future pregnancies, that your blood group is known to all care providers you deal with. Being informed and aware of your blood group will give you peace of mind, and help you make the best choices for you and your baby.

Also see: “Anti-D in Midwifery: Panacea or Paradox,” by Sara Wickham

MicroBio 4

Third line of defence - the specific immune response (Acquired Immunity) is a mechanism that is activated by the presence of pathogens and foreign substances.

Invasins= Most are proteins (enzymes) that act locally to damage host cells and/or have the immediate effect of facilitating the growth and spread of the pathogen.

These include your skin, tears, mucus, cilia, stomach acid, urine flow, 'friendly' bacteria and white blood cells called neutrophils.

The skin is the largest organ of your body. It forms a waterproof mechanical barrier.

PAMPs are small molecular sequences consistently found on pathogens that are recognized by Toll-like receptors (TLRs) and other pattern recognition receptors (PRRs). PAMPs include bacterial lipopolysaccharide "endotoxin" (LPS→TLR4), bacterial flagellin, lipoteichoic acid, lipoproteins and peptidoglycan

Antibodies - globulin proteins aka immunoglobulins (Ig) Molecules which bind to antigens and are recognized by lymphocytes

Epitope=specific regions or top portion on antigen that stimulates the immune response.

MHC=a collection of genes that encode molecules of genetically diverse glycoproteins that are found on mammalian cell membrane.
These genes are responsible for tissue rejection
Proteins encoded by MHC genes

Antibody titer=the amount of antibody in serum of your blood
Antitoxin=some factors in the serum that neutralizes lethal toxin

Hapten=non-antigenic molecule with low molecular weight and cannot induce an immune response by itself, but does react with products of that response .eg,

1. Immunoglobulin A (IgA), found in high concentrations in the mucous membranes, particularly those lining the respiratory passages and gastrointestinal tract, as well as in saliva mucus milk and tears.

2. Immunoglobulin G (IgG), the most abundant crosses placenta is found in all body fluids and protects against bacterial and viral infections. Also provides long term immunity.

3. Immunoglobulin M (IgM), is found mainly in the blood and lymph fluid, is the first antibody to be made by the body to fight a new infection.

4. Immunoglobulin E (IgE), is bound to mast cells and basophils, when it binds, antigen causes cells to release histamine--alergic response.(when the immune system overreacts to environmental antigens such as pollen or pet dander). It is found in the lungs, skin, and mucous membranes.

How ABO Incompatibility Is Treated

The most common problem caused by ABO incompatibility is jaundice. Jaundice occurs when there's a buildup of an orangish-red substance in the blood called bilirubin that's produced when red blood cells break down naturally.   If more red blood cells are broken down at once than is normal, the bilirubin that results will deposit fatty tissue under the skin, causing the yellowish hue of the skin and whites of the eyes that are the tell-tale symptom of jaundice.

Not every baby with ABO incompatibility will develop jaundice, and not every baby with jaundice will require extensive treatment. It will depend on how much bilirubin collects in the baby's blood. Some infants with mild jaundice will get better on their own simply by being fed more often.   A temporary increase in feedings will lead to an increase in bowel movements, which is how excess bilirubin exits the body. Moms who breastfeed may need to supplement their baby's diet with a formula for a few days   if nursing alone doesn't do the trick.

For infants whose jaundice is more severe, phototherapy, or light therapy, is effective. The baby's skin is exposed to light waves that transform the bilirubin into a substance that can pass through the baby's system. The baby will literally be placed under the light wearing just a diaper and soft eye patches.   Instead of, or in addition to, phototherapy a baby with jaundice may be treated with biliblanket which uses fiber optics to break down bilirubin.

In rare cases, a baby with an HDN will need to be treated with a type of blood transfusion called an exchange transfusion.   This is when a portion of a baby's blood is replaced with type O blood. And a child who becomes severely anemic as a result of an HDN may need a more traditional transfusion in which he's given extra blood to replace blood that's lost.

What happens if there is a blood incompatibility during pregnancy? - Biology

Henry VIII, King of England and founder of the Anglican Church, was basically the Brad Pitt of his day when he was younger. Charming, attractive and even kind, for a member of the Royal family. Yet he is most remembered for being gluttonous, impaired and executing wives.

Research conducted by bioarchaeologist Catrina Banks Whitley while a graduate student at Southern Methodist University and anthropologist Kyra Kramer, leads them to speculate that the numerous miscarriages suffered by Henry's wives could be explained if the king's blood carried the Kell antigen. A Kell negative woman who has multiple pregnancies with a Kell positive man can produce a healthy, Kell positive child in a first pregnancy but the antibodies she produces during that first pregnancy will cross the placenta and attack a Kell positive fetus in subsequent pregnancies.

As they write in The Historical Journal, the pattern of Kell blood group incompatibility is consistent with the pregnancies of Henry's first two wives, Katherine of Aragon and Anne Boleyn. If Henry also suffered from McLeod syndrome, a genetic disorder specific to the Kell blood group, it would finally provide an explanation for his shift in both physical form and personality from a strong, athletic, generous individual in his first 40 years to the monstrous paranoiac he would become, virtually immobilized by massive weight gain and leg ailments.

"It is our assertion that we have identified the causal medical condition underlying Henry's reproductive problems and psychological deterioration," write Whitley and Kramer.

Henry married six women, two of whom he famously executed, and broke England's ties with the Catholic Church – all in pursuit of a marital union that would produce a male heir. Historians have long debated theories of illness and injury that might explain the physical deterioration and frightening, tyrannical behavior that he began to display after his 40th birthday. Less attention has been given to the unsuccessful pregnancies of his wives in an age of primitive medical care and poor nutrition and hygiene, and authors Whitley and Kramer argue against the persistent theory that syphilis may have been a factor.

Blood group incompatibility between Henry VIII and his six wives could have driven the Tudor king's reproductive woes, and a genetic condition related to his blood group could finally provide an explanation for his dramatic physical and mental changes at mid-life. Credit:

A Kell positive father frequently is the cause behind the inability of his partner to bear a healthy infant after the first Kell negative pregnancy, which the authors note is precisely the circumstance experienced with women who had multiple pregnancies by Henry. The majority of individuals within the Kell blood group are Kell negative, so it is the rare Kell positive father that creates reproductive problems.

Further supporting the Kell theory, descriptions of Henry in mid-to-late life indicate he suffered many of the physical and cognitive symptoms associated with McLeod syndrome – a medical condition that can occur in members of the Kell positive blood group.

By middle age, the King suffered from chronic leg ulcers, fueling longstanding historical speculation that he suffered from type II diabetes. The ulcers also could have been caused by osteomyelitis, a chronic bone infection that would have made walking extremely painful. In the last years of his life, Henry's mobility had deteriorated to the point that he was carried about in a chair with poles. That immobility is consistent with a known McLeod syndrome case in which a patient began to notice weakness in his right leg when he was 37, and atrophy in both his legs by age 47, the report notes.

Whitley and Kramer argue that the Tudor king could have been suffering from medical conditions such as these in combination with McLeod syndrome, aggravated by his obesity. Records do not indicate whether Henry displayed other physical signs of McLeod syndrome, such as sustained muscle contractions (tics, cramps or spasms) or an abnormal increase in muscle activity such as twitching or hyperactivity. But the dramatic changes in his personality provide stronger evidence that Henry had McLeod syndrome, the authors point out: His mental and emotional instability increased in the dozen years before death to an extent that some have labeled his behavior psychotic.

McLeod syndrome resembles Huntington's disease, which affects muscle coordination and causes cognitive disorder. McLeod symptoms usually begin to develop when an individual is between 30 and 40 years old, often resulting in damage to the heart muscle, muscular disease, psychiatric abnormality and motor nerve damage. Henry VIII experienced most, if not all, of these symptoms, the authors found.

Fetal mortality is the Kell legacy, not infertility

Henry was nearly 18 when he married 23-year-old Catherine of Aragon. Their first daughter, a girl, was stillborn. Their second child, a boy, lived only 52 days. Four other confirmed pregnancies followed during the marriage but three of the offspring were either stillborn or died shortly after birth. Their only surviving child was Mary, who would eventually be crowned the fourth Monarch in the Tudor dynasty.

The precise number of miscarriages endured by Henry's reproductive partners is difficult to determine, especially when various mistresses are factored in, but the king's partners had a total of at least 11 and possibly 13 or more pregnancies. Only four of the eleven known pregnancies survived infancy. Whitley and Kramer call the high rate of spontaneous late-term abortion, stillbirth, or rapid neonatal death suffered by Henry's first two queens "an atypical reproductive pattern" because, even in an age of high child mortality, most women carried their pregnancies to term, and their infants usually lived long enough to be christened.

The authors explain that if a Kell positive father impregnates a Kell negative mother, each pregnancy has a 50-50 chance of being Kell positive. The first pregnancy typically carries to term and produces a healthy infant, even if the infant is Kell positive and the mother is Kell negative. But the mother's subsequent Kell positive pregnancies are at risk because the mother's antibodies will attack the Kell positive fetus as a foreign body. Any baby that is Kell negative will not be attacked by the mother's antibodies and will carry to term if otherwise healthy.

"Although the fact that Henry and Katherine of Aragon's firstborn did not survive is somewhat atypical, it is possible that some cases of Kell sensitization affect even the first pregnancy," the report notes. The survival of Mary, the fifth pregnancy for Katherine of Aragon, fits the Kell scenario if Mary inherited the recessive Kell gene from Henry, resulting in a healthy infant. Anne Boleyn's pregnancies were a textbook example of Kell alloimmunization with a healthy first child and subsequent late-term miscarriages. Jane Seymour had only one child before her death, but that healthy firstborn also is consistent with a Kell positive father.

Several of Henry's male maternal relatives followed the Kell positive reproductive pattern.

"We have traced the possible transmission of the Kell positive gene from Jacquetta of Luxembourg, the king's maternal great-grandmother," the report explains. "The pattern of reproductive failure among Jacquetta's male descendants, while the females were generally reproductively successful, suggests the genetic presence of the Kell phenotype within the family."

During pregnancy, how does the mother's immune system know to avoid attacking the baby?

4 2

This is part of the reason why newly pregnant women suffer from morning sickness the brand new fetus (or whatever it's called at this early stage) secretes a hormone that suppresses the mother's immune system to stop it attacking the tiny bundle of foreign cells.

Ultimately it's not (usually) a problem, because the mother and fetus have completely separate, independent circulatory systems so the mom's white blood cells can't get to the baby and attack it. This is what the placenta is, it's how the baby's and mom's blood vessels get close enough for oxygen and nutrients to be exchanged, but without actually sharing blood.

Also edit: Anonymous Silver?! Cool! I'm not sure what that means, but I'll take it. Thanks, unnamed benefactor!

Edit part 3: And my very first Reddit Gold, too? What a day, what a day. . .

To add to this, IgG class antibodies are capable of crossing the placenta. This can cause problems for the fetus if the mother has an antibody against an antigen present on the baby's red blood cells.

An example of this would be if the mother has Rh negative blood type and the fetus has Rh positive, or the D antigen present on the blood cell. In some cases a mother could develop an antibody against the D antigen if the fetus blood mixes with the mother's blood, which can happen during birth. If the mother had a second child with Rh positive blood the D antibodies she developed in the previous birth could attack the baby's red blood cells causing hemolytic disease of the fetus/newborn. Which can cause miscarriages in the worst case scenario or the baby will be born with an anemia.

It is a fairly common case in pregnancies and the mothers are given Rhogam to suppress the antibodies to prevent this from happening.

Source: Currently studying blood banking in my Medical Lab Science Program

I’m afraid this is likely not the case in regards to hyperemesis. The factors underlying the immune system and pregnancy are massively complicated and still not understood fully. We do know that there is an element of immunosuppression that protects against maternal attack, and increases the mothers susceptibility to infections (this is why flu season is dangerous to a non immunised pregnant female - and can be up to 6 weeks postnatally too).

BetaHCG rapidly rises in the first 16 weeks or pregnancy and then plateaus, this matches the majority of hyperemesis issues. The molecule contains similar homology to thyroid stimulating hormone and can elicit a thyrotoxicosis like state, which can contribute to vomiting.

There is a likelihood that the BetaHCG can stimulate the chemoreceptors of the “vomiting centre” in the brain. Whilst infections such as urinary tract infections do cause symptoms such as vomiting, (as opposed to outside of pregnancy) and whilst these infections are more common in pregnancy, the immune component is not really related to the constant vomiting of early pregnancy.

This is close to true, but not 100%. The mother doesn’t actually get immunosuppressed, contrary to historical dogma (one of Sir Peter Medawar’s biggest mistakes). In fact, some inflammation at the fetomaternal interface is actually necessary for implantation, as well as eventual delivery (for instance, decidual NK cells promote angiogenesis that helps develop the blood vessels that feed the embryo). The progeny helps modulate what type of inflammation happens, but it’s only really the second trimester where there’s something more like true immune privilege around the developing fetus. We are still learning about exactly which signals control the switches in type of inflammation that occur, and the source of these signals it’s a very cool field that has the potential to help a lot of people with currently unexplainable infertility in the future.

There’s also (poorly understood) microchimerism where some cells from the embryo starting at about 6 weeks if I remember correctly seed the mother and persist in her long term, helping tolerize her to offspring from the same father in the future. So it’s not even completely accurate to say that there’s a perfect barrier between the mother and embryo/fetus

Fun fact: the immunology of pregnancy weirdly parallels the immunology of a developing tumor.

Learn More

  • Fetal-maternal erythrocyte distribution (Medical Encyclopedia) Also in Spanish
  • Hemolytic disease of the newborn (Medical Encyclopedia) Also in Spanish
  • Hydrops fetalis (Medical Encyclopedia) Also in Spanish
  • Hydrops Fetalis/Erythroblastosis Fetalis (Children's Hospital and Health System, Inc.)
  • Red Blood Cell Antibody Screen />(National Library of Medicine) Also in Spanish
  • Rh Disease (March of Dimes Birth Defects Foundation) Also in Spanish
  • Rh Factor Blood Test (Mayo Foundation for Medical Education and Research) Also in Spanish
  • Rh incompatibility (Medical Encyclopedia) Also in Spanish
  • Rh Incompatibility />(National Heart, Lung, and Blood Institute)
  • Rh Incompatibility (For Parents) (Nemours Foundation) Also in Spanish

Blood Types in Pregnancy

Every person has a blood type, (O, A, B, or AB) and an Rh factor, either positive or negative. The blood type and the Rh factor simply mean that a person's blood has certain specific characteristics. The blood type is found as proteins on red blood cells and in body fluids. The Rh factor is a protein that is found on the covering of the red blood cells. If the Rh factor protein is present on the cells, the person is Rh-positive. If there is no Rh factor protein, the person is Rh- negative.

The following are the possible combinations of blood types with the Rh factors:

Rh Positive Blood Types:
A+, B+, 0+ and AB+

Rh Negative Blood Types:
A-, B-, 0- and AB-

Rh factors are genetically determined. A baby may have the blood type and Rh factor of either parent, or a combination of both parents. Rh factors follow a common pattern of genetic inheritance. The Rh-positive gene is dominant (stronger) and even when paired with an Rh-negative gene, the positive gene takes over.

If a person has the genes + +, the Rh factor in the blood will be positive.

If a person has the genes + -, the Rh factor will also be positive.

If a person has the genes - -, the Rh factor will be negative.

A baby receives one gene from the father and one from the mother. More specifically, consider the following:

If a father's Rh factor genes are + +, and the mother's are + +, the baby will have one + from the father and one + gene from the mother. The baby will be:

If a father's Rh factor genes are + +, and the mother's are - -, the baby will have one + from the father and one - gene from the mother. The baby will be:

If the father's genes are + - Rh positive, and the mother's are + - Rh positive, the baby can be:

If the father's genes are - -, and the mother's are + -, the baby can be:

If the father's genes are - -, and the mother's are - -, the baby will be:

Problems with the Rh factor occur when the mother's Rh factor is negative and the baby's is positive. Sometimes, an incompatibility may occur when the mother is blood type O and the baby is either A or B.

Rh Factor and How it Works

We know that people have different blood types. What this means is some people have one “factor” and some don’t. Some have A, and some have B, and some don’t have either. We call them type A, B and O (think of “zero” if it helps). If you needed a blood transfusion you would have to get it from someone who has the same blood factors which you have — or else from someone who doesn’t have those blood factors, someone who is type “O” (without A or B). If you were given the wrong blood, your body would attack and destroy the new blood like a foreign invader — and you would get very sick very quickly.

A baby in the womb can be a different blood type from the mom because the blood very rarely mixes — and there is a natural mechanism, which usually protects both mom and baby if it does occur. The baby has completely different blood supply from the mom — and the mom’s body doesn’t reject or attack the baby even though his blood and tissue are “foreign” to her.

Well. .. aside from the major blood group, there are minor factors and proteins as well as the major ones, A and B. One of them is the Rh factor (called “Rh” because the first researchers were using “Rhesus” monkeys when they were trying to find out why some babies were being damaged in their mother’s wombs). A baby in the womb can have the same or a different blood type from his mom, and there won’t be problems — but some of the “minor factors” like “Rh” MIGHT cause problems.

A mom who is Rh “negative” doesn’t have the Rh factor. She might be type A, B or O, and is called “negative” if she lacks Rh. (She will be either A-, B- or O-).

If she gets pregnant with a baby who also doesn’t have the Rh-factor (an Rh-negative baby) then there is no problem. But if she gets pregnant with a baby who DOES have a blood type with Rh (an Rh-positive baby) then there might be problems. If there is any mixing of the mom’s and baby’s blood — as often happens during birth or sometimes in late pregnancy — then the mother’s body may make antibodies to destroy the “foreign invaders” – the Rh-positive blood cells. This process is similar (though much slower) to what might happen if someone were given the wrong type of blood during a blood transfusion.

This baby is usually born before the mom’s body can make this response, so there is no harm to this baby. But the NEXT time she becomes pregnant with an Rh-positive baby, the mom’s body may attack the new baby by sending these antibodies’ through the placenta and destroying the baby’s red blood cells. This can cause serious anemia — and if it goes on long enough can even cause the baby’s death.

We can protect the mom’s future babies by giving the mom an injection of Rhogam shortly after any birth of an Rh-positive baby — before her body has a chance to make antibodies to any Rh-positive blood cells which might have gotten mixed in her circulation during the birth. The next time she gets pregnant with an Rh-positive baby, it will be just like the first time — there won’t be any Rh-antibodies already formed waiting to attack the new baby in the womb.

A woman who is Rh-positive DOES have the Rh factor/protein. If she gets pregnant with an Rh-positive baby, then her blood already has this Rh factor and there will be no problem. If she gets pregnant with an Rh-negative baby, there will still be no problem, since the body mounts an immune response only if it detects a “foreign” factor. The Rh-negative baby has no factors to trigger the mother’s antibody response.

Sometimes are terms are confusing. When we call a mom “Rh-negative” it doesn’t mean she has a different type of Rh than the mom who is “Rh-positive”. It means she has NO Rh factor — no “rhesus factor”. This is why her body reacts when it detects the Rh factor from her baby — or from the wrong type of blood transfusion. She makes antibodies to the blood cells, which are “incompatible” with her own blood type. If a mom carries an Rh-negative baby, there will be no Rh-factor cells to trigger a response. And if mom is Rh-positive, she can safely carry a baby with any blood type — the Rh factor is not an issue at all for her. Her husband’s blood type isn’t important either since it doesn’t matter whether her babies will be Rh-positive or Rh-negative.

The father’s blood type is important only if a mom is Rh-negative. Her baby will inherit a blood type from her husband. The Rh factor is a dominant gene. If the mother is Rh-negative, it means she has no rh factor and can only contribute a gene with an Rh-negative blood type therefore her husband’s genes will be responsible for the blood type of the baby.

If the father is also Rh-negative, then all their babies will also be Rh-negative. There will never be a problem with Rh-disease in their pregnancies. But if the father is Rh-positive then this means he has the Rh factor and can father Rh positive babies, though he still “might” carry a recessive Rh-negative gene. (There is a blood test to discover this).

If he is Rh-positive but does not carry the recessive gene, then every one of their babies will be Rh-positive and at risk of Rh-disease. But if he carries the Rh-negative recessive gene, then there is a chance that some of their children will be Rh-negative, and also that some will be Rh-positive (but carry the recessive gene like their father).

This is why we test a mom’s blood to discover her blood type and her Rh factor. If the mom is Rh-positive, she never has to worry about developing a Rh blood incompatibility with her babies. But if we find she is Rh-negative, we also test her husband’s blood type as well. If she is Rh-negative and her husband is also Rh-negative, then there is no risk of having an Rh problem with their babies. Only if she is negative and if her husband is Rh-positive, will there be a risk of their babies developing an Rh- problem!

Evaluating bleeding

Bleeding during pregnancy can be evaluated by various tests as well as a pelvic examination. In addition to the possibility of pregnancy loss, a pelvic exam can help a health care provider rule out other potential causes of bleeding or spotting, such as infections, cervical trauma or cervical polyps (growths on the cervix that are usually not cancerous), Brown said.

One test given may be an ultrasound, a scan that uses sound waves to generate a black-and-white image of the developing fetus and placenta. Ultrasound can help detect a possible cause of a woman's bleeding, such as a fertilized egg developing outside the uterus (ectopic pregnancy), complications with the location of the placenta (placental abruption) or possible miscarriage, according to the March of Dimes.

Some women may receive a blood test to measure levels of human chorionic gonadotropin (hCG). A blood test may also check whether a woman needs treatment for Rh sensitization, a blood incompatibility between the mother and the fetus.

The treatment for bleeding during pregnancy will depend on its cause. Most of the time, treatment for bleeding or spotting is rest, according to the March of Dimes.


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