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Complications of Pregnancy Author: Evelyn M. Hickson, RN, MSN, CNS, WCC
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Objectives Describe and define the following complications of pregnancy; discuss predisposing factors, and management of: Preterm Labor Premature Rupture of Membranes Diabetes Thrombophelias Pulmonary Edema Bleeding Complications of Pregnancy (Placenta previa, Abruption, DIC)
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Preterm Labor Definition: Persistent uterine contractions that are accompanied by dilatation and/or effacement as detected by digital exam (Gonik and Creasy 1986)
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Preterm Labor One of the most common complications during pregnancy Issue is the appropriate diagnosis and monitoring Treatment modalities still have not been proven to work
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Definitions: Preterm Delivery Any birth, regardless of birth weight, that occurs before 37 completed weeks from the first day of the last menstrual period Beginning at 20 weeks and ending at 36 6/7 weeks (Creasy and Resnik, 2004)
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Risk Factors Contributing to Preterm Delivery Hypertension Systemic infections Pyelonephritis Drug abuse Maternal race Previous preterm birth Low prepregnancy weight Absent or inadequate PNC 35yrs Strenuous work High personal stress Anemia Smoking Bacteriuria Genital colonization or infection Cervical injury or abnormality Uterine anomaly Low socioeconomic status
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Risk Factors Contributing to Preterm Delivery Preterm labor Ruptured membranes Multiple gestation Preeclampsia Abrupto placenta Placenta previa Vaginal bleeding Growth restriction Oligo, polyhydramnios Fetal anomalies Uterine anomalies Chorioamnionitis Incompetent cervix Diabetes Connective tissue disorders Poor nutrition Peridonal disease Fibroids
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Spontaneous Preterm Labor Risk factors preterm rupture of membranes incompetent cervix amnionitis genital tract infection nonwhite race multiple gestation second trimester bleeding low prepregnancy weight previous preterm birth About 75% of preterm births fall into the spontaneous category (Creasy and Resnik)
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Epidemiology Poorly understood Recent Studies have theorized: Response to chronic intrauterine inflammatory insult Influenced by fetal and maternal immune response Infection induced activation for the fetal hypothalamic-pituitary-adrenal axis, the fetal membranes and decidua produce cytokines which initiate labor or rupture of membranes.
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Signs and Symptoms -Nonspecific and not necessarily those of labor at term -Pelvic pressure -Increased vaginal discharge -Backache -Menstrual-like cramps -Painful or painless contractions, different from Braxton-Hicks only in their persistence
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Difficulty with Accurate Diagnosis Fetal fibronectin test – can improve accuracy of diagnosis—negative Predictive value with dilatation <3cm and effacement <80% for delivery Within 7-14 days good, positive predictive value not good
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Difficulty with Accurate Diagnosis High prevalence of S&S among healthy women not in preterm labor Imprecision of digital exam Contraction frequency (4 or more per hour ) has low sensitivity and low positive predictive value Endovaginal ultrasonography cervical length of 30mm or greater has very high negative predictive value in symptomatic women
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Diagnosis Cervical effacement of 80% or greater Dilation of more than 2 cm Change in dilation of 1 cm or more Sonographic cervical length under 30mm or a positive fetal fibronectin
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Management Variety of drugs available-no clear first line drug-clinical situation and physician preference Antibiotics do not appear to prolong gestation, should be used for GBS prophylaxis if delivery is imminent Maintenance or repeated acute tocolysis doesn’t improve perinatal outcome used generally
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Managment Tocolytic drugs may prolong pregnancy 2- 7 days which may allow for steroids to improve lung maturity, and transport to a tertiary center Antenatal corticosteroids significantly reduce the incidence and severity of neonatal RDS. Also reduce incidence of IVH and necrotizing enterocolitis. Decrease neonatal mortality.
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Tocolytic Agent Dosage and Administration Contraindica- tions Maternal Side Effects Fetal and Neonatal Side Effects BetamimeticTerbutaline.25mg sub Q every 20 min to 3 hrs hold for pulse >120 Cardiac arrhythmias Cardiac arrhythmia Pulmonary edema Fetal tachycardia Hyperinsulinemia Hyperglycemia Myocardial and septal hypertrophy Myocardial ischemia Magnesium Sulfate 4-6 g bolus for 20 min, then 2-3 g/hr Myasthenia gravisFlushing,lethargy, Headache,muscle weakness, diplopia, dry mouth, pulmonary edema, cardiac arrest Lethargy, hypotonia, respiratory depression prolonged use demineral-ization with Tocolytics
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Calcium channel blockers Nifedipine 30mg loading dose, then 10-20mg q 4-6 hr Cardiac disease, use caution with renal disease, hypotension,90/50 mm HG avoid concomitant use with magnesium sulfate Flushing, headache, diaainess, nausea, transient hypotension None noted Prostaglandin gynthetase inhibitors Indomethacin loading dose of 50 mg rectally or 50- 100mg orally, then 25-50mg orally every 6hrx48hrs Sig. Renal or hepatic impairment Nausea, heartburnConstriction of ductus arteiosus, pulmanary hypertension, reversible decrease in renal function with oligo, IVH, hyperbilirubinemia, necrotizing enterocolitis Tocolytics
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Nursing Care: Evaluation for Preterm Labor History (risk factors) S&S of preterm labor S&S UTI S&S vaginitis/cervicitis/STDs S&S viral or bacterial infection S&S PROM Physical Exam VS Evaluate gestational age Electronic monitor and palpate contractions Electronic monitor of FHR and pattern Abdominal palpation for presentation, position, multiple gestation, EFW, pain Costovertebral angle tenderness Low back or suprapubic pain
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Evaluation for Preterm Labor Pelvic Exam Speculum exam for vaginitis,cervicitis,STDs,PROM, bloody show, meconium Digital exam for cervical changes (not done if PROM found on spec exam) Lab tests UA, urine culture and sensitivity Wet mount for Bacterial Vaginosis or Trichomonas GBS cultures and cultures of any lesions GC and chlamydia cultures CBC with differential Nitrazine and ferning if appropriate
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Nursing Care of Woman in Preterm Labor Bedrest, lateral position IV, hydration has not been shown to be effective in stopping labor and increases risk of pulmonary edema Continuous uterine and fetal monitoring Medications as ordered Arrange for transport if planned Arrange for care of infant, staffing, pediatrician, respiratory therapy, equipment
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Premature Rupture of Membranes (PROM) Definition: Rupture of membranes before the onset of labor Preterm premature rupture of membranes (PPROM)is rupture of membranes before the onset of labor at <37 weeks gestation
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Term PROM Complicates 8% of pregnancies Generally followed by onset of labor and delivery In a large randomized study, with expectant management, and ½ of women with PROM delivered within 5 hours, and 95% delivered within 28 hours. Risks—intrauterine infection—increases with duration of membrane rupture, umbilical cord compression (ACOG practice bulletin)
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Etiology of Membrane Rupture at Term Combination of stretching with uterine growth, strain from uterine contractions and fetal movement Biochemical changes, including a decrease in collagen content
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Management PROM May induce labor immediately Observe for the onset of spontaneous labor for up to 24-72 hours (if observing need to avoid digital exams which increase the risk of infection) Antibiotics if GBS positive or if rupture >18 hours
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Risk Factors Smoking Multiple gestation Abruptio placenta Cocaine use Previous PPROM Previous cervical operations or lacerations Occupational fatigue, long working hours Vitamin C and E deficiencies
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Management Antibiotics—prolongs latency period and improve perinatal outcome with expectant management prior to 35 weeks Administration of corticosteroids if <32 weeks (some recommend <34 weeks*) Avoid digital exams if not in labor and immediate induction is not planned
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Nursing Care Accurate history: time, amt, color, odor, intercourse Physical Exam: VS,FHR, contractions, abdominal palpation Sterile Speculum Exam: vulva, vaginal pooling, fluid from os, cord, fetal part, nitrazine, fFN, amnitoic protein, cervical cultures, GBS
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Nursing Care continued In labor assess temp q2 hrs, otherwise q 4 hrs Monitor FHR, cord compression or tachycardia Avoid unnecessary vaginal exams Watch hydration, dehydration can cause a temp elevation
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Diabetes Mellitus Definition: Gestational Diabetes is the presence of carbohydrate intolerance of varying degrees of severity with an onset or first recognition during pregnancy. (Varney) Incidence: Averages about 7%, varies with ethnicity Increased in Hispanic, African, Native American, South or Eastern Asian, or Pacific Islander Pregestational Diabetes: Diabetes which antedates the pregnancy
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Pre-Gestational Diabetes Type I or Type II Type I: True insulin-dependent, typically develops prior to adolescence, usually diagnosed prior to pregnancy.White classification of B,C,D,F and above Type II: Not necessarily insulin dependent and usually begins after age 40
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Risk Factors 1. Marked obesity 2. Hx GDM prior pregnancy 3. Strong family Hx 4. Previous infant >4000 gm 5. Hx unexplained stillbirth 6. Poor OB Hx, SABs, congenital anomalies 7. Recurrent glycosuria (2 positive tests) unexplained by diet
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Physiology Gestational Diabetes Similar to type II Diabetes: Insulin is available Hormonal changes alter receptivity to insulin <20 weeks cells more responsive to insulin >20 weeks, as placenta grows, production of human placental lactogen (HPL) increases
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Physiology of Gestational Diabetes HPL increases cellular resistance to insulin When production of insulin cannot keep up with rising need hyperglycemia results Peak effect of HPL 26 to 28 weeks
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Risks of Diabetes Pregestational Diabetes: Congenital anomalies,spontaneous AB, stillbirth, IUGR, HTN, preeclampsia Gestational Diabetes: If early pregnancy blood sugars not elevated, no increase in anomalies, but increase in macrosomic infants, protracted labor, shoulder dystocia, operative delivery HTN and preeclampsia, Type II Diabetes later in life
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Macrosomic Infant Insulin similar to Human Growth Hormone Glucose crosses the placenta Fetus increases insulin production to metabolize glucose Hyperplasia and hypertrophy of cells causing lifelong change increasing risk of obesity as well as diabetes
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Screening tests ADA recommends random nonfasting 1hour post 50 gram glucola <130-140 (early with risk factors, 24-28 weeks for everyone) 3 hour glucose tolerance test
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Management ADA diet—same nutrition requirements as nondiabetic women —2000 to 2200k cal diet, may consider caloric restriction in obese women no more than 33% Balance of calories from carbohydrate, fat and protein Home glucose monitoring Fasting <95mg/dl, 1 hr <140, 2hr <120 Careful evaluation of fetal size and fluid volume, ultrasound if necessary but poor predictor of EFW Optimal antenatal testing for diet controlled GDM with no other risk factors not established Usually recommend DFMC from 34 to 36 wks on at 40 weeks NST or BPP
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Management Mild to moderate exercise If well controlled with diet alone, await spontaneous labor Insulin or glyburide if poorly controlled with diet Consider C-Section if EFW >4500 gm 6 week postpartum glucose testing Labor management the same as nondiabetic with higher level of suspicion for shoulder dystocia IV fluids should not contain glucose
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Nursing Care Same as any woman in labor Notify pediatrician of diabetic mom Anticipate shoulder dystocia and be prepared to help Avoid glucose containing IV fluids unless on insulin drip and NPO If on insulin, periodic blood glucose checks and insulin as ordered Anticipate postpartum uterine atony/hemorrhage if macrosomic infant Watch vital signs closely and be aware of increased risk for HTN
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Thrombophilia Definition: Tendency toward blood clot formation Most common inherited are: 1. Factor V Leiden 2. Prothrombin G20210A mutation Less common inherited are: 1. Deficiency of anticoagulants protein C, proteinS, and antithrombin III
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Thrombophilia Most common acquired: 1. Antiphospholipid antibody syndrome 2. Lupus Anticoagulant 3. Anticardiolipin antibodies Less common acquired: 1. Lupus Anticoagulant 2. Anticardiolipin Antibodies
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Risk Factors for Deep Vein Thrombosis and Thromboembolic Disorders Hereditary thrombophilia Acquired thrombophilia Mechanical heart valve Atrial fibrillation Trauma/prolonged immobilization/major surgery History of deep vein thrombosis Strong family history of thrombosis or thromboembolic events Pregnancy Oral contraceptive use
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Testing for Thrombophilias History of thrombosis First degree relative with thrombophilia Recurrent fetal loss History of early or severe preeclampsia Severe unexplained IUGR
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Signs and Symptoms - Superficial Thrombophlebitis Leg pain Localized heat, tenderness or inflammation at site Palpation of knot or cord
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Signs and Symptoms DVT Slight temperature elevation Mild tachycardia Abrupt onset with severe leg pain worse with motion or standing Edema of ankle,leg,thigh Positive Homan’s sign Pain with calf pressure Tenderness along entire course of involved vessel with palpable cord
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Signs and Symptoms of Pulmonary Embolism Dyspnea Tachycardia Tachypnea Breath sounds few rales or wheezes Low PO2 and O2 saturation Hemoptysis Pleuritic chest pain
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Pleural friction rub or signs of effusion Hypoxia Hypotension Cyanosis Jugular venous distention Right ventricular heave (lower left sternal border) Signs and Symptoms of Pulmonary Embolism
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Management of Thrombophilias Appropriate testing for thrombophilias High index of suspicion with risk factors Occasional prophylactic anticoagulation with sub q heparin injection During labor, if anticoagulant therapy is required, IV heparin is used Postpartum, switch back to sub q heparin overlapping with coumadin With some anticoagulants neuraxial blocks should not be used for 24 hours after last injection
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Nursing Care Recognize increased risk for thromboembolic events and be prepared If on anticoagulants, recognize increased risk for bleeding and be prepared
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Pulmonary Edema Usually due to excess capillary pressure as in cardiomyopathy, mitral stenosis or due to a disruption of alveolar capillary membrane integrity as in pneumonia, ARDS (Gabbe, Niebyl, Simpson, 2002) Two general causes alveolar flooding: caused by heart failure or permeability edema from alveolar-capillary injury. In many OB cases both are present (Williams OB, 2001)
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Risk Factors for the Development of Pulmonary Edema Maternal cardiac disease (structural, ischemic or dysrhythmia) Eclampsia, severe preeclampsia, or other significant hypertensive disease Antepartum hemorrhage HELLP syndrome Use of tocolytics, Betamimetics, Magnesium Sulfate Fluid overload Infection - occult chorioamnionitis and sepsis Adult Respiratory Distress Syndrome
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Risk Factors/Acute Lung Injury Pneumonia: Aspiration, bacterial, viral Sepsis: Chorioamnionitis, pyelonephritis, puerperal infection, septic abortion Hemorrhage: Shock, massive transfusion therapy Arsenic poisoning Preeclampsia (Williams OB, 2001) Embolism: Amnionic fluid, trophoblastic disease, air Connective-tissue disease Substance abuse: Heroin, methadone Irritant inhalation and burns Pancreatitis Pheochromocytoma
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Signs and Symptoms Dyspnea Cough Orthopnea Tachycardia Hemoptosis (occasionally)
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Management O2 supplementation Diuretics Discontinuation of offending agent Ventilatory support Circulatory support Treatment of underlying cause
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Nursing Care Unless very mild, requires Intensive Care with invasive hemodynamic monitoring Labor and Delivery nurses role primarily in close monitoring of patient at risk, early recognition of signs of decompensation, prevention of iatrogenic causes
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Hypertensive Disorders of Pregnancy Chronic Hypertension Gestational Hypertension Preeclampsia Eclampsia HELLP syndrome
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Effects of HTN on Pregnancy Worsening or malignant HTN CNS involvement – stroke, hemorrhage Cardiac decompensation Renal deterioration or failure Decreased uteroplacental perfusion
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Hypertension in Pregnancy Chronic HTN: Present before the 20 th week of pregnancy or present before pregnancy Systolic greater than or equal to 140 and/or diastolic greater than or equal to 90 Mild=140/90 Severe=180/110 Use of antihypertensive meds before pregnancy Persistence of HTN beyond postpartum period
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Hypertension in Pregnancy Gestational Hypertension Replaces older term PIH (pregnancy induced hypertension) Describes cases in which elevated blood pressure without proteinuria develops after 20 weeks and returns to normal after delivery (ACOG Practice Bulletin 33) 25% of these women develop preeclampsia
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Complications of Gestational Hypertension and Pre-eclampsia At higher risk for pulmonary edema due to dramatic decrease in colloid osmotic pressure Highest risk is 6- 24 hours post- delivery prior to diuresis S & S of pulmonary edema: Decreased SaO2 Wheezing/SOB Neck vein distention Tachypnea Tachycardia Lungs dull to percussion Cough (Productive or Nonproductive) Anxiety
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Nursing Care Monitor: Signs and symptoms of decline in patient condition Maternal and Fetal Well-being (done by OB) Strict I & O Respiratory Status - Pulmonary Edema Renal and Hepatic Function Clotting Capability – potential for bleeding Psych-Social Support of patient and family
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Hypertension in Pregnancy Preeclampsia Definition: Pregnancy specific syndrome that usually occurs after 20 weeks (except in trophoblastic disease) Characterized by: BP elevation of 140 or greater systolic or 90 or greater diastolic in previously normotensive woman, accompanied by proteinuria of.3g or more in 24 hours, or 1+ or greater reading on dipstick Suspect preeclampsia if elevated BP without proteinuria but with HA, blurred vision, abdominal pain, low platelets, abnormal liver enzymes
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Risk Factors for Preeclampsia Nulliparity Trophoblastic disease Multiple pregnancy CHTN Preexisting renal disease Pregestational diabetes Family history of preeclampsia or eclampsia Hx of preeclampsia in previous pregnancy Multipara with new sexual partner African or Asian ethnicity Thrombophilia
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Signs and Symptoms Persistent HA Dizziness, blurred vision, scotomata Persistent epigastric pain BP elevation Ophthalmic Exam: Papilledema, A-V nicking, vessel; narrowing, hemorrhagic areas
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Lab Value Changes Platelets - Low > 100 K is severe disease Serum Uric Acid – High BUN – Normal to High Serum Creatinine – Normal to High Liver Function – Elevated Urine Protein – Increased 3-4+ with 5 Grams/L in 24 hrs = severe disease 2-3+ with 1 Grams/L in 24 hrs diagnostic of preeclampsia
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Treatment Magnesium Sulfate 4-6 Gram IV load over 20 minutes followed by 2 Grams /hr and maintained for 12-24 hours post partum Antihypertensive Medications for diastolic >105-110 If still pregnant with viable baby – determine severity of disease, risk to mother and to baby and determine if mom needs to be delivered If baby has demised, deliver
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Eclampsia Preeclampsia disease process that progresses to convulsions Most common prior to delivery but may occur to 10+ days post partum
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Seizure Aura “Worst Headache Ever” Feeling Weird Ringing in ears Visual Disturbance Epigastric / Right Upper Quadrant Pain
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Seizure Characteristics Fixation of diaphragm during seizure Respirations may cease during seizure Duration vary Cyanosis Fetal Bradycardia (if still pregnant) Potential for: Sudden Death Massive Cerebral Hemorrhage Blindness due to retinal detachment, occipital lobe ischemia, infarction or edema Cerebral Edema
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Treatment If still pregnant and baby alive and viable: Reload with Magnesium Sulfate 4-6 Grams Magnesium Sulfate drip rate at 2 Grams/hour No use of Valium – use Ativan Deliver
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HELLP Syndrome Combination of hemolysis(H), elevated liver enzymes(EL), and low platelets (LP) Liver involvement in preeclampsia- eclampsia May occur in as many as 20% of women with severe preeclampsia
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HELLP Syndrome Increased risk of averse outcomes Increased risk of abruptio placenta Renal failure Subcapsular hepatic hematoma Recurrent preeclampsia Preterm delivery Fetal and maternal death
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Signs and Symptoms Upper abdominal pain, epigastric or right upper quadrant Thrombocytopenia Elevated liver enzymes aspartate aminotransferase typically less than 200 to 500U/L Sometimes serum bilirubin is elevated, seldom greater than 2-4 mg/dL Intrahepatic and subcapsular hemorrhage Liver rupture, fatal hemorrhage
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Signs and Symptoms Most cases obvious preeclampsia Patients either present with or report having symptoms of “flu” Most have no symptoms relating to liver, but if there is pain liver more likely involved Hepatic failure with encephalopathy and consumptive coagulopathy are not usual Patient may become comatose if HELLP severe enough
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Management Prompt delivery Lab abnormalities peak by 23-48 hours and begin to normalize in 2-3 days
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References Burrow, G.N., MD; Duffy, T.D., MD (Eds.) (1999). Medical Complications During Pregnancy fifth edition. Pennsylvania: W.B. Saunders Company. Creasy, R.K., MD; Resnik, R., MD (Eds.) (2004) Maternal-fetal Medicine, Principles and Practice fifth edition. Pennsylvania: Saunders Cunningham, F.G., Gant, N.F., Leveno, K.J., Gilstrap III, L.C., Hauth, J.C., Wenstrom, K.D. (Eds.) (2001) Williams Obstetrics twenty first edition. New York: McGraw-Hill. Gabbe, S.G., Niebyl, J.R., Simpson J.L. (Eds.) (2002). Obstetrics, Normal and Problem Pregnancies fourth edition. Pennsylvania: Churchhill Livingstone. Netter, F.H., MD (Ed.) (1965) The CIBA Collection of Medical Illustrations Vol. 2 Reproductive System. New York: CIBA Pharmaceutical Company. Varney, H.; Kriebs, J.M.; Gegor, C.L., (2004) Varney’s Midwifery fourth edition. Canada: Jones and Bartlett Publishers. The American College of OB/GYN (Ed.) (2004) 2004 Compendium of Selected Publications. Washington D.C.: The American College of OB/GYN.
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