ST. ANTHONY COLLEGE OF ROXAS CITY, INC.

San Roque Extension, Roxas City, Capiz, Philippines 5800

Member, DC-SLMES Philippines
Emboldened...On Fire: Building a Culture of Innovation and Communion +inc
COLLEGE OF NURSING
S.Y. 2021-22

A CASE STUDY ON
RH INCOMPATIBILITY

Submitted by:
Mary Beth E. Abelido
BSN-2
Group-1

Submitted to:
Mrs. Nita Ammogao, RN
Clinical Instructor
 I. INTRODUCTION

The Rh factor (ie, Rhesus factor) is a red blood cell surface antigen that was named after

the monkeys in which it was first discovered. Rh incompatibility, also known as Rh disease,

is a condition that occurs when a woman with Rh-negative blood type is exposed to Rh-

positive blood cells, leading to the development of Rh antibodies. Rh incompatibility can

occur by 2 main mechanisms. The most common type occurs when an Rh-negative pregnant

mother is exposed to Rh-positive fetal red blood cells secondary to fetomaternal hemorrhage

during the course of pregnancy from spontaneous or induced abortion, trauma, invasive

obstetric procedures, or normal delivery. Rh incompatibility can also occur when an Rh-

negative female receives an Rh-positive blood transfusion. In part, this is the reason that

blood banks prefer using blood type "O negative" or "type O, Rh negative," as the universal

donor type in emergency situations when there is no time to type and crossmatch blood. The

most common cause of Rh incompatibility is exposure from an Rh-negative mother by Rh-

positive fetal blood during pregnancy or delivery. As a consequence, blood from the fetal

circulation may leak into the maternal circulation, and, after a significant exposure,

sensitization occurs leading to maternal antibody production against the foreign Rh antigen.

Once produced, maternal Rh immunoglobulin G (IgG) antibodies may cross freely from the

placenta to the fetal circulation, where they form antigen-antibody complexes with Rh-

positive fetal erythrocytes and eventually are destroyed, resulting in a fetal alloimmune-

induced hemolytic anemia. Although the Rh blood group systems consist of several antigens

(eg, D, C, c, E, e), the D antigen is the most immunogenic; therefore, it most commonly is

involved in Rh incompatibility.

I. OBJECTIVES

A. General Objective

After the case presentation, the student nurse will be able to deal with and care for patients with

RH incompatibility integrally by applying their knowledge, skills, and positive attitude.

B. Specific Objectives

At the end of the case presentation, the student nurse will be able to:

Knowledge
  Acquire sufficient information about the condition, its causes, preventive measures, and

treatment.

 Review the anatomy and physiology of the system affected.

 Identify the prescribed medication and its mechanism of action, indication, and nursing

responsibilities.

Skills

 Provide proper care and nursing interventions associated with recommended treatments

for Rh incompatibility.

 Formulate plan of care related to the nursing diagnosis identified.

Attitude

 Harness compassion and express empathy in caring for patients with ABO

incompatibility throughout the nursing process.

 II. ANATOMY AND PHYSIOLOGY

The Cardiovascular System: Blood

Blood transfusions in humans were risky procedures until the discovery of the major human

blood groups by Karl Landsteiner, an Austrian biologist and physician, in 1900. Until that point,

physicians did not understand that death sometimes followed blood transfusions, when the type

of donor blood infused into the patient was incompatible with the patient’s own blood.

Antigens are substances that the body does not recognize as belonging to the “self” and that

therefore trigger a defensive response from the leukocytes of the immune system.

Antigens are generally large proteins, but may include other classes of organic molecules,

including carbohydrates, lipids, and nucleic acids. Following an infusion of incompatible blood,

erythrocytes with foreign antigens appear in the bloodstream and trigger an immune response.

Proteins called antibodies (immunoglobulins), which are produced by certain B lymphocytes

called plasma cells, attach to the antigens on the plasma membranes of the infused erythrocytes

and cause them to adhere to one another.

Because the arms of the Y-shaped antibodies attach randomly to more than one nonself

erythrocyte surface, they form clumps of erythrocytes. This process is called agglutination.

The clumps of erythrocytes block small blood vessels throughout the body, depriving tissues of

oxygen and nutrients.

As the erythrocyte clumps are degraded, in a process called hemolysis, their hemoglobin

is released into the bloodstream. This hemoglobin travels to the kidneys, which are responsible

for filtration of the blood. However, the load of hemoglobin released can easily overwhelm the

kidney’s capacity to clear it, and the patient can quickly develop kidney failure.

More than 50 antigens have been identified on erythrocyte membranes, but the most

significant in terms of their potential harm to patients are classified in two groups: the ABO

blood group and the Rh blood group. However, we will be focusing more on the Rh blood group

for the sake of the case study.

The Rh blood group is classified according to the presence or absence of a second

erythrocyte antigen identified as Rh. Although dozens of Rh antigens have been identified, only

one, designated D, is clinically important. Those who have the Rh D antigen present on their

erythrocytes—about 85 percent of Americans—are described as Rh positive (Rh+) and those

who lack it are Rh negative (Rh−). The Rh group is distinct from the ABO group, so any
individual, no matter their ABO blood type, may have or lack this Rh antigen. When identifying

a patient’s blood type, the Rh group is designated by adding the word positive or negative to the

ABO type. For example, A positive (A+) means ABO group A blood with the Rh antigen

present, and AB negative (AB−) means ABO group AB blood without the Rh antigen.

Antibodies to the Rh antigen are produced only in Rh− individuals after exposure to the

antigen. This process, called sensitization, occurs following a transfusion with Rh-incompatible

blood or, more commonly, with the birth of an Rh+ baby to an Rh− mother. Problems are rare in

a first pregnancy, since the baby’s Rh+ cells rarely cross the placenta (the organ of gas and

nutrient exchange between the baby and the mother). However, during or immediately after

birth, the Rh− mother can be exposed to the baby’s Rh+ cells. After exposure, the mother’s

immune system begins to generate anti-Rh antibodies. If the mother should then conceive

another Rh+ baby, the Rh antibodies she has produced can cross the placenta into the fetal

bloodstream and destroy the fetal RBCs. This condition, known as hemolytic disease of the

newborn (HDN) or erythroblastosis fetalis, may cause anemia in mild cases, but the

agglutination and hemolysis can be so severe that without treatment the fetus may die in the

womb or shortly after birth.

The first exposure of an Rh− mother to Rh+ erythrocytes during pregnancy induces

sensitization. Anti-Rh antibodies begin to circulate in the mother’s bloodstream. A second

exposure occurs with a subsequent pregnancy with an Rh+ fetus in the uterus. Maternal anti-Rh

antibodies may cross the placenta and enter the fetal bloodstream, causing agglutination and

hemolysis of fetal erythrocytes.

III. TEXTBOOK DISCUSSION

Approximately 15% of Caucasians and 10% of African Americans in the United States are

missing the Rh (D) factor in their blood or have an Rh-negative blood type. Rh incompatibility

occurs when an Rh-negative mother (one negative for a D antigen or one with a dd genotype)

carries a fetus with an Rh-positive blood type (DD or Dd genotype). For such a situation to

occur, the father of the child must either be homozygous (DD) or heterozygous (Dd) Rh positive.

If the father of the child is homozygous (DD) for the factor, 100% of the couple’s children will

be Rh positive (Dd). If the father is heterozygous for the trait, 50% of their children can be

expected to be Rh positive (Dd). Although blood incompatibility is basically a problem that

affects the fetus, it can cause such concern and apprehension in a woman during pregnancy that

it becomes a maternal problem as well. Because people who have Rh-positive blood have a

protein factor (the D antigen) that Rh-negative people do not, when an Rh-positive fetus begins

to grow inside an Rh-negative mother who is sensitized, her body reacts in the same manner it

would if the invading factor were a substance such as a virus—she forms antibodies against the

invading substance. The Rh factor exists as a portion of the red blood cell, so these maternal

antibodies cross the placenta and cause destruction (i.e., hemolysis) of fetal red blood cells. A

fetus can become so deficient in red blood cells from this that a sufficient oxygen transport to

body cells cannot be maintained. This condition is termed hemolytic disease of the newborn or

erythroblastosis fetalis. Theoretically, there is no connection between fetal blood and maternal

blood during pregnancy, so the mother should not be exposed to fetal blood. In reality, a small

amount of fetal blood does enter maternal circulation (Kim & Makar, 2012). Procedures such as

amniocentesis or percutaneous umbilical blood sampling can allow this to occur. During a first

pregnancy, this effect is small. As the placenta separates after birth of the first child, however,

there is an active exchange of fetal and maternal blood from damaged villi. This causes most of

the maternal antibodies formed against the Rh positive blood to be formed in the first 72 hours

after birth. These become a threat in a second pregnancy.

IV. PATHOPHYSIOLOGY

When an Rh-negative mother is exposed to the Rh D antigen, the D antigen is perceived

as a foreign threat similar to how bacteria and viruses are perceived. This leads to a series of

activations of immunogenic pathways that culminates in the production of anti-D antibodies.

Those antibodies can bind to the D antigen present on the erythrocytes of Rh-positive fetuses

to further activate immunologic pathways that lead to the hemolysis of the fetal erythrocytes

It can cause symptoms, not to the mother but to the fetus, ranging from very mild to fatal.

Mild Rh disease involves limited destruction of fetal red blood cells, possibly resulting in

mild fetal anemia. The fetus can usually be carried to term and requires no special treatment

but may have problems with jaundice after birth. Mild Rh disease is more likely to develop in

the first pregnancy after sensitization has occurred.

Moderate Rh disease involves the destruction of larger numbers of fetal red blood cells.

The fetus may develop an enlarged liver and may become moderately anemic. The fetus may
need to be delivered before term and may require a blood transfusion before (while in the

uterus) or after birth. A newborn with moderate Rh disease is watched closely for jaundice.

Severe Rh disease (fetal hydrops) involves widespread destruction of fetal red blood

cells. The fetus develops severe anemia, liver and spleen enlargement, increased bilirubin

levels, and fluid retention (edema). The fetus may need one or more blood transfusions

before birth. A fetus with severe Rh disease who survives the pregnancy may need a blood

exchange. This procedure replaces most of the infant's blood with donor blood (usually type

O, Rh-negative).

With Rh incompatibility, an infant may not appear pale at birth despite the red cell

destruction that occurred in utero because the accelerated production of red cells during the

last few months in utero compensates to some degree for the destruction. The liver and

spleen may be enlarged from attempts to destroy damaged blood cells. If the number of red

cells has significantly decreased, the blood in the vascular circulation may be hypotonic to

interstitial fluid, causing fluid to shift from the lower to higher isotonic pressure by osmosis,

resulting in extreme edema. Finally, the severe anemia can result in heart failure as the heart

has to beat so fast to push the diluted blood forward. Hydrops fetalis is an old term for the

appearance of a severely involved infant at birth; hydrops refers to the edema and fetalis

refers to the lethal state. Most infants do not appear jaundiced at birth because the maternal

circulation has evacuated the rising indirect bilirubin level. With birth, progressive jaundice,

usually occurring within the first 24 hours of life, will begin, indicating in both Rh and ABO

incompatibility that a hemolytic process is at work. The jaundice occurs because, as red

blood cells are destroyed, indirect bilirubin is released. Indirect bilirubin is fat soluble and

cannot be excreted from the body. Under usual circumstances, the liver enzyme glucuronyl

transferase converts indirect bilirubin to direct bilirubin. Direct bilirubin is water soluble and

combines with bile for excretion from the body with feces. In preterm infants or those with

extreme hemolysis, the liver cannot convert all of the indirect bilirubin produced to direct

bilirubin, so jaundice becomes extreme. Normally, cord blood has a total serum bilirubin

(TsB) level of 0 to 3 mg/100 ml. An increasing bilirubin level becomes dangerous if the level

rises above 20 mg/dl in a term infant and perhaps as low as 12 mg/dl in a preterm infant

because brain damage from bilirubin-induced neurologic dysfunction (BIND), a wide

spectrum of disorders caused by increasingly severe hyperbilirubinemia ranging from mild

 dysfunction to ABE (invasion of bilirubin into brain cells), can occur. A second concern that

arises from excessive red blood cell destruction is that an infant is forced to use glucose

stores to maintain metabolism in the presence of anemia. This can cause a progressive

hypoglycemia, compounding the initial problem. A decrease in hemoglobin during the fi rst

week of life to a level less than that of the cord blood is a later indication of blood loss or

hemolysis.

An Rh-negative woman who conceives a child with an Rh-positive man is at risk for Rh

incompatibility and the baby has a 50 percent or more chance of having Rh-positive blood.

Mrs M.P. is Rh negative and her husband is Rh positive. If her husband is homozygous for

the D antigen, every fetus he fathers will be Rh positive and could potentially be affected. If

he is heterozygous, only half of his children will be affected.

Your risk of problems from Rh incompatibility is higher if you were exposed to Rh-

positive blood before the pregnancy which may have happened during an earlier pregnancy.

You also may have been exposed to Rh-positive blood if you had bleeding or abdominal

trauma during the pregnancy. An ectopic pregnancy, a miscarriage, or an induced abortion. A

mismatched blood transfusion or blood and marrow stem cell transplant. An injection or

puncture with a needle or other object containing Rh-positive blood.

V. VITAL INFORMATION

Name: M.P.
Age: 26 years old
Age of Gestation: 34 weeks and 3 days
Gravidity: 2
Parity: 1

VI. CLINICAL ASSESSMENT

General Survey Overall appearance reveals cleanliness, good nourishment.

Mother’s clothes are well-fitting, stature is appropriate for her age,
posture is straight, no signs of pain. Vital signs upon assessment were
the following: BP 120/80, PR 85bpm, Temp 36.5C,

Skin and Nails Skin color is even without obvious lesions. Skin pinches easily and
immediately returns to its original position. Linea Nigra is present.
Nails are clean and manicured. Nails are smooth and firm. Nailplate is
firmly attached to nailbed. There is normal capillary nailbed refill.

Head, Eyes,Ears,  Hair is black in color and smooth. Scalp is clean and dry. Head is
Nose,Throat(HEENT normocephalic and symmetric. Face is normally proportionate and
) symmetric. Pupils are equal and round, reactive to
Light and accommodation.
Tympanic membranes clear.
Nose is midline in face
 No lesions are present on the lips, tongue, and buccal mucosa. Throat
pink, no redness or exudate.

Neck Neck is short with skin folds between the head and shoulder. Trachea
is midline.

Breast Breast size is increased

and nodular. Breasts are more sensitive to
touch. Colostrum is excreted, especially
in the third trimester. Hyperpigmentation
of nipples and areolae is evident

Respiratory Thorax round and symmetric, hyperresonance percussed over lung

field.

Gastrointestinal The uterus contracts and feels firm. Fundic height is 35cm. Fetal
movement was felt during the assessment. Appetite excellent.

Urinary No history of urinary tract infections.

Genital Labia majora and minora are pink and moist. Enlarged labia and
clitoris. No discomfort or discharge during examination.

Peripheral/Vascular The upper extremities are symmetrically aligned, there is no lesion

and swelling. Varicose veins in the lower extremities noted.

Musculoskeletal  Feet and legs are symmetric in size, shape and movement. 

Neurologic  No tremors, unusual movements, or seizures.

Hematologic  Patient is Rh-positive.

Psychiatric  No developmental disorder.

VII. LABORATORY AND DIAGNOSTIC TEST

A simple blood test could be done during prenatal visit in order to know whether Mrs. M.P is

Rh-positive or Rh-negative. Her husband will be tested to find out his Rh type. Upon knowing

that Mrs. M.P. is Rh negative and the father is Rh positive, the baby has a 50 percent or more

chance of having Rh-positive blood. This depends whether her husband is homozygous for the D

antigen or heterozygous. Indirect Coombs Test can also be done. This is used to detect the

presence and amount of anti-D antibody in the maternal circulation. These antibodies could act

against certain red blood cells. This test will show if Mrs. M.P has an Rh antibody in her blood.

All women with Rh-negative blood should have an anti-D antibody titer done at a first pregnancy

visit. If the results are normal or the titer is minimal (normal is 0; a ratio below 1:8 is minimal),

the test is repeated at week 28 of pregnancy. If this is also normal, no therapy is needed. If a

woman’s anti-D antibody titer is elevated at a first assessment (1:16 or greater), showing Rh

sensitization, meaning that she have been exposed to Rh-positive blood before and she have

developed antibody for it, the well-being of the fetus in this potentially toxic environment will be
monitored every 2 weeks or more often by Doppler velocity of the fetal middle cerebral artery, a

technique that can predict when anemia is present or fetal red cells are being destroyed (Moise &

Argoti, 2012). If the artery velocity remains high, a fetus is not developing anemia and most

likely is an Rh-negative fetus. If the reading is low, it means a fetus is in danger, and immediate

birth will be carried out providing the fetus is near term. If the fetus is not near term, efforts to

reduce the number of antibodies in the woman or replace damaged red cells in the fetus are

begun.

In a pregnant woman with Rh-negative blood type, the Rosette screening test often is the first

test performed. The Rosette test can detect alloimmunization caused by very small amounts of

fetomaternal hemorrhage. When a high clinical suspicion of large fetomaternal hemorrhage is

present (>30 mL blood), the Kleihauer-Betke acid elution test can be performed. The Kleihauer-

Betke test is a quantitative measurement of fetal red blood cells in maternal blood, and it can be

valuable for determining if additional amounts of Rh IgG should be administered. The amount of

Rh IgG required for treatment after sensitization is at least 20 mcg/mL of fetal RBCs.

VIII. MEDICAL MANAGEMENT

One of the main principles of the management of Rh incompatibility is the prevention of

maternal sensitization. Rh IgG, first released for general use in 1968, has been remarkably

successful in the prevention of Rh incompatibility. In the Rh-negative mother, the preparation is

administered after a suspected fetomaternal hemorrhage. The exact mechanism by which passive

administration of Rh IgG prevents Rh immunization is unknown. The most likely hypothesis is

that the Rh immune globulin coats the surface of fetal RBCs containing Rh antigens. These

exogenous antibody-antigen complexes cross the placenta before they can stimulate the maternal

endogenous immune system B cells to produce IgG antibodies.

 a. Drug Tab

Generic Name: RHo (D) immune globulin

Brand name: RhoGAM
Drug Classification: Immune Globulins

Dosage and Indication Mechanism Side effect Contraindications Nursing

Frequency of Action Responsiblities
300 mcg Prevents The Fever, injection site If the pt has If Rh status of the
(1500 hemolytic mechanism soreness or hemolytic anemia infant is unknown
international disease of by which irritation, dizziness, or she has had an at 72 hours or >
units) IM at the fetus and RhIG or headache aller gic reaction 72 hours have
26—28 neonate, prevents to a shot of passed, do not
weeks which is the isoimmunizat immune globulin , withhold the dose.
gestation to result of ion is not or she already
be repeated transplacenta completely have Rh Monitor for side
within 72 l passage of understood sensitization, she effects and
hours of anti-D. but is likely should not get the hypersensitivity
delivery of a to suppress RhoGAM shot . reactions.
confirmed the immune
Rh- positive response and Do not receive
infant. antibody live vaccine
formation in within three
In case of Rh-negative weeks.
known or individuals
suspected exposed to
massive Rh-positive
fetomaternal RBCs.
hemorrhage
( > 15 ml fetal
red blood
cells or > 30
ml fetal
whole blood),
300 mcg
(1500
international
units) IM
should be
given for
every 15 ml
of fetal red
blood cells
(30 ml of
fetal whole
blood)
present. The
total dose
should be
administered
within 72
hours of the
exposure.
 IX. NURSING MANAGEMENT

Nursing care is focused on prevention through early assessment for risk and treatment of the

woman with each pregnancy. Upon receipt of test results, the nurse should report that the

pregnant woman is Rh-negative (indirect Coombs’ test is negative, nonsensitized) and fetus is

Rh-positive and follow through with RhoGAM treatment as ordered. Observation should be

continued to determine treatment effectiveness and absence of fetal distress due to

incompatibility and damage to fetal red blood cells from maternal antibodies.
 a. Nursing Care Plan

ASSESSMENT DIAGNOSIS PLANNI NURSING RATIONALE NURSING CORE EVALUATIO

NG INTERVENTIONS THEORY VALUE N
S
Risk for fetal After INDEPENDENT: Jean Compass Mrs. M.P was
Objective data: injury related nursing -Educate the patient For client to be Watson: ionate able to
to abnormal interventi with the advantages well-informed, Theory of Service undersand the
Blood Type: A- blood profile on, the of receiving Rh as a result, she Human benefits of
Blood Type of patient immunoglobulin can make Caring: Social receiving Rh
husband/father: will be and the rational “Nursing is Commit immunoglobuli
A+ able to: consequences if she decisions. concerned ment n and
Rh-negative - doesn’t. with Co-
participat - Confirm both the The coomb’s promoting responsib
e in maternal and test will indicate health, ility and
history newborn’s blood if there is a large preventing respect
taking type, and the number of illness, for
and maternal antibodies are caring for human
screening sensitization status present in the the sick, and dignity
procedure thru coomb’s test mother which restoring
s as result. means that she health.”
indicated has already been
-verbalize sensitized.
understan
ding of
individual
risk
factors or
condition
s that may DEPENDENT:
impact
pregnanc
y -Administer Rh - Rh-Ig may
immunoglobulin minimize the
(RhIgG) to client at incidence of
28 weeks maternal
gestation in Rh- isoimmunization
negative clients in non sensitized
with Rh-positive mother and may
partners and within help to prevent
72 hours after erythroblastosis
delivery. fetalis in
subsequent
pregnancies.
 X. Discharge Planning

Medications

1. Educate the patient to report immediately if she experience bleeding or an sensitizing

events.
2. Educate the patient on the prescribed medication, including doses, route, action, and side
effects.
3. Advise the client not to miss the intake of medications given by her physician, if there
are any, upon discharge.
Exercise

1. Educate the pregnant woman that it's not advised to start a high intensity exercise that
you haven't tried before.
2. Offer some exercise that are safe during pregnancy like walking, swimming and yoga.
Treatment
1. Teach the patient the dosages, routes, and side effects for all medications prescribe to
her, if there are any.
2. Discuss the importance of strict adherence to medication regimen to ensure complete
healing.
3. Advise parents about proper hygiene practices.
Health teaching

1. Provide information about the current illness of the patient.

2. Encourage the patient to maintain a comfortable and clean environment.
Outpatient

1. Go to all of the follow-up appointments.

2. Advice the patient to seek medical advice and inform the physician for any abnormalities
noted.
Diet
1. Mothers have increased nutritional needs after delivery, especially if they are
breastfeeding. Be sure to drink plenty of fluids and to eat foods from all four of the Basic
Food Groups.
2. Continue to take your personal vitamins and iron tablets as ordered by your doctor.

Spiritual

1. Encourage family to have faith and pray to God.

2. Introduce benefits of spiritual counselling and refer the client if she is interested.