ECTOPIC PREGNANCY

Ectopic pregnancy is implantation of a fertilized ovum in a site other than the endometrial lining of the uterus. This occurs when a fertilized egg implants in a location that can’t support its growth and it can rarely occur in the ovary and abdominal cavity or cervix. An ectopic pregnancy happens when a fertilized egg implants outside of the uterus, most commonly in the fallopian tube (95%)

Moreover, the other common site of ectopic pregnancy are the following such as:

Fimbrial - 8%

Interstitial - 8%

Ampulla – 80%

Isthmic – 12%

Cervical

Abdominal

Tubo-ovarian

ETIOLOGY

In most cases, conditions that slow down or block the movement of the egg down the fallopian tube cause ectopic pregnancy. This could happen due to:

The scar tissue, adhesions or inflammation from a prior pelvic surgery.

Fallopian tubes have damage, such as from a sexually transmitted infection (STI)

Born with an irregularly-shaped fallopian tube.

Having a growth blocking in the fallopian tube.

CLINICAL MANIFESTATIONS

The early symptoms of an ectopic pregnancy can be very similar to typical pregnancy symptoms. However, the patient may experience additional symptoms during an ectopic pregnancy, including:

Vaginal bleeding.

Amenorrhea

Dizziness or weakness.

Pain in the lower abdomen, pelvis and lower back.

If the fallopian tube ruptures, the pain and bleeding could be severe enough to cause additional symptoms. These can include:

Fainting.

Shoulder pain.

Low blood pressure (hypotension)

Rectal pressure or bowel problems.

Moreover, when a tube bursts, the patient may feel sudden, sharp lower abdominal pain and this is a medical emergency.

PATHOPHYSIOLOGY

An ectopic pregnancy happens when a fertilized egg implants outside of your uterus.

The egg is meant to travel down your fallopian tubes and embed itself into the wall of your uterus, where it can develop.

Anatomic distortion and obstruction of the fallopian tube are widely responsible for most ectopic implantations. In an ectopic pregnancy, the egg implants in one of the structures along the way.

It lodges on that constricted part and implantation takes place at that area instead of the uterus.

DIAGNOSTIC TEST:

Tests to determine the possibility of ectopic pregnancy must be performed first before the diagnosis.

PELVIC ULTRASOUND: An early pregnancy ultrasound is the most common determinant of an ectopic pregnancy.

MAGNETIC RESONANCE IMAGING: This is also another way to detect the presence of ectopic pregnancy

HYSTEROSALPINGOGRAPHY: ALSO KNOWN AS UTEROSALPINGOGRAPHY is a radiologic procedure to investigate the shape of the uterine cavity and the shape and patency of the fallopian tube

NURSING MANAGEMENT

Nurses must also have their own function when it comes to ectopic pregnancy, even without a direct order from the physician. These may include:

Assessing the vital signs to establish baseline data and determine if the patient is under shock.

Maintaining accurate intake and output to establish the patient’s renal function.

Upon the arrival at the emergency room, place the woman flat in bed.

MEDICAL MANAGEMENT

The medical management of a woman with an ectopic pregnancy should be initiated the moment she is brought to the emergency room. These can include:

Administration of methotrexate: Methotrexate is a chemotherapeutic agent that is a folic acid antagonist. It destroys rapidly growing cells such as the trophoblast and the zygote. This would be administered until a negative hCg titer result has been produced.

Administration of mifepristone: An abortifacient that causes sloughing off of the tubal implantation site. Both of these therapies would leave the tube intact and no surgical scarring.

Intravenous therapy :This would be performed when the ectopic pregnancy has already ruptured to restore intravascular volume due to bleeding.

Withdrawing of blood sample :A large amount of blood would be lost, so blood typing and crossmatching must be done in anticipation of a blood transfusion. The blood sample would also be used to determine the hemoglobin levels of the pregnant woman.

Moreover, surgical interventions would be performed after the rupture of the ectopic pregnancy to ensure that the reproductive system would still be functional and no complications would arise.

Laparoscopy: This will be performed to ligate the bleeding blood vessels and repair or remove the damaged fallopian tube.

Salpingectomy: This intervention would be performed if the fallopian tube is completely damaged. The affected tube would be removed and what would be left would be sutured appropriately.

NURSING DIAGNOSIS

The care provider should do a complete observation to diagnose any possible causes of ectopic pregnancy such as:

Risk for Deficient Fluid Volume: related to bleeding from a ruptured ectopic pregnancy.

Powerlessness: related to early loss of pregnancy secondary to ectopic pregnancy.

References

Belleza, M. (2017). Ectopic Pregnancy.

Cleveland Clinic. (2023). Ectopic Pregnancy.

GESTATIONAL ANEMIA

ETIOLOGY

Dietary factors (insufficient iron intake) Chronic blood loss from Gl bleeding.

Impaired Gl absorption of iron (prolonged diarrhea, gastrectomy) Increased iron requirements (rapid body growth, menstruation, pregnancy).

Iron-refractory deficiency anemia (IRIDA)

PATHOPHYSIOLOGY

The body stores of iron decreases as do the stores of transferrin which binds and transports iron. This leads to depletion of red blood cells, resulting in decreased hemoglobin concentration and decreased oxygen-carrying capacity of the blood.

DIAGNOSTIC TEST

Complete blood count (CBC) in the first trimester is recommended for all pregnant women to screen for anemia. The screening of pregnant women for IDA in absence of anemia is still debatable. If IDA is suspected, a ferritin level of <30 ng/ml is diagnostic.

NURSING MANAGEMENT

Administer prescribed medications which includes iron supplements (IV, IM, or oral)

Advise patients to take iron supplements an hour before meals for maximum absorption.

Advise patients to take liquid forms of iron using a straw to prevent teeth staining.

MEDICAL MANAGEMENT

Medical care starts with establishing the diagnosis and reason for the iron deficiency.

Iron therapy. Oral ferrous iron salts are the most economical and effective medication for the treatment of iron deficiency anemia; of the various iron salts available, ferrous sulfate is the one most commonly used.

Diet. The addition of nonheme iron to national diets has been initiated in some areas of the world.

NURSING DIAGNOSIS

Fatigue related to decreased hemoglobin and diminished oxygen-carrying capacity of the blood.

Deficient knowledge related to the complexity of treatment, lack of resources, or unfamiliarity with the disease condition.

GESTATIONAL DIABETES

ETIOLOGY

If your body is unable to produce enough additional insulin during pregnancy, gestational diabetes will develop. the body can use the hormone insulin, which is produced in the pancreas, to help utilize glucose as fuel and regulate blood sugar levels. Your body produces unique hormones and experiences other changes during pregnancy, such as weight growth. Insulin resistance is the result of these alterations, which cause your body's cells to poorly utilize insulin. Throughout their late pregnancy, all pregnant women experience some insulin resistance. Some pregnant women are unable to produce enough insulin to reverse insulin resistance, but most can. Pregnant diabetics are born to these women.

CLINICAL MANIFESTATIONS

Glycosuria on two successive office visits

Recurrent monilial vaginitis

Macrosomia of the fetus on ultrasound

Polyhydramnios

PATHOPHYSIOLOGY

1. In gestational diabetes mellitus (type III, GDM), insulin antagonism by placental hormones, human placental lactogen, progesterone, cortisol, and prolactin leads to increased blood glucose levels. The effect of these hormones peaks at about 26 weeks’ gestation. This is called the diabetogenic effect of pregnancy.

2. The pancreatic beta cell functions are impaired in response to the increased pancreatic stimulation and induced insulin resistance.

3. Pregnancy complicated by diabetes puts the mother at increased risk for the development of complications, such as spontaneous abortion, hypertensive disorders, and preterm labor, infection, and birth complications.

4. The effects of diabetes on the fetus include hypoglycemia, hyperglycemia, and ketoacidosis. Hyperglycemic effects can include:

Congenital defects

Macrosomia

Intrauterine growth restriction

Intrauterine fetal death

Delayed lung maturity

Neonatal hypoglycemia

Neonatal hyperbilirubinemia

DIAGNOSTIC TEST

Fasting blood sugar test will reveal elevated blood glucose levels.

A 50-g glucose screen (blood glucose level is measured 1 hour after client ingests a 50-g glucose drink) reveals elevated blood glucose levels. The normal plasma threshold is 135 to 140 mg/dL.

NURSING MANAGEMENT

1. Establish an initial database and maintain serial documentation of test results throughout the pregnancy.

2. Provide client and family teaching.

3. Arrange for the client to consult with a dietitian to discuss the prescribed diabetic diet and to ensure adequate caloric intake

4. Address emotional and psychosocial needs. Intervene appropriately to allay anxiety regarding diabetes and childbirth.

5. Prepare the client for intensive frequent intrapartum assessment, which may include:

Fetal monitoring

Intravenous infusion of glucose, insulin, and oxytocin

Evaluation for diabetic ketoacidosis (signs and symptoms include altered level of consciousness, labored breath sounds, fruity breath odor, and ketonuria)

Intravenous fluid and electrolyte replacement therapy

Invasive maternal cardiac monitoring

MEDICAL MANAGEMENT

Treatment for gestational diabetes aims to keep blood glucose levels equal to those of pregnant women who don't have gestational diabetes. The treatment always includes special meal plans and scheduled physical activity, and it may also include daily blood glucose testing and insulin injections.

NURSING DIAGNOSIS

Gestational Trophoblastic Disease

Gestational trophoblastic disease is the degeneration and abnormal proliferation of the trophoblastic villi. The cells become filled with clear fluid, giving them the appearance of grape-like vesicles.

ETIOLOGY

The most common types of gestational trophoblastic disease occur when a sperm cell fertilizes an empty egg cell or when two sperm cells fertilize a normal egg cell. Your risk is higher based on your:

Age: Gestational trophoblastic disease occurs in women of childbearing age.

History of molar pregnancy

Prior miscarriage(s) or problems getting pregnant

Blood type: Women with blood types A or AB are at slightly higher risk than those with types B or O.

Diet: A few studies have found that a low level of beta-carotene in the diet may be linked with a higher risk of molar pregnancy. More research is needed to confirm this connection.

CLINICAL MANIFESTATION

If you have gestational trophoblastic disease, you may not notice any signs or symptoms and your pregnancy may seem normal. Your doctor may notice signs of the disease during your routine prenatal care visits. Possible signs include:

Uterus expands faster than normal. Because the trophoblast cells proliferate abnormally, it does so in such a rapid pace that the uterus reaches its growth landmarks before the usual time.

Vaginal bleeding. When the H-mole is still not identified at the 16th week of pregnancy, it will identify itself through vaginal bleeding accompanied by clear fluid filled vesicles.

A larger-than-normal uterus or swollen abdomen

PATHOPHYSIOLOGY

Fertilization occurs as the sperm enters the ovum. In instances of a partial mole, two sperms might fertilize a single ovum.

Reduction division or meiosis was not able to occur in a partial mole. In a complete mole, the chromosome undergoes duplication.

The embryo fails to develop completely. There are 69 chromosomes that develop for the partial mole, and 46 chromosomes for the complete mole.

The trophoblastic villi start to proliferate rapidly and become fluid-filled grape-like vesicles.

DIAGNOSTIC TEST

Diagnostic tests are ordered to check for a presence that might indicate a positive gestational trophoblastic disease.

Pregnancy test. This may not be able to detect specifically the H-mole, but this will confirm if the woman is pregnant or not.

CT scan - CT scans use X-rays to create cross-sectional pictures of your abdominal area. They are useful in showing the size of the tumor, if lymph nodes are swollen, and if the tumor has spread to other organs.

PET scan - An imaging test that can help reveal the metabolic or biochemical function of your tissues and organs. The PET scan uses a radioactive drug called a tracer to show both typical and atypical metabolic activity.

NURSING MANAGEMENT

Nurses must also take action during the critical stages of the pregnancy. We must be able to function on our own while waiting for any orders from the physician.

Assess the abdominal girth of the pregnant woman to check if it is within the usual landmark of pregnancy.

Assess for signs and symptoms of pregnancy induced hypertension, because for a woman with H-mole, they occur earlier than the 20th week of pregnancy.

Instruct the woman to save all perineal pads containing any clots or tissue that has passed out of her during bleeding.

MEDICAL MANAGEMENT

The physician would order medications and other interventions that would ensure the safety of the woman during this complicated period.

Methotrexate: Physicians may order a prophylactic course of methotrexate, which attacks rapidly growing cells like the abnormally growing trophoblastic cells.

Dactinomycin: This is ordered by the physician once metastasis occurs.

NURSING DIAGNOSIS

Grieving be related to:

loss of pregnancy

anger

social detachment

GOAL: Resolves feelings about the loss.

References

Belleza, M. (2016, December 22). Gestational Trophoblastic Disease. Retrieved from Nurseslabs:

Cancer.Net. (2022, July 22). Gestational Trophoblastic Disease: Symptoms and Signs.

HYPEREMESIS GRAVIDANUM

Nausea and vomiting is a common occurrence in pregnancy, with at least 70 percent of women experiencing some form of it. It’s typically referred to as morning sickness, though it can happen at any time of day. But sometimes the symptoms are so extreme — severe, persistent nausea, vomiting, and weight loss during pregnancy — that it may be diagnosed as a less common disorder known as hyperemesis gravidarum. Hyperemesis gravidarum can lead to dehydration and nutrient loss, affecting both the health of a pregnant woman and the fetus she’s carrying. Nausea can be debilitating, interfering with daily activities and quality of life. It usually subsides at between 14 and 20 weeks (about 4 and a half months) of gestation. Women with hyperemesis gravidarum have an increased risk of preterm birth, preeclampsia, and eclampsia — a rare complication of preeclampsia that causes seizures during pregnancy — among other issues, but the risk is low.

ETIOLOGY

The etiology of hyperemesis gravidarum is largely unknown, but several theories exist (see pathophysiology). There are, however, risk factors associated with the development of hyperemesis during pregnancy. Increased placental mass in the setting of a molar or multiple gestations has been associated with a higher risk of hyperemesis gravidarum. Additionally, women who experience nausea and vomiting outside of pregnancy due to the consumption of estrogen-containing medications, exposure to motion, or have a history of migraines are at higher risk of experiencing nausea and vomiting during pregnancy. Some studies also suggest a higher risk of hyperemesis in women with first-degree relatives, for instance, if her mother or sister experienced hyperemesis gravidarum.

Experts don’t know for sure what causes hyperemesis gravidarum. However, rising hormone levels are most likely what causes it. Specifically, HCG (human chorionic gonadotropin), which your body makes during pregnancy — very quickly and in large amounts. HCG levels peak around 10 weeks of pregnancy, which is when most people report having the most severe symptoms. Estrogen, another hormone that increases during pregnancy, may also play a role in causing nausea and vomiting.

CLINICAL MANEFISTATIONS

The defining symptoms of hyperemesis gravidarum are gastrointestinal in nature and include nausea and vomiting. Other common symptoms include ptyalism (excessive salivation), fatigue, weakness, and dizziness. This vomiting can lead to:

Feeling dizzy, lightheaded, and faint

Losing more than 5 percent of body weight

Becoming dehydrated, with signs of dehydration such as dark urine and dry skin

PATHOPHYSIOLOGY

The exact cause of hyperemesis gravidarum remains unclear. However, there are several theories for what may contribute to the development of this disease process.

Hormone Changes: Levels of human chorionic gonadotropin (HCG) have been implicated. HCG levels peak during the first trimester, corresponding to the typical onset of hyperemesis symptoms. Some studies show a correlation between higher HCG concentrations and hyperemesis. However, this data has not been consistent.

Changes in the Gastrointestinal System: It is well-known that the lower esophageal sphincter relaxes during pregnancy due to the elevations in estrogen and progesterone. This leads to an increased incidence of gastroesophageal reflux disease (GERD) symptoms in pregnancy, and one symptom of GERD is nausea. Studies examining the relationship between GERD and emesis in pregnancy report conflicting results.

Genetics: An increased risk of hyperemesis gravidarum has been demonstrated among women with family members who also experienced hyperemesis gravidarum.

NURSING MANAGEMENT

1. Promote resolution of the complication.

2. Address emotional and psychosocial needs. Maintain a non-judgmental atmosphere in which the client and family can express concerns and resolve some of their fears.

MEDICAL MANAGEMENT

If you have severe symptoms of hyperemesis gravidarum, you may need to be hospitalized. Hyperemesis gravidarum is the second leading cause of hospitalization in early pregnancy. For less severe cases, you may be able to seek treatment at home or at a doctor’s office. While the course of treatment for hyperemesis gravidarum varies from person to person, your doctor may recommend one or more of the following:

Vitamin B6

Small, frequent meals that include dry, bland foods such as crackers

NURSING DIAGNOSIS

Nausea: Nausea is an uneasiness of the stomach that often comes before vomiting. Vomiting is the forcible voluntary or involuntary emptying ("throwing up") of stomach contents through the mouth.

Related to:

Pregnancy

Unpleasant sensory stimuli

Rise in hormone levels

Multiple gestation pregnancy

Genetic predisposition

As evidenced by:

Food aversion

Increased salivation

Gagging sensation

Sour taste

Increased swallowing

Vomiting

Expected outcomes:

Patient will verbalize the reduction of incidence and severity of nausea and vomiting.

Patient will demonstrate effective interventions that can help alleviate nausea and vomiting.

Patient will be able to eat small meals and/or consume fluids.

INCOMPETENT CERVIX

ETIOLOGY

A condition that refers to the inability of the cervix to hold the fetus any longer until term because it has dilated prematurely.

Uterine abnormalities and genetic disorders affecting a fibrous type of protein that makes up your body's connective tissues (collagen) might cause an incompetent cervix.

CLINICAL MANIFESTATION

Show. This is a pink-tinged vaginal fluid that is discharged from the vaginal opening as a sign that the cervix has dilated. Increased pelvic pressure. The fetus is already descending, causing a pressure felt by the mother on her pelvis. Cervical dilation. Upon inspection of the physician, the cervix would show dilation

NURSING INTERVENTIONS

Determine any factors that further contribute to the anxiety of the woman so it could be avoided.

Monitor vital signs to determine any physical responses of the patient that could affect her condition.

Convey empathy and establish a therapeutic relationship to encourage client to express her feelings.

Provide accurate information about the situation to help client back into reality.

PATHOPHYSIOLOGY

When the fetus reaches its 20th week, it starts to become heavy and gain fats.

The mother’s cervix is weak, and it could not hold the fetus’ weight anymore as it slowly starts to dilate.

This would cause the appearance of a show, a pink-tinged vaginal discharge.

Then, the membranes would rupture and amniotic fluid would be discharged.

Uterine contractions would start followed by a short labor, then the birth of the fetus.

DIAGNOSTIC TESTS

There are few diagnostic tests that could detect an incompetent cervix before it usually happens. It is usually diagnosed after the pregnancy has already been lost.

Ultrasound. This is the only test that the physician could order if an incompetent cervix is already suspected.

NURSING MANAGEMENT

As nurses, here is what we could do to help in our own way.

MEDICAL MANAGEMENT

Medical management by the physician would not include any medications that could hinder the dilation of the cervix. Surgical procedures are immediately enforced to prevent compromising the pregnancy.

NURSING DIAGNOSIS

Anxiety related to impending loss of pregnancy as evidenced by premature dilation of the cervix.

PLACENTA ACCRETA

Placenta accreta is an uncommon condition in which the chorionic villa adheres to the myometrium. It can be exhibited as:

Placenta accreta: the placental chorionic villi adheres to the superficial layer of the uterine myometrium.

Placenta increta: the placental chorionic villi invade deeply into the uterine myometrium.

Placenta percreta: the placental chorionic villi grow through the uterine myometrium and often adhere to abdominal structures (eg, bladder or intestine).

ETIOLOGY

Predisposing factors are prior uterine surgery and placenta previa

CLINICAL MANIFESTATIONS

Placenta fails to separate

Profuse hemorrhage may result depending on the portion of placenta involved.

PATHOPHYSIOLOGY

Implantation in an area of defective endometrium with no zone separation between the placenta and the myometrium.

DIAGNOSTIC TEST

Ultrasound

MRI

Note: Your health care provider can evaluate how deeply the placenta is implanted in your uterine wall.

MEDICAL MANAGEMENT

Placenta accreta is a rare condition and is associated with considerable maternal morbidity and mortality. Though the surgical approach of hysterectomy is a definitive therapy, there are occasions when conservation of the uterus is desired by the patient.

NURSING DIAGNOSIS

Risk for bleeding

Related to:

Disease process

Low-lying placenta

Sexual intercourse

Vaginal examinations

Labor

As evidenced by:

A risk diagnosis is not evidenced by signs and symptoms, as the problem has not occurred yet and nursing interventions are directed at the prevention of symptoms.

Expected Outcomes:

The patient discusses and demonstrates precautions to prevent bleeding complications

The patient is able to deliver the fetus without excessive bleeding

References

AWagrier M. (2022, October 21) Nurse Together Placenta Previa Nursing Diagnosis & Care Plan

RN Pedia Placenta Accreta Nursing Management

PLACENTA PREVIA

The placenta has implanted at the bottom of the uterus, over the cervix or close by, which means the baby can’t be born vaginally.

ETIOLOGY

Low implantation of the fertilised egg

Abnormalities of the uterine lining, such as fibroids

Scarring of the uterine lining (endometrium)

Abnormalities of the placenta

Multiple babies, such as twins

Multiple pregnancies - a woman who has already had six or more deliveries has a risk of one in 20.

CLINICAL MANIFESTATION

Painless vaginal bleeding - During the later stages of pregnancy, the bottom part of the uterus thins and spreads to accommodate the growing baby. If the placenta is anchored to the bottom of the uterus (as occurs with placenta previa), this thinning and spreading separates the placenta and causes bleeding.

Sexual intercourse can also cause bleeding from the placenta previa in later pregnancy. During labour, the cervix thins and dilates, which would normally allow the baby to exit into the vagina. In placenta previa, the dilation of the cervix further tears the placenta and causes bleeding.

PATHOPHYSIOLOGY

The placenta implants on the lower part of the uterus.

The lower uterine segment separates from the upper segment as the cervix starts to dilate.

The placenta is unable to stretch and accommodate the shape of the cervix, resulting in bleeding.

DIAGNOSTIC TEST

Ultrasound scan

Feeling the mother’s belly to establish the baby’s position (the baby is sideways or presenting bottom-first in around one in three cases of placenta previa)

NURSING MANAGEMENT

Assess baseline vital signs especially the blood pressure. The physician would order monitoring of the blood pressure every 5-15 minutes.

Assess fetal heart sounds to monitor the wellbeing of the fetus.

Monitor uterine contractions to establish the progress of labor of the mother.

MEDICAL MANAGEMENT

Medical interventions are necessary to ensure that the safety of both mother and fetus are still intact.

Intravenous therapy: This would be prescribed by the physician to replace the blood that was lost during bleeding.

Avoid vaginal examinations: This may initiate hemorrhage that is fatal for both the mother and the baby.

Attach external monitoring equipment: To monitor the uterine contractions and record fetal heart sounds, an external equipment is preferred than the internal monitoring equipment.

NURSING DIAGNOSIS

Fear related to outcome of pregnancy due to bleeding.

Reference: Belleza M., RN (2021, April 22) Placenta Previa

POSTPARTUM DEPRESSION

Postpartum depression (PPD) is a type of depression that affects new mothers after giving birth. It typically occurs within the first few weeks to months after delivery, but can develop at any time during the first year postpartum.

ETIOLOGY

The exact cause of postpartum depression (PPD) is not fully understood, but it is likely a combination of biological, psychological, and environmental factors. Some of the factors that may contribute to the development of PPD include:

1. Hormonal changes: During pregnancy, a woman's hormone levels, particularly estrogen and progesterone, increase significantly.

2. Genetics: Women with a family history of depression or other mood disorders may be at a higher risk for developing PPD.

3. Stressful life events: The transition to motherhood can be challenging, and women who experience significant stress during pregnancy or after childbirth, such as financial stress, relationship problems, or a difficult birth experience, may be more likely to develop PPD.

4. Lack of social support: Women who do not have adequate social support during and after pregnancy may be more vulnerable to developing PPD.

5. Previous history of depression: Women who have experienced depression or other mental health conditions in the past are at a higher risk for developing PPD.

CLINICAL MANIFESTATION

Postpartum depression (PPD) can manifest in a variety of ways, and symptoms may vary from person to person. Some common clinical manifestations of PPD include:

1. Mood changes: This may include feelings of sadness, irritability, anxiety, or hopelessness that are persistent and do not improve with time.

2. Sleep disturbances: Women with PPD may have difficulty sleeping or may sleep excessively.

3. Appetite changes: This may include a loss of appetite or an increase in appetite.

4. Fatigue and loss of energy: Women with PPD may feel extremely tired and have difficulty completing daily tasks.

PATHOPHYSIOLOGY

The exact pathophysiology of postpartum depression (PPD) is not fully understood, but it is believed to involve complex interactions between hormonal, genetic, environmental factors, and changes in brain function and structure.

1. Hormonal: After childbirth, hormone levels drop rapidly, which may contribute to the development of PPD

2. Environmental factors: Stress, lack of social support, and a history of trauma may also contribute to the development of PPD.

3. Changes in brain function and structure: Studies have shown that women with PPD have altered activity in certain areas of the brain, particularly in areas involved in emotional processing and regulation.

DIAGNOSTIC TEST

There is no single test to diagnose postpartum depression (PPD): Dagnosis is typically made based on clinical evaluation, which may include a physical exam, review of symptoms, and assessment of medical history and family history.

Edinburgh Postnatal Depression Scale (EPDS): Commonly used screening tool that can help healthcare providers identify women who may be at risk for PPD.

NURSING MANAGEMENT

Nursing management of postpartum depression (PPD) may include:

1. Assessing for risk factors: Nurses should assess for risk factors for PPD, including a history of depression or anxiety, a lack of social support, a difficult pregnancy or childbirth experience, and a history of trauma.

2. Educating the patient: Nurses should provide education to new mothers about PPD, including its symptoms, risk factors, and available treatments.

3. Providing emotional support: Nurses should provide emotional support to new mothers who are experiencing PPD, including active listening, validation of feelings, and empathy.

MEDICAL MANAGEMENT

Medical management of postpartum depression (PPD) may include:

1. Medication: Antidepressants such as selective serotonin reuptake inhibitors (SSRIs) may be prescribed to help alleviate symptoms of PPD.

2. Psychotherapy: Psychotherapy, such as cognitive-behavioral therapy (CBT) or interpersonal therapy (IPT), may be recommended to help new mothers manage symptoms of PPD and develop coping strategies.

3. Hormone therapy: In some cases, hormone therapy may be used to help regulate hormone levels and improve mood.

4. Referral to a specialist: Patients with severe or treatment-resistant PPD may be referred to a mental health specialist, such as a psychiatrist or psychologist, for further evaluation and treatment.

5. Support groups: Support groups or peer counseling may be recommended to help new mothers with PPD connect with others who are experiencing similar challenges.

POSTPARTUM HEMORRHAGE

ETIOLOGY

Postpartum hemorrhage has four main: uterine atony, trauma, retained placenta, and coagulopathy. The most common and challenging to treat is uterine atony, where a lack of uterine contractility leads to massive hemorrhage postpartum.

CLINICAL MANIFESTATION

Heavy vaginal bleeding.

Drop in blood pressure or signs of shock.

Tense and rigid uterus.

Inadequate blood coagulation.

PATHOPHYSIOLOGY

There are different main causes of postpartum hemorrhage, and they cause bleeding in different ways.

In uterine atony, the uterus stops contracting, which leads to bleeding because the placental sites have closed.

If the uterus has retained placental fragments, it can also cause massive bleeding postpartum.

DIAGNOSTIC TEST

Pelvic exam: Your provider checks your vagina, uterus, and cervix

Hematocrit: This is a blood test that checks the percent of your blood (called whole blood) that’s made up of red blood cells.

Ultrasound: Your provider can use ultrasound to check for problems with the placenta or uterus. Ultrasound is a test that uses sound waves and a computer screen to make a picture of your baby inside the womb or your pelvic organs.

NURSING MANAGEMENT

Need to intervene early or during the course of a hemorrhage to help the patient regain her strength and vitality.

Establish data that would give essential care to the patient with hemorrhage.

Address emotional and psychosocial needs.

Save all perineal pads used during bleeding and weigh them to determine the amount of blood loss.

Blood Replacement

NURSING DIAGNOSIS

Deficient fluid volume related to excessive bleeding after birth.

Risk for Infection.

Ineffective Tissue Perfusion

ADHD (Attention-deficit/Hyperactivity disorder)

One of the most prevalent neurodevelopmental diseases in children is ADHD. It frequently persists into maturity and is typically first diagnosed in infancy. Children with ADHD may struggle to focus, manage impulsive behaviors (doing without considering the consequences), or be extremely active.

ETIOLOGY

Recent research relates genetic causes to ADHD. Scientists are researching additional potential causes and risk factors, such as brain injury, in addition to genetics. environmental dangers (like lead) being exposed when pregnant or when young.

MANIFESTATIONS

Easily Distracted

Daydreaming

Forgetfulness

Excessive Talking

Careless Mistakes

Impatience

NURSING INTERVENTIONS

Accept the child or individual as what he is

Approach the child at his current level of functioning

Use simple and direct instructions.

Implement scheduled routine every day

Avoid stimulating or distracting settings

Give positive reinforcements

Encourage physical activity

PATHOPHYSIOLOGY

ADHD is linked to cognitive and functional problems. In those with ADHD, it is discovered that the anterior cingulate gyrus and the dorsolateral prefrontal cortex (DLFPC) are tiny.

NURSING MANAGEMENT

Nurses must possess the necessary expertise to care for patients with ADHD, and they must take behavioral and environmental factors into account.

MEDICAL MANAGEMENT

The therapeutic approach to ADHD has been shifting.

Behavioral psychotherapy: When combined with a successful pharmaceutical regimen, behavioral psychotherapy is frequently beneficial; behavioral therapy or behavior modification programs can assist reduce ambiguous expectations and improve organization.

Psychosocial interventions: Effective psychosocial interventions include behavioral parent training and behavioral classroom management, which work best when combined with psychopharmacological methods.

Cognitive therapy for adults with ADHD: Through the use of cognitive and behavioral therapy principles and techniques to improve time management, adult ADHD patients are now better equipped to combat the anxiety and depressive symptoms that interfere with task performance.

NURSING DIAGNOSIS

Defective Coping

Impaired social interactions

Altered thought processes

Risk for parental role conflict

Risk for injury

Risk for delay in growth and development

Reference: Belleza, M. (2017, September 23). Attention Deficit Hyperactivity Disorder: Pediatric Nursing Study Guide. Nurseslabs

ATRIAL SEPTAL DEFECT (ASD)

An abnormal opening in the atrial septum between the right and the left atria often caused by failure of foramen ovale to close.

ETIOLOGY

Every child is born with an opening between the upper heart chambers. It’s a normal fetal opening that allows blood to detour away from the lungs before birth. After birth, the opening is no longer needed and usually closes or becomes very small within several weeks or months.

Sometimes the opening is larger than normal and does not close after birth. Some children can have other heart defects along with Atrial Septal Defect (ASD).

In some cases, the tendency to develop ASD might be inherited (genetic). Genetic syndrome can cause extra or missing pieces of chromosomes that can be associated with ASD.

In most children the cause is not known. The exact cause of ASD is unknown.

CLINICAL MANIFESTATIONS

Manifestations depend on its size and its location Usually asymptomatic: small to moderate size and may not be diagnosed until preschool years or later. Children with larger, more severe ASDs, might have some of these signs or symptoms:

Shortness of breath, especially during physical activity.

Extreme tiredness

Palpitations or rapid heartbeat

Cyanosis, a bluish tint to the skin or lips due to decreased oxygenation.

Delayed growth and development in infants and children.

Frequent respiratory infections

Harsh systolic murmur.

Hypertrophy of the right side of the heart.

Congestive heart failure may occur depending on the size of the defect.

PATHOPHYSIOLOGY

The pathophysiology of ASD involves abnormal blood flow between the atria, which can lead to increased pressure and volume overload in the right atrium and the right ventricle.

Normally, oxygen-poor blood returns from the body to the right atrium and is then pumped into the right ventricle, which pumps it to the lungs for oxygenation. Oxygen-rich blood from the lungs returns to the left atrium and is then pumped into the left ventricle, which pumps it to the rest of the body.

In the case of ASD, there is a hole in the atrial septum, allowing blood to flow from the left atrium to the right atrium, instead of the normal unidirectional flow. As a result of the abnormal blood flow, there is increased blood volume in the right atrium and right ventricle, which cause the right side of the heart to work harder that normal, which can eventually lead to right ventricular hypertrophy (thickening of the right ventricular wall).

The increased volume in the right atrium and ventricle can also cause increased pressure in these chambers. Over time, this pressure can cause pulmonary hypertension (high blood pressure in the pulmonary arteries), which can lead to right heart failure.

Blood shunting from left to right can also lead to oxygen-rich blood being pumped back to the lungs, which can lead to an increased workload on the lungs, in some cases, to Eisenmenger syndrome, which is characterized by the development of pulmonary hypertension and a reversal of the shunt from right to left, resulting in cyanosis.

The severity of ASD and its impact on the heart and lungs depend on the size and location of the defect, as well as the age at which it is diagnosed and treated. Early diagnosis and intervention can prevent or minimize the potential complications associated with ASD.

DIAGNOSTIC TEST

Electrocardiogram (ECHO)

Echocardiogram (ECG/EKG)

Chest X-ray

Cardiac catheterization

Magnetic resonance imaging (MRI),

NURSING MANAGEMENT

Assess and monitor vital signs frequently, including heart rate, blood pressure, and oxygen saturation to detect any changes or signs of complications. Promote rest and activity limitation. Nurse can educate patient about the importance of rest and activity limitations, and help them develop strategies to conserve energy.

Administer medications as prescribed, such as diuretics to manage symptoms like fluid overload. Ensure medications are administered on schedule and monitor for any adverse effects. Provide emotional support and health education.

Monitor for potential complications. Prepare client for surgery or interventional procedures. Provide education about the procedure and postoperative care, as well as assist with preoperative preparation and postoperative monitoring.

After surgery:

Closely monitor vital signs, central venous and intra-arterial pressures, intake and output.

Give an antibiotic and an analgesic, as ordered.

MEDICAL MANAGEMENT

Medication to treat symptoms, namely diuretics will be attempted first in an effort to allow the defect to close spontaneously.

Defect that remain 5 mm or greater with persistent shunting after an observation period should be referred for closure to decrease the incidence of supraventricular dysrhythmias and prevent pulmonary vascular disease. Secundum ASD, defect that is located in the center of the atrial septum, is typically closed in the catheterization lab with a device that sits in the defect space.

Cardiac Catheterization, a thin, flexible tube (a catheter) is inserted into a blood vessel in the leg that leads to the heart. A special implant is positioned into the hole and is designed to flatten against the septum on both sides to close and permanently seal the ASD. Taking a low dose of aspirin for 6 months is needed to prevent the risk of blood clots. Less physical activity for a few days or weeks.

Sinus venosus, found high in the septum where the pulmonary veins enter the left atrium, and primum defects, found low in the atrial septum near the inferior vena cava (IVF), are referred for surgical closure, they cannot be closed in the catheterization lab because of their anatomy. When the ASD is very large or too close to the wall of the heart, surgery is needed to close the defect. Surgical closure involves a median sternotomy incision and cardiopulmonary bypass.

NURSING DIAGNOSIS

Risk for decreased cardiac output related to the defect structure.

Impaired gas exchange related to decreased pulmonary blood flow secondary to shunting of blood from the right atrium to the left atrium through the ASD.

Risk for injury related to the risk of stroke or embolism due to the shunting of blood through the ASD.

References:

American Heart Association. (2019). Atrial septal defect (ASD).

Straight Nursing. (n.d). Atrial septal defect nursing assessment and intervention.

AUTISM

Autism spectrum disorder (ASD) is a developmental disability caused by differences in the brain. People with ASD often have problems with social communication and interaction, and restricted or repetitive behaviors or interests. People with ASD may also have different ways of learning, moving, or paying attention.

ETIOLOGY

Autism spectrum disorder has no single known cause. Given the complexity of the disorder, and the fact that symptoms and severity vary, there are probably many causes. Both genetics and environment may play a role.

GENETICS: Several different genes appear to be involved in autism spectrum disorder. For some children, autism spectrum disorder can be associated with a genetic disorder, such as Rett syndrome or fragile X syndrome. For other children, genetic changes (mutations) may increase the risk of autism spectrum disorder. Still other genes may affect brain development or the way that brain cells communicate, or they may determine the severity of symptoms. Some genetic mutations seem to be inherited, while others occur spontaneously.

ENVIRONMENTAL FACTORS: Researchers are currently exploring whether factors such as viral infections, medications or complications during pregnancy, or air pollutants play a role in triggering autism spectrum disorder.

PATHOPHYSIOLOGY

1. Dysfunction of neural functions: Some findings on the pathophysiology of autism are based on the brain’s ability to perform neural functions efficiently. Our brain’s neural function is best assessed based on its ability to build healthy neural circuits, and this is granted by a process called synaptic pruning. A synapse is the point on a nerve that transmits information from one neuron to the next. A synapse allows for neural communication between cells. When there’s too many synaptic connections, the brain goes through a process of cutting down; known as synaptic pruning.

2. Genetic and epigenetics factors in autism: Epigenetics is the study of how the environment and our behaviors affect how our genes work. Although epigenetic changes are reversible, and do not change your DNA sequence, they can however change your body reads a DNA sequence. In addition, some epigenetic changes can be hereditary.

3. The endocrine system: The endocrine system consists of glands that secrete hormones, namely: the thyroid gland, the parathyroid glands, the hypothalamus, pituitary gland, and pineal gland in the brain, the thymus, the pancreas, ovaries (in women), and testes (in men), and the adrenals.

DIAGNOSTIC TESTS

Autism Diagnosis Interview – Revised (ADI-R) A clinical diagnostic instrument for assessing autism in children and adults.

Autism Diagnostic Observation Schedule – Generic (ADOS-G)

Childhood Autism Rating Scale (CARS)

Gilliam Autism Rating Scale – Second Edition (GARS-2)

NURSING MANAGEMENT

1. The nurse must be able to familiarize the combination of symptoms associated with autism of the patient.

2. The nurse is the coordinator of therapies and interventions that meet the specific needs of individual children.

3. During the treatment session, the nurse’s main goal is to provide safety. The nurse must ensure that unnecessary may harm the child, and are removed from the area. It is also important to let the other staff members know of the child’s special needs.

4. Apply appropriate behavioral strategies. One example is the applied behavioral analysis (ABA). This program uses a one-on-one teaching approach that reinforces the practice of various skills. The goal is to get the child close to normal developmental functioning.

5. Listen to the child, his parents and the caregivers. As a nurse, you have to be an effective channel of communication among these people.

MEDICAL MANAGEMENT

Special education for the child

Behavioral management

Medications

Biomedical and complementary therapies

Antipsychotic drugs

Minerals, vitamins and dietary interventions

NURSING DIAGNOSIS

Impaired verbal communication related to reduced ability to read body language

At risk for injury

Impaired social interaction

Family and caregiver lack of knowledge regarding autism

Ineffective therapeutic regimen related to economic difficulties

CEREBRAL PALSY

Cerebral palsy is a group of disorders that affect normal movement in different parts of the body. This condition can cause problems with posture, manner of walking (gait), muscle tone, and coordination of movement. The word “cerebral” refers to the brain’s cerebrum, which is the part of the brain that regulates motor function. “Palsy” describes the paralysis of voluntary movement in certain parts of the body. There are several types of cerebral palsy that are characterized by the location of the brain injury. Symptoms can vary depending on where and how badly the brain was damaged. The types of cerebral palsy include:

Ataxic cerebral palsy: This type is caused by cerebellum damage resulting in issues with motor control and movement.

Athetoid/dyskinetic cerebral palsy: Caused by basal ganglia and/or cerebellum damage; symptoms include fluctuating muscle tone and involuntary movements.

Hypotonic cerebral palsy: This rare type, also caused by cerebellum damage, is characterized by floppy muscles, excess flexibility, and poor mobility.

Spastic cerebral palsy: The most common type of cerebral palsy, caused by damage to the motor cortex or pyramidal tracts and characterized by tight muscles and jerking movements.

Mixed cerebral palsy: Multiple areas of brain damage can cause patients to have more than one type of cerebral palsy.

ETIOLOGY

Cerebral palsy is caused by damage or abnormal development in the parts of the brain that control movement. These events can happen before, during, or shortly after birth or in the first few years of life, when the brain is still developing. In many cases the exact cause of cerebral palsy is not known.

CLINICAL MANEFISTATIONS

The symptoms of cerebral palsy vary from person to person and range from mild to severe. Some people with cerebral palsy may have difficulty walking and sitting. Other people with cerebral palsy can have trouble grasping objects. The effects of the condition can become more or less obvious or limiting as a child grows and develops motor skills. They also vary depending on the part of the brain that was affected.

Developmental delay. History of gross motor developmental delay in the first year of life.

Abnormal muscle tone. The most frequently observed symptom; the child may present as either hypotonic or, more commonly, hypertonic, with either decreased or increased resistance to passive movements, respectively; children with cerebral palsy may have an early period of hypotonia followed by hypertonia; a combination of axial hypotonia and peripheral hypotonia is indicative of a central process.

PATHOPHYSIOLOGY

Cerebral palsy (CP), defined as a group of nonprogressive disorders of movement and posture, is the most common cause of severe Neurodisability in children. Understanding its physiopathology is crucial to developing some protective strategies. Interruption of oxygen supply to the fetus or brain asphyxia was classically considered to be the main causal factor explaining later CP. However, several ante-, peri-, and postnatal factors could be involved in the origins of CP syndromes. Congenital malformations are rarely identified. CP is most often the result of environmental factors, which might interact with genetic vulnerabilities, and could be severe enough to cause the destructive injuries visible with standard imaging (i.e., ultrasonographic study or MRI), predominantly in the white matter in preterm infants and in the gray matter and the brainstem nuclei in full-term newborns. Moreover, they act on an immature brain and could alter the remarkable series of developmental events. Biochemical key factors originating in cell death or cell process loss, observed in hypoxic-ischemic as well as inflammatory conditions, are excessive production of proinflammatory cytokines, oxidative stress, maternal growth factor deprivation, extracellular matrix modifications, and excessive release of glutamate, triggering the excitotoxic cascade. Only two strategies have succeeded in decreasing CP in 2-year-old children: hypothermia in full-term newborns with moderate neonatal encephalopathy and administration of magnesium sulfate to mothers in preterm labor.

DIAGNOSTIC TEST

A doctor will diagnose cerebral palsy by taking a complete medical history, performing a physical exam that includes a detailed neurological exam, and evaluating the symptoms. The following additional testing may also be used:

Electroencephalogram (EEG). An EEG is used to evaluate electrical activity in the brain. A doctor may order it when someone is showing signs of epilepsy, a primary cause of seizures. Learn more about epilepsy and seizures.

MRI. An MRI uses powerful magnets and radio waves to produce detailed images of the brain. A healthcare professional may perform an MRI in order to identify brain irregularities or injuries.

CT scan. A CT scan creates clear, cross-sectional images of the brain. It can also reveal brain damage.

Ultrasound. A cranial ultrasound is a method of using high-frequency sound waves to get basic images of a young infant’s brain. It’s relatively quick and inexpensive. Learn more about ultrasound.

Blood tests. A healthcare professional may take and test a sample of blood to rule out other possible conditions, such as bleeding disorders.

NURSING MANAGEMENT

Use of communication board or computer-assisted communication

Self-care is the goal of care for children

Provide adequate nutrition and rest

Increase calorie intake

Maintain a safe environment

Provide headgear or padded bed

NURSING DIAGNOSIS

Based on the assessment data, the major nursing diagnoses include:

Risk for injury related to spasms, uncontrolled movements, and seizures.

Impaired physical mobility related to spasms and muscle weakness.

Changes in growth and development related to neuromuscular disorders.

Impaired verbal communication related to difficulty in articulation.

Risk for aspiration related to neuromuscular disorders.

Disturbed thought processes related to cerebral injury, learning disabilities.

Self-care deficit is related to muscle spasms, increased activity, cognitive changes.

Deficient knowledge related to home care and therapeutic needs.

CLEFT LIP AND PALATE

ETIOLOGY

Cleft lip occurs as a familial tendency or most likely occurs from the transmission of multiple genes. It is twice as prevalent in the Japanese population and occurs rarely. A formation may be aided by teratogenic factors present during weeks 5 to 8 of intrauterine life, such as viral infection or possibly a deficiency of folic acid.

Most cases appear to be consistent with the concept of multifactorial inheritance as evidenced by an increased incidence in relatives and monozygotic twins

Environmental. In some cases, babies inherit a gene that makes them more likely to develop a cleft, and then an environmental trigger actually causes the cleft to occur.

CLINICAL MANIFESTATIONS

These defects are readily apparent at birth.

Cleft lip involves a notched upper lip border, nasal distortion, and may include unilateral or bilateral involvement.

Cleft palate is a visible or palpable gap in the uvula, soft palate, hard palate, and/or incisive foramen with exposed nasal cavities and associated nasal distortion.

Difficulty swallowing. The newborn has a hard time in swallowing, with the potential for liquids or foods to come out the nose.

PATHOPHYSIOLOGY

During embryonic development the lateral and medial tissues forming the upper lip fuse between weeks 7 and 8 of gestation; the palatal tissues forming the hard and soft palate fuse between 7 and 12 weeks of gestation.

Cleft lip and cleft palate result when these tissues fail to fuse

The cleft may be a simple notch in the vermilion line, or it may extend up into the floor of the nose.

DIAGNOSTIC TEST

Cleft lip may be detected by a sonogram while the infant is in utero. If not detected then, it is readily apparent on inspection at birth.

Cleft palate can be determined by depressing the newborn’s tongue with a tongue blade. This reveals the total palate and the extent of the cleft palate. Be sure to have clear lighting to visualize the palate clearly.

NURSING MANAGEMENT

Assess for problems with feeding, breathing, parental bonding, and speech.

Ensure adequate nutrition and prevent aspiration.

Provide special nipples of feeding devices (e.g., soft pliable bottle with soft nipples with enlarged opening) for a child unable to suck adequately on standard nipples.

Hold the child in a semi-upright position; direct the formula away from the cleft and toward the side and back of the mouth to prevent aspiration.

Feed the infant slowly and burp frequently to prevent excessive swallowing of air and regurgitation.

NURSING DIAGNOSIS

Risk for aspiration related to a reduced level of consciousness after surgery.

Risk of injury to the operative site related to newborns' desire to suck thumb or fingers and anatomical changes.

Imbalanced nutrition less than body requirement related to food intake

Deficient knowledge (mother) regarding proper feeding techniques

COLIC

Colic is paroxysmal abdominal pain that generally occurs in infants under 3 months of age. Colic is most common during the first 6 weeks of life. It is also when a healthy baby cries for a very long time, for no obvious reason. In most infants, colic disappears almost magically at 3 months of age, probably because it becomes easier to digest foods and an infant maintains a more upright position by this time which allows less gas to form

ETIOLOGY

The exact cause of Colic is still unclear. However, some potential causes why it happens are being explored. These include:

Having a milk allergy or intolerance

Being sensitive to gas

Unable to calm themselves

CLINICAL MANIFESTATIONS

Colic often begins suddenly, with loud and mostly nonstop crying like a colicky crying. It is louder with a high-pitched, and more urgent sounding than regular crying. Colicky babies can be very hard to calm down. Moreover, babies with colic are often fussy and gassy. The face of the infants with colic becomes red and flushed. If offered a bottle, the infant will suck vigorously for a few minutes a s if starved, then stop as another wave of intestinal pain occurs. Additionally, colic is defined as when a baby’s crying lasts for more than 3 hours a day, happens more than 3 days a week, and occurs for more than 3 weeks. Babies who have colic may also show manifestations such as:

Burping often or passing a lot of gas

Having a tight belly

Curling up their legs toward their belly when crying

Clenching their fists when the abdomen become tense.

PATHOPHYSIOLOGY

It may occur in susceptible infants from overfeeding or from swallowing too much air while feeding

Formula-fed babies are more likely to have colic than breast-fed babies possibly because they swallow more air while drinking or because formula is harder to digest.

DIAGNOSTIC TEST

Thorough assessment of the signs and symptoms of colic that may be present to the infant.

Observe the duration and frequency of the problem (usually lasts up to 3 hours a day and occurs at least 3 days every week)

A family medical history is also important to obtain because allergy to milk may stimulate colic.

Thorough history taking on the feeding practices of the baby and the preparation of the mother.

Blood tests and X-rays or other imaging tests may be done (these can help find out if your baby has other health problems)

NURSING MANAGEMENT

Ask parents about the duration of the problem and its frequency.

Ask what happens just before the attack and describe the attack itself.

Document the number and type of bowel movements.

Determine the baby’s feeding pattern.

Offering a pacifier may be comforting.

Help parents plan relief time from infant care to relieve stress.

NURSING DIAGNOSIS:

The care provider should do a complete physical exam to diagnose any possible causes for the baby's distress. The exam will include:

Measuring baby's height, weight and head circumference

Listening to the heart, lungs and abdominal sounds

Examining the limbs, fingers, toes, eyes, ears and genitals

Assessing reaction to touch or movement

Looking for signs of rash, inflammation, or other signs of infection or allergies