PRENATAL CLIENT HIGH RISK Is one in which a concurrent disorder, pregnancy related complication, or external factor jeopardizes the health of the woman, the fetus or both. Poverty Lack of support people circumstances that Poor coping mechanisms causes women to be Genetic inheritance high- risk Past history of pregnancy complications
Should be seen more frequently for prenatal care
A. IDENTIFYING CLIENTS AT RISK
1. ASSESSMENT OF RISK FACTORS Factors Effects Demographic factors 1. Age (<16 or >35 years)
2. Poverty
3. Mulitiparity ( >4 pregnancies) Less than 18: increased risk for LBW and preterm labor, PIH, anemia,CS for CPD.
More than 35 years: increased risk of chromosomal abnormalities, PIH
Associate with LBW, preterm infants
Hemorrhage, CS and fetal loss
Personal social factors/lifestyle 1. Weight
2. Height ( <5 feet)
3. Smoking
4. Alcohol/illegal drug use <100 lbs: associated with LBW >200 lbs: PIH, LGA infants, difficult labor, CS due to CPD Increased risk for CS due to CPD
Obstetric factors 1. Birth of previous infant with weight >8.5 lbs
Increased risk for CS, birth injury, maternal gestational diabetes and neonatal hypoglycemia
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2. Previous stillbirth
3. Rh sensitization
4. Cervical insufficiency
5. Multiple gestations Increased risk of maternal psychological distress
Increased risk for fetal anemia, eryhroblastosis and kernicterus Associated with delivery of previable fetus
Associated with nutritional anemia, preeclampsia, preterm labor, malpresentation, CS, postpartum hemorrhage Existing medical conditions 1. DM
2. Hypothyroidism
3. Cardiac disease
4. Renal disease
5. Concurrent infection
6. Seizure disorders
7. Liver disease Increased risk of PIH. CS, LGA, SGA , neonatal hypoglycemia, fetal or neonatal death, congenital anomalies
Increased risk of spontaneous abortion, congenital anomalies, congenital hypothyroidism
Increased risk of fetal or neonatal death Watch out for signs of worsening heart disease such as edema, crackles, activity intolerance, SOB , irregular heart rate.
Associated with maternal renal failure, preterm delivery, intrauterine growth retardation
Severe fetal effects if maternal disease occurs in the first trimester Increased risk for spontaneous abortion and congenital anomalies
Increased risk of fetal malformation, increased incidence of cerebral palsy, seizure disorder and mental retardation in offspring
Preterm and stillbirths
Environmental agents Impair fertility, interfere with normal placental function and may be toxic to the fetus leading to fetal death B. FACTORS THAT CATEGORIZES A PREGNANCY AS HIGH RISK Psychological Social Physical Prepregnancy History of drug dependence ( including alcohol) History of intimate partner abuse Occupation involving handling of toxic, substances ( including radiation and anesthesia gases) Visual or hearing challenges Pelvic inadequacy or misshape Uterine incompetency, 3
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History of mental illness History of poor coping mechanisms Cognitively challenged Survivor of childhood sexual abuse
Environmental contaminants at home Isolated Lower economic level Poor access to transportation for care High altitude Highly mobile lifestyle Poor housing Lack of support people position or structure Secondary major illness ( heart disease, diabetes mellitus, kidney disease, hypertension. Chronic infection such as tuberculosis, hemopoietic or blood disorder, malignancy) Poor gynecologic or obstetric history History of previous poor pregnancy outcome ( miscarriage, stillbirth, intrauterine fetal death) History of child with congenital anomalies Obesity ( BMI >30) Underweight ( BMI <18.5) Pelvic inflammatory disease History of inherited disorder Small stature Potential of blood incompatibility Younger than age 18 years or older than 35 years Cigarette smoker Substance abuser
Pregnancy Loss of support person Illness of a family member Decrease in self esteem Drug abuse ( including alcohol and cigarette Refusal of or neglected prenatal care Exposure to environmental teratogens Disruptive family incident Conception less Subject to trauma Fluid or electrolyte imbalance Intake of teratogen such as a drug Multiple gestation A bleeding 4
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smoking) Poor acceptance of pregnancy than 1 year after last pregnancy disruption Poor placental formation or position Gestational diabetes Nutritional deficiency of iron, folic acid, or protein Poor weight gain Pregnancy- induced hypertension Infection Amniotic fluid abnormality Postmaturity
Labor and birth Severely frightened by labor and birth experience Inability to participate because of anesthesia Separation of infant at birth Lack of separation for labor Birth of infant who is disappointing in some way ( such as sex, appearance, or congenital anomalies) Illness in newborn Lack of support person Inadequate home for infant care Unplanned cesarean birth Lack of access to continued health care Lack of access to emergency personnel or equipment Hemorrhage Infection Fluid and electrolyte imbalance
C. MEDICAL CONDITIONS AFFECTING PREGNANCY OUTCOMES ( PRE- GESTATIONAL CONDITIONS)
1. Assessment of a woman with CARDIAC DISEASE: Thorough health history---to document her prepregnancy cardiac status Ask her level of exercise performance 5
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Ask if she has cough or edema Instruct the woman to report coughing during pregnancy---bec pulmonary edema from heart failure may first manifest itself as a simple cough. Normal edema of pregnancy involves only the feet and ankles Edema of pregnancy induced hypertension usually begins after week 20.
Sign of heart failure: o Edema o Irregular pulse o Rapid or difficult respirations o Chest pain on exertion Making comparison assessment for nail bed ( should be <5 seconds) Jugular venous distention Assess liver size ( heart dss involves right sided heart failure)- difficult to assess, since the uterus presses the liver upward under the ribs and difficult to palpate. Echocardiography Chest radiograph----- abdomen is covered with lead apron during exposure ECG------ less accurate because ty tHe enlarge uterus presses upward on the diaphragm and displaces the heart
Four categories of heart disease: 1. Class 1 and II can expect to experience a normal pregnancy and birth. 2. Class III can complete a pregnancy by maintaining almost complete bed rest. 3. Class IV are poor candidates for pregnancy because they are in cardiac failure even at rest and when they are not pregnant. - Advised to avoid pregnancy. HEPARIN drug of choice for early pregnancy . Anticoagulant - No teratogenic effect - Does not cross the placenta and the fetus SODIUM WARFARIN (COUMADIN) can be used after week 12 but a woman will returned to heparin therapy during the last month of pregnancy======for the fetus not to develop a coagulation disorder at birth. Fetal assessment Cardiac failure affect fetal growth o Maternal blood pressure becomes insufficient to provide an adequate supply of blood and nutrients to the placenta. o Low birth weight o acidotic fetal environment o Preterm labor o Immaturity o Infant may not respond to labor ( late decelerations)
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Note: When cardiac output is not enough to meet systemic body demands---peripheral vasoconstriction occurs because the uterus is a peripheral organ that causes the uterine/placental constriction. Interventions: 1. Promote healthy nutrition Must gain weight but not so much weight ( burden to her heart) 2. Take iron supplements to prevent anemia 3. Educate regarding medication Digoxin= administered to a woman during pregnancy to slow the Fetal heart if fetal tachycardia is present Adenosine beta blockers and angiotensin convertine enzyme ( ACE) inhibitors = to reduce hypertension, safe during pregnancy Nitroglycerin= a compound often prescribed for angina, safe A valid exception to the rule No medicine during pregnancy
4. Educate regarding the avoidance of infection Caution a woman with heart disease to avoid visiting or being visited by people with infection
Interventions during labor and birth 1. Monitpr FHR and uterine comntractions in all women with heart dss 2. Assess BP, pulse and RR frequently A rapid increasing PR ( >100 beats/min) is an indication that a heart is pumping ineffectively and has increased its rate in an effort to compensate. Advise the woman to assume a side lying position to reduce the possibility of supine hypertension syndrome If she has pulmonary edema= have her chest and head elevated ( semi-fowlers ) to ease the work of breathing. Fatigue is a symptom of heart decompression 3. Oxygen administration 4. Swan ganz catheter- to monitor the heart function 5. Epidural anesthesia If epidural anesthesia is used, low forcep or vacuum extractor can be used for birth 6. Should not push with contractions
Interventions during postpartum 1. Decreased activity 2. Anticoagulant and digoxin therapy 3. Antiembolic stockings and ambulation may be needed to increase venous return from the legs 4. If prophylactic antibiotics had not been started prior to birth, they will be started immediately after birth to discourage subacute bacterial endocarditis 5. Close inspection of the baby Acrocyanosis normal in newborn 6. Oxytocin (pitocin) for uterine involution, used with caution=tend to increase BP 7
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7. Kegel exercise for perineal strengthening but NOT postpartum exercises to improve abdominal tone.wait for the dr or midvives order. 8. Stool softener As a rule, woman with heart disease can brestfeed without difficulty
RHEUMATIC ENDOCARDITIS/RHEUMATIC HEART DISEASE Is an acue, recurrent inflammatory disease that causes damage to the heart as a sequel to group. A beta hemolytic streptococcal infection, particularly the valves, resulting in valve leakage ( insufficiency) and or obstruction ( narrowing or stenosis). There are associated compensatory changes in the size of the hearts chambers and the thickness of chamber walls. Pathophysiology and etiology Rheumatic fever is a sequel to group A streptococcal infection that occur in about 3% of untreated infections. It is a preventable disease through the detection and adequate treatment of streptococcal pharyngitis. Connective tissue of the heart, blood vessels, joints and subcutaneous tissues can be affected. Lesions in connective tissue are known as aschoff bodies which are localized areas of tissue necrosis is surrounded by immune cells. Heart valves are affected, resulting in valve leakage and narrowing Compensatory changes in the chamber sizes and thickness of chamber walls occur. Heart involvement ( carditis) also includes pericarditis, myocarditis and endocarditis. Myocarditis inflammatory process involving the myocardium Pericarditis inflammation of the pericardium, the membranous sac enveloping the heart
Clinical manifestations 1. Symptoms of streptococcal pharyngitis may precede rheumatic symptoms a. Sudden onset of sore throat, throat reddened with exudate b. Swollen, tender lymph nodes at angle of jaw c. Headache and fever 101 -104 F ( 38.9 -40C) d. Abdominal pain ( children) e. Some cases of streptococcal throat infection are relatively asymptomatic 2. Warm and swollen joints ( polyarthritis) 3. Chorea ( irregular jerky, involuntary, unpredictable muscular movements) 4. Erythema marginatum (transient meshlike mascular rash on trunk an dextremities in about 10% of patients) 5. Subcutaneous nodules ( hard, painless nodules over extensor surfaces of extremities ) 6. Fever 8
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7. Prolonged PR interval demonstrated by ECG 8. Heart murmurs, pleural and pericardial rubs Diagnostic evaluation 1. Throat culture to determine presence of streptococcal organisms 2. Sedimentation rate, WBC count and differential, and CRP increased during acute phase of infection 3. Elevated antistreptolysin O ( ASO) titer 4. ECG prolonged PR interval or heart block Management 1. Antimicrobial therapy- penicillin is the drug of choice a. Note that missed doses of antibiotics due to the patients unavailability while off of the unit for diagnostic tests are given after return to the unit. b. Missed antibiotic doses may have irreversible deleterious consequences. c. Notify heath acre provider if doses will be missed to make sure that appropriate alternative measure are taken. 2. Rest to maintain optimal cardiac function 3. Salicylates or NSAIDS to control fever and pain 4. Prevention of recurrent episodes through long term penicillin therapy for 5 years after initial attack in most adults, periodic prophylaxis throughout life if valvular damage. Complications 1. Valvular heart disease 2. Cardiomyopathy 3. Heart failure Nursing Assessment 1. Ask patient about symptoms of fever or throat or joint pain. 2. Ask patient about chest pain, dyspnea, fatigue 3. Observe for skin lesions or rash on trunk and extremities. 4. Palpate for firm, nontender movable nodules near tendons or joints. 5. Auscultate heart sounds for murmurs and rubs Nursing Diagnosis 1. Hyperthermia related to disease process. 2. Decreased cardiac output relate to decreases cardiac contractility 3. Activity intolerance related to joint pain and easy fatigability. Nursing Interventions Reducing Fever 1. Administer penicillin therapy as prescribed to eradicate hemolytic streptococcus ; an alternative drug may be prescribed if patients is allergic to penicillin or sensitivity testing and desensitization may be done. 2. Give salicylates/NSAIDS as prescribes to suppress rheumatic activity by controlling toxic manifestations. To reduce fever and to relieve joint pain. 3. Assess for effectiveness of drug therapy a. Take and record temperature every 3 hours. b. Evaluate patients comfort level every 3 hours. 9
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Maintaining adequate cardiac output 1. Assess for signs and symptoms of acute rheumatic carditis. a. Be alert to patients complaint of chest pain, palpitations, and or precordial tightness b. Monitor for tachycardia ( usually persistent when patient sleeps) or bradycardia. c. Be alert to development of second degree heart block or wenckebachs disease ( acute rheumatic carditis causes PR interval prolongation). 2. Auscultate heart sounds every 4 hours. a. Document presence of murmur or pericardial friction rub. b. Document extra heart sounds ( S3 gallop, S4 gallop). 3. Monitor for development of chronic rheumatic endocarditis, which may include valvular disease and heart failure. Maintaining Activity 1. Maintain bed rest for duration of fever or if signs of active carditis are present. 2. Provide ROM exercise program. 3. Provide diversuonal activities that prevents exertion. 4. Discuss needs for tutorial services with parents to help child keep up with school work. Patient education and health maintenance 1. Counsel patient to maintain good nutrition. 2. Counsel patient on hygienic practices. a. Discuss proper hand washing, disposal of tissues, laundering of handkerchiefs ( decrease risk of exposure to microbes) b. Discuss the importance of using patients own toothbrush, soap and washcloths when living in group situations. 3. Counsel patient on importance of receiving adequate rest. 4. Instruct patient to seek treatment immediately should sore throat occur. 5. Support patients in long-term antibiotic therapy to prevent relapse ( 5 years for most adults) 6. Instruct patient with valvular disease to use prophylactic penicillin therapy before certain procedures and surgery. 7. Explore with patient his ability to pay for medical treatment. If appropriate, contact social services for patient.
2. DIABETES MELLITUS Is an endocrine d/o in which the pancreas cannot produce adequate insulin to regulate body glucose levels. NOT a good candidate for oral contraceptive because progesterone interferes with insulin activity and therefore increases blood glucose levels estrogen has the potential increasing lipid and cholesterol levels and blood coagulation NOT a candidate for using IUD Associated with higher rates of Pelvic inflammatory disease Have problems fighting infections Subcutaneous implanted or IM injections of progestin may be good choice 10
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Clinical Presentation Polyuria Polydypsia Polyphagia Weight loss Frequent UTI Large fetus
3 Classification of Diabetes Mellitus Type Description Type 1 Formerly known as insulin dependent diabetes mellitus A state characterized by the destruction of the beta cells in the pancreas that usually leads to absolute insulin deficiency. A. immune mediated diabetes mellitus resulys from autoimmune destruction of the beta cells. B. Idiopathic type I refers to forms that has no cause Type 2 Formerly known as non-insulin dependent diabetes mellitus. A state that usually arises because of insulin resistance combined with a relative deficiency in the production of insulin Gestational diabetes
Risk factors: Obesity Age over 25 years Hx of large babies (10 lb or more) Hx of unexplained fetal or perinatal loss Hx of congenital anomalies in previous pregnancies Hx of polycystic ovary syndrome Family hx of diabetes ( one close relative or two distant ones) Member of a population with a high risk for diabetes A condition of abnormal glucose metabolism that arises during pregnancy. ( 24 th -28 th weeks) Impaired glucose homeostasis A state between normal and diabetes in which the body is no longer using and or secreting insulin properly. A. impaired fasting glucose- a state when fasting plasma glucose is at least 110 but under 126mg/dl B. impaired glucose tolerance- a state 11
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when the results of the oral glucose tolerance test are at least 140 but under 200 mg/dl in the 2 hour sample.
TEST 1. 50 g oral glucose challenge test To confirm diabetes = fasting plasma glucose of 126 mg/dl or above or a nonfasting plasma glucose of 200 mg/dl or above = with diabetes After the oral 50 g glucose load- a venous sample is taken for glucose determination 60 minutes later. Done during the first prenatal visit and repeat at 24-28 weeks AOG 2. If negative: use 100g Glucose Tolerance test at 32-34 weeks If the serum glucose level at 1 hour is more than 140 mg/dl, the woman is scheduled for a 100 g , 3 hour fasting glucose tolerance test. If 2 of the 4 blood samples collected for this test are abnormal or the fasting value is above 95 mg/dl diabetes is present
Oral glucose challenge test values (fasting plasma glucose values) for pregnancy Test type Pregnant glucose level (mg/dl) by carpenter and coustan Fasting 95 1 hour 180 2 hours 155 3 hours 140 Following a 100 g glucose load. Rate is abnormal if two values are exc Nursing care and management: 1. Complete patient database and document test results during pregnancy. 2. Educate both the patient and her family Assess patients understanding of her condition and ite effects on daily life Discuss and demonstrate self administration of insulin Demonstrate self monitoring of blood glucose level before meals and at bedtime. Stress the importance of recording blood glucose levels insulin dose dietary intake periods of exercise periods of hypoglycemia kind and amount of treatment 12
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urine test results daily 3. Explain importance of continued evaluation even during the postpartum period ( monitor glucose levels every 4-6 hours for 24 hours, administer insulin subcutaneously when needed) and even when blood glucose levels are normal. 4. Arrange for patients consultation with a dietician Diet: 20% CHON, 40-50% CHO, 30% fats 5. Encourage regular exercise ( 3-4x /week, duration of 15-30 minutes, HR maintains between 130-160 bpm) 6. Attend to patients emotional and psychological needs and provide assurance. 7. Ensure patients preparation for intensive and regular intrapartun assessment: Fetal monitoring Intravenous glucose Insulin and oxytocin infusion Evaluation for diabetic hetoacidosis IVF replacement Invasive maternal cardiac monitoring 8. Identify and refer the patient and her family to possible support groups and resources 9. Advise contraception in diabetic women 10. Monitor BP and lipid levels 11. Woman who is type 1 0r 2 should meet with her obstetrician before she becomes pregnant. 12. Use home test kit to determine if she is pregnant to know it at earliest time. 13. Glycosylated hemoglobin is used to detect the degree of hyperglycemia Glucose circulates in the blood, binds to a portion of hemoglobin in the blood. Measuring glycosylated hemoglobin is advantageous because it reflects the average blood glucose levels over the past 4-6 weeks ( the time the RBC were picking up glucose) 14. Ophthalmic examination is done during pregnancy 15. Urine culture may be done each trimester to detect asymptomatic UTI as the increased glucose concentration in urine leads to increased infection. Therapeutic management 1. Insulin Regular = short acting insulin ( Lispro or insulin aspart) 2/3 given in the morning 1/3- evening Self administered 30 minutes before breakfast in aratio 2:1 ( intermediate to regular) Again before dinner: ratio 1:1 Human insulin is recommended bec it has lesser antibody response than beef or pork insulins. 2. Blood glucose monitoring To determine if hypoglycemia or hyperglycemia exists
Signs and symptoms of hypoglycemis and hyperglycemia
hunger blurred vision nervousness weakness, fatigue shallow breathing, but normal PR urine negative for glucose and ketones blood glucose level <60 mg/dl
Rapid, deep breathing, fruity breath odor Depressed reflexes Drowsiness, headache
3. ANEMIA Normally: blood volume expands during pregnancy ( pseudo anemia) True anemia 1 st and 3 rd trimester: hemoglobin concentration is less than 11g/dl ( hematocrit <33%) 2 nd trimester: hemoglobin is less than 10.5g/dl (hematocrit <32%) a. Iron deficiency anemia A microcytic ( small red blood cell), hypochromic ( less hemoglobin than the average red cell) anemia because when an inadequate supply of iron is ingested, iron is unavailable for incorporation into red blood cells. Most common anemia of pregnancy Hemoglobin level is below 12 mg/dl Hematocrit <33% Low serum iron level confirms iron deficiency anemia Increased iron binding capacity Causes: o Diet low in iron o Heavy menstrual flow o Unwise weight reduction programs o Pregnant less than 2 years o Low socio economic levels Made available to the body by absorption from the duodenum into the bloodstream after it is ingested. In the blood stream------transferrin----for transport to the liver, spleen and bone marrow------------and incorporated into hemoglobin or stored as ferritin.
Effects: o LBW o Preterm birth o Pica ( food craving) like ice or starch Management: 1. Women should take prenatal vitamins Iron supplement of 60 mg 2. Diet high in iron and vitamins * green leafy vegetables, meat, legumes , fruit) 3. Therapeutic levels of medications * 120-200 mg elements iron/day)in the form of Ferrous sulfate or ferrous gluconate Iron is best absorbed from an acid medium Side effects: o Constipation 14
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o Gastric irritation Mgt: increase roughage diet Always take the pills with food If iron deficiency anemia is severe and a woman has difficulty with oral iron therapy, IM or IV iron dextran can be prescribed.
b. Folic acid deficiency anemia Folic acid/ folacin- B vitamins= necessary for the normal formation of red blood cells in the mother. Associated with preventing neural tube defects in the fetus. High- risk: Occurs most in multiple pregnancies bec of increased fetal demand Women with secondary hemolytic illness---there is rapid destruction and production of new red blood cells Women taking hydantoin an anticonvulsant agent that interferes with folate absorption Women taking oral contraceptives Women who had gastric bypass for morbid obesity Megaloblastic anemia enlarged red blood cells Anemia common in this type The mean corpuscular volume will ne elevated in contrast to the lowered level seen with iron deficeiency Take several weeks to develop Apparent during 2 nd trimester A contributory factor in early miscarriage or premature separation of the placenta. Occur in the 1 st few weeks of fetal development Advised the woman to begin 400 microgram folic acid daily Eat folacin food (green leafy vegetables, oranges, dried beans. During pregnancy Folic acid requirement increases to 600 microgram daily c. Sickle cell anemia An inherited hemolytic anemia caused by abnormal aminmo acid in the beta chain of hemoglobin. If an abnormal amino acid replaces the amino acid valine, sickle hemoglobin (HbS) results If it is substituted for the amino acid lysine, nonsickling hemoglobin ( HbC) results. An individual is heterozygous ( has only one gene in which the abnormal substitution has occurred) has the sickle cell trait ( HbAS) If the person in homozygous ( has 2 genes in which the substitution has occurred) sickle cell disease results. ( HbSS) Majority of the red blood cells are irregular or sickle shaped------cannot carry as much hemoglobin as a normally shaped red cells do. oxygen bld becomes viscid ( dehydrated) cells clump
hemolysis blood flow to organs vessel blockage
decrease # of RBC severe anemia 15
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Effects of homozygous disease: 1. Prematurity 2. Miscarriage 3. Perinatal mortality 4. Increased incidence of asymptomatic bacteriuria resulting in increase incidence of pyelonephritis.
Sickle cell anemia is a threat to life if vital blood vessels such as those to the liver, kidneys, heart, lungs or brain become blocked. In pregnancy, blockage to the placental circulation can directly compromise the fetus, causing low birth weight and possibly fetal death. Assessment: 1. Monitor hemoglobin level 2. Clean catch urine sample Since they are susceptible to bacteriuria 3. Monitor diet throughout pregnancy 4. Fluid intake carefully monitored Should consume at least 8 glasses of fluids daily If nauseated ----decrease fluid intake, dehydration then sickle cell crisis occurs. 5. Assess for presence of varicosities during prenatal visits Due to uterine pressure during pregnancy/pooling of blood in leg veins Pooling and pressure can lead to red blood cell destruction Standing for long time causes this pressure 6. Encourage woman to elevate legs while sitting 7. Sims position to encourage venous return from the lower extremities 8. Monitor fetal health by a. UTZ at 16-24 weeks to assess for intrauterine growth restriction b. NST by weekly beginning at 30 weeks c. Blood flow velocity to measure blood flow to the uterus and placenta If reduced ------ intrauterine growth restriction Therapeutic Management: 1. Periodic exchange transfusion throughout pregnancy----to replace sickled cells with non sickled cells 2. O2 administration 3. Increase fluid volume Hypotonic (0.45 saline)---to keep plasma tension low because of the difficulty of a woman concentrating urine to remove large amounts of fluids. As a rule women with sickle cell anemia are not given iron supplement during pregnancy Sickle cells cannot incorporate with iron same manner as non sickled cell cell can, so excessive iron buildup may result 4. Hospitalization If with fever to rule out the development of sickle cell crisis With infection and hemolysis 16
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If a woman has the disease and her partner has the trait----50% child born with the dss, and all of their child will have the disease. Symptoms of sickle cell disease do not become apparent until an infants fetal hemoglobin converts to a largely adult pattern ( in 3 -6 months). Fetal hgb= 2 alpha 2 gamma chains Adult hgb = 2 alpha 2 beta chains Bec sickle cell trait is carried on the beta chain, symptoms will be manifested until this chain appears. 5. Electrophoresis of RBC---obtained thru percutaneous umbilical blood sampling/amniocentesis----can reveal the presence of the disease. NB have 15% adult hgb at birth-----so electrophoresis at birth can reveal if the dss is present.
6. HIV Risk factors: Multiple sexual partners of the individual or sexual partner Bisexual partners Intravenous drug used by the individuals or sexual partner Assessment: a. Reproductive tract irritation b. Mild flu symptoms c. Seroconversion- in which a woman converts from having no HIV antibodies in her blood serum ( HIV serum negative) to having antibodies against HIV ) HIV serum positive Happens 6 weeks to 1 year after exposure d. Weight loss e. fatigue higher risk of developing toxoplasmosis and cytomegalovirus infections HIV positive woman may invade the cerebrospinal fluid and cause extreme neurologic involvement. f. Tuberculis ELISA or Western blot analysis Zidovudine ( ZVD)- administerd to the woman beginning with the 14 th week of pregnancy And newborns receives antiviral therapy beginning with birth. And a follow- up of 6weeks .
Therapeutic Mgt: 1. Advised not to be pregnant 2. Trimethoprin with sulfamethoxazole (bactrim)- with pneumonia Teratogenic in early pregnancy Sulfamethoxazole ( gantanol)- may lead to increase bilirubin levels in newborn if administered late in pregnancy 3. Chemotheraphy for those with Kaposis sarcoma- contraindicated during early pregnancy bec of potential for fetal injury but can be used later in pregnancy to halt the malignant growth. 4. Cs delivery