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S A B Xu

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S A B Xu

  1. 1. Early Pregnancy Complications <ul><li>Spontaneous abortion </li></ul><ul><li>Ectopic pregnancy </li></ul>
  2. 2. Spontaneous Abortion
  3. 3. Definition of abortion <ul><li>Before 20 weeks gestation </li></ul><ul><ul><li>Based on LMP </li></ul></ul><ul><li>Or delivery of fetus </li></ul><ul><ul><li>Weight less than 500 grams </li></ul></ul>
  4. 4. Etiology of spontaneous abortion <ul><li>50% of SA during the first 12 weeks with abnormal karyotype (Aneuploidy) </li></ul><ul><li>Abnormal development noted in majority of cases </li></ul><ul><li>Incomplete cervix cause of second trimester loss </li></ul>
  5. 5. Etiology of spontaneous abortion <ul><li>Maternal factors </li></ul><ul><ul><li>Systemic disease </li></ul></ul><ul><ul><li>Uterine defects </li></ul></ul><ul><ul><li>Immunologic disorders </li></ul></ul><ul><ul><li>Malnutrition </li></ul></ul><ul><li>Toxic factors </li></ul><ul><li>Trauma </li></ul>
  6. 6. Abortion classification <ul><li>Threatened abortion </li></ul><ul><li>Inevitable abortion </li></ul><ul><li>Incomplete abortion </li></ul><ul><li>Complete abortion </li></ul><ul><li>Missed abortion </li></ul><ul><li>Septic abortion </li></ul><ul><li>Recurrent abortion </li></ul>
  7. 7. Threatened abortion <ul><li>Bleeding during early pregnancy </li></ul><ul><li>Prognosis worse with pain or cramping </li></ul><ul><li>Rule out other course of bleeding </li></ul><ul><ul><li>Cervical lesions </li></ul></ul><ul><ul><li>Polyps </li></ul></ul><ul><ul><li>Implantation bleeding </li></ul></ul>
  8. 8. Management of threatened abortion <ul><li>Serial hCG </li></ul><ul><li>Serial progesterone </li></ul><ul><li>Vaginal sonograms </li></ul><ul><li>Pelvic rest </li></ul><ul><li>Bed rest </li></ul>
  9. 9. Inevitable abortion <ul><li>Certain to occur </li></ul><ul><li>Rupture of membranes </li></ul><ul><li>Cervical dilation </li></ul>
  10. 10. Management of inevitable or incomplete abortion <ul><li>Evacuation of the uterus by suction D and C </li></ul><ul><li>Prognosis is excellent if the retained tissue is promptly and completely evacuated. </li></ul>
  11. 11. ECTOPIC PREGNANCY
  12. 12. Yanwen Xu , M.D., PhD The First Affiliated Hospital of Sun Yat-sen University ECTOPIC PREGNANCY
  13. 14. <ul><li>Definition: </li></ul><ul><li>A fertilized ovum implants in an area other than the endometrial lining of the uterus. </li></ul>
  14. 15. Sites of ectopic pregnancies
  15. 21. Residual uterus pregnancy Uterus
  16. 22. Tubal ectopic pregnancy
  17. 23. Etiology <ul><li>Tubal factor </li></ul><ul><ul><li>Ovarian factors </li></ul></ul><ul><ul><ul><li>Other factors </li></ul></ul></ul><ul><ul><ul><ul><ul><li>IUD </li></ul></ul></ul></ul></ul>
  18. 24. Time of Rupture <ul><li>Rupture is usually spontaneous </li></ul><ul><ul><li>Isthmic pregnancies 6-8 week’s gestation </li></ul></ul><ul><ul><li>Ampullary pregnancies 8-12 week’s gestation </li></ul></ul><ul><ul><li>Interstitial pregnancies 12-16 weeks’s gestation </li></ul></ul>
  19. 25. Pathology <ul><li>Little or no decidual reaction and minimal defense against the permeating trophoblast in the ectopic implantation sites. </li></ul><ul><li>A hematoma in the subserosal space enlarges as pregnancy progress. </li></ul><ul><li>Bleeding is of uterine origin and is caused by endometrial involution and decidual sloughing. </li></ul><ul><li>The Arias-Stella reaction in endometrium is non specific. </li></ul>
  20. 26.   Clinical findings <ul><li>    Three major symptoms : </li></ul><ul><ul><ul><li>Amenorrhea </li></ul></ul></ul><ul><ul><ul><ul><li>Pain </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Vaginal bleeding </li></ul></ul></ul></ul></ul>
  21. 27. Clinical findings <ul><li>Dizziness, lightheadedness, and/or syncope is present in one-third to one-half cases. </li></ul>
  22. 28. Signs <ul><li>General condition </li></ul><ul><li>Abdominal examination </li></ul><ul><ul><li>Diffuse or localized abdominal tenderness </li></ul></ul><ul><li>PV : </li></ul><ul><ul><li>A unilateral adnexal mass </li></ul></ul><ul><ul><li>Adnexal and/or cervical motion tenderness </li></ul></ul><ul><ul><li>Uterus may undergo typical changes of pregnancy </li></ul></ul>
  23. 29. Laboratory findings <ul><li>Hematocrit </li></ul><ul><ul><li>Depending on the degree of intraabdominal bleeding </li></ul></ul><ul><li>White blood count </li></ul><ul><li>Pregnancy tests </li></ul><ul><ul><li>The β -HCG is positive. </li></ul></ul><ul><ul><li>Two-thirds of ectopic pregnancy have abnormal serial titers. </li></ul></ul><ul><li>Ultrasound </li></ul><ul><li>Culdocentesis </li></ul>
  24. 30. Normal Pregnancy Ectopic Pregnancy
  25. 31. Culdocentesis
  26. 32. Culdocentesis <ul><li>Nonclotting blood shows intra-abdominal bleeding. </li></ul><ul><li>If the blood clots, it is likely from a punctured vessel in the vaginal wall. </li></ul><ul><li>If culdocentesis is positive, laparoscopy or laparotomy should be performed immediately . </li></ul><ul><li>A negatively result may rule out a ruptured or leaking ectopic but not an intact one. </li></ul>
  27. 33. Differential Diagnosis <ul><li>Abortion </li></ul><ul><li>Acute salpingitis </li></ul><ul><li>Hemorrhagic corpus luteum </li></ul><ul><li>Acute appendicitis </li></ul><ul><li>Ovarian cyst torsion </li></ul>
  28. 34. Treatment <ul><li>Expectant management </li></ul><ul><ul><li>The β -HCG titers are low (<200 mIU/mL) or decreasing. </li></ul></ul><ul><ul><li>The risk of rupture is low. </li></ul></ul><ul><li>Surgical treatment </li></ul><ul><ul><li>Conservative surgery in the hemodynamically stable patient with an ampullary pregnancy. </li></ul></ul><ul><ul><li>Laparoscopy is preferred over laparotomy in stable pregnancy. </li></ul></ul>
  29. 35. Treatment in hemodynamically unstable patients----Salpingectomy
  30. 36. Treatment <ul><li>Interstitial pregnancies require a corneal wedge resection, with uterine reconstruction and sometimes salpingectomy on the affected side. </li></ul><ul><li>Cervical ectopics with methotrexate or hysterectomy. </li></ul><ul><li>Ovarian pregnancy requires oophorectomy and sometimes salpingectomy on the affected side. </li></ul><ul><li>Abdominal pregnancy involves delivery of the fetus with ligation of the umbilical cord. The placenta is left. </li></ul>
  31. 37. Medical management <ul><li>① Small (<3cm) </li></ul><ul><li>② Intact </li></ul><ul><li>③ Extr-auterine gestation with no </li></ul><ul><li>fetal heart motion </li></ul><ul><li>MTX or 5-FU </li></ul>
  32. 38. Pre-eclampsia & eclampsia Yanwen Xu , M.D., PhD The First Affiliated Hospital of Sun Yat-sen University
  33. 39. Patient history <ul><li>謝 x 芳, 30 y/o F </li></ul><ul><li>Chief complain: Twin pregnancy at 32+ gestational weeks with elevated BP and vaginal watery discharge since 8/8 12:00am </li></ul><ul><li>Past history:denied any systemic disease, such as HTN, DM, CAD, pulmonary dx </li></ul><ul><li>Allergy history:denied </li></ul><ul><li>Drug use history:denied </li></ul><ul><li>OP and anesthesiology history:denied </li></ul>
  34. 40. Present pregnancy history and menstrual history <ul><li>G1P0, got this pregnancy by ET </li></ul><ul><li>LMP:94-12-26, EDC:95-10-12 </li></ul><ul><li>Routine pregnancy exam. no abnormality was told such as GDM, PIH before 8/2 </li></ul>
  35. 41. Symptom and sign <ul><li>8/2 8/3 8/4 8/5 8/6 8/7 8/8 </li></ul>Epiphora Proteinuria Abdominal edema at lower abdomen Fetal movement decrease in right side Dyspnea, orthopnea Insomnia, urinary frequency BP:136/80 BP:210/100
  36. 42. Events at 8/8 <ul><li>12am 4pm 5pm 18am </li></ul>watery discharge BP : 210/100mmHg BT:1’30”, CT:1’40” WBC:8.4x10 3 /ul RBC:3.19x10 6 /ul Hb : 10g/dl , Hct:29% Plt : 9.7K/μL O2, adalate, trandate(5mg) refer to ER BT:37.6 HR:129 BP:198/118 SpO2:100% RR:27/min Admission to 5FD BT:37.6 HR:120 BP:181/102 RR:22/min 5:40pm BP:161/104 HR:110 SaO2:100% MgSO4:10ml/hr
  37. 43. <ul><li>6pm 6:30 6:40 </li></ul>接獲通知,前往探視 送入 DR O2 mask 3L, SaO2:93% room air, SaO2:97%  70%  97% BP:232/148 , HR:105 dyspnea could not lie down , edema , difficult in breathing , cough with frothy sputum Induction Etomidate:20mg laryngoscopy Trandate:15mg LMA Cisatracurium:10mg laryngoscopy ENT standby 備 fiber ASA VE
  38. 44. <ul><li>6:40 7:00 8:00 </li></ul>Maintenance Sevoflurane:0.2-0.3MAC add N 2 O Lasix:40mg Morphine:10mg midazolam:5mg bicarbonate:5amp ventilation: volume control ,PEEP:8 cmH 2 O suction 6:42 Operation 6:47 twin A F 1510g , 1  7 twin B F 1698g , 4  8 7:45 finish, IV:150ml blood loss:200ml On A-line ABG :7.05/77.3/162/21.5/-9.4/12.3/37/98.4/193/5.2/144/4.4/112.8/1.03 Endo:6.5mm fix 21cm
  39. 46. Lab data 8/8 pre OP <ul><li>WBC:11.55 K/uL </li></ul><ul><li>RBC:3.75M/uL </li></ul><ul><li>Hb:11.1 g/dL </li></ul><ul><li>HCT:34.4% </li></ul><ul><li>PLT:107K/uL </li></ul><ul><li>PT:11sec </li></ul><ul><li>PTT:29.5sec </li></ul><ul><li>INR:0.93 </li></ul>
  40. 47. Lab data <ul><li>AST:36U/l </li></ul><ul><li>ALT:18U/l </li></ul><ul><li>CRP:0.52mg/dl </li></ul><ul><li>Alb:2.67g/dL </li></ul><ul><li>D-Bil:0.1mg/dl </li></ul><ul><li>Na:140mmole/l </li></ul><ul><li>K:3.5mmole/l </li></ul><ul><li>Cl:110mmole/l </li></ul><ul><li>Mg:0.74mmole/l </li></ul><ul><li>BUN:6.4mg/dl </li></ul><ul><li>Cre:0.8mg/dl </li></ul><ul><li>FDP:53.2ug/mL </li></ul><ul><li>D-Dimer:2978 </li></ul><ul><li>Random urine: </li></ul><ul><li>Sp.Gr.:1.01 </li></ul><ul><li>pH:5.5 </li></ul><ul><li>protein:1+ (70mg/dL) </li></ul><ul><li>Glu.:- </li></ul>
  41. 48. Definitions - pre-eclampsia <ul><li>Persistent hypertension from gestation 20 th week onwards defined by either : </li></ul><ul><ul><li>Diastolic bp >90 Torr </li></ul></ul><ul><ul><li>Systolic bp >140 Torr </li></ul></ul><ul><ul><li>Or relative increase diastolic bp >15 Torr or systolic bp>25 Torr </li></ul></ul><ul><li>Proteinuria > 0.3g in 24 hours </li></ul><ul><li>Generalised oedema (mainly lower extremities, hands) </li></ul>
  42. 49. Definition of Eclampsia <ul><li>One or more convulsion , not caused by other cerebral condition, in a patient with pre-eclampsia </li></ul>
  43. 50. Definition of severe pre-eclampsia <ul><li>Features of pre-eclampsia plus one the following : </li></ul><ul><ul><li>Systolic bp > 160 Torr </li></ul></ul><ul><ul><li>Diastolic bp >110 Torr </li></ul></ul><ul><ul><li>Proteinuria > 2 g per 24 hours </li></ul></ul><ul><ul><li>Cerebral or visual disturbances </li></ul></ul><ul><ul><li>Oliguria ≤ 500ml per 24 hours </li></ul></ul><ul><ul><li>Epigastric pain </li></ul></ul><ul><ul><li>Pulmonary oedema </li></ul></ul><ul><ul><li>Haemolysis, elevated liver enzymes and low platalet syndrome = HELP syndrome </li></ul></ul>
  44. 51. Mild and severe preeclampsia <100000 >100000/mm 3 Platelet count Yes No HELLP Yes No cynosis Yes No Pulmonary edema Yes No RUQ pain Yes No Epigastric pain Yes No Visual disturbances Yes No headache <500 >500ml/24hr Urine output >=5 3+or4+ <5g/24hr 1+or2+ Urinary protein >=110 <110mmHg DAP >=160 <160mmHg SAP severe mild
  45. 52. Epidemiology <ul><li>Incidence pre-eclampsia 6 % all pregnancies </li></ul><ul><li>Incidence eclampsia 2-5 in 1000 deliveries </li></ul><ul><li>PEE is associated with 1.8 % maternal mortality and 7 % fetal/ neonatal mortality </li></ul>
  46. 53. Pathogenesis <ul><li>Factors predisposing </li></ul><ul><ul><li>Increase Oxygen demand states e.g. </li></ul></ul><ul><ul><ul><li>Multiple pregancies </li></ul></ul></ul><ul><ul><ul><li>Fetal macrosomia </li></ul></ul></ul><ul><ul><li>Decrease Oxygen transfer </li></ul></ul><ul><ul><ul><li>Maternal anemia, High altitude (Tibet,Nepal,Peru) </li></ul></ul></ul><ul><ul><ul><li>Microvascular di s ease e.g. Hypertension, Diabetes, collagen disease , smoking </li></ul></ul></ul><ul><ul><ul><li>Abnormal placentation </li></ul></ul></ul><ul><ul><li>Genetic e.g. Angiotensin gene </li></ul></ul><ul><ul><li>Immune mechanism e.g. antiphospholipid syndrome </li></ul></ul>
  47. 54. Pathogenesis <ul><li>Primary defect involves abnormal migration of extravillous trophoblast in placenta </li></ul><ul><ul><ul><li>Myometrial vessels retain musculoelastic architecture instead of being converted into sinusoidal vessels( as occurs in normal pregnancy) </li></ul></ul></ul><ul><ul><ul><li>Defect occurs with the inhibition of second wave of migration i.e. in second trimester </li></ul></ul></ul><ul><ul><ul><li>Consequence of this defect includes </li></ul></ul></ul><ul><ul><ul><ul><li>Hypoperfusion and hypoxia of placenta endothelial cells </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Change in ratio of vasopressor substances tromboxane prostacyclin ratio by endothelium causing vasospasm </li></ul></ul></ul></ul>
  48. 55. Faulty placentation Genetic, immunologic, inflammatory factors Maternal vascular disease Excessive trophoblast Reduced uteroplacental perfusion Endothelial activation Capillary leak hemoconcentration edema proteinuria Vasospasm Activation of coagulation thrombocytopenia Vasoactive agents: Prostaglandins nitric oxide endothelins Noxious agents: Cytokines Lipid peroxidases oliguria HTN seizures abruption liver ischemia
  49. 56. Pathophysiology - cerebral <ul><li>Cerebral involvement include </li></ul><ul><ul><li>Eclamptic convulsions – principal sequlae </li></ul></ul><ul><ul><li>pathogenesis may be due to: </li></ul></ul><ul><ul><ul><li>Focal cerebral vasospasm and hypoperfusion causing abnormal electrical activity with hypertension occurring as secondary response – most likely explanation </li></ul></ul></ul><ul><ul><ul><li>Hypertension causes breakdown in cerebral autoregulation, leading to overdistension of vessels and extravasation of fluid </li></ul></ul></ul><ul><ul><li>Visual disturbances i.e. cortical blindness (rare) </li></ul></ul><ul><ul><li>Cerebral haemorrhage </li></ul></ul>
  50. 57. Pathophysiology - circulation <ul><li>Circulation </li></ul><ul><ul><li>Uteroplacental vascular resistance increases with decrease in blood flow , leading to placental ischaemia and fetal growth retardation </li></ul></ul><ul><ul><li>Systemic circulation – 2 models </li></ul></ul><ul><ul><ul><li>Traditional model – occurs in 80% pre-eclampsia with picture of </li></ul></ul></ul><ul><ul><ul><ul><li>Decreased plasma volume </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Vasoconstriction </li></ul></ul></ul></ul><ul><ul><ul><li>and therefore hypoperfusion of placenta and kidney </li></ul></ul></ul><ul><ul><ul><li>Hyperdynamic model – high CO with compensatory vasodilation </li></ul></ul></ul>
  51. 58. Pathophysiology - renal <ul><li>Renal involvement occurs in 2 stages: </li></ul><ul><ul><li>Impairment of tubular function occurs early – reflected by development of hyperuricaemia . </li></ul></ul><ul><ul><ul><li>Serum uric acid levels are a sensitive marker of progression and risk </li></ul></ul></ul><ul><ul><li>Glomerular filtration impaired later in disease – reflected by proteinuria > 0.5g in 24 hours or in severe pre-eclampsia > 2 g in 24 hours </li></ul></ul><ul><ul><li>Acute renal failure (rare) due to: </li></ul></ul><ul><ul><ul><li>Acute tubular necrosis (more common and reversible) </li></ul></ul></ul><ul><ul><ul><li>Acute cortical necrosis (permanent) </li></ul></ul></ul>
  52. 59. Pathophysiology – Blood <ul><li>Platelets </li></ul><ul><ul><li>usually associated with thrombocytopaenia ( < 100,000/mm 3 ) and increase in mean platelet volume </li></ul></ul><ul><ul><ul><li>Immune mediated </li></ul></ul></ul><ul><ul><li>Increase platelet activation </li></ul></ul><ul><ul><ul><li>Possibly due to endothelial activation or intrinsic changes in platelets </li></ul></ul></ul>
  53. 60. Pathophysiology – blood <ul><li>Coagulation cascade activated to greater extent than normal pregnancy </li></ul><ul><ul><li>Increase factor VIII consumption </li></ul></ul><ul><ul><li>Increase thrombin activity </li></ul></ul><ul><ul><li>All leads to heightened risk of thrombosis </li></ul></ul><ul><li>Anticoagulant protein levels decreased </li></ul><ul><ul><li>Decreased antithrombin III </li></ul></ul><ul><ul><li>Decreased protein C and S </li></ul></ul><ul><li>Fibrinolytic system – conflicting results </li></ul>
  54. 61. Pathophysiology – liver <ul><li>Liver complications consists of: </li></ul><ul><ul><li>Impaired liver function tests due to vasoconstriction of hepatic bed causing </li></ul></ul><ul><ul><ul><li>Periportal fibrin deposition </li></ul></ul></ul><ul><ul><ul><li>Hepatocellular necrosis </li></ul></ul></ul><ul><ul><li>Hepatic infarction and rupture – worst but rare condition </li></ul></ul><ul><ul><li>HELLP syndrome-hemolytic anemia, elevated liver enzymes, and low platelet count </li></ul></ul>
  55. 62. Pathophysiology – HELLP syndrome <ul><li>Constellation of laboratory findings in pre-eclampsia </li></ul><ul><ul><li>H aemolysis - seen on peripheral blood smear and bilirubin levels > 1.2mg/dL </li></ul></ul><ul><ul><li>E levated L iver enzymes – serum aspartate aminotransferase (AST) levels > 70 U/L </li></ul></ul><ul><ul><li>L ow P latelets < 100,000/mm 3 </li></ul></ul><ul><li>Pathogenesis uncertain but may be due to vasospasm </li></ul>
  56. 63. Pathophysiology –pulmonary system <ul><li>Pulmonary edema occur with severe pre-eclampsia or eclampsia. </li></ul><ul><ul><li>Excessive fluid administration </li></ul></ul><ul><ul><li>Delayed mobilization of extravascular fluid </li></ul></ul><ul><ul><li>Decreased plasma colloid oncotic pressure from proteinuria </li></ul></ul><ul><ul><li>Decreased hepatic synthesis of albumin </li></ul></ul>
  57. 64. <ul><li>Hypertension </li></ul><ul><li>Proteinuria </li></ul><ul><ul><li>An indicator of fetal jeopardy </li></ul></ul><ul><li>Edema </li></ul><ul><ul><li>Weight gain >2 lb/wk or a sudden weight gain over 1 to 2 days </li></ul></ul>Clinical Findings
  58. 65. Symptoms <ul><li>Headache </li></ul><ul><li>Oedema </li></ul><ul><li>Visual disturbance </li></ul><ul><li>Focal neurology, fits, anxiety, amnesia </li></ul><ul><li>Abdo pain </li></ul><ul><li>Decreased urine output </li></ul><ul><li>None </li></ul>Multisystem disease with varying clinical presentations.
  59. 66. Signs <ul><li>Hypertension </li></ul><ul><li>Tachycardia and tachypnoea </li></ul><ul><li>Creps or wheeze on auscultation </li></ul><ul><li>Neurological deficit </li></ul><ul><li>Hyperreflexia </li></ul><ul><li>Petechiae, intracranial haemorrhage </li></ul><ul><li>Generalised oedema </li></ul><ul><li>Small uterus for dates </li></ul>
  60. 67. Complications <ul><li>Early delivery and fetal complications due to prematurity. </li></ul><ul><li>Chronic uteroplacental insufficiency increases the risk of IUGR and oligohydraminos. </li></ul><ul><li>Abruptio placentae </li></ul>
  61. 68. Treatment-mild preeclampsia <ul><li>Maternal treatment should include: </li></ul><ul><ul><li>Bed rest </li></ul></ul><ul><ul><li>Serial or continuous blood pressure monitoring </li></ul></ul><ul><ul><li>Urinanalysis for proteinuria – quantification for degree of severity </li></ul></ul><ul><ul><li>Blood test include </li></ul></ul><ul><ul><ul><li>B P + platelet count and morphology </li></ul></ul></ul><ul><ul><ul><li>Haemocoagulation system </li></ul></ul></ul><ul><ul><ul><li>Uric acid, creatinin for renal function </li></ul></ul></ul><ul><ul><ul><li>Serum uric acid – useful early and for progression </li></ul></ul></ul><ul><ul><ul><li>Hepatic enzymes (AST,ALT, GMT) </li></ul></ul></ul><ul><ul><li>Fluid balance – urine output, CVP, Sa02 etc </li></ul></ul><ul><ul><li>ECG , medical Management Consulting ( neurologists, internists) </li></ul></ul>
  62. 69. Assessment of fetal status <ul><li>Fetal monitoring: </li></ul><ul><ul><li>Regular fetal HR monitoring NST – for acceleration, loss of variability or decelerations </li></ul></ul><ul><ul><li>Fetal ultrasound may be useful for fetal size and morphology, amniotic fluid volume estimation , placenta maturation </li></ul></ul><ul><ul><li>Amniocentesis to determine the L:S ratio </li></ul></ul><ul><ul><li>Corticosteriods to accelerate fetal lung maturity </li></ul></ul><ul><ul><ul><li>If delivery may occur in the next 2-7 days </li></ul></ul></ul>
  63. 70. Treatment-severe preeclampsia <ul><li>Goals of management: </li></ul><ul><ul><li>Prevention of convulsions </li></ul></ul><ul><ul><li>Control of blood pressure </li></ul></ul><ul><ul><li>Maintain placental perfusion with delivery timed appropriately </li></ul></ul>
  64. 71. Management – Anticonvulsant therapy <ul><li>Magnesium sulphate : anticonvulsant of choice </li></ul><ul><ul><li>Action by : </li></ul></ul><ul><ul><ul><li>antagonism of calcium and hence decreased systemic and cerebral vasospasm </li></ul></ul></ul><ul><ul><ul><li>Increase release of PGI 2 by vascular endothelium </li></ul></ul></ul><ul><ul><li>Other effects in parturient include: </li></ul></ul><ul><ul><ul><li>Tocolysis </li></ul></ul></ul><ul><ul><ul><li>Decreased cathecholamine release </li></ul></ul></ul><ul><ul><ul><li>Mild antihypertensive </li></ul></ul></ul><ul><ul><ul><li>Increases renal and uterine blood flow </li></ul></ul></ul>
  65. 72. Management – anticonvulsant therapy <ul><li>Magnesium continued </li></ul><ul><ul><li>Renally excreted – so reduce dose in renal failure </li></ul></ul><ul><ul><li>Therapeutic level 4.8-8.4mg/dL ; must monitor for toxicity </li></ul></ul><ul><ul><li>Repeated seizures despite therapeutic levels need to consider others </li></ul></ul><ul><li>Monitoring during MgSO 4 treatment </li></ul><ul><ul><li>Deep tendon reflex </li></ul></ul><ul><ul><li>Urine output at least 100mL during the preceding 4 hours </li></ul></ul><ul><ul><li>Respirations 12/min </li></ul></ul><ul><ul><li>10mL of 10% calcium chloride or calcium gluconate </li></ul></ul>
  66. 73. Management – Anticonvulsant therapy <ul><li>Diazepam : effective especially if needed acutely but causes fetal/ neonatal complications </li></ul><ul><ul><li>Adverse effect </li></ul></ul><ul><ul><ul><li>depression of muscle tone and breath centre </li></ul></ul></ul><ul><ul><ul><li>Competing with bilirubin for albumin bingding, predisposing the infant to kernicterus </li></ul></ul></ul>
  67. 74. Management of eclamptic seizures <ul><li>Airway protection </li></ul><ul><li>Maintain oxygenation (O2 inhalation via mask) </li></ul><ul><li>Control of seizures </li></ul><ul><ul><li>Continued convulsions may indicate other cerebral pathology </li></ul></ul><ul><ul><li>Management may involve treatment cerebral oedema (CS) </li></ul></ul><ul><li>Delivery of fetus when mother is in stable condition, even in some situation SC is needed acutely </li></ul>
  68. 75. Management – Antihypertensive therapy <ul><li>Treatment required when : </li></ul><ul><ul><li>Diastolic bp > 110 mmHg </li></ul></ul><ul><ul><li>The goal is to bring Bp into 90-100 mmHg </li></ul></ul><ul><li>Hydralazine : agent of choice </li></ul><ul><ul><li>Causes direct arteriolar vasodilation </li></ul></ul><ul><ul><li>Improves renal and uteroplacental blood flow </li></ul></ul><ul><li>Labetalol : nonselective beta blocker </li></ul><ul><ul><li>causes rapid decrease in arterial bp without compromising uteroplacental flow </li></ul></ul><ul><ul><li>May cross placenta but fetal complications rare </li></ul></ul>
  69. 76. Management – Antihypertensive therapy <ul><li>Nifedipine : causes direct relaxation of arteriolar smooth muscle </li></ul><ul><ul><li>Maintains uterine perfusion </li></ul></ul><ul><ul><li>Can cause uterine muscle relaxation – increase risk of post partum haemorrhage </li></ul></ul><ul><ul><li>Contra-indicated with use of Mg </li></ul></ul><ul><li>Sodium nitroprusside : hypertensive emergencies </li></ul><ul><li>Nitroglycerin : useful especially when pulmonary oedema complicates situation </li></ul>
  70. 77. Management – Antihypertensive therapy <ul><li>Unsuitable therapies : </li></ul><ul><ul><li>α - Methyldopa – slow onset </li></ul></ul><ul><ul><li>Clonidine – rebound hypertension on cessation </li></ul></ul><ul><ul><li>B-blockers – risk of hepatotoxicity, decrease uteroplacental perfusion, fetal complications </li></ul></ul><ul><ul><li>ACE-Inhibitors – contraindicated in pre-delivery because of intrauterine death, oliguria, renal failure in mum and neonate </li></ul></ul><ul><ul><li>Diuretics –avoid - because deplete intravascular volume </li></ul></ul>
  71. 78. Conclusion <ul><li>Pre-eclampsia due to a primary disturbance of placental vasculature is leading to increase systemic vascular resistance and bears a potential for multiorgan disturbances / failure secondary to vasospasm. </li></ul><ul><li>Mainstay of management is early diagnosis, prevention of hypertension and seizures. </li></ul><ul><li>Severe pre-eclampsia requires intensive management and the ultimate cure being delivery of fetus. </li></ul><ul><li>Eclamptic seizures and pulmonary oedema often occur in the post-partum period (strict patient control after delivery) . </li></ul>
  72. 79. Maternal Mortality - Obstetrical Hemorrhage - 4(4%) D.I.C. 9(10%) Couvelaire uterus 17(16%) Abruptio placenta 7(7%) Placenta previa 66(63%) Uterine atony Patients (n=103) Indication
  73. 80. Placenta Previa
  74. 81. The placenta provides the fetus with oxygen and nutrients and takes away waste such as carbon dioxide via the umbilical cord.
  75. 82. <ul><li>Definition     </li></ul><ul><ul><li>Placenta previa is a condition that may occur during pregnancy when the placenta implants in the lower part of the uterus and obstructs the cervical opening to the vagina (birth canal). </li></ul></ul>
  76. 83. Incidence <ul><li>The incidence of placenta previa is approximately 1 out of 200 births. </li></ul><ul><li>Increases with each pregnancy , and it is estimated that the incidence in women who have had 6 or more previous deliveries may be as high as 1 in 20 births. </li></ul><ul><li>Doubled in multiple pregnancy (such as twins and triplets). </li></ul>
  77. 84. <ul><li>Risk factors </li></ul><ul><ul><li>Multiparity (previous deliveries) </li></ul></ul><ul><ul><li>Multiple pregnancy </li></ul></ul><ul><ul><li>Previous myomectomy (removal of uterine fibroids through an incision in the uterus) </li></ul></ul><ul><ul><li>A previous C-section (if the scar is low and close to the vaginal cervix region). </li></ul></ul>
  78. 85. Etiology <ul><li>Endometrium factors: </li></ul><ul><ul><li>a scarred endometrium (lining of the uterus) </li></ul></ul><ul><ul><li>Curretage for several times </li></ul></ul><ul><ul><li>an abnormal uterus </li></ul></ul><ul><li>Placental factors </li></ul><ul><ul><li>Large </li></ul></ul><ul><ul><li>Abnormal formation of the placenta (succenturiate lobe or placenta diffusa). </li></ul></ul><ul><li>Development retardation of fertilized egg </li></ul>
  79. 86. Mechanisms of bleeding <ul><li>Mechanical separation of the placenta from its implantation site </li></ul><ul><li>Placentitis </li></ul><ul><li>Rupture of poorly supported venous lakes in the deciduas basalis </li></ul>
  80. 87. Classification <ul><li>Total placenta previa </li></ul><ul><li>The internal cervical os is covered completely by placenta </li></ul><ul><li>Partial placenta previa </li></ul><ul><li>The internal os is partially covered by placenta </li></ul><ul><li>Marginal placenta previa </li></ul><ul><li>The edge of the placenta is at the margin of the intenal os. </li></ul>
  81. 88. classification
  82. 89. Clinical findings <ul><li>Symptoms     </li></ul><ul><ul><li>Spotting during the first and second trimesters </li></ul></ul><ul><ul><li>Sudden, painless, and profuse vaginal bleeding in pregnancy during the third trimester (usually after 28 weeks) </li></ul></ul><ul><ul><li>--Bleeding may not occur until after labor starts in some cases </li></ul></ul><ul><ul><li>--Anemia, shock </li></ul></ul>
  83. 90. <ul><li>Signs </li></ul><ul><ul><li>The uterus is usually soft, relaxed and nontender. </li></ul></ul><ul><ul><li>The infant position is oblique ( // ) or transverse ( == ) in about 15% of cases. </li></ul></ul><ul><ul><li>Fetal distress is not usually present unless vaginal blood loss has been heavy enough to induce maternal shock , placenta abruptio , or a cord accident occurs. </li></ul></ul><ul><ul><li>No vaginal and rectal examination  </li></ul></ul>
  84. 91. Accessory examinations <ul><li>Ultrasonography: </li></ul><ul><ul><li>Accuracy 95% </li></ul></ul><ul><ul><li>34 th week </li></ul></ul><ul><li>Postpartum examination of placenta and membrane </li></ul><ul><ul><li>7cm </li></ul></ul>
  85. 92. <ul><li>Differential diagnosis </li></ul><ul><ul><li>Placental abruption </li></ul></ul><ul><ul><li>vagina bleeding with pain, tenderness of uterus. </li></ul></ul><ul><ul><li>Vascular previa </li></ul></ul><ul><ul><li>Abnormality of cervix </li></ul></ul><ul><ul><li>cervical erosion or polyp or cancer </li></ul></ul>
  86. 93. Complications     <ul><li>Maternal complications </li></ul><ul><ul><li>major hemorrhage, shock , and death. </li></ul></ul><ul><ul><li>Implanted placenta </li></ul></ul><ul><ul><li>Anemia and infection </li></ul></ul><ul><li>Fetal complications </li></ul><ul><ul><li>Prematurity (infant is less than 36 weeks gestation) is responsible for about 60% of infant deaths secondary to placenta previa. </li></ul></ul><ul><ul><li>Fetal blood loss or hemorrhage may occur because of the placenta tearing away from the uterine wall during labor. It may also occur with entry into the uterus during a C-section delivery. </li></ul></ul>
  87. 94. Treatment <ul><li>The course of expectant treatment depends on </li></ul><ul><ul><li>The amount of abnormal uterine bleeding </li></ul></ul><ul><ul><li>Whether the fetus is developed enough to survive outside the uterus </li></ul></ul><ul><ul><li>The amount of placenta over the cervix </li></ul></ul><ul><ul><li>The position of the fetus </li></ul></ul><ul><ul><li>The parity (number of previous births) for the mother </li></ul></ul><ul><ul><li>The presence or absence of labor. </li></ul></ul>
  88. 95. Treatment <ul><li>Early in pregnancy, transfusions may be given to replace maternal blood loss . </li></ul><ul><li>Medications may be given to prevent premature labor, prolonging pregnancy to at least 36 weeks. </li></ul><ul><li>Beyond 36 weeks, the benefits of additional infant maturity have to be weighed against the potential for major hemorrhage. </li></ul>
  89. 96. Treatment <ul><li>In selecting the optimum time for delivery, tests of fetal lung maturation are invaluable adjuvants. </li></ul><ul><li>Cesarean section is the method for delivery. It has proven to be the most important factor in reducing maternal and infant death rates. </li></ul>
  90. 97. Expectations (prognosis) <ul><li>The maternal prognosis (probable outcome) is excellent when managed appropriately. </li></ul><ul><ul><li>This is done by hospitalizing those at risk who are exhibiting signs and symptoms, and by performing C-section delivery. </li></ul></ul>
  91. 98. ABRUPTIO PLACENTAE
  92. 99. Definition <ul><li>Abruptio Placentae( placental abruption): </li></ul><ul><li>premature separation of the normally implanted placenta from the uterine wall. </li></ul><ul><li>Incidence : </li></ul><ul><ul><li>1/77-89 deliveries </li></ul></ul><ul><ul><li>Severe form (resulting in fetal death)1/500-750 </li></ul></ul>
  93. 100. Classification <ul><li>Concealed separation : no vaginal bleeding </li></ul><ul><li>Apparent separation : vaginal bleeding will be </li></ul><ul><li>Mixed separation : vaginal bleeding will be apparent </li></ul>
  94. 102. Classification <ul><li>Concealed form (20%) </li></ul><ul><ul><li>Detachment of the placenta may be complete </li></ul></ul><ul><ul><li>Complications are often severe. About 10% with DIC. </li></ul></ul><ul><li>External form (80%) </li></ul><ul><ul><li>Placenta detachment is more likely to be incomplete </li></ul></ul><ul><ul><li>Complications are fewer and less severe. </li></ul></ul>
  95. 103. Etiology <ul><li>Mechanism: hemorrhage into the decidua basalis, leading to premature placental separation and further bleeding. </li></ul><ul><li>Associated factors: </li></ul><ul><li>Maternal hypertension </li></ul><ul><li>Sudden decompression of the uterus </li></ul><ul><li>Maternal age and multiparity </li></ul><ul><li>trauma </li></ul>
  96. 104. Pathophysiology and pathology <ul><li>Local vascular injury that results in vascular rupture into the decidua basalis, bleeding, and hematoma formation. </li></ul><ul><ul><li>Preeclampsia-eclampsia, chronic hypertension, DM, chronic renal disease </li></ul></ul><ul><li>An abrupt rise in uterine venous pressure transmitted to the intervillous space. </li></ul><ul><ul><li>Vasodilatation secondary to shock, compensatory hypertension and the paralytic vasodilation of conduction anesthesia. </li></ul></ul>
  97. 105. Pathophysiology and pathology <ul><li>Uteroplacental apoplexy </li></ul><ul><ul><li>Extensive intramyometrial bleeding, resulting in a purplish and copper-colored, ecchymotic, indurated organ that all but loses its contractile power because of disruption of muscle bundles. </li></ul></ul>
  98. 106. Pathophysiology and pathology <ul><li>Coagulation abnormalities </li></ul><ul><li>Hypofibrinogenemia </li></ul><ul><li>Increaseing levels of fibrin degradation products </li></ul><ul><li>decreasing platelet count </li></ul><ul><li>Increasing prothrombin time and partial thromboplastin time </li></ul><ul><li>Decreasing other serum clotting factors </li></ul>
  99. 107. Diagnosis <ul><li>Classic clinical presentation : </li></ul><ul><li>vaginal bleeding 80% </li></ul><ul><li>Tender uterus 2/3 </li></ul><ul><li>Uterine contractions 1/3 </li></ul><ul><li>Fetal distress 50% </li></ul>
  100. 108. <ul><li>Ultrasonography: </li></ul><ul><li>Placental examination </li></ul><ul><li>The extent of placental abruption of the maternal surface of the placenta on which a clot is detect at the time of delivery. </li></ul>
  101. 109. <ul><li>Complication </li></ul><ul><li>DIC </li></ul><ul><li>Shock </li></ul><ul><li>Amniotic fluid embolism </li></ul><ul><li>Acute renal dysfunction </li></ul>
  102. 110. Management <ul><li>Maintain hemodynamic stabilization ( Transfusion therapy) </li></ul><ul><li>Crystalloid transfusion </li></ul><ul><li>Whole blood therapy </li></ul><ul><li>Component therapy </li></ul><ul><li>Correct coagulation status </li></ul>
  103. 111. <ul><li>Delivery </li></ul><ul><li>When the fetus is mature, vaginal delivery is preferable unless there is evidence of fetal distress or hemodynamic instability. </li></ul><ul><li>When the fetus is not mature and placental abruption is limited, observation with close monitoring of both fetal and maternal status. </li></ul>
  104. 112. Delivery <ul><li>Cesarean section is indicated : </li></ul><ul><ul><li>Fetus exhibits persistent evidence of distress. </li></ul></ul><ul><ul><li>Situation is not favorable for rapid delivery. </li></ul></ul><ul><ul><li>Uncontrollable hemorrhage </li></ul></ul><ul><ul><li>A rapid expanding uterus with hemorrhage. </li></ul></ul><ul><ul><li>Uterine apoplexy </li></ul></ul>
  105. 113. Thank you for your attention!

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