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Chapter 26

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Rich Kroll

on 23 February 2015

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Transcript of Chapter 26

Pregnancy can alter the care of concurrent disorders in two ways:
Pregnancy may alter the course of the disease
The disease or treatment may alter the pregnancy

Furthermore, some disorders which are mild or even unnoticeable by the mother may have serious fetal effects
This chapter will discuss some of these diseases

Cardiac Disease
Alterations in cardiovascular function are necessary in pregnancy to meet additional maternal metabolic demands and the needs of the fetus.
Anemias
Anemia is a condition in which a decline in circulating RBC mass reduces O2 carrying ability to mother's organs and the fetus
One of the most common problems of pregnancy
Affecting 15%-25% of women
Associated with preterm labor and low birth weight
Pregnant woman is considered anemic if hgb < 10.5 or 11 g/dL
Iron
Deficiency Anemia
Total iron requirement in pregnancy is about 1,000 mg
Insufficient stores due to menstrual blood loss
Meeting iron needs by diet alone is difficult
Found in meat, fish, chicken, liver, & green leafy vegetables
Medical Conditions
Women with preexisting conditions must be aware of the effects the pregnancy will have on their condition, and the effect the condition will have on the pregnancy
Diabetes Mellitus
Chapter 26
Concurrent Disorders during Pregnancy

Infections
During Pregnancy

Pathophysiology
Etiology
Effect of Pregnancy on Fuel Metabolism
Classification
Incidence
Preexisting
Diabetes Mellitus
Early Pregnancy
Late Pregnancy
Birth
Postpartum Period
Maternal Effects
Fetal Effects
Congenital Malformation
Variations in Fetal Size
Neonatal Effects
Hypoglycemia
Hypocalcemia
Hyperbilirubinemia
Respiratory Distress Syndrome
Maternal Assessment
History
Physical Examination
Laboratory Tests
Fetal Surveillance
Therapeutic Management
Preconception Care
Diet
Self-Monitoring of Blood Glucose Levels
Insulin Therapy
First Trimester
Second and Third Trimesters
During Labor
Postpartum Period
Oral Therapy
Timing of Delivery
Gestational Diabetes Mellitus
Risk Factors
Identifying
Gestational Diabetes
Screening
Glucose Challenge Test
Oral Glucose Challenge Test
Maternal, Fetal, and Neonatal Effects
Therapeutic Management
Diet
Exercise
Blood Glucose Monitoring
Fetal Surveillance
Nursing Considerations
Increasing Effective Communication
Providing Opportunities for Control
Providing Normal Pregnancy Care
The glucose accumulates in the blood resulting in hyperglycemia. The body attempts to rid the glucose by polydipsia, causing blood volume to increase. The kidneys now work to rid the vascular system through polyuria the excess fluid and glucose. When glucose cannot get into the cell the cell starves causing polyphagia.
1 to 20 weeks gestation
There is little change in the metabolic rates and energy needs for the mother at this time. However, insulin release in response to serum glucose levels accelerates which may cause hypoglycemia. This particularly occurs in women experiencing morning sickness.
Understanding the way pregnancy and diabetes alter the metabolism of food.
20 to 40 weeks gestation
During this time fetal growth accelerates and placental hormones rise sharply, particularly estrogen, progesterone, and human placental lactogen (hPL). Causing a resistance to insulin in maternal cells and increasing the availability of glucose for the fetus. Thus, having a diabetogenic effect that may leave the woman insufficient of insulin and hyperglycemic.
Maintenance of normal maternal glucose levels is essential during birth to reduce neonatal hypoglycemia.
Women will continue with glucose testing and administration of insulin the day before a scheduled induction or c-section.
After the admission and the diet is NPO glucose levels will be monitored hourly and a continuous infusion of glucose and insulin is started.
The need for insulin falls during this period
Breatfeeding is encouraged, not only because of the fetus, but the caloric intake by the mother lowers the need for insulin. The woman with gestational diabetes usually needs no insulin after birth.
The mother needs an intervention pertaining to her risk for developing type II diabetes before discharge.
The fetus continually draws glucose and amino acids from maternal blood, causing an earlier than normal switch from carbohydrate metabolism to gluconeogenesis. (the formation of glycogen from noncarbohydrate s such as proteins and fat)
There are three types of diabetes mellitus
Type 1: insulin deficient, beta cells do not produce insulin
Type 2: insulin resistant, there is production of insulin but not enough for carbohydrate metabolism.
Gestational diabetes: glucose intolerance begins during pregnancy
Diabetes mellitus is a common medical condition
90% to 95% of all reported cases are type 2
10% of all pregnancies are affected by GDM.

incidence varies with different ethnic groups, with African American, Latino, and American Indians having a higher prevalence for developing GDM.
Women who have had GDM are 30% to 65% more likely to develop diabetes in the next 10 to 20 years
Incidence and Classification
Rheumatic Heart Disease
Congenital Heart Disease
Left-to-Right Shunt
Atrial Septal defect
Ventricular Septal Defect
Patent Ductus Arteriousus
Right-to-Left Shunt
Tetralogy of Fallot
Eisenmenger's Syndrome
Mitral Valve Prolapse
Peripartum and Postpartum Cardiomyopathy
Diagnosis and Classification
Therapeutic Management
Class I or II Heart Disease
Class III or IV Heart Disease
Drug Therapy
Anticoagulants
Antidysrhythmics
Antiinfectives
Drugs for Heart Failure
Intrapartum Management
Postpartum Management
Maternal Effects
Fetal and Neonatal Effects
Therapeutic Management
Folic Acid Deficiency
(Megaloblastic Anemia)
Maternal Effects
Fetal and Neonatal Effects
Therapeutic Management
Sickle Cell Disease
Maternal Effects
Fetal and Neonatal Effects
Therapeutic Management
Thalassemia
Maternal Effects
Fetal and Neonatal Effects
Therapeutic Management
Immune Complex Diseases
Systemic Lupus Erythematosus
Antiphospholipid Syndrome
Hashimoto's Thyroidosis
Rheumatoid Arthritis
Neurologic Disorders
Seizure Disorders
Bell's Palsy
Viral
Infections

Cytomegalovirus
Fetal and Neonatal Effects
Therapeutic Management
Rubella
Fetal and Neonatal Effects
Therapeutic Management
(Chickenpox)
Varicella-Zoster Virus
Fetal and Neonatal Effects
Therapeutic Management
Herpes Simplex Virus
Fetal and Neonatal Effects
Therapeutic Management
Parovirus B19
Fetal and Neonatal Effects
Therapeutic Management
Hepatitis B
Fetal and Neonatal Effects
Therapeutic Management
Human
Immunodeficiency Virus
Fetal and Neonatal Effects
Prevention
Therapeutic Management
Non-viral Infections
Toxoplasmosis
Fetal and Neonatal Effects
Therapeutic Management
Group B Streptococcus Infection
Fetal and Neonatal Effects
Therapeutic Management
Tuberculosis
Fetal and Neonatal Effects
Therapeutic Management
References
Infections for pregnant women with type 1 DM often causes ketoacidosis.
Thresholds of hyperglycemia may be lower in pregnant women than in non-pregnant women.
Untreated ketoacidosis can progress to death for mother and fetus.
Hypoglycemia, hyperglycemia, and ketosis may lead to spontaneous abortion in the first trimester.
Preeclampsa is 2 to 3 times more likely to develop when the woman has DM
UTI's are more common, possibly due to the large amount glucose in the urine.
Macrosomia, fetus larger than (8.8lbs) can cause maternal tissue injury at birth.
Labor dystocia, cesarean birth, uterine atony with hemorrhage after birth due to:
hydramnios- resulting from fetal hyperglycemia and consequent fetal diuresis
premature rupture of the membranes- caused by over distention of the uterus by hydramnios or macrosomia
Fetal effects depend on the severity of maternal
hyperglycemia and the degree of vascular impairment
that has occurred
2 to 6 times more likely if maternal hyperglycemia is poorly controlled in the first trimester
Most common defects are neural tube defects, caudal regression syndrome (failure of the sacrum, lumbar spine, and lower extremities to develop), and cardiac defects
Fetal macrosomia results when elevated levels of blood glucose stimulate excessive production of fetal insulin, which acts as a powerful growth hormone.
Intrauterine growth restriction (IUGR) is impaired placental perfusion decreased by vasoconstriction and it causes an infant born small for gestational age (SGA).
There are four major effects
Caused by neonatal hyperinsulinemia after birth when maternal glucose is no longer available and insulin production remains high
The transfer of calcium is high during the last half of pregnancy. At the time of birth it is abruptly stopped leading to a dramatic decrease in ionized calcium.
Hypocalcemia is associated with preterm birth and perinatal aphyxia .
S/S include pallor, fatigue, lethargy, H/A
May include inflammation of lips / tongue
Pica
Labs - RBCs microcytic and hypochromic
Plasma iron and serum ferritin levels low
Total iron-binding capacity high
Multifetal pregnancies or bleeding complications put mother at higher risk for anemia
All effects on fetus and Neonate unclear
Fetus will generally receive adequate iron stores at the expense of the mother
If mother is severely anemic fetus with have reduced RBC volume, hgb, and iron stores
Profound maternal anemia will reduce fetal O2 supply
Routine supplementation, rather than based on anemia, is controversial
Ferrous Sulfate 325 mg PO 1-3 times per day is common supplementation
Taken with 500 mg Vitamin C or a glass of orange juice enhances absorption
Continued for 6 months after anemia has been corrected
Parenteral therapy may be needed for severe anemia or hgb < 8.5 g/dL
Folic acid is a coenzyme in the synthesis of DNA
Essential for cell duplication and fetal and placental growth
Essential for formation of RBCs
Needs double during pregnancy due to greater production of erythrocytes and fetal / placental growth
Deficiency results in reduction of DNA synthesis and mitosis resulting in large immature erythrocytes (megaloblasts)
Inadequate folate intake is primary cause
Nonfood factors include: hemolytic anemias with increased RBC turnover, multifetal pregnancy, some medications, and malabsorbtion problems
Folic acid deficiency is often present in association with iron deficiency anemia
Associated with increased risk of:
Spontaneous abortion
Abruptio placentae
Fetal anomalies
Increase in neural tube deficiencies
Recommended daily folic acid intake doubles with pregnancy
Best sources are fortified greens, legumes (black beans, lentils, peanuts, etc), dark green leafy vegetables
Folic acid often destroyed during cooking
Supplementation recommended to women of childbearing age of 400 mcg daily
Increase to 600 mcg daily with confirmed pregnancy
Most prenatal vitamins contain 1 mg of folate
Murray, S., & McKinney, E. (2014).
Foundations of maternal-newborn
and women's health nursing
(6th ed.). St Louis, MO: Elsevier.
A fetus experiencing recurrent hypoxia produces additional erythrocytes (polycythemia). After birth the excess erythrocytes are broken down, which releases large amount of bilirubin into the neonate's circulation without the ability to metabolize and excrete the bilirubin.
Autosomal recessive disorder
Production of hgb S
Become sickle-shaped in hypoxic, acidotic, and dehydrated conditions
Occludes small vessels and occludes perfusion
Affects those of African, Sub-Saharan decent
90,000 - 100,000 Americans annually
Cortisol production, slowed by fetal hyperinsulinemia, is needed for the synthesis of surfactant.
Delayed maturation of fetal lungs
inadequate production of pulmonary surfactant
slowed absorption of fetal lung tissue.
It is ideal for a woman with preexisting DM to receive preconception
care.
A detailed history covering the onset and management of the disease. What was her glycemic control before pregnancy? Was the patient compliant with her past plan of care? What does the patient and her partner know about the disease? Can she mix and inject her insulin?
Her emotional status will also be assessed for coping with her pregnancy.
Physiologic anemia, increased coagulation factors, venous stasis (normal in pregnancy) can precipitate sickle cell crisis
Prone to pyelonephritis, bone infection, and heart disease
Preeclampsia occurs in 15% of these women
Preterm birth and intrauterine growth restriction (IUGR) are common
The nurse needs to know what type of medications are being taken. Oral agents are not used during pregnancy, it has not been proven but they may cause adverse fetal effects
In absence of sickle cell crisis the fetus usually fares well
Instance of fetal weight loss is high if sickle cell crisis occurs due to placental infarctions
Higher instance of prematurity and IUGR
Seek preconception care and early prenatal care
Folic acid supplimentaion 400 mcg PO daily due to erythrocyte turnover
Frequent CBC monitoring
Urinalysis for culture / sensitivity
In addition to routine prenatal examination, specific efforts will be made to assess the effects of diabetes. An electrocardiogram will be obtained for baseline cardiovascular status. A retinopathy should be
performed. Weight and blood pressure will be obtained and monitored for development of preclampsia. Fundal height will be measured, for abnormal increase in size, indicating macrosomia or hydramnios and for lower than expected growth,
indicating
fetal growth restriction
or fetal death.
In addition to routine prenatal laboratory tests, baseline renal function will be assessed with a 24-hour urine collection for total protein excretion and creatinine clearance. A urine sample will be taken at every visit for possible UTI. Glucose, ketones, and protein will also be checked. Thyroid function test will be performed, diabetic women are at risk for coexisting thyroid disease. Hemoglobin A1c (HbA1c) is monitored for glycemic control and compliance of diet.
Women with preexisting DM surveillance should begin early due to increased risk for congenital anomalies or fetal death
Testing will include multiple-marker screening for neural tube or other open defects or chromosome abnormalities. ultrasonography and fetal echocardiography an 20 to 22 weeks to determine the integrity of the fetal body and cardiac structure.
During the third trimester surveillance is done to identify a worsening intrauterine environment this may include "kick counts", biophysical profiles, nonstress tests, and contraction stress tests. Ultrasound will be performed for growth rates. Doppler is also done to identify vascular complications or if hypertension develops.
Genetic disorder
Involves abnormal synthesis of alpha and beta chains of hgb
Alterations in cell membrane causing decreased lifespan of RBCs
Beta-Thalassemia most common in US, often in those of Mediterranean, Middle Eastern, and Asian decent
Beta-Thalessemia Minor inherits gene from one parent
Beta-Thalessemia Major inherits gene from both parents
Females with B-T Major often die in young adulthood
Those who survive are often sterile
Women with Beta-Thalassemia Minor often mildly anemic, otherwise healthy
Lab values indicate mild hypochromic and microcytic anemia
Iron often not supplemented as these patients absorb and store iron in excess and require a chelating agent to rid the body of excess
Chelating therapy is often paused during pregnancy as the safety of this treatment during pregnancy is not known
Science is inconclusive on if maternal Beta-Thalessemia impacts rates of fetal and neonatal morbidity, prematurity, low birth weight, or abnormal size
Serious fetal anemia may develop of inadequate fetal hbg is produced
Fetus may inherit the serious problem of Beta-Thalassemia Major if both parents have Beta-Thalassemia Minor
No specific therapy during pregnancy
Maternal and fetal outcome are generally satisfactory
Infections that affect the production of RBCs or accelerate destruction need to be identified and treated promptly
Chronic, inflammatory, autoimmune disease that can affect any organ or system
Body attacks its own tissues as non-self
S/S include: inflammation of multiple organ systems, "butterfly rash", joint pain, photosensitivity
Periods of exacerbation and remission
Females affected 6-10 times more than males
Exacerbation can worsen during pregnancy
SLE mother have higher risk of spontaneous abortion and fetal death during 1st trimester
After 1st trimester, prognosis for live birth is improved if no exacerbation occurs
Newborn risks include preterm birth, growth restriction, and permanent congenital heart block
Autoimmune condition characterized by the production of antiphospholipid antibodies combined with certain clinical features
Special clinical features include confirmed thrombosis by imaging or pathalogic studies, abnormal and recurrent pregnancy outcomes, and elevated anticardiolipin antibody or presence of lupus anticoagulant
Pregnancy problems may include: unexplained fetal death after 10 weeks, preterm birth of normal infant at or before 34 weeks due to severe preeclampsia or severe placental insufficiency
Most common concurrent with another autoimmune disease such as SLE
Women with APS should be informed of possible OB complications including risk of CVA
Treated with a combination of low-dose ASA and heparin
Characterized by antithyroid antibodies
Causes most cases of hypothyroidism in women
Hypothyroidism increases risk for miscarriage, preterm birth, and preeclampsia
Can adversely effect child's mental development
Thyroid-Stimulating Hormone level should be checked and corrected within the first trimester
Chronic inflammatory disease
Unknown cause, but is believed to be autoimmune
Usually affects synovial joints
Symptoms often markedly improve during pregnancy
Reason for improvement is unclear but is suspected to be related to a pregnancy-specific protein which suppresses inflammation
Joints become unstable late in pregnancy
Relapse of RA occurs 6 weeks to 6 months after birth
Obstetric problems rare
Most common form of epilepsy, a recurrent disorder of cerebral function
Seizures may occur during pregnancy even if mother has been seizure-free for years
Effect of pregnancy on epilepsy is variable and unpredictable
Serum levels of anticonvulsants may rise, fall, or stay the same
Higher-than-normal risk for stillbirth and preterm labor
Anticonvulsants compete with folate for absorption, leading to a risk of folate deficiency
Seizures during pregnancy result in fetal hypoxia and acidosis
Anticonvulsant therapy often cannot be stopped during pregnancy, however:
Anticonvulsants have many teratogenic effects such as craniofacial abnormalities, limb reduction deficits, growth restriction, intellectual disability, and cardiac abnormalities
Consult a neurologist before conception
Establish optimal time for pregnancy, this is based on maintenance of maternal blood glucose levels for reducing risk factors of fetal malformation.
Identify if diabetes complications exist in other organ system.
Determine the degree of glycemic control based on client records or laboratory studies.
Have woman take 400mcg. of folic acid, if there has been a previous pregnancy with a neural tube 4mg. is recommended
Instruct woman how to use glucometer and have her teach back.
A sudden unilateral neuropathy of the seventh cranial nerve that causes facial paralysis with weakness of the forehead and lower face
No known cause
Three times more common during pregnancy, often in the third trimester
Most woman recover 3 to 6 weeks after birth
Face feels stiff and pulled to one side
Closing eye on affected side may be difficult or impossible
Eating may be difficult
Disturbed sense of taste
Treatment: Steroids may be prescribed
Protect cornea from injury with an eye patch and ointment or eye drops
Chew carefully to prevent mouth trauma
Psychological support
Condition is temporary
Infection during pregnancy can have have benign or severe effects on the mother, the fetus or both
Some infections may also increase the risk for pregnancy complications

While pregnancy often doesn't worsen the effect of viral infections in the mother, the effects on the fetus can be severe.
The following have the greatest potential to cause harm in the fetus or newborn.
Widespread virus in the herpesvirus group that eventually infects most humans
Can be transmitted by most bodily fluids including urine, saliva, blood, cervical mucus, semen, breast milk, and stool
Symptoms are so vague woman is often unaware of infection
After primary infection virus becomes latent, however periodic reactivation and shedding may occur
Primary infection is more likely to cross placenta than reactivation infection
Most infections are asymptomatic
Diagnosis of neonatal testing done by urine culture
About 90% of newborns are not affected
10% are symptomatic at birth
10% of those who are symptomatic will demonstrate full cytomegalic disease
Another 10% of those who are symptomatic at birth will develop late-onset signs such as developmental delay, seizure activity, enlargement of spleen and liver, retinal inflammation,dental defects, and hearing loss
No therapy is available for treatment of congenital CMV infection
Ultrasound may identify manifestations of infection
Antiviral agents may be used during active shedding, but these drugs are toxic and should only be used short-term
Prevention by emphasizing handwashing and limiting sexual partners
Virus is transmitted from person to person through droplets and contact with nasopharangeal secretions
Rubella infection after birth is a mild disease
Congenital rubella can be severe
S/S include fever, general malaise, characteristic maculopapular rash that begins in the face and migrates over the body
Incidence of infection has declined since the vaccine became available in 1969, however outbreaks are becoming more frequent as more parents choose not to vaccinate their children
Maternal rubella can cross placental barrier at any time during pregnancy
Greatest risk is exposure during first trimester as organs develop
If mother is infected during first trimester approximately 1/3 will result in spontaneous abortion, while the remaining 2/3 of fetuses may be severely compromised
Most common complications include deafness, developmental delay, cataracts, cardiac defects, IUGR, and microcephaly
Mothers infected during pregnancy pose a threat to other infants and susceptible populations
Prevention is the only effective protection for the fetus
Women who are immune do not become infected
Determining immunity status of all women of childbearing age is critical
Titer provides evidence of immunity
Vaccination is recommended prior to conception for those who are not immune
Vaccination during pregnancy is not recommended due to a low risk of fetal compromise from the live-virus vaccine
Recommendations for diet are individualized. Women with DM that are of normal weight follow a 30 kilocalories per kilogram of body weight per day 40-45% should be from carbohydrates 12-20% should be from protein and up to 40% from fat. Diets will be based on weight for higher or lower caloric needs.
(SMBG)
Herpesvirus transmitted by direct contact or through respiratory tract
Over 90% of people with have had VZV by the time they reach puberty
Virus becomes latent after primary infection and can reactivate later in life as shingles
Maternal complications of active infection include preterm labor, encephalitis, and pneumonia
Available vaccine has resulted in a decrease in the number of childhood infections
One common testing regimen requires obtaining fasting and 2-hour postprandial levels.Another includes testing six times per day: a fasting capillary glucose level, 1 to 2hours after breakfast, before and after lunch, before dinner, and at bedtime. Normal fasting and postprandial glucose levels have been associated with better outcomes.
Fetal and neonatal effects depend on the time of maternal infection
If during 1st trimester fetus has a small (0.4%) risk for congenital varicella syndrome
Greatest risk between 13 and 20 weeks (2% of births)
Clinical findings include limb hypoplasia, cutaneous scars, chorioretinitis, cataracts, microcephaly, and IUGR
Later in pregnancy, maternal antibodies protect fetus
Infant infected 5 days before or 2 days after birth are not protected by maternal antibodies, infection during this time is life threatening. Varicella-zoster immune globin (VZIG) is indicated
VZIG is also indicated in infants born before 28 weeks or less than 1 kg as maternal antibodies have not yet passed the placental barrier
Most treatment regimens rely on three daily injections with a combination of short-acting (regular) insulin and intermediate-acting (neutral protamine Hagedorn [NPH]) insulin given before breakfast, regular insulin before dinner, and NPH insulin at bedtime.
Immune testing is recommended for pregnant women
VZIG should be administered to those who have been exposed
Report respiratory problems immediately
Hospitalization is required if varicella-zoster pneumonia develops
Acyclovir is primary drug used to treat varicella
For infants born to mother who have an infection administer VZIG within 96 hours of birth for passive immunity
Women and infants with varicella are highly contagious and should be placed in airborne and contact isolation
Only staff with known immunity should come in contact with these patients
Vaccine is recommended for those who are not immune and those who live with the non-immune pregnant woman
The live-virus vaccine in contraindicated during pregnancy
Insulin needs generally decline during the first trimester because the secretion of placental hormones antagonistic to insulin remains low. In addition, the fetus receives its share of glucose, which reduces maternal plasma glucose levels and decreases the need for maternal insulin.
Insulin needs increase markedly during the second and third trimesters when placental hormones,which initiate maternal resistance to the effects of insulin, the nausea of early pregnancy usually resolves, and the diet includes additional calories per day to meet the increased metabolic demands of pregnancy.
Maintenance of tight maternal glucose control during birth is desirable to reduce neonatal hypoglycemia. Continuous infusion of a regular insulin solution combined with a separate intravenous solution containing glucose allows titration to maintain blood glucose levels between 80 and 110 mg/dl.
Insulin needs should decline rapidly after the delivery of the placenta and abrupt cessation of placental hormones. However, blood glucose levels should be monitored at least four times daily so that the insulin dose can be adjusted to meet individual needs.
Genital herpes is one of the most common STDs in the herpes simplex virus group
Can be caused by HSV type 1 or 2
Most genital infections are caused by type 2. Type 1 is most common in the mouth or upper body
Spread through direct contact with skin or mucus membrane with an active lesion.
Many women are asymptomatic and may shed the virus unknowingly
Transmission from mother to infant can occur after water breaks or through contact with a lesion in the birth canal during birth
Diagnosis based on clinical S/S
Pregnancy complications from a recurrent infection are rare
If primary infection occurs during pregnancy it can result in spontaneous abortion, IUGR, and preterm labor
Neonatal herpes infection is uncommon, but serious
Neonate infection can be limited to lesions or systemic
Symptoms appear in first week and progress rapidly
Likelihood of death or serious complication for infected neonate is 50%
No known cure exists
Acyclovir may be given during late pregnancy to reduce risk of lesions during labor
Vaginal birth is allowed of infected woman has no lesions present
Cesarean birth is recommended for women with active genital lesions
Expectant mothers need information on how to deal with emotional and physical effects of herpes
Many are concerned about privacy and don't want their family to know why a C-section was necessary
Acyclovir is prescribed for infected neonates
Erythema infectiosum, caused by human parovirus B19, is an acute, communicable disease characterized by a distinctive rash
Starts with a redness of the cheeks then progresses to a generalized maculopapular rash
Other s/s include fever, malaise, and joint pain
Most contagious before the first rash appears
Prognosis is usually excellent, however if contracted during pregnancy, the disease can be deadly for the fetus
Titers can test for immunity
If maternal infection occurs during pregnancy, fetal death can result from failure to produce fetal RBCs, followed by severe fetal anemia, generalized edema, and heart failure
Ultrasonography can detect generalized fetal edema
Intrauterine transfusion is an option to treat severe fetal anemia
Risk to fetus is greatest when mother becomes infected during the first 20 weeks
The affected offspring is assessed and reassessed for years to follow due to delayed onset of complications
No specific treatment exists
Analgesics may be used for joint pain
Transmitted via blood, saliva, vaginal secretions, semen, and breast milk
Can cross the placental barrier
Mortality for acute hepatitis is about 1%
85%-90% of adults recover
10%-15% of adults develop chronic hepatitis
Maternal infection increases risk of prematurity, low birth weight, and neonatal death
Newborn of infected mother must be carefully bathed prior to any injections
Breastfeeding from infected mother is safe if baby has been vaccinated
All pregnant women should be screened for Hepatitis B
No specific treatment exists
Infection of the neonate of an infected mother can usually be prevented with administration of HBIG
Prevention through the use of safer sex practices
Prevention through universal precautions
Vaccine is recommended for any population at risk including the young, the elderly, those in close contact with an infected person, women of childbearing age, and healthcare workers
Vaccine for newborns is recommended at birth, 1-2 months, and 6-18 months
Acquired immunideficiency syndrome (AIDS) is a failure of the immune system caused by HIV
Transmitted through contact with infected blood or tissues, sexual contact, exposure to maternal genital secretions during childbirth
Breast milk or prechewed food of an infected person can cause infant infection
There is a period of 3-12 months after exposure before first, flu-like symptoms appear. Usually lasting 1-2 weeks
The patient then becomes relatively asymptomatic, sometimes for many years before the disease further progresses
Once the disease further progresses, it is ultimately fatal due to opportunistic infections
Infant infection may occur during pregnancy, during labor or birth, or after birth if baby is breastfed
Infected newborns are typically asymptomatic after birth, but symptoms may appear during first year of life including: enlargement of liver or spleen, failure to thrive, persistent thrush, and extensive seborrheic dermatitis (cradle cap)
Infected infants often have bacterial infections such as meningitis, pneumonia, osteomyelitis, septic arthritis, and septicemia
There is no cure
Prevention through:
Safer sex practices
Refraining from IV drug use
Universal precautions
Multiple antiretroviral drug treatment may extend life and delay symptoms
Antiretroviral drug therapy may be started on infected infants at birth to slow progression of the disease
Protein infection caused by Toxoplasmosa Gondii
Transmitted through raw or undercooked meat, contact with cat feces, soil, and across the placental barrier
Poor handwashing and sanitation practices when handling food increases risk of illness
Those affected may be unaware of the disease
May experience a few days of fatigue, muscle pains, and swollen glands
Although disease may go unnoticed in women, it may result in spontaneous abortion or result in passing the disease to the fetus
About 40% of infants born to mothers with primary infection during pregnancy have congenital toxoplasmosis
About 50% of affected infants may be asymptomatic at birth
Others may have serious side effects such as low birth weight, enlarged liver and spleen, jaundice, anemia, or coagulation disorders
Other complications may develop years later such as chorioretinitis leading to blindness, deafness, seizures, hydrocephalus, and microcephaly
Cook meat thoroughly until juice runs clear
Avoid touching mucus membranes while handling raw meat
Wash all surfaces that contact raw meat
Wash hands after handling raw meat
Avoid uncooked eggs and unpasteurized milk
Wash fruits and vegetables
Avoid contact with materials that could possibly be contaminated with cat feces (litter box, sandboxes, soil)
If infected, maternal treatment is essential to prevent spread of disease to baby
Sulfonamides can be used in conjunction with other drugs
Spiramycin may be used under specific guidelines
Insulin therapy is the accepted treatment for diabetes because it does not cross the placental barrier, however studies are being done for oral agents in treatment of Gestational diabetes mellitus (GDM).
Studies show that Glyburide improved maternal fasting and postpartum glucose levels. There is no difference in newborn outcomes
The failure rate for glyburide to control GDM glucose level were 15% to 20% and failure rates are higher in women with earlier diagnosis. There has also been significant cost savings with glyburide.
Pregnancy, if possible is allowed to go until full term. If there is evidence of fetal compromise such as nonreassuring biophysical profile delivery may be required. If this is before 38 weeks an amniocenteses will be done to assess fetal lung development
GDM is an added risk factor that a woman may develop type 2 after child bearing years. Risk factors associated with GDM are obesity, inactivity, abnormal cholesterol levels, vascular disease, or family members with type 2.
All pregnant women will be screened for GDM, history and risk factors associated with type 2 diabetes and blood glucose testing will be used for identification.

Two types are used Glucose Challenge Test (GCT) and Oral Glucose Tolerance Test (OGTT)
Leading cause of life-threatening perinatal infections in the US
Colonizes rectum, vagina, cervix, and urethra of pregnant and non-pregnant women
Approx 15%-40% of pregnant women are colonized in rectum or vagina
Often asymptomatic
Infections include UTI, chorioamnionitis, & metritis
Most women respond quickly to antimicrobial therapy
Women who have GBS in the rectovaginal area have a 60% chance of passing it to the newborn during birth
Approx 1%-2% of exposed newborns will develop early-onset GBS disease within the fist 2-7 days after birth
Disease includes sepsis, pneumonia, and meningitis
Late-onset GBS disease occurs after the fist week of life
Meningitis is the most common manifestation
Neurologic consequences are likely in those who survive the primary infection
Optimal identification of maternal GBS is obtained via vaginal and rectal culture between 35 and 37 weeks
Women who have previously had GBS at birth or had GBS in a urine culture will be considered GBS positive for delivery
Women who deliver before 37 weeks, has ruptured membranes for >18 hours, or has a temp higher than 100.4 degrees F will be considered GBS positive for delivery
Penicillin is first-line treatment
Cephazolin is alternative for mother with non-life threatening PCN allergy
Clindamycin is used for women at risk for anaphylaxis
TB is a infection caused by the colonization of mcyobacterium tuberculosis in the lungs
Transmitted by droplet
Women at risk should be screened via PPD test
If positive CXR is needed with a lead shield over ABD, preferable after first trimester
Diagnosis confirmed by sputum culture
Penicillin is first-line treatment
Cephazolin is alternative for mother with non-life threatening PCN allergy
Clindamycin is used for women at risk for anaphylaxis
Fetal infection is rare, but may be acquired from swallowing or aspirating infected amniotic fluid
Diagnosis is made by identifying bacilli in neonatal gastric aspirate or placental tissue
Signs of congenital TB include failure to thrive, lethargy, respiratory distress, fever, and enlargement of the spleen, liver, and lymph nodes
If mother remains untreated, newborn is at risk for acquiring TB by droplet from mother
Treatment based on two principals
First, more than one drug must be used to prevent the growth of resistant organisms
Second, treatment must continue for a prolonged period
Preferred Rx for pregnant women with active TB is isoniazid, rifamopin, and ethambutol daily for 2 months, followed by rifamipn and rifampin daily or twice weekly for 7 months
Vitamin B6 should be given with isoniazid to prevent fetal neurotoxicity
Drug resistance in the TB strain may require addition drugs, however the following are not recommended during pregnancy: steptomycin, kanamycin, capreomycin, and fluoroquinolones
Management of the infant born to a mother with TB focuses on prevention
If maternal sputum test is negative, isolation from baby is not required
Breastfeeding is safe, although some anti-TB meds will pass through breastmilk
Infant skin test at birth and possible isoniazide therapy initiated and continued until mother's TB has been inactive for 3 months
Retest in 3 months
If infant skin test is positive, full course of antiinfective therapy will be required
GCT is administered between 24 and 28 weeks.The women does not need to fast. She is to ingest 50g. of oral glucose solution and a blood sample is taken 1 hour later. When the blood glucose concentration is 140mg/dl or greater a 3 hour glucose tolerance test is ordered.
The OGTT is the gold standard for diagnosing diabetes. The woman must fast on the day of the test. A fasting plasma glucose level is determined and the woman is to ingest 100g. of oral glucose solutions. Plasma glucose levels are then determined at 1, 2, and 3 hours. GDM is diagnosed if the fasting level is abnormal or 2 or more of the following values occur
Fasting, greater than 95 mg/dl
1 hour, greater than 180mg/dl
2 hours, greater than 155 mg/dl
3 hours, greater than 140 mg/dl
OGTT values
With a few important exceptions, the effects of GDM are similar to those associated with preexisting diabetes.
GDM is associated with:
increased neonatal morbidity and mortality.
macrosomia, hypoclacemia, hyperbilirubinemia, and respiratory distress.
GDM is not associated with:
increased risk for maternal ketoacidosis
spontaneous abortion
congenital malformations
GDM occurs in the third trimester
Breast feeding may reduce later development of
type 2 diabetes in the infant.
The diet should provide the calories and nutrients needed for maternal and fetal health, result is eughycemia, avoid ketosis, and promote appropriate weight gain. Simple sugars should be avoided. Carbohydrates at breakfast may be limited to 30g due to increased levels of cortisol and growth hormones at that time of day. Protein at breakfast helps to satisfy hunger. Evening snack is usually needed to prevent ketosis at night. Calories should be divided between 3 meals and 3 snacks.
A graduated physical exercise program should be recommended by physician taking into account each woman's risk factors, exercise has been shown to be safe with GDM. Research results are mixed about whether exercise reduces the need for insulin in the woman with GDM.
Blood glucose levels should be monitored. Fasting capillary blood glucose levels repeatedly exceed 95 mg/dl or postprandial values exceed 120 mg/dl will begin insulin therapy
May begin as early as 28 weeks if the woman has poor glycemic control or 34weeks gestation in lower-risk women with GDM. "Kick counts", ultrasonography, amniotic fluid volume, biophysical profile, non-stress, contraction stress test, or amniocentesis help identify fetal compromise.
There is a rigid schedule of controlling the diet, performing blood glucose tests, administering insulin, and performing regular fetal surveillance.
A woman often does not volunteer information about her feelings and concerns, The nurse must ask specifically about them that she and her family may have. Asking about her concerns will often offer information about her emotional well-being.
Allow the woman to make as many decisions as possible increases her sense of being in control. Some women resent being "treated as though ill," even though their diabetes control is excellent. Allow her to help with choices in diet and exercise.
Women with diabetes experience the same discomforts as women without, they need education and counseling regarding the normal aspects of pregnancy as well.
Rheumatic heart disease is a complication that sometimes follows streptococcal pharyngitis (strep-throat). One infection of rheumatic fever may cause stenosis of the heart valves.Early diagnosis and treatment of strep-throat has resulted in a near-eradication of rheumatic fever.Mitral stenosis obstructs free flow of blood from the left atrium to the left ventricle. The left atrium becomes dilated, resulting in chronically elevated left atrium, pulmonary veins, and pulmonary capillaries. This may lead to pulmonary hypertension, pulmonary edema, or CHF. The first warning signs of heart failure include persistent rales at the base of the lungs, dyspnea on exertion, cough, and hemoptysis. Additional signs are Progressive edema and tachycardia.
Atrial septal defect often is first discovered in women of childbearing age because symptoms are absent of vague. This defect produces a left-to-right shunt because pressure in the left side of the heart is higher than that in the right side. Pregnancy is well tolerated by women with an uncomplicated atrial septal defect, and no specific treatment is recommended. Pulmonary hypertension may develop in uncorrected atrial septal defects because the additional blood that moves to the right side of the heart is transported to the lungs through the pulmonary artery.
They are more common than AVD and usually close without treatment. Most women are asymptomatic,but fatigue or symptoms of pulmonary congestion may occur. Pregnancy is well tolerated with small to moderate left-to-right shunts. However, pregnancy occasionally precipitates heart failure or a dysrhythmia, both are managed as in nonpregnant patients. Bacterial endocarditis is common with unrepaired defects, and antibacterial prophylaxis is recommended.
The communicating shunt between the pulmonary artery and aorta is usually discovered and treated in childhood. If untreated, the physiologic effects are related to size. If small the lesion may be tolerated during pregnancy unless complicated by pulmonary hypertension. The patent ductus arteriosus tends to become infected, so antibiotic prophylaxis before labor is recommended.
Tetralogy of fallot is the most common cause of right-to-left shunting and it is a combination of 4 defects; ventricular septal defect, pulmonary valve stenosis, right ventricular hypertrophy, and displacement of the aorta toward the right ventricle.
A cyanotic heart condition that develops when pulmonary resistance equals or exceeds systemic resistance to blood flow and a right-to-left shunt develops. Several congenital defects may underlies the equalization of pressures within the ventricles, such as a large ventricular septal defect or a large patent ductus arteriosus (PDA). The defects must be closed as soon as possible. Late surgical correction often results in the woman's death. If she survives pregnancy carries a 50% survival rate and are preterm and small for gestational age.

Plasma volume, venous return, and cardiac output all increase. Heart rate and stroke volume, the components of cardiac output, increase during pregnancy.
Heart rate gradually increases in the 3rd trimester.
Stroke volume increases are primarily responsible
for the overall rise in cardiac output early during
early pregnancy.

For women with preexisting or underlying heart disease, changes can impose an additional burden on an already compromised heart. When this is the case cardiac decompensation and congestive heart failure(CHF) may be the result.
Heart disease complicates about 1%of pregnancies and is a significant cause of maternal death. The two main causes are rheumatic heart disease and congenital heart disease. Cardiomyopathy may occur during late pregnancy to 5 months postpartum with no identifiable cause and no known previous heart disease.
can be grouped into those that cause left-to-right shunt and right-to-left shunt.
The fetus is more likely to inherit congenital defects, although the risk does very depending in the maternal defect.
The defects of Left-to-right shunting include atrial and ventricular septal defects and patent ductus arteriosus.
right-to-left shunt defects occurs when a cyanotic heart defect such as tetralogy of Fallot is present. It may also occur through a septal defect or patent ductus arteriosis when pulmonary vascular resistance exceeds peripheral vascular resistance and pulmonary hypertension occurs.
Mitral valve prolapse is one of the most common cardiac conditions among the general population. This is an inherited condition that may be associated with a variety of cardiac disorders such as atrial septal defects and Marfan syndrome. Most pregnant women with this disease are asymptomatic and tolerate pregnancy well, others experience dysrhythmias or chest pain. Many physicians feel mitral valve prolapse to be a significant risk factor for bacterial endocarditis and administer prophylactic antibiotics before and during labor.
is exclusively associated with pregnancy
women with this condition have no underlying heart disease
symptoms appear at the end of pregnancy or up to 20 weeks postpartum
symptoms are the same as CHF (dyspnea, edema, weakness, chest pain, and heart palpitations.)
50% of women will recover with persistent CHF or other cardiac dysfunction
about 20% of the women need a heart transplant
peripartum cardiomyopathy often recurs with subsequent pregnancies
anticoagulation with low-molecular-weight heprin is used to prevent clot formation during pregnancy along with fluid restriction for pulmonary edema
and treatment of CHF
S&S are dyspnea, syncope with exertion, hemoptysis, paroxysmal nocturnal dyspnea, and chest pain with exertion. Signs that confirm diagnosis are cyanosis, clubbing, diastolic presystolic or continuous heart murmur, cardiac enlargement, a loud harsh systolic murmur associated with a thrill, and serious dysrhythmias. Clinical confirmation will usually be done with transesophageal echocardiography.

Class I: uncompromised. no limitations
Class II: slightly compromised. requiring some limitation of physical activity
Class III: Larked limitation of physical activity. Comfortable at rest, but less than normal activity causes excessive fatigue.
Class IV: Inability to perform any physical activity without discomfort. table 26-2 pg.548
New York Heart Association functional classification of Heart Disease
limit physical activity: she should remain free of symptoms of cardiac stress such as dyspna, chest pain and tachycardia.
Avoid excessive weight gain: diet adequate in protein, calories, and sodium will be advised
Prevent anemia: Iron and folic acid will be prescribed.
Prevent infection: Immunizations for influenza, pertussis, and pneumonia are available, antibiotics may also be ordered. It is necessary to avoid ill people when times for upper respiratory tract infections are prevalent.
careful assessment for the development of CHF, pulmonary edema, and cardiac dysrhythmias
primary goal is to prevent decompensation and CHF
prevent infant from hypoxia and IUGR
bed rest especially during last trimester, she has little reserve to meet metabolic demands
elastic compression stocking to prevent thrombus formation
prophylactic anticoagulation may be used.
The medical team must consider risk and benefit when treating the pregnant woman with cardiac disease.
Warfarin causes fetal malformations

Heparin does not cross the placental barrier and is effective, PTT and aPTT, platelet count will be monitored.
Enoxaparin (Lovenox) can also be used and requires less monitoring
Beta-blockers and calcium channel blockers are used for maternal hypertension
Digixin, adenosine, and calcium channel blockers appear to be safe.
Beta-blockers can cause neonatal respiratory depression, sustained bradycardia, and hypoglycemia when taken late in pregnancy. Atenolol and matoprolol are preferred, they do not cause the uterine stimulation
In 2007 the American Heart Association released a new set of guidelines for use of prophylaxis to prevent infective endocarditis in persons that are high risk. Complete list is on pg. 549
women with an increased risk for bacterial endocarditis may receive amocicillin, penicillin, ampicillin, and gentamicin at delivery.
Vancomycin and Certriaxone are given for acute endocarditis
Diuretics: furosemide and thiazide, careful monitoring for fluid and electrolyte balance
Beta-blockers
Ace inhibitors
angiotensin receptor blockers
digoxin
Furosemide is associated with IUGR,
Thiazide is associated with fetal jaundice, thrombocytopenia, anemia and hypoglycemia
Every effort is made to minimize the effects of labor on the cardiovascular system.
IV fluids are monitored to prevent fluid overload.
Position is on side, with head and shoulders elevated
Oxygen is administered to promote blood oxygen saturation and monitored with pulse oximetry
discomfort is kept to a minimum and relaxation is promoted
The fetus is monitored electronically
mom is monitored for cardiac decompenstion
Vacuum extraction or forceps are used to minimize pushing
Valsalva maneuver is used
minimize abrupt positional changes after delivery of placenta
do not massage uterus to expedite placental separation
assess throughout labor and postpartum period for circulatory overload, bounding pulse, distended neck and peripheral veins,and moist rales in lung
Monitor for cardiac decompensation due to increased blood returning to the right side of heart
Continue to observe for CHF
Assess for infection, hemorrhage, and thromboembolism, urine output
Breast feeding is advised on an individual bases
Diabetes mellitus is a complex disorder of carbohydrate metabolism. There is a partial or complete lack of insulin secretion by the beta cells of the pancreas. Cells like cardiac, skeletal, and adipose tissue rely on insulin to carry glucose across the cell membrane.
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