Complications of Pregnancy

1. Complications of Pregnancy Spring 2012

2. 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

3. 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

4. Gestational Onset Disorders

5. Bleeding Disorders

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

7. Types of Abortions • Threatened • Imminent • Complete • Incomplete • Missed • Recurrent/Habitual

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

9. Cerclage procedure -- purse-string suture placed around the internal os to hold the cervix in a normal state

10. 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

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

12. 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

13. 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

14. Gestational Trophoblastic DiseaseHydatiform 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.

15. 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

16. 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

17. 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?

18. 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

19. 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

20. 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

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

22. 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; FHT’s countable and uterus is not hypertonic • Blood clotting defect absent Abruptio Placenta • Bleeding accompanied by 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

23. 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

24. 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? • Assess the fundal height for a decrease • Place a hand on the abdomen to assess if hard, board-like, tetanic • Place a clean pad under the patient to assess the amount of bleeding • Prepare for an emergency cesarean delivery

25. Disseminated IntravascularCoagulation (DIC) Anti-coagulation and Pro-coagulation effects existing at the same time.

26. Etiology Defect in the Clotting Cascade • An abnormal overstimulation of the coagulation process Activation of Coagulation with release of thromboplastin into maternal bloodstream ê Thrombin (powerful anticoagulant) is produced ê Fibrinogen fibrin which enhances platelet aggregation and clot formation • ê • Widespread fibrin and platelet deposition in capillaries and arterioles

27. 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

28. 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

29. Hyperemesis Gravidarum

30. 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

31. Nursing Care / InterventionsHyperemesisGravidarium • 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

32. Hypertenison during pregnancy

33. 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

34. Predisposing Factors • Primigravida • Multiple gestation pregnancy • Vascular Disease • Age >35 • Obesity

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

36. 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

37. 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

38. 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

39. Significant Lab WorkChanges 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)

40. 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

41. 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.

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

43. 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

44. Central Nervous System Changes • Cerebral edema -- forcing of fluids to extracellular • Headaches -- severe, continuous • Hyper-reflexia • LOC changes – changes in affect • Convulsions / seizures

45. Visual Changes Retinal Edema and spasms leads to: • Blurred vision • Double vision • Retinal detachment • Scotoma (areas of absent or depressed vision)

46. Nausea and Vomiting • Epigastric pain –often sign of impending coma

47. Pre-Eclampsia Mild Severe • 140/90 • Protien 1+ to 2+ • Edema 1+ to lower legs • < 1lb/ week • Reflexes 1+ to 2+ • 160/90 • Protein 3+ to 4+ • Edema 3+ to 4+ • >2 lb/ week • Reflexes 3+ to 4+ (hyperreflexia) • Clonus present • Blurred vision or Scotoma • Retinal detachment • N&V, Epigastric pain • Elevated Liver enzymes • Headache or change in LOC • Premature aging of placenta, IUGR, & or late decelerations

48. 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

49. 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

50. Hospital ManagementNursing Care Goal 1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant