Uterine inversion and retained placenta are obstetric emergencies that require prompt recognition and management to prevent life-threatening complications like hemorrhage and shock. Uterine inversion occurs when the uterus turns inside out, and can be classified based on the extent of inversion and time since delivery. Retained placenta is defined as failure to deliver the placenta within 30 minutes of childbirth. Both conditions require urgent evaluation and treatment to replace the inverted uterus or manually remove the retained placenta while resuscitating the patient.

1. • Uterine Inversion
• Retained placenta
• Amniotic Fluid Embolism
Dr Sushma Sharma
Professor
Department of Obstetrics & Gynaecology
MIMER Medical College, Talegaon(D), Pune

2. Uterine Inversion
Dr

3. Introduction
• Uterine inversion occurs when the uterine fundus collapses into the
endometrial cavity, turning the uterus inside out.
• A rare complication of vaginal delivery /cesarean
• Life threatening obstetric emergency
• Needs prompt recognition and management
• Less than 5% maybe spontaneous

4. Classification
By the extent of inversion:
• First degree (Incomplete) – The fundus
is within the endometrial cavity
• Second Degree (Complete) – The
fundus protrudes through the os.
• Third Degree (Prolapsed) – The fundus
protrudes into or beyond the introitus
• Fourth Degree (Total) – Both the uterus
and vagina inverted

5. Classification-contd.
By time of occurrence:
• Acute – within 24 hours of delivery
• Subacute – more than 24 hours but less than four weeks post partum
• Chronic – more than one month post partum

6. Incidence -
Ranges from 1 in 3500 to 1 in 20,000
Pathogenesis -
Incompletely understood.
Maybe attributed to:
• Use of excessive cord traction
• Fundal pressure
• Crede’ manoeuvre
• Fundal implantation of placenta
• Likely that other factors play a role – eg connective tissue disorders like
Marfan’s syndrome

8. Risk factors –
• Short cord
• Prolonged labour
• Precipitate labour
• Macrosomia
• Use of uterine relaxants
• Uterine anomalies
• Retained placenta
• Placenta accreta spectrum

9. Clinical Features
Depends on extent and time of occurrence. May include:
• Mild to severe vaginal bleeding
• Mild to severe lower abdominal pain
• Mass protruding from cervix/ vagina
• Urinary retention
Commonest presentation of complete inversion is Shock- out of
proportion to blood loss- attributed to Neurogenic shock.

10. Clinical Features
On examination:
Features of shock:
• P/A- Atonic uterus and fundal notch
or dimple in the area of normally
globular fundus
• Local examination smooth round
mass protruding from cervix or
vagina

11. Diagnosis
Bases upon clinical findings:
• Imaging is rarely necessary
maybe used for confirmation in
subacute/ chronic variety
• Ultrasound, MRI maybe used

12. Differential Diagnosis
• Fibroid Polyp
• Cervical Polyp
• Uterine Prolapse

13. Management
Goals:
• Replace the fundus to its anatomical position.
• Manage PPH and shock
• Prevent recurrent inversion

14. Management
Uterine Inversion
Remove placenta
Oxytocic infusion
(40 units/500mls
NS)
Antibiotics observe
O’Sullivan hydrostatic method
-dependent part replace into
vagina
-5L or more physiological
solution deposited onto
posterior fornix
-assistant create water tight
seal
Manual reduction
-apply pressure to
dependent part of
uterus
-simultaneous
pressing with other
hand on other part
which inverted last
GA/ stabilize
patient
UTERUS
REPLACED
Immediate
replacement
Resuscitate, IV
access, fluids/ bolus
replacement
NO
YES

15. ⦿Teamwork = resuscitation + uterine repositioning
simultaneously
⦿postpartum hemorrhage drill.
⦿The quickest way to treat neurogenic shock - to replace the
uterus.

16. ⦿ Delay in treatment increases the mortality, So number of
steps are taken immediately and simultaneously.
Before shock develops :
⦿ When one is on the spot when the inversion happens TRY
IMMEDIATE MANUAL REPLACEMENT, even
without anesthesia if not easily available.
Principle :
“ The part of the uterus which has come down last , should go back first. “
Mx of Acute Inversion of Uterus

17. Manual
reposition-
Johnson’s
technique
Procedure
⦿ If the diagnosis is made immediately after the
inversion has occurred, then that same degree
of relaxation of myometrium and cervix (which
is required for the inversion to occur) will allow
uterine replacement easily…
1. The gloved hand is lubricated with suitable antiseptic cream
and placed inside the vagina.
2. The uterine fundus with or without the attached placenta, is
cupped in the palm of the hand. The fingers and thumb of the hand
are extended to identify margins of the cervix.

18. 3. The whole uterus is lifted
upwards towards and beyond
umbilicus
4. Additional pressure is exerted
with the fingertips
systematically and sequentially
to push and squeeze the
uterine wall back through the
cervix.

19. 5. Sustained pressure for 3-5 mins to achieve complete replacement
6. Apply counter support by the other hand placed on the abdomen
7. Once the fundus has been replaced keep the hand in the uterus
while rapid infusion of oxytocin is given to contract the uterus.
Initially, bimanual compression aids in control of further
hemorrhage until uterine tone is recovered.

20. 8. When the uterus is felt contracting, the hand is slowly
withdrawn.
If placenta is attached, it is to be removed only after the uterus
becomes contracted.
If the placenta is partially attached , it should be peeled out
before replacement of uterus.

21. ⦿ Tube passed into the posterior fornix
⦿ Assistant close vulva around
operator’s wrist
⦿ Warm saline run in until pressure
gradually restores position of uterus
O’Sullivan’s hydrostatic method

23. Surgical techniques
• When conservative management fails. Usually because the
constriction ring gets too tight
Surgery
Abdominal Vaginal
Huntington ; Haultain Kustner ; Spinelli

24. Modifications
of the classical
abdominal techniques
– use of ventouse cup

25. Last resort -

26. Prevention
 Do not employ any method to expel the placenta when
the uterus is relaxed
 Patient should not be instructed to change her position.
 Pulling the cord simultaneously with fundal pressure
should be avoided
 Manual removal of placenta should be done in proper manner.

27. Retained Placenta
• Definition : failure of separation and delivery of placenta within 30
minutes post partum

28. Aetiology
• Abnormality of lower segment / internal os behavior
• ? Premature injudicious oxytocics usage
• Adherent placenta – commonest , most dreaded. Also called morbidly
adherent placenta (MAP )

29. Adherent placenta occurs
when there is a defect in the decidua basalis ,
Resulting
in an abnormal invasion of the placenta
directly into the substance of the uterus.

30. Types
1 ) Simple Adherent Placenta.
2 ) Morbidly Adherent Placenta :
i ) Placenta Accreta
ii ) Placenta Increta
iii) Placenta Percreta

31. INCIDENCE
 It varies widely all over the world.
Increased dramatically over the last 3 decades
( Because of Increase in LSCS rate … ).
 A.C.O.G.  1 Per 2500 deliveries. Accreta : 75
-78 %
Increta : 15 – 18 %
Percreta : 5 -7 %

32. Associated Conditions :
 Placenta Previa
 Previous Surgeries such as …
- Cesarean Section
- Myomectomy
- Synecolysis
- D & C
- M.R.P.
- Cornual Resection
 Uterine Malformation
 Septic Endometritis

33. Risk Factors :
 High Parity
 Advanced Maternal Age
 Down Syndrome
 High level of Maternal Serum AFP.
 High level of Maternal free Beta HCG.

34. ETIOLOGY :
 Defective decidual formation :
- Partial / total absence of decidua basalis
- Imperfect development of fibrinoid layer (Nitabuch layer)
- Placental villi are attached to the myometrium

35. Significance :
 Increased Maternal Morbidity ( 2 – 7 % )
 Increased Maternal Mortality ( 7 – 10 % )
from,
- Severe Hemorrhage
- Infection
- Inversion of Uterus

36. DIAGNOSIS
Earliest diagnosis of Adherent Placenta is must to
avoid any catastrophic emergency in future.
Antenatal diagnosis is the single most important factor
in improving the outcome in MAP.

37. METHODS…
 Clinical suspicion
 Ultrasound
 Color Doppler
 MRI
 Biochemical Marker
 Histopathology

38. USG
First-line investigation for suspected
placental invasion of the myometrium.
• Both transabdominal and transvaginal
ultrasonography

39. USG CRITERIA
 1st Trimester :
G. Sac located in the lower uterine segment
(rather than the fundus), next to or lower than
the Prev. CS scar.
 2nd & 3rd Trimester :
 Presence of irregular lacunae within the placenta
 Loss of retro placental clear space
 Loss or disruption of the white line – Bladder line

40. Moth – eaten OR
Swiss Cheese
Appearance
• Obliteration of clear space between
placenta and uterine wall

41. Reliability :
• Sensitivity - 93%
• Specificity - 79%
The use of power Doppler, color Doppler, or three- dimensional
imaging does not significantly improve the diagnostic
sensitivity compared with that achieved by grayscale
Ultrasonography alone.
[ Chou MM, Ho ES, Lee YH. Prenatal diagnosis of placenta previa accreta by transabdominal color
Doppler ultrasound. Ultrasound Obstet Gynecol 2000;15:28–35. ]

42. 3 D USG
Diagnostic Criteria :
Irregular intraplacental vascularization with
tortuous confluent vessels crossing placental
width.
Hypervascularity of uterine serosa– bladder
wall interface.

43. Colour Doppler
 Diffuse or focal
intraparenchymal lacunar
flow.
 Vascular lakes with
turbulent flow.
 Hypervascularity of serosa-
bladder interface.
 Prominent subplacental
venous complex.

44. M.R.I.
 No more sensitive than USG , But used as an adjunct
to USG , when there is strong clinical suspicion of
accreta.
 MRI achieves better images than Ultrasonography in
- Posteriorly sited MAP and
- With prior myomectomy,
( Because the ultrasound beam is impeded by the fetal
head in the former and by the scar tissue in the latter )

45. M.R.I. Criteria
Uterine bulging into the
bladder
Heterogeneous signal
intensity within the placenta
Presence of intra placental
bands on the T2W imaging
Abnormal placental vascularity
Focal interruption of the
myometrium

46. Laboratory Findings :
•
• Several series and case reports have reported an association
between placenta accreta and otherwise unexplained elevations in
second trimester MSAFP concentration (>2 or 2.5 multiples of the
median [MOM]).
Although an elevated MSAFP level supports an ultrasound-
based diagnosis of placenta accreta, it is an inconsistent finding and
is not useful by itself for diagnosis of accreta.

47. Histology
 Post Partum specimen shows :
Placental villi anchored directly on, or invading into
or through, the myometrium, without an intervening
decidual plate.

48. Treatment :
A multidisciplinary team approach is relevant
in managing these patients in order to reduce
morbidity and mortality associated with MAP.

49. Particular consideration should be given to
anticipation and management of massive
hemorrhage,
including
- availability of packed cells,
- platelets,
- fresh frozen plasma,
- cryoprecipitate, and
- activated factor VII.
Interventional Radiology and cell saver
technology are useful.

50. At present , placenta accrete can be managed in three ways:
( 1 ) Carry out a hysterectomy;
( 2 ) Leave the placenta in situ ; and
( 3 ) Resect the invaded tissues with the entire placenta
restoring uterine anatomy.
 Each one has weaknesses and strengths,
dependent on the condition itself and the specific
preferences taken by the surgeon and the team.

51. Women who have had a previous CS who also
have either placenta previa or an anterior placenta
underlying the old CS scar at 32 weeks of gestation
are at increased risk of placenta accreta and should
be managed as if they have placenta accreta, with
appropriate preparations for surgery made.
(RCOG 2011)
Elective delivery by caesarean section at 34–35
weeks of gestation for suspected placenta accreta
(ACOG 2012).

52. Conservative
/ moderate blood Loss / fertility to be
 In case of
( focal defect
preserved )
 Localized Resection with uterine repair
 Over sewing of the ut. Defect
 Blunt dissection followed by curetting the uterine cavity
• Uterus fails to contract (Multipara) :
Hysterectomy

53. Non Surgical
Leave the Placenta in situ to resorb with methotrexate
therapy
Ligation of the Ut. And Int. iliac artery
Fluoroscopic bilateral UAE
Argon beam coagulation for haemostasis
Insertion of occluding Balloons in the Int. iliac art. (Bilat)

54. Surgical
 Cesarean Hysterectomy.
Hysterectomy and partial / total resection of
bladder
Subtotal Hysterectomy with removal of large part
of placenta and Prophylactic occlusive Balloon
catheter in int. iliac art.

55. An Elective controlled condition is preferred rather
than an emergency condition without adequate
preparations.
A midline incision will facilitate better exposure, especially
if placenta Percreta is suspected.
Leaving the placenta undisturbed until completion of
the hysterectomy would prevent unnecessary
hemorrhage.
In cases where MAP is associated with placenta previa,
total hysterectomy is preferred to a subtotal hysterectomy.

56. Uterine Incision:
It is best to avoid cutting through a MAP because of the
possibility of massive haemorrhage.

57. Various modifications of the uterine
incision to avoid the placenta have been
reported…
- Classical incision,
- High transverse incision,
- Fundal incision,
- Fundal transverse incision

58. Remember

 The presence of pericervical or lower-segment varicose veins
proper of placenta praevia can be confused with the
neovascularization of placenta accreta.
Surgical exploration will make a differential diagnosis, thus
avoiding unnecessary hysterectomies.

59. Excision of placental site
 It is possible to "excise the placental site".
This is done by inverting the uterus in order to provide
good access to the placental site.
If the area of placental attachment is focal and the
majority of the placenta has been removed, then a
"wedge resection" of the area can be performed.

60. Balloon Catheterization
Pre-operative placement of arterial catheters in internal iliac
artery
After delivery balloons are inflated to achieve temporary
homeostasis
Selective arterial embolization (SAE) if necessary. . .
Bil. Int. iliac artery ligation is performed prior to peripartum
hysterectomy where Interventional Radiology is not
available.

61. Placement of occlusion balloon catheters
into both internal iliac arteries.

62. Methotrexate
 A folate antagonist, acts primarily against
rapidly dividing cells and therefore is effective
against proliferating trophoblasts.
First described by Arulkumaran et al in
1986. They reported administration 50 mg of
methotrexate as an intravenous infusion on
alternate days and the placental mass was
expelled on 11th postnatal day.
However, more recently, others have
argued that, after delivery of the fetus, the
placeta is no longer dividing and therefore,
methotrexate is of no value.

63. Methotrexate has been used in varying
doses and routes, however, there are no
randomized trials and no standard protocol
regarding its dosage.
The outcome when the placenta is left in
place after methotrexate administration varies
widely; it ranges from expulsion at 7 days to
progressive resorption in roughly 6 months.
Mtx – 50 mg IM + Folic Acid 6mg IM on
alternate day till β HCG comes to zero.

64. Other Modalities


Tamponade of the placental implantation site
with inflated Intra Uterine balloon catheter bags.
Lower Segment Compression Sutures
Pelvic pressure sponge packing.

65. Follow up…
1.- Ultrasound for Vascularity
2.- hCG titers weekly till it becomes Zero.
3.- Monitor for infection
4.- Bleeding
5.- Coagulation profile
Antibiotics till needed

66. 99099 44160. 41
Resources Patient, clinical and
anatomic features
Decision Definitive treatment
Limited
experience
or expertise, poor
resources or no
facilities for safe
patient transfer
lower segment invasion
vaginal bleeding with high
suspicion of accreta
Possibility of percreta
Extraplacental
hysterotomy,
Placental left in
situ
Followed by
uterine closure
Delayed hysterectomy
or conservative procedure
according clinical
and surgical status
Qualified and
experienced
team, adequate
hospital
resources
No desire for future
pregnancy
Tissue destruction> 50% of
uterine circumference
Intractable haemorrhage
DIC
Resective surgery
Subtotal hysterectomy
for upper segment lesions
Total hysterectomy
for lower segment
and cervical involvement
Qualified and
experienced
team,
adequate
hospital
resou
22
r-c
De
ecs
-14
Desire for future
pregnancy
Destruction < 50% of
uterineaxial circumference
Minor coagulation
disorders
Dr Shashwat Jani.
Conservative
surgery
1Placenta in situ with or wi
MXT
2 One step surgery
OR
3- Two step surgery

67. Bladder Involvement
 Involve UROLOGIST.
Preoperative Ureteric
stenting aids in identifying
the ureters, which will
help reduce ureteric
injuries.

68. Care must be taken during
surgery not to attempt to
dissect the bladder off the
lower uterine segment
which results in torrential
bleeding.
Anterior bladder wall
incision is particularly
helpful in defining
dissection planes and the
location of the ureters.

69. Reality :
Even today, the ground reality is that a
majority of morbidly adherent placenta are
diagnosed during the third stage of labour
or during caesarean section and which
results in adverse consequences including
exanguinating haemorrhage.

70. To Conclude…
Caesarean hysterectomy was the
cornerstone in the management in the past.
Antenatal diagnosis permits effective and
safe conservative approaches today.
The use of methotrexate, monitoring with
serum hCG and follow up with USG is backed
only by conflicting evidence.

71. Amniotic Fluid Embolism
• Protects the unborn fetus from its surrounding environment.
• Isolated from the maternal intravascular compartment.
• When this isolation is disrupted in one way or another, a
systemic maternal reaction can ensue, affecting the heart,
lungs, and brain.
• This reaction can be lethal to both mother and fetus.
Amniotic Fluid

72. • The syndrome is know as amniotic fluid embolism (AFE)
and is one of the most serious complications of pregnancy
and delivery.
• Given the unpredictable and unexpected nature of AFE, every
obstetrician should be prepared to include this condition in
differential diagnosis to optimize the chances for survival of
both mother and infant.

73. Background
• The presence of fetal cellular debris in the maternal circulation,
associated with maternal complications, was reported for the first
time in the 1920s by Ricardo Meyer from Brazil.
• In an effort to better understand this condition, several animal
models have been developed.
• Studies to human beings cannot be easily made, since not all the
findings in animals are consistent with the clinical manifestations.
• Recently, the term Anaphylactoid syndrome of pregnancy has
been proposed instead of AFE.

74. Incidence
• The true incidence of AFE may not be known.
• The disparity between reported figures is large, with rates ranging
from 1 in 8,000 to 1 in 83,000 deliveries.
• A recent study from California reports an incidence of 1 per
20,646 deliveries.

75. Mortality
• AFE constitutes the leading cause of mortality during
labor and the first few postpartum hours.
• 5% and 18% of all maternal deaths are due to AFE, a rate
of about 7.8 to 12 deaths per million births.
• Maternal death usually occurs because of
*sudden cardiac arrest,
*hemorrhage due to coagulopathy,
*acute respiratory distress syndrome (ARDS)
*multiple organ failure.

76. • It’s rare enough that despite systematic research in an
autopsy series, no evidence of AFE was noted among 14
maternal deaths from 26,000 deliveries.
• For women diagnosed as having AFE, mortality rates ranging
from 26% to as high as 86% have been reported.
• Intensive care management of affected patients can
cause improvements.

77. Pathophysiology
• For years, it was thought that microscopic fetal debris
particles during an AFE episode caused acute occlusion
of a large part of the mother's pulmonary
microvasculature.
• This was assumed because of respiratory distress and
cyanosis were the manifestations.

78. The first hemodynamic assessments of patients with AFE
revealed
1. Elevated pulmonary capillary wedge pressure (PCWP),
2. Decreased left ventricular stroke work index (LVSWI),
3. Mild to moderate increases in mean pulmonary arterial
pressures (MPAP), and
4. Variable increases in central venous pressure (CVP).
• These findings are consistent with left-sided heart failure.

79. • The initial reaction of the pulmonary vasculature to
amniotic fluid exposure may be -transient vasospasm,
-pulmonary hypertension, and
-profound hypoxia.
• To date, however, no direct evidence of these reactions
has been documented, probably due to the delay between
the onset of symptoms.

80. • Clinically, the reaction to AFE comprises 3 distinct phases.
1. Respiratory, including respiratory distress and cyanosis;
2. Hemodynamic, with pulmonary edema and shock; and
3. Neurologic, including seizures, confusion or coma.
• These presentations can occur separately or in combination,
and in different degrees.

83. Cause
• AFE is very rare and complex.
• The disorder occurs during the last stages of labor when amniotic fluid
enters the circulatory system of the mother.
• When the fetal cells and amniotic fluid enters the
bloodstream, the immune system responds by releasing products that cause
an inflammatory reaction this causes severe changes in the mechanisms
that affect blood clotting.
• Intravascular coagulation (DIC) occurs and results in serious bleeding.

84. • The condition can also develop after elective
abortion, amniocentesis, cesarean delivery or
trauma.
• The use of drugs to induce labor, such as misoprostol,
nearly doubles the risk of AFE.
• A maternal age of 35 years or older is associated with AFE.

85. Diagnosis
• Until now, the diagnosis of AFE was made by a pathologist, based on a
finding in :- maternal tissue of epithelial squamous cells,
- fat derived from vernix caseosa,
- mucin derived from infant's intestinal mucus,
- bile derived from meconium.
• Increased awareness of the syndrome's existence has resulted in earlier
diagnoses, aggressive intervention, and better chance of survival.
• Diagnosis is also based upon the signs and symptoms observed
during the birth or procedures.

86. Symptoms & Signs
• Suspect AFE when confronted with any pregnant patient who has
sudden onset of - respiratory distress,
- cardiac collapse,
- seizures,
- unexplained fetal distress, and
- abnormal bleeding
• AFE is suspected when a woman giving birth experiences very
sudden insufficient oxygen to body tissues, low blood pressure,
and profuse bleeding due to defects in blood coagulation.
• They also can be entirely absent.

89. Clinical Conditions Associated With AFE
• The most frequently cited are
- onset of labor,
- fetal death, trauma, and
- uterine over distention by multiple gestation,
- polyhydramnios or fetal macrosomia.
• Cited risk factors are not consistent.

90. Management
• AFE is a rapidly lethal condition.
• To limit its associated mortality and morbidity,
supportive care must be initiated with the same
promptness and aggressiveness as the presentation of
AFE itself.

92. Medications
• Pharmacologic treatment
• The goals of therapy are:
(1) maintenance of systolic blood pressure above 90 mm Hg
(2) maintenance of arterial PO2 over 60 mm Hg
(3) correction of coagulation abnormalities.
• Use inotropics (ß adrenergics) and pressors (ephedrine,
dopamine, dobutamine, norepinephrine infusions).

93. Prognosis
• The neonatal survival rate after a delivery affected by
AFE was 79% according to the Registry, and only half
of the surviving infants were neurologically normal.
The infant's prognosis was adversely affected by
maternal cardiac arrest.
• National AFE Registry indicate a maternal mortality
rate of 61%.

94. Summary
• AFE is a sudden and unexpected complication of
pregnancy.
• It has a complex pathogenesis and serious implications
for both mother and infant.
• Continues to be associated with high rates of
morbidity and mortality.
• Obstetricians should be alert to the symptoms of AFE
and strive for prompt and aggressive treatment.