My study notes for all forensic pathologists

1. Hazem Ali

2. Hazem Ali

3. Commonly used “traditional” definition:
 Blood loss of ≥ 500ml following vaginal delivery
 Blood loss of ≥ 1,000mL following C.S
More recent “less popular” definition:
 Any bleeding causing 10% drop in hematocrit from admission
Approximately 5% of all deliveries
One of the leading cause of maternal mortality
 Especially in developing countries

4. Either early (1ry) or delayed (2ry)
 1ry: bleeding onset < 24 hours of delivery
 Atony ‘tone’
 Genital tract laceration ‘trauma’
 Retained placenta ‘tissue’
 Coagulopathy ‘thrombin’
 2ry: bleeding onset > 24 hours of delivery
 Placental site sub-involution
 Retained placenta
 Infection (endometritis)
4T

5.  Patient’s parity and gestation
 Any abnormality of the antepartum and delivery course
 Pre-eclampsia or polyhydramnios,……
 Radiological studies
 Fibroid, placenta creta or congenital abnormality,……
 History of the use of instruments
 Forceps,…..
 Trials to control hemorrhage
 Bimanual massage, uterine packing, suturing, artery
embolization,…..
 Operative report if hysterectomy done
 Postoperative condition

7.  Identify the specimen
 Total/subtotal hysterectomy, with/without/unilateral salpingeophrectomy
 Photography of every step
 Detailed description of any gross abnormalities
 Especially sutures and tears
 Try to examine the uterus before fixation (if possible)
 better identification, better description, better photography
 Open the uterus with any approach, but DO NOT open through
sutures and tears
 Clamp marks on the broad and round ligaments should be inspected
 Residual hematoma from uterine/ovarian artries can be present
 Ask about the placenta (it should be sent for examination)

9.  Failure of contraction and retraction of myometrium following
delivery (Uterus like dough)
 Most common cause of 1ry PPH (80%)
 Risk factors:
 Rapid “stimulated” or prolonged labor
 Uterine overdistension (Polyhydramnios, Multiple pregnancy,
Macrosomia)
 Use of uterine-relaxing agents (MgS04, Beta-adrenergic agonists,
Halothane anesthesia)
 Infection (Bacterial toxins)
 High parity

10.  It a clinical diagnosis, pathology will not help
 Gross: The uterus is enlarged, edematous and soft
 Microscopic: edema and hemorrhage
 Only diagnosed by exclusion
 The diagnosis will depend on clinical information, combined with adequate
histologic sampling to exclude other causes
Non-specific

12.  If PPH continues despite adequate uterine tone “firm uterus”, think
of lacerations of genital tract (cervix, vagina, perineum)
 2nd most common cause of 1ry PPH (15%)
 Risk factors:
 Assisted vaginal delivery (forceps or vacuum)
 Episiotomy
 Malpresentation
 Macrosomia
 Prolonged labor

13. Points to remember
Site
Length
Depth
Extension
Complications
 Hematoma
 Discharge
 Others…….
Surgical intervention

14. Gross
 Lateral sides
 Superficial or Deep
 Localized to cervix or extended:
 Upward  lower uterine segment
 In this case can involve large uterine arteries, bleeding into broad ligament
 Downward  vagina
Be careful, Dührssen incision
 Cervix is purposefully incised at the 2- and/or 10-o’clock positions
 Aim to facilitate delivery of an entrapped fetal head during a breech delivery
 Very rarely done

15. Microscopic (nonspecific)
 Edema, hemorrhage
 Torn muscle fibers, torn vessels
 Complications??
 Amniotic fluid embolism
 DIC
Extensive sampling
may be required
• Amniotic debris fills not only vessels adjacent to the surface
mucosa and tears, but also seen in deep stromal vessels
• This is helpful to distinguishes it from contamination of
the surface mucosa by meconium and amniotic fluid at
delivery

16. Middle or upper third, commonly anterior wall
 Lower vaginal tear can extend to vulva/perineum
Commonly Small, superficial
 But can be deep
Nonspecific microscopic findings
 Edema, hemorrhage, torn muscles/vessels

17.  First-degree:
 Involves the fourchette, the perineal skin, and vaginal mucous membrane
 But not the underlying fascia and muscle
 Second-degree:
 In addition to skin and mucous membrane, it involves the fascia and muscles of
the perineal body
 But not the anal sphincter
 Third-degree:
 In addition to skin, mucous membrane, and perineal body, it involves the anal
sphincter
 If rectal mucosa is involved  complete laceration
 If rectal mucosa NOT involved  incomplete laceration

18. Total or partial disruption of uterine wall
One in 2,000 deliveries
The most predisposing factor to uterine rupture are
separation of a previous cesarean / surgical scar
Risk factor in non-scarred uterus are similar to those of
genital tract lacerations

19. Gross
 Lower uterine segment
 At site of previous C scar (i.e. anterior wall)
 Can be vertical, horizontal, or oblique
 Can extend upward to body of uterus, or downward to cervix
 With/without hematoma
Differentiate between rupture and dehiscence
Rupture Dehiscence
Layers of separation Entire thickness Myometrium
Uterine serosa Disrupted Intact
Communication between uterine and
peritoneal cavities
Present Absent

20. Microscopic
 Nonspecific (edema, hemorrhage, …..)
 Previous CS ??
 Suture material ( + giant cell reaction)
 Fibrosis
 Endometriosis and adenomyosis
 Predisposing factors ??
 Infection
 Extensive fibrosis + thinned muscle fibers

22. If PPH continues despite adequate uterine tone and
without laceration/rupture, think about retained placental
tissue
Rare cause of 1ry PPH (5%)
Risk factors:
 Accessory lobe
 Abnormal placentation (placenta creta)
 Preterm gestations (especially < 24 weeks)
 Pre-eclampsia

23. Full placental examination is very important
 Maternal surface  Look for missed cotyledon
Succenturiate “accessory” lobe is another cause
 Fetal surface  look if fetal vessels coursing to the placental edge and abruptly
ending at a tear in the membranes

24. Gross: retained placental fragments
Where to look?
 Commonly  upper (fundus), Posterior wall
 Abnormally  attached to previous CS / Surgical scar or placenta
previa (lower uterine margin)
Approach?
 Two parallel longitudinal anteroposterior sections, about 2–3 cm
apart on either side of the midline
 AVOID if tear/rupture will be disrupted
Placenta creta?

25. Abnormally adherent or ingrowing placenta that does not
detach with full contraction of the uterus after expulsion
of the fetus.
The most important risk factors:
 Previous CS / Surgery
 Placenta previa
Types:
 Accreta (abnormal attachment to the wall)
 Increta (extension into the myometrium)
 Percreta (extension up to the serosa)

26. Microscopic: look for villi / trophoblasts
Placenta creta:
 Acreta  direct contect of villous tissue to myometrium
without intervening decidua
 only fibrin and RBCs can be seen in between
 Increta  extension of villi into the superficial myometrium
 Percreta  extension of villi into the deep myometrium up to the serosa
Invasive mole can be differentiated from placenta increta/percreta by
presence of abnormal “molar” villi with abnormal trophoblastic
proliferation

28. Very rare cause of 1ry PPH (< 1%)
Congenital:
 Von Willebrand disease
 Idiopathic thrombocytopenic purpura (ITP)
Acquired:
 Anticoagulant therapy
 Consumptive coagulopathy (DIC)
 Clinical history and laboratory investigations are important
Obstetric risk factors of DIC:
• Preeclampsia (HELLP)
• Intrauterine fetal death
• Sepsis
• Placental abruption
• Amniotic fluid embolism

30.  Delayed / incomplete sloughing / closure of the modified spiral arteries
in the superficial myometrium beneath the placental attachment site
 One of the important causes of 2ry PPH
 Maximal in the 2nd week postpartum
 Risk factors:
 Old age
 Multiparty
 Unknown etiology, may be due to abnormal immunologic relationship
between trophoblast and the uterus
 But NOT Iatrogenic

31. During pregnancy:
 The extravillous trophoblast (EVT) modifies spiral artries by:
 Replace arterial endothelium
 Replace arterial media with hyaline fibrinoid material
 Loss of elastic lamina

32. During pregnancy:
 The end result is forming of large-caliber, high-flow, but low-resistance
arteries
 sufficient to meet the demands of the growing placenta and fetus

33. After delivery:
 Involution events occur within the uteroplacental vasculature:
 Decrease in the lumen size
 Disappearance of trophoblast
 Thickening of the intima “occlusive fibrointimal thickening”
 Re-growth of endothelium
 Regeneration of internal elastic lamina
 These changes normally occur within 3 weeks of delivery

34. Fibrointimal obliteration of the uteroplacental artery lumen
“Normal involution”

35. Gross:
 Soft
 Larger than expected
 May show extensive bleeding
 Large dilated vessels beneath the placental site
may be seen

36. Microscopy:
 Uterine vessels:
 Large, dilated
 Partially / completely thrombosed “variably aged”
 Lack a medial coat “replaced by hyaline material”
 Lack of elastic lamina
 Confirmed by special stains “von Gieson”

37. Microscopy:
 Interstitial or endovascular Trophoblasts
may be seen:
 Polygonal
 Abundant amphophilic cytoplasm
 Vesicular nuclei
 Can be confirmed by IHC
 CK
 Inhibin-alpha
 Mel-CAM
 Human placental lactogen
 rarely HCG

38. Remember:
 Avoid temptation to only record the presence or absence of villous tissue
without exclusion of subinvolution at first
 Physiologic patency of uteroplacental arteries will be seen in the
immediate (< 24 h) postpartum period
 Should NOT be interpreted as subinvolution
 A-V malformation is one of the differential diagnosis
 Variable sized, dilated vessels
 Presence of media and elastic lamina
 Absence of trophoblasts

39. Endometritis
Uterine inversion
Leiomyomas
Unexplained

40. Hazem Ali