summer 2013. risk factors age – under 17 over 35 gravida and parity socioeconomic status ...

Summer 2013

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, gestational hypertension

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

Abortions Termination of pregnancy at any time before the fetus has reached the age of viability Either: spontaneous occurring naturally induced artificial

Types of Abortions Threatened Imminent Complete Incomplete Missed Recurrent/Habitual

Question??? What are two main complications related to a missed abortion? 1. 2.

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 trendelenberg position Teach Assess for leakage Assess for contractions Assess fetal movement and report decrease movement Assess temperature for elevation

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

Ectopic Pregnancy Implantation of the blastocyst in ANY site other than the endometrial lining of the uterus (5) Cervical ovary

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 Cullens sign -- bluish discoloration around umbilicus Nausea, Vomiting Faintness

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 grape- size 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 doesnt 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

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

Abruptio Placenta Premature separation of the placenta from the implantation site in the uterus Etiology: Chronic Maternal Hypertension Short umbilical cord Trauma History of previous delivery with separation Smoking / Caffeine / Cocaine Vascular problems such as with diabetes Multigravida status Defined as marginal, partial or complete

Treatment and Nursing Care Abruptio Placenta Cesarean delivery immediately Combat shock blood replacement / fluid replacement Blood work assessment for complication of DIC

Placenta Previa PAINLESS vaginal bleeding 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; FHTs countable and uterus is not hypertonic Blood clotting defect absent Abruptio Placenta Bleeding accompanied by PAIN Bleeding accompanied by PAIN Dark red bleeding Dark red bleeding First episode of bleeding usually profuse First episode of bleeding usually profuse Signs of blood loss out of proportion to visible amount Signs of blood loss out of proportion to visible amount Uterus board-like, painful and low back pain Uterus board-like, painful and low back pain Fetal parts non-palpable, FHTs non-countable and high uterine resting tone (noted with IUPC) Fetal parts non-palpable, FHTs non-countable and high uterine resting tone (noted with IUPC) Blood clotting defect (DIC) likely 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

Critical Thinking Mrs. A., G3 P2, 38 weeks gestation is admitted to L & D with scant amount 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 coagulant) is produced Fibrinogen fibrin which enhances platelet aggregation and clot formation Widespread fibrin and platelet deposition in capillaries and arterioles

Etiology continued 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

Assessment & Intervention Precipitating factors Abruption PIH/HELLP syndrome Sepsis Anaphylactoid Syndrome Labs to review PT, PTT, Platelets, D-Dimer, FSP Interventions Remove the cause Replace fluids (Blood or blood products) Meds

Assessment/Signs and Symptoms Spontaneous bleeding from gums and nose (epistaxis, injection and IV sites, incisions) Excessive bleeding Petechiae and ecchymosis at site of blood pressure cuff, pulse points Tachycardia, diaphoresis, restlessness, hypotension Hematuria, oliguria, occult blood in stool Altered LOC if cerebral circulation is decreased or cerebral bleed

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, thrombocytopenia Fibrin Split Product increased An increase in both FSP and D-dimer are indicative of DIC

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 = 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 = Progression of pre-eclampsia to generalized seizures not attributable to other causes Chronic HTN = BP > or equal to 140/90 that was known to exist before pregnancy or develops prior to 20 weeks gestation or does not resolve after 6 weeks after delivery

Predisposing Factors Primigravida Multiple gestation pregnancy Vascular Disease Age >35 Obesity Hydatiform Molar Pregnancy Family History Lower SES (poor nutrition,/decreased protein intake, inadequate prenatal care)

PATHOLOGICAL CHANGES Gestational Hypertension due to: GENERALIZED ARTERIOLAR CYCLIC VASOSPASMS INCREASED PERIPHERAL RESISTANCE; IMPEDED BLOOD FLOW ( in blood pressure) Endothelial CELL DAMAGE Intravascular Fluid Redistribution (decrease in diameter of blood vessel) Decreased Organ Perfusion Multi-system failure Disease

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

The difference between dependent edema and generalized edema is important. The patient with pre-eclampsia has generalized edema because fluid is in all tissues. The Nurse Must Know

Placenta Due to Vasospasms and Vasoconstriction of the vessels in the placenta. Decreased Placental Perfusion and Placental Aging Fetal Growth is retarded - IUGR, SGA Positive CST / __________Decelerations With Prolonged decreased Placental Perfusion:

Oliguria 100ml/4 hrs or less than 30 ml. / 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 Hyperreflexia 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

Systolic> or = to 140/90 but or = to 90 but < 110 mm Hg Protein > or = to 0.3 g but < 2 g in 24 hr specimen (1-2+ dipstick) Creatinine, serum normal Platelets normal ALT/AST normal or minimal increase Urine output normal No HA Absent RUQ pain/ no N/V Absent to minimal visual changes No pulmonary edema or heart failure Normal fetal growth > or = to 160 mm Hg 2 readings 6 hrs apart on bedrest > or = to 110mm Hg Protein > or = to 5 g in 24 hr specimen (3+ or higher dipstick) Creatinine elevated > 1.2 mg/ dL Platelets decreased < 100, 000 cells/mm3 ALT/AST Elevated levels Oliguria common, often

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, ALT, 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. Vasodilator-- 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 for hyporeflexia -- D/C if hyporefexia 3. Measure Urinary Output >100ml in 4 hrs. 4. Measure Magnesium levels normal is 1.5-2.5 mg/dl per hr 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

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.Do NOT want to decrease the B/P too low or too rapidly. Best to keep diastolic ~90. WHY?WHY?

Promote Diuresis ** Dont give Diuretic, masks the symptoms of Gestational Hypertension Bed rest in left or right lateral position Check hourly output -- foley catheter with urimeter Dipstick for Protein Weigh daily -- same time, same scale

Monitor Fetal Well-Being FETAL MONITORING-- assessing for late decelerations. NST -- Non-stress test CST contraction stress test BPP biophysical profile If all else fails ---- Deliver the baby!!

HELLP Syndrome A multisystem condition that is life threatening and complicates 10% of pregnancies in women with severe HTN and may occur during PP period H = hemolysis of RBC EL = elevated liver enzymes LP = low platelets

summer 2013. risk factors age – under 17 over 35 gravida and parity socioeconomic status ...

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