HOLY FAMILY COLLEGE OF NURSING , DELHI

MATERIAL FOR CONTINUING NURSING EDUCATION

ON

“ OBSTETRICAL HAEMORRHAGE ”
Obstetrical hemorrhage or bleeding is bleeding in pregnancy that occurs before , during or after child
birth. Bleeding before childbirth is that which occur after 24 weeks of pregnancy. Bleeding which occurs
before 24 weeks is known as early pregnancy bleeding. An obstetric hemorrhage may occur before or
after delivery , but more than 80% of cases occur postpartum .

Broadly obstetrical hemorrhage is divided into two :

A. Antepartum Hemorrrhage
B. Post partum Hemorrhage

A. ANTEPARTUM HEMORRHAGE:

INTRODUCTION:
Antepartum haemorrhage or prepartum hemorrhage is genital bleeding during pregnancy from
the 24th week (sometimes defined as from the 20th week) gestational age to term.
It can be associated with reduced fetal birth weight.
In regard to treatment, it should be considered a medical emergency (regardless of whether there
is pain) and medical attention should be sought immediately, as if it is left untreated it can lead
to death of the mother and/or fetus.
DEFINITION
It is defined as bleeding from or into the genital tract after the 28th week of pregnancy but before
the birth of the baby (the first and second stage of labor are thus included). The 28th week is
taken arbitrarily as the lower limit of fetal viability. The incidence is about 3% amongst hospital
deliveries.
CAUSES OF THE ANTEPARTUM HEMORRHAGE:

APH

Placental bleeding Unexplained (25%) Extra placental

(70%) excluding placental - Implantation
Bleeding and local lesions bleed
Placenta praevia - Carcinoma of
Abruptio placenta Cervix
-Cervical ectropion
- Varicose vein
- Local trauma
- Cervical polyps

DEFINITION OF ABRUPTIO PLACENTA:

It is one form of antepartum hemorrhage where the bleeding occurs due to premature separation
of normally situated placenta. Out of the various nomenclatures, abruptio placenta seems to be
appropriate one.

TYPE/ VARIETIES OF ABRUPTIO PLACENTA:

(1) Revealed: Following separation of the placenta, the blood insinuates downwards between the
membranes and the decidua. Ultimately, the blood comes out of the cervical canal to be visible
externally. This is the commonest type.
(2) Concealed: The blood collects behind the separated placenta or collected in between the
membranes and decidua. The collected blood is prevented from coming out of the cervix by the
presenting part which presses on the lower segment. At times, the blood may percolate into the
amniotic sac after rupturing the membranes.
In any of the circumstances blood is not visible outside. This type is rare.
(3) Mixed: In this type, some part of the blood collects inside (concealed) and a part is expelled
out (revealed). Usually one variety predominates over the other. This is quite common.
Bleeding is almost always maternal. But placental tear may cause fetal bleeding.

INCIDENCE OF ABRUPTIO PLACENTA:

The overall incidence is about 1 in 200 deliveries. Depending on the extent (partial or complete)
and intensity of placental separation, it is a significant cause of perinatal mortality (15–20%) and
maternal mortality (2–5%). More and more cases of placental abruption are being diagnosed in
the recent years

ETIOLOGY OF THE ABRUPTIO PLACENTA:

The prevalence is more with
(a) high birth order pregnancies with gravida 5 and above — three times more common than in
first birth
(b) advancing age of the mother
(c) poor socio-economic condition
(d) malnutrition
(e) Smoking (vaso-spasm).

 Hypertension in pregnancy is the most important predisposing factor. Pre-eclampsia,

gestational hypertension and essential Hypertension, all are associated with placental
abruption. The association of pre-eclampsia in abruptio placenta varies from 10-50
percent. The mechanism of the placental separation in pre-eclampsia is : Spasm of the
vessels in the utero placental bed (decidual spiral artery) → anoxic endothelial damage
→ rupture of vessels or extravasation of blood in the decidua basalis (retroplacental
hematoma).
 Trauma: Traumatic separation of the placenta usually leads to its marginal separation
with escape of blood outside. The trauma may be due to:
(i) Attempted external cephalic version specially under anaesthesia using great force
(ii) Road traffic accidents or blow on the abdomen
(iii) Needle puncture at amniocentesis.
 Sudden uterine decompression: Sudden decompression of the uterus leads to diminished
surface area of the uterus adjacent to the placental attachment and results in separation of
the placenta. This may occur following—(a) delivery of the first baby of twins
(b) Sudden escape of liquor amnii in hydramnios and
(c) Premature rupture of membranes.
 Short cord, either relative or absolute, can bring about placental separation during labor
by mechanical pull.
  Supine hypotension syndrome: In this condition which occurs in pregnancy there is
passive engorgement of the uterine and placental vessels resulting in rupture and
extravasation of the blood.
 Placental anomaly: Circumvallate placenta.
 Sick placenta: Poor placentation, evidenced by abnormal uterine artery Doppler
waveforms is associated with placental abruption.
 Folic acid deficiency even without evidence of overt megaloblastic erythropoiesis — this
has been observed to be associated.
 Uterine factor: Placenta implanted over a septum (Septate Uterus) or a submucous
fibroid.
 Torsion of the uterus leads to increased venous pressure and rupture of the veins with
separation of the placenta.
 Cocaine abuse is associated with increased risk of transient hypertension, vasospasm and
placental abruption.
 Thrombophilias inherited or acquired have been associated with increased risk of
placental infarcts or abruption.

Prior abruption: Risk of recurrence for a woman with previous abruption varies between 5 to
17%.

PATHOPHYSIOLOGY OF THE ABRUPTIO PLACENTA:

Depending upon the etiological factors,

Premature placental separation is initiated by hemorrhage into the decidua basalis.

The collected blood (decidual hematoma) at the early phase hardly produces any morbid
pathological changes in the uterine wall or on the placenta.

However, depending upon the extent of pathology, there may be degeneration and necrosis of the
decidua basalis as well as the placenta adjacent to it.

Rupture of the basal plate may also occur, thus communicating the hematoma with the
intervillous space.

The decidual hematoma may be small and self limited; the entity is evident only after the
expulsion of the placenta (retroplacental hematoma).
The features of retroplacental hematoma are :
(a) Depression found on the maternal surface of the placenta with a clot which may be found
firmly attached to the area
(b) Areas of infarction with varying degree of organization.

CLINICAL FEATURES OF THE ABRUPTIO PLACENTA:

COMPLICATIONS OF ABRUPTIO PLACENTA:

MATERNAL: In revealed type—maternal risk is proportionate to the visible blood loss and
maternal death is rare.
In concealed variety—The following complications may occur either singly or in combination.
(1) Hemorrhage which is either totally concealed inside the uterus or more commonly, part is
revealed outside. There may be intraperitoneal or broad ligament hematoma
(2) Shock may be out of proportion to the blood loss. Release of thromboplastin into the
maternal circulation results in DIC or there may be amniotic fluid embolism
(3) Blood coagulation disorders
(4) Oliguria and anuria due to—(a) hypovolemia (b) serotonin liberated from the damaged
uterine muscle producing renal ischemia and (c) Acute tubular necrosis. However, a severe
case may lead to (d) cortical necrosis and renal failure
(5) Postpartum hemorrhage due to — (a) atony of the uterus and (b) increase in serum FDP
(6) Puerperal sepsis.

The complicating factors those are responsible for increased maternal death varies from 2–8%.
However, with better understanding in the management of shock, coagulation failure and renal
failure, maternal death has been reduced markedly. Some cases who manage to survive may
develop features of ischemic pituitary necrosis. There is failure of lactation (Sheehan’s
syndrome) later on.

FETAL: In revealed type, the fetal death is to the extent of 25-30%. In concealed type, however,
the fetal death is appreciably high, ranging from 50-100%. The deaths are due to prematurity and
anoxia due to placental
Separation. With same degree of placental separation, the fetus is put to more risk in abruptio
placenta than in placenta previa. This is due to the presence of pre-existing placental pathology
with poor functional reserve in the former, in contrast to almost normal placental functions in the
latter. Risk of recurrence in subsequent pregnancy is about tenfold with high perinatal mortality.

PREVENTIVE MEASURES OF THE ABRUPTIO PLACENTA:

The prevention aims at—
(1) elimination of the known factors likely to produce placental separation
(2) correction of anemia during antenatal period so that the patient can withstand blood loss and
(3) Prompt detection and institution of the therapy to minimise the grave complications namely
shock, blood coagulation disorders and renal failure.
Prevention of known factors likely to cause placental separation are

 Early detection and effective therapy of pre-eclampsia and other hypertensive disorders
of pregnancy.
 Needle puncture during amniocentesis should be under ultrasound guidance.
 Avoidance of trauma—especially forceful external cephalic version under anaesthesia.
 To avoid sudden decompression of the uterus— in acute or chronic hydramnios,
amniocentesis is preferable to artificial rupture of the membranes.
 To avoid supine hypotension the patient is advised to lie in the left lateral position in the
later months of pregnancy.

Routine administration of folic acid from the early pregnancy — of doubtful value.

MANAGEMENT OF THE ABRUPTIO PLACENTA:

AT HOME: The patient is to be treated as outlined in placenta previa and arrangement should be
made to shift the patient to an equipped maternity unit as early as possible.
IN THE HOSPITAL: Assessment of the case is to be done as regards:
(a) amount of blood loss
(b) maturity of the fetus and
(c) whether the patient is in labor or not (usually labor starts)
(d) presence of any complication and
(e) Type and grade of placental abruption.

Emergency measures:
(i) Blood is sent for hemoglobin and hematocrit estimation, coagulation profile
(fibrinogen level, FDP, prothrombin time, activated partial thromboplastin time and
platelets), ABO and Rh grouping and urine for detection of protein
(ii) Ringer’s solution drip is started with a wide bore cannula and arrangement for blood
transfusion is made for resuscitation. Close monitoring of maternal and fetal
condition is done.

Management options are:

(a) Immediate delivery
(b) Management of complications if there is any
(c)Expectant management (rare).

Definitive treatment (immediate delivery): The patient is in labor: Most patients are in labor
following a term pregnancy: The labor is accelerated by low rupture of the membranes. Rupture
of the membranes with escape of liquor amnii accelerates labor and it increases the uterine tone
also. Oxytocin drip may be started to accelerate labor when needed.
Vaginal delivery is favoured in cases with:
(i) Limited placental abruption
(ii) FHR tracing is reassuring
(iii) Facilities for continuous (electronic) fetal monitoring is available
(iv) Prospect of vaginal delivery is soon or
(v) Placental abruption with a dead fetus.
The advantages of amniotomy are:
(a) Initiates myometrial contraction and labor process
(b) Expedites delivery
(c) Better compression of spiral artery to arrest hemorrhage
(d) Reduces entry of thromboplastin into maternal circulation and thereby (e) Reduces the risk of
renal cortical necrosis and DIC.
The patient is not in labor:
(i) Bleeding continues
(ii) > Grade I abruption :

Delivery either by
(A) Induction of labor or (B) Cesarean section.

(A) Induction of labor is done by low rupture of membranes. Oxytocin may be added to
expedite delivery. Labor usually starts soon in majority of cases and delivery is
completed quickly (4-6 hours). Placenta with varying amount of retroplacental clot is
expelled most often simultaneously with the delivery of the baby. Inj. oxytocin 10.IU IV
(slow) or IM or Inj. Methergin 0.2 mg IV is given with the delivery of the baby to
minimise postpartum blood loss. Oxytocics should be used to improve the uterine tone
along with blood transfusion.
(B) Cesarean section: Indications are :
(a) Severe abruption with live fetus
(b) Amniotomy could not be done (unfavorable cervix)
(c) Prospect of immediate vaginal delivery despite amniotomy is remote
(d) Amniotomy failed to control bleeding
(e) Amniotomy failed to arrest the process of abruption (rising fundal height)
(f) Appearance of adverse features (fetal distress, falling fibrinogen level, oliguria).
Anesthesia during cesarean section: Regional anesthesia is generally avoided when there is
significant hemorrhage. This is to avoid profound and persistent hypotension Expectant
management in a case of placental abruption is an exception and not the rule. Cases where
bleeding is slight and has stopped (Grade I abruption), fetus reactive (CTG) and remote from
term, may be considered. The goal of expectant management is to prolong the pregnancy with
the hope of improving fetal maturity and survival. Continuous electronic fetal monitoring is
maintained. Patient should be observed in the labor ward for 24-48 hours to ensure that no
further placental separation is occurring. Meanwhile betamethasone is given to accelerate fetal
lung maturity in the event preterm delivery has to be contemplated. Further separation of
placenta at any moment may cause fetal death or maternal complications. This is the major risk
of conservative management.
Management of complications : The major complications of placental abruption are:
 (a)Hemorrhagic shock.
(b) DIC.
(c) Renal failure and
(d) Uterine atony and postpartum hemorrhage.
Hypovolemia should be corrected early. Blood pressure may not be a correct guide to assess
shock, as it may be high due to severe degree of vasospasm. Irrespective of the patient’s general
condition, at least one litre of blood transfusion should be the minimum when the diagnosis of
concealed accidental hemorrhage is made. The best guide to monitor the patient is the use of
central venous pressure (CVP), which is maintained at
10 cm of water. Hematocrit should be at least 30% and urinary output > 30 mL/h.
A. Hemorrhagic shock—Classification of obstetric hemorrhagic is based upon volume deficit.
B. DIC—Release of tissue thromboplastin in placental abruption causes consumptive
coagulopathy. Diagnosis is based on the coagulation profile assessment. Treatment is to restore
the hematologic deficiency (fibrinogen level > 150 mg/ dL), 1 unit (500 mL) of fresh blood
contains 0.5 mL g of fibrinogen and raises the fibrinogen level by 12.5 mg/dL. Platelet count
Increases by 10,000–15,000/cu mm to replenish the volume deficit and to arrest the pathologic
process (delivery).
Feto-maternal hemorrhage is common with traumatic variety of placental abruption. To combat
feto-maternal hemorrhage 300 μg of anti-D immunoglobulin is administered to all Rh-negative
women. The amount of fetal to maternal bleed is usually < 15 Ml

INDETERMINATE BLEEDING:
The exact cause of vaginal bleeding in late pregnancy is not clearly understood in few cases. The
diagnosis of unclassified bleeding should be made after exclusion of placenta previa, placental
abruption and local causes. Rupture of vasa previa, marginal sinus hemorrhage, circumvallate
placenta, marked decidual reaction on endocervix or excessive show may be a possible cause of
such bleeding.
VASA PREVIA: The unsupported umbilical vessels in velamentous placenta, lie below the
presenting part and run across the cervical os. These vessels are torn either spontaneously or
during rupture of membranes.
Color-flow Doppler is helpful for antenatal diagnosis. Fetal mortality is high (50%) due to fetal
exsanguination. Detection of nucleated red blood cells (Singer’s alkali denaturation test) or fetal
hemoglobin is diagnostic.
Vaginal bleeding is often associated with fetal distress (tachycardia, sinusoidal FHR tracing).
MANAGEMENT: Management depends on fetal gestational age, severity, persistence or
recurrence of bleeding, and the presumed cause of bleeding.
A) Pregnancy > 37 weeks and bleeding recurrent — delivery is recommended. The mode of
delivery depends on the state of the fetus, and other associated factors (cervix).
B) Expectant management can be done in selected cases for fetal maturity similar to placenta
previa. Fetal monitoring must be carefully done. Intrapartum diagnosis of vasa previa, needs
expeditious delivery. Neonatal blood transfusion may be needed.

EXTRA PLACENTAL CONDITIONS OF ANTEPARTUM HEMORRHAGE:

1. IMPLANTATION BLEED

A small vaginal bleed can occur when the blastocyst embed in the endometrium. This usually
occurs 5-7 days after fertilization and if the timing coincides with the expected menstruation this
may cause confusion over the dating of the pregnancy if the menstrual is used to estimate the
date of birth.

2. CERVICAL POLYPS

These are small, vascular, pedunculated growths on the cervix, which consist of squamous or
columnar epithelial cells over a core of connective tissue rich with blood vessels. During
pregnancy, the polyps may be a cause of bleeding but require no treatment unless the bleeding is
severe or a smear test indicates malignancy.

3. CARCINOMA OF THE CERVIX

Carcinoma of the cervix is the most common gynaecological malignant disease occurring in
pregnancy with an estimated incidence of 1 in 2200 pregnancies .The condition presents with
vaginal bleeding and increased vaginal discharge. On speculum examination the appearance of
the cervix may lead to a suspicious of carcinoma, which is diagnosed following colposcopy or a
cervical biopsy.
The precursor to cervical cancer is cervical intraepithelial neoplasia (CIN), which can be
diagnosed from an abnormal papanicolaou (PAP) smear. Where this is diagnosed at early stage,
treatment can usually be postponed for the duration of the pregnancy. The Pap smear is not
routinely carried out during pregnancy , but the midwife should ensure
that pregnant women know about the National Health Service Screening Programme(2013),
recommending a smear 6 weeks postnatally if one has not been carried out in the previous 3
years.
Treatment for cervical carcinoma in pregnancy will depend on the gestation of the pregnancy and
the stage of the disease, and full explanations of treatments and their possible outcomes should
be given to the woman and her family. For carcinoma in the early stages, treatment may be
delayed until the end of the pregnancy, or a cone biopsy may be performed under general
anaesthetic to remove the affected tissue. However there is risk of hemorrhage due to the
increased vascularity of the cervix of the cervix in the pregnancy, as well as the risk of
miscarriage. Where the disease is more advanced and the diagnosis made in early pregnancy, the
woman may be offered a termination of pregnancy in order to receive the treatment, as the
effects of chemotherapy and radiotherapy on the fetus cannot be accurately predicted at the
present time. During the late second and third trimester the obstetric and oncology teams will
consider the optimal time for birth in order to achieve the best outcomes for both mother and the
baby.

1. CERVICAL ECTROPION

More commonly known as cervical erosion. The changes seen in cases of cervical ectropion are
as a physical response to hormonal changes that occur in pregnancy. The number of columnar
epithelial cells in the cervical canal increase significantly under the influence of estrogen during
pregnancy to such an extent that they extend beyond to the vaginal surface of the cervical os,
giving it a dark red appearance. As this area is vascular, and the cells form only a single layer,
bleeding may occur either spontaneously or following sexual intercourse. Normally, no
treatment is required, and the ectropion reverts back to normal cervical cells during the
puerperium.
NURSING MANAGEMENT OF ANTEPARTUM HEMORRHAGE:
1. ASSESSMENT:

Assess for the following clinical manifestation:

 Scant or profuse vaginal bleeding.

 Uterine irritability, tenderness and rigidity.
 Abdominal pain that is intermittent or continuous.
 Signs of maternal shock- hypotension, rapid pulse, dyspnoea
 Violent fetal activity followed by inactivity
 FHR- slow to absent
 Late deceleration noted in monitor strip
 May have blood stained amniotic fluid ( port wine stain)
2. ANALYSIS/ NURSING DIAGNOSIS:
 Risk for fetal injury
 Risk for infection
 Ineffective airway clearance
 Actual/ risk for aspiration
 Anxiety
 Anticipatory grieving
 Altered family process
 Actual/ risk for altered parenting
 Health seeking behaviour
3. PLANNING:
 Promote safe care environment
 Monitor for presence of pre existing conditions.
 Assess maternal – fetal status and initiative emergency care
 Provide encouragement and support.
 Administer measures to treat shock and blood loss
4. IMPLEMENTATION:
 Monitor maternal and fetal vital signs.
 Treat shock symptoms
 Assess vital signs every 5-15 mins
 Administer oxygen by face mask at 7-10 L/min
 Increase IV flow rate
 Administer blood
 Monitor urinary output
 Monitor FHR continuously
 Observe for signs and symptoms of coagulation problems
 Measure abdominal girth
 Remain with woman
 Monitor labor pattern continuously if allowed to progress or prepare for cessarean
section.
5. EVALUATION
 The woman and her spouse understand the treatment plan
 The physiological status of the women and the fetus remains within the normal limits.
 The women and her spouse verbalizes, decrease of anxiety and feelings of support.

ANTEPARTUM HAEMORRHAGE

Definition:Antepartum haemorrhage (APH) is defined as bleeding from or in to the genital tract,

occurring from 28 weeks (>500g) of pregnancy and prior to the birth of the baby.

By RCOG 2011

Epidemiology :

 Affects 3–5% of all pregnancies

 Leading cause of perinatal and maternal mortality worldwide.
 Up to one-fifth of very preterm babies are born in association with APH occurs in 2.8/1000
singleton pregnancies and 3.9 /1000 twin pregnancies
 Most of the time unpredictable

CAUSE

 Placenta praevia – most common pathological cause ( 1/100)

 Abruptio placenta: second most common pathological cause (1/200)
 Vasa praevia: often difficult to diagnose frequently leads to fetal demise ( 1/2000 – 3000)
 Uterine rupture – (<1% in scarred uterus)
 Bleeding from the lower genital tract

 Cervical bleeding – cervicitis

  Cervical neoplasm
 Cervical polyp
 Cervical ectropion
 Vaginal bleeding - trauma
o Neoplasm
o Vulval varices
o Infection
 Inherited bleeding problems – very rare , 1 in 10,000 women.
 Unexplained – no definite cause is diagnosed in about 40% of APH
 Excessive show
 Local causes ( bleeding from cervix, vagina and vulva )

COMPLICATIONS OF APH

Maternal complications

•Anaemia

•Infection

•Maternal shock

•Renal tubular necrosis

•Consumptive coagulopathy

•Postpartum haemorrhage

•Prolonged hospital stay

•Psychological sequelae

•Complications of blood transfusion

Fetal complications

•Fetal hypoxia

•Fetal growth restriction

•Prematurity (iatrogenic & spontaneous)

•Fetal death

PLACENTA PREVIA :

Definition : Placenta praevia is when the placenta attaches inside the uterus but near or over the cervical
opening.

 The placenta is implanted partially and completely over the lower uterine segment ( over or
adjacent to the internal os) it is called Placenta Previa.
 ( DC Dutta )
 In placenta previa the placenta is implanted in the lower uterine segment such that is completely
or partially cover the cervix or is close enough to the cervix to cause bleeding when cervix is
dilated or the lower uterine segment effaces.
( Hull and Resnik, 2009_)

INCIDENCE :

 In 80% cases it is found multiparous women.

 the incidence is increased beyond the age of 35, with high birth order pregnancies and in multiple
pregnancy.
 The incidences approximately 4-5 per thousand pregnancies.

RISK FACTORS :

Risk factors with their odds ratio

Risk factor Odds ratio

Illicit drugs 2.8

≥ 1 previous Cesarean section 2.7

Parity ≥ 5 (vs. para 0) 2.3

Parity 2–4 (vs. para 0) 1.9

Prior abortion 1.9

Smoking 1.6

Congenital anomalies 1.7

Male fetus (vs. female) 1.1

Pregnancy-induced hypertension 0.4

RISK FACTORS
The following have been identified as risk factors for placenta previa:

 Previous placenta previa (recurrence rate 4–8%), caesarean delivery, myomectomy or endometrium
damage caused by D&C.
 Women who are younger than 20 are at higher risk and women older than 35 are at increasing risk as
they get older.
 Alcohol use during pregnancy was previous listed as a risk factor, but is discredited by this article.
 Women who have had previous pregnancies ( multiparity ), especially a large number of closely
spaced pregnancies, are at higher risk due to uterine damage.
 Smoking during pregnancy; cocaine use during pregnancy.
 Women with a large placentae from twins or erythroblastosis are at higher risk.
 Race is a controversial risk factor, with some studies finding that people from Asia and Africa are at
higher risk and others finding no difference.
 Placental pathology (Vellamentous insertion, succinturiate lobes, bipartite i.e. bilobed placenta etc.)
 Number of curettage for spontaneous or induced abortion.
 Residence at higher altitudes.

CAUSE
Exact cause of placenta previa is unknown.
It is hypothesized to be related to abnormal vascularisation of the endometrium caused by scarring
or atrophy from previous trauma, surgery, or infection. These
factors may reduce differential growth of lower segment, resulting in less upward shift in placental
position as pregnancy advances.

Placental growth slows down in later

monthsLower segment
progressively dilates

Inelastic placenta sheared off the wall of

lower segmentOpening up of
uteroplacental vessels

Bleeding
CLASSIFICATION:

Traditionally, four grades of placenta previa were used, however now it is more common to simply
differentiate between 'major' and 'minor' cases.

Type Description

Minor Placenta is in lower uterine segment, but the lower edge does not cover the internal os

Major Placenta is in lower uterine segment, and the lower edge covers the internal os

Other than that placenta previa can be also classified as :

Complete : When the placenta completely covers the cervix.
Partial : When the placenta partially covers the cervix.
Marginal : When the placenta ends near the edge of the cervix, about 2 cm from the internal cervical os.

Traditionally placenta previa is divided into four types –

1 Low lying placenta previa:In this type placenta is extended into the lower uterine segment but does
not reach the internal orifice of cervix. In most of cases it often moves upward in the uterus as the
due date approaches

2 Marginal placenta previa: When placenta just reaches the internal orifice of cervix, but does not
cover it then the condition is known as marginal placenta

3 Partial placenta previa: In this type placenta partially covers the internal orifice of cervix

4.Complete placenta previa: In this the internal orifice of cervix is completely covered by placenta
SIGNS AND SYMPTOMS
Vaginal bleeding :
 Sudden in onset and painless
 Revealed bleeding ( fresh blood )
 Bright red or dark colored
 Unrelated to activity.
Vaginal bleeding with uterine contraction : (10-20%)
General condition and anaemia are proportionate to the visible blood loss.

Abdominal examination :
 The uterus feel relaxed, soft and elastic without any localised area of tenderness.
 Persistence of malpresentation like breech or transverse or unstable lie is more frequent. There
is also increased frequency of twin pregnancy.
 The head is floating in contrast to the period of gestation Peristent displacement of the fetal head
is very suggestive. The head cannot be pushed down into the pelvis.
 Fetal heart sound is usually present, unless there is major separation of the placenta with the
patient in exsanguinated condition slowing of the fetal heart rate on pressing the head down into
the pelvis which soon recovers promptly as the pressure is released is suggestive of the presence
of low lying placenta specially of posterior type (stallworthy’s sign). But this signis not always
significant because it may be due to fetal head compression even in an otherwise normal case.

Vulval inspection:

Only inspection is to be done to note whether the bleeding is still occurring or has ceased,
character of the blood – bright red or dark coloured and the amount of blood loss – to be assessed from
the blood stained clothing. In placenta praevia, the blood is bright red as the bleeding occurs from the
separated utero-placental sinuses close to the cervical opening and escapes out immediately.

Vaginal examination must not be done outside the operation theatre in the hospital, as it can provoke
further separation of placenta with torrential haemorrhage and may be fatal. It should only be done prior
to termination of pregnancy in the operation theatre under anaesthesia, keeping everything ready for
caesarean section.

Asymptomatic (ultrasound ) : 10%

1/3rd of pregnant women present with bleeding prior to 30 wks : blood transfusion and prenatal delivery
and perinatal mortality.
Bleeding after delivery occurs in about 22% of those affected.
Women may also present as a case of failure of engagement of fetal head.

DIAGNOSIS:
a) History may reveal antepartum haemorrhage.
b) Abdominal examination usually finds the uterus non-tender, soft and relaxed.
c) Leopold's Maneuvers may find the fetus in an oblique or breech position or lying transverse as a
result of the abnormal position of the placenta.
d) Malpresentation is found in about 35% cases.
Vaginal examination is avoided in known cases of placenta previa

CONFIRMATORY

1.Ultrasonography

 Trans vaginal : gold standard , safe and effective technique.

 Trans labial ultrasonography : excellent images.
 Trans abdominal : accuracy 95%

False negative rate 7%

An over distended bladder for anterior previa

For posterior previa : Trendelburg position.

2. color Doppler flow study

3. magnetic resonance
4. vaginal examination
CONFIRMATION OF DIAGNOSIS

DIAGNOSIS: Painless and recurrent vaginal bleeding in the second half of pregnancy should be taken as
placenta praevia unless proved otherwise. Ultrasonographyis the initial procedure either to confirm or to
rule out the diagnosis.

1. LOCALISATION OF PLACENTA 2. CLINICAL

(PLACENTOGRAPH) - By internal
- Sonography . Magnetic resonance examination (double
imaging(MRI) set up examination)n
- Transabdominal - Direct visualization
Ultrasound(TAS) during caesarean
- Transvaginal section
Ultrasound(TVS) - Examination of the
- Transperineal ultrasound placenta following
- Coloue Doppler flow study vaginal delivery.

PLACENTOGRAPHY
1. Sonography : Sonography is the diagnostic technique of choice (RCOG-2001). It provides
the simplest, most precise and safest method of placental localization.
In addition, it is helpful for assessing the fetal size and status. It also provides information pertaining
to maturity and well being of the fetus for guiding the management.

a. Transabdominal (TAS) : The accuracy after 30th week of gestation is about 98 percent. False
positive result may be due to full bladder or myometrial contractions. Poor imaging could be due
to maternal obesity and posteriorly situated placenta.

b.Transvaginal (TVS) :Transducer is inserted within the vagina without touching the cervix.

c.Transperineal (TPS) :this is well accepted by patients. Internal os is visualized in 97-100% of

cases.

Colour Doppler flow study :prominent venous flow in the hypoechoic areas near the cervix is
consistent with the diagnosis of placenta praevia.
Magnetic Resonance Imaging (MRI) : it is a non invasive method without any risk of
ionising radiation. Quality to placental imaging is excellent. Limitation of MRI are : more time
consuming, lack of portability and the cost.

Advantages of ultrasonography and MRI :

(1) Need of vaginal examination with the risk of haemorrhage is avoided
(2) The need of prolonged and unnecessary hospital stay in patients with clinical diagnosis of APH can be
reduced

(3)Diagnosis of placenta praevia can bemade even before the bleeding starts

(4) Diagnosis of morbid adherent placenta (specially in a woman with placenta praevia and prior
caesarean delivery) can be made

(5) plan to delivery can be organized accordingly.

CLINICAL CONFIRMATION
Double set-up examination (vaginal examination): It is less frequently done these days.
The indications are

(1) Inconclusive USG report

(2) USG revealed type I placenta or

(3) USG facilities not available. It is done in the operation theatre under anaesthesia keeping everything
ready for caesarean section. Palpation of the placenta on the lower segment not only conclusively
confirms the clinical diagnosis but also identifies its degree.

MANAGEMENT

 Prevention
 Immediate management
 Expectant management
 Active management
Prevention

 Adequate antenatal care to improve the health status of the women & correction of
anemia.
 Antenatal diagnosis of low-lying placenta at 20 weeks with routine ultrasound.
 Significance of warning hemorrhage
 Family planning & limitation of births
 TREATMENT ON ADMISSION

1. IMMEDIATE
2. FORMULATION OF LINE OF ATTENTION

1. IMMEDIATE ATTENTION : overall assessment of the case is quickly made as regard:

a. Amount of blood loss – by noting the general condition , pallor , pulse rate , and blood
pressure.
b. Blood sample are taken for group, cross matching and estimation of haemoglobin.
c. A large-bore IV cannulal is sited and an infusion of normal saline is started and compatible
cross matched blood transfusion should be arranged.
d. Gentle abdominal palpation to ascertain any uterine tenderness and auscultation to note the
fetal heart rate
e. Inspection of the vulva to note the presence of any active bleeding.

FORMULATION OF LINE OF TREATMENT

The definitive treatment depends upon the duration of pregnancy, fetal and maternal status and extent of
the haemorrhage.

 Expectant management
 Active management

Expectant management :

The aim : to continue pregnancy for fetal maturity without compromising the maternal health.

Vital prerequisites :

1. Availability of blood for transfusion whenever required

2. Facilities for caesarean section should be available throughout 24 hours, should it prove
necessary.

Suitable case :

1. Mother is in good health status ( haemoglobin >10gm, haematocrit > 30 %)

2. Duration of pregnancy is less than 37 weeks
3. Active vaginal bleeding is absent
4. Fetal well being is assured ( USG)

Conduct of expectant treatment :

1. Bed rest
2. Investigation : like Hb, blood grouping and urine for protein
3. Periodic inspection : of the vulval pads and fetal surveillance with ISG at intervsl of 2-3 wks
 4. Supplementary haematinics: and blood loss is replaced by adequate cross matched blood
transfusion, if the patient is anaemic.
5. When the patient is allow to out of the bed ( 2-3 days after the bleeding stops) , a gentle Cusco’s
examination is made to exclude local cervical and vaginal lesions for bleeding.
6. Use of tocolysis (MgSo 4 ) can be done if vaginal bleeding is associated with uterine contractions.
7. Use of cervical cerclage to reduce bleeding and to prolong pregnancy is not helpful.
(RCOG2005)
8. Rh immunoglobin should be given to all Rh negative women

TERMINATION OF THE EXPECTANT TREATMENT : the expectant treatment is carried upto 37

weeks of pregnancy. By this time baby become sufficiently mature.

Steroid therapy : is indicated when the duration of pregnancy is less than 34 weeks . Betamethasone
reduces the risk of respiratory distress of the new born when preterm delivery is considered.

ACTIVE MANAGEMENT

The indication of delivery are :

1. Bleeding occurs at or after 37weeks od pregnancy.

2. Patient is in labour
3. Patient is in exsanguinated state on admission
4. Bleeding is continuing and of moderate degree
5. Baby is dead or known to be congenital deformed

DEFINITE MANAGEMENT :

A. CAESAREAN SECTION : is done for all women with sonographic evidence of placenta previa
where placental edge is within 2cm from the internal os. It is specially indicated if it posterior or
thick (RCOG2005)
B. VAGINAL DELIVERY : may be considered where placenta edge is clearly 2-3 cm away from
the internal cervical os.
Precaution during vaginal delivery

1. All the possible steps should be taken to restore the blood volume.
2. Methergin 0,2 mg should be given IV with the delivery of anterior shoulder to prevent blood loss
in third stage
3. Proper examination of the cervix should be done soon following delivery to detect any evidence
of tear
4. Baby’s blood haemoglobin level is to be checked and if necessary arrangement are to be made
for blood transfusion.

SHCHEME OF ACTIVE MANAGEMENT OF PLACENTA PREVIA IN HOSPITAL

 All APH patients are to be admitted

 General and abdominal examination

 Clinical assessment of blood loss
 Hb%, haematocrit, ABO and Rh group
 Resuscitation, if necessary ( IV
infusion/transfusion using wide bore cannula)
 Localisation of placenta (USG)

Expectant treatment active interference

 No active bleeding bleeding continue

 Preg.>37wks preg < 37wks
 Pt- stable pt in labour
 FSH – good FSH – absent
 CTG – reactive fetus

Ultrasonographic evidence

Placenta edge is clearly 2-3 cm placenta edge within 2cm

Away from the internal os

Internal exa in OT. No internal examination

ARM +- oxytocin caesarean section

Satisfactory progress bleeding continue , no labour initiation

Vaginal delivery caesarean delivery

 COMPLICATIONS

Maternal.

1.During pregnancy –

 APH with shock

 Malpresentation
 Premature labor either spontaneous or induced

2.During labor –

 Early rupture of membranes

 Cord prolapse
 Intrapartum haemorrhage
 Increased operative interferance
 Postpartum haemorrhage
 Imperfect retraction of the lower uterine segment on which the placenta is implanted.
 Large surface area of placenta with atonic uterus due to preexisting anemia
 Trauma to cervix and lower segment because of extreme softness and vascularity.
Retained placenta(increased surface area,morbid adhesion)

PUERPERIUM Sepsis is increased due to –

 Increased operative interference –

 Placental site near to vagina –
 Anemia & devitalized state of the patient Subinvolution embolism

Fetal

 Low birth weight

 Asphyxia
 Early separation of placenta
 Compression of the placenta
 Compression of cord
 Intrauterine death
 Severe degree of separation of placenta
 Maternal hypovolaemia
 shock•
 Birth injuries-
 increased intraoperative interference•
 Congenital malformation

PROGNOSIS•
 a. Reduction of maternal deaths in placenta praevia due to
 Early diagnosis
 Omission of internal examination
 Free availability of blood transfusion facilities.
 Potent antibiotics
 Wider use of caesarean section with expert anaesthetist
 Skill & judgment with which the cases are managed
b. Fetal
 Fetal mortality ranges from10-25%.
 Reduction of deaths is principally due to judicious extension of expectant treatment
thereby reducing loss from prematurity, liberal use of LSC’s which greatly lessens the loss
from anoxia and improvement in the NICU.

NURSING DIAGNOSIS

 Risk for Impaired Fetal Gas Exchange r/t Disruption of Placental Implantation
 Fluid Volume Deficit r/t Active Blood Loss Secondary to Disrupted Placental Implantation
 Active Blood Loss (Hemorrhage) r/t Disrupted Placental Implantation• Fear r/t Threat to
Maternal and Fetal Survival Secondary to Excessive Blood Loss
 Activity Intolerance r/t Enforced Bed Rest During Pregnancy Secondary to Potentiafor
Hemorrhage
 Altered Diversional Activity r/t Inability to Engage in Usual Activities Secondary to Enforced
Bed Rest and Inactivity During Pregnancy

NURSING INTERVENTIONS

 If continuation of the pregnancy is deemed safe for patient and fetus administer magnesium
sulfate as ordered for premature labor
 Obtain blood samples for complete blood count and blood type and cross matching
 Institute complete bed rest
 If the patient and placenta previa is experiencing active bleeding, continuously monitor her blood
pressure, pulse rate, respiration, central venous pressure, intake and output, and amount of
vaginal bleeding as well as the fetal heart rate and rhythm
 Assist with application of intermittent or continuous electronic fetal monitoring as indicated by
maternal and fetal status.
 Have oxygen readily available for use should fetal distress occur, as indicated by bradycardia,
tachycardia, late or available decelerations, pathologic sinusoidal pattern, unstable baseline, or
loss of variability.
 If the patient is Rh-negative and not sensitized, administer Rh (D) immune globulin (RhoGAM)
after every bleeding episode.• Administer prescribed IV fluids and blood products.
 Provide information about labor progress and the condition of the fetus.

 Prepare the patient and her family for a possible caesarian delivery and the birth of a preterm
neonate, and provide thorough instructions for postpartum care.
 If the fetus less than 36 weeks gestation expect to administer an initial dose of betamethasone:
explain that additional doses may be given again in 24 hours and possibly for the next 2 weeks to
help mature the neonates lungs.
  Explain that the fetus survival depends on gestational age and amount of maternal blood loss.
Request consultation with a neontologist or pediatrician to discuss a treatment plan with the
patient and her family.• Assure the patient that frequent monitoring and prompt management
greatly reduce the risk of neonatal death.

 Encourage the patient and her family to verbalize their feelings helps them to develop effective
coping strategies, and refer them for counseling, if necessary.

 Anticipate the need for a referral for home care if the patient bleeding ceases and she’s to return
home in bed rest.

Research evidence
1. Kishor S, Naiknaware. Antepartum Haemorrhagecauses and its effects on mother and child.
Indian journal of obstetric and gynaecology.2017 Nov 24;321(19):118-124

Objective: Aim of the present study was to find the demographic profile, type of APH, maternal and
perinatal complications.
Method: It is a prospective study carried out in a tertiary care hospital, Mumbai, India over a period
of 2 yrs from Sept 2010 to Aug 2012 on 124 women admitted with the diagnosis of APH.
Results: The incidence of APH was 1.31%. 73 % cases of APH were associated with Pregnancy
induced hypertension suggesting PIH is one of the major risk factors. Maternal and perinatal
morbidity was very high with increased rates cesarean section 90%, post partum hemorrhage (36%),
need of blood transfusion (75%), preterm deliveries (65%), low birth weight (40%) and NICU
admission (44%). Though there is no maternal mortality due to timely intervention but 3% patients
underwent Obstetric Hysterectomy and 6.4% required CCU admission. Perinatal mortality was very
high (21%).
Conclusion: There is very high maternal and perinatal morbidity and perinatal mortality in APH

INTRODUCTION
in the developing world about 1.2% of deliveries are associated with PPH and when PPH
occurred about 3% of women died.Globally it occur about 8.7% million times and result in
44,000 to 86,000 death per year making it the leading cause of death.

DEFINITION
Postpartum hemorrhage is defined as any amount of bleeding from or into the genital tract
following child birth up to the end of puerperium, which adversely affects the general condition
of the patient evidenced by rise in pulse rate and falling BP.

ACCORDING TO WHO {2003}

Mild PPH- loss of 500-999ml in a healthy women
Severe -loss of greater than 1000ml
TYPES OF PPH
 PRIMARY PPH

Hemorrhage occurs within 24hrs following the birth of the baby.in majority, it occurs within two
hours following the delivery
 Third stage hemorrhage –bleeding occurs before placental expulsion

 True postpartum hemorrhage –bleeding occurs subsequent to expulsion of placenta

 SECONDARY PPH

It is any abnormal bleeding from the genital tract occurring after 24hrs -12 wks. in postnatal
period
INCIDENCE–It is about 4-6% of all deliveries
It is one of the most alarming and serious emergencies and accounts for MMR-(2004)- WHO -
severe bleeding 27%
And MMR/lakh in India in 2015 is 100.according to health information of India

CAUSES OF PPH
 ATONIC UTERUS :With the separation of placenta the uterine sinuses, which are torn,
cannot be compressed effectively due to imperfect contraction and retraction of the uterine
musculature and bleeding continues.

 Grand multi para inadequate retraction and frequent adherent placenta

 Overdistention of uterus:As in a multiple pregnancy, hydramnious and big baby (>4kg).

Imperfect retractions and large placental site are responsible for excessive bleeding
 Antepartum hemmorhage: Both placenta previa and abruption
 Prolonged labour{>12HRS} may cause poor retraction, infection,dehydration may result
from muscle exhaustion
 General anesthesia –anesthetic agents may cause uterine relaxation
 Incomplete placental separation: if placenta remains fully adherent to uterine wall, it is
unlikely to cause bleeding. Once separation has begun,maternal vessels are torn. If placental
tissue remains partially embedded in the spongy decidua, efficient contraction and retraction
are interrupted.
 Polyhydramnious, macrosomia or multiple pregnancies:The myometrium becomes
excessively stretched and therefore less efficient.
 Placenta previa: Placental site is partly or wholly in the lower segment where the thinner
muscles layer contains few oblique fiber results in poor control bleeding
 Induction or augmentation of labour:Oxytocin sometimes may result in hyper stimulation
of the uterus and causes a precipitate, expulsive birth of baby, in this instance the uterus may
 still be responding in a stimulated,but ineffective manner in terms of contracting the empty
uterus.
 Malformation of uterus: Implantation of the placenta in the uterine septum of a septate
uterus or in the corneal region of a bicornuate uterus may cause bleeding.
 Uterine fibroid: It may cause imperfect retraction mechanically.
 Mismanaged third stage of labor:This includes-
 Too rapid delivery of the baby preventing the uterine wall to adapt to the diminishing
contents
 Premature attempt to deliver the placenta before it is separated
 Kneading and fiddling the uterus
 Pulling the cord.
 Manual removal of placenta increases blood loss during C-Section.
 Placenta: placenta accrete, percreta, partially or completed separated or retained placenta
cause PPH.
 Precipitate labor:In rapid delivery, separation of placenta occurs following the birth of the
baby. Bleeding continues before the onset of uterine retraction
 TRAUMATIC (20%): trauma to the genital tractfollowing operative delivery. Trauma
involves the cervix, vagina, perineum, paraurethral region, rupture of uterus.
 RETAINED TISSUES: Bits of placenta, blood clots cause PPH due to imperfect uterine
contraction.
 DRUGS: Use of tocolytic drugs, MgSO4, Nifedipine.
 COMBINATION OF ATONIC AND COMBINED:
 BLOOD COAGULATION DISORDERS: Acquired or congenital, are less common causes
of PPH. It may be due to diminished procoagulants (washout phenomenon) or increased
fibrinolytic activity. The firmly retracted uterus can prevent bleeding. Specific therapy
following coagulation screen including recombinant activated factor VII may be given.

 Episiotomy and need for perineal sutures-blood loss from perinea trauma in addition to
even a normal blood loss from the uteruscan together equal a mild PPH

PREDISPOSING FACTORS THAT INCREASES THE RISK OF PPH

 Previous history of PPH or retained placenta

 Anemia
 HIV /AIDS-is a state of compromised immunity which lowers the platelet to such a degree
that even a relatively minor loss may cause severe morbidity or death

 Caesarean section

SIGNS OF PPH
 Visible bleeding

 Maternal collapse

 Pallor

 Falling BP

 Altered level consciousness, drowsiness or restlessness

 On palpation the uterus feels bloggy –soft ,distended and lacks tone or no visible loss of
blood

PREVENTION OF PPH
Antenatal –
 Improvement of the health status

 Screening of high risk patients

 Early blood grouping and typing

 Placental localization

Intranatal-
 Active management of third stage for all women in labor to reduce risk

 In induction or augmentation of labor the oxytocin infusion should be continued for at least 1
hour after delivery

 After caesarian section , syntocin 5IU slow IV to be given to reduce blood loss

 Placental examination to be done to detect any missing lobes or retained placenta

 Observation for about 2hours after delivery makes sure that the uterus is hard and well
contracted before sending to ward
MANAGEMENT OF PPH
PRINCIPLES
 To empty the uterus of its contents and to make it contract

 To replace the blood-to prevent shock

 To ensure effective hemostasis in traumatic bleeding

PLACENTAL SITE BLEEDING

 To palpate the fundus and massage the uterus to make it hard. The massage is done by
placing four fingers behind the uterus and thumb. However if the bleeding persists the
bleeding is from genital tract.

 Start crystalloids [NS,RL] with oxytocin [1l with 20 u ] at 60 drops per min and arrange for
blood transfusion

 Oxytocin 10u IM or methergin 0.2mg IV

 Catheterize the bladder

 Give antibioticsuch as – metronidazole – 500mg, ampicillin -2g IV

During this procedure, the placental separation feature are evident, then expression of placenta is
to be done either by fundal pressure or controlled cord traction method.
If placenta is not separated then manual removal of placenta under general anesthesia is to be
done.

TRAUMATIC PPH
Genital tract injuries can also lead to PPH and include lacerations of the cervix, vagina and
perineum. Vulvovaginal hematomas may be concealed cause.
Predisposing factors
 Instrumental delivery
 Vaginal birth after caesarean
 Face to pubis delivery
 Precipitate labor
 Macrosomia

COAGULOPATHY
Disseminated intravascular coagulopathy and hypofibrinogenesis is a relatively rare cause for
haemorrhage, but should be considered in all patients at high risk for coagulopathy.
Disseminated Intravascular coagulation can complicate haemorrhage due any other cause and so
simultaneous correction of the coagulation deficit is essential.
Predisposing factors
 Abruption
 Sepsis
  Intrauterine death
 Severe pre-eclampsia with HELLP syndrome
 Amniotic fluid embolism

Management of coagulopathy
If there is evidence of coagulation defects, blood products like fresh frozen plasma, platelet
concentrates and cryoprecipitate are made available.
For every 6 units of red cells, 4 units of fresh frozen plasma can be given.
Each unit of FFP will restore procoagulant activity by about 10% and will also raise the
fibrinogen level by 25mg/dl.
Cryoprecipitate contains Factor VIII, fibrinogen and Von Willebrand factor and is indicated if
the fibrinogen level below 100mg/dl.
Each adult dose of cryoprecipitate will raise the fibrinogen level by 100mg/dl.
The FFP and cryoprecipitate should ideally be of the same group as the recipient.
If unavailable, FFP of different ABO group is acceptable, provided that is does not have high
anti A or anti B activity.
Platelet concentrates should be given if the platelet count goes below 50,000/L.
Each adult dose of platelet concentrate will raise the platelet count by 20,000/L.
Rh negative woman must receive Rh negative platelets.
Recombinant factor VIIahas been reported to be effective in controlling life threatening
haemorrhage. This therapy is expensive and the evidence is not conclusive and hence, it should
be reserved for women with severe haemorrhage in which common protocols have failed.

STEPS OF MANUAL REMOVAL OF PLACENTA

 STEP 1-IT IS DONE UNDER GENERAL ANESTHESIA after obtaining a written consent.
Position is lithotomy and the bladder is emptied

 STEP II-One hand is introduced into the uterus in a cone shaped manner, following the cord,
which is made taut by other hand while introducing the hand the labia are separated by
fingers of the other hand. The uterine hand should locate the margin of the placenta

 STEP III-Counter pressure on the uterine fundus is applied by other hand placed over the
abdomen. The abdominal hand should be steady on the fundus and guides the movement of
fingers of the uterine cavity until the placenta is completely separated

 STEP IV-As soon as placental margin is reached, the fingers are insinuated between the
placenta and uterine wall with the back of the hand in contact with the uterine wall. The
placenta is gradually separated with a sideways sliding movements of the fingers,until the
separation of placenta
 STEP V- When the placenta is separated completely, it is extracted by traction of cord by
other hand. The uterine hands are still inside the uterus for exploration of the cavity to be
sure that nothing is left inside

 STEP VI- IV methergin 0.2mg is given and the uterine hand is gradually removed while
massaging the uterus by external hand to make it hard

 STEP VII- The placenta and membranes are inspected for completeness and be sure that the
uterus remains hard. and contracted

MANAGEMENT OF TRUE PPH

The bleeding occurs subsequent to expulsion of placenta
PRINCIPLES-
 Simultaneous approach of
 Communication
 Resuscitation
 Monitoring
 Arrest bleeding

APPLY ABC :
 Call for medical AID

 Stop BLEEDING by rubbing a contraction giving a uterotonic and emptying the uterus by
palpating the fundus and massage the uterus to make it hard. The massage is done by placing
four fingers behind the uterus and thumb. however if the bleeding persists the bleeding is
from genital tract

 Resuscitate the mother as necessary-Circulation

 Lift the legs to allow blood to draw from legs to central circulation

 Catheterize the bladder

 Estimation of hemoglobin, cross matching is done. Blood transfusion as ordered

 Administer oxygen at 10-15l/min

 Administration of uterotonic agents such as oxytocin 20u in one lite of RL /NS at 60 drops
/min or plasma substitutes- haemaccel

 Vital signs and intake and output monitoring

ACTUAL MANAGEMENT
Control the fundus and note the feel of uterus. If the uterus is flabby, the bleeding is likely from
atonic uterus. If it is firm the bleeding is likely to be from the traumatic site.

ATONIC UTERUS:-
STEP-I
 Massage the uterus to make it hard and express the blood clots

 Methergin 0.2mg is given intravenously

 Inj. synto 10u in 500ml ns at 40-60 drops /min

 Foleys cauterization

 To examine the expelled placenta and membranes, for missing cotyledon or pieces of
membranes. If uterus fails to contract, proceed to the next step

STEP – II
The uterus is to be explored under general anesthesia. Inspection of cervix, vagina especially
paraurethral region to be done to exclude co-existent bleeding sites from injured area.

STEP – III-Uterine massage and bimanual compression

 BIMANUAL COMPRESSION

If bleeding continues bimanual compression is to be given. The fingers of one hand are inserted
into vagina like a cone , the hand is formed into a fist and placed into the anterior vaginal fornix,
the elbow resting on the bed. The other hand is placed behind the uterus abdominally the fingers
pointing towards the cervix. The uterus is brought forward and compressed between the palm of
hand positioned abdominally and the fist in the vagina.
If bleeding persists then uterine artery ligation or hysterectomy may be considered.
STEP - IV-UTERINE TAMPONADE:
TIGHT INTRAUTERINE PACKING: It is kept high up in the fundal area first while the
uterus is steadied by the external hand. Gradually the rest of the cavity is packed so that no
empty cavity is left. A separate pack is used to pack vagina. Antibiotic should be administered
and the pack should be removed by 24hours.

BALLOON TAMONADE- tamponade using various types of hydrostatic balloon catheters are
used. Mechanism of action is similar to uterine packing.

TRAUMATIC UTERUS

STEP – V-SURGICAL INTERVENTIONS

 Undersewing:
Undersewing the placental bed with figure of eight or purse string sutures can be done at
ceasarean section for placenta previa.
 Cho’s multiple block sutures:
Block sutures involve approximation of the anterior and posterior uterine walls with
multiple squares until no space is left in the uterine cavity. It is useful in atonic and
placental site bleeding.
 B-Lynch or brace suture:
It is a simple surgical method which involves the use of vertical brace sutures, which will
appose the anterior and posterior walls of the uterus, this will lead to compression of the
fundus and lower uterine segment, thereby controlling hemorrhage. It is very easy to
perform and many a time, may obviate the need of hysterectomy.
 Modified B Lynch or Haymen:
This utilizes two vertical compression sutures placed on either side of the fundus. The
advantage is that it is quicker and does not require lower transverse incision.
 Systematic pelvic devascularisation:

 Ligation of uterine arteries-the ascending branch of uterine artery is ligated at the lateral
border between upper and lower uterine segment.

 Ligation of ovarian and uterine artery anastomosis –if bleeding continues, it is done just
below the ovarian ligament

 Ligation of anterior division of internal iliac artery-unilateral or bilateral, reduces the distal
flow

 Hysterectomy-when the uterus fails to contract and bleeding continues in spite of other
measures. It is the last resort.
MANAGEMENT OF SECONDARY PPH
bleeding occurs beyond 24hrs and within puerperium, also called as delayed or late PPH.

CAUSES
 Retained bits of placenta

 Infection or laceration of cervico-vaginal canal

 Endometritis and subinvolution of placental site

 Secondary hemorrhage from caesarean section

DIAGNOSIS
The bleeding is bright red and varying amount. Rarely it may be risk .varying degree of anemia
and evidences os sepsis are present. Internal examination reveals- sepsis , subinvolution of uterus
Ultrasonography helps in detection retained bits of placenta inside the uterine cavity.

MANAGEMENT
Principles:
 To assess the amount of blood loss and to replace it

 To find out cause and to take appropriate steps to rectify it.

SUPPORTIVE THERAPY
 Blood transfusion

 Methergin 0.2mg IM

 Antibiotic therapy

CONSERVATIVE :if bleeding is slight and no apparent cause is detected , a careful watch for
period of 24hours or so is done in the hospital
ACTIVE TREATMENT: As the common cause is due to retained bits of placenta, it is
preferably to explore uterus urgently under general anesthesia.the product is then removed.

NURSING DIAGNOSIS FOR PPH

 Deficient fluid volume related to excessive of blood loss

 Ineffective tissue perfusion related to lack of haemoglobin concentration
 Risk for infection related to haemorrhage
 Risk for pain related to post partum haemorrhage
 Anxiety related to excessive bleeding
 Knowledge deficit related to disease condition