A.

FOLIC ACID DEFICIENCY

DEFINITION:

Folate-deficiency anemia is the lack of folic acid in the blood.

Folic acid is a B vitamin that helps your body make red blood

cells. If you don’t have enough red blood cells, you have anemia.

Red blood cells carry oxygen to all parts of your body. When you

have anemia, your blood can’t bring enough oxygen to all your

tissues and organs. Without enough oxygen, your body can’t work

as well as it should.

Low levels of folic acid can cause megaloblastic anemia. With

this condition, red blood cells are larger than normal. There are

fewer of these cells. They are also oval-shaped, not round.

Sometimes these red blood cells don’t live as long as normal red

blood cells.

ETIOLOGY:

Folic acid deficiency can arise from multiple causes including

inadequate dietary intake. Heating during cooking destroys folic

acid. Folate is absorbed in the jejunum by active and passive

transport mechanisms across the intestinal wall. Hence, diseases

such as celiac disease, tropical sprue, short bowel syndrome,

amyloidosis, gastric bypass or mesenteric vascular insufficiency

can inhibit folate absorption resulting in a deficiency. Elevated

pH as occurs in achlorhydria can also lead to poor folate

absorption. Drugs such as methotrexate, phenytoin, sulfasalazine,

and trimethoprim can antagonize folate utilization, inhibit its

absorption or conversation to its active form resulting in folate

deficiency. Congenital deficiencies of enzymes required in folate

metabolism can lead to folate deficiency. Folic acid deficiency

can occur subsequent to vitamin B-12 deficiency due to an

impairment of methionine synthase resulting in the trapping of

folate as methyltetrahydrofolate whereby methylene THFA

accumulates in serum leading to folate trap phenomenon and

increased urinary excretion of folate. Alcoholism is a

significant cause of folate deficiency. Pregnancy, hemolytic

anemia, and dialysis can also result in folate deficiency.

NSG INTERVENTIONS:

1. Educate the patient about her condition, its risk factors

and it’s probable outcomes.

2. Discuss the importance and function of folic acid to the

pregnant woman’s body and the fetus’ CNS development.

3. Discuss foods required for a well-balanced diet, as well as

dietary sources of folic acid.

4. Develop a dietary plan with the patient that includes food

preferences that are rich in folic acid and foods that are

easy and quick to prepare.

 5. Make sure the patient does not have megaloblastic anemia

before giving folic acid supplement.

6. Discuss the importance of taking the folic acid supplement

and complying to the doctor’s order.

7. Advice to continue take Folic acid supplements until the

12th week of pregnancy.

8. Educate the patient about the different daily activities

that she could do like light exercises and yoga.

9. Advise the patient to take rests in between activities.

10. Advise the patient to avoid strenuous activities.

B.THALASEMIA

DEFINITION:

Thalassemia is an inherited blood disorder in which the body

makes an abnormal form of hemoglobin. Hemoglobin is the protein

molecule in red blood cells that carries oxygen.

The disorder results in excessive destruction of red blood cells,

which leads to anemia. Anemia is a condition in which your body

doesn’t have enough normal, healthy red blood cells.

Thalassemia is inherited, meaning that at least one of your

parents must be a carrier of the disorder. It’s caused by either

a genetic mutation or a deletion of certain key gene fragments.

Thalassemia minor is a less serious form of the disorder. There

are two main forms of thalassemia that are more serious. In alpha

thalassemia, at least one of the alpha globin genes has a

mutation or abnormality. In beta thalassemia, the beta globin

genes are affected.

Each of these forms of thalassemia has different subtypes. The

exact form you have will affect the severity of your symptoms and

your outlook.

ETIOLOGY:

Thalassemia is caused by mutations in the DNA of cells that make

hemoglobin — the substance in red blood cells that carries oxygen

throughout your body. The mutations associated with thalassemia

are passed from parents to children.

Hemoglobin molecules are made of chains called alpha and beta

chains that can be affected by mutations. In thalassemia, the

production of either the alpha or beta chains are reduced,

resulting in either alpha-thalassemia or beta-thalassemia.

In alpha-thalassemia, the severity of thalassemia you have

depends on the number of gene mutations you inherit from your

parents. The more mutated genes, the more severe your

thalassemia.
In beta-thalassemia, the severity of thalassemia you have depends

on which part of the hemoglobin molecule is affected.

NSG INTERVENTIONS:

1. Health education. Explain the importance of the diagnostic

procedures (such as complete blood count), bone marrow

aspiration and a possible referral to a hematologist; and

2. Explain the hematological vocabulary and the functions of

blood elements, such as white blood cells, red blood cells,

and platelets.

3. Prevent infection. Assess for local or systemic signs of

infection, such as fever, chills, swelling, pain, and body

malaise; instruct the client to avoid contact with people

with existing infections; instruct the client to avoid

eating raw fruits and vegetables and uncooked meat; stress

the importance of daily hygiene, mouth care, and perineal

care; and teach the client and visitors the proper hand

washing.

4. Prevent bleeding. Assess for any frank bleeding from the

nose, gums, vagina, or urinary or gastrointestinal tract and

monitor platelet count.

5. Activity. Assist the client in planning and prioritizing

activities of daily living (ADL); assist the client in

 developing a schedule for daily activity and rest; and

stress the importance of frequent rest periods.

C.MALARIA

DEFINITION:

Malaria is a mosquito-borne disease caused by a parasite. People

with malaria often experience fever, chills, and flu-like

illness. Left untreated, they may develop severe complications

and die. In 2017 an estimated 219 million cases of malaria

occurred worldwide and 435,000 people died, mostly children in

the African Region. About 1,700 cases of malaria are diagnosed in

the United States each year. The vast majority of cases in the

United States are in travelers and immigrants returning from

countries where malaria transmission occurs, many from sub-

Saharan Africa and South Asia.

ETIOLOGY:

Malaria is caused by Plasmodium parasites. The parasites are

spread to people through the bites of infected female Anopheles

mosquitoes, called "malaria vectors." There are 5 parasite

species that cause malaria in humans, and 2 of these species – P.

falciparum and P. vivax – pose the greatest threat.

Malaria is an acute febrile illness. In a non-immune individual,

symptoms usually appear 10–15 days after the infective mosquito

bite. The first symptoms – fever, headache, and chills – may be

mild and difficult to recognize as malaria. If not treated within

24 hours, P. falciparum malaria can progress to severe illness,

often leading to death.

Children with severe malaria frequently develop one or more of

the following symptoms: severe anaemia, respiratory distress in

relation to metabolic acidosis, or cerebral malaria. In adults,

multi-organ failure is also frequent. In malaria endemic areas,

people may develop partial immunity, allowing asymptomatic

infections to occur.

NSG INTERVENTIONS:

1. Monitor the trend of increase in body temperature.

Rational: that the fever caused by endotoxin effects on the

hypothalamus and hypothermia are important signs that reflect the

status of the development of shock / decrease in tissue

perfusion.

2. Give warm compresses bath, avoid the use of alcohol.

Rational: to help reduce the fever, the use of ice / alcohol may

cause freezing. Addition of alcohol can also cause dry skin.

3. Give a cooling blanket.

Rationale: This blanket is used to reduce fever with

hyperthermia.

4. Observe the chills and diaphoresis.

Rational: chills often precedes temperature peaks that occur in

the general infection.

5. Monitor signs of deviation conditions / failure to improve

during therapy.

Rational: may indicate inaccuracy antibiotic therapy or growth of

the organism.

6. Give anti-infective drugs as directed.

Rational: could root out / give temporary immunity to common

infections.

7. Get blood sample.

Rational: for identifying the causes of malaria infections.

D.COAGULATION DISORDERS

DEFINITION:

Coagulations disorders are conditions that affect the blood’s

clotting activities. Hemophilia, Von Willebrand disease, clotting

factor deficiencies, hypercoagulable states and deep venous

thrombosis are all coagulations disorders. Hemophilia and Von

Willebrand disease are among the best known.

ETIOLOGY:

 Hemophilia. This condition is a bleeding disorder in which

blood does not clot normally. Children with hemophilia have

low levels of a clotting factor protein necessary for

clotting.

 Von Willebrand disease. This condition takes its name from a

clotting factor protein in the blood called von Willebrand

factor. This disorder is often genetic (passed down from

parent to child) and causes excessive bleeding when von

Willebrand factor is low.

 Other clotting factor deficiencies. Low levels of clotting

factor proteins other than those leading to hemophilia may

also result in bleeding.

 Disseminated intravascular coagulation. This condition

causes overactive clotting that obstructs blood vessels.

 Liver Disease. Liver disease comprises a number of

conditions in which liver function is impaired.

 Overdevelopment of circulating anticoagulants. This

condition causes diminished clotting that creates a

condition with symptoms similar to hemophilia.

 Vitamin K deficiency. A deficiency in this vitamin, which is

common in breast-fed infants, can impair blood clotting.

  Platelet dysfunction. Platelets are important cells needed

to make blood clots. If platelets are too low or if they do

not work properly, bruising and bleeding may occur.

 Factor V Leiden. In this genetic disorder, a blood clotting

protein called factor V Leiden overreacts causing the blood

to clot too often or too much.

 Antithrombin III (ATIII) deficiency. ATIII helps to regulate

the bleeding and clotting system. Also a genetic disorder,

low levels of ATIII cause the blood to clot too much.

 Protein C or protein S deficiency. Protein C and protein S

help to regulate the bleeding and clotting system. Low

levels of either protein cause the blood to clot too much.

 Prothrombin (PT) gene mutation. This is also called factor

II mutation. PT gene mutation is a genetic disorder. This

mutation results in too much clotting factor being made, and

too much clotting factor can result in too much clotting.

 Antiphospholipid antibody syndrome. This is an autoimmune

disorder resulting in an increase in certain blood proteins

that may increase the risk of clotting.

NSG INTERVENTIONS:

1. Monitor the coagulation assays for factor VIII AND IX.

Because Decreased value indicate that factor replacement

therapy is subtherapeutic.
2. Monitor the partial thromboplastin time (PTT). PTT is

prolonged because of a deficiency in the clotting system

factors. The prothrombin time will be normal.

3. Assess for any signs of bruising and bleeding (note the

extent of bleeding). Assess for prolonged bleeding after

minor injuries. Usual sites of external bleeding may include

the bleeding in the mouth from a cut, bite, or from cutting

or losing a tooth; nosebleeds for no obvious reasons; heavy

bleeding from a minor cut, or bleeding from a cut that

resumes after stopping for a short time. Hemophiliacs do not

bleed faster or more frequently. Instead, they bleed longer

due to a deficiency of clotting factor. Clients are often

aware of bleeding before clinical manifestation. Bleeding

can be life-threatening to these clients.

4. Assess for any pain and swelling over the entire body. A

headache, in the presence of a trauma history, may suggest

intracranial hemorrhage. Abdominal pain may indicate an

internal bleeding. Bleeding into a joint is usually reported

as a peculiar tingling sensation felt well before pain or

swelling is detected.

5. If spontaneous or traumatic bleeding is evident, monitor

vital signs. Hypovolemic shock can happen due to decreased

circulatory volume with blood loss. Signs include

hypotension and tachycardia.

 6. Anticipate the need for blood replacements. Volume expanders

and O-negative blood should be immediately available in the

event of life-threatening hemorrhage.

E.EARLY POSTPARTAL HEMORRHAGE

DEFINITION:

Early postpartum haemorrhage is defined as bleeding that occurs

within 24 hours (usually immediately) after delivery of the

placenta. The volume exceeds the normal 500 ml third stage blood

loss.

ETIOLOGY:

 Uterine atony (70% of cases): the placenta has been

expelled, but the uterus fails to retract. The uterus gets

larger, extends, and becomes soft. Factors for uterine atony

include: overstretching (polyhydramnios, multiple pregnancy,

foetal macrosomia), prolonged labour and infection

(chorioamniotitis). It can be the cause or an aggravating

factor of the PPH.

 Obstetric trauma (20% of cases): uterine rupture,

particularly in case of vaginal delivery in women with a

scarred uterus but also in women without uterine scarring;

cervical and vaginal lacerations; uterine inversion.

  Retained placenta (10% of cases): the entire placenta or a

fragment of the placenta remains in the uterus.

 Coagulation disorders (< 1% of cases)

NSG INTERVENTIONS:

1. Close delivery room monitoring is crucial for 2 hours post-

partum, in order to rapidly identify and treat postpartum

haemorrhage (PPH).

2. Blood loss is often underestimated (up to 50%).

3. Delay in treatment can lead to coagulation disorders, with a

risk of massive, diffuse bleeding.

4. Evaluate and monitor blood loss.

5. Remove the placenta manually if it has not yet delivered.

6. Perform uterine massage to expel any clots and aid uterine

contraction (to be repeated every 15 minutes for the first 2

hours after PPH).

7. Insert a Foley catheter: keeping bladder empty facilitates

uterine retraction.

8. Perform uterine exploration to remove any blood clots or

placental fragments and check for absence of uterine

rupture.

9. Administer oxytocin to correct potential uterine atony or

ensure uterine retraction: 5 to 10 UI by slow IV then, start

an IV infusion with 20 IU in 1 litre of Ringer lactate or

 0.9% sodium chloride, administered over 2 hours (160

drops/minute).

10. Inspect the birth canal, check for injury to the cervix

or vagina using retractors.

F.LATE POSTPARTAL HEMORRHAGE

DEFINITION:

Late or delayed hemorrhage, secondary postpartum hemorrhage

occurs between 24 hours and 6 weeks postpartum. Typically

occurring after discharge, it's the leading cause of readmission

in postpartum patients.

ETIOLOGY:

Infection and retained products of conception are the leading

causes of secondary postpartum hemorrhage. Pelvic ultrasound may

be done to detect retained placental fragments. Clinicians should

suspect retained fragments in a patient with delayed

lactogenesis.

Retained products of conception can lead to uterine atony failure

of effective uterine contraction after delivery. This condition

accounts for 75% to 80% of postpartum hemorrhage cases

NSG INTERVENTIONS:
1. Observe for reports of persistent perineal pain or feeling

of vaginal fullness. Apply counterpressure on labial or

perineal lacerations. Hematomas often result from continued

bleeding from laceration of the birth canal.

2. Perform external uterine massage and bimanual compression.

These compression techniques encourage uterine contractions

that counteract atony and assist with expulsion of retained

placenta or clots. Aortic compression is another compression

technique that has been used for severe PPH.

3. Administer uterotonic agents, which cause the uterus to

contract. These medications include oxytocin, misoprostol,

methylergonovine, carboprost tromethamine, and dinoprostone

as ordered by the physician.

4. Monitor vital signs including systolic and diastolic blood

pressure, pulse and heart rate. Check for the capillary

refill and observe nail beds and mucous membranes. Increased

heart rate, low blood pressure, cyanosis, delayed capillary

refill indicates hypovolemia and impending shock. Decrease

fluid volume of 30-50% will reflect changes in the blood

pressure.

5. Prepare for surgical intervention if indicated; e.g.,

evacuation of hematoma and ligation of a bleeding point,

laceration or episiotomy extension, D & C, abdominal

hysterectomy or bilateral ligation of hypogastric artery.

 Surgical repair of lacerations/episiotomy, evacuation of

hematoma and removal of retained tissues will stop the

bleeding

6. Maintain a bed rest with an elevation of the legs by 20-30° and

trunk horizontal. The position increases venous return, making

sure a greater availability of blood to the brain and other vital

organs. Bleeding may be decreased with the bed rest.

G.SUBINVOLUTION

DEFINITION:

Failure of the uterus (or, occasionally, an associated organ or

structure) to return to its expected size after the end of a

pregnancy; incomplete involution; an instance of this.

ETIOLOGY:

Endometritis, retained placental fragments, pelvic infection, and

uterine fibroids may cause uterine subinvolution.

Predisposing factors

1. Grand multiparity

2.Overdistension of uterus as in twins and hydramnios

3.Ill maternal health

4. Caesarean section

5. Uterine prolapse
 6. Retroversion after the uterus becomes pelvic organ

7. Uterine fibroid

Aggravating factors

 Retained products of conception

 Uterine sepsis, endometritis

NSG INTERVENTIONS:

1. Monitor daily the fundal height to document involution.

2. Promote early ambulation postpartum.

3. Prevent excessive blood loss, infection, and other

complications.

4. Massage uterus, facilitate voiding, and report blood loss.

5. Administer oxytocic medication to improve uterine muscle

tone as ordered by the physician. Oxytocic medication

includes oxytocin & pitocin.

6. Monitor the patient’s vital signs particularly the blood

pressure and pulse rate. The vital signs are the indicator

for any significant changes that’s in need of immediate

response.

7. Administer prescribed medications such as anti-biotic as

prescribed by the physician. This is to prevent the patient

from getting infections.

 8. Be prepared for possible Dilation and curettage (D&C) to

remove any placental fragments.

H.POSTPARTAL PUERPERAL INFECTION

DEFINITION:

Postpartum infections, also known as childbed fever and puerperal

fever, are any bacterial infections of the female reproductive

tract following childbirth or miscarriage. The most common

infection is that of the uterus and surrounding tissues known as

puerperal sepsis, postpartum metritis, or postpartum

endometritis.

ETIOLOGY:

Postpartum infections are less common since the introduction of

antiseptics and penicillin. However, skin flora such as

Streptococcus or Staphylococcus and other bacteria still cause

infections. These thrive in moist and warm environments.

Postpartum infections often start in the uterus after delivery.

The uterus can become infected if the amniotic sac becomes

infected. The amniotic sac the membranes that contain the fetus.

NSG INTERVENTIONS:
1. Inspect the perineum twice daily for redness, edema,

ecchymosis, and discharge.

2. Evaluate for abdominal pain, fever, malaise, tachycardia,

and foul-smelling lochia.

3. Obtain specimens for laboratory analysis; report the

findings.

4. Offer a balanced diet, frequent fluids, and early

ambulation.

5. Demonstrate and maintain a strict hand-washing policy for

staff, client, and visitors. This helps prevent cross-

contamination.

6. Administer prescribed antibiotics or medications as ordered

by the physician; document the client’s response.

7. Demonstrate correct perineal cleaning after voiding and

defecation, and frequent changing of peripads. Cleaning

removes urinary/fecal contaminants. Changing pad removes

moist medium that favors bacterial growth.

8. Demonstrate proper fundal massage. Review importance and

timing of the procedure. Enhances uterine contractility;

promotes involution and passage of any retained placental

fragments.

9. Monitor temperature, pulse, and respirations. Note presence

of chills or reports of anorexia or malaise. Elevations in

vital signs accompany infection; fluctuations, or changes in

 symptoms, suggest alterations in client status. Note:

Persistent fever unresponsive to antibiotic therapy may

indicate pelvic thrombophlebitis.

I.ENDOMETRITIS

DEFINITION:

Endometritis is an inflammatory condition of the lining of the

uterus and is usually due to an infection. It’s usually not life-

threatening, but it’s important to get it treated as soon as

possible. It will generally go away when treated by your doctor

with antibiotics.

Untreated infections can lead to complications with the

reproductive organs, issues with fertility, and other general

health problems. To minimize your risks, read on to learn what

they are, the symptoms, and your outlook if diagnosed.

ETIOLOGY:

An infection of the uterine lining causes endometritis. The

cervix, which is the opening to the uterus, usually keeps

bacteria out of the uterus. However, when the cervix is open,

such as during childbirth or surgery, bacteria can get into the

womb. Both the bacteria normally found in the vagina and abnormal
bacteria can be the cause of endometritis. Possible risk factors

for endometritis include:

 Childbirth or miscarriage. These are the most common reasons

for the uterus lining to become inflamed.

 Cesarean delivery. Uterus inflammation is more common after

a cesarean section than a vaginal delivery, and after an

unscheduled versus a scheduled cesarean.

 Sexually transmitted infections (STIs) and other

bacteria. Sexually transmitted infections are passed on

during sexual activity. These

include chlamydia or gonorrhea, which can cause an infection

in the uterus lining. It is important to always practice

safe sex.

 Bacteria in the uterus. Bacteria normally found in the

vagina and cervix can cause endometritis if they are found

in the uterus.

 Pelvic procedures. Some surgical or medical procedures can

let bacteria into the uterus. This is especially so when

they are performed through the cervix or uterus, such as

o dilation and curettage (D&C), or surgery involving the

uterus

o endometrial biopsy, where a sample of uterus lining

tissue is taken
 o hysteroscopy, where a small telescope is inserted into

the uterus to look for abnormalities

o inserting an intrauterine device (IUD)

o cesarean section

 Pelvic inflammatory disease. Pelvic inflammatory disease, or

PID, is an infection in the pelvis. It is often associated

with, or a cause of, endometritis. PID can be serious if not

treated and requires quick medical attention and a possible

stay in the hospital.

NSG INTERVENTIONS:

1. Monitor the patient’s Vital signs especially the temperature

and the pulse rate.

2. Inspect the perineum twice daily for redness, edema,

ecchymosis, and discharge.

3. Evaluate for abdominal pain, fever, malaise, tachycardia,

and foul-smelling lochia.

4. Obtain specimens for laboratory analysis; report the

findings.

5. Offer a balanced diet, frequent fluids, and early

ambulation.

6. Administer prescribed antibiotics or medications as ordered

by the physician; document the client’s response.

 7. Be prepared for possible Dilation and curettage (D&C) to

remove any placental fragments.

8. Demonstrate and maintain a strict hand-washing policy for

staff, client, and visitors. This helps prevent cross-

contamination.

9. Demonstrate correct perineal cleaning after voiding and

defecation, and frequent changing of peripads. Cleaning

removes urinary/fecal contaminants. Changing pad removes

moist medium that favors bacterial growth.

10. Discuss to the patient the importance of strictly complying

with her anti-biotic medications.

J.WOUND INFECTION

DEFINITION:

An infected wound is a localized defect or excavation of the skin

or underlying soft tissue in which pathogenic organisms have

invaded into viable tissue surrounding the wound. Infection of

the wound triggers the body's immune response, causing

inflammation and tissue damage, as well as slowing the healing

process.

ETIOLOGY:

Most infected wounds are caused by bacterial colonization,

originating either from the normal flora on the skin, or bacteria

from other parts of the body or the outside environment. The most
common infection-causing bacteria is Staphylococcus aureus and

other types of staphylococci.

NSG INTERVENTIONS:

1. Assess changes in body temperature, specifically increased

in body temperature. Fever is a systemic manifestation of

inflammation and may indicate the presence of infection.

2. Monitor white blood cell (WBC) count. Very low WBC count may

indicate a severe risk for infection. In older patients,

infection may be present without an increased WBC count.

3. Assess and monitor nutritional status, weight, history of

weight loss, and serum albumin. Patients with poor

nutritional status may be anergic or unable to muster a

cellular immune response to pathogens making them

susceptible to infection.

4. Investigate the use of medications or treatment modalities

that may cause immunosuppression. Antineoplastic agents,

corticosteroids, and so on, can reduce immunity.

5. Check for redness, swelling, increased pain, purulent

discharge from incisions, injury, and exit sites of tubes

(IV tubings), drains, or catheters. These are the classic

signs of infection. Any suspicious drainage should be

 cultured; antibiotic therapy is determined by pathogens

identified.

6. Know signs of itching and scratching. The patient who

scratches the skin in attempts to alleviate extreme itching

may open skin lesion and increase risk for infection.

K.URINARY TRACT INFECTION

DEFINITION:

A urinary tract infection (UTI) is an infection in any part of

your urinary system — your kidneys, ureters, bladder and urethra.

Most infections involve the lower urinary tract — the bladder and

the urethra.

Women are at greater risk of developing a UTI than are men.

Infection limited to your bladder can be painful and annoying.

However, serious consequences can occur if a UTI spreads to your

kidneys.

Doctors typically treat urinary tract infections with

antibiotics. But you can take steps to reduce your chances of

getting a UTI in the first place.

ETIOLOGY:

Urinary tract infections typically occur when bacteria enter the

urinary tract through the urethra and begin to multiply in the

bladder. Although the urinary system is designed to keep out such

microscopic invaders, these defenses sometimes fail. When that

happens, bacteria may take hold and grow into a full-blown

infection in the urinary tract.

The most common UTIs occur mainly in women and affect the bladder

and urethra.

 Infection of the bladder (cystitis). This type of UTI is

usually caused by Escherichia coli (E. coli), a type of

bacteria commonly found in the gastrointestinal (GI) tract.

However, sometimes other bacteria are responsible.

Sexual intercourse may lead to cystitis, but you don't have

to be sexually active to develop it. All women are at risk

of cystitis because of their anatomy — specifically, the

short distance from the urethra to the anus and the urethral

opening to the bladder.

 Infection of the urethra (urethritis). This type of UTI can

occur when GI bacteria spread from the anus to the urethra.

Also, because the female urethra is close to the vagina,

sexually transmitted infections, such as herpes, gonorrhea,

chlamydia and mycoplasma, can cause urethritis.

NSG INTERVENTIONS:
1. Assess changes in body temperature, specifically increased

in body temperature. Fever is a systemic manifestation of

inflammation and may indicate the presence of infection.

2. Monitor white blood cell (WBC) count. Very low WBC count may

indicate a severe risk for infection. In older patients,

infection may be present without an increased WBC count.

3. Monitor the bacterial count in the urine. Bacterial counts

of 105 are usually considered diagnostic for UTI, although

lower counts may also indicate UTI.

4. Assess and monitor nutritional status, weight, history of

weight loss, and serum albumin. Patients with poor

nutritional status may be anergic or unable to muster a

cellular immune response to pathogens making them

susceptible to infection.

5. Investigate the use of medications or treatment modalities

that may cause immunosuppression. Antineoplastic agents,

corticosteroids, and so on, can reduce immunity.

6. Administer prescribed antibiotics or medications as ordered

by the physician; document the client’s response.

7. Assess the appearance of urine. Cloudy, turbid, foul-

smelling urine with visible sediment is indicative of

urinary tract or bladder infection.

8. Encouraged the client to void often every 2 to 3 hours a day

and completely empty the bladder. This will prevent bladder

 distention, facilitate flushing of the bacteria and avoid

reinfection.

9. Encouraged increased oral fluid intake (2 to 3 liters a day

if no contraindication). Fluid intake facilitates urine

production and flushes bacteria from the urinary tract.

10. Suggest drinking of cranberry juice (four to six 8

ounce glasses per day). Cranberry juice has been shown to

reduce adherence of bacteria to the uroepithelial cells in

the urinary tract.

L.THROMBOEMBOLITIC DISORDERS

DEFINITION:

In thromboembolic disorders, blood clots (thrombi) form in blood

vessels. An embolus is a blood clot that travels through the

bloodstream and blocks an artery. In the United States,

thromboembolic disorders are a common cause of death in pregnant

women.

ETIOLOGY:

The risk of developing a thromboembolic disorder is increased for

about 6 weeks after delivery. Most complications due to blood

clots result from injuries that occur during delivery. The risk

is much higher after cesarean delivery than after vaginal

delivery.
Blood clots usually form in the superficial veins of the legs as

thrombophlebitis or in the deep veins of the legs as deep vein

thrombosis. Symptoms can include leg swelling, pain, and

tenderness. These symptoms may be hard to recognize because

pregnancy can cause similar symptoms. The severity of the

symptoms does not correlate with the severity of the disease.

Deep vein thrombosis may also develop in the pelvis. There, it

may not cause symptoms. A clot can move from the deep veins of

the legs or pelvis to the lungs. There, the clot may block one or

more lung (pulmonary) arteries. This blockage, called pulmonary

embolism, can be life threatening.

NSG INTERVENTIONS:

1. Monitor vital signs, noting increased temperature. Elevations in

heart rate may indicate increased discomfort or may occur in

response to fever and inflammatory process. Fever can also

increase client’s discomfort.

2. Assess for the signs and symptoms of deep vein thrombosis (DVT).

The signs and symptoms occur in the leg affected by the deep vein

clot which includes swelling, pain or tenderness, increased

warmth, and changes in skin color (redness).

3. Measure the circumference of the affected leg with a tape

measure. Unilateral leg and thigh swelling can be assessed by

measuring the circumference of the affected leg 10 cm below the

tibial tuberosity and 10 cm to 15 cm above the upper edge of the

 patella. Deep vein thrombosis is suspected if there is a

difference of >3 cm between the extremities.

4. Provide warm, moist heat to the affected site. Heat promotes

comfort and reduces inflammation.

5. Administer analgesics as prescribed. Analgesics relieve pain and

promote comfort.

6. Administer anticoagulants as (heparin/warfarin [Coumadin]) as

prescribed. Treatment with anticoagulant is used primarily to

prevent the formation of new clots by decreasing the normal

activity of the clotting mechanism. Heparin IV or subcutaneous

low-molecular-weight heparin is started initially. Oral

anticoagulant therapy (warfarin) will be initiated while the

client is still receiving heparin because the onset of action for

warfarin can be up to 72 hours. Heparin will be discontinued once

the warfarin reaches therapeutic levels.

7. Maintain bed rest during the acute phase. Decreases discomfort

associated with muscle contraction and movement.

8. Provide foot cradle. Cradle keeps the pressure of bedclothes off

the affected leg, thereby reducing pressure discomfort.

9. Encourage client to change position frequently. Reduces muscle

fatigue, helps minimize muscle spasm and maximizes circulation to

tissues.

10. Apply a warm compress to the affected leg using a 2-hour-on,

2-hour-off schedule around the clock. Moist heat may be applied to

the affected region to relieve pain and improve circulation

through vasodilation.
M.MASTITIS

DEFINITION:

Mastitis is an inflammation of breast tissue that sometimes

involves an infection. The inflammation results in breast pain,

swelling, warmth and redness. You might also have fever and

chills.

Mastitis most commonly affects women who are breast-feeding

(lactation mastitis). But mastitis can occur in women who aren't

breast-feeding and in men.

Lactation mastitis can cause you to feel run down, making it

difficult to care for your baby. Sometimes mastitis leads a

mother to wean her baby before she intends to. But continuing to

breast-feed, even while taking an antibiotic to treat mastitis,

is better for you and your baby.

ETIOLOGY:

Milk that is trapped in the breast is the main cause of mastitis.

Other causes include:

 A blocked milk duct. If a breast doesn't completely empty at

feedings, one of your milk ducts can become clogged. The

 blockage causes milk to back up, leading to breast

infection.

 Bacteria entering your breast. Bacteria from your skin's

surface and baby's mouth can enter the milk ducts through a

crack in the skin of your nipple or through a milk duct

opening. Stagnant milk in a breast that isn't emptied

provides a breeding ground for the bacteria.

NSG INTERVENTIONS:

1. Assess vitals for signs of systemic infection. Mastitis may or

may not be the result of infection. Monitor for fever.

2. Assess breasts and note swelling, erythema and tenderness

3. Assess for baseline and note location of symptoms. Mastitis

generally occurs on only one breast at a time.

4. Note skin quality and presence of cracked nipples that may

indicate potential for infection. Monitor for signs of potential

abscess development

5. Encourage hydration. Drinking water helps to promote milk

production and flow.

6. Apply warm compresses before breastfeeding or milk expression

(pumping. This helps dilate the milk ducts to allow for the

expression of breastmilk. Standing in a warm shower may also

help.

7. Apply cool compresses after breastfeeding or milk expression

(pumping). This helps relieve pain and sooth sore breasts

 8. Administer medications: Ibuprofen or acetaminophen may help

reduce pain, inflammation and fever, Antibiotics may be given to

treat infection.

9. Examine patient breastfeeding; observe position and baby’s latch.

Improper positioning or bad latch can cause nipple pain and

irritation and discourage the patient from fully emptying the

breast. Make sure baby has no anatomical cause for bad latching.

10. Provide lactation education: Pump or manually express milk

after each feeding, Alternate breasts when feeding, Adjust or

alternate positions for feedings.

N.POSTPARTAL PSYCHIATRIC DISORDER

DEFINITION:

It appears that about 50 to 85% of women experience postpartum

blues during the first few weeks after delivery. Given how common

this type of mood disturbance is, it may be more accurate to

consider the blues as a normal experience following childbirth

rather than a psychiatric illness. Rather than feelings of

sadness, women with the blues more commonly report mood lability,

tearfulness, anxiety or irritability. These symptoms typically

peak on the fourth or fifth day after delivery and may last for a

few hours or a few days, remitting spontaneously within two weeks

of delivery. While these symptoms are unpredictable and often

unsettling, they do not interfere with a woman’s ability to

function. No specific treatment is required; however, it should

be noted that sometimes the blues heralds the development of a

more significant mood disorder, particularly in women who have a

history of depression. If symptoms of depression persist for

longer than two weeks, the patient should be evaluated to rule

out a more serious mood disorder.

PPD typically emerges over the first two to three postpartum

months but may occur at any point after delivery. Some women

actually note the onset of milder depressive symptoms during

pregnancy. Postpartum depression is clinically indistinguishable

from depression occurring at other times during a woman’s life.

ETIOLOGY:

The postpartum period is characterized by a rapid shift in the

hormonal environment. Within the first 48 hours after delivery,

estrogen and progesterone concentrations fall dramatically. As

these gonadal steroids modulate neurotransmitter systems involved

in the regulation of mood, many investigators have proposed a

role for these hormonal shirts in the emergence of postpartum

affective illness. While it appears that there is no consistent

correlation between serum levels of estrogen, progesterone,

cortisol, or thyroid hormones and the occurrence of postpartum

mood disturbance, some investigators hypothesize that there is a

subgroup of women who are particularly sensitive to the hormonal

changes that take place after delivery. This population of women

may be more vulnerable to PPD and to other hormonally driven mood

disturbances, such as those occurring during the premenstrual

phase of the menstrual cycle or during the perimenopause.

NSG INTERVENTIONS:

1. Debriefing: It is brief version of client-centered therapy for

postpartum depression using health visitors over a period of 8

weeks. Debriefing is being introduced for women after childbirth

with the aim of improving psychological recovery. This gives

women an opportunity to discuss their experiences of delivery

with an empathetic listener.

2. Cognitive behave Therapy: It is a psychotherapeutic approach

based on the idea that behavior is secondary to thinking.

Short-term cognitive-behavioral therapy (CBT) was as

effective as treatment with Fluoxetine in women with

postpartum depression.

3. Interpersonal therapy: It is effective for the treatment of

women with mild to moderate postpartum depression and

improving the quality of their interpersonal relationship.

4. Assess the women thoughts and ensure the safety of mother

and her child and delusions, compounded with feelings of

irritability and difficulty in controlling emotions

psychiatric disorders.

5. Be alert for signs of dysfunction and be prepared to help

promote attachment between mother and baby, referral of the

 mother and family for support services and counseling and

assisting the family prioritizing and performing necessary

family functions.

6. Assist the mother in breast feeding techniques.

7. Maintain a therapeutic relationship and a community

8. Educate the mothers about available services if symptoms

services if symptoms develop and of the serious consequences

of untreated illness.

9. Ensure effective communication and understand detail of the

client specially including the both antenatal and postnatal.

O.POSTPARTAL PREGNANCY-INDUCED HYPERTENSION

DEFINITION:

Postpartum preeclampsia is a rare condition that occurs when you

have high blood pressure and excess protein in your urine soon

after childbirth. Preeclampsia is a similar condition that

develops during pregnancy and typically resolves with the birth

of the baby.

Most cases of postpartum preeclampsia develop within 48 hours of

childbirth. However, postpartum preeclampsia sometimes develops

up to six weeks or later after childbirth. This is known as late

postpartum preeclampsia.
Postpartum preeclampsia requires prompt treatment. Left

untreated, postpartum preeclampsia can cause seizures and other

serious complications.

ETIOLOGY:

 High blood pressure during your most recent pregnancy.

You're at increased risk of postpartum preeclampsia if you

developed high blood pressure after 20 weeks of pregnancy

(gestational hypertension).

 Obesity. The risk of postpartum preeclampsia is higher if

you're obese.

 Having multiples. Having twins, triplets or more increases

your risk of preeclampsia.

 Chronic high blood pressure. Having uncontrolled high blood

pressure before pregnancy increases your risk of

preeclampsia and postpartum preeclampsia.

 Diabetes. Having type 1 or type 2 diabetes increases your

risk of preeclampsia and postpartum preeclampsia.

NSG INTERVENTIONS:

1. Monitor the patient’s vital signs. The vital signs will provide

base line data about the patient’s condition.

2. Assess for signs of impending eclampsia: hyperactivity of deep

tendon reflexes (3+ to 4+), ankle clonus, decreased pulse and

respirations, epigastric pain, and oliguria (less than 50 ml/hr).

 Generalized edema/vasoconstriction, manifested by severe CNS,

kidney, liver, cardiovascular, and respiratory involvement,

precede convulsive state.

3. Establish measures to lessen likelihood of seizures; i.e., keep

room quiet and dimly lit, limit visitors, plan and coordinate

care, and promote rest. Lessens environmental factors that may

stimulate irritable cerebrum and cause a convulsive state.

4. Administer anti-hypertensives as prescribed by the doctor. This

is regulate the patient’s Blood pressure.

5. Administer MgSO4 drip as prescribed by the doctor. MgSo4 is a

drug that lessn the patient’s chance of acquiring seizures.

6. Administer Nicardipine Drip as prescribed by the doctor.

Nicardipine drip will help in the reduction of the patient’s

Blood pressure.

7. Make sure to monitor the patient’s Blood pressure while on the

nicardipine drip. This is to make sure when to titrate the drip.

8. Check on BP and side effects of antihypertensive drugs.

Administer propranolol (Inderal), as appropriate. Side effects

such as tachycardia, headache, nausea, and vomiting, and

palpitations may be treated with propranolol.

P.INFERTITLITY IN THE MALES AND FEMALES

DEFINITION:

In humans, infertility is the inability to become pregnant after

one year of intercourse without contraception involving a male

and female partner. ... Male infertility is responsible for 20–

30% of infertility cases, while 20–35% are due to female

infertility, and 25–40% are due to combined problems in both

parts.

ETIOLOGY:

All of the steps during ovulation and fertilization need to

happen correctly in order to get pregnant. Sometimes the issues

that cause infertility in couples are present at birth, and

sometimes they develop later in life.

Infertility causes can affect one or both partners. In general:

 In about one-third of cases, there is an issue with the man

 In about one-third of cases, there is an issue with the

woman

 In the remaining cases, there are issues with both the man

and the woman, or no cause can be found

Male infertility

 Abnormal sperm production or function due to undescended

testicles, genetic defects, health problems such as

diabetes, or infections such as chlamydia, gonorrhea, mumps

 or HIV. Enlarged veins in the testes (varicocele) also can

affect the quality of sperm.

 Problems with the delivery of sperm due to sexual problems,

such as premature ejaculation; certain genetic diseases,

such as cystic fibrosis; structural problems, such as a

blockage in the testicle; or damage or injury to the

reproductive organs.

 Overexposure to certain environmental factors, such as

pesticides and other chemicals, and radiation. Cigarette

smoking, alcohol, marijuana, anabolic steroids, and taking

medications to treat bacterial infections, high blood

pressure and depression also can affect fertility. Frequent

exposure to heat, such as in saunas or hot tubs, can raise

body temperature and may affect sperm production.

 Damage related to cancer and its treatment, including

radiation or chemotherapy. Treatment for cancer can impair

sperm production, sometimes severely.

Female infertility

 Ovulation disorders, which affect the release of eggs from

the ovaries. These include hormonal disorders such as

polycystic ovary syndrome. Hyperprolactinemia, a condition

 in which you have too much prolactin — the hormone that

stimulates breast milk production — also may interfere with

ovulation. Either too much thyroid hormone (hyperthyroidism)

or too little (hypothyroidism) can affect the menstrual

cycle or cause infertility. Other underlying causes may

include too much exercise, eating disorders or tumors.

 Uterine or cervical abnormalities, including abnormalities

with the cervix, polyps in the uterus or the shape of the

uterus. Noncancerous (benign) tumors in the uterine wall

(uterine fibroids) may cause infertility by blocking the

fallopian tubes or stopping a fertilized egg from implanting

in the uterus.

 Fallopian tube damage or blockage, often caused by

inflammation of the fallopian tube (salpingitis). This can

result from pelvic inflammatory disease, which is usually

caused by a sexually transmitted infection, endometriosis or

adhesions.

 Endometriosis, which occurs when endometrial tissue grows

outside of the uterus, may affect the function of the

ovaries, uterus and fallopian tubes.

 Primary ovarian insufficiency (early menopause), when the

ovaries stop working and menstruation ends before age 40.

 Although the cause is often unknown, certain factors are

associated with early menopause, including immune system

diseases, certain genetic conditions such as Turner syndrome

or carriers of Fragile X syndrome, and radiation or

chemotherapy treatment.

 Pelvic adhesions, bands of scar tissue that bind organs that

can form after pelvic infection, appendicitis, endometriosis

or abdominal or pelvic surgery.

 Cancer and its treatment. Certain cancers — particularly

reproductive cancers — often impair female fertility. Both

radiation and chemotherapy may affect fertility.

NSG INTERVENTIONS:

1. Discuss Healthy eating habits like Adding more whole-grain

products, fruits, vegetables.

2. Limiting processed foods and foods with added sugars, eating

a diet low in cholesterol and saturated fats

3. Encourage patient to do regular exercise

4. No smoking (avoid passive smoking)

5. Limit alcohol intake

6. Maintain healthy weight

7. Folic acid supplementation in women

8. Advice on rubella vaccination if seronegative

References:
https://www.mayoclinic.org/diseases-conditions/infertility/symptoms-
causes/syc-20354317
https://www.mayoclinic.org/diseases-conditions/postpartum-
preeclampsia/symptoms-causes/syc-20376646

https://nurseslabs.com/pregnancy-induced-hypertension-nursing-care-plans/#Risk-for-Maternal-Injury
https://womensmentalhealth.org/specialty-clinics/postpartum-
psychiatric-disorders/ https://juniperpublishers.com/gjo/pdf/GJO.MS.ID.555844.pdf
https://www.mayoclinic.org/diseases-conditions/mastitis/symptoms-
causes/syc-20374829
https://www.americannursetoday.com/secondary-postpartum-hemorrhage-
risk-factors-assessment-intervention/

https://www.msdmanuals.com/home/women-s-health-issues/pregnancy-
complicated-by-disease/thromboembolic-disorders-during-pregnancy
https://www.mayoclinic.org/diseases-conditions/urinary-tract-
infection/symptoms-causes/syc-20353447
https://www.woundsource.com/patientcondition/infected-wounds
https://www.medicalnewstoday.com/articles/321298.php#causes
https://www.healthline.com/health/endometritis#causes
https://www.healthline.com/health/puerperal-infection#causes

https://nurseslabs.com/puerperal-infection-nursing-care-plans/#Risk-For-Infection
https://www.who.int/news-room/fact-sheets/detail/malaria
https://www.cdc.gov/parasites/malaria/index.html
https://medicalguidelines.msf.org/viewport/ONC/english/8-2-early-
postpartum-haemorrhage-51417782.html

https://www.rileychildrens.org/health-info/coagulation-disorders
https://www.healthline.com/health/thalassemia#causes
https://www.mayoclinic.org/diseases-conditions/thalassemia/symptoms-
causes/syc-20354995

https://www.ncbi.nlm.nih.gov/books/NBK535377/
https://www.healthline.com/health/folate-deficiency