Medical Complication Of Pregnancy

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Medical Complication Of Pregnancy

  1. 1. Medical complications of pregnancy
  2. 2. Introduction <ul><li>Physiology adaptation to pregnancy involves the Cardiovascular, pulmonary, endocrine, hematologic, neurologic, renal, and gastrointestinal systems. </li></ul><ul><li>In a normal healthy woman, the adaptive responses are approciate and well tolerated. </li></ul><ul><li>When underlying pathology is present, organ failure may occur. </li></ul><ul><li>Chapter ninth, maternal physiology </li></ul>
  3. 3. Cardiovascular system
  4. 4. Physiologic changes during pregnancy <ul><li>During human pregnancy, cardiac output increases by almost 40%: 5000ml/min for normal nonpregnant woman, and 7000ml/min for pregnant woman. </li></ul><ul><ul><li>most of this increase is due to an increase in stroke volume </li></ul></ul><ul><ul><li>Heart rate increase by only about 10 beats/min during the third trimester. </li></ul></ul><ul><li>Cardiac output peaks at around 18 to 24 weeks, and then stabilizes. </li></ul>
  5. 5. Heart disease <ul><li>Internal medicine </li></ul><ul><li>Types of CVS </li></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Coronary heart disease </li></ul></ul><ul><ul><li>Pulmonary heart disease </li></ul></ul><ul><ul><li>Arrhythmia </li></ul></ul><ul><ul><li>Rheumatic heart disease </li></ul></ul><ul><ul><li>Congenital heart disease </li></ul></ul><ul><ul><li>Cardiomyopathy </li></ul></ul><ul><ul><li>Pleral cavity problem </li></ul></ul><ul><ul><li>Heart failure </li></ul></ul>
  6. 6. Rheumatic heart disease <ul><li>The leading factor of heart disease of pregnant women </li></ul><ul><li>Mitral stenosis </li></ul><ul><ul><li>At higher risk of developing heart failure , subacute bacterial endocarditis, and thrombolic disease </li></ul></ul><ul><ul><li>Cardiac output increases and the mechanical obstruction worsens. Patients may develop cardiac decompensation and pulmonary edema </li></ul></ul><ul><ul><li>Atrial fibrillation </li></ul></ul>
  7. 7. Congenital heart disease <ul><li>The anatomic defects of most of the patients has been corrected </li></ul><ul><li>The anatomic defect has not been corrected </li></ul><ul><ul><li>Well tolerate </li></ul></ul><ul><ul><li>Less well tolerate </li></ul></ul><ul><li>Patients with primary pulmonary hypertension or cyanotic heart disease with residual pulmonary hypertension are in danger of undergoing decompensation during pregnancy. </li></ul><ul><ul><li>pulmonary hypertension from any cause is associated with a 25% to 50% maternal mortality during pregnancy. </li></ul></ul>
  8. 8. What is the right to left shunt for the congenital heart disease?
  9. 9. Cardiac arrhythmia <ul><li>Superventricular tachycardia is the most common arrhythmia </li></ul><ul><ul><li>Pregnancy (weight gain) </li></ul></ul><ul><ul><li>Anemia </li></ul></ul><ul><ul><li>labor </li></ul></ul><ul><li>Ventricular premature constriction </li></ul><ul><li>The cause of the arrhythmia and the hemodynamic changes due to the arrhythmia </li></ul><ul><ul><li>Structural and functional </li></ul></ul><ul><ul><li>Asymptomatic and symptomatic </li></ul></ul>
  10. 10. Peripartum and postpartum cardiomyopathy <ul><li>It is very rare, but it is exclusively associated with pregnancy. </li></ul><ul><li>Patients have no underlying cardiac disease, and symptoms of cardiac decompensation appear during the last weeks of pregnancy or 2 to 20 weeks postpartum </li></ul><ul><li>Patient with a history of pre-eclampsia or hypertension and poorly nourished are at high risk. </li></ul>
  11. 11. Management of cardiac disease during pregnancy <ul><li>New York heart association’s functional classification of heart disease </li></ul><ul><li>Cardiac decompensation may occur at any phase of pregnancy, it is most likely occur during the period of peak increase in cardiac output (18-24weeks), during labor or delivery, or during the immediate postpartum period. </li></ul><ul><ul><li>Prenatal management </li></ul></ul><ul><ul><li>Management of labor </li></ul></ul><ul><ul><li>Management of delivery and the immediate postpartum period </li></ul></ul>
  12. 12. New York heart association’s functional classification of heart disease <ul><li>Class 1 no signs or symptoms of cardiac decompensation </li></ul><ul><li>Class 2 no symptoms at rest, but minor limitation of physical activity </li></ul><ul><li>Class 3 no symptoms at rest, but marked limitation of physical activity </li></ul><ul><li>Class 4 symptoms present at rest, discomfort increased with any kind of physical activity </li></ul>
  13. 13. Prepregnant counseling and prenatal care <ul><li>The maternal and fetal risk for patients with class 1 and 2 disease is small </li></ul><ul><ul><li>Permitted to conception </li></ul></ul><ul><ul><li>Intensive care </li></ul></ul><ul><ul><ul><li>Normal :term pregnancy </li></ul></ul></ul><ul><ul><ul><li>Abnormal:Abortion or induction of labor </li></ul></ul></ul><ul><li>whereas they are greatly increased with class 3 and 4 disease. </li></ul><ul><ul><li>Not permitted to pregnancy </li></ul></ul><ul><ul><li>Abortion or induction of labor </li></ul></ul>
  14. 14. Prenatal management <ul><li>A general principle: all pregnant cardiac patients should be managed with the help of a cardiologist. </li></ul><ul><li>A number of guidelines: </li></ul><ul><ul><li>Avoidance of excessive weight gain and edema </li></ul></ul><ul><ul><li>Avoidance of strenuous activity </li></ul></ul><ul><ul><li>Avoidance of anemia </li></ul></ul><ul><ul><li>Early detection of a problem </li></ul></ul><ul><ul><ul><li>Infection </li></ul></ul></ul><ul><ul><ul><li>cardiac decompensation </li></ul></ul></ul><ul><ul><ul><li>pulmonary edema </li></ul></ul></ul>
  15. 15. Management of labor <ul><li>During labor, cardiac output increase by about 40%-50% when compared with prelabor levels, and by about 80% to 100% when compared with prepregnancy levels </li></ul><ul><li>The increase in the cardiac output is due to catecholamine release brought about by pain and apprehension, most of the increase is due to abdominal and uterine muscle contraction. </li></ul><ul><li>Sedation, epidural anesthesia, prophylactic antibiotics, aterial and Swan-Ganz catheters, cardiac rhythm, fluid intake and urine output, arterial blood gas, hemoglobin concentration, electrolytes. </li></ul>
  16. 16. Management of delivery and the immediate postpartum period <ul><li>cardiac patients should be delivered vaginally unless obstetric indication for cesarean section are present. </li></ul><ul><ul><li>Second stage of labor </li></ul></ul><ul><li>Avoid pushing during uterine contraction </li></ul><ul><li>Cardiac output increase to 80% above prelabor values in the first few hours after a vaginal delivery and up to 50% after cesarean section. </li></ul><ul><ul><li>After delivery of the placenta, the uterine contracts and about 500ml of blood is added to the effective blood volume. </li></ul></ul><ul><li>If cardiac decompensation occurs, it should be managed as a medical emergency. </li></ul>
  17. 17. Cardiac dysfunction associated with pregnancy and labor <ul><li>during the period of 18-24weeks peak increase in cardiac output </li></ul><ul><li>during labor or delivery especially the the second stage of labor </li></ul><ul><li>during the immediate postpartum period. </li></ul>
  18. 18. Thromboembolic disorder <ul><li>superficial thrombophlebitis </li></ul><ul><li>deep venous thrombosis </li></ul><ul><li>pulmonary embolism </li></ul>
  19. 19. Conditions and mechanism of blood clots formation (pathology) <ul><li>Endothlial damage of the blood vessels </li></ul><ul><li>Decreasing of the velocity of the blood flow </li></ul><ul><li>High blood coagulating status </li></ul><ul><ul><li>Platelet </li></ul></ul><ul><ul><li>Coagulation factors </li></ul></ul>
  20. 20. superficial thrombophlebitis <ul><li>Incidence </li></ul><ul><ul><li>1/600 during antepartum period </li></ul></ul><ul><ul><li>1/95 in the immediate postpartum peroid] </li></ul></ul><ul><li>High risk factors </li></ul><ul><ul><li>Varicose vein </li></ul></ul><ul><ul><li>Obese patient </li></ul></ul><ul><ul><li>Limited physical activity </li></ul></ul><ul><li>Calf area is the most common site </li></ul>
  21. 21. Diagnosis of superficial thrombophlebitis <ul><li>Symptoms </li></ul><ul><ul><li>Swelling and tenderness of the involved extremity </li></ul></ul><ul><li>Signs </li></ul><ul><ul><li>Erythema, tenderness, warmth, and a palpable cord over the course of the involved superficial veins </li></ul></ul>
  22. 22. Treatment of superficial thrombophlebitis <ul><li>Pain medication </li></ul><ul><li>Local Heat application </li></ul><ul><li>Elevation of the lower extremities </li></ul><ul><li>Anti-inflammatory agents </li></ul><ul><li>Anticoagulants is not indicated </li></ul><ul><li>Superficial thrombophlebitis is not lifethreatening and does not lead to pulmonary embolization; but the inflammatory process might extent to the deep veins </li></ul><ul><li>5-7 days is sufficient </li></ul>
  23. 23. deep venous thrombosis <ul><li>Incidence </li></ul><ul><ul><li>1/2000 antepartum period </li></ul></ul><ul><ul><li>1/700 postpartum period </li></ul></ul><ul><li>It is a high risk condition </li></ul><ul><li>High risk factors </li></ul><ul><ul><li>Vascular damage, infection, tissue trauma </li></ul></ul><ul><ul><li>Hypercoagulability and venous stasis of the pregnancy </li></ul></ul>
  24. 24. The site of deep venous thrombosis <ul><li>The deep calf venus and the iliofemoral veus </li></ul><ul><li>The pelvic venous (Ovarian venus) </li></ul><ul><ul><li>The leading cause of pulmonary embolism </li></ul></ul><ul><li>Most of the deep venous thrombosis occurred in the left leg and thigh </li></ul>
  25. 27. The pathologic type and outcome of thrombosis <ul><li>Pathologic type </li></ul><ul><ul><li>Red </li></ul></ul><ul><ul><li>Mixed </li></ul></ul><ul><ul><li>White </li></ul></ul><ul><li>Pathologic outcome </li></ul><ul><ul><li>Thrombolysis </li></ul></ul><ul><ul><li>New clot formation </li></ul></ul><ul><ul><li>Organization </li></ul></ul><ul><ul><li>Calcification </li></ul></ul><ul><ul><li>Recanalization </li></ul></ul><ul><ul><li>Shedding and leading to pulmonary embolism </li></ul></ul>
  26. 29. Diagnosis of the deep venous thrombosis <ul><li>Clinical diagnosis </li></ul><ul><ul><li>Hotman sign: Pain in the calf areas in association with dorsiflexion of the foot is a clinical sign of deep venous thrombosis in the calf vein </li></ul></ul><ul><ul><li>Acute swelling and pain in the thigh area and in the femoral triangle are suggestive of iliofemoral thrombosis </li></ul></ul>
  27. 30. Assistant diagnostic methods for deep venous thrombosis <ul><li>Ultrasonography </li></ul><ul><li>MRI </li></ul><ul><li>venogram </li></ul>
  28. 31. Treatment of the deep venous thrombosis <ul><li>Surgery </li></ul><ul><ul><li>Forgarty catheter </li></ul></ul><ul><ul><li>Within 48hr </li></ul></ul><ul><li>Medical therapy </li></ul><ul><ul><li>Thrombolysis (within 72hr) </li></ul></ul><ul><ul><li>Anticoagulation </li></ul></ul><ul><ul><li>antiaggregation </li></ul></ul>
  29. 32. Thrombolysis <ul><li>Tissue type plasminogen activitor (short half life time, and specific action on the clots sticking fibrin not the fibrin ) </li></ul><ul><li>Urokinase </li></ul><ul><li>streptokinase </li></ul>
  30. 33. Anticoagulation[1] <ul><li>Heparin </li></ul><ul><ul><li>Low molecular and Large molecular </li></ul></ul><ul><ul><li>Do not cross the placenta </li></ul></ul><ul><ul><li>PPT (partial prothrombin time)[2 to 2.5 times of normal control] </li></ul></ul><ul><ul><li>PT-INR </li></ul></ul><ul><ul><li>Stopped before active labor phase and continued 12 hours after delivery </li></ul></ul><ul><ul><li>Hemorrhage tendency, thrombocytopenia, osteoporosis </li></ul></ul>
  31. 34. Anticoagulation[1] <ul><li>Warfarrin </li></ul><ul><ul><li>Inhibit the production of coagulation factors 2,7,9 and 10 </li></ul></ul><ul><ul><li>Cross the placenta leading to fetal hemorrhage </li></ul></ul><ul><ul><li>Stopped after the 36 gestational weeks and continued after delivery </li></ul></ul><ul><ul><li>PT (Prothrombin time) </li></ul></ul>
  32. 35. Antiaggregation <ul><li>Low molecular dextran </li></ul><ul><ul><li>500ml bid </li></ul></ul><ul><li>Aspirin </li></ul>
  33. 36. The aim of treatment of deep venous thrombosis
  34. 37. pulmonary embolism <ul><li>Incidence </li></ul><ul><ul><li>1/2500 during pregnancy </li></ul></ul><ul><ul><li>The maternal mortality is less than 1% if treated early and greater than 80% if left untreated </li></ul></ul><ul><li>The source of the emboli </li></ul><ul><ul><li>70% come from the deep venous thrombosis </li></ul></ul>
  35. 38. Diagnosis of pulmonary embolism <ul><li>Clinical features </li></ul><ul><ul><li>Symptoms </li></ul></ul><ul><ul><ul><li>Pleuritic chest pain, shortness of breath, air hunger, palpitation, hemoptysis, and syncope episode </li></ul></ul></ul><ul><ul><li>Signs </li></ul></ul><ul><ul><ul><li>Tachypnea, tachycardia, low grade fever, a fleural friction rub, chest splinting, pulmonary rales, accentuated pulmonic valve second heart sound, signs of right ventricular failure </li></ul></ul></ul><ul><li>Assistant methods </li></ul><ul><ul><li>Chest X film </li></ul></ul><ul><ul><li>Blood gas SPO2 </li></ul></ul><ul><ul><li>Computerized tomography and MRI </li></ul></ul>
  36. 39. Treatment of pulmonary embolism <ul><li>It is similar to the treatment of deep venous thrombosis </li></ul><ul><li>But it more emergent than the deep venous thrombosis </li></ul><ul><li>Hemorrhage of uterine,birth canal, abdominal incision and other site(nose,brain,gastric) </li></ul><ul><ul><li>Acute </li></ul></ul><ul><ul><li>Chronic or later onset </li></ul></ul>
  37. 40. Pulmonary disorders
  38. 41. The basic function of respiratory system <ul><li>The basic function is inspiration of the oxygen and expiration of the carbon dioxide. </li></ul><ul><li>The types of respiratory dysfunction </li></ul><ul><ul><li>Central nerve </li></ul></ul><ul><ul><li>Spinal nerve </li></ul></ul><ul><ul><li>Skeleton muscle </li></ul></ul><ul><ul><li>Pleural cavity </li></ul></ul><ul><ul><li>Perfusion of the lung </li></ul></ul><ul><ul><li>Air and blood barrier [pulmonary edema] </li></ul></ul><ul><ul><li>Airway [asthma] </li></ul></ul>
  39. 42. bronchial asthma <ul><li>The incidence during pregnancy 1% </li></ul><ul><li>About 15% of these individuals have one or more severe attacks during pregnancy </li></ul><ul><li>Mild asthma </li></ul><ul><li>Moderate asthma </li></ul><ul><li>Severe asthma is associated with an increased abortion rate and an increased incidence of intrauterine fetal death and fetal growth restriction, most probably as a result of intrauterine hypoxia </li></ul><ul><li>The effect of pregnancy on bronchial asthma is variable </li></ul>
  40. 43. Obstetric management[1] <ul><li>Pregnant asthmatics should be followed closely during pregnancy to ensure adequate maternal and fetal assessment </li></ul><ul><li>In most asthmatics, no drug treatment is needed. </li></ul><ul><ul><li>Adequate bed rest </li></ul></ul><ul><ul><li>Early and aggressive treatment of respiratory infection </li></ul></ul><ul><ul><li>Avoidance of hyperventilation </li></ul></ul><ul><ul><li>Avoidance of excessive physical activity </li></ul></ul><ul><ul><li>Avoidance of allergens </li></ul></ul>
  41. 44. Obstetric management[2] <ul><li>For outpatient treatment of occasional mild asthma attacks, inhaled beta-agonist are often sufficient </li></ul><ul><ul><li>Relaxation of the bronchial smooth muscle cells </li></ul></ul><ul><ul><li>Inhibiting the releasing of the histamine from the mast cell </li></ul></ul><ul><li>Albuterol, pirbuterol, terbutaline </li></ul><ul><li>Uterine relaxation effect </li></ul>
  42. 45. Obstetric management[3] <ul><li>If the asthma could not controlled adequately with beta-agonists, a regimen of inhaled corticosteroids or cromolyn should be started. </li></ul><ul><li>Inhaled cromolyn </li></ul><ul><ul><li>The asthma is triggered by inhaled agents </li></ul></ul><ul><ul><li>The asthma is induced by excise </li></ul></ul>
  43. 46. Obstetric management[3] <ul><li>If the asthma could not controlled adequately with beta-agonists, a regimen of inhaled corticosteroids or cromolyn should be started. </li></ul><ul><li>Inhaled cromolyn </li></ul><ul><ul><li>The asthma is triggered by inhaled agents </li></ul></ul><ul><ul><li>The asthma is induced by excise </li></ul></ul>
  44. 47. Obstetric management[4] <ul><li>For severe exacerbation or for patients not responding to acute bronchodilator therapy, a course of oral corticosteroids is indicated </li></ul><ul><li>The dose is tappered gradually and is replaced by inhaled steroids for maintenance therapy </li></ul><ul><li>For patients with refractory disease, a low to moderate daily dose of oral corticosteroids may be continued for an indefinite period. </li></ul>
  45. 48. Obstetric management[5] <ul><li>Mild status </li></ul><ul><ul><li>No drug] </li></ul></ul><ul><ul><li>Inhaled beta2-agonists </li></ul></ul><ul><li>Moderate status </li></ul><ul><ul><li>Inhaled steroids </li></ul></ul><ul><ul><li>Inhaled cromolyn </li></ul></ul><ul><li>Severe status </li></ul><ul><ul><li>Oral steroids </li></ul></ul>
  46. 49. Obstetric management[6] <ul><li>Fetal assessment </li></ul><ul><ul><li>Fetal growth by ultrasonography </li></ul></ul><ul><ul><li>Biophysical score </li></ul></ul><ul><li>The timing of delivery is dependent on the status of both the mother and the fetus </li></ul>
  47. 50. Management of labor and delivery <ul><li>If the patient taking oral steroids during pregnancy, the intravenous administration of glucocorticoids is recommended during labor, delivery, and postpartum period. </li></ul><ul><li>A selective epidural block is beneficial </li></ul><ul><ul><li>Pain </li></ul></ul><ul><ul><li>Anxiety </li></ul></ul><ul><ul><li>Hyperventilation </li></ul></ul><ul><ul><li>Respiratory work </li></ul></ul><ul><li>Vaginal delivery should be anticipated. Cesarean section is indicated only for obstetric reasons. </li></ul>
  48. 51. pulmonary edema <ul><li>Pulmonary edema is very common in the patients with hypertensive disorder during pregnancy especially during the immediate postpartum period </li></ul><ul><li>Low SPO2, and chest X-film </li></ul><ul><li>Benign and self-limited </li></ul><ul><li>Within the first three days, the edema should diappear </li></ul><ul><li>Low albuminemia, increased capillary permeabilty, increased interstitial colloid osmolarity, magnesium and fluid expansion. </li></ul>
  49. 52. Endocrine and metabolism disorders <ul><li>diabetes mellitus </li></ul><ul><li>thyroid disease </li></ul><ul><li>Adrenal gland disease </li></ul><ul><li>Other endocrine glands and tissues or cells </li></ul>
  50. 53. Diabetes Mellitus <ul><li>Incidence and classification </li></ul><ul><li>Complications </li></ul><ul><li>Diagnosis </li></ul><ul><li>Management </li></ul>
  51. 54. Incidence and definition <ul><li>Incidence 0.5% </li></ul><ul><li>Definition </li></ul><ul><ul><li>Pregnancy complicated with diabetes mellitus (type 1 and type 2) [10%] </li></ul></ul><ul><ul><ul><li>Before pregnancy, during pregnancy, and after pregnancy </li></ul></ul></ul><ul><ul><ul><li>Random glucose >200mg/dl, FPG >126mg/dl </li></ul></ul></ul><ul><ul><li>Gestational diabetes mellitus[90% ] </li></ul></ul><ul><ul><ul><li>Before pregnancy, during pregnancy , and after pregnancy </li></ul></ul></ul>
  52. 55. Classification <ul><li>Class onset FPG 2h-PPG therapy </li></ul><ul><li>A1 GDM <105 <120 diet </li></ul><ul><li>A2 GDM >105 >120 insulin </li></ul><ul><li>Class onset of age duration vascular disease therapy </li></ul><ul><li>B >20 <10 None insulin </li></ul><ul><li>C 10~19 10~19 none insulin </li></ul><ul><li>D <10 >20 benign retinopathy insulin </li></ul><ul><li>F any any nephropathy insulin </li></ul><ul><li>R any any roliferative retinopathy insulin </li></ul><ul><li>H any any heart insulin </li></ul>
  53. 56. The first step: 50 glucose loading test <ul><li>the aim of the test is to screen the gestational diabetes mellitus </li></ul><ul><li>it is usually carried out during 24-28 gestational week for the first time </li></ul><ul><li>the screening test: </li></ul><ul><ul><li>50g glucose load </li></ul></ul><ul><ul><li>1 hour, 130~140mg/dl[7.2~7.8mmol/L] </li></ul></ul><ul><ul><li>Without regard to the time of the day or the time of the meal </li></ul></ul>
  54. 57. blood glucose test performed before the 24 gestational weeks <ul><li>older than 25 years old </li></ul><ul><li>Obesity </li></ul><ul><li>family history of DM </li></ul><ul><li>previous infant weight no less than 4000g </li></ul><ul><li>previous stillbirth infant </li></ul><ul><li>previous congenitally deformed infant </li></ul><ul><li>previous polyhydranmios </li></ul><ul><li>history of recurrent abortions </li></ul>
  55. 58. The second step: 100g glucose load test <ul><li>glucose level(mmol/l) </li></ul><ul><li>Fast 5.8 </li></ul><ul><li>1hour 10.55 </li></ul><ul><li>2hour 9.16 </li></ul><ul><li>3hour 8.05 </li></ul><ul><li>if two values are abnormal, excluding the fasting blood glucose,the patients is classified as having gestational diabetes mellitus </li></ul>
  56. 59. Only one step diagnostic method: 75g glucose load test <ul><li>Normal value Impaired tolerance DM </li></ul><ul><li>Fast <6.1 ≥6.1 ≥7.0 </li></ul><ul><li>2h </li></ul><ul><li>postprandial <7.8 ≥7.8~<11.1 ≥11.1 </li></ul>
  57. 60. Maternal complications <ul><li>Obstetric complications </li></ul><ul><ul><li>Polyhydramnios </li></ul></ul><ul><ul><li>Pre-eclampsia </li></ul></ul><ul><li>Diabetic emergency </li></ul><ul><ul><li>Hypoglycemia </li></ul></ul><ul><ul><li>Ketoacidosis </li></ul></ul><ul><ul><li>Diabetic coma </li></ul></ul><ul><li>Vascular and end-organ involvement [cardiac, renal, ophthalmic, and peripheral vascular] </li></ul><ul><li>Neurologic [peripheral neuropathy and GIT disturbance] </li></ul><ul><li>Infection(antepartum and postpartum) </li></ul>
  58. 61. Fetal complications <ul><li>Spontaneous abortion </li></ul><ul><li>premature delivery (premature preterm rupture of the membrane) </li></ul><ul><li>Unexplained intrauterine fetal demise and stillbirth </li></ul><ul><li>Macrosomia with traumatic delivery such as cesarean section and shoulder dystocia </li></ul><ul><li>Delayed organ maturity (lung) </li></ul><ul><li>Congenital anomalies </li></ul><ul><li>Intrauterine growth restriction </li></ul>
  59. 62. Neonatal complications <ul><li>Respiratory distress </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Hypocalcemia </li></ul><ul><li>Hyperbilirubinemia </li></ul><ul><li>Cardiac hypertrophy </li></ul><ul><li>Long-term cognitive development </li></ul><ul><li>Inheritance of diabetes </li></ul><ul><li>Altered fetal growth </li></ul>
  60. 63. The pathogenesis of the gestational diabetes mellitus <ul><li>Only maternal insulin decrease the plasma glucose </li></ul><ul><li>The glucagon and hormones produced by the placenta disturb the equilirium of the glucose metabolism </li></ul>
  61. 64. Diabete mellitus with the fetus <ul><li>High glucose and Ketoacidosis[across the placenta] </li></ul><ul><ul><li>First trimester </li></ul></ul><ul><ul><li>The second trimester </li></ul></ul><ul><ul><li>Third trimester </li></ul></ul><ul><ul><li>labor </li></ul></ul><ul><li>Oral hypoglycemic agents </li></ul><ul><ul><li>Pancreatic island </li></ul></ul><ul><ul><li>Anomalies during the first trimester </li></ul></ul>
  62. 65. Management <ul><li>The diabetic team </li></ul><ul><li>Achieving euglycemia </li></ul><ul><li>Antepartum obstetric management </li></ul><ul><li>Timing of delivery </li></ul><ul><li>Intrapartum management </li></ul><ul><li>Postpartum period </li></ul>
  63. 66. The diabetic team <ul><li>Patient </li></ul><ul><li>Obstetrician </li></ul><ul><li>Clinical nurse specialist </li></ul><ul><li>Psychosocial worker </li></ul><ul><li>dietitian </li></ul>
  64. 67. Achieving euglycemia <ul><li>Diet </li></ul><ul><li>exercise </li></ul><ul><li>Oral hypoglycemic agents </li></ul><ul><li>Insulin </li></ul><ul><ul><li>Subcutanieous </li></ul></ul><ul><ul><li>Intravenous </li></ul></ul><ul><ul><li>Pump </li></ul></ul><ul><ul><li>adjustment of the dosage and the administration methods </li></ul></ul>
  65. 68. Antepartum obstetric management <ul><li>Maternal status </li></ul><ul><ul><li>Plasma glucose </li></ul></ul><ul><ul><li>Ketouria </li></ul></ul><ul><ul><li>Hypetension </li></ul></ul><ul><ul><li>Renal, cardiac, ophthalmic </li></ul></ul><ul><li>Fetal growth and development </li></ul><ul><ul><li>Ultrasonagraphy </li></ul></ul><ul><ul><li>Non-stimulating test </li></ul></ul><ul><ul><li>Biophysical profile score </li></ul></ul>
  66. 69. Timing of delivery <ul><li>Well controlled </li></ul><ul><ul><li>Term and spontaneous labor onset </li></ul></ul><ul><li>Uncontrolled and bad controlled </li></ul><ul><ul><li>Fetal status </li></ul></ul><ul><ul><li>Maternal status </li></ul></ul><ul><ul><li>Gestational week </li></ul></ul><ul><ul><li>Other things </li></ul></ul>
  67. 70. Intrapartum management <ul><li>Pain, anxiety, nervous, fautigue, diet, insulin </li></ul><ul><li>Intravenous nutrition and intravenous insulin </li></ul><ul><li>Fetal and maternal monitoring </li></ul><ul><ul><li>Maternal plasma glucose level 80~100mg/dl </li></ul></ul><ul><ul><li>Ketouria </li></ul></ul><ul><ul><li>Maternal blood gas </li></ul></ul><ul><ul><li>Continuous contraction stimulating test for the fetus </li></ul></ul>
  68. 71. Postpartum period <ul><li>The dosage of insulin decreased rapidly,even stopped </li></ul><ul><li>Infection </li></ul>
  69. 72. Long term things of GDM <ul><li>Almost all of the GDM patients will get rid of the intolerance glucose test status for several years or for all the life. </li></ul><ul><li>Almost all of the patients will develop GDM during the following pregnancy </li></ul><ul><li>About 50 percent of the GDM patients will become the overt 2 type diabetes mellitus 20 years later. </li></ul>
  70. 73. Emphasis of GDM <ul><li>Predisposing factors </li></ul><ul><li>24-28 gestation week </li></ul><ul><li>The glucose intolerance and insulin </li></ul><ul><ul><li>Prepregnant, the first/sencond and third trimester, intrapartum, postpartum </li></ul></ul><ul><ul><li>Insulin dosage </li></ul></ul><ul><li>Oral hypoglycemic agents </li></ul><ul><li>The emergent status </li></ul><ul><ul><li>diabetes ketoacidosis </li></ul></ul><ul><li>The fetal, neonatal and maternal complications </li></ul>
  71. 74. thyroid disease <ul><li>Normal thyroid physiology during pregnancy </li></ul><ul><li>maternal hyperthyroidism </li></ul><ul><li>maternal hypothyroidism </li></ul>
  72. 75. Normal thyroid physiology during pregnancy <ul><li>Goiter during pregnancy </li></ul><ul><ul><li>Renal glomerular filtration rate increase </li></ul></ul><ul><ul><li>renal excretion of iodine increase </li></ul></ul><ul><ul><li>plasma inorganic iodine nearly halved </li></ul></ul><ul><ul><li>benign hypertrophy of thyroid gland compensating for the iodine deficiency </li></ul></ul>
  73. 76. Maternal thyroid function tests during pregnancy <ul><li>Hypothylamus (TRH and TIH) </li></ul><ul><li>Pitutary (serum thyroid stimulating hormone: sTSH) </li></ul><ul><li>Thyroid gland </li></ul><ul><ul><li>Total serum thyroixine(T4): bound and free </li></ul></ul><ul><ul><li>Serum triiodothyroning (T3): bound and free </li></ul></ul><ul><ul><li>Thyroxine binding globin (TBG) </li></ul></ul><ul><li>Thyroid stimulating immunoglobulins (TSIG) </li></ul><ul><li>Nuclear action sites of the target cells: free T3 and T4, especially free T3 </li></ul>
  74. 77. Fetal thyroid function test <ul><li>Fetal thyroid stimulating hormone, T4, and free thyroxine levels suggests that a mature and autonomous thyroid pitutary axis exists as early as 12 weeks gestation </li></ul><ul><li>Placenta transfer </li></ul><ul><ul><li>Thyroid stimulating immunoglobulins (TSIG) </li></ul></ul><ul><ul><li>Minimal transfer of T3 and T4 </li></ul></ul><ul><ul><li>Thyroid hormone analogues with smaller molecular weight, decreased protein binding, and increased fat solubility may transfer the placenta and influence the fetal thyroid status </li></ul></ul>
  75. 78. Maternal hyperthyroidism <ul><li>The incidence: 1/500 </li></ul><ul><li>Grave disease or toxic diffuse goiter is the most common cause of hyperthyroidism during pregnancy </li></ul>
  76. 79. Diagnosis of hyperthyroidism <ul><li>Prepregnant hyperthyroid history </li></ul><ul><li>Clinical signs and symptoms </li></ul><ul><ul><li>Tachycardia </li></ul></ul><ul><ul><li>Eye changes </li></ul></ul><ul><ul><li>Weight loss </li></ul></ul><ul><ul><li>Heat intolerance </li></ul></ul><ul><li>Laboratory test </li></ul><ul><ul><li>sTSH </li></ul></ul><ul><ul><li>Free T3 and T4 </li></ul></ul>
  77. 80. Therapy of hyperthytoidism <ul><li>Medical </li></ul><ul><ul><li>thiamides [Propylthioruacil and metimazole(tapazole)] </li></ul></ul><ul><ul><ul><li>Propylthioruacil cross the placenta freely, but the children exposed to thiamides in utero attain full physical and intellectual development and have normal thyroid function test </li></ul></ul></ul><ul><ul><li>Beta receptor blocker </li></ul></ul><ul><ul><ul><li>Propranolol </li></ul></ul></ul><ul><ul><ul><li>Fetal effects </li></ul></ul></ul><ul><li>Radioactive iodine(contraindicated during pregnancy) </li></ul><ul><li>Surgery: partial ablation </li></ul>
  78. 81. Thyroid storm <ul><li>Precipitating factors </li></ul><ul><ul><li>Infection,Labor,Cesarean section,Noncompliance with medications </li></ul></ul><ul><li>Clinical signs and symptoms </li></ul><ul><ul><li>Hyperthermia, marked tachycardia, perspiration, sever dehydration </li></ul></ul><ul><li>Special treatment </li></ul><ul><ul><li>Propranolol: beta receptor blocker </li></ul></ul><ul><ul><li>Sodum iodine: thyroid hormone secretion blocker </li></ul></ul><ul><ul><li>Propylthiouracil: thyroid hormone synthesis blocker </li></ul></ul><ul><ul><li>Dexamethasome: transfer of T4 to T3 blocker </li></ul></ul><ul><ul><li>Replacing fluid losses </li></ul></ul><ul><ul><li>Hypothermic techniques </li></ul></ul>
  79. 82. Neonatal thyrotoxicosis <ul><li>1% of maternal hyperthyroidism results from Grave disease </li></ul><ul><li>Placental transfer of the thyroid stimulating immunoglobulins </li></ul><ul><ul><li>Long acting thyroid stimulators </li></ul></ul><ul><li>The newborns may require antithyroid treatment for several weeks until the TSIGs are degraded </li></ul>
  80. 83. maternal hypothyroidism <ul><li>Uncommon during pregnancy </li></ul><ul><li>Fetal and neonatal outcome are normally good </li></ul><ul><li>Elevated serum TSH </li></ul><ul><li>Cretinism(congenital hypothyroidism) </li></ul><ul><ul><li>1/4000 births </li></ul></ul><ul><ul><li>Etiologic factors </li></ul></ul><ul><ul><ul><li>Thyroid dysgenesis </li></ul></ul></ul><ul><ul><ul><li>Inborn errors of thyroid function </li></ul></ul></ul><ul><ul><ul><li>Drug induced endemic hypothyroidism </li></ul></ul></ul><ul><li>The most common cause of neonatal goiter is maternal ingestion of iodides present in cough syrup </li></ul>
  81. 84. Hematologic disorders
  82. 85. Anemia <ul><li>Definition </li></ul><ul><ul><li>The homoglobin level is lower than 11g/dl during the nonpregnant status </li></ul></ul><ul><ul><li>10g/dl during the pregnant status </li></ul></ul><ul><li>Physiologic anemia in pregnancy </li></ul><ul><ul><li>The blood volume increase by 40% to 50% </li></ul></ul><ul><ul><li>The red cell mass increase by 25% </li></ul></ul>
  83. 86. Classification and common causes of anemia during pregnancy <ul><li>Lower production by bone marrow (MATERIAL DEFICIENCY) </li></ul><ul><ul><li>Iron deficiency anemia </li></ul></ul><ul><ul><ul><li>(80%) </li></ul></ul></ul><ul><ul><ul><li>Iron supplement </li></ul></ul></ul><ul><ul><ul><li>Preventive methods during antepartum period </li></ul></ul></ul><ul><ul><ul><li>Lower than 6g/dl is dangerous for the fetus </li></ul></ul></ul><ul><ul><li>Folic acid deficiency anemia </li></ul></ul><ul><ul><li>Combined iron and folate deficiency </li></ul></ul><ul><li>Hemalysis </li></ul><ul><ul><li>DIC </li></ul></ul><ul><li>Blood loss </li></ul><ul><ul><li>Antepartum, intrapartum and postpartum hemorrhage </li></ul></ul><ul><li>HEMORRHAGE AND SHOCK AND DIC </li></ul>
  84. 87. Leukemia <ul><li>RARE </li></ul><ul><li>VERY VERY POOR MATERNAL AND FETAL OUTCOME </li></ul>
  85. 88. Hemoglobinopathies <ul><li>SICKLE CELL DISEASE </li></ul><ul><li>RARE </li></ul><ul><li>DANGEROUS TO THE MOTHER AND FETUS </li></ul>
  86. 89. disorders of blood coagulation <ul><li>Inherited disorders of plasma coagulation factors </li></ul><ul><ul><li>Hemophilia A </li></ul></ul><ul><ul><li>Hemophilia B </li></ul></ul><ul><ul><li>von Willebrand disease </li></ul></ul><ul><ul><li>Congenital fibrinogen deficiency </li></ul></ul>
  87. 90. Thrombocytopenia <ul><li>idiopathic </li></ul><ul><li>Hypertensive disorders during pregnancy </li></ul><ul><ul><li>HELLP SYNDROME </li></ul></ul><ul><li>Other factors </li></ul><ul><ul><li>Immunologic </li></ul></ul><ul><li>DIC (disseminated intravascular coagulation status) </li></ul>
  88. 91. Clincal features of thrombocytopenia <ul><li>Lower than 100X10 9 /L,Lower than 30-50X10 9 /L,Lower than 10X10 9 /L,Lower than 2X10 9 /L </li></ul><ul><li>Maternal cerebral hemorrhage, and postpartum hemorrhage </li></ul><ul><li>Fetal effects </li></ul><ul><ul><li>Anti-platelet antibody </li></ul></ul><ul><ul><li>rare </li></ul></ul>
  89. 92. Treatment for thrombocytopenia <ul><li>Corticosteroid hormone </li></ul><ul><li>Platelet infusion </li></ul><ul><li>Immunoglobin infusion (1g/kg.day) </li></ul><ul><li>splenoectomy </li></ul>
  90. 93. DIC <ul><li>Very very common and dangerous disease in obstetric practice </li></ul><ul><li>Common cause </li></ul><ul><ul><li>High coagulation status during pregnancy </li></ul></ul><ul><ul><li>Abruptio placentae, severe preeclampsia and eclampsia,intrauterine fetal demise, sepsis, transfusion reaction, and amniotic fluid embolism </li></ul></ul><ul><li>Clinical and laboratory features </li></ul><ul><ul><li>Thrombocytopenia </li></ul></ul><ul><ul><li>Hypofibrinemia </li></ul></ul><ul><ul><li>increased D-dimers </li></ul></ul><ul><ul><li>intra vascular hemolysis </li></ul></ul><ul><ul><li>and hemorrhage tendency </li></ul></ul><ul><ul><li>Increased PT AND PPT </li></ul></ul>
  91. 94. Neurologic disorders <ul><li>Seizures </li></ul><ul><ul><li>Medication </li></ul></ul><ul><ul><li>Injury to the pregnancy </li></ul></ul><ul><ul><ul><li>Physical attack(maternal, uterus, placenta, and even the fetus) </li></ul></ul></ul><ul><ul><ul><li>hypoxia </li></ul></ul></ul><ul><li>Eclampsia: cerebral edema and hemorrhage </li></ul><ul><li>Cerebral tumor or vascular deformity </li></ul><ul><li>Intracranial venous thrombosis due to high coagulation status </li></ul><ul><ul><li>Easily mixed with eclampsia </li></ul></ul>
  92. 95. Pregnancy complicated with cerebral vascular disease (a very emergent condition) <ul><li>Hemorrhage or ischemia </li></ul><ul><li>Aterial or venous </li></ul><ul><li>Etiology and pathogenesis </li></ul><ul><li>Severity </li></ul><ul><li>Gestational week </li></ul><ul><li>The attitude of the woman and her families </li></ul><ul><li>Cooperation of the obstetrician and neurologists </li></ul>
  93. 96. Renal disorders
  94. 97. Acute renal failure <ul><li>Prerenal,Renal and postrenal </li></ul><ul><li>Postpartum hemorrhage and DIC are the most common causes </li></ul><ul><li>Causal manigement, recovery of the circulation and dialysis are the most important methods </li></ul><ul><li>Reversible and irreversible </li></ul><ul><ul><li>Age </li></ul></ul><ul><ul><li>Severity and Duration of DIC </li></ul></ul><ul><ul><li>Treatment protocol </li></ul></ul>
  95. 98. Chronic renal failure <ul><li>Covert </li></ul><ul><li>Associated and mixed with pregnancy induced hypertensive disorders </li></ul><ul><li>Magnesium sulfate toxicity </li></ul><ul><ul><ul><li>Orthostatic or postural hypotension (vascular smooth muscle) </li></ul></ul></ul><ul><ul><ul><li>Dyspnea (skeletal muscle) </li></ul></ul></ul><ul><ul><ul><li>Muscle relxation (skeletal muscle) </li></ul></ul></ul>
  96. 99. Pregnancy following renal transplantation <ul><li>RARE </li></ul><ul><li>Main concerns </li></ul><ul><ul><li>Bad effects of Immunosuppressive agents to the fetus </li></ul></ul><ul><ul><li>Infection </li></ul></ul><ul><li>Refer to the table in page 257 </li></ul>
  97. 100. Gastrointestinal disorders <ul><li>nausea and vomiting during pregnancy </li></ul><ul><li>hyperemesis gravidarum </li></ul><ul><li>reflux esophagitis </li></ul><ul><li>peptic ulcer </li></ul><ul><li>acid aspiration syndrome </li></ul><ul><li>gastrointestinal bypass and pregnancy </li></ul><ul><li>chronic inflammatory bowel disease </li></ul>
  98. 101. Nausea and vomiting during pregnancy <ul><li>Morning sickness </li></ul><ul><li>60%~80% </li></ul><ul><li>During first 8~12 gestational weeks </li></ul><ul><li>Mild and disappear during the early part of the second trimester </li></ul><ul><li>The underlying causes are not well delineated </li></ul><ul><li>A small part of patients with severe symptoms necessitates hospital admission </li></ul>
  99. 102. Hyperemesis gravidarum <ul><li>Intractable nausea and vomitting </li></ul><ul><li>1% </li></ul><ul><li>More frequent with first pregnancy </li></ul><ul><li>Pregnancy outcome is usually good </li></ul><ul><li>Electrolyte disturbance </li></ul><ul><ul><li>Hypokalemia </li></ul></ul><ul><ul><li>Hyponatremia </li></ul></ul><ul><ul><li>Hypochloremia alkalosis </li></ul></ul><ul><li>Low energy and nutrition intake </li></ul><ul><li>Vitamin B1 deficiency </li></ul><ul><ul><li>Glucose metabolism </li></ul></ul><ul><ul><li>Central and peripheral nervous damage </li></ul></ul><ul><ul><li>Lethal condition </li></ul></ul>
  100. 103. Treatment <ul><li>Symptomatic </li></ul><ul><ul><li>Antiacids </li></ul></ul><ul><ul><li>Avoidance of recumbent position </li></ul></ul><ul><li>H2 blocker </li></ul><ul><ul><li>Cimetidine </li></ul></ul><ul><li>Proton pump blocker </li></ul><ul><ul><li>Omeprazole </li></ul></ul><ul><li>Intravenous hydration </li></ul><ul><li>Correction of electrolytes and and acid base imbalance </li></ul><ul><li>Intravenous nutrition and vitamins </li></ul><ul><li>Psychological counseling </li></ul>
  101. 104. Hepatic disorders <ul><li>Main factors associate with hepatic disorders </li></ul><ul><ul><li>Albumin </li></ul></ul><ul><ul><li>Coagulationg factors (bleeding) </li></ul></ul><ul><ul><li>Bilirubin </li></ul></ul><ul><ul><li>Drug metabolism </li></ul></ul><ul><ul><li>Nutrition material metabolism </li></ul></ul><ul><li>Intrahepatic cholestasis of pregnancy </li></ul><ul><li>Acute fatty liver of pregnancy </li></ul><ul><li>DIC </li></ul><ul><li>HELLP syndrome </li></ul>

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