Fall 2011 Risk Factors Age – under 17 over 35 Gravida and Parity Socioeconomic status Psychological well-being Predisposing chronic illness – diabetes, heart conditions, renal Pregnancy related conditions – hyperemesis gravidarum, PIH Goals of Care for High Risk Pregnancy © Provide optimum care for the mother and the fetus © Assist the client and her family to understand and cope through education Initial Data Chief complaint: moderate amount vaginal bleeding Vital Signs: T. 98.4; P. 100, R. 22, B/P 100/66 G1 P0 Last menstrual period: 8/12; EDC: May 19 Allergies: none known Nauseated Mild pain HCG levels – WNL for pregnancy Abortions Termination of pregnancy at any time before the fetus has reached the age of viability Either: spontaneous – occurring naturally induced – artificial Etiology / Predisposing Factors Chromosomal abnormalities - Faulty germ plasm -imperfect ova or sperm, genetic make-up (chromosomal disorders), congenital abnormalities Faulty implantation Decrease in the production of progesterone Drugs or radiation Maternal causes -- infections, endocrine disorders, malnutrition, hypertension, cervix disorder Types of Abortions Threatened Signs and Symptoms vaginal bleeding, spotting Mild cramps, backache Cervix remains CLOSED Intact membranes Treatment and Nursing Care Bed rest, sedation Avoid stress and intercourse Progesterone therapy A period of “watchful waiting” Imminent Abortion Signs and Symptoms Loss is certain Bleeding is more profuse Painful uterine contractions Cervix DILATES Treatment and Nursing Care Assess all bleeding. Save all pads. (May need to weigh the pads) Use the bedpan to assess all products expelled Treated by evacuation of the uterus usually be a D & C or suction Provide Psychological Support Complete Abortion All products of conception are expelled No treatment is needed, but may do a D & C Incomplete Abortion Parts of the products of conception are expelled, placenta and membranes retained and intact Treated with a D & C or suction evacuation Provide support to the family Missed Abortion The fetus dies in-utero and is not expelled Uterine growth ceases Breast changes regress Maceration occurs Treatment: D&C Hysterotomy Question??? What are two main complications related to a missed abortion? 1. 2. Recurrent / Habitual Abortion Premature Cervical Dilation Abortion occurs consecutively in _____ or more pregnancies Usually due to an Incompetent Cervical Os Occurs most often about 18-20 weeks gestation. Habitual Abortion Treatment Cerclage procedure -- purse-string suture placed around the internal os to hold the cervix in a normal state Nursing Care post cerclage Bedrest in a slight trendelenburg position Teach: Assess for leakage of fluid, bleeding Assess for contractions Assess fetal movement and report decrease movement Assess temperature for elevations Delivery options: When time for delivery there are several options: physician will clip suture and allow patient to go into labor on her own induce labor cesarean delivery Key Concepts Related to Bleeding Disorders If a woman is Rh-, RhoGam is given within 72 hours of abortion Provide emotional support. Feelings of shock or disbelief are normal Encourage to talk about their feelings. It begins the grief process Bleeding Disorders Ectopic Pregnancy Implantation of the blastocyst in ANY site other than the endometrial lining of the uterus ovary (5) Cervical Etiology / Contributing Factors Salpingitis Pelvic Inflammatory Disease, PID Endometriosis Tubal atony or spasms Imperfect genetic development History of sexually transmitted disease Contributing Factors Failed tubal ligation Intrauterine device Multiple induced abortions Maternal age > 35 years History of previous ectopic Assessment Ectopic Pregnancy Early: • Missed menstruation followed by vaginal bleeding (scant to profuse) • Unilateral pelvic pain, sharp abdominal pain • Referred shoulder pain • Cul-de-sac mass Acute: • Shock – blood loss poor indicator • Cullen’s sign -- bluish discoloration around umbilicus • Nausea, Vomiting • Faintness Diagnostic Tests Ectopic Pregnancy Diagnosis: • Ultrasound • Culdocentesis • Laparoscopy Treatment Options / Nursing Care Combat shock / stabilize cardiovascular • Type and cross match • Administer blood replacement • IV access and fluids Laparotomy Psychological support Linear salpingostomy Methotrexate – used prior to rupture. Destroys fast growing cells Gestational Trophoblastic Disease Hydatiform Molar Pregnancy A DEVELOPMENTAL ANOMALY OF THE PLACENTA WITH DEGENERATION OF THE CHORIONIC VILLI As cells degenerate, they become filled with fluid and appear as fluid filled grapesize vessicles. Assessment: Vaginal Bleeding -- scant to profuse, brownish in color (prune juice) Possible anemia due to blood loss Enlargement of the uterus out of proportion to the duration of the pregnancy Vaginal discharge of grape-like vesicles May display signs of pre-eclampsia early Hyperemesis gravidarium No Fetal heart tone or Quickening Abnormally elevated level of HCG Question 6 Interventions and Follow-Up Empty the Uterus by D & C or Hysterotomy Extensive Follow-Up for One Year • Assess for the development of choriocarcinoma • Blood tests for levels of HCG frequently • Chest X-rays • Placed on oral contraceptives • If the levels rise, then chemotherapy started usually Methotrexate Critical Thinking Exercise A woman who just had an evacuation of a hydatiform mole tells the nurse that she doesn’t believe in birth control and does not intend to take the oral contraceptives that were prescribed for her. How should the nurse respond? Placenta Previa Low implantation of the placenta in the uterus Etiology • Usually due to reduced vascularity in the upper uterine segment from an old cesarean scar or fibroid tumors Three Major Types: • Low or Marginal • Partial • Complete Question 8 Abruptio Placenta Premature separation of the placenta from the implantation site in the uterus Etiology: ª Chronic Maternal Hypertension ª Short umbilical cord ª Trauma ª History of previous delivery with separation ª Smoking / Caffeine / Cocaine ª Vascular problems such as with diabetes ª Multigravida status ª Defined as marginal, partial or complete Recently Identified Risk Factor Autoimmune antibodies including resulting in various coagulopathies: Anticardiolipin Lupus anticoagulant Placenta Previa • PAINLESS vaginal bleeding Abruptio Placenta Bleeding accompanied by • Bright red bleeding • First episode of bleeding is slight then becomes profuse Signs of blood loss comparable to extent of bleeding Uterus soft, non-tender Fetal parts palpable; FHT’s countable and uterus is not hypertonic Blood clotting defect absent • • • • PAIN Dark red bleeding First episode of bleeding usually profuse Signs of blood loss out of proportion to visible amount Uterus board-like, painful and low back pain Fetal parts non-palpable, FHT’s non-countable and high uterine resting tone (noted with IUPC) Blood clotting defect (DIC) likely Signs of Concealed Hemorrhage Increase in fundal height Hard, board-like abdomen High uterine baseline tone on electronic fetal monitoring Persistent abdominal pain and low back pain Systemic signs of hemorrhage Interventions and Nursing Care Placenta Previa Bed-rest Assessment of bleeding Electronic fetal monitoring If it is low lying, then may allow to deliver vaginally Cesarean delivery for All other types of previa Treatment and Nursing Care Abruptio Placenta Cesarean delivery immediately Combat shock – blood replacement / fluid replacement Blood work – assessment for complication of DIC Critical Thinking Mrs. A., G3 P2, 38 weeks gestation is admitted to L & D with scant amoutn of dark red bleeding. What is the priority nursing intervention at this time? A. Assess the fundal height for a decrease B. Place a hand on the abdomen to assess if hard, board-like, tetanic C. Place a clean pad under the patient to assess the amount of bleeding D. Prepare for an emergency cesarean delivery Disseminated Intravascular Coagulation (DIC) Anti-coagulation and Pro-coagulation effects existing at the same time. Etiology Defect in the Clotting Cascade An abnormal overstimulation of the coagulation process Activation of Coagulation with release of thromboplastin into maternal bloodstream Thrombin (powerful anticoagulant) is produced Fibrinogen fibrin which enhances platelet aggregation and clot formation Widespread fibrin and platelet deposition in capillaries and arterioles Resulting in Thrombosis (multiple small clots) Excessive clotting activates the fibrinolytic system Lysis of the new formed clots create fibrin split products These products have anticoagulant properties and inhibit normal blood clotting A stable clot cannot be formed at injury sites Hemorrhage occurs Ischemia of organs from vascular occlusion of numerous fibrin thrombi Multisite hemorrhage results in shock and can result in death Disseminated Intravascular Coagulation (DIC) Precipating Factors: Abruptio placenta PIH Sepsis Retained fetus (fetal demise) Retained fetal placenta fragments Amniotic embolism Maternal liver disease Septic abortion HELLP and preeclampsia Assessment Signs and Symptoms Spontaneous bleeding -- from gums and nose (Epistaxis), injection and IV sites, incisions Excessive bleeding -- Petechiae at site of blood pressure cuff, pulse points. Ecchymosis Tachycardia, diaphoresis, restlessness, hypotension Hematuria, oliguria, occult blood in stool Altered LOC if cerebral bleeding or significant blood loss Diagnostic Tests Lab work reveals: PT – Prothrombin time is prolonged PTT – Partial Thromboplastin Time increased D-Dimer – increased Product that results from fibrin degradation. More specific marker of the degree of fibrinolysis Platelets -- decreased Fibrin Split Products – increase An increase in both FSP and D-Dimer are indicative of DIC DIC Interventions and Nursing Care Remove Cause Evaluate vital signs Replace blood and blood products Fluid replacement May give Heparin – Why? Question 9-D: E HYPEREMESIS GRAVIDARIUM **Pernicious vomiting during Pregnancy Hyperemesis Gravidarium Etiology Increased levels of HCG Assessment Persistent nausea and vomiting Weight loss from 5 - 20 pounds May become severely dehydrated with oliguria AEB increased specific gravity, and dry skin Depletion of essential electrolytes Metabolic alkalosis -- Metabolic acidosis Starvation Nursing Care / Interventions Hyperemesis Gravidarium Control vomiting Maintain adequate nutrition and electrolyte balance Allow patient to eat whatever she wants If unable to eat – Total Parenteral Nutrition Combat emotional component – provide emotional support and outlet for sharing feelings Mouth care Weigh daily Check urine for output, ketones Classification of HTN in Pregnancy Gestational HTN = Systolic BP > or equal to 140/90 after 20 weeks (replaces term of PIH), protein negative or trace Pre-eclampsia = BP > or equal to 140/90 after 20 weeks, proteinuria, edema considered nonspecific Eclampsia = other signs plus convulsions not attributable to other causes Chronic HTN = BP > or equal to 140/90 that was known to exist before pregnancy or does not resolve after 6 weeks after delivery PRIMIGRAVIDA UNDER 17 AND OVER 35 MULTIPLE PREGNANCY HYDATIFORM MOLE PREDISPOSING FACTORS FAMILY HISTORY VASCULAR DISEASE Diabetes, renal LOWER SOCIOECONOMIC STATUS Severe malnutrition, decrease Protein intake Inadequate or late prenatal care PATHOLOGICAL CHANGES PIH is due to: GENERALIZED ARTERIOLAR CYCLIC VASOSPASMS (decrease in diameter of blood vessel) INCREASED PERIPHERAL RESISTANCE; IMPEDED BLOOD FLOW ( in blood pressure) Endothelial CELL DAMAGE Intravascular Fluid Redistribution Decreased Organ Perfusion Multi-system failure Disease Clinical Manifestation HYPERTENSION Earliest and The Most Dependable Indicator of PIH Hypertension B/P = 140 / 90 if have no baseline. 1. 30 mm. Hg. systolic increase or a 15 mm. Hg. diastolic increase (two occasions four to six hours apart) 2. Increase in MAP > 20 mm.Hg over baseline or >105 mm. Hg. with no baseline Rationale for HYPERTENSION The blood pressure rises due to: ARTERIOLAR VASOSPASMS AND VASOCONSTRICTION causing (Narrowing of the blood vessels) an increase in peripheral resistance fluid forced out of vessels HEMOCONCENTRATION Increased blood viscosity = Increased hematocrit Key Point to Remember ! HEMOCONCENTRATION develops because: Vessels became narrowed forcing fluid to shift out of the vascular space Fluid leaves the intravascular space and moves to extravascular spaces Now the blood viscosity is increased (Hematocrit is increased) **Very difficult to circulate thick blood Proteinuria With renal vasospasms, narrowing of glomerular capillaries which leads to decreased renal perfusion and decreased glomerular filtration rate PROTEINURIA Spilling of 1+ of protein is significant to begin treatment Oliguria and tubular necrosis may precipitate acute renal failure Significant Lab Work Changes in Serum Chemistry Decreased urine creatinine clearance (80-130 mL/ min) Increased BUN (12-30 mg./dl.) Increased serum creatinine (0.5 - 1.5 mg./dl) Increased serum uric acid (3.5 - 6 mg./dl.) Weight Gain and Edema Clinical Manifestation: Edema may appear rapidly Begins in lower extremities and moves upward Pitting edema and facial edema are late signs Weight gain is directly related to accumulation of fluid WEIGHT GAIN AND EDEMA Albumin is lost due to the damage to the tubules allowing larger solutes to pass in the urine This leads to a decreased colloid osmotic pressure A in COP allows fluid to shift from from intravascular to extravascular by osmosis Fluid accumulates in the extravascular space Activation of angiotensin and release of aldostersone =retention of sodium and water and vasoconstriction The Nurse Must Know The difference between dependent edema and generalized edema is important. The patient with PIH has generalized edema because fluid is in all tissues. Placenta Due to Vasospasms and Vasoconstriction of the vessels in the placenta. Decreased Placental Perfusion and Placental Aging Positive OCT / __________Decelerations With Prolonged decreased Placental Perfusion: Fetal Growth is retarded - IUGR, SGA Condition is Worsening Oliguria – 100ml/4 hrs or less than 30 cc. / hour Edema moves upward and becomes generalized (face, periorbital, sacral) Excessive weight gain – greater than 2 pounds per week Central Nervous System Changes Cerebral edema -- forcing of fluids to extracellular Headaches -- severe, continuous Hyper-reflexia LOC changes – changes in affect Convulsions / seizures Visual Changes Retinal Edema and spasms leads to: Blurred vision Double vision Retinal detachment Scotoma (areas of absent or depressed vision) Nausea and Vomiting Epigastric pain –often sign of impending coma Pre-Eclampsia Mild B/P Protein Edema Weight Reflexes Severe 140/90 1+ 2+ 1+, lower legs <1 lb. / week 1+ 2+ brisk Retina 160/110 3+ 4+ 3+ 4+ >2lb. / week 3+ 4+ (Hyperreflexia) Clonus present Blurred vision, Scotoma Retinal detachment GI, Hepatic CNS Fetus N & V, Epigastric pain, changes in liver enzymes Headache, LOC changes Premature aging of placenta IUGR; late decelerations Interventions and Nursing Care Home Management Decrease activities and promote bed rest Sedative drugs Lie in left lateral position Remain quiet and calm – restrict visitors and phone calls Dietary modifications increase protein intake to 70 - 80 g/day maintain sodium intake Caffeine avoidance Weigh daily at the same time Keep record of fetal movement - kick counts Check urine for Protein Hospitalization If symptoms do not get better then the patient needs to be hospitalized in order to further evaluate her condition. Common lab studies: CBC, platelets; type and cross match Renal blood studies -- BUN, creatinine, uric acid Liver studies -- AST, LDH, Bilirubin DIC profile -- platelets, fibrinogen, FSP, D-Dimer Hospital Management Nursing Care Goal 1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant Decrease CNS Irritability Provide for a Quiet Environment and Rest 1. MONITOR EXTERNAL STIMULI Explain plans and provide Emotional Support Administer Medications 1. Anticonvulsant -- Magnesium Sulfate 2. Sedative -- Diazepam (Valium) 3. Apresoline (hydralazine) Assess Reflexes Assess Subjective Symptoms Keep Emergency Supplies Available Magnesium Sulfate ACTION CNS Depressant, reduces CNS irritability Calcium channel blocker- inhibits cerebral neurotransmitter release ROUTE IV effect is immediate and lasts 30 min. IM onset in 1 hour and lasts 3-4 hours Prior to administration: Insert a foley catheter with urimeter for assessment of hourly output Magnesium Sulfate NURSING IMPLICATIONS 1. Monitor respirations > 14-16; < 12 is critical 2. Assess reflexes for hypo-reflexia -- D/C if hypo-refexia 3. Measure Urinary Output >100cc in 4 hrs. 4. Measure Magnesium levels – normal is 1.5-2.5 mg/dl Therapeutic is 4-8mg/dl.; Toxicity - >9mg/dl; Absence of reflexes is >10 mg/dl; Respiratory arrest is 12-15 mg/dl; Cardiac arrest is > 15 mg/dl. Have Calcium Gluconate available as antagonist Test Yourself ! A Woman taking Magnesium Sulfate has a respiratory rate of 10. In addition to discontinuing the medication, the nurse should: a. Vigorously stimulate the woman b. Administer Calcium gluconate c. Instruct her to take deep breaths d. Increase her IV fluids Nursing Care: Hospital Management 1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant Control Blood Pressure Check B / P frequently. Give Antihypertensive Drugs Hydralazine Labetalol Nifedipine Check Hematocrit •Do NOT want to decrease the B/P too low or too rapidly. Best to keep diastolic ~90. •WHY? Nursing Care: Hospital Management 1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant Promote Diuresis **Don’t give Diuretic, masks the symptoms of PIH Bed rest in left or right lateral position Check hourly output -- foley catheter with urimeter Dipstick for Protein Weigh daily -- same time, same scale Nursing Care: Hospital 1. Decrease CNS Irritability Management 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant Monitor Fetal Well-Being FETAL MONITORING-- assessing for late decelerations. NST -- Non-stress test OCT --oxytocin challenge test BPP –biophysical profile If all else fails ---- Deliver the baby!! Key Point to Remember ! SEVERE COMPLICATIONS OF PIH: PLACENTAL SEPARATION - ABRUPTIO PLACENTA; DIC PULMONARY EDEMA RENAL FAILURE CARDIOVASCULAR ACCIDENT IUGR; FETAL DEATH HELLP SYNDROME HELLP Syndrome A multisystem condition that is a form of severe preeclampsia eclampsia H = hemolysis of RBC EL = elevated liver enzymes LP = low platelets <100,000mm (thrombocytopenia) Etiology of HELLP Hemolysis occurs from destruction of RBC’s Release of bilirubin Elevated liver enzymes occur from blood flow that is obstructed in the liver due to fibrin deposits Vascular vasoconstriction endothelial damage platelet aggregation at the sites of damage low platelets. HELLP Syndrome Assessment: 1. Right upper quadrant pain and tenderness 2. Nausea and vomiting 3. Edema 4. Flu like symptoms 5. Lab work reveals – a. anemia – low Hemoglobin b. thrombocytopenia – low platelets. < 100,000. c. elevated liver enzymes: -AST asparatate aminotransferase (formerly SGOT) exists within the liver cells and with damage to liver cells, the AST levels rise > 20 u/L. - LDH – when cells of the liver are lysed, they spill into the bloodstream and there is an increase in serum > 90 u/L/ HELLP Intervention: 1. Bedrest – any trauma or increase in intra- abdominal pressure could lead to rupture of the liver capsule hematoma. 2. Volume expanders 3. Antithrombic medications Urinary Tract Infection Most common infection complicating Pregnancy Etiology Pressure on ureters and bladder causing Stasis with compression of ureters Reflux Hormonal effects cause decrease tone of bladder Assessment Dysuria, frequency, urgency lower abdominal pain; costal vertebral pain fever Interventions Monthly cultures Oral Sulfonamides; Amoxicillin, Ampicillin, Cephalosporins, NO tetracyclines Increase fluid intake to 3 – 4 liters / day Knee chest position Complication Premature labor T O R C H A Infections T = Toxoplasmosis O = Other Syphilis, Gonorrhea, Chlamydial,Hepatitis A or B R = Rubella C = Cytomegalovirus H = Herpes A = Aids Toxoplasmosis Etiology Protozoan infection. Raw meat and cat litter Maternal and Fetal Effects Mom - flu-like symptoms, lymphadenopathy Fetus – stillborn, premature birth, microcephaly; Interventions / Nursing Care mental retardation * Instruct to cook meat thoroughly * Avoid changing cat litter * Advise to wear gloves when working in the garden Treatment: Sulfa drugs Syphilis Etiology • Spirochete – Treponema Pallium Maternal and Fetal Effects May pass across the placenta to fetus causing spontaneous abortion. Major cause of late, second trimester abortion Infant born with congenital anomalies Syphilis Intervention: • 1. Penicillin • 2. Advise to return for prenatal visits monthly to assess for re-infection • 3. Advise that if treated early, fetus may not be infected Gonorrhea Etiology – Neisseria Gonorrhoeae Maternal and Fetal Effects: May get infected during vaginal delivery causing Ophthalmia neonatorium (blindness) in the infant Mom will experience dysuria, frequency, urgency Major cause Pelvic Inflammatory Disease which leads to infertility. Treated with Rocephin Spectinomycin Treat partner!! Chlamydia Three times more common than gonorrhea. Etiology - Chlamydia trachomatis Maternal and Fetal Effects Mom – pelvic inflammatory disease, dysuria, abortions, pre-term labor Fetus -- Stillbirth, Chylamydial pneumonia Interventions Erythromycin, doxycycline, zithromax Advise treatment of both partners is very important Hepatitis A or B Highly contagious when transmitted by direct contact with blood or body fluids Maternal and Fetal Effects: • All moms should be tested for Hep B during pregnancy • Fetus may be born with low birth weight and liver changes\ • May be infected through placenta, at time of birth, or breast milk Intervention: • Recommend Hepatitis B vaccination to both mother and baby after delivery. Rubella Etiology Spread by droplet infection or through direct contact with articles contaminated with nasopharyngeal secretions. Crosses placenta Maternal and Fetal Effects Mom– fever, general malaise, rash Most serious problem is to the fetus--causes many congenital anomalies (cataracts, heart defects) Intervention Determine immune status of mother. If titer is low, vaccine given in early postpartum period CYTOMEGALOVIRUS Etiology -- Member of the Herpes virus • Crosses the placenta to the fetus or contracted during delivery. Cannot breast feed because transmitted through breast milk Effects on Mom and Fetus • Mom – no symptoms, not know until after birth of the baby Fetus -- Severe brain damage; Eye damage • Intervention No drug available at this time Teach mom should not breast feed baby Isolate baby after birth Herpes Simplex Type 2 Maternal and Fetal Effects Painful lesions, blisters that may rupture and leave shallow lesions that crust over and disappear in 2-6 weeks Culture lesions to detect if Herpes, No cure If mom has an outbreak close to delivery, then cannot deliver vaginally. Must deliver by Cesarean birth *Virus is lethal to fetus if inoculated at birth Intervention: Zovirax HIV/AIDS Etiology: Human Immunodeficiency Virus, HIV Transmission of HIV to the fetus occurs through: The placenta; birth canal Through breast milk **The virus must enter the baby’s bloodstream to produce infection. Maternal and Fetal Effects Mom - brief febrile illness after exposure to with symptoms of fatigue and lymphadenopathy Fetus has a 2-5% chance of being infected. No symptoms until about 1 year of age Diagnosis: ELISA test – identifies antibodies specific to HIV. If positive = person has been exposed and formed antibodies Western Blot – used to confirm seropositivity when ELISA is positive. Viral load - measures HIV RNA in plasma. It is used to predict severity – lower the load the longer survival. CD4 cell count – markers found on lymphocytes to indicate helper T4 cells. HIV kills CD4 cells which results in impaired immune system. Goal: reduce viral load to below 50 copies /ml. and increase the CD4 cell count. Nursing Care: **Provide Emotional Support **Teach measures to promote wellness AZT oral during pregnancy IV during labor liquid to newborn for 6 weeks. **Provide information about resources Fetal Demise / Intrauterine Fetal Death DEFINITION: Death of a fetus after the age of viability Assessment: 1. First indication is usually NO fetal movement 2. NO fetal heart tones Confirmed by ultrasound 3. Decrease in the signs and symptoms of pregnancy Treatment: Deliver the fetus How??? Diabetes in Pregnancy Diabetes creates special problems which affect pregnancy in a variety of ways. Successful delivery requires work of the entire health care team Endocrine Changes During Pregnancy There is an increase in activity of maternal pancreatic islets which result in increase production of insulin. Counterbalanced by: a. Placenta’s production of Human Chorionic Somatomammotropin (HCS) b. Increased levels of progesterone and estrogen-antagonistic to insulin c. Human placenta lactogen – reduces effectiveness of circulating insulin d. Placenta enzyme-- insulinase GESTATIONAL DIABETES Diabetes diagnosed during pregnancy, but unidentifable in non-pregnant woman Known as Type III Diabetes - intolerance to glucose during pregnancy with return to normal glucose tolerance within 24 hours after delivery Glucose tolerance test: 1 hr oral GTT – if elevated, do 3 hour GTT Gestational diabetes if: Fasting – 95 mg / dl 1 hour - 180 mg/ dl 2 hour - 155 mg/ dl 3 hour – 140mg/dl Treatment Treatment - controlled mainly by diet No use of oral hypoglycemics Effects of Diabetes on the Pregnancy MATERNAL Increase incidence of INFECTION Fourfold greater incidence of Pre-eclampsia Increase incidence of Polyhydramnios Dystocia – large babies Rapid Aging of Placenta FETAL COMPLICATIONS Increase morbidity Increase Congenital Anomalies neural tube defect (AFP) Cardiac anomalies Spontaneous Abortions Large for Gestation Baby, LGA Increase risk of RDS Effects of Pregnancy on the Diabetic Insulin Requirements are Altered First Trimester--may drop slightly Second Trimester-- Rise in the requirements Third Trimester-- double to quadruple by the end of pregnancy Fluctuations harder to control; more prone to DKA Possible acceleration of vascular diseases Key Point to Remember! If the insulin requirements do not rise as pregnancy progresses that is an indication that the placenta is not functioning well. Interventions /Nursing Care I. Diet Therapy dietary management must be based on BLOOD GLUCOSE LEVELS Pre-pregnant diet usually will not work Need ~300kcal/day Divide among three meals and three snacks II. Insulin Regulation maintaining optimal blood glucose levels require careful regulation of insulin. Sometimes placed on insulin pump. III. Blood Glucose Monitoring teach how to keep a record of results of home glucose monitoring IV. EXERCISE A consistent and structured exercise program is O.K. V. MONITOR FETAL WELL-BEING The objective is to deliver the infant as near to term as possible and prevent unnecessary prematurity NST Ultrasound L / S ratio Heart Disease in Pregnancy Cardiac Response in All Pregnancies Every Pregnancy affects the cardiovascular system ¤ Increase in Cardiac Output 30% - 50% ¤ Expanded Plasma Volume ¤ Increase in Blood (Intravascular) Volume A woman with a healthy heart can tolerate the stress of pregnancy,but a woman with a compromised heart is challenged Hemodynamically and will have complications Effects of Heart Disease on Pregnancy Growth Retarded Fetus Spontaneous Abortion Premature Labor and Delivery Effects of Pregnancy on Heart Disease The Stress of Pregnancy on an already weakened heart may lead to cardiac decompensation (failure). The effect may be varied depending upon the classification of the disease Classification of Heart Disease Class 1 Uncompromised No alteration in activity No anginal pain, no symptoms with activity Class 2 Slight limitation of physical activity Dyspnea, fatigue, palpitations on ordinary exertion comfortable at rest Class 3 Marked limitation of physical activity Excessive fatigue and dyspnea on minimal exertion Anginal pain with less than ordinary exertion Class 4 Symptoms of cardiac insufficiency even at rest Inability to perform any activity without discomfort Anginal pain Maternal and fetal risks are high Nursing Care - Antepartum Decrease Stress teach the importance of REST! watch weight assess for infections - stay away from crowds assess for anemia assess home responsibilities Teach signs of cardiac decompensation Key Point to Remember Signs of Congestive Heart Failure ª Cough (frequent, productive, hemoptysis) ª Dyspnea, Shortness of breath, orthopnea ª Palpitations of the heart ª Generalized edema, pitting edema of legs and feet ª Moist rales in lower lobes, indicating pulmonary edema Teach about diet high in iron, protein low in sodium and calories ( fat ) Watch weight gain Teach how to take their medicine Supplemental iron Heparin, not coumarin – monitor lab work Diuretics – very careful monitoring Antiarrhythmics –Digoxin, quinidine, procainamide. *Beta-blockers are associated with fetal defects. Reinforce physicians care Key point to remember ! Never eat foods high in Vitamin K while on an anticoagulant! ( raw green leafy vegetables) Nursing Care: Intrapartum ª Labor in an upright or side lying position ª Restrict fluids ª On O2 per mask throughout labor and cardiac monitoring. ª Sedation / epidural given early Report fetal distress or cardiac failure ª Stage 2 - gentle pushing, high forceps delivery Nursing Care Postpartum The immediate post delivery period is the MOST significant and dangerous for the mom with cardiac problems Following delivery, fluid shifts from extravascular spaces into the blood stream for excretion Cardiac output increases, blood volume increases Strain on the heart! Watch for cardiac failure Test Yourself ! Mrs. B. has mitral valve prolapse. During the second trimester of pregnancy, she reports fatigue and palpitations during routine housework. As a cardiac patient, what would her functional classification be at this time? a. Class I b. Class II c. Class III d. Class IV