2. MISCARRIAGE THREATENED SILENT INEVITABLE INCOMPLETE TROPHOBLASTIC DISEASES ECTOPIC PREGNANCY LOCAL CAUSE
3. Clinical presentation
4. Clinical Presentation Amount of bleeding Pain Passage of products
5. MISCARRIAGE SPORADIC MISCARRIAGEDefinitionIn UK : loss of an intrauterine pregnancy before 24 completed weeks of gestation. WHO : expulsion of fetus / embryo wt < 500 g & gestation limit of < 22 completed wks of pregnancy.
6. MISCARRIAGE SPORADIC MISCARRIAGE A distressing complication of pregnancy Occur ~ 20% of pregnancies Majority of sporadic miscarriage occur in 1st trimester = early pregnancy loses Only 2-5% of pregnancy miscarry after FH activity has been detected by USG
7. Spontaneous MiscarriageIncidence 10-15% in clinically evident pregnancy 30% in chemically evident pregnancy 80% of spontaneous miscarriage occurred in gestational age less than 14 weeks.
8. Miscarriage Threatened – 25% of all pregnancies ~ uterine bleeding prior to 24 w of pregnancy Inevitable – complete or incomplete depending on whether all or not POC expelled from the uterus. Early fetal/embryonic demise (missed/anembryonic/blighted ovum) ~ failure of pregnancy is identified before the expulsion of fetal and placental tissue.
9. Miscarriage Septic Recurrent miscarriage ~ primary – no previous live birth ~ secondary – at least one previous successful pregnancy.
10. AETIOLOGY No demonstrable cause – commonest MORPHOLOGIC AND GENETIC ABNORMALITY Abnormal karyotype~ 50% in first trimester 20 – 30% in 2nd trimester 5- 10% in 3rd trimester
11. AETIOLOGY 50% of spontaneous miscarriage is due to aneuploidy 50% of aneuploidy is autosomal trisomies eg: trisomy 16 during first trimester- commonly trisomy 16 or monosomy X (45XO Turner Syndrome – 20%) polyploidy (triploidy) 20%, producing blighted ovum or partial mole
13. Infective Causes of Miscarriage Mechanisms – unclear but postulated due to maternal pyrexia/ bacteraemia Recent prospective study found : Women experience 1st trimester miscarriage – no more likely to have a clinical infection than those having a successful pregnancy In recurrent miscarriage : Infective causes (> genital tract infection) is unclear
14. Infective Causes of Miscarriage HIV Remains unknown Syphillis & Parvovirus B19 Commonly cause late 2nd trimester miscarriage & stillbirth Group B Streptococcus (GBS) In late miscarriages & preterm labour
15. Structural causes of Miscarriage Mullerian duct defects – Anatomical uterine abn Prevalence : 3% (in lap sterilisation) Prevalence in recurrent miscarriers: 3 – 27% Most sensitive method of Ix : Hysteroscopy > HSG > ? USG In early preg loss, embryo must be presumed to implant in an avascular area of endometrial cavity – lead to arrested dev & early preg failure. This process is unlikely in recurrent preg loss
16. Structural causes of Miscarriage Open surgical / abd resection : Risk of pelvic & intrauterine adhesion formation(Asherman’s Syndrome) myomectomy Hysteroscopic resection of intrauterine septa More promising but lack of randomised studies Cervical incompetence Def : Painless dilatation of the cx lead to miscarriage in the absence of uterine contractions / haemorrhage Aetiology of 2nd trimester loss
17. Other causes of miscarriage Fetal sex More in males, but sex ratio remain unknown Multiple pregnancy Assoc with an increased risk of fetal loss (either by resorption, post- implantation loss / 2nd trimester miscarriage) Risk of miscarriage 2x singleton preg Monochorionic twin preg – 12% risk Parity Rises risk with parity Results of reproductive compensation & related with maternal age (assoc with trisomic pregnancies)
18. Maternal health in miscarriage Cigarete smoking Correlated with miscarriage Nicotine has adverse effect on trophoblastic invasion Cocaine – increased risk of miscarriage Alcohol – higher in women ended up with miscarriage Caffeine – high level ass. with miscarriage Chemicals : lead,ethylene oxide, solvents, pestisides, vinyl chloride & anaesthetic gases – ass. with fetal loss Radiotherapy & Chemotherapy May cause miscarriage & fetal abnormality in a dose of > 25 rads – 0.1% risk
19. CLINICAL FINDINGS Threatened Minimal vaginal bleeding + pain (usually painless) Closed cervical os, Without expulsion of POC Viable pregnancy by USG soft, non-tender abdomen, uterus=POA Continued vomiting ass. with increased chance of life birth
20. CLINICAL FINDINGS Inevitable fresh vaginal bleeding with abdominal/back pain with cx dilatation and effacement 50% will miscarry Diagnosis determined by confirmation of cervical dilatation at VE Occasionally severe shock – may be due to massive haemorrhage / vasovagal reaction – cervical shock syndrome due to distension of the cervix by POC (Treatment is by quick removal of the POC from os by bedside)
21. CLINICAL and USG FINDINGS Incomplete heavy bleeding & abd cramps with open cx os POC partially expulsed & USG showed hyperechoic material in the uterine cavity Complete A hx of pain + bleeding + POCs seen bleeding and pain cease afterwards as POCs completely expelled. USG ~ empty uterus Recent studies of women showed around 20-30% of all miscarriage is complete(Chung et al 1994; Mansur 1992) Expectant mx of early fetal demise has demonstrated that, with time, up to 25% women go on to have complete miscarriage (Jurkovic et al 1998)
22. CLINICAL FINDINGS Early Embryonic / Fetal Demise* (Missed / Silent) Failure of preg is identified before any expulsion of POC occur Disappearance of sn/sx of pregnancy with ut < gest age & closed cervical os An USG dx of non-viable preg in the absence of PV bleeding / pain(accidental finding) A fetal pole > 5 mm w/out FH activity or when USG I / 2 wks apart have shown no growth / no FH activity: Missed / silent miscarriage
23. CLINICAL FINDINGS w/out a fetal pole : A sac > 20 mm in diameter a blighted ovum* Goldstein – most of anembryonic pregnancy are not truly without embryos. They lose viability before our ability to image them. Many initially had early embryonic dev. with subsequent loss of viability, followed by embryonic resorption and thus ,appearance of empty sac. * An embryonic pregnancy / blighted ovum has been replaced with early embryo/ fetal demise in UK
24. CLINICAL FINDINGS Septic A complication of incomplete miscarriage where the remaining POCs become infected by ascending organisms + instrumentation of the uterus Presented with suprapubic pain, malaise, fever + PV bleeding O/E : Fever, suprapubic pain/abd rigidity, uterine & adnexal tenderness and closed cervix. Around 3-6% following termination of pregnancy Common organisms : E.Coli,Bacteroides, streptococci Clostridium welchii Complications : Septicaemia → bactaremic shock → maternal death
25. INVESTIGATIONS USG ~ is essential in the diagnosis – usually TVS. ~ will determine on-going pregnancy/failing pregnancy/rule out ectopic and trophoblastic disease. Pregnancy test – by urinary or serum hCG to distinguish an early complete miscarriage or on- going ectopic pregnancy. Blood grouping and Rh typing – Rh neg. should receive anti-D Ig regardless of gestational age.
26. Management of miscarriage Tx aim : to reduce the potential complication of miscarriage (i.e prolonged pain & bleeding, sepsis & rh- iso-sensitisation) Conservative Expectant Mx ~ avoids surgical procedure & anaesthetic. Appropriate for pts with an incomplete miscarriage with POC < 50mm in diameter on TVS In cases without haemodynamic compromise / maternal anaemia, spontaneous resolution occurred within 3 days in up to 80% of cases with minimal retained POC No evidence of impairment of future fetility
27. Management of miscarriage Conservative Management less useful for blighted ovum because bleeding appears to be heavier & more prolonged than surgical management 60% which treatment conservatively require ERPOC at some stage
28. Management of miscarriage Surgical Evacuation of retained POC (ERPOC) – most common form of tx for miscarriage Cx is dilated & retained POC removed by S+C Cpx : Perforation of the uterus (by dilator / currete), infection (commonest) & incomplete emptying of the cavity ~ in up to 6% of cases, tearing of cervix Incidence of serious morbidity : 2.1% (RCOG 1985) Potential anaesthetic cpx Asherman syndrome (intrauterine adhesions) Incidence of mortality : 0.5 / 100 000 (Lawson et al 1994)
29. Threatened Miscarriage Mx 97-98% chance of a live birth Women > 40s, miscarriage rate : 15-30% – even after FH present by USG Tx : reassurance & continued medical & emotional support Advise bedrest & avoiding SI Bedrest ↓pressure & improve outcome – but no clinical evidence Progesterone supplementation However, several meta-analysis trial unable to demonstrate beneficial effect of progesterone tx (Goldstein et al 1989)
30. Incomplete Miscarriage Mx Tx : Surgical evacuation of POC Without tx : maternal mortality of 1.6% Due to haemodynamic compromise of cervical shock. Suction evacuation >safer technique than sharp curettage Lower rate of perforation, blood loss & subsequent intrauterine adhesion formation (Edmonds 1992, Verkuyl & Crowther 1993) Routine use of syntocinon / ergometrine – no benefits in ↓blood loss during surgical tx of 1st trimester miscarriage (Beeby et al 1984) Screening for chlamydia infection is recommended
31. Early Fetal Demise Mx Same for incomplete miscarriage Tx : Surgical tx after cervical ripening (with mifepristone/ prostaglandin) To ↓ risk of cx trauma / ut perforation assoc with forced cx dilatation Expectant mx : < effective than cases of incomplete miscarriage With only 25% proceeding to complete miscarriage Efficacy of medical tx also < inc miscarriage Complete miscarriage rate can be up to 90% with higher dose of mifepristone & misoprostol
32. Coronal TVUS of the uterus shows a gestational sac withhyperechoic margins (arrow) and endometrial cavity (curvedarrow).
33. Double Decidual Sac Sign. Coronal TVUS of the uterus reveals anintrauterine gestational sac (straight arrow), decidua capsularis(curved arrow), decidua parietalis (arrowhead), and effacedendometrial cavity (asterisks)
34. Yolk sac (thin arrow) outside the amniotic membrane(arrowhead), which has not yet fused with the chorion (curvedarrow). Embryo (thick arrow) is seen within the amniotic sac
35. Anembryonic Pregnancy
36. Abnormal Shape of the GS
37. Abortion in Progress
38. Missed Abortion
39. Subchorionic Haemorrhage
40. Retained Products of Conception
41. Retained Products of Conception
42. Introduction Leading cause of death of pregnancy related deaths during first trimester 13 maternal deaths resulting from ectopic pregnancy in the UK in 1997–99. Incidence of ectopic pregnancy has remained static in recent years (11.1/1000 pregnancies) 32000 ectopic pregnancies are diagnosed in the UK within a three year period.
43. Clinical presentation Clinical suspicion – positive pregnancy test, pain, bleeding and adnexal mass Clinical triad – pain, bleeding, adnexal mass ~ 45% of patients Pain Clinical Triad Bleeding Adnexal mass
44. Clinical presentation Location of pain lower abdominal ~ 74% generalised abdominal ipsilateral lower quadrant contralateral lower abdomen shoulder tip back pain vaginal
45. Risk Factors for Ectopic pregnancy High Risk Tubal surgery Sterilization Previous ectopic pregnancy Use of IUCD Documented tubal disease In utero exposure to diethylstilbesterol
46. Risk Factors for Ectopic pregnancy High Risk Moderate Risk Infertility Multiple sexual partners Previous genital infections Slight Risk Cigarrette smoking Previous pelvic / abdominal surgery
47. Pregnancy testing Urine pregnancy test – Sensitive radioimmunoassays are widely available – +ve at approximately 23 menstrual days (9 days postconception)
48. Pregnancy testing Beta hCG quantitation (serum B hCG) Normal intrauterine pregnancy – hCG doubling time of 2 days (66%) – Intrauterine GS (US Scan) with hCG 1000 – 2000 mIU/ml
49. Pregnancy testing Beta hCG quantitation (serum B hCG) Ectopic pregnancy – hCG doubling time is different – hCG doubling time increased – disproportionately high level of hCG in correlation ultrasound findings
50. Diagnosis of Ectopic Pregnancy Clinical Biochemical Ultrasound Diagnostic laparoscopy ~ GOLD STANDARD
51. SONOGRAPHY Early intrauterine pregnancy Earliest sign ~ small fluid collection in the endometrium
52. SONOGRAPHY Gestational sac Early intrauterine pregnancy intradecidual sign with echogenic ring formed by chorionic villi double decidua sac sign (DSS) eccentric to the endometrial cavity Uterus Bladder
53. SONOGRAPHY Gestational sac Early intrauterine pregnancy presence of yolk sac & the embryo Yolk Sac
54. No identifiable intrauterine GS One of three possibilities – Very early intrauterine pregnancy – recent spontaneous miscarriage – Ectopic pregnancy Bladder Cervix Uterus
60. SONOGRAPHY Ectopic Pregnancy UterusAdnexal mass Mass
61. SONOGRAPHY Ectopic Pregnancy LIVERLIVER Kidney Kidney Free fluid at Morrison’s Pouch Normal
62. MANAGEMENT OF ECTOPIC PREGNANCY Surgical option – Laparotomy VS Laparoscopy – Salpingotomy VS salpingectomy• Nonsurgical treatment – Expectant management – Metrotrexate• Combined medical-surgical treatment
63. MANAGEMENT OF TUBAL ECTOPIC PREGNANCY Laparoscopy VS Laparotomy A laparoscopic should be the surgical management of tubal pregnancy, in the haemodynamically stable patient.
64. MANAGEMENT OF TUBAL ECTOPIC PREGNANCY Laparoscopy VS Laparotomyshorter operation times,less intraoperative blood loss,shorter hospital staylower analgesic requirements
65. MANAGEMENT OF TUBAL ECTOPIC PREGNANCY Laparoscopy VS Laparotomy no difference in overall tubal patency rates Similar subsequent intrauterine pregnancy rates Lower repeat ectopic pregnancy rates in laparoscopic approach laparoscopic salpingotomy was less successful than an open approach in elimination of the tubal pregnancy (higher rates of persistent trophoblast)
66. MANAGEMENT OF TUBAL ECTOPIC PREGNANCYIn haemodynamically unstable, management should beby the most expedient method.In most cases, this will be laparotomy.
67. MANAGEMENT OF TUBAL ECTOPIC Medical Management – Methotrexate Patient selection : Compliant Adnexal mass < 3.5 cm Beta hCG < 3000 mIU/ml Absent fetal heart activity Minimal symptom 15% of women will require more than one dose of methotrexate 7% will experience tubal rupture during follow up. 75% will experience abdominal pain following treatment
68. MANAGEMENT OF TUBAL ECTOPIC Medical Management – Methotrexate im methotrexate as a single dose calculated from patient body surface area (50 mg/m2) – 75 mg and 90 mg. Serum hCG levels checked on days four and seven a further dose is given if hCG levels have failed to fall > than 15% between day four and day seven. < 10% of women treated with this regimen will require surgical intervention
69. MANAGEMENT OF TUBAL ECTOPIC Medical Management – Methotrexate 2 X weekly hCG measurements (ideally < than 50% of its initial level within seven days) weekly transvaginal US examinations (reduction in the size of adnexal mass by seven days) Thereafter, weekly hCG and transvaginal US examinations until serum hCG levels are < than 20 mIU/ml
70. Pregnancy of unknown location Conservative Management clinically stable women with minimal symptoms Beta hCG level < 1500 to 2000 mIU/ml 44–69% of pregnancies of unknown location resolve spontaneously with expectant management – small ectopic pregnancies which were : spontaneously absorbed or resolved by tubal abortion. – early intrauterine pregnancies that miscarried. 14-28% lead to ectopic pregnancy
71. Remember !!!Rhesus Negative women Nonsensitised women who are rhesus negative with a confirmed or suspected ectopic pregnancy should receive anti-D immunoglobulin.
72. WORK-UP FOR ECTOPIC PREGNANCY Qualitative Beta HCG (UPT) negative positive TVS Pregnancy excludedIntrauterine pregnancy(normal / abnormal) No IUP & Tubal mass No IUP & stable unstable No adnexal mass / Free Fluid Laparoscopy / Laparotomy Medical Follow up
73. WORK-UP FOR ECTOPIC PREGNANCY Empty uterus & no adnexal mass / Free fluid Serum Beta HCG Serum Beta HCG < 1500Serum Beta HCG > 1500 Repeat 48 hours laterLaparoscopy 66% or more rise Rise by < 66% or condition worsen Repeat scan in 1 week unless condition worsen
