This document provides an overview of ectopic pregnancy. It begins with an introduction defining ectopic pregnancy and reviewing anatomy and physiology related to implantation. It then covers epidemiology, risk factors, clinical presentation, diagnostic tools like beta-hCG and ultrasound, and management options including expectant, medical, and surgical approaches. The focus is on tubal ectopic pregnancy as the most common type. Key points include the discriminatory hCG level for diagnosing ectopic versus intrauterine pregnancy and criteria for medical management with methotrexate versus surgical intervention.

1. Ectopic Pregnancy
Presenter:
Dr. Bwire Innocent Resident Obsgyn KIU
Mentor:
Dr. Balungi Charles Consultant Obs/Gyn HRRH

2. Outline
• Introduction
• Anatomy and physiology
• Epidemiology
• Common sites/classification
• Risk factors
• Diagnosis
• Management
• Ovarian, cervical, abdominal, caesarean scar ectopic pregnancy
• Prognosis

3. Introduction
• Ectopic pregnancy is a pregnancy in which the blastocyst
implants anywhere other than the endometrial lining of the
uterine cavity.
• Ectopic- Greek= ektopos “out of place”
• Occasionally, a multifetal pregnancy contains one
conceptus with normal uterine implantation and the other
implanted ectopically is termed a heterotopic pregnancy

4. Review Of Physiology
Fertilization of the ovum normally takes place in the
ampullary portion of the fallopian tube.
The fertilized ovum is carried down the tube by ciliary and
peristaltic action.
The fertilized ovum reaches the uterine cavity 5-6 days
after ovulation.
Implantation-usually at the fundus

5. Ampullary tubal pregnancy (arrow) seen during
laparoscopy.

6. Epidemiology
• EP accounts for approximately 2% of all reported pregnancies(ACOG)
• Accounts for 3% of all pregnancy-related death (Creanga,2017)
• The prevalence of EP among women presenting to an emergency
department with first-trimester vaginal bleeding, or abdominal pain, or
both, has been reported to be as high as 18% (ACOG)
• Prevalence 2-5% in patients who utilized ART (panelli , 2015)
• In Uganda EP prevalence is 1.9% (Teziita 2013)

7. Sites
• Tubal ectopic pregnancy (95%)
• Non-tubal (5%)
• Uterus
• Extrauterine

9. Rare sites
• Ovarian ectopic pregnancy (3.2%)
• Abdominal ectopic pregnancy (1.3%) on omentum,
liver and retroperitoneum
• Cesarean scar pregnancy (CSP)
• Cervical ectopic pregnancy (rare)
• Cornual in mullerian agenesis vs interstitial
(Cornual)
• Intraligamentous

10. Risk factors
• High risk factors
• Tubal corrective surgery
• Tubal sterilization
• Previous ectopic- 15%, 30%
• ART
• PID-9%
• Documented tubal pathology
• Other risk factors
• Endometriosis
• Fibroids
• Diethylstilbestrol (DES) exposure
• Congenital anomalies of the uterus
• Maternal age 35-44
• One third no risk factor found
Moderate risk factors
• Infertility & ovulation induction
• Contraception failure- IUDs, POPs, BTL
• Previous genital infections
• Multiple sexual partners
Slight risk factors
• Previous pelvic or abdominal surgery
• Smoking
• Douching
• Intercourse before 18 years

11. Tubal pregnancy
• Risks : Abnormal fallopian tube anatomy underlies most cases
• Prior tubal pregnancy (highest risk),
• Tubal Surgery ,
• prior tubal infection
• peritubal adhesions from salpingitis,appendicitis and endometrisosis
• Infertility and ART,
• Contraceptive failure (IUD, COCs,POP )
• smoking

12. pathogenesis
• With tubal pregnancy, because the fallopian tube lacks a submucosal
layer, the fertilized ovum promptly burrows through the epithelium.
• The zygote comes to lie near or within the muscularis, which is
invaded by rapidly proliferating trophoblast.
• Potential outcomes from this include tubal rupture, tubal abortion, or
pregnancy failure with resolution.

13. Pathophysiology
• Acute and chronic intraluminal inflammation that leads tubal damage
with subsequent fibrin deposition, and tubal scarring
• Also delayed hypersensitivity reaction from persistent chlamydial
antigen leads to slower, continued tubal damage
• Intraluminal inflammation results in arrest of embryo transport and
provide a premature preimplantation signal
• Interference of normal function of oviduct interstitial cells of Cajal
(specialized pacemaker cells) responsible for oviduct motility and egg
transport also implicated

14. Pathophysiology
• Cannabinoid receptor (CB1) also involved with oviductal transport of
embryos, mediated by endocannabinoid signaling mechanism
• Chronic exposure to nicotine can affect endocannabinoid levels and
lead to fallopian tube dysfunction
• E-cadherin, an adhesion molecule, has also been implicated
• The E-cadherin strongly localized to the tubal embryo implantation
site only in women who underwent ART
• Destruction of normal tubal anatomy & hence transport, resulting in
delayed or prevention in passage of blastocyst uterine cavity

15. Pathophysiology
• Fallopian tube lacks a submucosal layer beneath its epithelium and this
results in faster root for the blastocyst to invade & implants in the
mascularis layer hence erosion, bleeding
• Thereafter it causes acute or chronic ectopic presentation
• Aris stella reaction : hormone related atypical endometrial change
with hypertrophy and vacuolization of glandular epithelial cells. Arias
Stella Reaction is not specific for ectopic pregnancy but for
blightening of conceptus either intra uterine or extrauterine.

16. Outcomes of tubal ectopic pregnancy
• Tubal rupture(35%)- isthmic pregnancy. Intercourse or bimanual
examination can lead to rupture
• Tubal abortion (65%)- especially in cases of Fimbrial pregnancy
(distal implantation) resulting in complete absorption, complete or
incomplete detachment or tubal mole
• Secondary abdominal pregnancy if extruded pregnancy continue to
grow while still maintain trophoblastic connection to tubal epithelium
• Pregnancy failure with resolution

17. Risk factors for tubal rupture
• Ovulation induction
• Serum β-human chorionic gonadotropin (β-hCG) level > 10,000 IU/L,
• Never having used contraception
• “Ring of fire” placental blood flow within the periphery of the
complex adnexal mass

18. Clinical Presentation
• Consider ectopic as a diagnosis in any patient of reproductive age
with vaginal bleeding and or abdominal pain with x-tics
• Pregnancy not yet confirmed, conceived by IVF, unknown pregnancy
status, in rare cases hemodynamic instability and an acute abdomen
that’s is not explained by another diagnosis
• Before rupture, symptoms and signs are often subtle or absent
• Isthmic rupture usually occurs at 6–8 weeks, the ampullary one at 8–
12 weeks and the interstitial one at about 16 weeks.

19. Clinical presentations
• The classic triad is amenorrhea (80%) that is followed by pain (90%)
and vaginal bleeding(70%).
• Symptoms of early pregnancy: breast tenderness, nausea….less
• Referred pain to shoulder/neck may suggests sizable hemoperitoneum
• Symptoms of Anaemia: malaise, weakness, dizziness, sense of passing
out on standing/syncope, fainting

20. Tubal ectopic presentation
• Acute ectopic: more common
• characterized by a high serum β-hCG level at presentation, rapid
growth, higher risk of rupture & rapid diagnosis
• Chronic ectopic:
• characterized by earlier death of trophoblast with resultant negative,
low or static serum β-hCG level, complex pelvic mass, late rupture if
ever at all and requires surgical diagnosis

21. Examination findings
• General examination:
• Pallor, dehydration , early signs of pregnancy, evidence of hemodynamic
instability- hypotension, tachycardia, tachypnea, hypothermia
• Abdominal examination:
• abdominal tenderness (80%), worse on affected side
• Signs of peritoneal irritation: guarding, rigidity, rebound tenderness
• Pelvic examination:
• vaginal bleeding (70%), Bulky enlarged & soft uterus
• cervical motion tenderness, Adnexal mass (50-90%)- tender or non-
tender, Bulging posterior fornix

22. Shock index
• Shock index is the heart rate divided by systolic blood pressure
• can be used assess the severity of ruptured ectopic pregnancy, trauma
patients or hypovolemic or septic shock.
• The normal range lies between 0.5 and 0.7 for nonpregnant patients.
• A shock index > 0.85 and a systolic blood pressure < 110 mm Hg are
highly suggestive of a potentially life-threatening gynecologic
emergency, such as a ruptured ectopic pregnancy

23. Investigations
• an initial urine β-hCG assay, urinalysis, and Hb or hematocrit are
routine. ABO & Rh type and cross-matching
• CBC to assess WBC count if serious infection is a possible diagnosis.
• A positive urine pregnancy test result should prompt a serum β-hCG
assay for those with pain or bleeding
• For women with a positive pregnancy test result plus bleeding or pain,
an initial TVS is typically performed to locate the gestation

24. Beta Human Chorionic Gonadotropin
• Lower limits of detection are 20 to 25 mIU/mL for urine and ≤5
mIU/mL for serum (Greene, 2015).
• The initial β-hCG level sets expectations for anticipated TVS Finding.
• With values above a discriminatory threshold, a normal IUP is
expected to be seen within the uterus
• TVS discriminatory threshold at ≥1500 mIU/ mL, whereas others use
≥2000 mIU/mL. Connolly and associates (2013) suggested an even
higher threshold >3510 mIU/mL.

25. Discriminatory level
β-hCG level above which IUP is reliably visualized in nearly 100%
cases.
Suspect ectopic if:
Transabdominal sonography shows no IUP & hCG >6500mIU/mL or
IU/L and Transvaginal sonography with >1500mIU/mL
Follow up serial serum β-hCG : rising, falling or plateauing

26. Discriminatory zone
• Lack of IUP when β-hCG is above discriminatory zone may suggest
1. Ectopic pregnancy
2. Multiple gestation
3. Failing IUP
4. Recent completed abortion
• After serial β-hCG endometrial sampling is informative looking for
chorionic villi or sac

27. Progesterone
• Aids in ectopic pregnancy diagnosis when serum β-hCG levels and TVS
fndings are inconclusive (Stovall, 1992).
• A single value is sufcient. From studies, a serum progesterone level <6
ng/mL (<20 nmol/L) has a pooled specifcity of 98 % to predict a nonviable
pregnancy in women with a PUL (Verhaegen, 2012)
• A value >25 ng/mL suggests a live IUP and excludes ectopic pregnancy
with 97-percent sensitivity (Carson, 1993).
• With most ectopic pregnancies, progesterone levels range between 10 and
25 ng/mL and thus have limited diagnostic utility (ACOG 2019c).

28. Imaging
• TVS: accurate and initial investigation of choice
• Definitive IUP, definitive ectopic, probable IUP, Probable ectopic, PULs
• Features IUP: eccentrically placed ovoid fluid filled sac (gestational sac)
with sonolucent center >5mm in Diameter, surrounded by thick concentric
bright echogenic ring within the endometrium. It contains fetal pole, yolk
sac or both. Positive decidual sign
• Decidual sign: echogenic rim around gestational sac
• Features probably Abnormal pregnancy: irregular, crenated gestational Sac
>10mm with out fetal pole or with fetal pole but no cardiac activity

29. Placental blood flow within the periphery of
the complex adnexal mass—the ring of fire

30. Features of definitive ectopic
1. A definitive gestational sac outside the uterus (with intact well defined tubal
ring= Doughnut or Bagel sign),
2. empty uterus or centrally placed pseudogestational sac; negative Decidual sign
3. cystic or solid adnexal or tubal mass,
4. hematosalpinx,
5. free fluid or clotted blood in cul-de-sac or intraperitoneal gutters (Morrison’s
pouch),
6. Trillaminar endometrial pattern
7. Endometrial stripe thickness <8mm
8. Decidual cyst
• TVS ectopic diagnostic criteria- Rottem et al (1991)

31. Other diagnostic modalities
• Laparoscopy- “Gold standard”
• Culdocentesis-
• presence of non-clotted blood in POD, Free fuid in this pouch
typically is not seen until accumulated volumes reach 400 to 600 mL
• If sonography is unavailable, culdocentesis is a simple technique and
was used commonly in the past
• Endometrial sampling

32. Differential diagnosis
• Obstetrics: Threatened, incomplete or septic abortion
• Gynecological: delayed menses, PID, ruptured or hemorrhagic corpus
luteum, adnexal torsion, DUB, endometriosis, Salpingitis,
degenerating fibroids, ovarian torsion, Tubo-ovarian abscess,
• Non-gynecologic: appendicitis, urinary calculi, gastroenteritis,
perforated peptic ulcers, intraperitoneal Haemorrhage
• Arias- stella reaction

33. Treatment
• Treatment option include: Expectant, Medical & Surgical management
• Option taken will depend on
1. Patient age
2. Future reproductive capacity
3. Nature of lesion: rupture status, location of the ectopic, & its size
4. Patients hemodynamic status

35. Expectant management :
• Only observation is done in hope of spontaneous resolution.
• no treatment is given, patient is admitted & vitals are monitored. b-
hCG levels are measured every 48 hours till they become ‘N’
• Indication:
• Decreasing serial β-HCG titres
• Tubal pregnancies only
• No evidence of intraabdominal bleeding or rupture assessed by vaginal
sonography
• Diameter of the ectopic mass< 3.5 cm (Preferably < 3 cm)
• Baseline hCG < 1000 IU/L and falling , best results are obtained if b-
hCG < 200 MIU/ml.

36. When to abandoned expectant management
• Significant increase in symptoms e.g. abdominal pain
• Serum hCG start to raise or fails to decrease
• Signs of tubal rupture
• Nb; A commitment to surveillance visits and relative proximity to
emergency care are safeguards

37. Medical management
• Fails in 5-10%
• Consider if surgical risk is unacceptably high & patient meets medical
criteria
• Single outpatient therapy versus multiple inpatient therapy
• Drug of choice: methotrexate
• Other experimental agents: potassium chloride, hyperosmolar glucose,
antiprogestin mifepristone (RU 480), prostaglandins
• Tubal rupture in 5-10% requiring emergency surgery

39. prerequisite for medical management
Ectopic <4cm with no cardiac activity
or <3.5cm with cardiac activity Plus
absence of free fluid in POD
Desire for future fertility
No evidence of tubal rupture
Serum hCG <3000- 15000 IU/L
Not breast feeding
Does not have coexisting intrauterine
pregnancy
Does not have known contraindication
to methotrexate
Hemodynamically stable & Has no
pelvic pain
Patient reliable & compliant: will
return for follow up
Availability of facility for follow up
care
No underlying severe medical
condition
Patient agrees to use reliable
contraception for 3-4 month post
treatment
No abnormalities of LFTs, RFTs &
CBC, showing normal liver, kidney &
bone marrow
Currently not taking NSAIDS,
diuretics, penicillin & tetracycline
group of drugs

40. Contraindications to medical management
Absolute
 Active Intraabdominal bleeding
 Breast feeding
 Alcoholism
 Immunodeficiency
 Liver & renal disease
 Blood dyscrasias
 Acute pulmonary disease
 Peptic ulcers
 Folic acid supplements
Relative
 Sexual intercourse
 Alcohol intake

41. Methotrexate
• Folic acid antagonist which inhibit DNA synthesis in actively dividing
cells. Binds to DHFR blocking active folate formation (THF)
• Success rate 94% in 3-7 weeks
• Side effects: bone marrow suppression, elevated liver enzymes,
alopecia, rash, stomatitis, nausea & vomiting
• Best predictor of success: hCG <5000IU/L
• Multiple dose superior to single dose
• Single dose: less expensive, lower side effects (29% vs 48%), require
less extensive monitoring, does not require rescue folinic acid

42. Contraindications to methotrexate
Absolute Relative
Pregnancy & lactation
Hepatic (>2 normal transaminase) , renal
(creatinine >1.5mg/dl) & hematological
dysfunction
Over or laboratory evidence of
immunosuppression with WBC <1.5 *109
Peptic ulcer disease
Alcoholism, alcoholic liver disease or other
chronic liver disease
Active pulmonary disease
Preexisting blood dyscrasias such as bone
marrow hypoplasia, leukopenia,
thrombocytopenia & significant Anaemia
Known sensitivity to methotrexate
Gestational sac > 3.5cm
Presence of cardiac activity
strenuous exercise

43. Methotrexate protocol
Single dose Multiple/variable dose
 Pretreatment investigation: CBC, LFTs, KFTs, serum hCG, ABO typing & Rh
antibody, TVS
 Pretreatment prerequisites: signed informed consent by partner & patient,
weight & height measurement and calculate BSA
 Mosteller formula: BSA (M2)= square root of {height (cm)* weight (kg)
divided by 3600}
 Dose= IM methotrexate 50mg/m2 on day 1 (day of treatment) plus RhoGAM
300mcg with the following instructions: avoid folic acid supplements, refrain
from strenuous exercise, alcohol and intercourse. Discontinue folinic acid
 Day 4 hCG measurement: baseline for subsequent measurements if >15% ok
 If<15% repeat dose then begin new day 1
 Day 7 hCG measurement: drop of >15% is ok. If day 7 hCG decline is < 15%
may give a second dose or if cardiac activity still present
 Weekly hCG till negative results or < 15 IU/L. if weekly hCG increase or
plateau second dose may be given
 Day 14 hCG measurement: if no drop in hCG surgical intervention indicated
 If symptoms worsen repeat TVS for possible rupture, AST levels, CBC,
 Any time perform Laparoscopy if severe abdominal pain, acute abdomen or
rupture develops
Indications: cervical ectopic &
Cornual ectopic
 Dosage: every alternate day of
1mg/kg of I.M Methotrexate
alternating with 0.1mg/kg of
I.M Leucovorin calcium for a
total of 4 doses (30 hours after
MTX dose)
{MTX days 1, 3, 5 & 7 and
Leucovorin on days 2,4,6 & 8}
 Follow up with CBC, LFTs,
RFTs, serum hCG at baseline,
day 1, day 3, day 5 and day 7
till hCG drops
 Weekly serum hCG till
undetectable or <5IU/L

44. Other measures in ectopic management
• Blood transfusion in anemia
• Analgesics
• Antibiotics if history of infection- doxycycline recommended
• Antiglobulin D 300mg if mother Rhesus negative With incompatibility
• Slow fluid infusion
• Until resolved avoid coitus, alcohol, folic acid supplements, NSAIDS ,
Sunlight(ACOG 2019)

45. Surgical treatment
• Surgical approach: open surgery (laparotomy) or minimally invasive
(laparoscopy)
• Surgical options: Salpingostomy, salpingectomy, salpingotomy
• Indications for surgical therapy
• Candidates not suitable for medical therapy
• Failed medical therapy
• Heterotopic pregnancy with viable intrauterine pregnancy
• Hemodynamically unstable patient & requires immediate treatment
• Preoperative preparation

46. Factors influencing surgical approach
• Choice of Laparotomy vs laparoscopy influenced by:
Prior multiple surgeries
Pelvic adhesions
Skills of the surgeon & surgical staff
Availability of the equipment's
Condition of the patient
Size & location of the ectopic

47. Pre-operative preparation
• Written informed consent
• Typed & crossed matched blood (ABO &Rh)- at least 4 units
• CBC
• RhoGAM be administered if Rh negative
• If hemodynamically unstable immediate resuscitation
• Inform theatre staffs, anesthetist
• Catheterization

48. Surgical approach
Laparoscopy Laparotomy
Advantages:
 fewer postoperative morbidity
 less postoperative pain hence less analgesic
use
 short Hospital stay
 reduced complication rates such as wound
infection & adhesion formation and
 faster recovery & return to normal activity
Possible laparoscopic complication
 Missed diagnosis
 Bleeding
 Incomplete removal of ectopic pregnancy
 Visceral injury
 Leakage of purulent exudates
 Intraabdominal abscess
Indications & advantages:
 Hemodynamically unstable patient
 Cervical, interstitial or abdominal ectopic
 Presence of >1500mls of hemoperitoneum or
large hematoma
 Underlying cardiac disease & COPD
 Prior abdominal surgery

49. Surgical options
Salpingectomy- removal of affected tube Salpingotomy-
indications:
 Severely damaged tube
 Uncontrolled bleeding
 Recurrence of ectopic on the same tube
 Tubal pregnancy wit Size >5cm
 Ruptured ectopic
 Completed family ( future pregnancy not
desired)
 Ectopic follows sterilization procedure or
tubal reconstructive surgery
 Patient requests sterilization
 Bleeding continues after salpingotomy
 Chronic tubal pregnancy
 no longer done but has same outcome
comparable to salpingostomy
 Here incision sutured
 Abandoned due to increased operation time
Salpingostomy
 Opening of the tube
 Incision over the ectopic, extract the ectopic & allow
healing without closure
 10-15% risk of persistent ectopic
Segmental resection & anastomosis (partial
salpingectomy)
 Used in unruptured isthmic tubal pregnancy because
salpingostomy may cause scarring & subsequent
narrowing of small isthmic lumen

52. Ovarian ectopic pregnancy
• Spielberg’s (1878) criteria for diagnosis of primary ovarian pregnancy
1. The tube on the affected side must be intact & distinct from ovary
2. Fetal sac must occupy the position of the ovary
3. The ovary must be connected to the uterus by the ovarian ligament
4. Ovarian tissue must be located in the sac wall
• Highest risk factors ART & IUD failure (24%)
• Clinical presentation: one third rupture may occur earlier
• Diagnosis: mostly surgical
• Treatment: mostly ovarian wedge resection or cystectomy for small lesion
and oophorectomy for larger lesions

53. Cervical ectopic pregnancy
• Cervical gland found histologically opposite placental attachment site
& part or all placenta found below the entrance of uterine vessels or
below peritoneal reflection on anterior uterus
• Incidence 1 in 8600- 1 in 12400, on rise due to ART
• Risk factor: D & C (70%), ART
• Presentation: painless PV bleeding (90%), massive hemorrhage,
• Medical treatment: offer medical if hemodynamically stable. Direct
injection of MTX or IM 50-75mg/m2 BSA into the sac +/- uterine
artery embolization +/- kill fetus in utero using 2ml of KCl

54. Cervical ectopic pregnancy
• Ultrasound criteria for cervical pregnancy (Paalman’s)
1. Echo-free uterine cavity or the presence of a false gestational sac
only
2. Hourglass uterine shape
3. Ballooned cervical canal
4. Gestational sac in the endocervix
5. Placental tissue in the cervical canal
6. Closed internal os

56. Management of cervical ectopic
• Surgical option: suction curettage or hysterectomy for advanced pregnancy
& unstable
• Failure rate higher for gestational age> 9 weeks, β-hCG levels > 10,000
IU/L, crown-rump length> 10 mm, and fetal cardiac activity
• Minimizing bleeding in cervical ectopic
1. uterine artery embolization
2. Local methotrexate injection into the amnionic sac before D & C,
3. ligation of the descending branches o the uterine arteries, or
4. Cerclage placement at the internal os to compress feeding vessels
5. Placement of 26F Foley catheter post D & C

57. Abdominal ectopic pregnancy
• May be primary or secondary implantation
• Studdiford’s criteria for diagnosis of primary abdominal pregnancy
1. Presence of normal tubes & ovaries with no evidence of recent or
past pregnancy
2. No evidence of uteroperitoneal fistula
3. Presence of a pregnancy related exclusively to the peritoneal surface
and early enough to eliminate the possibility of secondary
implantation after primary tubal nidation

58. Management of abdominal ectopic
• Diagnosis is difficult due to absent or vague symptoms, uninformative
laboratory, abnormal fetal positions & uninformative sonography
• Oligohydramnios common
• MRI best
• Conservative management carries risk for massive hemorrhage, fetal
malformation & deformation (20%) hence terminate if <24 weeks
• If reached viability deliver the baby & choose your option carefully in
managing the placenta

59. Cesarean scar pregnancy
• Incidence 1 in 2000 pregnancies, increased with increases cs rates
• Pathogenesis follows similar to placenta accrete
• Diagnosis: sonographic criteria for diagnosis
1. An empty uterine cavity
2. An empty cervical canal
3. A gestational sac in the anterior part of the uterine isthmus
4. Absence of healthy myometrium between the bladder and
gestational sac

60. Management of CSP
• Treatment standards lacking
• Expectant management: 57% live birth report but risk of hemorrhage,
placenta accreta syndrome & uterine rupture
• Hysterectomy better initial option if done with family or fertility-
preserving medical & surgical options
• Uterine artery embolization to minimize bleeding, balloon tamponade
• Long term complications: uterine arteriovenous malformations

61. Interstitial pregnancy
• Implantation within the proximal part of the tube
• Occasionally carried to viability due to greater distensibility of the
myometrium covering interstitium but can cause severe bleeding due
to proximity to uterine ad ovarian vessels
• Mortality as high as 2.5%
• Also referred incorrectly to as cornual pregnancy
• Risk factors: prior ipsilateral salpingectomy
• Presentation: rupture may occur at 8-16 weeks,

62. Management interstitial ectopic
• Diagnosis difficult but the following criteria is helpful
• Empty uterus
• Gestational sac seen separate from the endometrium& > 1cm away
from the most lateral edge of the uterine cavity
• Thin, <5mm myometrial mantle surrounding the sac
• “Interstitial line sign” echogenic line extending from the sac to the
endometrial cavity
• Laparoscopic evidence of enlarged protuberance outside the round
ligament

63. Management
• Cornual wedge resection or cornuostomy with intraoperative
intramyometrial vasopressin injection to limit bleeding
• Also a role for medical management but protocol lacking
• Needs longer follow up with β-hCG due to higher initial β-hCG
• Consider caesarian for subsequent pregnancy
• Angular pregnancy sometimes carried to term displaces the round
ligament upward & outward but interstitial does not

64. Heterotropic pregnancy
• A uterine pregnancy in conjunction with an extrauterine pregnancy
• Earlier incidence 1 per 30,000 pregnancies, now 1 per 7000 following
ART & 1 per 900 with ovulation induction
• Suspect if
1. Persistent or rising hCG following D& C
2. More then one corpus luteum
3. Absence of vaginal bleeding with signs & symptoms of ectopic
pregnancy
• Mgt – surgical resection/aspiration, intralesional KCL or Glucose
(hyperosmolar) MTX avoided

65. Complication
• Usually results from late diagnosis
• Tubal rupture
• Hemorrhagic shock, DIC, death
• Surgery &Recurrent ectopic pregnancy
• Persistent trophoblast (5-15%)
• anaesthesia: infection, visceral injury
• Infertility

66. Prognosis
• Haemorrhage is the main cause of death
• >60% will become pregnant again
• Presence of contralateral tubal damage reduces chances of successful
conception
• Risk of subsequent pregnancy becoming ectopic is 10-20% compared
to 1% in general population

67. Reference
• William obstetrics 26th edition
• William gynecology 3rd edition
• Llewellyn- Jones Fundamentals of obstetrics and Gynaecology 10th
edition by Jeremy Oats and Suzanne Abraham
• ACOG :Tubal Ectopic Pregnancy 2018
• UP TO DATE