1. Ambo University
College of Health Sciences
Department of Medicine
1
Obstetric Emergency
By : Aregahegn T & Aster.A
July,2014
Ambo,Ethiopia
2. Outline
Before delivery
-Hyperemesis G
-PROM
-Abortion
-Ectopic P
-Preeclampsia & E
-Abreptio P
-Placenta P
During delivery
-Obstructed labour
-Uterine rupture
-Cord prolapse
After delivery
-Retained P
-Placenta accreta
-Injury to the cervix
2
3. Hyperemesis Gravidarum
It is the actual vomiting in the morning , which
leads to dehydration & significant amount of wt
loss
It is usually start between the 4th and 6th weeks
of pregnancy and improves or disappears about
the 12 th week.
The vomiting is not confined to the morning but
it is repeated throughout the day until it affects
the general condition of the patient
3
4. Etiology
1 Hormonal:
High human chorionic gonadotrophin (hCG)
stimulates the chemoreceptor trigger zone in
the brain stem including the vomiting center
in the conditions where the hCG is high as in:-
a. early in pregnancy,
b. vesicular mole and
c. multiple pregnancy.
4
5. Cont’d
2.Allergy: to the corpus luteum or the released
hormones.
3. Deficiency of:
a. adrenocortical hormone and /or,
b. vitamin B6 and B1
4.Nervous and psychological:
a due to psychological rejection of an
unwanted pregnancy,
b fear of pregnancy or labour so it is more
common in primigravidae
5
6. Diagnosis
Symptoms:
>The patient cannot retain anything in her
stomach,
> vomiting occurs through the day and night even
without eating.
>Thirst, constipation and oliguria.
>In severe cases, vomitus is bile and/ or blood
stained.
> Finally, there is manifestations of Werniche’s
encephalopathy as drowsiness, nystagmus and
loss of vision then coma.
6
7. Cont’d
Signs:
Manifestations of starvation and dehydration:
*Loss of weight.5%
* Sunken eyes.
* Dry tongue and inelastic skin.
* Pulse: rapid and weak.
* Blood pressure: low.
* Temperature: slight rise
7
9. PROM
Premature ROM is defined as rupture of the
chorioamnionic membranes prior to the onset
of labor
Prolonged ROM usually refers to ROM for
more than 24 hours
It is a complication in one quarter to one
third of preterm births
9
10. Cont’d
• May or may not be associated with PTL
(preterm labor)
• Complicates 1/3 of all preterm deliveries
• Around 1-2% of pregnancies
• Majority of patients delivery within 1 week
10
12. Diagnosis
History
– Gush of fluid
– Constantly wet
Physical
– Pooling fluid - posterior fornix
– Fluid per os
– Examine with sterile speculum to prevent/limit
digital exam of cervix, to minimize risk of
ascending infection and amnionitis
12
14. Complication
Maternal effects
Increase in chorioamnionitis
Increase in Cesarean delivery
Spontaneous labor in ~ 90% within 48 hr. of
membrane rupture
Increased risk of placental abruption
Thromboembolic disease
14
15. Cont’d
Fetal effects
Increase in RDS
Increase in intraventricular hemorrhage
Increase in neonatal sepsis and subsequent
cerebral palsy
Increase in perinatal mortality
Increase in cord prolapse
Abruption
Oligohydramnios
15
16. Management
Considerations
When?
• If later than 34 weeks, consider induction
• If <34 weeks, consider tocolysis for steroid
course, then expectant management or
delivery?
• Chorioamnionitis necessitates immediate
delivery
16
17. Cont’d
Supported Interventions
- Tocolysis for steroid administration if no
contraindications and fetus 24 – 34 weeks
- Prophylactic antibiotics
May prolong latent period by an average of
5-7d
May reduce maternal amnionitis and
neonatal sepsis
- Ultrasound for fetal weight
- Expectant management for any gestational age
17
18. Cont’d
• Steroids
– To enhance fetal lung maturation and
decrease RDS
• Tocolytics
– Randomized trials have shown no pregnancy
prolongation
18
19. ABORTION
Spontaneous abortion, or “miscarriage,” is
defined as pregnancy loss before 20 weeks of
gestation.
Most of these occur before 12 weeks.
10-15% of clinically recognized pregnancies
terminate in spontaneous abortion.
19
20. Cont’d
The causes of spontaneous abortion are both
fetal and maternal.
Chromosomal anomalies such as aneuploidy,
polyploidy, and translocations are present in
approximately 50% of early abortuses.
Maternal factors include luteal-phase defect,
poorly controlled diabetes, and other
uncorrected endocrine disorders.
20
21. Cont’d
Physical defects of the uterus, such as
submucosal leiomyomas, uterine polyps, or
uterine malformations may prevent
implantation adequate to support fetal
development.
Systemic disorders affecting maternal
vasculature, such as antiphospholipid
antibody syndrome, coagulopathies, and
hypertension, may predispose to miscarriage.
21
22. Cont’d
Finally, infections with bacteria such as
Toxoplasma, Mycoplasma, and Listeria, as
well as viral infections, have also been
implicated as causes of abortion.
Ascending infection is particularly common in
second-trimester losses.
Clinically the patient may have bleeding or
shock.
22
23. Essentials of Diagnosis
Suprapubic pain, uterine cramping, and/or back pain
Vaginal bleeding
Cervical dilatation
Extrusion of products of conception.
Disappearance of symptoms and signs of pregnancy.
Quantitative -HCG
Abnormal ultrasound findings
23
24. Ectopic pregnancy
The term applied to implantation of the fetus
in any site other than a normal intrauterine
location.
The most common site is within the fallopian
tubes (∼90%).
Other sites include the ovary, the abdominal
cavity, and the intrauterine portion of the
fallopian tube (cornual pregnancy).
24
25. Cont’d
The most important predisposing condition
are:
- Prior pelvic inflammatory disease resulting in
fallopian tube scarring
- Factors leading to peritubal scarring and
adhesions such as endometriosis, and
previous surgery.
- Intrauterine contraceptive devices
- Fallopian tube may normal in some cases
25
26. Cont’d
Ovarian pregnancy is presumed to result from
the rare fertilization and trapping of the ovum
within the follicle just at the time of its
rupture.
Abdominal pregnancies may develop when
the fertilized ovum fails to enter or drops out
of the fimbriated end of the tube.
26
27. Cont’d
In all these abnormal locations, the fertilized
ovum undergoes its usual development with
the formation of placental tissue, amniotic
sac, and fetus, and the host implantation site
may develop decidual changes.
27
28. Cont’d
Morphology. Tubal pregnancy is the most
common cause of hematosalpinx (blood-filled
fallopian tube) and should always be suspected
when a tubal hematoma is present.
Initially the embryonal sac, surrounded by
placental tissue composed of immature chorionic
villi, implants in the lumen of the fallopian tube.
With time trophoblastic cells and chorionic villi
start to invade the fallopian tube wall as they do
in the uterus during normal pregnancy.
28
29. Cont’d
However, proper decidualization is lacking in
the fallopian tube, and growth of the
gestational sac distends the fallopian tube
causing thinning and rupture.
Fallopian tube rupture frequently results in
massive intraperitoneal hemorrhage.
29
30. Cont’d
Less commonly the tubal pregnancy may
undergo spontaneous regression and
resorption of the entire conceptus.
Still less commonly, the tubal pregnancy is
extruded through the fimbriated end into the
abdominal cavity (tubal abortion).
30
31. Risk Factors
High risk
• Tubal surgery
• Sterilization
• Previous ectopic pregnancy
• In utero exposure to diethylstilbestrol
• Use of IUD
• Documented tubal pathology
Moderate risk
Infertility ,Previous genital infections ,Multiple sexual
partners
Slight risk
• Previous pelvic/abdominal surgery, Cigarette smoking,
Vaginal douching ,Early age at first intercourse (< 18 years)
31
32. Clinical Features
The clinical course of ectopic pregnancy is
punctuated by the onset of severe abdominal
pain, most commonly about 6 weeks after a
previous normal menstrual period, when
rupture of the tube leads to pelvic
hemorrhage.
32
33. Cont’d
Rupture of a tubal pregnancy constitutes a
medical emergency.
In such cases the patient may rapidly develop
hemorrhagic shock with signs of an acute
abdomen, and early diagnosis is critical.
Chorionic gonadotropin assays, ultrasound
studies, and laparoscopy may be helpful to
diagnose.
33
34. PREECLAMPSIA AND ECLAMPSIA
Preeclampsia refers to a systemic syndrome
characterized by widespread maternal
endothelial dysfunction presenting clinically
with hypertension, edema, and proteinuria
during pregnancy.
Preeclampsia should be distinguished from
gestational hypertension that can develop in
pregnancy without proteinuria.
34
35. Cont’d
Minimum criteria
– BP ≥ 140/90 mm Hg after 20 weeks' gestation
– Proteinuria ≥ 300 mg/24 hours or ≥ 1 +
dipstick
Increased certainty of preeclampsia
– BP ≥ 160/110 mg Hg
– Proteinuria 5.0 g/24 hours or ≥ 2+ dipstick
35
36. Cont’d
– Serum creatinine > 1.2 mg/dL unless known
to be previously elevated
– Platelets
– Microangio< 100,000/mm3pathic hemolysis
(increased LDH)
– Elevated ALT or AST
– Persistent headache or other cerebral or
visual disturbance
– Persistent epigastric pain
36
37. Risk factors
• Primigravida
• Multipara with change
of partner
• Chronic hypertension
• Chronic renal disease
• Diabetes mellitus
• Multifetal gestation
• Polyhydramnios
• RH Isoimmunized
pregnancy
• Hydatidiform mole
• Previous history of
preeclampsia
• Family history of
pregnancy induced
hypertension
37
38. Types
Mild pre-eclampsia: blood pressure ≥ 140/90 mmHg ± oedema.
Severe pre-eclampsia:
- blood pressure >140/90 mmHg + proteinuria ± oedema or
- diastolic blood pressure>110 mmHg or
- cerebral or visual disturbances.
N.B.
Imminent eclampsia : It is a state in which the patient is about to
develop eclampsia. Usually there are :
- blood pressure much higher than 160 /110 mmHg ,
- heavy proteinuria (+++or ++++),
- hyperreflexia,
- severe continuous headache,
- blurring of vision,
- epigastric pain.
Fulminating pre-eclampsia: a rapidly deteriorating pre-eclampsia to
be imminent eclampsia.
38
39. Classification
39
Criteria Mild preeclampsia Severe preeclampsia
Blood pressure < 160/110 > 160/110
Symptoms Absent Present
Proteinuria < 5 g/dl 24 hours collection > 5 g/dl; > 2+ on dipstick
Liver and Renal function Normal Abnormal
Platelet count Normal Thrombocytopenia
Pulmonary edema Absent Present
Convulsions Absent Present
HELLP syndrome Absent Present
Fetal growth restriction Absent Present
The presence of any one of the above findings is sufficient to lead to a classification of the
preeclampsia into the severe category
40. Pathogenesis
The exact mechanisms leading to
development of preeclampsia are still being
investigated; however, it is clear that the
placenta plays a central role in the
pathogenesis of the syndrome, since the
symptoms disappear rapidly after delivery of
the placenta.
The placenta reveals various microscopic
changes, most of which reflect malperfusion,
ischemia, and vascular injury
40
41. Clinical Feature
The onset is typically insidious, characterized
by hypertension and edema, with proteinuria
following within several days.
Headaches and visual disturbances are
serious events and are indicative of severe
preeclampsia, often requiring delivery.
Eclampsia is heralded by central nervous
system involvement, including convulsions
and eventual coma.
41
42. Symptoms
• Visual disturbances: blurring of vision, flashes of
light or blindness.
• Epigastric or right upper quadrant pain: due to
enlargement and subcapsular haemorrhage of
the liver.
• Nausea and vomiting : due to congestion of
gastric mucosa and/ or cerebral oedema.
• Oliguria or anuria: due to kidney pathology. 5
42
43. Investigations
• Complete urine examination: for proteinuria,
pus cells, RBCs, casts,specific gravity, culture
and sensitivity .
• Kidney function tests: serum uric acid > 6 mg
% is abnormal during pregnancy. It is more
specific for pre-eclampsia than creatinine.
• Coagulation status :Platelet count, fibrinogen
and FDP as DIC may develop.
43
44. cont’d
• Eye fundus examination.
• Tests for foetal well being: as
- ultrasound,
- daily foetal movement count,
- non-stress test,
- oxytocin challenge test (if needed)
44
46. Management
46
Mild preeclampsia Severe preeclampsia
Management depends on:
•Gestational age
•Fetal well being
If at term :
•Admission
•Ascertain fetal maturity
•Terminate pregnancy via the most appropriate
route
If preterm : Conservative management
•Admission
•Bed rest
•Follow vital signs; organ function tests; platelet
count; development of symptoms; level of
proteinuria; evidence of hemolysis; fetal well being
tests
•If severe disease develops during conservative
management or achieve fetal maturity; proceed to
delivery
If any one of the evidences of severe
preeclampsia develop or are present,
conservative management option is
not possible.
Conservative management is
contraindicated.
Management of severe preeclampsia
includes:
•Admission
•Administration of anticonvulsants-valium;
magnesium sulphate;
phenytoin
•Control of severe hypertension by IV
antihypertensives such as hydralazine
or labetalol
•After mother is stabilized, proceed to
delivery irrespective of fetal gestational
age
47. Abruptio placenta
Detachment of placenta after 24 weeks of
gestation and before delivery
Predisposing factors:
• Multiparity
• Hypertension
• Blunt external abdominal trauma (direct)
• Cocaine use
• Previous third trimester bleeding
• Age older than 35 years
47
49. Management
• Management is influenced by gestational age
and degree of abruption
• Indicators for delivery-
– Fetal intolerance
– DIC
– Labor
• Vaginal delivery is acceptable
49
50. Cont’d
• Correct SHOCK- IV access – 2 large bore
cannulae
-Crystalloids IV – emergency
-BLOOD as soon as possible
• Correct DIC - Heparin
• Catheterize - hourly urine output chart
• Assess for delivery
50
51. Placenta previa
Placenta attached in the lower segment
There are four grades
1) Low lying - lower than upper implantation
2) Marginal – placental edge approaches
cervical os
3) Partial – implantation occludes portion of the
cervical os
4) Total – implantation totally obstruct cervical
os
51
53. Types
• Minor – Enters LUS but does not cover os
• Major – Covers internal os completely
53
54. Etiology
• Unclear
• Any damage to endometrium or myometrium
Scar tissue impedes migration away from
os
• Multiple pregnancy- large surface area
• Cigarette smoking- vasoconstriction
• Cocaine Use – Vasoconstriction-hypertrophy
• Rh issoimmunization
• Syphilis
54
55. Cont’d
• Previous Placenta Praevia
• Maternal Age – reduced uterine blood flow
needs greater surface area
• Parity - 3 previous deliveries 2.6 fold
Vessels at site of previous placenta reduced
flow discourage implantation
55
56. Presentation
• Antepartum Haemorrhage
- Late pregnancy
- Painless bleeding ( most common)
• Malpresentation
-Breech/High Head/Unstable lie in 3rd
trimester
56
57. Diagnosis
• The clinically important diagnosis of placenta
previa is therefore a late second or early third
trimester diagnosis (after 24-26 weeks
gestation)
• Ultrasound is the easiest, most reliable way to
diagnose (95-98% accuracy)
• Pelvic examination is contraindicated
57
58. Management
Antenatal
• Bed rest indicated
• Inpatient vs Outpatient
• Major Vs minor
• Anaemia
-Regular Hb
-X-match/Transfuse
58
59. Cont’d
• Delivery should depend upon type of previa
– Complete previa = c/section
– Low lying = probable attempted vaginal
delivery
– Marginal/partial = it depends!Consider
“double setup” for uncertain cases
59
60. Obstructed labor
Obstructed labor is failure of progressive
descent of the presenting part of the fetus in
the birth canal for mechanical reasons inspite
of good uterine contraction.
The prevalence in developing countries is
about 1-2% in the referral hospitals
60
61. Risk Factors
Ht <150 cm
Previous Hx of prolonged or OL
Clinical pelvimetry
Soft tissue anomalies
Estimate size of fetus late in Pregnancy
61
62. Etiology
A. Maternal causes
Cephalo-pelvic disproportion (CPD)
• Contracted pelvis
• Bone deformities
• Soft tissue obstruction
62
63. Contracted pelvis
Generally contracted pelvis involves contracture
of:-
- the pelvic inlet
- the mid pelvis
- the pelvic outlet, or by combinations of
these.
Inlet contracture-
-AP diameter of < 10 cm – normally 11cm
-Transverse diameter of < 12cm ---normally
–13.5cm
-Diagonal conjugate <11.5cm,normally-12.5cm
63
65. Cont’d
Clinical pelvic assessment done after emptying
the bladder & putting the woman in lithotomy
position.
• Then we assess the following:-
-Reachability of sacrum promontory.
-Smoothness &concavity of sacrum.
-Straightness of sidewalls and projection of
ischial spine.
-Size of pubic angle & intertuberous distance
65
66. Bone deformity
Small pelvis -developmental or congenital
Abnormal shape of the pelvis due to:
-Diseases like rickets & osteomalacia or
tuberculosis
-Previous accidents.
-Tumors of the bones.
-Childhood poliomyelitis affecting shape of the hips.
-Spine: -Lumbar kyphosis.
- Lumbar scoliosis
66
67. Soft tissue obstruction
Tight perineum in primi
Vaginal abnormalities- septa, scar, tumors
Cervical stenosis- infection, surgery, tumors
Uterine factors- fibroids, congenital anomalies
Ovarian tumor- impacted in the pelvis
67
68. B. Fetal causes
Large sized fetus / Macrocosmic
Congenital anomalies- Hydrocephalus
Locked and conjoined twins
Shoulder dystocia
Malpositions and Malprsentation
– Breech
– Transverse lie
– Brow presentation
– Mento- posterior position (face)
68
69. Diagnosis
History
– The patient is usually young teenage
– Abnormally prolonged labor
General examination
– Tired, exhausted and anxious.
– Tachycardic, tachypenic .
– Dehiydrated
-Temprature increase(>38)
69
70. Cont’d
Abdominal examination
– Hypertonic or hypotonic uterine contraction.
– Uterus is hard and tender
– FHR abnormality – tachycadia, bradycardia
or may be absent
– Bladder often distended.
– Catheterization may be often difficult
and the urine is blood stained.
70
71. Cont’d
Vaginal examination
-Vulva is edematous.
- Cervix fully or partially dilate& edematous
-The liquor is meconium stained and often
foul smelling.
-The presenting part is high, not engaged,
with excessive moulding and Large caput.
71
72. Complication
Maternal
- Maternal distress
– Uterine rupture – UNcommon in primi
– PPH- atonic or traumatic
– Infection -sepsis, abscess and peritonitis
– Infertility
– Psychological trauma
72
74. Management
Prevention
• Good nutritional supply since childhood
• Avoid early marriage
• Universal ANC
–To screen out the " at risk mothers "
–Pelvic assessment at 38-39wks
• Promote family planning services
• Elective caesarean delivery when
indicated
74
75. Cont’d
Specific treatment
• Resuscitation
• Broad spectrum antibiotics
• Operative delivery
– Episiotomies for some primis with tight perineum.
– Vacum / Forceps delivery
• Alive fetus and head < 1/5 above pelvic brim (+1)
• Mild-moderate moulding
– Destructive delivery
• Dead fetus, fully dilated cervix and no evidence of
rupture or imminent rupture of the uterus
75
76. Cont’d
- Caesarean delivery
• Alive fetus with incomplete cervical dilatation or
high station.
• Alive fetus with Brow or Mento posterior
position or face
• Alive or dead fetus with evidence of imminent
uterine rupture.
- Caesarean Hysterectomy
• Severely bruised lower uterine segment
• Major uterine vessels torn
76
77. Uterine Rupture
Tear in the wall of the uterus w/c commonly
occurs in the lower uterine segment.
Common in multiparas and rarely occurs in
primiparas.
Peak incidence is 3rd /4th pregnancy.
It can occur anteriorlly , posteriorlly , laterally
or combination of these.
-anterior rupture is the commonest
77
78. In obstructed labour:
- It is usually in lower uterine segment.
- Usually oblique or transverse.
- More on the left side due to;
i) dextrorotation of the uterus.
ii) left occipito-positions are more common.
In rupture scar:
At the site of the scar.
78
79. Cont’d
Can be complete or incomplete
1 Complete(true) uterine rupture
-includes the entire thickness of the uterine wall
and serosa resulting in direct communication
with peritoneal cavity.
2 Incomplete (uterine dehiscence)
-is the defect of the uterine wall that is
contained by the visceral peritoneum or broad
ligament.
-common in patients with prior C/S scar
79
80. Cont’d
Incidence
0.05% for all pregnancies.
0.8% for women with low-transverse uterine
scar.
4-8% -prior classic scar.
all pregnancies following myomectomy may
be complicated by uterine rupture.
80
81. Causes
• OL specially in multis
• Rupture or dehiscence of previous c/s scar
• Excessive stimulation
• Difficult instrumental delivery
• Internal podalic version -particularly after
drainage of the liquor
• Difficult manual removal of placenta
• Sharp penetrating trauma
81
82. Clinical features
History
• History of prolonged labor
• Worsening abdominal pain (supra pubic)
persisting b/n contraction
• Sudden cessation of uterine contraction
• Absent fetal movement
• Variable degree of vaginal bleeding
• Shoulder pain on lying down due to irritation of the phrenic
nerve by accumulating blood under the diaphragm
82
83. Cont’d
P/E-reduced BP
-feeble and rapid pulse/impalpable
-Signs of severe anemia-pallor
• Abdomen -tender & distension
-Scar of the previous operation.
-easily palpable fetal parts
-absent FHB & uterine contraction
-signs of fluid collection/variable shifting dullness
• Pelvic examination
-active vaginal bleeding
-the presenting part may be impacted or
retracted in to peritoneal cavity.
83
84. Differential Diagnosis
• Abruptio placentae.
• Disturbed advanced extrauterine pregnancy.
• Other causes of acute abdomen.
84
85. Management
1 Supportive management
• Secure IV line with two lines
• Vigorous infusion of crystalloids
• Do HCT ,B/g
• Broad spectrum IV antibiotics
• Catheterize
85
86. 2 Definitive management
• Repair- If it is amenable for repair and the
patient did not complete her family.
-usually with tubal ligation if future
fertility is not desired.
• Hysterectomy-total/subtotal if posterior,
lateral
• Subtotal hysterectomy is less time consuming
so it is done if there is no cervical tear.
86
87. Cord presentation and prolapse
Cord presentation and prolapse describe a
situation in which the umbilical cord is felt
anterior to the fetal presenting part on vaginal
examination.
If the membranes are intact it is a cord
presentation while with ruptured membranes
it is identified as a prolapsed cord.
As long as the membranes are not ruptured,
the risk of compression and asphyxia is low.
87
88. Cont’d
Cord prolapse can be:
1 Overt- being felt inside the cervix, the
vagina or even hanging outside the introitus.
2 Occult- with the cord anterior to
the presenting part in the lower segment but
not felt on digital vaginal exam
88
89. Cont’d
Cord prolapse can occur in:
– vertex and frank breech presentations-0.5%
– complete breech -5%
– footling breech -15% and
– shoulder presentation -20%.
89
90. Etiology
• Malpresentations in labor
• PROM
• Amniotomy with a high fetal station
• Polyhydramnios with sudden membrane
rupture
• Second twin delivery
• Internal podalic version
• Cephalopelvic disproportion in labor
90
91. Complications
• Cord compression and constriction of umbilical
vessels due to cold exposure outside the introitus
can lead to fetal asphyxia and death.
• Partial cord occlusion may give the fetus some
time but in complete cord occlusion the fetus can
die of asphyxia in 5-7 minutes if cord
compression is not immediately relieved.
• There is increased maternal risk from cord
prolapse because of emergency operative vaginal
or abdominal delivery performed in order to
salvage the fetus
91
92. Diagnosise
• In the vagina or inside the cervix anterior to the presenting
part
– Check for pulsation and its rate
– Replace the cord immediately into the vaginal ( not inside
the uterus) canal if outside the introitus
• If membrane is intact, cord presentation is diagnosed
• In all malpresentations, a careful search for cord presentation
or prolapse should be made
• Occult cord prolapse can only be diagnosed by detection of
abnormal fetal heart rate patterns
• In cases of malpresentations, sonographic search can also be
made for cord anterior to the fetal presentation
92
93. Management
Immediate management
If cord is pulsating:
• Put mother in knee-chest position
• Initiate oxygen administration by face mask
5L/min
• Insert bladder catheter and infuse the bladder
with 0.5L of saline
• Replace the cord into the vaginal canal
• Push fetal presenting part upwards via the
examining hand in the vagina to relieve
compression of the cord by the presentation
• Prepare for immediate delivery
93
94. Cont’d
Delivery :
Non-pulsatile cord:
• Manage as any other labor as the cord prolapse will
not alter the course of labor (dead fetus)
Pulsatile cord:
Second stage of labor:
• Expedite delivery by forceps delivery if other
conditions for forceps delivery are met.
• Breech extraction if other conditions for breech
extraction are met (full cervical dilation)
First stage of labor:
• caesarean delivery.
94
95. Postpartum hemorrhage
Excess blood loss after delivery (>500ml )
It is the leading cause of maternal mortality
Types
- Primary PPH in the first 24 hours
- Secondary PPH the first 24 hrs to 6 weeks.
Massive PPH may be truly terrifying
95
96. Etiology
• The “4 T’ s” : tone, tissue, trauma, and
thrombosis
• Uterine atony, i.e., failure of the uterine
contraction and retraction of myometrial muscle
fibers following delivery of the baby.
• PPH in a previous pregnancy is a major risk
factor and every effort should be made to
determine its severity and cause.
• Birth weight, labor induction and augmentation,
chorioamnionitis
96
97. Cont’d
Primary PPH
The most important cause of massive PPH is uterine
atony when the uterus is not contracted
Steps to stop bleeding
1. Massaging the uterus to cause it to contract
2. Bimanual compression-Under general anaesthesia,
the uterus is firmly compressed for 5-30 minutes
3. Uterine contraction is maintained by oxyitocin
4. Prostaglandin -through the anterior abdominal wall.
97
98. Aetiology:
(A) Placental site haemorrhage:
(I) Atony of the uterus(90%)
II) Retained placenta.
(III) Disseminated intravascular coagulation
(B) Traumatic haemorrhage:
Rupture uterus, cervical, vaginal , vulval or
perineal lacerations.
98
99. Complications
1- Maternal death in 10% of postpartum
haemorrhages.
2- Acute renal failure.
3- Embolism.
4- Sheehan’s syndrome.
5- Sepsis.
6- Anaemia.
7- Failure of lactation
99
100. Cont’d
Secondary PPH
1. Retained products or conception
2. Uterine infection
3. placenta accrete
4. Injury to cervix
100
101. Retained placenta
Incidence
Retained placenta is found in 2% of deliveries.
The frequency of retained placenta is markedly
increased at gestation <26 weeks
At term, 90% of placentas will be delivered within 15
minutes.
Once the third stage exceeds 30 minutes, there is a
ten-fold increase in the risk of hemorrhage
101
102. Causes:
• Atony of the uterus :due to causes mentioned
before.
• Constriction ring.
• Rupture uterus :where the placenta passes to the
peritoneal cavity.
• Abnormal adherence of the placenta which may be:
i) Simple adhesion: Manual separation can be done
easily.
ii) Morbid adhesion: Placenta accreta
102
103. Clinical Picture
• Bleeding :occurs only if the placenta is separated
partially or completely.
• Uterus :is lax in case of atony.
• Vaginal examinationmay reveal:
i- Constriction ring.
ii- Rupture uterus.
iii- Morbid placental adherence where there is
no plane of cleavage
103
104. Management
When the placenta is delivered, it should be
inspected for completeness.
Manual exploration of the uterine cavity as
required.
If the placenta is retained, the operator
should use the fingers of one hand or
Curettage with a blunt instrument.
Antibiotics should be routinely administered
104
105. Manual Removal of The Placenta
• The procedure is done under general anaesthesia.
• The right hand is introduced along the umbilical
cord into the uterus.
• The lower edge of the placenta is identified and by
a sawing movement from side to side the placenta
is separated from its bed.
• Grasp the placenta and deliver it out.
• Examine the placenta and membranes for
completeness.
• The left hand is supporting the uterus abdominally
throughout the procedure.
105
106. Complications of Retained Placenta
1- Shock.
2- Postpartum haemorrhage.
3- Puerperal sepsis.
4- Subinvolution
5- Retained parts with subsequent haemorrhage,
infection, placental polyp formation or
choriocarcinoma.
6- Complications of the methods used for its
separation
106
107. Placenta accreta
Placenta accreta is a retained placenta that is
morbidly adherent to the uterine wall.
Types
1.Accreta vera (75-85%)- in which the placenta
adheres to the myometrium without invasion into
the muscle.
2.Increta (17%)-, in which it invades into the
myometrium.
3.Percreta (5%)- in which it invades the full
thickness of the uterine wall and possibly other
pelvic structures, most frequently the bladder
107
108. Cont’d
In a patient with a previous cesarean
section
-Previous one has 14% risk of placenta a.
-Previous two has 24% risk of placenta a.
-Previous three has 44% risk of placenta a.
108
109. Management
1. Hysterectomy
2. Simple excision of the site of trophoblast
invasion with over sewing of the area to the
uterine
3. Internal iliac artery ligation
109
110. Injury to the cervix
After a vaginal delivery, the majority of
women will have lacerations or bruising
of the cervix.
Bleeding which continues despite a well-contracted
uterus is an indication for
examining the cervix.
110
111. Etiology
• Forceps, ventose or breech extraction before full
cervical dilatation.
• Manual dilatation of the cervix.
• Improper use of oxytocins.
• Precipitate labour.
Predisposing Factors:
• 1- Cervical rigidity.
• 2- Scarring of the cervix.
• 3- Oedema as in prolonged labour.
• 4- Placenta praevia due to increased vascularity.
111
112. Types:
1- Unilateral :more common on the left side due
to:
i) Dextro-rotation of the uterus.
ii) Left occipito-anterior position is the
commonest.
2- Lateral.
3- Stellate:multiple tears extending radially from
the
external os like a star.
4- Annular detachment
112
113. Diagnosis:
• Postpartum haemorrhage,in spite of well
contracted uterus.
• Vaginal examination :The tear can be felt.
• Speculum examination : using a posterior wall self
retaining speculum or vaginal retractors and 2 ring
forceps to grasp the anterior and posterior lips of
the cervix so the tear can be visualised.
113
114. Complications
• Postpartum haemorrhage.
• Rupture uterus due to upward extension.
• Infection: cervicitis and parametritis.
• Cervical incompetence leading to future
recurrent abortion or preterm labour.
• Ureteric injury: from the extension of the tear or
during its repair.
114
115. Vaginal Lacerations
Causes:
(I) Primary lacerations less common and caused by :
1- Forceps application.
2- Destructive operations.
3- Vacuum extraction if the cup sucks a part from
the vaginal wall.
(II) Secondary lacerations :more common and are
due to extension from perineal or cervical tears.
115
116. Management
Immediate repair :Continuous locked cut gut
sutures are taken starting from above the
apex to control bleeding from the retracted
blood vessels.
Tight pack :may be needed to control bleeding
from a raw surface area. Foley's catheter
should be inserted before packing and both
are removed after 12-24 hours.
116
117. Cont’d
Deep lacerations, and particularly those that
involve the vaginal vault, need to be
managed under anaesthesia.
A laceration into the vault could extend
forward to the bladder or laterally towards
the uterine artery at the base of the broad
ligament
117
118. Management
• Prompt recognition of the injury and action to
control the bleeding
• Repair
118
119. References
Current Obstetrics and Gynecologic diagnosis
Williams Obstetrics 23rd edition
Management of common problems in GYN
and Obs 5th edition
Simplified Obstetrics
Aptudate
119