Practical Manual of Obstetrics Amitava Pal, Rupali Modak
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SpecimensCHAPTER 1

 
ECTOPIC PREGNANCY
 
Specimen of Tubal Pregnancy
Que. How do you identify the tubal ectopic pregnancy?
Ans. Identify the fallopian tube and confirm it by fimbrial end and look carefully, whether ovary is attached with it or not and the ectopic pregnancy is in tube, so this specimen is unruptured tubal ectopic pregnancy (Figure 1.1A).
Que. Which operation is performed here?
Ans. Salpingectomy of the affected tube.
Que. Do you know any other management of unruptured tubal ectopic pregnancy?
Ans.
  1. Medical management (discussed later).
  2. Conservative surgery by salpingostomy or laparoscopic aspiration.
Que. What is ectopic pregnancy?
Ans. Any pregnancy, where the fertilized ovum is implanted in any site other than normal uterine cavity is called ectopic pregnancy.
Que. What is the incidence of ectopic pregnancy in fallopian tube?
Ans. 95% to 99%.
zoom view
Figure 1.1A: Unruptured tubal ectopic pregnancy
zoom view
Figure 1.1B: Tubal mole (Black spot marked by arrow) on cut section
2Que. What is the commonest site of tubal ectopic pregnancy?
Ans. Ampulla (78%) as it is the normal site of fertilization.
Que. What is the incidence of ectopic pregnancy in other part of the tube?
Ans. Fimbrial—5%; Isthmic—12%; Interstitial—2% to 3%.
Que. What are the causes of ectopic pregnancy?
Ans.
  1. Acquired causes:
    1. Pelvic inflammatory disease (PID).
    2. Surgical:
      • Surgical reconstruction of tube (Tuboplasty)
      • Spontaneous recanalization occurs after ligation
    3. Intrauterine contraceptive device (IUCD).
    4. Endometriosis.
    5. Broad ligament tumor and ovarian tumor—kinking of the tube.
    6. In vitro fertilization (IVF) and gamete intrafallopian transfer (GIFT).
  2. Congenital
    Hypoplasia, undue tortuosity of the tube and accessory lumina.
Que. What is the outcome of ectopic pregnancy?
Ans.
  1. Tubal abortion—complete or incomplete.
  2. Tubal mole—the dead ovum remains in the tube and subjected to repeated small choriodecidual hemorrhage, which convert it to carneous mole. If pregnancy is small, the mole absorbed partially and give rise to a small and often symptomless hematosalpinx.
  3. Tubal rupture—intraperitoneal/extraperitoneal (Common in isthmic ectopic pregnancy).
  4. Secondary/abdominal pregnancy.
Que. What are the clinical types of ectopic pregnancy?
Ans. Chronic (common) and acute type.
Que. How do you diagnose chronic ectopic pregnancy?
Ans. History
  1. The patient has a short period of amenorrhea.
  2. Symptoms of early pregnancy—nausea, breast tenderness.
  3. Abdominal pain due to:
    • Distension of the tube
    • Choriodecidual hemorrhage
    • Escape of blood in the peritoneal cavity (associated with syncope).
      (Combination of abdominal pain and syncopal attack is the most important symptom of ectopic pregnancy).
      3
  4. Vaginal bleeding—mild, following pain. This is uterine in origin due to separation of decidua.
  5. Shoulder tip pain may occur in heavy peritoneal collection of blood and when the patient is lying down.
  6. A large pelvic hematocele may cause retention of urine.
On examination (O/E)
  1. Pallor+, pulse rate (PR) is high, intermittent pyrexia.
  2. Early pregnancy change of breast.
  3. Tenderness and muscle guard over lower abdomen.
  4. Intestinal distention by peritoneal fluid.
  5. Hemoperitoneum of 2 to 3 weeks causes bruising around umbilicus (cullen's sign)—not so common.
Per vaginal (P/V)
  1. Irregular tender mass on the affected side felt through the fornix.
  2. Ill-defined tender semisolid swelling in pouch of douglas (POD).
  3. Arterial pulsation through the fornix (occassionally).
Investigations
  1. Hemoglobin percent (Hb%)—lower, leukocyte count is high, pregnancy test is positive in 50 percent of cases.
  2. Ultrasonography (USG)—Bagel sign—on endovaginal sonography (EVS) hyperechoic ring around the gestational sac in the adnexal region, but more often they are seen as a small inconglomerate mass near the ovary with no evidence of sac or embryo—blob sign. Hemoperitoneum may also be found. Transvaginal sonography (TVS) can diagnose 80 percent of ectopic pregnancy.
  3. Laparoscopy—is helpful for diagnosis of ectopic pregnancy (EP).
  4. Culdocentesis:
    • +ve inference—0.5 mL of unclotted blood
    • -ve inference—0.5 mL of serous blood
    • Indeterminate—no fluid.
  5. Final diagnosis—by laparotomy.
Important finding
If beta-human chorionic gonadotropin (β-hCG) is not detected in serum, the diagnosis of ectopic pregnancy is ruled out. In 90 percent of ectopic pregnancy, β-hCG level is less than 6,500 m IU/mL. It has also shown that if percent increase in β-hCG during 2 days period (48 hours) is less than 66 percent, the chance to ectopic pregnancy is high.
4Que. How do you diagnose a case of ruptured ectopic pregnancy?
Ans. History
  1. Short period of amenorrhea.
  2. Excruciating pain in the hypogastrium.
  3. Features of shock (pallor, low blood pressure (BP), PR increased, cold clammy skin, oliguria).
O/E
  1. Features of shock.
  2. Presence of free fluid may cause dullness of lower abdomen.
P/S
Vagina is pale.
P/V
  1. Acute tenderness and pain due to movement of cervix by vaginal examination is the leading sign.
  2. POD is often felt soft, fluctuant, full and tender due to pelvic hematocele.
Investigations
  1. Complete blood count (CBC), Hb%—low.
  2. USG—empty cavity with fluid in POD/abdomen.
  3. Culdocentesis—Aspiration contains blood.
Que. How do you manage a case of ectopic pregnancy?
Ans. Resuscitation and operation will go side by side. Resuscitation is done by moist oxygen, intravenous (IV) fluid (by ringer lactate [RL], normal saline [NS] or plasma expander, blood) operation— Laparotomy is followed by:
  1. Salpingostomy: A linear incision over ectopic pregnancy along the antimesosalpinx border provided the pregnancy is in ampullary part and size is less than 5 cm. It is not suitable in the isthmic pregnancy.
  2. Segmental excision and end to end anastomosis for isthmic pregnancy.
  3. Milking of the tube—in ampullary pregnancy, where pregnancy can be easily dislodged.
  4. Salpingectomy: Removal of the affected tube is the usual procedure.
    (Portion of the tube should always be examined histologically and bacteriologically for tuberculosis [TB]).
Note: See gynecological part for details of operation on ectopic pregnancy.
5Que. Do you remove ovary during salpingectomy operation?
Ans. No, It is always preserved for future pregnancy, but it is removed if it is pathological.
Que. How do you diagnose early unruptured ectopic pregnancy and how do you manage it?
Ans. The likelihood of EP is suspected in woman who has just missed period and experience abdominal pain or vaginal bleeding, especially when a patient has a past history of PID/infertility/tubal surgery/medical termination of pregnancy (MTP) or using IUCD.
Diagnosis
  1. By USG (EVS)—empty uterine cavity and adnexal mass.
  2. β-hCG—in normal pregnancy, this hormone level doubles every 2 days; in abnormal gestation, the rate is much lower or absent.
  3. Color flow dopplor—see USG in obstetrics.
Note: Vaginal USG can detect EP at 5 to 6 weeks when β-hCG value is lower than 2,500 IU/mL.
Que. What are the criteria for medical treatment?
Ans. The criteria for the medical treatment are as follows:
  1. Patient is of good health, hemodynamically stable and able to follow-up examination
  2. Unruptured EP
  3. No evidence of intrauterine pregnancy
  4. Ectopic mass is less than 3.5 cm
  5. hCG less than 10,000 IU/l
  6. No yolk sac seen
  7. No fetal heart tone.
Que. What are the agents used for medical management of EP?
Ans. Methotrexate, mifepristone, potassium chloride, actinomycin, prostaglandins (PGs), hyperosmolar glucose, anti-hCG antibodies.
Que. How methotrexate is used?
Ans.
  1. Intrasac methotrexate by EVS guidance, where reduced dose is required.
  2. Systemic injection of methotrexate is used, 50 mg/m2 is administered on day 0. Up to 13 percent of cases required second dose if the hCG level does not reduce by 15 percent between 4 to 7 days.
Another regime—injection methotrexate, 1 mg/kg body weight (BW) should be given on day 1, 3, 5 with folinic acid on day 2, 4, 6.
6Que. How methotrexate act?
Ans. Methotrexate is a folic acid antagonist and folate is essential for deoxyribonucleic acid (DNA) synthesis and effective against rapidly dividing cells.
Que. What are the contraindications of methotrexate therapy?
Ans. Intrauterine pregnancy, severe anemia, leucopenia (< 3 × 109/l), thrombocytopenia, active infection, human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), renal and liver disease, peptic ulcer and ulcerative colitis. Other relative contraindications—gestational sac >3.5 cm, embryonic cardiac activity present.
Que. What will you do in case of failure of methotrexate therapy?
Ans. Repeat the dose; if fails to resolute, go for surgery.
Que. When do you choose the procedure for laparoscopic surgery?
Ans.
  1. The EP sac must be less than 4 cm in diameter
  2. It is easily approachable.
Que. What are the indications of hysterectomy in case of disturbed ectopic pregnancy?
Ans. Patient's age greater than 40 years when associated with:
  1. Ectopic pregnancy due to widespread pelvic adhesion.
  2. Uterus is diseased.
  3. When the patient is in a good condition.
  4. Interstitial pregnancy.
Que. What is interstitial pregnancy?
Ans. When the implantation occurs in the interstitial portion of the tube.
Que. When does it rupture?
Ans. It ruptures around 16 to 20 weeks.
Que. How do you diagnose this condition?
Ans. Diagnosis is very difficult and confused with pregnancy in bicornuate uterus, pregnancy with fibroid uterus, pregnancy in a rudimentary horn.
There may be asymmetrical enlargement of one cornu.
Que. How do you treat this case?
Ans. Surgical
  1. Patient does not wish for further pregnancy—Total abdominal hysterectomy (TAH).
    7
  2. If patient wishes for further pregnancy—partial hysterosalpingectomy, but there is a risk of rupture of the uterus in future pregnancy.
Que. What is the incidence of ovarian pregnancy?
Ans. 1 Percent of all EP.
Que. What are the types of ovarian pregnancy?
Ans. Intrafollicular, extrafollicular or combined.
Que. Can you diagnose ovarian pregnancy preoperatively?
Ans. It is very difficult to diagnose it preoperatively with certainty.
Que. What are Spielberg's criteria?
Ans.
  1. The tube on the affected side must be intact.
  2. The fetal sac must occupy the position of ovary.
  3. The ovary and the sac must be connected with the uterus by ovarian ligament.
  4. Definite ovarian tissue must be present in the wall of the sac.
Que. What is the treatment of ovarian pregnancy?
Ans. At operation, the affected ovary usually has to be sacrificed.
Que. What is the cornual pregnancy?
Ans. Implantation occurs in the rudimentary horn of the uterus. This horn does not always communicate with the rest of the uterine cavity. Spermatozoa ascends through the other horn of uterus and tube and fertilize in the peritoneal cavity, this then enter the tube of rudimentary horn.
Que. What is the fate of cornual pregnancy?
Ans. Rupture of the horn occurs at 12 to 20 weeks of pregnancy with intraperitoneal hemorrhage and shock.
Que. What is the D/D of cornual pregnancy?
Ans. Uterine fibroid, ovarian tumor, interstitial type of tubal pregnancy.
Que. How can you differentiate it from interstitial pregnancy?
Ans. Position of the round ligament, which is attached lateral to the sac and the long pedicle by which it is attached to the uterus.
Que. What is the treatment?
Ans.
  1. Remove the rudimentary horn.
  2. If the pedicle is short and attachment is wide, hysterectomy is the treatment of choice.
8Que. Which abdominal pregnancy is common?
Ans. Secondary due to ruptured tubal pregnancy (1 in 15,000 births).
Que. How do you diagnose secondary abdominal pregnancy?
Ans.
  1. X-ray of abdomen:
    • Absence of uterine outline and placental shadow
    • Intermingling of maternal gas shadow with the fetal parts (Bishop's sign)
    • An abnormal high position of fetus
    • Fetal parts overlapping maternal spine in the lateral view (Weinberg's sign).
  2. USG of abdomen.
Que. How do you treat such patient?
Ans.
  1. As soon as diagnosis is made laparotomy should be done as the delay may lead to spontaneous intraperitoneal hemorrhage.
    • Removal of the placenta, if it is not adherent to any vital organ.
    • If adherent to broad ligament and uterus, go for hysterectomy.
    • If placenta is adherent to bowel then cut the cord, close to the placenta and leave it. It usually gets absorbed or occasionally forms abscess.
    • The place of methotrexate is doubtful in this case.
Que. What are nontubal ectopic pregnancies?
Ans. They are cervical pregnancy, abdominal pregnancy, and ovarian pregnancy.
Que. What is cervical pregnancy?
Ans. Cervical pregnancy is one that implants entirely within the cervical canal.
Que. What is the incidence of cervical pregnancy?
Ans. 1:250 to 1:18000 deliveries (0.2% of ectopic pregnancies).
Que. What are the predisposing factors of cervical pregnancy?
Ans.
  1. Therapeutic abortion previously
  2. Previous cesarean section
  3. Asherman's syndrome
  4. IUI and IVF.
Que. What are the clinical criteria of diagnosis of cervical pregnancy?
Ans.
  1. The distended cervix is smaller on P/V examination
  2. On curettage, no evidence of trophoblastic tissue
  3. The product of conception is confined within the cervix
  4. The internal os is closed.
9Note: Cervical pregnancy is associated with profuse vaginal bleeding without abdominal pain.
Que. What is the USG criteria for diagnosis of cervical pregnancy?
Ans.
  1. Ballooning of cervical canal
  2. Gestational sac is within the endocervix
  3. Internal os is closed
  4. No evidence of intrauterine pregnancy.
Que. What is Rubin's criterion for diagnosis of cervical pregnancy?
Ans.
  1. There must be cervical gland opposite to placental attachment
  2. The placental attachment to the cervix must be intimate
  3. The whole or a portion of the placenta must be situated below the entrance of uterine vessels or below the peritoneal reflection of the anterior and posterior surface of the uterus
  4. No fetal element should be present in the corpus uteri.
Que. Management of cervical ectopic pregnancy?
Ans.
  1. Hysterectomy is the only treatment of choice
  2. Other surgical alternatives less radical to hysterectomy are sometime helpful
    1. D and C operation
    2. To control bleeding
      1. Packing of the uterus and cervix
      2. Intracervical 30 mL Foley's catheter
      3. Deep lateral cervical stitches or placement of cervical circlage
      4. In some cases bilateral internal iliac artery ligation.
  3. Medical—Some patients may be treated with methotrexate either intraamniotically or systematically. Therapeutic success has been reported with the use of etoposide or combination chemotherapy.
 
RUPTURE OF UTERUS
The specimen is of uterus (subtotal hysterectomy) where tubes and ovaries are absent, cervix is also absent.
Que. Why this operation was done?
Ans. This was done for rupture of uterus.
Que. What are the causes of uterine rupture during pregnancy?
Ans. Spontaneous rupture (rare)
  1. Congenital maldevelopment of uterus—rupture commonest at mid trimester.
  2. Spontaneous rupture at last trimester
    10
    zoom view
    Figure 1.2: Rupture of uterus (Subtotal hysterectomy done)
    • Previous operation (myomectomy or classical cesarean section [CS])—common
    • Old perforation (MTP).
Traumatic (rarest)
Fall, crushing accident or blow on abdomen.
Que. How do you diagnose rupture of uterus during pregnancy?
Ans.
  1. Acute abdominal pain with features of shock
  2. Contracted uterus is felt as a suprapubic mass
  3. Easily palpable fetus.
  4. Fetal heart sounds (FHS)—absent.
Que. What are the causes of rupture of uterus during labor?
Ans. Spontaneous
  1. Obstructed labor—malpresentation, malposition, cephalopelvic disproportion (CPD), hydrocephalus.
  2. Multiparity—causes more fibrous tissue and malnutrition produces certain changes in myometrium and susceptible to rupture.
  3. The cesarean or hysterotomy scar rupture (very common).
  4. Injudicious use of oxytocics.
Traumatic
  1. Internal version.
  2. Extraction of fetus through the incomplete dilated cervix
  3. Operative delivery like difficult forceps, craniotomy, decapitation.
Que. What are the different types of rupture pathologically?
Ans.
  1. Complete: When all the coats of the uterus are involved including peritoneum.
    11
  2. Incomplete: When peritoneum is not involved.
    • Spontaneous rupture is more often complete than incomplete
    • Traumatic rupture is more often incomplete than complete.
Que. Is rupture of lateral wall of uterus complete or incomplete?
Ans. Lateral wall of pregnant uterus is uncovered by peritoneum. Rupture of this site may include whole thickness of muscular wall of uterus and still be incomplete, as it only opens up the broad ligament, but does not tear the peritoneum.
Que. Why incomplete rupture and broad ligament hematoma is more common on left side of the uterus?
Ans.
  1. Dextrorotation of the uterus expose lateral wall to increased stress of labor.
  2. Passive venous congestion in the left broad ligament due to left ovarian vein draining into the left renal vein at right angle.
Que. Rupture is more common in classical CS than LSCS, why?
Ans. Rupture of classical CS is 2 percent and half of these cases occur before the onset of labor. Rupture in lower segment cesarian section (LSCS) is rare (0.4% or less).
Note: Two previous sections carry 3 to 5 folds increased risk over one previous section.
Rupture occurs due to the following reasons:
  1. Defective healing of classical scar due to contraction and relaxation in uterine involution.
  2. Difficulty in approximation of edges.
  3. Incomplete hemostasis and infection.
  4. Placenta on the scar makes the scar tissue weak.
Que. What are the signs and symptoms of rupture uterus in labor?
Ans.
  1. Signs of prolonged and difficult labor.
  2. Acute pain on lower abdomen.
  3. Previous labor pain stops when rupture occurs.
  4. Shock appears due to intraabdominal hemorrhage.
  5. The uterine outline is completely lost and fetus is felt most superficially when palpating the patient's tender abdomen.
  6. FHS is absent.
Vaginal examination
  1. Hemorrhage through the cervical orifice (os).
  2. The presenting part often goes up.
  3. Hematuria on catheterization if bladder is involved.
  4. Cervix hangs like a curtain.
12In an atypical case
  1. General condition is satisfactory.
  2. The uterine outline is intact if rupture is incomplete.
  3. Tenderness and fullness in suprapubic and iliac region.
  4. The FHS is absent or irregular.
  5. An unexplained collapse during the late first and early second stage of labor with tender inert uterus with slight bleeding should suggest rupture of uterus and not accidental hemorrhage.
  6. When a patient collapse after difficult vaginal delivery, it is advisable to explore the uterus after manual removal of placenta (MRP).
Que. How do you manage the case?
Ans. General:
  1. Stop oxytocin, if running.
  2. Start IV fluid (NS/RL).
  3. Blood transfusion in severe hemorrhage.
  4. Continuous maternal monitoring.
  5. Emergency laparotomy with rapid operative delivery.
Definitive repair of the tear:
  1. If the tear is small.
  2. There must be strong reason to preserve the uterine function.
  3. Clean wound and edges are not ragged as in rupture of LSCS scar.
  4. If patient does not want issue perform tubal ligation with repair.
Note: If patient wishes to have pregnancy go for elective CS in future before term in tear repair cases without ligation.
Hysterectomy:
  • When the tear is irregular, irreparable and edges are friable.
  • In colporrhexis.
  • Lateral tears with broad ligament hematoma.
  • When the uterus is infected.
    If bladder is involved—repair of bladder in two layers followed by hysterectomy and Foley's catheter is kept in bladder for 10 days.
Que. What are the postoperative complications?
Ans. Hemorrhage, shock, peritonitis, rarely pulmonary embolism.
 
HYDATIDIFORM MOLE (SYNONYMS VESICULAR MOLE, GESTATIONAL TROPHOBLASTIC DISEASE)
Que. What is this specimen?
Ans. This is the specimen of hydatidiform mole.
(Description of the specimen—cystic grape-like structures from pin head to large size).
13Que. What is the histology? What is the histological classification?
Ans.
  1. Trophoblastic proliferation of cytotrophoblast and syncytiotrophoblast.
  2. Hydropic changes in the stroma with cistern formation.
  3. Absence of fetal blood vessels.
Histologically:
  1. Hydatidiform mole (Complete and partial)
  2. Invasive mole (chorioadenoma destruens)
  3. Chorio-carcinoma
  4. Placental site trophoblastic tumor.
Que. What are the risk factors of H mole?
Ans.
  1. Maternal age greater than 40 years.
  2. Teen age less than 19 years.
  3. Asian woman.
  4. Malnutrition.
  5. Immunologic and genetic factors are also responsible.
Que. What is the complete mole?
Ans. Complete mole (without embryo or fetal remnants) has 90 percent of 46 XX karyotype.
In 10 percent of cases, 46 XY are present. Chances of malignancy are high in this case.
zoom view
Figure 1.3: Specimen of hydatidiform mole
zoom view
Figure 1.4: Complete mole
14
zoom view
Figure 1.5: Partial mole
Que. What is partial mole (with embryo-fetus)?
Ans. Karyotype is 69 XXY. Fertilization by two sperms, one with 23 X and another with 23 Y (dispermy) with normal ovum containing 23 X.
Fetal tissue is present.
Less likely to develop malignant change
Que. Define H mole.
Ans. It is a non-invasive abnormal placenta charecterized by enlarged, edematous chorionic villi with variable amounts of proliferative trophoblast.
Que. Why H mole is formed?
Ans.
  1. Primary death of fetus results in failure in villus circulation and consequence edema and liquefaction of stroma.
  2. Primary error in the development of the vessels in the core causing villus to become overloaded with fluid and food staffs, the later then provide epithelial cells with excessive growth stimulus for proliferation.
  3. Anoxia causes active fluid secretion into the core of the villus, as well as cellular hyperplasia.
Que. How does the patient present?
Ans.
  1. Period of amenorrhea—8 to 12 weeks or more.
  2. Vaginal bleeding.
  3. Pain abdomen.
  4. Passage of grape-like vesicles.
  5. Excessive vomiting, hypertension.
  6. Fetal movement is absent if gestational age (GA) greater than 20 weeks.
Que. How will you diagnose H mole?
Ans.
  1. History
  2. General survey—anemia, BP (may increase), hyperthyroidism in 1 percent case.
P/A
  1. Uterine size is enlarged than period of amenorrhea in 50 percent of cases, in some cases size correspond or even less, due to discharge of moles per vagina.
    15
    zoom view
    Figure 1.6: USG—H mole
  2. Doughy feeling, i.e. no fetal part felt.
  3. FHS—absent.
P/V
  1. Os—closed, internal ballottement is absent.
  2. Bilateral cystic enlarged ovary in 25% to 50% of cases (Lutein cyst).
  3. Bloody discharge.
  4. Discharge of vesicles (50%).
Investigations
  1. β-hCG level is very high, both in urine and blood—urinary hCG level, of 3,50,000 to 5 million IU/L above 100 days, is strongly indicative. Biweekly rising titer is helpful.
  2. Sonography—‘snow storm appearance’
    • Sonolucent area due to blood clot
    • Absence of gestational sac at 5 to 7 weeks
    • Repeat scan a week later.
      (D/D of snowstorm appearance—missed abortion, degenerated fibroid).
  3. Others—Renal, hepatic and thyroid function test, chest radiography.
Que. What are the complications of H mole?
Ans.
  1. Hemorrhage
  2. Shock
  3. Sepsis
  4. Perforation
  5. Malignant change (5%).
16
Que. What are the high-risk factors for malignancy in H mole?
Ans.
  1. Complete mole
  2. Bilateral theca lutein cyst (& 6 cm)
  3. Age above 40 years
  4. Serum hCG—1 million U/L before starting treatment.
Que. How do you treat a case of H mole?
Ans.
  1. Start IV drip with RL oxytocin is administered only after dilatation of cervix and partial evacuation to aid hemostasis.
  2. Grouping and cross matching for blood
  3. Antibiotic by IV route
  4. Early evaluation
  5. Partial expulsion:
    • Os open—suction evacuation by cannula with 10 units of syntocinon
    • Os closed—Slow dilatation by—laminaria tent and cerviprime (intracervical) gel or misoprostol per vagina and then suction curettage.
    At the end of first week, repeat curettage for complete evacuation of uterus and sending the material for histopathological (H/P) examination is not mandatory. It is done only in presence of persisting trophoblast in the uterine cavity. Repeated evacuation may cause high chance of requiring chemotherapy and may increase rate of complications.
Total hysterectomy (surgical extirpation of adenexa even for benign indication)
  1. If patient's age greater than 35 years
  2. Elderly with completed family
  3. Perforating mole and placental site trophoblastic tumor
  4. Patient not responding to chemotherapy.
Hysterotomy
Seldom done now-a-days, done in case of excessive bleeding, vomiting, oliguria, but tightly closed cervix.
Patient should be followed up for 2 years.
Theca lutein cysts: It disappears after several weeks of molar evacuation. Enlarged cyst may undergo torsion, infraction or rupture, and oophorectomy should be considered in these conditions.
Que. What is the risk of recurrence in H mole?
Ans. 0.8% to 2.9% risk of recurrence after one mole and 15% to 18% after two moles.
17Que. When will you start chemotherapy?
Ans.
  1. In high-risk groups (as mentioned above)
  2. When the patient cannot be followed up properly
  3. High level of hCG persisting for 2 months after evacuation
  4. Any detectable hCG in the serum after 6 weeks
  5. Persistent uterine bleeding, even if trophoblastic tissues are not available by curettage. This is the indication of myometrial invasion
  6. Evidence of metastasis in brain and lungs.
Que. Which drug is used in prophylactic chemotherapy?
Ans. Oral methotrexate 5 mg TDS × 5 days. A total of 3 courses are given at a gap of 5 to 7 days.
Que. How do you follow up a case of H mole?
Ans. Protocol:
Weekly for 8 weeks, monthly for 10 months and 3 monthly for 2 years and patient should not conceive for 1 year.
Procedure
At each visit, history relevant to:
  1. Irregular bleeding P/V
  2. Central nervous system (CNS) disturbances like headache, vomiting
  3. Hemoptysis and breathlessness.
A full abdominal and pelvic examination for:
  1. Vaginal secondaries
  2. Subinvolution of uterus
  3. Theca lutein cyst.
A chest X-ray is advised routinely on diagnosis of H mole, if it is normal it is repeated monthly, until hCG becomes normal. Serum. β—hCG assay at each visit—becomes negative after 6 weeks in majority of cases; in few cases, the titer becomes high, even after normal level of β—hCG later on. When it is high, exclude:
  1. Pregnancy
  2. Choriocarcinoma
  3. Enlarged ovary.
Que. What are the criteria for repeat curettage?
Ans.
  1. Irregular bleeding P/V
  2. The uterus does not involutes satisfactorily
  3. If β—hCG level is still positive, 6 weeks after evacuation.
18Que. What is the contraceptive practice in H mole?
Ans.
  • Patient should not be allowed to become pregnant for 1 year
  • IUCD—no, for irregular bleeding
  • Condom—preferable
  • Low-dose oral contraceptive pill (OCP)—use, after β—hCG level becomes normal.
FOR POSTGRADUATES
Que. What are the different types of gestational trophoblastic neoplasia?
Ans.
  1. Non-metastatic: No evidence of disease outside the uterus. (Treatment: Single agent chemotherapy—methotrexate—0.4 mg/kg day IV or intramuscularly [IM] for 5 days course and repeat the same dose after 7 to 10 days). [Day 1, 3, 5, 7 with methotrexate Injection with folinic acid 0.1 mg/kg per day on 2, 4, 6, 8th day]
  2. Metastatic: Any disease outside the uterus.
Good prognosis of metastatic disease
  1. Short duration less than 4 months.
  2. Urinary hCG less than 1,00,000 IU/24 hours or serum β-hCG less than 40,000 IU/mL.
  3. No metastasis to brain or liver.
  4. No significant prior chemotherapy.
Metastatic poor prognosis
  1. Long duration greater than 4 months.
  2. Urinary hCG greater than 1,00,000 IU/24 hours or serum β-hCG greater than 40,000 IU/mL.
  3. Metastasis to brain and liver.
  4. Unsuccessful prior chemotherapy.
  5. Gestational trophoblastic tumor following term pregnancy.
Que. What is the protocol of MAC regime?
Ans. Chemotherapy of poor-prognostic disease
  1. Methotrexate—10 to 15 mg/day IV or IM
    Dactinomycin—10 to 12 µg/kg/day IV
    Chlorambucil—8 to 10 mg/day per mouth or Cyclophosphamide—3 to 5 mg/kg/day IV
    1. Give the course for 5 days
    2. Repeat the cycle with minimum interval of 10 to 14 days as toxicity allows.
    1. Continue repetitive chemotherapy three courses after negative serum β-hCG titer.
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    2. Remission is defined as three consecutive normal weekly β—hCG titer.
Switch on to alternative chemotherapy
  1. Titer rise (10 fold or more)
  2. The plateau after two courses of MAC regime
  3. New metastasis appear
Do not begin or continue a course of chemotherapy, if white blood cell (WBC) count less than 3,000/µL
Granulocytes less than 1,500/µL
Platelet count less than 1, 00,000/µL
Blood urea nitrogen (BUN), serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT) serum bilirubin significantly elevated, laboratory values obtain daily during treatment cycle.
Que. What is alternative chemotherapy for poor prognosis patient of choriocarcinoma?
Ans. EMA-CO (E—etoposide, M—methotrexate, A—dactinomycin, C—cyclophosphamide, O—vincristine).
Que. What is invasive mole?
Ans. It is a type of invasive mole that penetrates the uterine wall and causes internal hemorrhage.
Que. Differences between invasive mole and choriocarcinoma.
Ans. Invasive mole
  1. Villus structure is present. Trophoblastic invasion of uterine wall and not the blood vessels.
  2. Locally malignant and does not kill the patient by distant metastasis.
Choriocarcinoma
Villus structure is absent. Invasion of myometrium, blood vessels, tissue necrosis and hemorrhage, kills the patient by distant metastasis to lungs and brain.
Que. What is the treatment?
Ans.
  1. Correction of anemia, multiparity—total hysterectomy
  2. Conservative chemotherapy till the lesion regresses and pulmonary deposit disappear spontaneously
  3. Vaginal deposits removed and pulmonary deposit disappears spontaneously.
Que. What is the partial molar degeneration of placenta?
Ans. In this case, only a part of the placenta undergoes molar changes, the rest of it remains normal. So, a fetus is usually present. This 20condition may occur in singleton pregnancy, but more common in multiple pregnancies. USG helps to diagnose the condition.
Que. What will you do if complete hydatidiform mole coexists with two fetuses?
Ans. In the past, it was terminated immediately following the diagnosis. The circumstances have been changed in recent years. The absolute indication of immediate evacuation of pregnancy includes:
  1. Development of pre-eclampsia (severe, not managed by medical treatment)
  2. Intractable vaginal bleeding
  3. Severe hyperemesis gravidarum
  4. Hyperthyroidism
  5. Evidence of trophoblastic embolism.
Some authors have also suggested that, in the absence of fetal anomalies, the pregnancy can be allowed to continue upto term irrespective of the development of persistent gestational trophoblastic disease (PGTD) provided there are no other complications as mentioned above.
Que. What is the incidence of H mole with a coexistent fetus?
Ans. The incidence is very rare; 1 in 22,000 to 1,00,000 pregnancies.
Que. What is placental site trophoblastic tumor (PSTT)?
Ans. This is an uncommon trophoblastic tumor composed principally of cytotrophoblast cells and the lesion is microscopic to follow a soft, brown, partly hemorrhagic mass, which protrude in the uterine cavity and infiltrate the uterine musculature. In addition to vaginal bleeding, cytotrophoblast cells produce hPL producing hyperprolactinemia which can result amenorrhea and galactorrhea.
Que. How does it differ from choriocarcinoma?
Ans. This produces relatively little hCG than choriocarcinoma in relation to the size of tumor. There is typical myometrial invasion with rare systemic metaslatis.
Que. How do you treat placental site trophoblastic tumor?
Ans. Curettage is not generally done as it causes perforation due to uterine muscle infiltration. Treatment of choice is hysterectomy.
Que. What is the fate of placental site trophoblastic tumor?
Ans.
  1. It may be benign with a capacity for spontaneous regression.
  2. It may be highly malignant with resistance to cytotoxic drugs.
21Que. Is there any requirement of anti-D globulin in Rh -ve mother with molar pregnancy?
Ans. Anti-D globulin should be given to the mother if she is Rh -ve for all practical purpose, irrespective of complete or partial mole.
Note: See also the specimen of chorio carcinoma in gynecological part.
 
PLACENTA WITH UMBILICAL CORD
zoom view
Figure 1.7A: Placenta—Fetal surface (umbilical cord and umbilical blood vessels)
Que. What is this specimen?
Ans. This is the specimen of placenta with umbilical cord.
Que. What is its weight?
Ans. 500 g or in relation to fetal body weight is 1/6th to 1/7th of the weight of fetus.
Que. In which condition the size of the placenta increases?
Ans. Syphilis, diabetes and erythroblastosis (placental weight—2,000 gm).
Que. What is its shape?
Ans. It is disc shaped (15 to 20 cm in diameter). It is thickest in the center, with maximum thickness of about 25 mm and then diminished towards periphery.
Que. What is the type of human placenta?
Ans. Hemochorial, because of direct contact of human blood and chorion.
22Que. How does it develop?
Ans. Chorionic frondosum and decidua basalis form the discrete placenta.
Que. What are the surfaces and how do you identify it?
Ans.
  1. Maternal surface—spongy, 15 to 20 lobes or cotyledons, which are limited by fissures. Each fissure is occupied by decidual septum. Only the decidua basalis and the blood in the intervillus space are of maternal origin.
  2. Fetal surface is glistened with the umbilical cord attached near the center. At term, 4/5th of placenta is of fetal origin.
zoom view
Figure 1.7B: Maternal surface of placenta (rough due to cotyledons)
Que. What are the structures of placenta?
Ans. From fetal side to maternal side:
  1. Amniotic membrane
  2. Chorionic plate
  3. Choriodecidual space—contains stem villi with their branches, the space is filled with maternal blood.
  4. Basal plate—from outside inward
    1. Part of compact and spongy layer of deciduas basalis
    2. Nitabuch's layer of fibrinoid degeneration of the outer syncytiotrophoblast at the junction of cytotrophoblastic shells and deciduas
    3. Cytotrophoblastic shell
    4. Syncytiotrophoblast.
Que. What is choriodecidual space?
Ans. It is bounded on inner side by chorionic plate, outside by basal plate, limited on the periphery by fusion of two plates. It is lined internally on all sides by syncytiotrophoblasts and is filled with 23maternal blood. Numerous branching villi arising from stem villi enter into the space and contribute the chief content of choriodecidual space.
Que. What are primary, secondary and tertiary villi?
Ans. Primary villi contains only the syncytiotrophoblast and cytotrophoblast cells.
Secondary villi contains outer syncytiotrophoblast and cytotrophoblast cells with mesoderm.
Tertiary villi contains:
  1. Outer syncytiotrophoblast
  2. Cytotrophoblast
  3. Basement membrane
  4. Central stroma contains fetal capillaries, primitive mesenchymal cells and hofbauer (phagocytic cells)) from outside inward).
zoom view
Figures 1.8A and B: (A) Placenta of uniovular twin pregnancy (fetal surface); (B) Placenta of twin pregnancy (maternal surface) (single placenta with 2-cords and no vessel anastomosis on fetal surface)
24Que. How many spiral arteries are in normal placenta?
Ans. 200.
Que. What is the rate of blood flow through uteroplacental unit?
Ans. 500 mL/minute at term.
Que. What is the rate of fetal blood flow through the placenta?
Ans. 400 mL/minute.
Que. What is placental barrier?
Ans. In the villi—maternal and fetal blood flow are separated by a barrier (0.25 mm thick) and consist of:
  1. Syncytiotrophoblast
  2. Cytotrophoblast
  3. Basal membrane
  4. Stromal tissue
  5. Endothelium of fetal capillaries with basement membrane.
Que. What is α-zone and β-zone of the placental membrane?
Ans. The thin zone of terminal villi (0.002 mm) ‘α-zone’ for fetomaternal exchange and the thick zone of terminal villi, i.e. β-zone are for hormone synthesis.
Que. What is Nitabuch's membrane?
Ans. It is a fibrinoid deposit in the outer syncytiotrophoblast adjacent to the decidua. This membrane limits further invasion of decidua by trophoblasts.
Que. When this membrane is absent?
Ans. It is absent in placenta accreta.
Que. What are the functions of placenta?
Ans.
  1. Transport:
    1. Oxygen is transported by diffusion
    2. Water, glucose, sodium ions (Na+), potassium ions (K+), calcium ions (Ca2+) and phosphorus pass from maternal to fetal side by passive diffusion
    3. Amino acid is transported by active process
    4. Iron and water soluble vitamin are transported by active mechanism to the fetus.
  2. Synthesis:
    1. Enzyme—heat stable alkaline phosphatase, cysteine aminopeptidase (CAP)
    2. Protein hormone—hCG and human placental lactogen (HPL)
    3. Steroid hormone—estrogen and progesterone
      25
    4. Pregnancy-associated placental protein—pregnency associated plasma protein A (PAPP-A), pregnancy associated plasma protein-B (PAPP-B), etc.
  3. Respiratory
  4. Nutritive
  5. Excretory
  6. Barrier and immunological function
Que. What are the abnormalities of placenta?
Ans.
  1. Placenta succenturiate
    An accessory lobe, which remains at a distance from main placenta and is connected to the main placenta by membrane containing umbilical blood vessels.
    Significance: It causes postpartum hemorrhage (PPH), shock, sepsis and placental polyp.
    zoom view
    Figure 1.9A: Placenta succenturiata
  2. Placenta bipartia or tripartia
    Placenta is divided incompletely at the periphery into two or three lobes and this has no obstetrical significance.
    zoom view
    Figure 1.9B: Placenta bipartia
  3. Placenta duplex or triplex
    Here, the placenta is completely divided into two or more lobules. The small lobules are attached with the main placenta by membrane or blood vessels. 26Significance: Antepartum hemorrhage (APH), PPH, retained bits.
    zoom view
    Figure 1.9C: Placenta duplex
  4. Placenta membranacea—large, 15 inch in diameter. Here, the placenta develops from chorion laeve and from chorion frondosum.
    zoom view
    Figure 1.9D: Placenta circumvallate
  5. Placenta circumvallate: Partial or complete ring divide the fetal surface into the distinct central and peripheral portion. The rim is raised yellowish-white in color and ½ inch broad and is composed of double layer of chorion, which undergoes infraction when the ring coincide with the placental margin. The condition is called placenta marginata.
    zoom view
    Figure 1.9E: Circumvallate placenta (Schematic diagram)
    Central zone is slightly depressed and normal appearance, but peripheral zone may be 5 to 7.5 cm in breadth. Placental 27tissue is thicker over peripheral zone. Vessels radiate from the cord up to the ring and then disappear.
    The probable explanation is that during early development, the chorionic frondosum is too restricted for nutrition of the fetus, to compensate for this the peripheral villi grow outwards splitting the deciduas basalis into two layers.
    Significance: Abortion, APH, Preterm labor, intrauterine growth restriction (IUGR), intrauterine fetal death (IUFD).
  6. Battledore placenta:
    Cord is attached to the margin of the placenta.
    Significance: Cord presentation and cord prolapse.
    zoom view
    Figure 1.9F: Battledore placenta
  7. Velamentous insertion of the cord
    Cord is inserted in the membrane and cord vessels traverse some distance along the membrane to reach the placent.
    Significance: Vasa previa is associated with placenta previa. (Here, the fetal blood loss is significant). Here intrapartum bleeding is common rather than antipartum bleeding.
    zoom view
    Figure 1.9G: Velamentous insertion of the cord
Que. What are the diseases of placenta?
Ans. Placental polyp, cyst, hydatidiform degeneration, edema and infraction and placental tumor (hemangioma—rare).
Que. How do you examine the placenta?
Ans. Maternal surface
  1. Lobules of the placenta
  2. The lobules should fit together
  3. he margins should be regular
  4. If there is missing of lobules, they do not fit together.
    28
Fetal surface
  1. Attachment to umbilical cord to placenta
  2. The umbilical vessels passing from the cord and fades into the margin
  3. Look for free ending vessels, which may indicate succenturiate lobe has been left behind in uterus.
Membrane
  1. The chorion is the layer in contact with the uterus—rough and thick.
  2. The amnion is the inner layer—thin and shiny.
  3. The amnion can be peeled up to the insertion of the cord.
  4. If the membrane is ragged, place them together and ascertain their completeness.
Umbilical cord
Look for artery and vein (normal A2, V1). If only one artery is found, look for congenital defect of the baby.
Que. What is normal length of the cord?
Ans. 50 to 60 cm and diameter is 12 mm.
Que. What are the structures of the cord?
Ans.
  1. Amnion
  2. Wharton's jelly
  3. Umbilical artery (2) and umbilical vein (1). [A2V]
Que. What is short cord and mention its clinical significance?
Ans. Short cord, length—35 to 46 cm.
  1. Malpresentation (breech)
  2. Temporary arrest of descent
  3. Separation of placenta
  4. Inversion of uterus
  5. Fetoplacental hematoma
  6. Tearing of the cord.
Que. Why there is twisting of the cord?
Ans. Due to the embryonic/fetal movement
Note: Two vessels cord is associated with aplasia or atrophy, 30 percent with single umbilical artery may have congenital defect.
Que. How umbilical cord develops?
Ans. The umbilical cord begins to develop in the 5th postmenstrual week, when a bridge of mesenchymal tissue condensed between ventral surface of the embryo forming connecting stalk. The connective tissue of the cord is Wharton's jelly, a ground substance made up of predominantly mucopolysaccharide.
29Que. Which type of major fetal anomalies are associated with SUA (single umbilical artery)?
Ans.
  1. Fetal heart anomaly
  2. CNS defect
  3. Kidney problem
  4. Chromosomal anomalies like trisomy 13 and 18.
Note: SUA on USG should thoroughly search fetal anomalies and if anomaly is found the risk of aneuploidy also increases, amniocentesis may be needed later on.
 
ANENCEPHALY
Que. What is this specimen?
Ans. This is the specimen of anencephaly.
zoom view
Figure 1.10: Anencephaly
Que. What is the cause of anencephaly?
Ans. Due to absence of cranial vault and much of the forebrain.
Note: Female baby is at increased risk, aneuploidy and folic acid deficiency may be the underlying etiology.
Que. How can you diagnose anencephaly?
Ans. By USG and X-ray.
Note: For other questions and answers see the chapter of X-ray, USG and flying oral questions on hydramnios.