Ambo UniversityCollege of Health SciencesDepartment of Medicine

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By : Aregahegn T & Aster.A

July,2014Ambo,Ethiopia

Obstetric Emergency

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

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Hyperemesis GravidarumIt 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

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Etiology1 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.

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Cont’d2.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

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DiagnosisSymptoms:

>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.

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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

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Management

Hospitalization

For observation, fluid therapy

Intravenous fluids

Drugs

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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

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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

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Risk Factors

• Previous preterm PROM

• Incompetent cervix

• Alterations in vaginal pH

– Infections

• Smoking

• Multiple gestation

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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

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Cont’dTest

– Fern - cervical mucus broad fern vs. amniotic fluid narrow fern

– pH (Nitrazine) - turns blue

– Cervicovaginal fetal fibronectin > 50 ng/ml

– Val-salvaImaging-Ultrasound

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ComplicationMaternal 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

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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

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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

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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

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Cont’d

• Steroids

– To enhance fetal lung maturation and

decrease RDS

• Tocolytics

– Randomized trials have shown no pregnancy

prolongation

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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.

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Cont’dThe 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.

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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.

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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.

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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

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Ectopic pregnancyThe 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).

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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 cases25

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.

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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.

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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.

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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.

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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).

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Risk FactorsHigh risk• Tubal surgery• Sterilization• Previous ectopic pregnancy• In utero exposure to diethylstilbestrol• Use of IUD• Documented tubal pathology

Moderate riskInfertility ,Previous genital infections ,Multiple sexual

partners

Slight risk• Previous pelvic/abdominal surgery, Cigarette smoking,

Vaginal douching ,Early age at first intercourse (< 18 years)

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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.

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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.

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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.

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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

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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

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Risk factors

• Primigravida

• Multipara with change of partner

• Chronic hypertension

• Chronic renal disease

• Diabetes mellitus

• Multifetal gestation

• Polyhydramnios

• RH Isoimmunizedpregnancy

• Hydatidiform mole

• Previous history of preeclampsia

• Family history of pregnancy induced hypertension

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TypesMild 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 tobe imminent eclampsia.

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Classification

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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

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

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Clinical FeatureThe 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.

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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. 542

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.

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cont’d

• Eye fundus examination.

• Tests for foetal well being: as

- ultrasound,

- daily foetal movement count,

- non-stress test,

- oxytocin challenge test (if needed)

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Complication

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Fetal

• IUGR

• Oligohydramnios

• Placental infarcts

• Placental abruption

• Prematurity

• Uteroplacentalinsufficiency

• Perinatal death

Maternal

• CNS seizures & stroke

• DIC

• ↑↑ CS

• Renal failure

• Hepatic failure or rupture

• Death

Management

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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

Abruptio placentaDetachment 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

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Types

Revealed (80%)

- Pain + Vaginal bleeding

Concealed (20%)

-Pain/Shock

-No vaginal bleeding

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Management

• Management is influenced by gestational age and degree of abruption

• Indicators for delivery-

– Fetal intolerance

– DIC

– Labor

• Vaginal delivery is acceptable

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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

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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

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Cont’d

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Types

• Minor – Enters LUS but does not cover os

• Major – Covers internal os completely

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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

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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

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Presentation

• Antepartum Haemorrhage

- Late pregnancy

- Painless bleeding ( most common)

• Malpresentation

-Breech/High Head/Unstable lie in 3rd

trimester

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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

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Management

Antenatal

• Bed rest indicated

• Inpatient vs Outpatient

• Major Vs minor

• Anaemia

-Regular Hb

-X-match/Transfuse

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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

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Obstructed labor

Obstructed labor is failure of progressive descent of the presenting part of the fetus in the birth canal for mechanical reasons inspiteof good uterine contraction.

The prevalence in developing countries is about 1-2% in the referral hospitals

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Risk Factors

Ht <150 cm

Previous Hx of prolonged or OL

Clinical pelvimetry

Soft tissue anomalies

Estimate size of fetus late in Pregnancy

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Etiology

A. Maternal causes

Cephalo-pelvic disproportion (CPD)

•Contracted pelvis

•Bone deformities

• Soft tissue obstruction

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Contracted pelvisGenerally 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

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Cont’d

Mid cavity contracture –

-AP < 11.5cm ---normally -11.5cm

-Transverse diameter < 9.5cm

Outlet contracture-

-Inter tuberous diameter <8cm- normally-10cm

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Cont’d

Clinical pelvic assessment done after emptying the bladder & putting the woman in lithotomyposition.

• 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

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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

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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

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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)

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Diagnosis

History

– The patient is usually young teenage

– Abnormally prolonged labor

General examination

– Tired, exhausted and anxious.

– Tachycardic, tachypenic .

– Dehiydrated

-Temprature increase(>38)

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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.

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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.

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Complication

Maternal

- Maternal distress

–Uterine rupture – UNcommon in primi

–PPH- atonic or traumatic

– Infection -sepsis, abscess and peritonitis

– Infertility

–Psychological trauma

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Cont’d

Fetal

• Cerebral birth trauma

• Asphyxia

• Early neonatal infection

• Congenital pneumonia

• Intracranial hemorrhage from excessive moulding.

• Birth injuries

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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

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Cont’dSpecific 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

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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

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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

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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.

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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 scar79

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.

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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

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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

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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.

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Differential Diagnosis

• Abruptio placentae.

• Disturbed advanced extrauterine pregnancy.

• Other causes of acute abdomen.

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Management

1 Supportive management

• Secure IV line with two lines

• Vigorous infusion of crystalloids

• Do HCT ,B/g

• Broad spectrum IV antibiotics

• Catheterize

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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.

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Cord presentation and prolapseCord 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

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

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

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

Complications

• Cord compression and constriction of umbilical vessels due to cold exposure outside the introituscan 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

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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

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

Cont’dDelivery :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

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

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

Cont’d

Primary PPHThe most important cause of massive PPH is uterine

atony when the uterus is not contracted

Steps to stop bleeding1. Massaging the uterus to cause it to contract2. Bimanual compression-Under general anaesthesia,

the uterus is firmly compressed for 5-30 minutes 3. Uterine contraction is maintained by oxyitocin4. Prostaglandin -through the anterior abdominal wall.

97

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

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

Cont’d

Secondary PPH

1. Retained products or conception

2. Uterine infection

3. placenta accrete

4. Injury to cervix

100

Retained placenta

IncidenceRetained 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

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

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

Management

When the placenta is delivered, it should beinspected for completeness.

Manual exploration of the uterine cavity asrequired.

If the placenta is retained, the operatorshould use the fingers of one hand orCurettage with a blunt instrument.

Antibiotics should be routinely administered

104

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

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

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Placenta accretaPlacenta accreta is a retained placenta that is

morbidly adherent to the uterine wall.

Types1.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

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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.

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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

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Injury to the cervix

After a vaginal delivery, the majority ofwomen will have lacerations or bruisingof the cervix.

Bleeding which continues despite a well-contracted uterus is an indication for examining the cervix.

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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

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

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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.

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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.

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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.

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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.

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Cont’d

Deep lacerations, and particularly those thatinvolve the vaginal vault, need to bemanaged under anaesthesia.

A laceration into the vault could extendforward to the bladder or laterally towardsthe uterine artery at the base of the broadligament

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Management

• Prompt recognition of the injury and action to control the bleeding

• Repair

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References

Current Obstetrics and Gynecologic diagnosis

Williams Obstetrics 23rd edition

Management of common problems in GYN and Obs 5th edition

Simplified Obstetrics

Aptudate

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